Veterinary Parasitology by Valsoriml

E-LEARNING RESOURCES IN VETERINARY PARASITOLOGY
1. DIAGNOSIS OF VETERINARY ENDOPARASITIC INFECTIONS
2.LIFE CYCLES OF SOME IMPORTANT PARASITES
3. Parasites and Parasitism in Livestock
4. Laboratory Demonstrations in Parasitology Useful Biological Prefixes and Suffixes
Diagnosis of Veterinary Endo-parasitic Infections

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Laboratory techniques - Fecal Samples Laboratory techniques - Blood Samples Parasitological Drug Index
As per Hosts
Click on the host of choice: Domesticated Mammals Poultry and other birds Reptiles top
As per Diagnostic Techniques Click on the procedure for further details:

Techniques for Fecal Samples
Comparison of Fecal Examination Techniques Frequently found artifacts in fecal smears Direct Smear Zinc Sulfate Flotation Ethyl Acetate Sedimentation Baermannization
Modified Wisconsin Sugar Flotation Method
Stoll Egg Counting Technique McMaster Egg Counting Technique Saturated salt flotation method top
Techniques for Blood Samples
Filtration Method Smears Procedure for concentration of blood (Knott's Test)
Therapeutic Index Index of common drugs used in treatment endoparasitic infections of Animals top
This section is intended to reinforce important principles
in the diagnosis, epidemiology, pathology, and treatment and control of selected parasites of significance in veterinary medicine. This is not intended to be a primary source of information about any of the parasites, but rather serve as a reference and reminder of the application of the life cycle to the practice of veterinary medicine.
Parasites and Parasitism in Livestock
Contents
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Introduction to Parasitology Introduction to Nematodes Trichostrongyloidea Strongyloidea Ascaridoidea Oxyuroidea Trematodes Siphonaptera (fleas) Anthelmintics & their Uses Heartworm
Veterinary Parasitology Laboratory Demonstrations
In each Parasitology lab, the teaching staff will put out numerous displays of the parasites which you are required to know. Next to each display is a card that explains the display. Photocopies of all these cards are available in the library. In the past, students would make a photocopy and then use it to make notes on as they progressed through each lab station. The only problem was that some of the twice photocopied cards were of poor quality. Therefore, we have made the contents of these cards available on this web site.
Laboratory 1 - Introduction to the Parasitology Laboratory Nematode Taxonomy Laboratory 2 - Strongyles Laboratory 3 - Hookworms, Lungworms and Strongyloides Laboratory 4 - Ascarids, Oxyuris, and Trichocephalids Laboratory 5 - Spirurids and Filariids LAB EXAM 1 Laboratory 6 - Trematodes Laboratory 7 - Cestodes, Acanthocephalans Laboratory 8 - The Arachnids Laboratory 9 - Insects of Veterinary Importance Laboratory 10 - Protozoa
Useful Biological Prefixes and Suffixes

Prefix or suffix aabacantho-adalbi-algia ambyl- or amblyo amylananaancyloangioanteanti- (ant) apoaqua-ase autobibiobrachyMeaning not, without from, away spine to, toward white pain blunt starch not, without up, upon bent vessel before, in front of against, opposed to off, from, away from water designating an enzyme self two, twice life short Examples atypical abnormal Acanthocephala dorsad, adhere albicans neuralgia Ambylocera amylopsin anhydrous anabolism ancylostoma angiocarditis anterior antitoxin, anthelmintic apoplexy aquatic amylase autosuggestion biceps, bifocal biology brachycardia
bradycalor-cara -cardia-cephalus -cera -cerca cerebrochrom-cidal corpuscteno-cyst -cyte, cyto-dermic didiadys-ectomy em-, en-, endo-emia enteroepi-
slow heat head heart head horn tail brain color killing body like a cockle bladder cell skin two, twice through, between bad, difficult cut out in, into blood intestine on, above, upon
bradycardia calorimeter Toxocara bradycardia Ctenocephalides brachycera Onchocerca cerebrospinal chromosome bacteriocidal corpuscle Ctenocephalides oocyst cytoplasm hypodermic dichromic diaphragm dyspepsia appendectomy embolism, endoskeleton anemia enterokinase epiglottis
erythro-fer-fract-gastro-gen-glossoglyc-gnath-gnosis -graph -helminth hemoheterohomohydrohyperhypo-iasis interintrairischn or ischno -itis kata-, cata-
red to carry, to transport to break stomach to produce, to begin tongue glucose, sugar jaw, cheek knowledge, to know to write worm blood different, other alike, same water over, more than under, less than infestation between, together within not long, thin inflammation down
erythrocyte afferent, efferent fracture, refraction pneumogastric genetics, glycogen hypoglossal glycosuria gnathostoma diagnosis cardiograph anthelminthic hemorrhage heterozygous homozygous hydrolytic hypersecretion hyposecretion onchocerciasis intercostal intrathoracic irregular Ischnocera appendicitis catabolism
kin-lacleuco-, leuko-ology lymph-, lympho-lysin, -lysis, -lytic macro-meter micromonomyonemaneurnephr-oid -ole -oma onchooncooo-opia -osis os-, oste-, osteoovi-
to move or activate milk white science, knowledge lymph dissolve, destroy large measure small one muscle thread relating to nerves kidneys like small swelling, tumor hook mass, bulk egg sight condition or process bone egg
kinetic lactase, prolactin leucocyte physiology lymphocyte hemolysis macrophage manometer microorganism
monocyte, monosacchar myosin, myoglobin nematode neurilemma nephritis lymphoid, ameboid bronchiole sarcoma Onchocerca oncosphere oocyst myopia, hyperopia cyanosis, phagocytosis osteology, osteocyte oviducy, ovipositor
parapathoperiphago-phil-plasmplaty-pnea pneumo-ped polypostpropropriopseudopsychopulmo-renal -rrhea sarco-
near, by, beside disease, suffering around, near to eat loving substance broad breathing air, lungs foot many after, behind before, giving rise to one's own false mind lung kidney flow flesh, muscle
parathyroid pathology pericardium phagocyte basophil, eosinophil cytoplasm, plasmolysis Platyhelminthes dyspnea pneumonia pseudoped polysaccharide postganglionic proenzyme proprioceptors pseudoped psychology pulmonary adrenal diarrhea sarcoplasm
soma-some stoma-
body body mouth
somatic cell chromosome ancylostoma
-strongyle -thrombo-tode -tome, -tomy toxi-, toxotricho-trophic -tropic -ule -uria -uris vaso-
cylinder clot, coagulation like to cut poison hair-like feeding attached to small pertains to urine tail pertains to blood vessel
trichostrongylus thrombosis nematode tonsillectomy toxin trichostrongylus autotrophic phototropic saccule glycosuria trichuris vasodilation
Index of Commonly Used Pharmaceuticals in the Treatment of Veterinary Parasitic Infections

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Drug
trade names.)
Trade names
(may also be available under other
Amprolium Butamisole Hyrdochloride Clindamycin Dichlorvos
Corid Styquin Antirobe Task
Diethylcarbamazine
Disophenol Sodium Epsiprantel Febantel Fenbendazole Imidocarb dipropionate
Nemacide
DNP Cestex Drontal Plus Panacur
Imizol
Ivermectin
Plus, etc.
Ivomec, Heartgard, Heartgard
Mebendazole
Melarsomine dihydrochloride
Telminic
Immiticide
Flagyl Interceptor ProHeart, ProHeart 6 Navigator
Metronidazole Milbemycin oxime Moxidectin Nitazoxanide Piperazine Praziquantel Pyrantel Pamoate Pyrantel embonate Selamectin Sulfadimethoxine Thiacetarsamide sodium
Pipa-tabs, Tasty Paste, WRM Rid, etc.
Droncit, Drontal, Drontal Plus

Nemex, Heartgard plus, Strongid T, etc.
Drontal, Drontal Plus Revolution Albon, Bactrovet
Carparsolate
Web-link
www.fda.gov/cvm/greenbook/greenbook.html of currently approved drugs. The FDA's searchable list
Diagnosis of Veterinary Endoparasitic Infections
Domesticated Mammals
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Cat Dog Cow Ferret Goats Sheep Horse Llama Pig Rabbit
Birds
Robin - Turdus migratorius
Reptiles
Loggerhead turtle - Caretta caretta
Comparison of Fecal Examination Techniques
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TECHNIQUE
Direct Smear
ADVANTAGES
Quick to prepare. No distortion of parasites if isotonic saline is used as diluent. Only way to see live trophozoites (isotonic saline must be used as the diluent). Useful for examining feces of small birds and reptiles (where trematode eggs are common). Procedure floats the most common helminth ova and coccidian oocyst . Solutions are inexpensive. There is little debris to obscure the view of the parasite.
DISADVANTAGES
Can miss parasite if concentration is too low or if too much debris or fat is present. Sand, seeds, or other fecal debris can make apposition of coverslip onto slide difficult. May take a long time to examine.
Saturated Sucrose or Salt
Procedure will not float trematode ova and some tapeworm (pseudophyllidian) ova. Distorts Giardia cysts. Time consuming if centrifugation not performed. Unsuitable for fatty stool samples.
Zinc Sulfate Flotation
Recommended procedure for most fecal exams Procedure floats most helminth eggs. Best method for protozoan cysts, especially Giardia. There is little debris to obscure view of parasites. Procedure recovers ALL types of helminth ova, larvae, and most protozoan cysts. It is the best technique for formalin - fixed samples and for stools with high fat content.
Procedure will not float some trematode ova, and some tapeworm (pseudophyllidian) ova. Unsuitable for fatty stool samples. ZnSO4 is expensive and a hydrometer should be used to make up the solution.
Ethyl Acetate Sedimentation
It is more difficult to perform than other techniques. Ethyl acetate is flammable and expensive. There is more debris in preparation preps than in flotation preps - therefore it will take longer to read.
Artifacts
Scroll down to see an assortment of artifacts commonly found in fecal smears and floats of dogs and cats.
Free living mite and mite egg (dog feces)
Above: Stained with iodine Below: unstained and at a higher magnification
Yeast (Saccharomycopsis gutulatus): this is a normal inhabitant of the gut of rabbits, it is commonly found in fecal floats done on dogs that ate rabbit feces. It is not pathogenic and it just passes through the dog.
Plant cells
Free living mites and mite egg (dog feces)
Monocystis sp. sporocyst and plant nematode in dog feces (10X).
Monocystis sp. sporocyst (40X)
(100X)
Monocystis sp. is a protozoan parasite of earthworms. The sporocysts appear in the feces of animals (usually dogs and turtles) that have eaten infected earthworms. The sporocysts are not infectious to dogs and the dog is not infected with the parasite. Plant nematodes also just "pass through" the dog; they can be identified as a plant nematode if the "spears" they use to puncture plant cell-walls can be seen in the buccal cavity.
Pollen in dog feces
Pine pollen in dog feces
Air bubble
Eimeria sp. oocyst in dog feces. Eimeria spp. do not infect dogs, this oocyst (~ 40 m) was ingested with something the dog ate (maybe horse or cattle manure!) and just passed through the dog. (Photo by Terri Jarratt and used with permission.)
Plant spine Fiber
Plant
Plant cell
Fungal spores
Note the small piece of the hypha still attached to one end of each of the spores.
Direct Fecal Smear Examination
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Direct Smear Fecal Exam

1. Place a small amount of feces on a microscope slide. 2. Add a drop of liquid to the feces and mix thoroughly. The type of liquid added depends on what you hope to accomplish with the technique. If you are examining a liquid fecal sample for the presence of protozoan trophozoites (live active protozoa) then use saline (if any extra liquid is needed). If you are looking for helminth eggs and protozoan cysts in a small sample (bird droppings, rectal smear, etc) then either water or iodine may be used. 3. Cover with a cover slip. Move the cover slip around until it lays flat. You should be able to read through the smear (light from the microscope must be able to pass through the sample in order for you to examine it). 4. Examine the slide using the 10X objective, and then go over it with the 40X objective. Because this technique examines only a very small amount of feces, it should only be used in the following circumstances: a. Liquid feces where protozoan trophozoites may be present. b. Fecal samples where the amount of feces obtained is too small to handle with any other technique. c. As an adjunct to a flotation technique where you are looking for eggs that do not float. (In this case you probably would be better off running an ethyl acetate sedimentation and examining the resultant pellet using the direct smear method.) Note: Circumstances "b" and "c" occur frequently when dealing with small fish, birds, amphibians and reptiles and thus the direct smear has some utility in dealing with fecal samples from these
animals.
Fecal Examination Using the Zinc Sulfate Centrifugal Flotation Method
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Below is a description of how to test fecal samples using the Zinc Sulfate Centrifugal Flotation Method: Fill a 15 ml centrifuge tube with ZnSO4 solution (1.18 specific gravity)* and pour into a glass dish. Using a tongue depressor, push the feces (2 to 3 grams about 1 cm in diameter) through a strainer into the ZnSO4 solution in the dish. Using a funnel, pour the ZnSO4-fecal mixture back into the centrifuge tube. Centrifuge for 2 minutes at high speed (1500 - 2000 rpm). Using a headed-rod or loop, remove a sample from the surface of the solution and place on a microscope slide. You may have to take several samples with the rod or loop to get enough material to examine - you want the equivalent of a large drop on the slide. Add a drop of iodine (to stain the cysts and the ova) and a coverslip. Examine at 10X on a microscope.
Note: If the sample contains a large amount of fat or other

material that floats in water, you may want to wash the sample before doing the flotation. To do this, start at step 1 but use water instead of ZnSO4. When you centrifuge the water-fecal mixture, the eggs will sink but the fat will remain afloat as the eggs are heavier than water. After centrifugation pour off the supernatant and add the ZnSO4 solution - mix well. Centrifuge as in step 5. * ZnSO4 solution (1.18 specific gravity) is made by adding 386 grams of ZnSO4 to 1 liter of water. The mixture should be checked with a hydrometer and adjusted to 1.18 specific gravity.. The ZnSO 4 solution should be stored tightly capped to prevent evaporation (and the resulting change in specific
gravity of the solution).
Fecal Examination Using the Ethyl Acetate Sedimentation Method
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Below is description of how to test a fecal sample using the Ethyl Acetate Sedimentation Method:
Pass a piece of feces (about 5x5 mm) through a sieve into about 9 ml of water, then pour solution into a 15 ml centrifuge tube. Add about 3 ml of ethyl acetate, and plug the tube with a rubber stopper. Shake the tube vigorously, and then centrifuge it.
CAUTION: Test materials before placing Ethyl Acetate into them. This solvent will dissolve many types of plastic!! The white plastic centrifuge tubes (Polypropylene) used in the lab are OK, but clear plastic tubes (polystyrene) and the disposable polystyrene cups will dissolve.
Using a stick, "ring" the plug of fat at the water-ethyl acetate interface (the plug adheres to the side of the tube and must be detached before the liquid contents of the tube can be poured off). Pour off the supernatant, being careful to leave the pellet at the bottom of the tube intact.
Transfer some of the sediment from the bottom of the tube to a slide and examine. The sediment can be transferred in several ways: 1)If some liquid remains, the pellet can be resuspended and a drop transferred with a pipette. 2) Add a drop of iodine to the pellet to resuspend it and then transfer with a pipette. 3) Use a stick to remove some of the pellet and smear it on a slide as you would when making a direct smear.
NOTE:When removed from the centrifuge, your tube

will have clearly defined layers: A. An ethyl acetate layer on top. B. A plug of dissolved fat in the middle. C. A layer of water. D. A pellet of sediment at the bottom. Because formalin fixed eggs and cysts may not float (they may now have a specific gravity of greater than 1.2) this technique is preferred for formalin fixed samples.
NOTE: If you did this technique just to remove fat,

you can re-suspend the pellet in flotation solution, centrifuge, and remove the material from the top of the float to examine for eggs.
Fecal Examination Using The Baermannization Method
Below is description of how to test a fecal sample using Baermannization Method. The Baermannization method is used for the extraction of live larval stages of nematode parasites from the feces. Place a sieve in a custard dish or other similar container. Spread about one gram of feces on a piece of tissue paper and place it into the sieve Place warm* water in the dish until it just covers the feces. Be careful not to disrupt the feces. Allow mixture to sit for one hour** Lift off sieve Pour liquid into a 50 ml centrifuge tube. Let sit for 20 minutes Using a Pasteur pipette, remove a drop of sediment at the bottom of the tube and place it on a microscope slide for examination. Be careful not to resuspend the sediment before you take a sample from it. * This procedure makes use of two characteristics of parasitic larval nematode behavior. First, the warmer it is, the more active the larva will be (however, you do not want to over heat them! - 37 to 40oC is the upper limit). Second, Most parasitic larval nematodes are poor swimmers. Therefore, the following events take place when the sieve is placed in the water. The larvae will move around in a random fashion and within time, some of them will migrate through the tissue paper and fall into the water. Because the larvae can't
swim, they sink to the bottom of the dish and accumulate there. ** The longer you wait the more larvae will accumulate at the bottom of the dish, but with time the fecal sample breaks down and begins to pass through the paper tissue leading to an accumulation of sediment along with the larvae.
Modified Wisconsin Sugar Flotation Method This method of determining the EPG is probably the most commonly used method. It is the most accurate as it counts all the eggs in 3 grams of feces and because it is a flotation method it has little debris to interfere with the count. However, if the EPG is high, there may be too many eggs to count. 1. Fill a 15 ml test tube with 10 ml of Sheathers* solution. 2. Weigh 3 grams of feces and place into a cup. 3. Pour the Sheathers solution from the test tube into the cup and mix well. 4. Place a funnel into the test tube tube, place a strainer into the funnel and pour the fecal-sugar solution mixture through the strainer into the test tube. Using a tongue depressor, squeeze the liquid out of the feces that is left in the strainer. 5. Centrifuge the tube for 2 to 4 minutes. 6. Fill the tube to just over the top and place a cover slip onto the meniscus. 7. Let sit for about 5 minutes, then remove the cover slip and place on a slide. 8. Examine the entire cover slip and count the number of eggs that you find. 9. The number of eggs counted is the number per 3 grams of feces, so divide by 3 to find the EPG.
* Sheathers Solution: Add 454 gm (1 lb) of table sugar to 355 ml of very hot water. Stir until dissolved and allow to cool. This solution will grow mold if left out, so keep refrigerated and use quickly.
Fecal Examination Using the Stoll Egg Counting Method
The Stoll Egg Counting Technique is a method for determining the number of nematode eggs per gram of feces in order to estimate the worm burden in an animal. The advantage of this technique is that it requires no specialized equipment. The disadvantage is that the counting takes a long time because of the amount of extra (non-egg) material on the slides. Weigh out 3 grams of feces Measure out 42 ml of water and place it into a dish. Using a tongue depressor, push the 3 grams of feces through a sieve into the water. Lift the sieve and hold over the dish. Push out any remaining water from the feces. While stirring the water-feces mixture, take 0.15 of the suspension and spread over 2 slides. Cover each slide with a long coverslip (or 2 regular coverslips). Examine both slides for worm eggs. The total amount of eggs counted X 100 represents the number of eggs per gram of feces. The mathematics: 0.15 ml is 1/300 of 45 ml (42 ml water and 3 grams of feces) so the number of eggs in 0.15 ml X 100 is equal to 1/3 of the total number of eggs in the original 3 grams (and thus equal to eggs per gram = EPG).
Fecal Examination Using the McMaster Egg Method
The McMaster Egg Counting Technique is a method for determining the number of nematode eggs per gram of feces in order to estimate the worm burden in an animal. The advantage of this technique is that it is quick as the eggs are floated free of debris before counting. The disadvantage is that you must use a special counting chamber. Weigh out 2 grams of feces Pass the feces through a sieve into a dish containing 60 ml of ZnSO4 or saturated salt solution. Lift the sieve and hold over the dish. Push out any remaining solution from the feces. While stirring vigorously (you may want to put the solution in a flask to prevent spillage), take a sample of the mixture with a pipette and transfer it to one of the chambers of the McMaster slide. Repeat the procedure and fill the other chamber. Wait 30 seconds then count the total number of eggs under both of the etched areas on the slide. Multiple the total number of eggs in the 2 chambers by 100, this is the eggs per gram (EPG). The mathematics: The volume under the etched area of each chamber is 0.15 ml (the etched area is 1 cm X 1 cm and the chamber is 0.15 cm deep), so the volume examined is 0.3 ml. This is 1/200 of 60 ml. Since you started with 2 grams of feces and then multiplied by 100, the final result is "eggs per gram of feces".
Above: McMaster slide
Sources for McMaster slides are:

1. Chalex Corporation 5004-228th Ave SE, Issaquah, WA. USA 98029 http://www.vetslides.com/ ;
2. Focal Point, Onderstepoort, South Africa (http://www.mcmaster.co.za/) Prof. Antanas Vysniauskas, M.Marcinkeviciaus No 17-14, Vilnius LT-08412, Lithuania Tel.: +370 698 87699, fax: +370 5 2729727, e-mail: helmint@ktl.mii.lt.
3.
If you want to have one of these slides made for you here are the particulars: They are usually made of Glass or Plexiglass: 2 pieces (2.5 cm by 7.5 cm) with 2 etched boxes (1 cm by 1 cm) on the under side of the top piece. Some people make the bottom piece a little wider than the top piece to make it easier to load. The etched boxes usually have 5 additional etched lines (subdividing the box into 6 sections) to make counting easier. The etched lines should be as thin as possible so eggs are not hidden under them. The 2 pieces are separated by pieces (0.15 cm thick) placed at both edges and in the center between the etched boxes. See the photo above.
Fecal Examination Using the Saturated Salt Flotation Method
Saturated Salt Flotation

There are numerous devices for doing this type of flotation now in use in local veterinary hospitals. Below are a few examples. Ovatector system Ovassay Plus Fecalyzer
Filtration Method to Detect Microfilariae in Blood
1. Collect a 1 ml blood sample into EDTA or heparin and add to 10 ml lysing solution within a syringe. Mix thoroughly. (Lysing solution consists of 5.0 ml Triton X-100, 8.0 grams of NaCo3, 1 liter of water.) 2. Attach syringe to a filter unit (see drawing below). The lysed blood solution is pushed through an 8 um pore filter membrane. 3. Remove the filter from the filter holder, place it on a microscope slide and add one drop of 1:10,000 Methylene Blue Stain. Cover filter with a cover glass and examine under microscope.
Procedure for Making Blood Smears
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Procedure for making Blood smears (thin films) : To do a blood smear you need two slides. On one slide the blood sample is placed - this is the "sample" slide. The second slide is used to smear the drop of blood - this the "spreader" slide. Clean the sample slide by wiping it with alcohol. Handle slides by edges only. (any grease on the slide will cause the dried blood to flake off during staining). Place a very small drop of blood near the end of the sample slide. Place the end of the spreader slide on the sample slide so that the short sided edge of the spreader is just below the drop of blood. The next two steps should be done quickly to avoid smears that are too thick. Holding the spreader at an angle of 30 o (relative to the sample slide), push the spreader so that the edge just barely touches the drop of blood. By capillary action, a thin line of blood will spread along the edge of the spreader . Quickly drag the spreader along the entire length of the sample slide in one fluid motion. Note that the blood is being dragged by the spreader. To view a Quick Time Video of the procedure click here. If the correct amount of blood was used, and the technique was performed correctly, the smear should end before the end of the sample slide. The smear should also end in a "feathered edge" - a region where the blood cells are well separated. Air dry the sample slide. Fix and stain the slide. Various methods may be used. Normally a commercial staining kit is utilized following the manufacturer's instructions.
Modified Knott Method
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Add 1 ml of freshly drawn blood to 9 ml of 2% formalin (aqueous) in a centrifuge tube. Mix well to lyse red blood cells. Centrifuge for 5 minutes at 1500 rpm. Pour off the supernatant fluid. Note: Invert the tube completely when decanting the supernatant. Add a drop of 1% aqueous methylene blue. Adjust the amount to suit yourself, it stains the microfilariae blue and makes them easier to view). Then stir or mix up the sediment in the bottom of the tube. Place a drop of the stained mixture on a microscope slide and add a cover slip. Examine under a microscope.
Please choose a parasite: Ancylostoma caninum Dictyocaulus viviparus Dirofilaria immitis Echinococcus granulosus Eimeria bovis Giardia Haemonchus contortus Toxocara canis
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You may navigate between c tab. Click on the appropriate life cycle for that category. For more information about highlighted item. This will po one) containing pertinent inf diagrams, or other informati windows using the 'Close W clicking the appropriate butt otherwise, you will be lost in uncertain terms, please see
A|B|C|D|E|F| G|H|I |J |K|L|M |N|O |P|Q |R|S| T|U|V|W|X|Y -AAlae: Flattened, wing-like expansions of the cuticle of nematodes (cervical, caudal or lateral).
Apical complex: A complex set of organelles found at the anterior end of the protozoans of the Ph has a role in the penetration of host cells. Arrested development: See hypobiosis. Return to top of page
-B-
Bradyzoite: A stage in the life cycle of protozoa of the family Sarcocystidae (tissue-cyst-forming c to describe the merozoite which forms within the tissue cyst in the intermediate host (and rarely wit stage rarely infects new cells within the intermediate host, rather it is the infectious stage for the de Return to top of page
-C-
Cercaria: In the trematode life cycle, the cercaria is a larval trematode (which may or may not have cercaria develops from the germinal cells of the sporocyst or redia and emerges from the snail (int species) the metacercaria.
Coenurus: Larva of Taenia multiceps which is a fluid filled cyst containing many invaginated scole
Control: Reduction of disease incidence, prevalence, morbidity or mortality to a locally acceptable Continued intervention measures are required to maintain the reduction. Cysticercoid: A single, evaginated scolex that is embedded in a small solid cyst that are typically arthropods (Cyclophyllidian tapeworms).
Cysticercus: Larval stage in the cestode life cycle which is a fluid filled cyst containing an attache in mammal intermediate hosts (cyclophyllidian tapeworms) Return to top of page
-D-
Definitive Host: Found in all parasitic life cycles. The definitive host is the host in which the sexual If there are no sexual stages in the life cycle, then the definitive host is the host in the life cycle con
-D-
Definitive Host: Found in all parasitic life cycles. The definitive host is the host in which the sexual If there are no sexual stages in the life cycle, then the definitive host is the host in the life cycle con
Direct Parasite Life Cycle: A life cycle of a parasite in which the pre-parasitic larvae develop in the which the eggs will EITHER hatch and the pre-parasitic larvae are entirely free-living (e.g. Ostertag usually an L3 and infection occurs via ingestion of infective stage or skin penetration OR the eggs d develop inside their eggs (e.g. Ascaris suum) and infective stage is usually the egg containing the definitive host occurs via ingestion of the infective stage. Return to top of page
-E-
Embryonated egg: (Also called a "Larvated egg"): A nematode egg with a developed larva insi in the morula stage and develop in the environment to the embryonated stage (the stage just befor Strongyloides spp., Dictyocaulus arnfieldi) are embryonated at the time they leave the host. Ensheathed: A larval nematode that is within the retained cuticle of the previous stage.
Eradication: Permanent reduction to zero of the worldwide incidence of infection caused by a spec Intervention measures are no longer needed. Exsheathment: The final step in molting of the infective stage when the old cuticle (sheath) is lost inside the definitive host. It is a requirement for the establishment for infection in the host. Extinction: The specific organism no longer exists in nature or the laboratory. Return to top of page
-FReturn to top of page
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Gametocyte: The stage in the life cycle of some protozoa (Apicomplexa) which is destined to beco Return to top of page
-H-
Helminths: A general term referring to the nematodes (roundworms), trematodes (flat worms, fluke acanthocephalans (thorny-headed worms).
Hydatid Cyst: Larva of Echinococcus spp. which is a large fluid filled cyst containing many invagin also contain many invaginated scolecies. There are two types of hydatid cysts: E. granulosus has multilocularis has a multi-locular (many chambered) cyst.
Hypobiosis: In parasitology: A temporary halt in nematode development within the host at an early cycle in nematodes with direct life cycles only. Nematodes arrest as immature forms in the definitiv
Hydatid Cyst: Larva of Echinococcus spp. which is a large fluid filled cyst containing many invagin also contain many invaginated scolecies. There are two types of hydatid cysts: E. granulosus has multilocularis has a multi-locular (many chambered) cyst.
Hypobiosis: In parasitology: A temporary halt in nematode development within the host at an early cycle in nematodes with direct life cycles only. Nematodes arrest as immature forms in the definitiv external environment pose a hazard to survival of free living pre-parasitic stages (usually in winter o more favorable, the arrested development resume their development to adults the life cycle continu Return to top of page
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Intermediate host: A stage in the life cycle that is essential to parasite development (with some ex of the parasite to the definitive host is usually by predation. Intermediate hosts are not required for
Indirect Life Cycle: A life cycle of a parasite in which the pre-parasitic larvae develop inside an ap Return to top of page
-JReturn to top of page
-KReturn to top of page
-L-
Life cycle: The stages an organism goes through over time containing a possible pre-parasitic and as a circle beginning with the formation of a individual and ending with the production of the next ge the parasite gives the investigator predictive value for understanding pathogenesis and clinical sign and control of the parasite. Life cycles can either be direct or indirect. Return to top of page
-MMeront: See schizont. Merozoite: The invasive stage that is the end result of schizogony.
Metacercaria: Stage of trematode life cycle that the cercaria after invading the second intermediat develop into. When ingested by the definitive host, the metacercaria will develop to the adult stage Metacestode: Mature tapeworm larvae.
Miracidium: The pyriform, ciliated larva of a trematode that developed in and hatched from the egg and undergo development to the next stage in the lifecycle. Myiasis: Infestation of organs and tissues of vertebrates by larval dipterans (true flies).
Miracidium: The pyriform, ciliated larva of a trematode that developed in and hatched from the egg and undergo development to the next stage in the lifecycle. Myiasis: Infestation of organs and tissues of vertebrates by larval dipterans (true flies). Return to top of page
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Occult infection: An infection with adult worms but no corresponding diagnostic stage. For exam (heartworm) some hosts may not have circulating microfilaria (this may be a result of immune-medi single-sex infection, chemosterilization of the adult worms by drug treatment, or senescent adults). heartworm infection".
Oncosphere: In a cestode life cycle, the oncosphere is the hexacanth (6-hooked) embryo found in
Oviparous: Laying eggs in which the embryos have developed little or not at all. Seen, for examp Ancylostoma caninum.
Ovoviviparous: Condition in which the organism develops in an egg and hatches within the adult emerges from the adult female. Seen, for example, in the nematode Dirofilaria immitis and in some Return to top of page
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Paedogenesis: A process in the molluscan intermediate host which involves the production of new which one trematode egg may eventually develop into hundreds of adults.
Parasite: Organisms that live temporarily or permanently on or within other living organisms (plant obtaining food.
Parasitic Phase of Life Cycle: The development and maturation to adult males and females occu cycle.
Parasitism: A two species association in which one species, the parasite, lives on or in a second s its life and obtains nourishment from it. The parasite may or may not cause disease in the host.
Parasitology: The study of host-parasite relationships. Traditionally this area of study has focused helminths and arthropods.
Paratenic host (transport host): A type of intermediate host in which immature helminths may su undergo development. Further parasitic development depends upon infection of the definitive host, paratenic host. Completion of a life cycle may happen with or without a paratenic host, but the pres make infection of the definitive host by the parasite more efficient.
Periparturient Rise in Fecal Egg Counts (PPR): An increase in the number of parasite eggs in th This can be pronounced in ewes, sows, and goats.
paratenic host. Completion of a life cycle may happen with or without a paratenic host, but the pres make infection of the definitive host by the parasite more efficient.
Periparturient Rise in Fecal Egg Counts (PPR): An increase in the number of parasite eggs in th This can be pronounced in ewes, sows, and goats. Phagolysosome: A phagosome that has fused with a lysosome within the phagocyte. Phagosome: A vacuole within a cell that was formed during phagocytosis.
Pre-parasitic Phase of Life Cycle: The development to the infective stage occurring outside the d second (intermediate) host of the parasite life cycle. Predilection site: The site within a host where the parasite is normally found.
Prepatent Period (PPP): The period of time from infection until mature adult parasites are produci
Procercoid: The larvae of Pseudophyllidian tapeworms in which after a crustacean ingests a ciliate the body cavity of the crustacean.
Pleurocercoid: Second larval type in Pseudophyllidian tapeworms in which after the crustacean is procercoid is liberated, the pleurocercoid is develops in the muscles of the new host and possesse stage which is infective to final host.
Procercoid: The larvae of Pseudophyllidian tapeworms in which after a crustacean ingests a ciliate the body cavity of the crustacean.
Proglottid: One segment of the body (strobila) of a tapeworm. Proglottids may be immature, matu present) or gravid (full of eggs). . Return to top of page
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Redia: In the trematode life cycle, the redia is the larval form (possessing an oral sucker) that deve give rise to the cercariae in the snail (intermediate host). Return to top of page
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Schizogony: In schizogony the nucleus of the original invading protozoan undergoes repeated divisions to form man
becomes surrounded by cytoplasm and a cell membrane forms around each new organism. These new stages within t
Scolex: The anterior end ("head") of the adult cestode, it is the hold-fast organ that anchors the w
Somatic Migration: Migration in the host by a parasite through the lungs into the systemic circulat
Schizogony: In schizogony the nucleus of the original invading protozoan undergoes repeated divisions to form man
becomes surrounded by cytoplasm and a cell membrane forms around each new organism. These new stages within t
Scolex: The anterior end ("head") of the adult cestode, it is the hold-fast organ that anchors the w
Somatic Migration: Migration in the host by a parasite through the lungs into the systemic circulat encyst in the tissues.
Spicules: Chitinous structures found in male nematodes, usually paired. They are inserted in the f
Sporocyst: In the trematode life cycle, the miracidium will invade a snail, lose the cilia and develo sporocyst, from which the redia will develop (in some species the sporocyst gives rise to a daught Sporozoite: The initial invasive stage of most of the Apicompexan protozoa. Strobila: The string of proglottides which make up the "body" of a tapeworm.
Strobilocercus: A type of larva of cyclophyllidian tapeworms (i.e. the larva of Taenia taeniaeformi Return to top of page
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Tachyzoite: Extra-intestinal stage of Toxoplasma that are found in in vacuoles muscle, liver, brain, definitive hosts. Sporulated oocysts are ingested and liberated sporozoites rapidly penetrate the in the invasive and proliferative stage of Toxoplasma. Tetrathyridium: Worm like larva with an invaginated scolex found only in Mesocestoididae.
Tracheal Migration: Migration in the host by a parasite into alveoli up the respiratory tree and then intestine. Transport host: See paratenic host.
Trophozoite: The stage of the protozoa in the host which feeds and grows until division commence
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Vector: An intermediate host in a parasitic life cycle, that may or may not (paratenic host) be esse A vector will seek out the definitive host in the life cycle to prey on it, whereas other intermediate h
Visceral Larva Migrans: Nematode larvae migration in hosts that are suitable for long survival but adult stage. The larva worms wander for a time in the hosts tissues.
Viviparous: Condition in which the embryo develops within the female and is nourished by the mo example: mammals.
Visceral Larva Migrans: Nematode larvae migration in hosts that are suitable for long survival but adult stage. The larva worms wander for a time in the hosts tissues.
Viviparous: Condition in which the embryo develops within the female and is nourished by the mo example: mammals. Return to top of page
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Links to online Parasitology resources:

http://www.biosci.ohio-state.edu/~parasite/home.html--Parasites and Parasitological Resources: A site maintained by The Ohio State University with images and descriptions of over 500 parasites. www.ivis.org--Another source of information on veterinary parasites is "Companion and Exotic Animal Parasitology" (Last updated: 29-June-00) edited by D. D. Bowman. This web based text can be found on the site maintained by The International Veterinary Information Service (IVIS). http://asp.unl.edu/--The American Society of Parasitologists web site www.heartwormsociety.org--The American Heartworm Society web site www.aavp.org--The American Association of Veterinary Parasitologists web site
Introduction to Parasitology
Topics
Parasites and parasitism The spectrum of parasitism Parasite life cycles Defined stages in life cycles The importance of life cycles - pathogenesis The importance of life cycles - epidemiology Important questions about life cycles Table 1 Table 2 The concepts of infection and disease Parasitism and disease
The Nematodes
Topics
Introduction Classification - overview External Morphology - cuticle modifications Internal Morphology - general anatomy Digestive System Reproductive System Basic Nematode Life Cycle Life Cycle Variations Exsheathment The Infective and Diagnostic Stages Arrested Development Table 1 - Classification of Nematodes of Veterinary Importance
The Trichostrongyloidea
Topics
The Order Strongylida The Superfamily Trichostrongyloidea Classification Life cycles of the family Trichostrongylidae Arrested Development and the Periparturient Rise Genus Trichostrongylus Morphology and species Life cycles Pathogenesis and clinical signs Epidemiology and diagnosis Genus Haemonchus Morphology and species Life cycle Pathogenesis Epidemiology Clinical signs and diagnosis Genus Ostertagia Morphology and species Abomasal nematodes - male spicules Life cycle Pathogenesis Epidemiology Clinical signs and diagnosis Genus Nematodirus Life cycle Genus Cooperia Life cycle Genus Hyostrongylus Life cycle Genus Dictyocaulus Morphology and species Life cycle Pathogenesis Epidemiology Clinical signs and diagnosis
The Strongyloidea
Topics
The Order Strongylida The Superfamily Strongyloidea The Syngamidae Stephanurus dentatus Morphology Life cycles Pathogenesis Epidemiology, clinical signs and diagnosis Syngamus trachea Morphology, pathogenesis, epidemiology, clinical signs, diagnosis Life cycle The Chabertiidae Chabertia ovina Morphology, pathogenesis, epidemiology, clinical signs, diagnosis Genus Oesophagostomum Morphology and species Life cycles Pathogenesis and epidemiology Clinical signs and diagnosis Intestinal strongyles of horses - The strongylidae The large strongyles Morphology and species Life cycles - Strongylus vulgaris Life cycles - Strongylus edentatus and Strongylus equinus Pathogenesis - adults feeding in the cecum and colon Pathogenesis - migrating stages of Strongylus vulgaris Pathogenesis - migrating stages of Strongylus equinus and Strongylus edentatus The small strongyles Morphology and species Life cycles Pathogenesis Epidemiology of equine strongyles Hatching, development of larvae and arrested development Seasonal changes in strongyle egg counts and pasture L3 levels Development of strongyle infections in foals Treatment and control of equine strongyles The use of anthelmintics to control strongyle infections Control of small strongyles with anthelmintics
The Ascaridoidea
Topics
Introduction to the Ascarids Species, hosts and importance Ascarids of dogs and cats Toxocara canis Toxocara cati Toxascaris leonina Ascaris suum Introduction and description Life cycle Pathogenesis and disease Epidemiology and diagnosis Parascaris equorum Introduction and description Life cycle Pathogenesis and disease Epidemiology and diagnosis Schematic life cycles Toxocara canis Toxocara cati Toxascaris leonina
The Oxyuroidea
Topics
Introduction and description Oxyuris equi Life cycle Pathogenesis and disease Epidemiology and diagnosis Treatment and control
PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS
The Siphonaptera - Fleas

Topics
Life cycles

Parasiticides - the Anthelmintics
Topics
Terminology, Introduction and Properties Spectrum of activity Safety considerations The issues of cost and residues Routes of administration Anthelmintic groups Macrocyclic Lactones Ivermectin

Heartworm
Topics
Dirofilaria immitis The Worm and its Life Cycle Host Species Epidemiology Pathophysiology of Heartworm in Dogs Cardiopulmonary Disease Caval Syndrome Secondary Complications: Renal and Hepatic Disease Ectopic Infections Hypersensitivity Reactions and Occult Infections Diagnosis Clinical Signs and Laboratory Findings Radiographic Findings Parasitological Examination and Immunodiagnostics Another Filarial Infection : Dipetalonema reconditum Treatment and Prevention in Dogs Pharmaceuticals Surgery Heartworm Disease in Cats
Laboratory 1
INTRODUCTION TO PARASITOLOGY
Click on the text below to jump down to the desired section of this page. Taxonomy scheme Nematodes Trematodes Cestodes Arthropods Protozoa Techniques Review Question

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The taxonomy scheme on the card above is the one we will use in
this course as it is the one used in the text book. Note that it differs from the one given in the introductory lectures in that the protozoa are listed in the animal kingdom and not in the Protista. Taxonomists are not in agreement as to the number of kingdoms and how organisms are divided among them, as can be seen by a the third scheme shown below where the prokaryotes are divided into two kingdoms and the eukaryotes are lumped into one.

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Members of the Phylum NEMATHELMINTHES have a straight intestine, composed of only epithelial cells, with a posterior anus. The body cavity is a pseudocoel (i.e. lacking a mesodermal lining).
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The nematodes (phylum NEMATHELMINTHES, Class NEMATODA) are cylindrical in shape tapering at both ends and have a complete digestive system. The body is covered by an acellular cuticle. These helminths (worms) are commonly known as "roundworms" because of the shape of their cross-section
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Ascaris suum - Adult nematodes from the small intestine of a pig. This species is one of the larger nematodes.
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Ascaris suum - The diagnostic stage of this nematode is the egg which is passed out in the feces. The eggs will float in a saturated salt solution, therefore a standard fecal floatation can be used to diagnose an infection with this worm.
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Dirofilaria immitis ("Heartworm") - These adult nematodes are found primarily in the pulmonary arteries and sometimes in the right ventricle. Large numbers of adult heart worms (as seen here) can so damage the lining of the pulmonary vasculature that pulmonary hypertension and right-sided heart failure can result.
This museum specimen represents the classic picture of heartworm. In actual fact, a large mass of worms in the right ventricle is an artifact of death. In the living animal the worms are usually forced down into the pulmonary arteries by the blood flow.

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Members of the Phylum PLATYHELMINTHES (the "flatworms") are usually flattened dorso-ventrally and are bilaterally symmetrical. They lack true body segmentation, a body cavity and an anus.
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The Trematodes (Phylum PLATYHELMINTHES, Class TREMATODA), as adults, are flattened dorso-ventrally, have a blind gut and no coelom. They also have suckers for attachment to the host. They are commonly referred to as "flukes".
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Dicrocoelium dendriticum - This small trematode is found in the bile ducts of sheep and cattle.
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Dicrocoelium dendriticum - The egg, which passes in the feces, is the diagnostic stage of this trematode. This egg, like many trematode ova, is operculate (has a cap on one end) and contains the next life-cycle stage, the miracidium.
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Fasciola hepatica - An adult specimen taken from the bile duct of an infected sheep. Note the size, distinct cone at the anterior end, "shoulders", and the "leaf-shaped" outline.
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Fasciola hepatica - The adults of this trematode are found in the bile ducts of the liver. This specimen is from a cow, but these flatworms may also infect sheep, man, and most other mammals. Note the thickening of the bile ducts caused by the parasite infection.
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Fasciola hepatica - The diagnostic stage of this trematode is the egg which is passed in the feces. Like many fluke eggs it has an operculum (cap) at one end and does not float in the standard saturated salt solution. You must use a sedimentation method to concentrate the feces in order to diagnose an infection with this parasite.

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The Cestodes (Phylum PLATYHELMINTHES, Class CESTODA), as adults, are ribbon shaped organisms whose "body" is made up of many repeating segments. They have no digestive tract or coelom and the adults are always found in some part of the host's digestive
tract.
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Taenia saginata - The diagnostic stage for an infection caused by the adult tapeworm in humans is usually the gravid proglottid (an egg filled segment of the worm) which passes out with the feces. Identification of the type of tapeworm can be made by examining the morphology of the proglottid and the eggs it contains. This slide shows an egg which was removed from a proglottid (although these eggs sometimes may be found in the feces by a standard fecal flotation).
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Taenia saginata - This gross specimen shows the larval stages of T. saginata in the muscle of a cow. The larva is a cysticercus. The cysticerci appear as white, fluid-filled bodies throughout the muscle tissue.
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Taenia saginata - The adult is found in the small intestine of humans and may be quite long.
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Phylum ARTHROPODA Arthropods are bilaterally symmetrical animals with paired, multi-jointed appendages and an exoskeleton (outer covering) of secreted, non-cellular material (usually chitin or calcium carbonate). They have a dorsal heart and a ventral nerve cord. Their bodies are more or less segmented, and they are cold-blooded. The veterinary medical importance of these animals stems from their ability to act as pathogenic ecto- and endoparasites and from their ability to transmit other parasites or microbial pathogens.
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Class HEXAPODA (INSECTA) Insects have all of the characteristics of the phylum Arthropoda. Specifically, their exoskeletons are composed of chitin and cross-linked proteins. The adult stages have three pairs of legs, and their bodies are divided into three segments: head, thorax, and
abdomen. We will study three groups or orders of insects in this course. These orders are constituted by the true flies, the fleas, and the lice.
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Gasterophilus sp. These insects are the larval stage of a fly. The adult flies are free-living, and the larvae live attached to the wall of the horse's stomach. (This museum specimen shows the larvae attached to the mucosa of a horse's stomach.)
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Culex sp. This mosquito is an insect that may act as a vector and intermediate host for several different parasites. The larva, pupa, and male and female adults are seen here.
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Class ARACHNIDA Arachnids have all the characteristics of the phylum Arthropoda. They share a chitinous exoskelton with the insects, but differ from those animals in that they have four pairs of legs in the adult stage. Also, their bodies exhibit fusion of two of the insect segments, the head and thorax, into a single body region known as the cephalothorax. We will deal with only one Order in the class Arachnida, the Order ACARINA, which includes the ticks and mites.
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Notoedres cati This tiny skin burrowing mite was recovered in a skin scraping from a cat exhibiting symptoms of mange as illustrated in the museum specimen to the right.
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Notoedres sp. Note the damage that this skin burrowing mite (arachnid) has caused to this cat's head.
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Dermacentor variabilis ("American Dog Tick") These adult ticks (arachnids) were removed from the skin of a dog. Ticks not only suck blood from their hosts, they also are vectors for several parasitic diseases, such as Rocky Mountain Spotted Fever.

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The protozoa (Phylum PROTOZOA) are single cell animals which fall into several classes. In general the classes of protozoa are organized around structures used for locomotion (flagellum, pseudopodium, and cilia) or the lack of such structures. Most of the protozoa are microscopic.
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Eimeria stieda This protozoan infects the liver of rabbits. The white nodules you see in this rabbit's liver are part of the pathology caused by this parasite.
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Eimeria stieda The diagnostic stage of this coccidian is the oocyst which passes in the feces, it will float in a standard salt solution.
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Haemoproteus The stage of the protozoan seen in this red blood cell of a pigeon is one of the sexual forms of the parasite. This parasite is in the same group of protozoans as malaria.

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BAERMANN APPARATUS This device is used to recover nematode larvae from a fecal sample. The larvae under the microscope at the right were recovered using a Baermann apparatus. (right: modified Baermann apparatus, left: Baermann apparatus).
Review Question
This parasite was recovered from the bile duct of a deer. Its eggs (the diagnostic stage) are found in the host's feces. A.) To what Phylum and Class does this parasite belong? B.) Which of the diagnostic methods learned in today's laboratory would be the best one to use to detect the eggs of this parasite in the deer's feces. Click here for the answer. Return to top of page
Nematode Taxonomy
Back to Index
Class: Nematoda
Superfamily: Trichostrongyloidea Strongyloidea Metastrongyloidea Rhabditoidea Oxyuroidea Ascaridoidea Subuluroidea Spiruoidea Filarioidea Trichuroidea Dioctophymatoidea
Back to Index
Laboratory 2
THE STRONGYLES
Click on the text below to jump down to the desired section of this page. Haemonchus sp. Ostertagia sp. Trichostrongylus sp. Cooperia sp Chabertia sp. Nematodirus sp. Oesophagostomum dentatum Stephanurus dentatus Strongylus sp. Cyathostomum sp. Syngamus trachea Review Question

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Haemonchus sp.
This nematode is common in the abomasum of sheep, goat, cattle, and other ruminants. Note the spirally wound ovaries in the female worms which gives them their common name the "Barber pole worm". Size 20 to 30 mm (this is the largest of the abomasal trichostrongyles)
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Haemonchus contortus
This is the common "barber pole" worm of the abomasum of sheep. This slide shows the bursa of a male worm. Note the asymmetrical dorsal ray which is characteristic of this genus.
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This slide shows the vulva flap of a female worm.

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Ostertagia sp.
This trichostrongyle of the abomasum is intermediate in size (smaller than Haemonchus and larger than Trichostrongylus). Male 7.5 to 8.5 mm Female 10 to 12 mm

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Trichostrongylus sp.
One of the many species of Trichostrongylus found in horses and ruminants. Note the very small size of the worm. Male 4 to 5 mm Female 5 to 7 mm

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Cooperia curticei
Male and Female worms. This worm is commonly found in the small intestine of sheep. Note the small size of these nematodes and their coiled ("watch spring") appearance. Male 4.5 to 5.5 mm Female 5.8 to 7.2 mm
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Cooperia curticei
This female specimen demonstrates the characteristic "watch spring" appearance of the parasite. The anterior end shows the cervical inflation which is finely striated.
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Chabertia ovina
This parasite is commonly found in the large intestine of sheep and cattle. Note the buccal capsule can be seen with the naked eye Male 13 mm Female 18 mm
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Chabertia ovina
Mounted specimen to show the large buccal capsule which is directed ventrally. Note the leaf crowns.

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Nematodirus sp.
This is a relatively long trichostrongyle found in the intestine of ruminants. Note that the anterior end of this worm is thinner than the posterior. Also note the size: Male 10 to 15 mm Female 15 to 23 mm
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Nematodirus sp.
This slide shows the bursa of the male worm. Note the long spicules which are joined together at the tip by a narrow membrane. These characteristic spicules can be used to identify this nematode as Nematodirus sp. Male 7.5 to 8.5 mm Female 10 to 12 mm
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Nematodirus sp. Egg

Because of its size (200 X 90 um; about twice as large as other strongyle-type eggs) and shape, this egg is easily identifiable to genus. A = Nematodirus sp. egg B = typical strongyle egg
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Oesophagostomum dentatum
One of the species of nodular worms of pigs. Note the size: Male 7.5 to 8.5 mm Female 10 to 12 mm
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Note the small buccal capsule (A), leaf crowns (B) and a definite cephalic vesicle (C), which is terminated by a ventral groove.
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This is a section through a nodule produced in the intestine of a pig by O. dentatum.
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Sheep colon infected with Oesophagostomum sp. Note the thickened intestinal wall and the many nodules.

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Stephanurus dentatus
This is the kidney worm of swine and is found in cysts which open to the hilus of the kidney and the ureters. Note the thin cuticle and visible internal organs. Male 25 mm Female 35 mm

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Strongylus vulgaris
Whole worms. The females have pointed tails while the males have a bursa at the caudal end. Note the robust nature of these nematodes and their size (smaller than the other species of Strongylus).
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Strongylus vulgaris
A common nematode of the large intestine of horses. Note the large buccal capsule (A) and the leaf crowns at the anterior end. Two ear shaped teeth (B) are in the buccal capsule and a dorsal "gutter" (C) runs down the dorsal side of the buccal capsule.
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Parasitic thrombi of the arteries of a horse due to the larval stages of Strongylus vulgaris. Note the marked thickening of the arterial wall and the thrombus formation.
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Strongylus equinus
Whole worms. Note the size and the robust nature of these nematodes.
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Strongylus equinus
Note the large buccal capsule and the leaf crowns (C) at the anterior end. There is a dorsal "gutter" (D) with a bifid dorsal tooth (B) at its base and two smaller ventral teeth (A) at the base of the buccal capsule. (You will have to focus up and down to see both ventral teeth.)
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Strongylus edentatus
Whole worms. Note the size and the robust nature of these nematodes.
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Strongylus edentatus
One of the largest of the nematodes of the large intestine of the horse. Note the leaf crowns (A) surrounding the mouth, which opens into a large buccal capsule (B). There are no teeth in the buccal capsule of this species, however a dorsal "gutter" (C) is present. The purpose of this gutter is to allow enzymes secreted by glands in the esophagus to make their way into the buccal capsule which would be filled with host tissue while the worm is feeding. Return to top of page
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Small strongyles (Cyathostomum spp. Trichonema spp., etc.)

Whole worms. Note the size (much smaller than Strongylus spp.) A large number of genera and species exist and they vary in size from 5 mm to 15 mm. The males may have large bursa.

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Syngamus trachea
Occurs in the trachea of turkey, goose, fowl and various wild birds. The sexes are found in permanent copulation, hence the "Y"-shaped appearance of the worm pair. Male 2 to 6 mm Female 5 to 20 mm

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Review Question
A. The worms in the dish were removed from the colon of a horse which died with severe colic. Give the genus and, if possible, the species of each. B. Indicate which is the more important pathogen. CLICK HERE FOR THE ANSWER Return to top of page
Laboratory 3
HOOKWORMS, LUNGWORMS AND STRONGYLOIDES
Click on the text below to jump down to the desired section of this page. Ancylostoma caninum Ancylostoma braziliense Uncinaria stenocephala Bunostomum trigonocephalum Oslerus (Filaroides) osleri Muellerius capillaris Dictyocaulus viviparus Metastrongylus apri Strongyloides spp. Review Question

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Ancylostoma caninum
Whole worms. A fresh specimen of A. caninum is often colored red by the blood in its gut (the color fades on fixation in alcohol). Compare the size of these worms (10 to 16 mm) with the smaller U. stenocephala.
.
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Ancylostoma caninum
Specimen showing the mouth capsule. Note the deep capsule (bent dorsally) and 3 pairs of teeth (3 on each side of the ventral margin).
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Ancylostoma caninum
First-stage larva. Note the mouth tube, bulbed rhabditiform esophagus and straight tail (no genital rudiment is visible).

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Ancylostoma braziliense
This hookworm occurs in both cats and dogs. It is endemic in the gulf coast states, but may be transported north in pets that travel with their owners. It is the major etiological agent of cutaneous larval migrans in humans in the United States. Note the deep mouth (buccal) capsule, which is bent dorsally, and the pair of large lateral teeth.

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Uncinaria stenocephala
Whole worms. Note that these hookworms are smaller and thinner than A. caninum. Male 5 to 8.5 mm Female 7 to 12 mm
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Uncinaria stenocephala
This adult worm is mounted to show the buccal capsule. Remember that this nematode is similar to A. caninum but instead of teeth there are cutting plates, one on each side of the ventral surface of the mouth. Because the head is bent to the dorsal side, the ventral surface appears to be the anterior end of the worm.

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Bunostomum trigonocephalum
Whole worms. This species occurs in sheep and is similar in size and appearance to the cattle hookworm (B. phlebotomum). Because there are other bursate nematodes in the small intestine of sheep and cattle, identification of the hookworms will depend on seeing the buccal capsule and cutting plates. Male 14 mm Female 24 mm
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Bunostomum trigonocephalum
Specimen mounted to show the buccal capsule. Note the cutting plates seen on the ventral aspect of the mouth.

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Oslerus (Filaroides) osleri L1

The first stage larvae of this lungworm can be found in the feces or tracheal washes of infected dogs. Note the kinked tail (A).
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Oslerus (Filaroides) osleri

This slide is a cross-section of one of several nodules removed from the trachea of a dog. Note the accumulation of fibrous tissue around numerous nematodes (seen in cross-section). Numerous L1 can be seen within the uteri of the female worms.
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This is a preserved specimen of a trachea of a dog infected with O. osleri. Note the numerous wart-like nodules present at the bifurcation of the trachea and extending into the bronchi.
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PATIENT: 1 1/2 year old male schnauzer. HISTORY: During the last 2-3 weeks there was periodic respiratory distress, the dog would have labored breathing, become cyanotic, and pass out. Taken to 3 different veterinarians who diagnosed: 1) allergy 2) pneumonia 3) normal dog. PHYSICAL EXAMINATION: Dog sits on front elbows abducted, "gasping for breath". During attacks the dog became cyanotic. Decreased lung sounds on the right side. TENTATIVE DIAGNOSIS: 1) Diaphragmatic hernia, 2) Tension pneumothorax, 3) Allergy. COURSE OF THERAPY: 1. Hospitalized for 8 days (10/24 to 11/2), radiographs indicated a pneumothorax, given antibiotics and had air removed from thorax periodically. A thoracotomy (10/27) showed nothing abnormal. Dog sent home 1/2. 2. Returned 11/5 for removal of more air from thorax. Radiographs indicated air in the mediastinum (possibly leaking from trachea). 3. Readmitted 11/10. Radiographs indicated a spherical density of the ventral aspect of the trachea at the level of the right cardiac border. A blood smear showed many microfilariae*. Broncoscopy showed numerous nodular growths (1 to 5 mm) from the mid-trachea into both main stem bronchi. Several were large enough to obstruct bronchi during deep inspiration. Removed enough to make a patent opening. (Several nodules sent to pathology). Pathology indicated granulomas containing numerous nematodes. Dog was sent home. 4. Re-examined 11/23: Breathing normally. removed several nodules from trachea. 5. Re-examined 12/17: Dog normal. DIAGNOSIS: Pneumothorax due to leakage of air from the trachea. Wall of trachea weakened due to Oslerus osleri infection. NOTE: At the time this dog was seen there were no anthelmintics which were active against O. osleri. Today we have several effective drugs to kill this worm and one of them would have been used in this dog along with the surgery. *This indicated that the dog had heartworm in addition to the Oslerus osleri infection.

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Muellerius capillaris
This slide shows this lungworm in the lung of a goat. The worm is associated with small, nodular lung lesions which contain adult worms and larvae.

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Dictyocaulus viviparous
Whole specimens. These nematodes occur in the bronchi of cattle. Note the large size (4 to 8 cm) and the white color (the intestine may show through as a dark line).
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Metastrongylus apri
Whole specimens. Note they are long (up to 6 cm), slender, white nematodes found in the bronchi of pigs.
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Metastrongylus apri
This is an autopsy specimen from a pig infected with Metastrongylus apri. Note the presence of several worms (seen in cross-section) in the bronchi and the normal lung tissue surrounding the bronchi.

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Strongyloides ransomi
Adult females from the intestine of a pig. (see card3:23 for comparable image)
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Strongyloides stercoralis
This is a parasitic (parthenogenic) female recovered from a mucosal scraping of the small intestine of a dog. Note the small size, and long esophagus. There are no males in the parasitic portion of the life-cycle.
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This is a first-stage larva as passed in the feces. Note the rhabditiform esophagus, which is short (much less than 40% of the body) and distinctly bulbed, the short mouth capsule, and the large genital rudiment (GR). (The latter 2 characteristics distinguish these larvae from those of the hookworms.) Note also the simple pointed tail (this separates these larvae from lungworm L1).
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Infective L3. these occur on the soil surface or in fecal cultures. L3 can sometimes be found in tracheal washes of an infected dog. Note the filariform esophagus which extends to 40% of the body length. Focus carefully and notice the notched tail. The length of the esophagus and the notch in the tail allow you to distinguish between the L3 and the L1. Living L3 are infectious for dogs, primates and humans.

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Review Question
These worms were some of the many removed from the small intestine of a 6 week old puppy that died of severe anemia. A. Identify the nematode (Genus and species). B. How did the puppy most likely acquire this infection? Click here for the answer Return to top of page
Laboratory 4
ASCARIDS, OXYURIS, AND TRICHOCEPHALIDS
Click on the text below to jump down to the desired section of this page. Ascaris suum Parascaris equorum Toxocara canis Toxascaris leonina Toxocara cati Baylisascaris procyonis Ascaridia galli Heterakis gallinarum Oxyuris equi Trichinella spiralis Trichuris vulpis Capillaria spp. Dioctophyma renale Review Question

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Ascaris suum
This is the ascarid of swine. Note its size and shape. The male is smaller than the female and has a curved tail with spicules.
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Ascaris suum
This slide shows the 3 lips at the anterior of the worm. (Focus up and down to see all 3.)
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Pig lung infected with
Ascaris suum
Note the marked degree of hemorrhage in the lung, most of the air spaces are filled with blood. In addition, there is edema and cellular infiltration.
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All of the ascarids in this 1 gallon jar came from one foal.

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Parascaris equorum
This is the ascarid of horses. Note its size and the 3 large lips at the anterior end. (three lips are a characteristic of all ascarids.)
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Parascaris equorum
This slide shows the 3 lips (1 dorsal and 2 ventral). Focus up and down to see all three.

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Toxocara canis
This is the common ascarid of dogs. Note the 3 lips (focus up and down to see all 3) and the cervical alae. The alae are clear cuticular flanges running along the lateral margins of the worm. They are similar in shape to those of Toxascaris leonina.

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Toxascaris leonina
The cervical alae of this ascarid of dogs and cats is similar to those of the dog ascarid T. canis. In both of these worms the alae merge gradually into the cuticle. In contrast, the alae of T. cati end abruptly.
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Toxocara canis and Toxascaris leonina

Adult worms. T. canis is much larger, the males measure up to 10 cm and the females up to 18 cm long T. leonina males are up to 7 cm and the females are up to 10 cm. Recall the biological differences between the two species: Host(s), transmission options, larval migration (or not) and the resulting differences in pathogenesis. Are both equally significant in public health.
Toxascaris leonina
Toxocara canis
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Toxocara canis
The worms in this bottle were recovered from the 3 lb. puppy described in the case report.
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Toxocara cati
These are the adults of the common ascarid of cats. Note that the cervical alae can be seen with the naked eye.
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Toxocara cati
Note that the cervical alae of this ascarid terminate abruptly, unlike those of T. leonina the other ascarid of cats. Thus, ascarids that are expelled in the feces of cats can be easily distinguished.
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Baylisascaris procyonis
Adults from the small intestine of a raccoon. This worm lacks cervical alae. As has been pointed out in the lecture, this is an increasingly important parasite in veterinary public health. Although its larvae are not as prevalent in humans as those of T. canis, they are large and highly neurotropic, causing this species to be especially pathogenic. The larvae (not adults) occur in humans (and other mammals and birds) where they are one of several causative agents of "larval migrans".

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Ascaridia galli
Adult worms. This parasite occurs in the small intestine of chickens, turkeys, geese, and many wild birds (e.g. crows). Males 50 - 76 mm Females 72 - 116 mm

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Heterakis gallinarum
These are adults. This is the most common caecal worm of ground-reared poultry. Note its size. The females are larger than the males.

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Oxyuris equi
These are adults of the pinworm of horses. Formerly a very common parasite of the large intestine, its susceptibility to modern anthelmintics has all but eliminated this nematode from horses in this part of the country. Note the females have long thin tails (a characteristic of the family) while the males have a blunt tail with caudal alae and a single spicule.

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Trichinella spiralis
This is a section of muscle from a Trichinella spiralis infected mouse in the acute phase. Observe the abundant inflammation. It is these larvae that cause the most characteristic symptoms of trichinosis. Trichinella spiralis is unique among the nematodes because the same individual serves as the definitive and intermediate host.

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Trichuris vulpis
These are adult dog whipworms. Note the size and the long, thin anterior end (the "lash") and the short, thick posterior end (the "whip-handle") of the worm. Hence, the common name: "whipworm".
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Trichuris vulpis
This museum specimen demonstrates an infection with the whipworm of dogs. Note that the thin anterior end is embedded in the mucosa, whereas the thick posterior end protrudes into the lumen.
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Trichuris vulpis
The egg of Trichuris sp. is brown in color, thick shelled, lemon-shaped, with a smooth surface and possesses a plug at each pole. It is unembryonated when passed in the feces. It measures 80 X 40 um. Note: Focus up and down to see the texture of the outer surface of the eggshell.

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Capillaria spp.
These nematodes are closely related to Trichuris, but they are small and slender. The posterior portion of the body is not conspicuously thicker than the anterior as in the case of the whipworms. Capillaria spp. occur in many species of birds, mammals and other vertebrates. In some species, larvae may occur in invertebrates as well.
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Capillaria aerophila
The sides of this egg are usually parallel and the polar plugs tend to be asymmetrical. The easiest way to distinguish this egg from that of a whipworm is to examine the surface of the egg. Capillaria spp. eggs have a rough surface while Trichuris spp. eggs have a smooth surface. Note: Focus up and down to see the texture of the outer surface of the eggshell.

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Dioctophyma renale
This nematode is one of the largest known and is found in the kidney of dogs and wild carnivores (especially fish eating carnivores, e.g. mink). It causes destruction of the kidney tissue until only a fibrous shell is left. Fortunately, only one kidney is usually parasitized. Note the very large size and its location (within the kidney).
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Dioctophyma renale
This slide shows the egg of the kidney worm of dogs and other carnivores. They are barrel shaped, thick shelled, pitted (except at the poles) and are unsegmented (unembryonated) when passed in the urine.

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Review Question
This slide under the microscope contains the product of a fecal exam on a young pup from Philadelphia which, some two weeks prior, had shown clinical signs of pneumonia, e.g., coughing, elevated respiratory rate, foamy nasal discharge, etc. A) Name the parasite(s) present on the slide. (Note : Please do not move the slide.) B) Which parasite(s) could have accounted for the pulmonary signs? Click here for Answer
Laboratory 5
SPIRURIDS AND FILARIDS
Click on the text below to jump down to the desired section of this page. Spirocerca lupi Dracunculus insignis Dirofilaria immitis Dipetalonema reconditum Ae. aegypti Onchocerca lienalis Setaria equina Gongylonema pulchrum Physaloptera sp. "Horse hair worm" Review Question

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Spirocerca lupi
The esophageal worm of dogs. These worms are large and usually coiled. Living specimens are pink to bright red in color.
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Spirocerca lupi
The eggs of this worm are small (40 X 15 um), oval, thick shelled with parallel sides. When passed in the feces they contain a larva bent in the shape of an "U". Some students have told us that these look like miniature paperclips.
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Spirocerca lupi
Mounted specimen showing the esophageal lesion caused by the worm. Note the fibrous nodule or tumor with the worms coiled inside. Tissues in these nodules have been known to undergo malignant transformation.
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Spirocerca lupi Radiographs

Note the granulomatous mass surrounding the esophagus (difficult to see here) in both the general survey and in the angiogram on the right. Also note that in the survey you can see the thickening of the bodies of the thoracic . vertebrae (red arrows). The angiogram clearly shows an aneurysm in the descending aorta.

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Dracunculus insignis
This is an adult spirurid worm removed from a dog. This parasite of wildlife lives subcutaneously in its host. The female worm will make a hole through the skin (usually of the leg) in order to deposit L1 when the skin gets wet.
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Dracunculus insignis
This slide shows the L1 of the "guinea worm" of wildlife. This is the stage that is infective to the intermediate host, Cyclops sp. If a tube of water is placed over the skin ulcer formed by the female worm, L1 will be discharged into the tube and can be used to diagnose the infection.
This slide shows the adult female worm discharging L1 into a test tube.

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Dirofilaria immitis
These worms are found mainly in the pulmonary arteries and, with heavy infections, in the right atrium. Females reach a size of 25-30 cm long, and are slender. Males are shorter (12-16 cm) and the tail (right) is spirally coiled.
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Dirofilaria immitis - microfilaria

Note the tapered anterior end. In most specimens you will see a straight body and straight (or slightly curved) tail. The width is > 6 um. From a Knott preparation.
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Dirofilaria immitis
Ultrasound showing caval syndrome. Numerous white spots can be seen in the uppermost section. These spots represent adult worms in the right ventricle.
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Dirofilaria immitis
Ultrasound showing two adult worms in the pulmonary arteries. The presence of the worms is easily identified. Each worm is seen as parallel white lines.
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Dipetalonema reconditum microfilaria

Note the "blunt" anterior end (the cephalic hook may or may not be seen). The tail is curved (usually). The width (4.7 to 5.8 um) is less than D. immitis.
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Dirofilaria immitis
Microfilariae stained by the acid phosphatase technique. NOTE that staining is "zonal". These zones correspond to the excretory (anterior) and anal (posterior) pores of the microfilariae.
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Dipetalonema reconditum
Microfilaria stained by the acid phosphatase technique. Note that the staining is uniform in these microfilariae.

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Females of Aedes aegypti mosquitoes feeding on blood containing microfilariae of Dirofilaria immitis via artificial membrane feeding apparatus.
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Digestive tract of blood-engorged female Ae. aegypti. A: Midgut with blood. B: Hindgut (may be pulsating). C: Malphigian tubules (white in color). Note: You can actually see the giant 1o cells of the tubules under the dissecting scope.
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Gut contents of female Ae. aegypti showing microfilariae of D. immitis.
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Larvae of D. immitis from malphigian tubules 6 days after infection. (Focus up and down). A: 2nd stage D. immitis larvae. B: Malphigian tubule.
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Third stage larvae (infective) in mouthparts (labial sheath) 13 days after infection.
Arrows point to emerging L3 from proboscis.
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This museum specimen is from a dog with D. immitis infection. The pulmonary arteries have been dissected open to reveal the primary predilection site of the adult parasite. This museum specimen also shows adults of D. immitis in the right atrium. Retrograde movement of large numbers of adults into the right heart, as seen here, is usually an artifact of death, but may occur in vivo in cases of caval syndrome. .
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This model depicts the primary predilection site of adult D. immitis - the pulmonary arteries. Note that the model also represents the formation of rough villus-like plaques in the arterial lining, a response to injury by the worms and the primary lesion responsible for pulmonary . hypertension in heartworm disease.
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This model depicts D. immitis adults in the right atrium of the canine heart. Such a situation may occur in caval syndrome when decreased cardiac output permits retrograde migration of adult worms from the pulmonary arteries. In many cases, finding adult worms in this location at necropsy is simply an artifact of death. When pulmonary blood flow ceases, the worms move into the right heart.
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Onchocerca lienalis - microfilariae from a bovine skin biopsy

To see the microfilariae, carefully remove the petri dish top and focus on the bottom of the dish. The worms often congregate around the edges of the dish or around the skin biopsy itself. They are tiny, less than 300 um in length, and should be highly motile.
Please do not readjust the microscope or light.

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Setaria equina
Removed from the peritoneal cavity of a horse. Males: 4 to 8 cm. Females: 7 to 14 cm.
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Setaria sp. microfilaria

These microfilariae are sheathed.

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Gongylonema pulchrum
The sinusoidal tracks on the mucus membrane of this sheep's esophagus indicates where the adult of this spirurid worm is located. This worm uses dung beetles as the intermediate host. This nematode is a non-pathogenic parasite of many domestic mammals.
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Physaloptera sp.
These spirurid nematodes are parasites of the stomach of carnivores. They are normally found in opossums and raccoons but can occasionally be found in dogs and cats. This parasite uses a coprophagous beetle as an intermediate . host.

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"Horse hair worms" Adult found in swimming pool

Phylum Nematomorpha Class Gordioidea Adults are free living inhabitants of fresh water. Larvae are parasitic in insects. The larvae mature to the adult stage in the insect and when the insect is in . contact with water the adult emerges. This is why the adult worm can be found swimming in a pet's water dish or the family swimming pool.

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Review Question
A dog was presented to a local veterinarian for a routine heartworm exam. The dog was not showing any clinical signs of infection. The results of a Knott concentration test are seen in the compound scope at the right. (Please do not move the specimen!) The results of . a serologic test for Dirofilaria immitis antigen are also seen at this station. This test is showing a negative. A. Based on the information you have and on the appearance of the specimen under the scope, what would be your diagnosis? B. What further testing might you do to confirm your diagnosis? C. What are the implications of this
B. What further testing might you do to confirm your diagnosis? C. What are the implications of this finding for the dog's health? Click here for the answers
PARASITOLOGY LAB EXAM

(This is an actual examination paper for your reference) (Click on the question to see the picture that goes with the question) Question 1. A. A local dairy farmer has just acquired some livestock and is concerned that they may have liver flukes (the trematode Fasciola hepatica). What fecal examination method will give you the best chance of finding the eggs of this parasite? (3 pts.) B. A 3-week-old puppy has watery diarrhea. Given its age and clinical signs you suspect a Giardia infection. What fecal examination method will give you the best chance of detecting this parasite? (3 pts.) C. A 4-year-old dog has a chronic cough and you have included the nematodes that live in the lungs on your list of possible causes. What fecal examination method(s) will give you enough information to rule out (or in) the presence of these "lungworms"? (3 pts.)
Question 2. A. The fecal sample in the device at your place came from a 4-year-old male Rottweiler as part of his yearly check-up. Examine the sample and identify the eggs of the parasite (give Genus and species). (7 pts.) B. What other similar looking egg could appear in dog feces and how could You tell it apart from the egg you identified in part A? (3 pts.) Question 3. A. The sample of meat in the dish at your place is beef hamburger that is thought to have been contaminated with pork. Is it likely that the hamburger has pork in it (yes, no, can't tell)? (4 pts.) B. Explain your answer to part A. (3 pts.)
Question 4. A. A saturated salt flotation was done on a fecal sample from a 4 month old Puppy which has been brought to you for its first check-up. The results of this test are shown under the microscope at Station #4. Identify the parasite egg (give Genus and species). (7 pts.) B. What other similar looking egg may be found the feces of a dog and how could you tell it apart from the egg you identified in part A? (3 pts.) Question 5. A. A 6-year-old male mix breed dog was brought in to your practice with the complaint that it had chronic vomiting. The results of a saturated salt flotation fecal examination is shown under the microscope at Station #5. Identify the egg (give Genus and species). (6 pts.) B. What pathologic changes may have been caused by this parasite and what other procedures would you do to determine if this dog had these pathologic conditions?
(3 pts.) Question 6. A. The egg seen under the microscope at Station #6 was recovered from the feces of a 1 month old foal which has diarrhea. Many of these eggs are present on the slide. Identify the parasite (give Genus and species). (6 pts.) B. Why would you expect to see eggs of this parasite in a young foal rather than in a mature horse? (3 pts.) Question 7. A. The egg seen under the microscope at Station #7 was recovered during a urine analysis of a pig. Identify the parasite (give Genus and species). (6 pts.) B. In what organ does the adult worm reside? (3 pts.)
Question 8. A. The worms seen under the microscope at Station #8 were recovered from the small intestine of a sheep which died of bacterial pneumonia. Identify the parasite (give Genus only). (6 pts.) B. Describe the egg you would expect to find in the feces. (3 pts.) Question 9. A. A number of adult nematodes, each about 1.5 cm long, were recovered from the large intestine of a horse which died suddenly. The anterior end of the worm is shown on the kodachromes at Station #9. Identify the parasite (give Genus and species). (6 pts.) B. Where in the horse would the fourth-stage larvae (L4) of this worm be found? (3 pts.) Question 10. A. The dish under the microscope at Station #10 contains a skin biopsy in saline. The biopsy was taken from the ventral midline of a horse with itching dermatitis in this area. Identify the parasite (give Genus only). (6 pts.) B. How is this parasite transmitted? (3 pts.)
Laboratory 6
TREMATODES
Click on the text below to jump down to the desired section of this page. Gyrodactylus sp. Fasciola hepatica Fascioloides magna Dicrocoelium dendriticum Paramphistomum cervi Paragonimus kellicotti Heterobilharzia americana

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Gyrodactylus sp.
This monogenean trematode is an ectoparasite of fish. Note the haptor ("holdfast organ") at the posterior of the worm.

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Fasciola hepatica - Eggs

Note the size, shape, color, and the operculum.
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Fasciola - miracidium
Note the cilia, eye-spots and the germ cells.
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Limnea spp.
One of the many snail intermediates hosts suitable for the development of Fasciola stages.
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Fasciola - Redia
Characterized by a primitive digestive tract made up of a pharynx and intestine. Note the developing cercariae within the redia.
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Fasciola - cercaria
Note the oral and ventral suckers. Also note the tail for swimming.
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Fasciola hepatica - metacercaria

The encysted metacercaria would normally be found on vegetation.
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Fasciola hepatica
Adult specimen taken from the bile duct of an infected animal. Note the size, distinct cone at the anterior end, " shoulders" and broad outline.
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Model of a Sheep Liver infected with Fasciola hepatica

Note the thickened, calcified bile ducts and the adult worms in the bile ducts (difficult to see in this photo).
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Fascioloides magna
Very large liver fluke. Indigenous to North Americana. Normal Host Deer: Adults encapsulated but eggs passed into bile ducts. Abnormal Host Cattle: Adults encapsulated, no eggs passed. Sheep: Uninterrupted migration in liver parenchyma. Host usually dies.
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Dicrocoelium dendriticum - Eggs

These eggs are small, dark brown and asymmetrical, they are thick walled with an indistinct operculum.
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Dicrocoelium dendriticum
Adult specimen taken from the bile duct of an infected animal. Note the small size, lancet shape, absence of distinct cone at the anterior end, no "shoulders", narrow outline. Compare with Fasciola hepatica
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Paramphistomum cervi
The rumen fluke of sheep and cattle. Note the thick, circular fleshy character of the specimens in the bottom of the jar. Also the flukes buried in the rumen papillae.

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Paragonimus kellicotti
This trematode occurs in the lungs of dogs, cats, and wild carnivores and is found in fibrotic lung cysts. The second intermediate host is a crayfish. (What is the first intermediate host?)
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Paragonimus kellicotti - Eggs

These are large yellowish-brown operculated eggs that are found in the feces (or demonstrated in the sputum). They measure 75-118 u X 42-67 u and have a marked "shoulder" or "ridge" surrounding the operculum. .

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Heterobilharzia americana
Adult worms from the mesenteric veins of a dog. The male is the larger of the two, and has the gynaecophoral groove where the female resides following mating. Separate sexes are the distinguishing feature of the schistosomes.
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Review Question: The worms at the left were recovered from the bile duct of a deer in upper New York state. A. Identify the worms (Genus and species) B. How did the deer acquire the infection? CLICK HERE FOR THE ANSWER
Comments: please e-mail Dr. Nolan at parasit@vet.upenn.edu
Laboratory 7
CESTODES AND ACANTHOCEPHALANS
Click on the text below to jump down to the desired section of this page. Diphyllobothrium latum Spirometra mansonoides Mesocestoides Dipylidium caninum Taenia taeniaeformis Taenia pisiformis Cysticercus of Taenia Taenia multiceps Echinococcus granulosus Echinococcus multilocularis Taenia sp. egg Anoplocephala Moniezia Macracanthorhynchus hiridinaceus Review question
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Diphyllobothrium latum
(Cestoda: Pseudophyllidea) Segments of the broad fish tapeworm of man and dogs.
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Diphyllobothrium latum - eggs

Note the light brown color, shape, size (approximately 60 X 45 microns), and they are operculated (the operculum is indistinct in a fresh preparation). The eggs are not embryonated when passed in the feces.
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Spirometra mansonoides
(Cestoda: Pseudophyllidea) Portions of an adult worm. Note the line of brown spots going up the center of the worm. These are the uteri of the proglottids filled with brown eggs. Eggs . (not segments) are found in the feces. From the small intestine of a cat.
Mesocestoides - gravid proglottid

(Cestoda: Cyclophyllidea) Uterus lies in the mid-line of the proglottid. The eggs pass from this to be stored in the parauterine organ which can be seen as a thick-walled structure at one end of the proglottid.
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Mesocestoides sp.
Tetrathyridia removed from the peritoneal cavity of a dog. Note the size, and gross appearance (resemble "cream of wheat" particles).
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Dipylidium caninum proglottid

(Cestoda: Cyclophyllidea) Found in the small intestine of the dog, cat, and occasionally man. Note the two sets of reproductive organs in each segment. The gravid segments contain numerous "egg packets", the other reproductive organs having degenerated.
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Dipylidium caninum - egg packets

The egg packets contain 15-20 eggs in each and are seldom seen free in the feces. They may, however, be readily expressed from the gravid proglottids.
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Cysticercoid
This tapeworm larval stage is found in arthropods. It is the metacestode stage of Dipylidium caninum, Anoplocephala spp., and Moniezia spp.
Taenia taeniaeformis - adults

(Cestoda: Cyclophyllidea) This is known as the "broad necked' tapeworm of cats. The neck is almost as broad as the scolex and segmentation begins immediately behind the scolex.
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Strobilocercus
This is the larval stage of Taenia taeniaformis which has been removed from the intermediate host (a mouse).
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Taenia taeniaeformis - Strobilocercus

Note the pea-sized nodules containing the larval worms embedded in the liver. These are young larvae and the protoscoleces are still invaginated.
Taenia pisiformis - Adult

(Cestoda: Cyclophyllidea) Adult from the small intestine of a dog. Note the lateral genital pore on the gravid proglottids and how it alternates sides irregularly.
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Cysticercus
This is the larval stage of members of the genus Taenia. Note in this specimen the protoscolex is everted. Normally it would be found inside of the "bladder".
Taenia crassiceps
(Cestoda: Cyclophyllidea) Cysticercus of T. crassiceps (left) from the peritoneal cavity of a groundhog. (Note the fluid filled bladder with protoscolex at one end). Cysticercus of T. pisiformis from a rabbit peritoneal cavity is similar to T. crassiceps, but larger (not shown). Image on right is a bottle filled with Taenia cysticerci from the peritoneal cavity of a groundhog.
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Taenia saginata- cysticercus

(Cestoda: Cyclophyllidea) Cysticercus of Taenia saginata in the skeletal muscle of a cow. Note the pea-sized cysts.
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Taenia multiceps - coenurus

(Cestoda: Cyclophyllidea) This slide shows a cross section through the larva (coenurus). Note the many protoscolecies growing from the germinal layer.
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Echinococcus granulosus
(Cestoda: Cyclophyllidea) Note the size and number of segments in this adult tapeworm. There is a scolex, and one immature, one mature, and one gravid proglottid.
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Echinococcus granulosus
(Cestoda: Cyclophyllidea) Numerous hydatid cysts in the liver of a horse. A horse may become infected with a number of cysts at one time (each . egg ingested will result in one cyst).
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Hydatid cyst
This is the larval stage of Echinococcus granulosus. Note the thick laminated cyst wall and the fibrous host response outside the cyst wall. Also note the daughter cyst with protoscolices within the main cyst.
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Diagram of structure associated with the Hydatid Cyst.

(Intermediate stage of Echinococcus granulosus).
Echinococcus multilocularis
(Cestoda: Cyclophyllidea) This animal was infected 9 weeks ago. Note the myriad of small cysts produced by exogenous budding of the mother cysts.
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Alveolar hydatid cyst

This is the larval stage of Echinococcus multilocularis. Note the thin walls, many protoscolices, and the lack of a host response.
Taenia sp. eggs

Thick-shelled, radially striated eggs, light brown in color and measures about 34 X 38 um.
Anoplocephala magna and Anoplocephala perfoliata

(Cestoda: Cyclophyllidea) These tapeworms are found in the small and large intestine (respectively) of the horse. The intermediate hosts are . oribatid mites. Note: 1) A. perfoliata is characterized by 4 lappets, one behind each sucker. There are no lappets on A. magna. 2) A. perfoliata is smaller than A. magna.
Moniezia expansa
(Cestoda: Cyclophyllidea) Found in the small intestine of sheep (particularly lambs) and other ruminants. The scolex has 4 prominent suckers and the segments are broader than long. The . intermediate host is an orbatid mite in which the cysticercoids develop.
Macracanthorhynchus hiridinaceus
(Phylum: Acanthocephala)
Proboscis of the Thorny-Headed worm (Acanthocephala) of pigs. Note the recurved hooks on the proboscis in which assist in the anchoring of the parasite to the intestinal wall.
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Macracanthorhynchus hiridinaceus
This slide shows the eggs of the thorny-headed worm of pigs. The eggs are thick shelled (4 shells in fact) dark brown, pitted and ellipsoidal. They contain a larval stage, the acanthor.
Review question
This worm was found in a pronghorn antelope at the zoo. A. Based on the shape of the proglottids (wide and short) to what family of ruminate cestodes are they related? B. What do you expect the eggs to look like? Click here for answer
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Laboratory 8 THE ARACHNIDS
Click on the text below to jump down to the desired section of this page. Ornithonyssus sylvarium Pneumonyssus caninum Cheyletiella parasitivorax Psorptes sp. Chorioptes bovis Otodectes cyanotis Sarcoptes sp. Notoedres cati Knemidocoptes sp. Demodex sp. Argas persicus Otobius megnini Ixodes sp. Haemaphysalis sp. Amblyomma americanum Dermacentor variabilis Rhipicephalus sangiuneus Review Question

Card 9:1
Ornithonyssus sylvarium"The northern fowl mite"

Here you see masses of eggs, adults, larvae and nymphs in the feathers of a leghorn pullet which died from blood loss. This parasite is extremely common in this area. It is very capable of transferring from wild birds into the chicken houses and is transferred from farm to . farm when eggs are collected. Once in a "chicken" house, it is more successful than Dermanyssus gallinae, the "red mite of poultry", in that its entire life cycle can occur on the host, but it also has the option of being a temporary parasite.

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Pneumonyssus caninum
Predilection site: Nasal cavity and sinuses. Distribution: USA, Hawaii, Australia, S. Africa. Effects: From none to hyperemia of mucosa, sneezing, shaking of head, nose rubbing. Note:
. 1. Pale color (yellow-white when alive) 2. Well-developed legs (large for the body size) terminated by claws 3. Size: 1 - 1.5 X 6 - .9 mm 4. Palps have 5 segments 5. Very small chelicerae (mouth parts)
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Cheyletiella parasitivorax "Rabbit Mite"

Note the oval body with a "waist" at mid-section, the stylet-like chelicerae and the large palps with pincers
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Psorptes ovis spp.

Note that the legs are elongated, coxae II and III are widely separated as in Sarcoptes, the segmented pedicles are present on the 1st, 2nd, and 4th pairs of legs but absent from the 3rd pair of legs.
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Psorptes sp.
Note that the pretarsal sucker is on a segmented stalk. A: Pretarsus B: Segmented stalk
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Psorptic mange
Ear of rabbit

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Chorioptes bovis
Note the ribbon-like setae on the anal tubercles; the copulatory suckers and the bell-shaped suckers on the first three pairs of legs. Note also that unlike Otodectes the anterior epimeres run more or less parallel. (Yellow arrow points to an epimere).
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Otodectes cyanotis
"The auricular mite" of dogs and cats Note the general outline and the fact that the epimeres (the grooves in the cuticle which extend from the base of each leg) converge toward each other.
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Sarcoptes scabei
Note the globular body shape, coxae II and III are widely separated, the simple, stalked pedicel and the suckers on 1st and 2nd pairs of legs. Also note the presence of long trailing setae.
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Sarcoptes sp.
Note that the pretarsal sucker is on a non-segmented stalk. (PLEASE DO NOT MOVE THE SLIDE)
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Sarcoptic mange
Leg of fox.

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Notoedres cati
Similar to Sarcoptes but considerably smaller and more globose. Anus postero-dorsal in position.
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Head of Cat with Mange

This cat was suffering from infection with burrowing sarcoptid Notoedres cati. Like Sarcoptes sp. this mite lives in the skin, burrows, and causes thickening of the skin and loss of hair. A skin scraping examined under the microscope would . show the mite.

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Knemidocoptes sp. The "scaly-leg" mite of chickens

Compare with Sarcoptes sp. and Notoedres sp. Note the absence of scales and spines on the dorsal surface. The tarsal segments have claw-like structures and tactile hairs instead of pediculated . suckers.

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Demodex sp.
Note the elongate shape, composed of: the head, the thorax bearing 4 pairs of stumpy legs, and the cigar-shaped abdomen. Also note the annular rings on abdominal cuticle. The top picture is the adult, the bottom picture is the egg. PLEASE DO NOT MOVE
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Argas persicus
Note: 1. The oval shape of the tick 2. The scutum is lacking in the family ARGASIDAE 3. The mouth parts are ventral on the body 4. The cuticle has a leathery texture

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Otobius megnini
"The spinose ear tick" Note: ARGASIDAE characters Spines on dorsum Mouth parts on ventral surface of body

Card 9:18
Ixodes scapularis - Adult

Note the posteriorly directed spine on 1st coxa (Fig. 6) and pre-anal groove (yellow arrow). The genital pore is present and . there are no festoons on the posterior margin of the body.
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Ixodes scapularis - Nymph

This is the stage most commonly encountered on middle-sized mammals (dogs and cats) and on humans. During lab (not seen in these pics), note the convergent palpi. The coxal spine is not as elongate as in the adult and the genital pore is absent (sexually immature).

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Haemaphysalis sp. Females and Nymphal Stages

Note the characteristics of the genus, especially the 2nd palpal segment which is laterally produced.
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Amblyomma americanum
"The Lone Star Tick" Males and Females Note the ornate scutum with a central white mark on the female and the long mouth parts (the 2nd palpal segment is elongated). The eyes are on the lateral margin of the scutum.
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Dermacentor variabilis
Examine specimens for characters of genus. Especially note the rectangular basis capitulum and the palpal segments of more or less uniform length and shape. Also note the coxae on the ventral aspect of the males: Coxae I are deeply cleft. Coxae IV are larger than coxae I.
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Rhipicephalus sanguineus
The "Brown Dog Tick" Note: 1. The anal groove surrounds the anus posteriorly. 2. The hypostome and palpi are short. 3. There is a marked hexagonal angulation in the basal part of the basis capituli. 4. Festoons are present along the posterior margin.
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5. In the genus Rhipicephalus all of the coxae are of approximately the same size.

Card 9:24
Review Question
The specimen in the dish was removed from the skin of a dog in southern Montgomery County, PA. A. Identify the specimen to Genus B. Knowing the ticks that occur commonly on dogs, . would your identification lead you to caution the clients about any public health concern? Click here for answer
Laboratory 9 INSECTS OF VETERINARY IMPORTANCE
Click on the text below to jump down to the desired section of this page. Simulian spp. Tabanus spp. Gasterophilus spp. Lucilia, Sarcophaga and Calliphora adults Wing veins Antenna of Cyclorrapha Oestrus ovis Cuterebra Hypoderma Melophagus ovinus Ctenocephalides spp. (fleas) Trichodectes canis Damalina caprae Linognathus setosus Hematopinus spp. Phthirus pubis Pediculus humanus Review Question

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Simulium spp. "Black Fly"

Eggs
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Simulium spp.
A) Under the microscope is an early larval stage. 1) It is cylindrical 2) It has a posterior sucker-like organ armed with hooks. It is used as a holdfast to anchor the larva in fast moving streams. 3) It has an anterior pair of mouth brushes. 4) The ventral proleg is armed with hooks on its anterior end. It is used to migrate in "inchworm" fashion. B) Compare the size of this early larval stage with a later larval stage in the dish next to the microscope.
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Card 8:3
Simulium spp.
PUPA A) It is enclosed in a cocoon which is spun by the salivary glands of the last larval stage. B) It is an exarate pupa, that is, it is not covered by the 3rd larval skin. (eg. Simulium, Tabanus, Culicoides). A pupa covered by the hardened 3rd larval skin is known as a coarctate pupa. (eg. Cyclorrhapa). C) It has respiratory filaments on the anterior end.
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Simulium spp.
A) The humpbacked appearance. B) The multisegmeted antennae. C) Short proboscis.
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Tabanus
Wing veins are important in identifying flies; however, you are not responsible for knowing the different wing vein patterns. But you should know the antenna types.
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Card 8:6
Tabanus spp.
LARVA Note the fleshy tubercles on each segment.
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Gasterophilus intestinalis and G. nasalis

Distinguish between the larvae using the key provided (figure #5 in lab book).
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Gasterophilus intestinalis
Larvae attached to the mucosa of the stomach of a horse. You can see lesions where the larvae have detached. Note the rings of inflammatory thickening with eroded centers where the larvae were . attached.
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Gasterophilus sp.
Left: egg on the hair of a horse leg. Right: bottle filled with horse hairs and attached eggs.
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Gasterophilus sp.
Adult

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Lucilia, Sarcophaga, and Calliphora adults

See lab handout.

Card 8:13
Wing veins are important in identifying flies; however, you are not responsible for knowing the different wing vein patterns. But you should know the antenna types.
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Card 8.13A
Cyclorrhapha: Fly head (enface) Note the typical club-shaped antennae laying in the groove between the eyes.

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Oestris ovis larvae - sheep nasal bot

These were removed from the nasal cavities and frontal sinuses of sheep at New Bolton Center on post-mortem examination at the beginning of March. Note: 1. Shape and size 2. Large black oral hooks 3. Posterior spiracles 4. Morphology of spiracular plate 5. Bands of spines on the ventral surface 6. As the larvae matures it develops the brown bands on the dorsal surface of its segments.

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Cuterebra larva
This is a mature larva which would be found in a dermal pocket in the host. Note: 1. The dark color of the mature larva. 2. The larva is covered with spines. 3. Morphology of spiracular plate.

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Leather damage due to Hypoderma

This piece of leather shows the lesions following the emergence of Hypoderma sp. larvae from the back of a bovine. When the lesions heal, light spots which . are scars form. The scars lower the price received for the hide.
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Hypoderma sp. - Mature larvae

H. bovis 28 mm Barrel shaped Spiracle plates ear shaped, surface depressed, opening narrow, spiracle button small. Ventral surface of penultimate segment unarmed. H. lineatum 25 mm Thinner, more pointed at ends Spiracle plates kidney-shaped. Surface level, opening wide, spiracle button well defined. Ventral surface of penultimate segment armed with spines

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Melophagus ovinus - sheep ked

(Fam: Hippoboscidae) Collected from lambs at New Bolton Center Note: 1. This is a wingless fly (order: Diptera). 2. Strong legs 3. Sac-like abdomen The adults live in the wool of sheep. The female lays mature larvae and cements them to the wool. The larvae immediately pupate. The adults irritate sheep by their bites and soil the fleece with feces and blood. Wool is damaged when the sheep scratch and rub themselves.
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Card 8:19
Flea Life-Cycle
Egg - larva - pupa - adult
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Ctenocephalides felis - larvae

These larvae are free-living. Live larvae may have a red color from feeding on the adult flea's feces and dried blood. Note the tuft of strong bristles at the posterior end.
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Ctenocephalides felis - the cat flea

The cat flea, the dog flea, and the human flea can act as intermediate hosts for Dipylidium caninum. The larval stage of the flea becomes infected eating D. caninum eggs, and cystercercoids then develop within the flea. The final host (dogs, cats, man) acquire the infection by swallowing the infected adult . flea. Note: 1. The head is longer (less blunt) than that of the dog flea, C. canis. 2. The first two spines on the genal ctenidium are almost the same size.
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Ctenocephalides canis
Note: General structure - head, thorax, abdomen and 3 pairs of legs. Presence of both genal and pronotal ctenidia (combs). Short first tooth on the genal ctenidium. The head is more rounded than that of C. felis.

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Trichodectes canis- biting louse of dogs

Note: General structure - Head, thorax, abdomen dorsoventrally flattened -Three pairs of legs with 1 claw at the end of each leg - Antennae extend laterally from head (Suborder Ischnocera) . - Head: anterior end is broad and flat: characteristic of the biting lice

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Damalinia caprae
Adult on goat hair This louse belongs to the suborder Ischnocera (see the characteristics of Trichodectes canis).

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Linognathus setosus - Nit (egg)

Egg glued to the hair of a dog.
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Linognathus sp.
Sucking lice of this genus are found on cattle, goats, sheep and dog.

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Haematopinus spp. - sucking louse

Note: General structure - Head, thorax, abdomen dorsoventrally flattened - Three pairs of strong legs each with a claw - Antennae extend laterally from head - 5 segments
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- Narrow, pointed head with recessed stylets (adapted for sucking).

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Phthirus pubis - crab or pubic louse of humans

- a sucking louse (Anoplura). Note: 1. Head bearing antennae 2. Thorax with 3 pairs of legs. (The first pair of legs is slender compared to the others.) 3. Broad abdomen.
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Pediculus humanis head or body louse of humans

- a sucking louse (Anoplura) Note: 1. The body is longer than that of Phthirus pubis. 2. Head bearing antennae 3. Thorax with 3 pairs of legs 4. Oval abdomen The nymphs are smaller but have a very similar structure to the adults.

Card 8:30
Review Question
This louse was removed from a dog that had tapeworm segments in its feces. A. Identify the louse (be specific as possible). B. Could the dog have gotten the tapeworm from this louse? Click here for answer
Laboratory 10 THE PROTOZOA
Click on the text below to jump down to the desired section of this page. Entamoeba histolytica Giardia sp. Trichomonas muris Trypanosoma brucei Leishmania donovani Babesia canis Haemoproteus columbae Leucocytozoon smithi Eimeria spp. Isospora spp. Sarcocystis sp. Toxoplasma gondii Cryptosporidium parvum Review Question

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Entamoeba histolytica - trophozoite

Note the single, spherical, vesicular nucleus (containing an endosome). The cyst is the diagnostic stage in monkeys and humans, but are almost never seen in infected dogs. In dogs the trophozoite is the diagnostic stage.
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Giardia - cysts
Cysts measure about 10 to 12 um in length and each contains two to four nuclei, an axostyles and a median body.
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Giardia - trophozoites
This trophozoite was found in the watery feces of an infected dog by a direct smear. Normally only cysts are found in the feces. Note the shape (pear shaped), and the size (10 to 18 um in length). The internal organelles are doubled (i.e. two nuclei, 2 median bodies, etc.) and there are 8 . flagella.

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Trichomonas muris
This flagellate is similar in appearance to T. foetus of cattle. Note the undulating membrane and free flagella.

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Trypansoma brucei
Pathogenic trypanosome of domestic animals in tropical Africa. Note the nucleus, kinetoplast, undulating membrane and the free flagellum.
Card 10:5a
Leishmania donovani
This slide is a tissue impression of the spleen (stained with Giemsa) of an infected dog. The spleen cells have ruptured during the making of the slide, leaving behind nuclear material (green arrows). The Leishmania amastigotes however are too small to be effected by the forces that ruptured the spleen cells so they remain intact (yellow arrows). Note the nucleus and kinetoplast that are present in each amastigote.

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Babesia canis
The trophozoites are pyriform and 4 to 5 um long, or amoeboid 2 to 4 um in diameter. They generally contain a vacuole and multiple infection of the erythrocytes is common.
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Haemoproteus columbae
This blood smear shows a gametocyte which is wrapped around the nucleus of an erythrocyte (which is not distorted). Remember that the schizonts are not found in the blood cells.
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Leucocytozoon smithi - gametocyte

This slide shows a typical gametocyte which has distorted the white blood cell into an elongate, elliptical body. Little evidence of the white blood cell morphology remains. Note that no schizonts appear in the blood.
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Eimeria tenella
These are sporulated oocysts, note that each contains 4 sporocysts each with 2 sporozoites.
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Eimeria tenella
This slide shows the 2nd generation schizonts E. tenella. In this species the 2nd generation schizont is large and subepithial in position. Note the many merozoites within the mature schizonts.
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This illustration shows the lesion site of E. tenella in the chicken - the ceca. The top image shows the swollen, thickened ceca found in an affected chicken, and the bottom illustration shows the location of the caeca in the intestinal tract. Diagnosis of coccidiosis in poultry is done by showing the presence of oocysts in the feces or other stages in the intestinal epithelium. Species identification is made by determining the location and type of lesions in the intestine.
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Eimeria sp.
Unporulated oocyst from the feces of a goat. Note the thinning of the wall (arrows) at one pole of the oocyst - this is the micropyle.
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Eimeria sp.
This is a cross section of the intestine of a goat infected with Eimeria sp. This section shows the gametes in the epithelial cells. The majority of these gametes are macrogametes (female). The small granules within the macrogametes are assumed to form the oocyst wall after fertilization has occured.
Card 10:12a Isospora felis oocyst (blue arrow, unsporulated, about 40 m) and a sporulated Isospora rivolta oocyst (red arrow, about 20 m). The oocyst of I. canis (dog) looks like that of I. felis (cat) and the oocyst of I. ohioensis (dog) is similar to that of I. rivolta (cat). .

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Sarcocystis sp.
This is a sporocyst recovered from the feces of a dog.
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Sarcocystis sp.
A mature cyst in the muscle of the intermediate host.

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Toxoplasma gondii
Sporulated and unsporulated oocyst. Oocysts sporulate within 48 hours after being passed from the cat. Note the small size (9 to 14 um) and the round shape.
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Toxoplasma gondii
The tachyzoites are elongate and crescent-shaped. They measure 4 to 6 um in length.
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Toxoplasma gondii
Note that this cyst contains many bradyzoites.
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Toxoplasma gondii
Schizonts in the intestinal cells of a cat. Note the tachyzoites radiating from the center of the schizont.

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Cryptosporidium parvum
This is a fecal smear stained by the acid fast technique. The oocysts are acid-fast and therefore stain red. Yeasts (which are about the same size as the oocysts, 5 um) stain a light blue or green (depending on the counter-stain used).
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Review Question
This slide shows the result of a zinc sulfate flotation of a fecal sample from an asymptomatic kitten. The object shown is 14 X 9 um. A. Identify the parasite (Genus only). B. The client's dog ate some of the kittens's feces just before this sample was collected from the litter box. Is the stage seen on this slide (red arrow) infectious to dogs? Click here for answer
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Amprolium
Chemical group: thiamine analog Trade names: Corid, Amprol Mode of action: thiamine analog, competitively inhibits the active transport of thiamine. The coccidia are 50 times as sensitive to this inhibition as is the host. Pharmacokinetics: Freely soluble in water. Dose: In dogs and cats: "extra label use": 300 to 400 mg/kg, SID for 5
days or 110 to 220 mg/kg SID for 7 to 12 days.

In chickens: For prevention of coccidiosis: 36.3 - 113.5 g/ton in the feed or in the drinking water at 0.012%. No withdrawal is needed. Toxicity: May cause thiamine deficiency if given at high rates. Parasite Targets: Isospora in dogs and cats, Eimeria in cattle and poultry.
Butamisole hydrochloride
Chemical group: Imidazothiazole Trade names: Styquin (no longer sold in the United States) Mode of action: Probably similar to other imidazothiazoles, i.e.: Acetylcholine agonist and depolarizing neuromuscular blocking agent Pharmacokinetics: ? Dose: 2.4 mg/kg (SC) Use in dogs over 8 weeks of age. Toxicity: Incoordination, emesis, tremors, convulsions, and death were seen in dogs given 3 to 4 times the recommended dose. LD50 in dogs is 11.25 mg/kg Parasite Targets: Trichuris vulpis, Ancylostoma caninum
Clindamycin
Chemical group: Trade name: Lincosamide antibiotic Antirobe
Mode of action: Binds to ribosomes in bacteria, in protozoa it is linked to the loss of the 35 kb plastid DNA which is necessary for production of the vacuole in which the parasites lives. (ME Fichera & DS Roos. 1997. A plastid organelle as a drug target in apicomplexan parasites. Nature 389:407-409.)
Pharmacokinetics: Rapidly absorbed from the gut, binds to plasma proteins, partially metabolized in the liver, exits body in urine and bile (feces). It will pass in the milk. Dose: Dogs: T. gondii: 10 to 40 mg/kg/day (PO) divided TID or QID. Babesia spp.: 25 mg/kg (PO) divided BID until cured or immunity develops. Cats: 25 mg/kg divided BID or TID for 28 days (PO)
Toxicity: Dogs tolerated 300 mg/kg daily for up to a year. Dogs receiving 600 mg/kg/day developed anorexia and vomiting. Parasite Targets: Toxoplasma gondii, Babesiaspp.
Dichlorvous
Chemical group: Organophosphate Trade names: Task Mode of action: Cholinesterase inhibitor Pharmacokinetics: Rapidly metabolized and excreted. Dose: 10 to 12 mg/kg (PO) Use in dogs and cats over 2 weeks of age and over 2 lbs. Toxicity: Minimum toxic dose in horses and sheep is 25 mg/kg. LD50 in dogs is between 28 and 45 mg/kg for drug grade, the LD1 for formulated Dichlorvous is 182 mg/kg.. Parasite Targets: Ascarids, hookworms, and Trichuris vulpis.
Diethylcarbamazine
Chemical group: Piperazine Trade names: Nemacide Mode of action: GABA agonist, causes hyperpolarization of nerve membrane and flaccid paralysis of the nematode, worms are removed by normal peristalsis. Pharmacokinetics: Rapidly absorbed from the gut and excreted in the urine. Elimination is virtually complete by 48 hours. Eliminated through the urine as metabolites. Dose: 11.4 to 22.7 mg/kg (25 to 50 mg/lb), PO. Toxicity: Shock-like reactions in dogs with circulating microfilaria. Vomiting common when given on an empty stomach. LD50 in rodents is 660 mg/kg (mice) and 1380 mg/kg (rats). Parasite Targets: Ascarids
Disophenol Sodium
Chemical group: Trade name: Mode of action: Substituted phenol DNP - no longer being sold in the United States Uncoupler of oxidative phosphorylation Binds to red blood cells, has a half life in the dog of about 2
Pharmacokinetics: weeks. Dose:
9 mg/kg (SC) in dogs and cats
Toxicity: Narrow safety range. Blindness, hyperventilation, convulsions, and death are seen with overdoses. Parasite Targets: Hookworms, Spirocerca lupi
Epsiprantel
Chemical group: Trade name: Isoquinoline-pyrazine Cestex
Mode of action: Unknown, may interfere with calcium metabolism leading to detachment and disruption of the tegument. Pharmacokinetics: compound. Dose: Poorly absorbed from gut. Leaves host in feces as parent
Cat: 2.75 mg/kg (Use in cats over 7 weeks of age.) Dog: 5.5 mg/kg (Use in dogs over 7 weeks of age)
Toxicity: Minimum lethal dose in rats was greater than 5000 mg/kg. No adverse reactions seen in kittens given 29.9 mg/kg and none in puppies given 100 mg/kg. Parasite Targets: Tapeworms
Febantel
Chemical group: Trade name: Mode of action: Pro-benzimidazole Drontal Plus* Binds to tubulin subunit and interferes with microtubule formation
Pharmacokinetics: Metabolized in the liver to fenbendazole, oxfendazole, oxfendazole sulphone and at least 7 other metabolites. These may circulate in the blood, but most leave in the bile. Dose: 25 mg/kg (PO) (Drontal Plus) one dose (3 doses (SID) for Giardia),
Toxicity: Acute toxicity: LD50 in dogs is over 10,000 mg/kg. Oxfendazole is teratogenic in rats and sheep. Parasite Targets: Ascarids, hookworms, Trichuris vulpis., Taenia sp., Giardia sp.
* also contains pyrantel pamoate and praziquantel
Fenbendazole
Chemical group: Trade names: Mode of action: benzimidazole Panacur Binds to tubulin subunit and interferes with microtubule formation.
Pharmacokinetics: Poorly absorbed from the gut, most leaves the dog in the feces as fenbendazole, some is metabolized to oxfendazole, probably in liver, and returns to gut in bile. Totally eliminated in 48 hours. Dose: 50 mg/kg, (PO) SID, for 3 days. For Giardia use for 5 days. Use in dogs and cats (use in cats is prohibited in some countries like the US) over 2 weeks of age. Toxicity: Toxic dose not found. 500 mg/kg not toxic in a single dose. 250 mg/kg daily for 30 days was not toxic to dogs. Parasite Targets: Ascarids, hookworms, Trichuris vulpis, Aelurostrongylus abstrusus, Capillaria sp., Strongyloides sp., Filaroides sp., Taenia sp., Paragonimus kellicotti, Giardia sp.
Imidocarb dipropionate
Chemical group: N,N'-bis (3-(4,5-Dihydro-1H-imidazol-2-yl)phenyl) urea Trade names: IMIZOL Mode of action: May interfere with polyamine synthesis and function. Pharmacokinetics: In dogs given an intravenous bolus, the plasma half-life was 207 min and 80% was eliminated in 8 hours. Residues were found mainly in the liver and some in the kidney (it seems to be eliminated through the urine and feces.) Dose: 6.6 mg/kg, 2 doses, 2 weeks apart, IM or subcutaneous injection. Toxicity: LD50 in rats was 450 - 1200 mg/kg. Safe in dogs up to 9.9 mg/kg. Causes pain upon injection. Acute toxicity symptoms are consistent with a cholinesterase inhibitor activity. Parasite Targets: Babesia spp.
Ivermectin
Chemical group: Trade names: Cats, Ivomec, etc. Avermectin, (Macrocyclic Lactone) Heartgard 30, Heartgard Plus*, Iverheart Plus, Heartgard for
Mode of action: Binds to glutamate gated chloride channels in the parasites nervous system, causing them to open. Pharmacokinetics: Rapidly absorbed from the gut, less rapidly from a subcutaneous site. Leaves the body in the feces as ivermectin. Half life in dogs is about 24 to 36 hours. Dose: For heartworm prevention:
Dogs: 0.006 mg/kg (PO), given monthly, in puppies 6 weeks of age and older. Higher doses not recommended for puppies. Cats: 0.024 mg/kg (PO) given monthly. For other nematodes and for mites: 0.2 to 0.4 mg/kg (PO [SQ in cats]), repeat as needed. Pigs: 10mg /75 lb body wt. Toxicity: In collies, Australian sheepdogs and some collie mixes: toxic signs (lethargy, ataxia, coma) appear above 0.1 mg/kg. In other dogs, toxic signs are seen at doses at and above 0.8 mg/kg. (Cats probably about the same as dogs). Subcutaneous administration of horse, pig and cattle preparations to dogs or cats may cause local problems due to the vehicle. Parasite Targets: and mites. Heartworm L4, most nematodes (except adult heartworms2),
1. Heartgard Plus also contains Pyrantel Pamoate 2. Prolonged monthly use may shorten the life span of the adult heartworm.
Mebendazole
Chemical group: benzimidazole Trade name: Telmintic Powder Mode of action: Binds to tubulin and interferes with microtubule formation. Pharmacokinetics: Poorly absorbed, thus action limited to gut. Dose: 22 mg/kg (PO), SID, for 3 days. Toxicity: Acute toxic dose not found (above 1000 mg/kg in dogs and cats). Parasite Targets: Hookworms, Ascarids, Trichuris vulpis, Physaloptera sp. (Stomach worm in dogs), Taenia sp., Echinococcus granulosus.
Melarsomine dihydrochloride
Chemical group: arsenical Trade name: Immiticide Mode of action: Unknown, presumably due to the arsenics effect on glycolysis. Pharmacokinetics: Absorbed very rapidly from the injections site, some metabolites and the parent compound are eliminated in the bile and other metabolites are passed in the urine. The drug is rapidly cleared from the body. Dose: 2.5 mg/kg (IM) twice, 24 hours apart. (Dogs with class 3 disease should receive one dose and allowed to recover for a few months before receiving the complete set of 2 doses.) Toxicity: LD50 in rats (IM) was 24 to 33 mg/kg, some mortality seen in dogs given 7.5 mg/kg. Injection site reactions are common, as are lethargy, vomiting and anorexia. (A 10% death rate can be expected in dogs with class 3 disease when 2 doses are given initially.) Doses between 2.5 mg/kg and 2.7 mg/kg were fatal to Heartworm infected river otters (Lontra canadensis) and red pandas (Ailurus fulgens fulgens) [Neiffer, et al., 2002, J. Zoo. Wildl. Med 33(3)242-248]. Parasite Targets: Heartworm adults
Metronidazole
Chemical group: 5-nitroimidazole Trade name: Flagyl Mode of action: Reduced in anaerobic organisms to reactive metabolites which release superoxide anions. Pharmacokinetics: Rapidly and completely absorbed from gut. Some returns to the gut in the bile and through the colon, most is excreted in the urine. Will pass in the milk. Dose: 30 mg/kg, SID, for 5 days (PO) Toxicity: Dog can tolerate doses of 100 mg/kg per day for a month. Higher doses produce neurological signs (tremors, ataxia, etc.) Parasite Targets: Giardia spp., Trichomonas spp.
Milbemycin Oxime
Chemical group: Macrocyclic lactone Trade names: Interceptor, Sentinel* Mode of action: Opens chloride channels in the nerve cells. Pharmacokinetics: Rapidly absorbed from the gut. Cleared from blood by 120 hours. Dose: 0.5 mg/kg (PO). Use in dogs over 4 weeks of age (Interceptor). Toxicity: Toxic dose is above 10 mg/kg. Parasite Targets: Heartworm L4, most nematodes (except adult heartworm and Uncinaria stenocephala), some mites.
* Sentinel contains Milbemycin and Lufenuron
Moxidectin
Chemical group: Macrocyclic lactone Trade name: ProHeart, ProHeart6 Mode of action: Probably works like other macrocyclic lactones and opens chloride channels in the nerve cells, causing paralysis. Pharmacokinetics: Dog: ProHeart6: Peak blood levels by 7 to 14 days post-injection, by 6 months post-injection little drug remains in the dog. Dose: Dog: ProHeart: 3 g/kg, once a month, (PO). For use in dogs over 8 weeks of age. ProHeart6: 0.17mg/kg, [microspheres] once every 6 months (SQ) For use in dogs over 6 months of age. Toxicity: Dog: Safe at up to 5 to 10 times the recommended dose, in a collie given 30 times the recommended dose, ataxia, salivation and mild depression were seen. Parasite Targets: Dirofilaria immitis L3 and young L4. ProHeart6 will kill hookworms for up to 2 weeks after it is injected.
Nitazoxanide
Chemical group: benzamide Trade names: Navigator (Idexx Pharmaceuticals, Inc.) Mode of action: Target organisms are able to reduce nitazoxanides nitro group to a toxic free radical which interferes with cellular respiration. Pharmacokinetics: Given a single 22.72mg/lb dose: Cmax = 0.51 ppm, Tmax = 2.13 hr. The active metabolite (deacetynitazoxanide) is undetectable in plasma by 24 hrs post dosing. Dose: 11.36 mg/lb once a day on days 1 to 5, then 22.72 mg/lb once a day on days 6 to 28. Toxicity: A single dose at 5X the regular dose lead to transient depressed appetite, loose stools and lethargy for 11 to 14 days post treatment. Multiple (4) 5X doses lead to the death of 5 of 8 horses. The drug can disrupt the normal microbial flora of the GI tract leading to enterocolitis even at the normal dose. It is important to monitor the horse for adverse signs during the course of treatment. Parasite Targets: Sarcocystis neurona in horses. (The above information came from the Navigator package insert)
Piperazine
Chemical group: Piperazine Trade names: Pipa-tabs, Tasty Paste, WRM Rid, etc. Mode of action: GABA agonist, causes hyperpolarization of nerve membrane and flaccid paralysis of the nematode, worms are removed by normal peristalsis. Pharmacokinetics: Rapidly absorbed from the gut and excreted in the urine. Elimination is virtually complete by 24 hours. Dose: About 60 mg/kg of piperazine base, actual dose varies with the salt. (100 mg/kg of piperazine adipate) (PO). Use in animals over 6 weeks of age. Toxicity: Acute oral: About 800 mg/kg. Signs: Depression, hind leg weakness or incoordination. Side effects apparently common in cats and dogs. Will kill microfilaria, therefore not safe to use in microfilaria positive dogs. Parasite Targets: Toxocara spp., Toxascaris leonina
Praziquantel
Chemical group: Acylated quinoline-pyrazine Trade names: Droncit, Tape Worm Tabs, Drontal1, Drontal Plus2 Mode of action: Modulates cell membrane permeability (calcium dependent), leads to a disintegration of the tapeworms tegument. Pharmacokinetics: Rapidly absorbed from the gut, metabolized in the liver, metabolites and unchanged parent compound pass out in the feces. Dose: Cyclophyllidean Tapeworms: 3 to 5 mg/kg (PO or SC) Pseudopyllidean Tapeworms: 35 mg/kg (SC)3
Intestinal Trematodes: 30 mg/kg (PO) Lung flukes in dogs: 25 mg/kg, TID for 2 days. 4
Toxicity: LD50 in rats is between 2000 and 3000 mg/kg. No clinical effects seen in dogs or cats dosed with 100 mg/kg. Parasite Targets: Tapeworms and trematodes.
1. Drontal contains Praziquantel and Pyrantel Pamoate. 2. Drontal Plus contains Praziquantel, Pyrantel Pamoate and Febantel. 3. Sakamoto, T. 1977. Veterinary Medical Review. 1:64-74. 4. Kirkpatrick and Shelly. 1985. Journal of the American Veterinary Medical Association. 187(1):75-6.
Pyrantel Pamoate, Pyrantel embonate

Chemical group: Imidazothiazole Trade names: Nemex II, Strongid T, Pyratabs, D-Worm, Evict Liquid wormer, Sure Shot, Drontal1, Drontal Plus2, Heartgard Plus3, etc. Mode of action: Acetylcholine agonist and depolarizing neuromuscular blocking agent. It produces rigid contraction of the muscles. It appears to act on the nerve ganglia and nematode muscle cell membranes. Pharmacokinetics: 40% of soluble salts (pyrantel citrate) passes in urine as metabolites, the rest passes in the feces unchanged. Most of the pamoate/embonate salts remains in the gut and will pass in the feces. Dose: 5 mg/kg (PO) Use in animals over 2 weeks of age. Toxicity: Cats: 100 mg/kg daily for 3 days produced no side effects, a single dose of 230.6 mg/kg produced vomiting and diarrhea in 2/92 cats. Dogs: Acute LD50 dose is over 690 mg/kg, dogs given 20 mg/kg daily for 3 months had no problems, although dogs given 50 mg/kg for the same length of time did have signs of toxicity. Parasite Targets: hookworms, ascarids, Physaloptera sp. (Stomach worm in cats and dogs)
1. Drontal contains Pyrantel and Praziquantel 2. Drontal Plus contains Pyrantel, Febantel and Praziquantel 3. Heartgard Plus contains Ivermectin and Pyrantel
Selamectin
Chemical group: Macrocyclic lactone Trade name: Revolution Mode of action: Binds to glutamate gated chloride channels in the parasites nervous system, causing them to open. Pharmacokinetics: Absorbed through the skin and distributed via the blood. Concentrates in sebaceous glands. Active concentrations are found in the plasma for at least 30 days. Most excreted unmetabolized in the feces, and a small amount in the urine. Dose: 6 mg/kg (topical) Use in animals over 6 weeks of age. Toxicity: Cats: 60 mg/kg (10 X dose) produced no adverse reactions when given to kittens (initially 6 wks old) for 7 monthly treatments. 18 mg/kg (3 X dose) produced no effect on reproduction in females or males and no problems in heartworm positive cats. Orally a 6 mg/kg dose caused 2 of 6 cats to vomit (probably due to the alcohol carrier). (See: Krautmann, MJ, et al. 2000. Safety of Selamectin in Cats. Vet. Parasitol. 91:393-403.) Dogs: 60 mg/kg (10 X dose) produced no adverse reactions when give to puppies (initially 6 wks old) for 7 monthly treatments. 18 mg/kg (3 X dose) produced no effect on reproduction in females or males and no problems in heartworm positive dogs (but it did reduce the levels of microfilaria to nil by the 3 rd monthly treatment). 3 monthly doses of 30 mg/kg produced no adverse effects in avermectin sensitive collies. (See: Novotny, MJ, et al. 2000. Safety of Selamectin in Dogs. Vet. Parasitol. 91:377-391). Humans: Has a 279 fold safety range. Parasite Targets: hookworms, ascarids, heartworm L3,4, fleas, ticks, scabies, Otodectes
Sulfadimethoxine
Chemical group: Sulfonamide Trade names: Albon, Bactrovet Mode of action: Folic acid synthesis inhibitor, coccidiastatic. Pharmacokinetics: Readily absorbed from the gut, eliminated in the urine (dog) or metabolized in the liver and excreted as acetylsulfadimethoxine in the bile (cat and other species). Dose: 55 mg/kg the first day, then 27.5 mg/kg, SID for 10 to 14 days (PO) Toxicity: low Parasite Targets : Isospora spp.
Thiacetarsamide sodium
Chemical group: Arsenical Trade names: Carparsolate Sodium - no longer sold in the United States Mode of action: Unknown, presumably due to the arsenics effect on glycolysis. Pharmacokinetics: Elimination half life in dogs is about 46 min, it is metabolized by the liver. Dose: 2.2 mg/kg BID for two days (IV). Toxicity: 3.7 mg/kg daily for 3 days produced serious side-effects in 1/3 of the dogs tested. Side-effects at the standard dose increase with the clinical severity of the heartworm disease. Parasite Targets: Dirofilaria immitis adults.
Diagnosis of Veterinary Endoparasitic Infections
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Cat Homepage
List of feline endoparasites

Feline parasitology Quiz
Image library of feline parasite diagnostic stages
(Felis catus)
Class : Mammalia Order : Carnivora Family: Felidae Genus: Felis Species: catus
Diagnosis Quiz
Choose a case a below to test your knowledge Quiz Case 1 Quiz Case 2 Quiz Case 3 Quiz Case 4 Quiz Case 5 Egg Quiz
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Here is a comprehensive list of canine endoparasites

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Go to an image library of canine parasite diagnostic stages
Dog (Canis familiaris)

Class : Mammalia Order : Carnivora Family: Canidae Genus: Canis Species: familiaris
Diagnosis Quiz
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Cow Homepage
(Bos taurus)
Class : Mammalia Order : Artiodactyla Family: Bovidae Genus: Bos Species: taurus
Ferret Homepage
(Mustella putorius furo)

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Class : Mammalia Order : Carnivora Family: Mustelidae Genus: Mustella Species: putorius Subspecies: furo
Goat Homepage
(Capra hircus)
Class : Mammalia Order : Artiodactyla Family: Bovidae Genus: Capra Species: hircus
Sheep Homepage
(Ovis aries) Sheep and Goat share almost the same

parasite classes to view their parasites click here
Class : Mammalia Order : Artiodactyla Family: Bovidae Genus: Ovis Species: aries
Horse Homepage
(Equus caballus)
Class : Mammalia Order : Perissodactyla Family: Equidae Genus: Equus Species: caballus
Horse parasite list
Llama Homepage
(Lama glama)
Class : Mammalia Order : Artiodactyla Family: Camelidae Genus: Lama Species: glama
Pig Homepage
(Sus scrofa)
Class : Mammalia Order :Artiodactyla Family: Suidae Genus: Sus Species: scrofa
Rabbit Homepage
(Oryctolagus cuniculus)
Class : Mammalia Order : Lagomorpha Family: Leporidae Genus: Oryctolagus Species: cuniculus
Robin Homepage
(Turdus migratorius)
Class : Aves Order : Passeriformes Family: Turdidae Genus: Turdus Species: migratorius
Loggerhead Turtle (Caretta caretta) Parasite List
Sulcascaris sulcata (Ascarid) Ozobranchus margoi (leech)
Fecal Examination Using "Ovatector" brand Fecal Float
Fecal Examination Using "Ovassay Plus" brand Fecal Float
Fecal Examination Using "Fecalyzer" brand Fecal Float
You will need Quick Time in order to view this video. The video will loop until you hit the Blood Smear Instructions button to return to the Blood Smear Page.
Note that the spreader slide is pulled up against the small drop of blood and then quickly pushed to the other end of the slide pulling the blood behind it. Also note the thin feathered edge that is left at the far end of the smear.
Ancylostoma caninum
Dictyocaulus viviparus (Directions for Use)
Dirofilaria immitis
Echinococcus granulosus (Directions for Use)
Eimeria bovis (Directions for Use)
Giardia (Directions for Use)
Haemonchus contortus (Directions for Use)
Toxocara canis (Directions for Use)
Key definitions
1. Veterinary Parasitology Veterinary Parasitology is the science that deals with the parasites of domestic animals. More specifically, it is the science that deals with the interactions between a host and the population of parasites that are found on or in that host. A more encompassing point of view, from an epidemiological perspective, would define Veterinary Parasitology as the science that deals with the interactions between host populations and the parasites that infect them. This broad definition means that Veterinary Parasitology covers many aspects of parasites of domestic animals and their hosts including: the morphology, biochemistry, physiology and life cycles of parasites, the immunological, pathological and clinical responses of the host to the presence of parasites, all aspects of treatment and control of parasitic infections and diseases and the public health aspects of parasites of domestic animals that may also infect humans. 2. Parasitism The term parasitism may be defined as a two-species association in which one species, the parasite, lives on or in a second species, the host, for a significant period of its life and obtains nourishment from it. This is a commonly accepted working definition of parasitism and using it we can emphasize several important features of the host-parasite relationship. a. Parasitism always involves two species, the parasite and the host. b. Many of these parasitic associations produce pathological changes in hosts that may result in disease. c. Successful treatment and control of parasitic diseases requires not only comprehensive information about the parasite itself but also a good understanding of the nature of parasites' interactions with their hosts. d. The parasite is always the beneficiary and the host is always the provider in any host-parasite relationship. This definition of parasitism is a general one but it tells us nothing about parasites themselves. It does not address which particular infectious organisms of domestic animals we might include in the realm of parasitology. The protozoa, arthropods and helminths are traditionally defined as parasites. However, there are members of the scientific community who designate all infectious agents of animals as parasites including viruses, bacteria and fungi. This broader definition of parasites includes viruses, bacteria and fungi as well as the arthropods, helminths and protozoa. Within this broad definition, parasites are further divided into microparasites and macroparasites. The following table summarizes their salient characteristics.
Microparasites
Macroparasites
Bacteria, Viruses, Fungi, Protozoa Unicellular or acellular organisms Usually multiply in the host so that a few infecting organisms may give rise to many in a non-immune host. Short generation time - hours or days Acute infections most commonly seen. Infected animals may succumb, may recover and show significant protective immunity or the infection may, in some cases revert to a chronic state
Arthropods, Helmi Multicellular organisms Rarely multiply in a host
Long generation time - usually w months
Chronic infections are most com acute infections may be seen in susceptible animals. Recovery infections does not necessarily protection on the host.
However, the consensus among parasitologists is to view the subjects of the discipline as including only the arthropods, helminths and protozoa.
The Spectrum of Parasitism
Parasites are an extremely varied group. They range from flies, such as the blood-sucking mosquitoes, nematodes such as the heartworm of dogs, liver flukes of cattle and sheep, fleas commonly found on dogs and cats, lice and ticks found on almost all domestic animals and protozoa such as Giardia which are found in most domestic animals but are of particular significance in cattle and dogs. The table below illustrates some of these parasites.
A female mosquito blood feeding. Mosquitoes serve as intermediate hosts of other parasites such as Dirofilaria immitis the dog and cat heartworm and Plasmodium species causing malaria in humans and birds. They are also vectors of viruses causing yellow fever and encephalitis.
A cluster of nematodes, the roundworm of dogs, Toxoca This parasite is common in puppies and may be transmi transplacentally as well as to nursing pups in their mothe This parasite has public health importance as a cause of larva migrans in man.
Fleas are common parasites of dogs and cats. They bite their hosts and feed on blood. Fleas are intermediate hosts of the tapeworm Dipylidium caninum and the filarid nematode Dipetalonema reconditum. The cat flea is a vector of feline parvovirus.
Fasciola hepatica, the liver fluke of ruminants. The para complex life cycle involving snail intermediate hosts. Mig developing flukes in the host liver provokes an intense in reaction with severe liver damage.
Hematopinus suis, the blood-sucking louse of swine is common in pigs raised indoors with transmission readily occurring from pig to pig. Infested pigs are restless and rub their skin frequently to relieve the itching.
Anoplocephala perfoliata, a tapeworm of horses, is oft clusters at the ileo-cecal junction. It is widespread in dist usually benign. However, cecal abscesses, and intussus have been reported.
The nematode Dirofilaria immitis, the heartworm has a complex life cycle involving mosquitoes as intermediate hosts. These worms are found in the cardio-pulmonary circulation and may cause severe heart disease in dogs and cats.
The protozoan Giardia is important as a cause of diarrh and cattle but is also found in other domestic animals as The trophozoite stage, shown here, attaches to the muco epithelium cells of the small intestine.
An important feature to note about parasites is that they are not equally parasitic. Parasitism is seen as a spectrum. It includes organisms at one of the spectrum that spend most or all of their lives as independent free-living creatures, seeking a host only to feed. The other end of the spectrum includes parasites that spend their entire lives in or on a host and cannot survive at any stage of their life cycles without a host. Between these two extremes we see a whole host of parasitic configurations with differing degrees of host dependency.
At one end of the spectrum, we see flies such as mosquitoes which are the least parasitic and visit their hosts only to feed. Fleas are slightly more parasitic in that they feed and often lay eggs on the host. Coccidial protozoans are even more parasitic with all the life cycle stages except two occurring inside a host. Ascaris suum, a nematode of pigs has two well defined phases to its life cycle - a parasitic phase in the swine host and a preparasitic phase consisting of three stages found free-living in the external environment. At the other
end of the spectrum, we find the lice which spend their entire lives on the hair or feathers of their hosts. Off the host they will surviv most one or two days. Dirofilaria immitis, the dog heartworm is entirely parasitic with all stages of the life cycle occurring either in th mosquito intermediate host.
Parasite Life Cycles
Despite their diversity, parasites do have some common features: all of them have unique life cycles and each major parasite group (arthropods, nematodes, cestodes, trematodes and protozoa) includes a set of well-defined and recognizable stages unique to each group. The multicellular nematodes, for example, have life cycles which include adult males and females. They reproduce sexually and eggs are laid by the female. Larvae develop, in these eggs, hatch and progress through a series of developing larval stages until they reach adulthood as sexually mature males and females and the cycle begins again. Most nematodes follow this basic life cycle pattern, although some may also include variations and additional complexities. Click here to view the life cycle of the small strongyles of horses, an uncomplicated cycle. Remember to use the back button of your browser to return to this page. Click here to view the life cycle of Dirofilaria immitis, the heartworm of dogs. This pattern is complicated by the inclusion of required intermediate hosts, mosquitos. Use the back button of your browser to return directly to this page. The protozoa are unicellular organisms. Most of them have a phase of sexual reproduction in their life cycles and also include an asexual reproductive phase. They lack recognizable male and female adult stages as we see in the nematodes but they do have male and female stages that are analogous to eggs and sperm. For example, the coccidia have the following stages in their life cycles: oocysts, sporozoites, schizonts, merozoites, microgamets, macrogametes, zygotes. In a simple coccidian life cycle, a host is infecte by an oocyst containgin sporozoites which leave the oocyst and infect host cells. Asexual multiplication occurs resulting in an intracellular schizont containing many merozoites. Asexual reproduction (schizogony) may be repeated several times and ends with the beginning of sexual reproduction. Merozoites transform into micro or macro gametocytes. Macrogametocytes are female and grow to occupy a single host cell when they are usually called macrogametes. Microgametocytes are male and divide to produce microgametes which leave the host cell in search of a macrogamete. The latter is penetrated by a microgamete, fusion of their nuclei occurs and a zygote is formed. A cyst wall is formed around the zygote resulting in an oocyst which sporulates, forming sporozoites. This sporulated occyst is the infective form for the host. Click here to view the life cycle of Eimeria bovis, a coccidian of cattle. (Use the back button of your browser to return to this page). The arthropods have different life cycles but like the others they also have distinct and recognizable life cycle stages.
A female louse lays eggs which attach to the hair or feathers of a host A miniature adult called a nymph hatches from each egg and grows to an adult. The whole life cycle takes approximately one month.
Fleas are also arthropods and although they have distinct life cycle stages they are different to those of their lice cousins. Female fleas lay eggs from which larvae hatch. Each larva metamorphoses first into a pupa which in turn transforms into an adult.
The Importance of Life Cycles
Life cycles of parasites may provide two important pieces of information. 1. Information that has predictive value with respect to the pathogenic importance of each particular parasite. 2. Information of epidemiological significance that is indispensable to developing effective control programs.
Pathogenesis If we know the migration patterns of a parasite's life cycle in its host, this information can be used to predict the parasite's involvement in disease. For example by knowing the migratory pathways of Ascaris suum in pigs we can predict where the significant pathological changes will occur. Ascaris suum larvae migrate from the small intestine (F) to the liver (G) via the hepatic portal vein and then to the lungs (H) via the heart. Knowing this, we can predict that important pathological changes will be found in the liver and lungs. Migrating larvae in the liver cause an inflammatory reaction, intralobular tissue destruction and hemorrhage. This is followed by an intense infiltration of eosinophils and collagen production. These lesions are visible at necropsy on liver surfaces as whitish areas and are commonly called "milk spots" since they resemble splashes of milk. Migration of larvae in the lungs also produces hemorrhagic lesions and intense infiltrations of eosinophils around alveoli into which larvae are migrating on their way up the bronchial tree. Repeated infections will produce more widespread hemorrhages, edema and emphysema. The image to the right shows significant hemorrhagic lesions in the apical and cardiac lobes of Ascaris- infected lungs.
The Importance of Life Cycles
Life cycles of parasites may provide two important pieces of information. 1. Information that has predictive value with respect to the pathogenic importance of each particular parasite. 2. Information of epidemiological significance that is indispensable to developing effective control programs.
Epidemiology
We can make generalizations about the epidemiology and control of many parasites from information about their life cycles, in particular the requirements for transmission. For example the strongyles of horses are transmitted directly by ingestion of infective third stage larvae from pasture while horses are grazing. The survival of these infective larvae as well as their development for eggs is controlled primarily by temperature combined with humidity. This is true, not only of the horse strongyles, but also of all nematodes with direct life cycles.
Below 8'C, horse strongyle eggs will not hatch and above 38'C, they die. The image to the right shows that between these two extremes, the proportion of eggs developing through to third stage infective larvae is directly dependent on temperature with the maximum number of L3s developing at 26'C. Not only is 26'C the temperature at which the maximum number of L3s will develop from eggs but it is also the temperature at which eggs will develop to L3s in the shortest possible time. In the case of horse strongyles this will be approximately 72 hours. % of infective stage larvae developing from viable eggs at various temperatures
As a result of this influence of temperature and moisture on the survival and development of preparasitic life cycle stages, the strongyles of horses show seasonal patterns of development in temperate areas of the world with distinct seasonal changes in weather. These effects are shown in this graph of seasonal changes in strongyle eggs in the feces of grazing horses This graph shows that maximum transmission of horse strongyles occurs in spring, summer and early fall(autumn) when temperatures are optimum for rapid development of infective L3s from strongyle eggs passed in horse feces. In winter minimum development occurs and the majority of eggs and larvae will not survive. The great majority (95%) of eggs passed are from the cyathostomes with only a small small contribution from the large strongyles such as Strongylus vulgaris. This reflects the number of cyathostomes (tens of thousands) present compared with the large strongyles (hundreds) in naturally infected horses. These cyclical patterns occur regularly from year to year, from grazing season to grazing season and are predictable because of the effects of temperature and moisture on the life cycles of these nematodes. Their predictability is valuable because it allows us to focus control programs at strategic times of the year with the maximum possible benefits.
Information from Life Cycles
The key to understanding Parasitology lies in a thorough knowledge of the life cycles whether the parasites are nematodes, cestodes, trematodes, arthropods or protozoa. However, these life cycles are extremely varied, ranging from the simple to the very complex. Learning them can be daunting to many veterinary students but it helps to distill them down to a few common questions as listed below. 1. How does an animal host acquire a parasitic infection? For example, does the host become infected by direct ingestion of an infective stage, by ingestion of an intermediate host or transport host containing infective stages, by skin penetration of an infective stage, by direct contact with an infected host, or via the bite of an intermediate host serving as a vector. An important question in the case of many parasites is whether the host can be infected by transmission from mother to fetus across the placenta or to nursing offspring via colostrum or milk. 2. The second question asks what the predilection site of the parasite is in its definitive host. The predilection site is the place in the host where adult males and females are found. In those parasites without recognizable male and female forms, it's the site(s) where sexual and/or asexual reproduction occurs. 3. A related third question asks how the parasite reaches the predilections site since this may involve extensive migration through the body of a host. 4. The fourth questions asks how a parasite leaves its definitive host to return either to the environment or to its intermediate host. 5. The fifth and final question asks for the identity two life cycle stages; the (infective) stage entering the host and the stage leaving the host. The latter is often called the diagnostic stage if it is valuable in diagnosing parasitic infections. The following tables answer these questions for eight different parasites across the spectrum of Parasitology. Table 1 - Toxocara canis, Dirofilaria immitis, Fasciola hepatica, Haemonchus contortus Table 2 - Dipylidium caninum, Isospora suis, Hematopinus suis, Babesia species If you go to these tables, please use the back button on your browser to return to this page.
Summary of important information about specific life cycles
Table 1
Toxocara canis
Dirofilaria immitis
Fasciola hepatica
Route(s) of 1. Ingestion of entry to the infective eggs 2. Ingestion of host mouse hosts (paratenic) 3. Transplacental migration of L2s to fetal liver 4. Transmammary transmission of L3s to nursing pups Predilection Small intestine site
1. Injection of 1. Ingestion of 1. Ingestion L3s by metacercariae of infective blood-feeding larvae female mosquitos (intermediate hosts)
Right Bile ducts of ventricle and the liver pulmonary arteries Migration through the body and vascular system Migration from the small intestine across the peritoneal cavity to the liver
Abomasum
Route to the predilection site
Direct development in the small intestine after ingestion of paratenic hosts and L3s from the mammary gland. Otherwise by tracheal migration. In the feces of the host
Direct development in the abomasum after ingestion
Route of exit from the host
In the blood meal taken by a mosquito feeding on the host. L3
In the feces of In the feces the host of the host
Life cycle stage(s) entering the host
Egg, L2 or L3 depending on the route of transmission
Encysted metacercaria
Ensheathed L3
Stage Egg leaving the host (diagnostic stage)
Microfilaria
Egg
Egg
Summary of important information about specific life cycles
Table 2
Dipylidium caninum - dog & cat tapeworm
Eimeria bovis - coccidian of cattle
Hematopinus Babesis canis suis - dogs - pig louse 1. Injection of sporozoites by feeding female ticks (Rhipicephalus)
Route(s) of 1. Ingestion 1. Ingestion Direct contact of sporulated with an entry to the of intermediate oocysts infested host host hosts (fleas and lice) containing cysticercoids. Predilection Small intestine site in the definitive host Small Skin and hair intestine coat (Asexual reproduction) Large intestine (sexual reproduction) Direct development in the intestine None -all life cycle stages occur on the host
Red cells (asexual reproduction)
Route to the predilection site
Direct development in the small intestine after ingestion of intermediate hosts. In the feces of the host
Invasion of red cells by sporozoites
Route of exit from the host
In the feces of the host
None - all life cycle stages occur on the host. Adults and nymphs move to another host via direct contact All stages except eggs
Infected red cells are ingested by feeding ticks
Stage Cysticercoid entering the host (infective stage)
Sporulated oocyst
Sporozoites
Stage Egg leaving the host (diagnostic stage)
oocyst
All stages except eggs
Trophozoite in host red blood cells
Infection and disease
The terms infection and disease are not synonymous. While an animal must be infected with a parasite to produce disease it does not necessarily follow that all infected animals will show clinical signs of disease. When susceptible animals are infected with viruses, bacteria and protozoa, the host's lack of immunity usually results in clinically obvious disease. The outcome of these infections will depend on an interaction of factors including the virulence of the organism and how rapidly and successfully the host can mount an effective immune response. Protozoa are unique among the parasites in that they multiply rapidly in their hosts such that they may overwhelm them. This is particularly true of susceptible animals such as the young or older animals whose immune system has been compromised in some way. For example in congenital infections with Toxoplasma and Neospora, the disease is usually more severe because the fetus lacks a fully developed immune system and the outcome is likely to be fetal death. In cats receiving kidney transplants their immune system will be compromised because they are being treated with immunosuppresive drugs like corticosteroids. These cats are at high risk for being overwhelmed by acute Toxoplasmosis, an infection that has lain dormant in these transplant recipients and kept in check by cell mediated immunity. Suppression of cmi by immunosuppressive drugs allows these dormant organisms to begin mutiplying again producing acute infections that may be severe enough to overwhelm transplant recipients causing their death. This example illustrates another possible outcome to parasitic diseases namely that the immune response allows a host to successfully overcome acute clinical disease but the infection is either not totally cleared or the animal remains susceptible to low level infections. In both cases, the animal may harbor chronic subclinical infections throughout its life. Subsequent events during its lifetime may compromise the immune response and allow these chronic infections to flare up as potentially life-threatening acute diseases or make the anima, once more, susceptible to a new infection with a parasite. Parturition and lactation are events that, in some cases, appear to make animals more susceptible to parasite infections probably resulting from compromise of the immune response. For example, it is well established that parturient and lactating ewes are more susceptible to infections with Haemonchus contortus and post- partum dairy cattle are more susceptible to coccidial infections. Nematodes are more complicated than protozoa partly because they do not multiply inside their hosts. One nematode egg can only produce one infective larvae that develops into one adult worm. Therefore the development of clinical disease in hosts infected with nematodes depends almost entirely on the actual number of larvae infecting a susceptible host. I other words, the outcome of nematode infections is generally more dependent on the parasite burden and that is, in turn, directly related to the infecting dose. Generally speaking there is a direct correlation between the number of infecting larvae and the severity of any disease produced; a small number of infective larvae will produce minor pathological changes and generally no obvious clinical disease. It will often take many larvae (thousands or even tens of thousands) to incite pathological changes severe enough to produce serious clinical signs. For example, a foal infected with 100 Parascaris equorum will show either no clinical signs or at worst some coughing and minor nasal discharge. Conversely, a foal infected with 5,000 P. equorum will show severe clinical signs and may succumb to the infection. However, like all general rules there are often exceptions. Within the nematodes there are some whose anatomical locations, in a host, are such that even a small number of nematodes will incite pathological changes that can have devastating consequences for
a host. One example is Strongylus vulgaris in horses. Migration of even a few larvae in the mesenteric arterial tree can produce pathological changes (thrombi and emboli) severe enough to block blood supply to significant portions of the large intestine. The outcome is often acute colic that may be fatal. These changes are shown in the images below.
Images illustrating the pathogenesis of Strongylus vulgaris infections in horses
The celiac axis and its branches and the cranial mesenteric artery and its branches showing thrombosis and thickening of arterial walls due to Strongylus vulgaris larval migrations. Image courtesy of Dr. Owen Slocombe and Merial Inc.
Necrosis of the cecum and ventral colon of a horse resulting from ischemis and infarctions due to lesions produced by migrating larvae of Strongylus vulgaris. Image courtesy of Dr. Harold Drudge and Hoechst-Roussel
The dorsal aorta of a horse showing fibrin tracks due to migrations of Strongylus vulgaris larvae beyond the root of the cranial mesenteric artery. Image courtesy of Merial Inc.
Arteriographic picture of the abdomen of a foal 30 days after infection with 50 third stage larvae of Strongylus vulgaris. Image courtesy of Dr Jay Georgi. The mesenteric artery and its branches show minor changes
Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris. Image courtesy of Dr Jay Georgi. The mesenteric artery and its branches show extensive changes.
Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris and treatment at 30 days with a larvicidal anthelmintic. The mesenteric artery is essentially normal. Image courtesy of Dr Jay Georgi
A second exception is Dirofilaria immitis (the heartworm) in cats. Infections with even one or two adult heartworms may cause severe pathophysiological changes and life-threatening disease.
Parasites and disease
Many parasites have complex life cycles that involve extensive migrations in their hosts. Others have simple life cycles with little or no migrations. The propensity of a parasite to cause disease (its pathogenic potential) is not a simple prediction since it may depend on a number of factors including the examples listed below. Factors influencing the pathogenic potential of a parasite 1. The migratory pathway in a host 2. The anatomical site where a parasite develops if it does not migrate in its host. 3. Feeding habits 4. The predilection site 5. The propensity to stimulate hyperactive immunological responses in the host that may lead to immunopathological changes such as fibrosis, granulomas, cachexia, autoimmuine reactions, allergic reactions and splenomegaly. 6. The potential of the parasite to transmit other infectious agents. This property is especially relevant to the arthropods. Despite the complexities of parasite interactions with their hosts, we can make certain predictions about the pathogenic potential of a parasite and the likely clinical signs if we know certain details about its life cycle, its predilection site and its feeding habits. The following table summarizes the relevant information about Ostertagia ostertagi, a nematode parasite of cattle found commonly throughout temperate areas of the world, and Haemonchus contortus a nematode of sheep found throughout the world in warm temperate and subtropical areas.
Factors influencing the pathogenic potential of parasites Migratory pathway Site of parasite development Predilection site Feeding habits Immunopathological changes Transmission of other infectious agents
Ostertagia ostertagi None Gastric glands Abomasum Ingestion of abomasal contents None None
Haemo
In close apposit mucosa Abomasum Blood feeder None None
With this information, we can make certain assumptions and predictions about the pathophysiological changes and the clinical signs in these infections.
Ostertagia ostertagi. The nematode grows and develops in the gastric glands of
the abomasum which it leaves just before it becomes an adult, approximately 17-21 days after infection. During its time in a gastric gland, the nematode grows about 100 fold. Therefore we can predict that this growth will result in erosion of the secretory epithelium and also that swelling of the gland will occur. In heavy infections these erosive effects can be widespread resulting in heavy losses of secretory cells and significant reductions in the output of HCL and pepsinogen. These changes are summarized in the table below.
Pathogenesis of Ostertagia ostertagi Morphological Biochemical changes changes Loss of chief cells Reduction in HCl in the abomasum and a rise in the pH of abomasal contents Physiological consequences Failure to convert pepsinogen to pepsin. Loss of the bacteriostatic effect of an acid pH Results Protein digestion impaired. Bacterial accumulation in the g.i. tract Loss of protein digestion
Loss of peptic Reduction in secretion of cells pepsinogen
These changes will result in the collection of osmotically active materials in the intestine (undigested protein and bacteria) and these, in turn, will promote the transfer of fluid from the extracellular spaces into the gut lumen and diarrhea (watery feces) will be the outcome of this process. Diarrhea is, in fact, the primary clinical sign in acute ostertagiosis and we can make this prediction from a small, but critical, amount of information about the parasitic phase of the nematode's life cycle.
Haemonchus contortus. In this example, unlike Ostertagia, the parasite matures

on the mucosal surface of the the abomasum. Therefore its growth and development has little effect on the mucosa and makes no contribution to its pathogenic potential. Despite the fact that adult Haemonchus are no more than 1cm long, they are voracious blood feeders and it is this blood loss that is entirely responsible for the pathophysiological changes and clinical signs we see in Haemonchosis.
Pathogenesis of Haemonchus contortus Feeding Impact of Biochemical Physiological habits feeding changes consequences Blood Severe blood Loss of red cells Anemia feeding by loss. A worm = drop in the PCV L4s and burden of adults may 1,000 worms Loss of plasma Edema remove may remove proteins 0.05ml 50ml blood = hypoproteinemia blood per per day from (hypoalbuminemia) worm. an infected host.
The magnitude of the red cells losses due to the feeding habits of this parasite makes it easy to predict that anemia of varying degrees of severity will be a constant feature of these infections and will usually be seen clinically as pale mucous membranes and lethargy. The latter can be explained by the reduced oxygen carrying capacity of the blood due to the loss of Hemoglobin along with red cells and a resultant reduction in oxygen perfusion of tissues such as muscles. Edema is usually seen in live sheep as a gathering of fluid in the submandibular space,
between the mandibles and for this reason is often called "bottle jaw". At necropsy a Haemonchus-infected sheep would show a general wetness of the tissues as well as fluid in the peritoneal (ascites) and thoracic (hydrothorax) cavities. Edema has a more complicated explanation than anemia and requires an understanding of the forces controlling fluid flow in tissues at the capillary level.
The exchange of fluid between blood and the interstitial spaces, at the capillary level, is controlled by the opposing effect of two forces, Hydrostatic Pressure (HP) and Plasma Colloid Osmotic Pressure (COP). HP tends to force fluid out of the capillaries and COP tends to draw fluid into the capillaries. The balance of these two forces will determine what occurs. At the arterial end of a capillary HP is greater than COP and fluid will leave the capillary to perfuse the interstitial spaces. At the venous end of a capillary, HP is lower than COP and fluid will return to the capillary from the interstitial spaces. The concentration of albumin in plasma is the most important contributor to colloid osmotic pressure and is, therefore, the most important determinant in regulating fluid flow at the capillary level. A reduction in the level of albumin, because of blood loss, in Haemonchosis will result in a corresponding reduction in the COP with a net outflow of fluid from blood, its accumulation in the interstitial spaces and this is called edema. We know that Haemonchus is a blood sucking parasite and causes significant blood loss including plasma proteins. Our knowledge of the physiological forces governing fluid flow at the capillary level (Starling's Principles) leads us to predict that edema will be a logical and likely outcome of Haemonchus infections
The Nematodes
Introduction
Nematodes are commonly called roundworms because, as the name suggests, they are round when viewed in cross section. However, they are in fact cylindrical in structure and taper towards their anterior and posterior ends. They are bilaterally symmetrical, and while the sexes are separate in most species, a few are hermaphrodite. Nematodes that parasitize our domestic animals are found in all parts of the body but are most commonly found in the digestive and respiratory tracts and the circulatory system. Nematode parasites of domestic animals vary greatly in size ranging from small hair-like worms (up to 2 cm long) in the Superfamily Trichostrongyloidea to large, robust worms ( up to 40cm long) in the Superfamily Ascaridoidea. The following six examples show the considerable variations in size and appearance seen among the nematodes
Species:
Toxocara canis
Dirofilaria immitis Filarioidea Spirurida Right heart, pulmonary arteries Dogs, cats, ferrets 23 - 30 cm
Trichostrongylus axei Trichostrongyloidea Strongylida Abomasum/stomach
Superfamily: Ascaridoidea Order: Location: Hosts: Size: Ascaridida Small intestine Dogs 10 - 18 cm
Ruminants, horses, swine 0.7 cm
Species: Superfamily: Order: Location: Hosts:
Parascaris equorum Ascaridoidea Ascaridida Small intestine Horses, donkeys
Syngamus trachea Strongyloidea Strongylida Trachea Fowl, game birds
Size:
15 - 40cm
0.5 - 2 cm
The Nematodes
Classification
All living organisms, plants and animals, are organized into a hierarchy of groups called taxa. This structure is based primarily on the degrees of similarity among members of the same group and also shows the contrasts among members of different taxa. The highest level of classification considered here is the Phylum and the lowest is the Species. Nematodes belong to the Animal Kingdom and their taxonomic hierarchy is expressed as follows: KINGDOM PHYLUM CLASS ORDER SUPERFAMILY FAMILY SUBFAMILY GENUS SPECIES Species are named using the binomial system of Linnaeus (1753) and are written in italics. A species is defined as a collection of similar organisms that will only interbreed among themselves. Examples of nematode species include Strongylus vulgaris in horses, Toxocara canis in dogs, and Haemonchus contortus in sheep. Even though many different species are morphologically similar and may share the same habitat in the same host they are still distinct species because they do not interbreed. For example, three members of the genus Strongylus inhabit the large intestines of horses: Strongylus vulgaris, Strongylus equinus, and Strongylus edentatus. They are similar in size and appearance and without the aid of a microscope they are not readily distinguishable from each other. Although they share the same host and the same habitat within that host, they do not breed with each other. However, their similarities (as species) allow us to group them in the same hierarchical tree of classification. In addition, these similarities allow us to conclude that the three Strongylus species share common ancestors and this phylogenetic relationship is also recognized by placing them in the same taxonomic hierarchical tree.
CLASSIFICATION
Strongylus species
Phylum: Nematoda Family: Strongylidae
Order: Strongylida
Subfamily: Strongylinae Genus: Strongylus
Superfamily: Strongyloidea
Within the nematodes, some of the taxonomic groups have suffixes (endings) that are specific for the particular group. Examples are shown in the following table.
SUFFIX ida oidea idae inae
TAXONOMIC GROUP ORDER SUPERFAMILY FAMILY SUBFAMILY
Most of the nematodes of veterinary importance are found in the six orders and thirteen superfamilies listed in the table below.
Order
Superfamily
Strongyloidea Ancylostomatoidea Metastrongyloidea
Comments
Strongylida Trichostrongyloidea "Bursate" nematodes
Ascaridida Oxyurida Rhabditida Spirurida
Ascaridoidea Oxyuroidea Rhabditoidea Spiruroidea Thelazioidea Filarioidea Habronematoidea Trichuroidea (Trichinelloidea) Dioctophymatoidea
"Non-bursate" nematodes
Enoplida
Nematodes in the order Strongylida are also called "bursate nematodes", a descriptive term referring to the fact that each male has a pronounced copulatory bursa at the tail (posterior) end. The two images below show nematodes with and without a copulatory
bursa.
Fig. 1 Cooperia (Order Strongylida, Superfamily Trichostrongyloidea). Tail end of male showing copulatory bursa, spicules and bursal rays.
Fig. 2 Heterakis (Order Ascaridida, Superfamily Ascaridoidea). Male without a copulatory bursa showing spicule (A), caudal ala (B) and pre-cloacal sucker (C).
Click here to view a table showing a more complete classification of nematodes of veterinary importance.
Sources
There are several good sources on the Internet that describe taxonomic hierarchy. One can be found on the Web site maintained by the Royal (Dick) School of Veterinary Medicine at the University of Edinburgh in Scotland. A second, more comprehensive, taxonomy database is maintained by "NCBI/Gen Bank" and includes a searchable index.
The Nematodes
External Structures - cuticle
Nematodes are covered by a protective outer skin called a cuticle which is naturally colorless and partly translucent. The cuticle also lines the buccal cavity, esophagus, excretory pore, vagina, cloaca and rectum. The cuticle is also resistant to host digestive enzymes and in most nematodes is relatively impervious, allowing only the passage of water molecules and certain small water- soluble ions. The cuticle also appears to function as part of what Noble et al describe as the "hydrostatic skeleton of nematodes". Since the body cavities of nematodes contain pressurized fluids the cuticle apparently serves to maintain the body at a constant diameter by resisting the internal pressure of these fluids. In keeping this fluid contained, the cuticle therefore maintains a nematode's form and structure and also provides an anchor for muscles. The patterns of the several cuticular layers and their contents appear to allow simultaneous radial strength and longitudinal flexibility. In other words, the cuticle layers are arranged so as to maintain a constant body diameter while, at the same time, allowing the nematode to stretch longitudinally. A variety of organic compounds have been identified in the cuticles of many nematodes. These include amino acids, proteins, carbohydrates, lipids, RNA, ascorbic acid, ATP and hemoglobin. Their presence and variety suggests that the cuticle is far from inert and is, in fact, metabolically activity most of the time. It is also known that the cuticle is antigenic and may play an important role in eliciting the immune responses of infected hosts. In many nematodes the cuticle is a smooth outer layer but in others the cuticle may have longitudinal and circular striations and may be modified to produce a variety of structures that can be useful in identification of specific nematodes.
Cuticular modifications at the anterior ends of many nematodes may include leaf crowns, vesicles, alae and papillae.
Leaf crowns (A) are rows of finger-like projections surrounding the rim of the opening to the buccal cavity. They are particularly obvious in the strongyles of horses. Vesicles are inflations of the cuticle around the mouth - cephalic (B) and the anterior
esophagus -cervical (C). Alae are, as the name suggests, "wing-like" expansions of the cuticle. Cervical alae (D) are located in the terminal half of the esophageal region when cervical vesicles are also present and cover most of the esophageal region in the absence of vesicles. Cervical papillae (E) are paired spine-like projections found in the esophageal region. Their function is believed to be tactile or sensory.
Click here to see a set of images showing specific nematodes with cuticle modifications of their anterior ends.
Cuticle modifications - posterior end

Cuticle modifications at the posterior ends of nematodes may include caudal papillae and caudal alae. Caudal papillae are cuticular protuberances believed to be sensory in function. They vary in shape from small "button-like" protuberances to longer "stalk-like" structures. Caudal alae are wing-like expansions of the cuticle and may be found at the tail ends of nematodes.
In male nematodes, of species belonging to the order Strongylida, caudal alae are greatly expanded to form a structure called a copulatory bursa - so called because it is used by the male to grasp the female during copulation. A bursa has two lateral lobes and in some species, a third dorsal lobe. The bursa is supported by finger-like structures called rays which are caudal papillae with associated muscle tissue. Each lateral lobe usually contains six rays and the dorsal lobe has one ray.The number and shape of these rays may be valuable characteristics for species identification of nematodes in the order Strongylida. When resting, the bursa looks like a relaxed, folded hand but during copulation it is greatly expanded and used to grasp the female.
Click here to see a set of images of specific nematodes showing modifications to the cuticle at their posterior ends.
The Nematodes
Basic Nematode Life Cycle
Despite the diversity and complexity of many nematode life cycles, all of them can be related to the same basic pattern.
This pattern is illustrated by the adjacent figure and consists of two phases, parasitic and pre-parasitic. The parasitic phase takes place inside the definitive host while the pre-parasitic phase occurs either as a freeliving phase in the external environment or inside a second host, called an intermediate host. This basic life cycle also consists of seven stages, an egg, four larval stages (L2, L2, L3, L4) and two adult stages comprising separate males and females. Sometimes the sexually immature adult stages are called L5's In most species sexual reproduction by adult nematodes is the norm and occurs within an infected definitive host. Eggs are laid by the female and pass from this host into the external environment. These eggs must pass through the three developmental stages (L1, L2, and L3) before the nematode is again infective for another host. This is an important point to emphasize - In the vast majority of nematode life cycles the stage that passes from the definitive host is not the same stage that is infective for another definitive host. The nematode stage (usually an egg or L1) that passes from a definitive host must develop through to a stage (usually the L3) that can then infect another host. A first stage larva develops inside an egg, then hatches. Initiation of the hatching process is controlled by several factors including temperature and moisture levels in the external environment. Hatching occurs only when environmental conditions are favorable for survival of hatched larvae. These conditions stimulate the enclosed larvae to assume its own role in hatching by secreting enzymes to digest the surrounding egg membranes, then exerting pressure against the weakened membranes to rupture them and escape. This newly hatched L1 feeds on bacteria and grows until constrained by its outer skin or cuticle. At this point further growth is possible only if the larva grows a new, more flexible, cuticle and casts off its old outer cuticle. This process is called molting and involves two steps. 1. Synthesis of a new cuticle by the hypodermis. At this stage the larva, with a new cuticle is completely enclosed by its old cuticle. 2. Exsheathment - a process by which the old cuticle is loosened and ruptured
followed by the larva wriggling out of the casing of the old cuticle. Nematodes molt four times during each life cycle with a molt occurring at the end of each larval stage. Therefore, molts separate the first and second larval stages (L1 and L2), the second and third larval stages (L2 and L3), the third and fourth larval stages (L3 and L4) and also the fourth larval stages and immature adults (L4 and L5). The L5 grows to the limit of its new cuticle, at the same time developing into a sexually mature adult male or female. This developmental cycle can be represented by a growth curve as shown in the following figure.
An (L1) develops inside the egg, hatches (H), grows rapidly then molts (M1) to an L2. This second stage larva also shows a rapid spurt of growth followed by a second molt (M2) to a third stage larva (L3) the infective stage for many nematode species. This (L3) grows then molts(M3) inside the host to an L4. This final larval stage grows and undertakes a final molt (M4) to an immature adult (L5). These L5's pass through a final growth phase to become sexually mature adult males and females.
The Nematodes
Life cycle variations
Although the basic nematode life cycle described previously holds true for many nematode species, it is also true that other species show a number of variations and complications in their life cycle patterns. Most of these variations are concerned with the infective stage and whether other hosts, in addition to the definitive host, may play a role in the life cycle. There are two types of life cycle in nematodes infecting domestic animals - Direct and Indirect. Direct life cycles - all preparasitic stages are found free-living in the environment and their development may take place either inside the egg or after hatching. In nematodes where first stage larvae hatch from their eggs subsequent development takes place in the environment and the third stage larva is the infective stage. Examples of this type of direct life cycle occur among members of the family Trichostrongylidae In nematodes where eggs do not hatch, preparasitic larvae develop inside their eggs so that the infective stage is an egg containing an infective larva. Hatching will take place after these eggs are eaten by another host and the infective larva escapes. Example: Ascaris suum, the roundworm of pigs. Indirect life cycles - larvae develop to the infective stage inside an appropriate intermediate host. In these life cycles there are two possible methods of transmission of infective larvae to the definitive host. The intermediate host is ingested by the definitive host and infective larvae are released by digestion in the alimentary tract. Example: Parelaphostrongylus tenuis, the brainworm of white-tailed deer. The intermediate host is a biting or sucking arthropod. In these cases transmission of infective nematode larvae occurs during feeding on the definitive host. Example: Dirofilaria immitis, the heartworm of dogs and cats.
The Nematodes
Exsheathment
The molting process in nematode growth and development involves two steps: synthesis of a new cuticle and exsheathment or shedding of the old. The process of exsheathment is particularly important in the order Strongylida since it plays a vital role in transmission to the definitive host. The infective stage for most stronglyid species is a third stage larva still enclosed in the loosely-fitting cuticle (sheath) from the preceding second stage. This outer sheath plays a protective role for these larvae but, because it completely encloses the larva, it also prevents feeding. In species infecting grazing ruminants transmission occurs by ingestion of ensheathed third stage larvae during grazing. The first process to occur is exsheathment since without it, infection can not proceed. The exsheathment process in Haemonchus contortus in ruminants has been reasonably well delineated. The actual exsheathment of Haemonchus third stage larvae takes place in the rumen and appears to be a three-stage process.
1. Environmental conditions in the rumen - primarily levels of dissolved carbon dioxide (influenced by pH, temperature and reducing agents) activate neurosecretory cells in the nerve ring, at the base of the esophagus. 2. These activated neurosecretory cells release hormones (including nor adrenaline) which act directly on the excretory cell to stimulate the uptake of water which, in turn, activates enzymes present in crystalline form. 3. The accompanying diagram shows the third, and final, stage in the exsheathment process. Activated enzymes, including leucine aminopeptidase, are released into the excretory duct and pass into the space between the two cuticles. Enzyme action weakens the cuticle (A). The cuticle breaks at this point and the anterior end detaches as a cap (B). The exsheathed L3 (C) wriggles out leaving the sheath (D) (second stage cuticle) behind.
The importance of exsheathment is because it initiates infection. Without exsheathment, in nematodes like Haemonchus, infection would not occur. The process of exsheathment during infection is not only host specific but is also site specific within the host. This ensures that nematodes will not exsheath when ingested by abnormal hosts. For example, Haemonchus contortus will not infect horses because they lack a rumen and therefore infective Haemonchus larvae ingested by horses will not receive the necessary stimulus to begin the infective process.
The accompanying image shows Haemonchus larvae exsheathing in a petri dish after stimulation with carbon dioxide. Larva A still retains its sheath while larva B is wriggling out of its sheath (C). A cast, empty sheath, its larva having escaped, is labeled D.
The Nematodes
Arrested Development
Arrested development is an important feature of the life cycles of a number of nematode species. It is of particular importance in the order Strongylida especially the Trichostrongyles of grazing ruminants, the small strongyles of horses and the hookworms of dogs and humans. Synonyms include the terms hypobiosis, larval inhibition, inhibited larval development and arrested larval development Arrested development may be defined as a temporary halt in the parasitic phase of development at a specific point in the nematode life cycle. Under normal circumstances when a host is infected with a nematode, parasitic development begins immediately and continues through to adult males and females in the normal prepatent period characteristic of the species. However, under certain circumstances larval development will be halted or arrested at a specific stage (usually L3 or L4) and the prepatent period is prolonged sometimes for weeks or months.
This image shows a histological section of an abomasum with an arrested larva (early L4) of Ostertagia ostertagi contained within a gastric gland.
Arrested larvae not only fail to grow but also their metabolic rate decreases significantly and they stop moving. In this state they can survive for weeks or months before resuming development and may also be resistant to some anthelmintics at doses that are usually lethal to adults and normally developing larval populations. Arrested development can only be diagnosed by examining the population of worms in a host animal at necropsy. If arrested stages are present, the worm population will show the following characteristics.
1. A significant percentage of larvae will be at the same stage of development. 2. The sizes of recovered worms will show a bimodal distribution. The smaller group will be Image courtesy of Dr. Jorge Guerrero, Merial Inc arrested larvae, and the larger group will be mature adults. (In the case of Ostertagia ostertagi, the nematode population will include adult males (~ 7 mm long & 0.12 mm wide) , adult females (~ 10 mm long and 0.14 mm wide) and arrested larvae in the early L4 stage (~ 1 mm long & 0.03 mm wide). The image shows the relative sizes of an arrested L4 and a mature adult male). 3. The most recent exposure of the host animal to infection will be at least prior to the prepatent periods of the nematode species present.
Initiating factors in arrested development

Epidemiological and experimental evidence has identified three factors responsible for the initiation of arrested development. 1. Seasonal influences on infective larvae on pasture. 2. Host immune responses inhibiting the normal development of the parasitic phase of the life cycle. 3. An overcrowding effect whereby the presence of adult worms causes the "feedback" inhibition of incoming infective larvae which go into arrest until the adult worm population decreases in number or is eliminated.
Seasonal Arrest
Hypobiosis is the term most often used for arrested development that has a seasonal basis. It is a biologically important feature since it seems to be of particular importance in nematodes with relatively short adult life spans. In these species hypobiosis is initiated by an environmental signal received by free-living L3s. When these L3s subsequently infect a host, they do not develop continuously through to adults but instead arrest in host tissues either as exsheathed L3s or as early L4s. In other words hypobiosis occurs inside the definitive host but results from
environmental signals received by free-living infective larvae. It is a mechanism for nematodes to survive a period of harsh climatic conditions, hostile to survival of their progeny, by arresting as immature stages until conditions improve to the point where free-living larval stages can again grow and develop to the infective stage. In regions of the northern hemisphere with cool, temperate climates and pronounced seasonal changes, arrested larvae accumulate inside grazing animals during the fall/autumn, with the onset of falling temperatures signaling the approach of winter, a season that is usually threatening to the survival of free-living stages on pasture. The resumption of development of these hypobiotic larvae occurs in late winter or early spring when environmental conditions are, once again, conducive to survival and development of free-living preparasitic stages. In warm temperate regions of the northern hemisphere, hypobiosis appears to be linked to the onset of a dry season since dry conditions also threaten both the survival and development of free-living stages. In the southern United States, for example, Ostertagia ostertagi arrests during spring and remains arrested during the following hot, dry summer. Hypobiosis in Spring thus allows Ostertagia to survive within the host, as early L4's, protected from the inhospitable external environment. Similarly, hypobiosis occurs in Spring in regions of the southern hemisphere where summers are also hot and dry. These regions include parts of Australia (coastal and adjoining tablelands), Chile, Peru, Brazil, Argentina and South Africa. In tropical regions, hypobiosis has been recorded at the onset of dry seasons. In Northern Nigeria, for example, with a six-month dry season, hypobiosis occurs in Haemonchus contortus and Cooperia species in cattle. Resumption of development begins at the onset of the rainy season when the environment is, once again, hospitable to the survival and development of free-living stages. In contrast, hypobiosis is much less important in Southern Nigeria and Southern Ghana where the dry season is short. Hypobiosis is clearly genetically controlled but is not an "all or none" phenomenon. In cold temperate climates such as are found in Maine and Eastern Canada, the great majority of trichostrongyle larvae ingested by grazing ruminants, in late fall (autumn), will undergo hypobiosis. In milder climates, for example southern England, only a proportion of such ingested larvae (usually no more than 60%) will arrest since England's milder winters will often allow preparasitic stages to survive on pasture. Several studies have shown that the propensity for hypobiosis is genetically based. For example, cattle from Ohio, infected with a "winter-arresting" strain of Ostertagia ostertagi were moved to Louisiana ( a region where hypobiosis occurs in Spring) and grazed on Ostertagia-free pastures thus contaminating them with free-living stages of the "winter-arresting" strain. Calves grazed on this newly contaminated pasture were subsequently shown to contain hypobiotic larvae in the fall (autumn), the season for hypobiosis in their original Ohio environment rather than Spring, the time for hypobiosis in their new environment. The converse was also true, i.e. Ostertagia in cattle transferred from Louisiana to Ohio continued to show hypobiosis in the Spring. This evidence confirmed other observations that several different strains exist in populations of nematodes where hypobiosis is a significant feature of the life cycle. The resumption of development (to adults) of these arrested larvae occurs once the environment is, again, suitable for preparasitic development of the next generation of eggs and larvae. The triggering mechanisms responsible for ending hypobiosis and allowing larvae to resume
development, are not really known. However, it has been hypothesized that seasonally arrested larvae are in a similar state to diapause in insects. If so, then some type of genetically programmed clock would trigger the ending of hypobiosis at a set time after induction. Evidence for this comes from New Zealand studies where it was found that hypobiotic larvae mature at the same rate as they undergo arrest leading to the conclusion that arrested larvae resume their development at a set time after they become arrested in the host. For example, we can assume that hypobiotic larvae begin to accumulate in September in cattle grazing pastures in cool temperate regions of the northern hemisphere and this accumulation ends when these cattle are housed for the winter at the end of November. If we further assume that these larvae will remain arrested for 4 months then resumption of development will begin in January and continue until the end of March. It appears that seasonal hypobiosis is an important option for the life cycles of a number of nematodes of grazing animals, particularly ruminants. This is particularly true of the Trichostrongyles such as Ostertagia, Haemonchus, Trichostrongylus, Cooperia and Dictyocaulus as well as Oesophagostomum and, also, the small strongyles of horses.
Immune arrest
Another form of arrested development is also recognized and is due to the influence of the immune response. As animals graze, they continually ingest infective third stage larvae which develop to adults in the normal prepatent period. As the grazing season progresses these animals develop a strong immune response to nematode infections and one of the manifestations of the immune response is the inhibition of larvae inside the host. Larvae infecting a host are more likely to arrest if there is already an established population of adult worms in that host. In sheep, goats and pigs maturation of these immunologically arrested larvae appears to be linked with parturition. An inhibition of the immune response, specifically associated with gut-dwelling nematodes, is related to serum levels of prolactin. Immune competence is restored when prolactin levels drop, at weaning, and worm burdens are usually expelled as a consequence of the restored immune response.
Quiescence
Hypobiosis and immunological arrest of parasitic larvae should be distinguished from other forms of developmental arrest seen in paratenic and intermediate hosts during the life cycles of many nematodes, particularly the ascarids and spirurids. This form of arrested development is often called quiescence since it is an intrinsic part of the life cycle, is not an option and is not triggered by extraneous influences.
Biological importance of arrested development

Whatever the triggering mechanisms are that initiate developmental arrest and induce resumption of development, the phenomenon has considerable biological importance to nematodes that incorporate it into their life cycle options. It also has considerable epidemiological implications to nematode hosts and must be considered when devising methods for prevention and control of nematode infections and disease. There are several reasons why arrested development is important.
1. Arrested development ensures survival of nematodes during times when conditions are hostile to their survival in the external environment. 2. Resumption of development of large numbers of larvae in a host may produce serious outbreaks of disease. 3. Development of adults from arrested larvae will produce significant contamination of pastures with nematode eggs at a time when environmental conditions are, once again, favorable for development of preparasitic stages to infective larvae. This contamination which begins at the start of the grazing season and reaches a peak several weeks later is particularly dangerous for young, immunologically naive animals grazing pastures for the first time. 4. Hypobiotic larvae are depressed metabolically and hence may be less susceptible to some anthelmintics. Clearly the choice of drugs to be used in a nematode control program will be influenced by the role of arrested development in specific nematode life cycles and by the susceptibility of arrested larvae to the range of available anthelmintics.
CLASSIFICATION OF NEMATODES OF VETERINARY IMPORTANCE

ORDER
STRONGYLIDA
SUPERFAMILY
TRICHOSTRONGYLOIDEA
FAMILY
TRICHOSTRONGYLIDAE
DICTYOCAULIDAE
STRONGYLOIDEA
STRONGYLIDAE
CHABERTIIDAE
SYNGAMIDAE
ANCYLOSTOMATOIDEA
ANCYLOSTOMATIDAE
METASTRONGYLOIDEA
METASTRONGYLIDAE PROTOSTRONGYLIDAE
FILAROIDIDAE
ANGIOSTRONGYLIDAE
ASCARIDIDA
ASCARIDOIDEA
ASCARIDIDAE
OXYURIDA RHABDITIDA SPIRURIDA
OXYUROIDEA RHABDITOIDEA SPIRUROIDEA THELAZIOIDEA FILARIOIDEA
OXYURIDAE STRONGYLOIDIDAE SPIROCERCIDAE THELAZIIDAE ONCHOCERCIDAE
HABRONEMATOIDEA ENOPLIDA TRICHUROIDEA (TRICHINELLOIDEA)
HABRONEMATIDAE
TRICHINELLIDAE TRICHURIDAE
DIOCTOPHYMATOIDEA
DIOCTOPHYMATIDAE
Strongylida
The order Strongylida includes many of the important nematodes found in the gastrointestinal tracts of ruminants, horses, and swine, as well as the lungworms of ruminants and, the hookworms of dogs and cats. The following table gives an overview of the classification of this order with an emphasis on the superfamily Trichostrongyloidea.
Their distinguishing features include a copulatory bursa in males and a buccal capsule of variable shape and size. Examples of direct (free living larvae) and indirect (intermediate host) life cycles can be found among the members of this order. There are four superfamilies of importance in domestic animals: Trichostrongyloidea Strongyloidea Ancylostomatoidea Metastrongyloidea
Females belonging to the superfamilies Trichostrongyloidea, Strongyloidea and Ancylostomatoidea produce smooth, thin-shelled, ellipsoidal "strongyle-type" eggs (A), approximately 80-100 microns long and 40-50 microns wide. One exception to this rule is Nematodirus, whose species produce eggs that are approximately twice the size of "strongyle-type eggs (B). Notice the difference between these eggs and the whipworm (Trichuris) egg (C).
A fifth (minor) superfamily, the Diaphanocephaloidea, are bursate nematodes found in the digestive tracts of terrestrial snakes and occasionally lizards. There are two genera and thirty three species in this superfamily. Females pass a "strongyle-type" egg and their life cycles are direct and similar to the Trichostrongyloidea but it is also believed that paratenic hosts (snails and slugs) may play a role in their life cycles.
Members of this superfamily are widespread throughout the world in all major stock raising areas. They are found in all terrestrial vertebrates especially mammals. In domestic animals they are common and important parasites of ruminants but a few species are also found in horses and swine.
Classification
The following table shows the classification of the trichostrongloidea of domestic animals to the genus level.
Superfamily
Family
Genera
Trichostrongylus Haemonchus Ostertagia Nematodirus Cooperia Hyostrongylus Dictyocaulus
Trichostrongyloidea Trichostrongylidae
Dictyocaulidae
Trichostrongylidae
Members of the family Trichostrongylidae are widely found in large domestic animals especially cattle, sheep, goats, swine and, to a lesser extent, horses. Their predilection sites are the stomach/abomasum or small intestine. They are small (~1/2 to 3cm long), and hair-like, with an extremely small buccal capsule, and a pronounced copulatory bursa. All species have direct life cycles (no intermediate hosts). There is no migration within the definitive host, and infection is by ingestion of ensheathed third stage larvae (L3's). Hypobiosis (seasonal arrested development) is an important feature of the life cycles of the trichostrongylids and is therefore an important factor when devising appropriate methods of controlling infection and disease caused by these nematodes.
Arrested Development and the Periparturient Rise (PPR)
In the trichostrongyles of ruminants, especially sheep and goats, arrested development and the subsequent maturation of arrested larvae has particular significance in pregnant and lactating female hosts. In the 1960s, several authors described a rise in nematode egg counts in the feces of lactating ewes. Since this occurred regularly in the spring, it was named the "spring rise". However, it was later concluded that these observations were related to the reproductive status of the ewes rather than the season of the year since the same rise in egg counts was observed in ewes in which parturition and lactation occurred in other seasons. Hence the term was re-named the "periparturient rise" or "PPR" to more accurately describe its association with parturition and lactation. Experimental observations in sheep have shown that the PPR is associated with a periparturient relaxation of immunity that is, in turn, also associated with hormonal changes in late pregnancy and lactation. Prolactin, the primary lactogenic hormone, which begins to rise in late pregnancy and is maintained at high levels during lactation, appears to interfere (directly or indirectly) with the immunological mechanisms responsible for expulsion of gut-dwelling nematodes in sheep and goats. This suspension of parasite-specific immune responsiveness has the following consequences. 1. Incoming larvae ( either previously arrested or newly ingested from pasture) will develop to egg-laying adults without any constraints from the host's immune response. 2. Immunological constraints on egg production by existing female worms will be suspended. The end result will be a rise in the output of nematode eggs which will be seen as an increase in fecal nematode egg counts of ewes in late pregnancy and lactation. Terminating lactation by weaning nursing lambs has four sequential results in the mother ewes. 1. Their circulating levels of prolactin drop. 2. Immunological responsiveness is restored. 3. The population of adult nematodes (responsible for the PPR) is expelled, a process often called self cure. 4. Fecal nematode egg counts drop to zero
This graph depicts the PPR as it occurs naturally in a flock of sheep, and also illustrates how the PPR can be controlled by appropriate anthelmintic treatments. In this particular flock, lambing occurred between January 1st
and February 15th. Ewes and their lambs were kept indoors until weaning on April 29th. The ewes were divided into two groups: one was left untreated (yellow line) while the other (green line) was treated, at parturition, with Ivermectin - a drug effective against both adult worms and arrested larvae. Six weeks after lambing began, the fecal egg counts of untreated ewes started to rise (the PPR) and peaked on April 29th, the day of weaning. At that point the fecal egg counts of these ewes dropped precipitously, reflecting a self cure of their worm population. In treated ewes, a PPR did not occur. Clearly, this was a reflection that the Ivermectin treatment eliminated those worms responsible for the eventual PPR (arrested larvae and existing adults). Both groups of ewes continued to graze on pastures after their lambs were weaned and showed a typical summer rise in egg counts. These resulted from the acquisition of infections from grazing pasture contaminated by third stage larvae which, in turn, developed from eggs deposited on the pasture by ewes showing a PPR.
Genus Trichostrongylus
Trichostrongylus spp are widely distributed throughout the world. There are four important species animals and these are listed in the table below. Nematode Species Host Species Predilection site Trichostrongylus axei ruminants, horses, and pigs Abomasum/stomach Trichostrongylus colubriformis ruminants small intestine Trichostrongylus vitrinus ruminants small intestine Trichostrongylus capricola goats and sheep small intestine
Trichostrongylus species are the smallest members of the family Trichostrongylidae. They are thin and with a length of 7 mm or less are difficult to see without a microscope
As the accompanying image shows, there is no buccal capsule (A) and the opening of the excretory pore (B) is easily seen in the anterior esophageal region of adult worms. Females have a tapered tail and are missing a vulva flap. Males are readily identified by their spicules. The life cycles of all three species are similar and follow the family pattern with a strongyle-type egg and a free living preparasitic phase. Infective larvae of ruminant species tend to migrate onto vegetation where they are available, for grazing animals, enclosed in a film of moisture.
The parasitic phase is non-migratory, and development to adults takes place in the mucosa of the abomasum or small intestine, depending on the species. The prepatent period is 2-3 weeks in ruminants, and approximately 25 days in horses (T. axei). One other important species, Trichostrongylus tenuis, is found in the small intestine and ceca of birds especially geese and grouse and is widely distributed throughout the world. It is particularly common in red grouse in Britain where it is the causative agent of "grouse disease". Prevalence rates in adult grouse can reach 100% and worm burdens have been reported to reach as high as 10,000 in adult birds. Adult worms may survive in birds for at least two years. Grouse chicks appear to acquire their infections early in life as their diet changes to heather from insects as the birds approach maturity. Field studies have shown that ensheathed infective L3s accumulate in films of moisture on the outer tips of heather. The prepatent period is 7-8 days and hypobiosis occurs during winter at the exsheathed L3 stage. Synchronized resumption of development of arrested L3s, in spring, produces a "Spring Rise" in strongyle-type egg output from the resulting adult worm population and is also responsible for the seasonal occurrence of grouse disease and associated mortality in red grouse during spring time.
Trichostrongylus species
Pathogenesis
In Trichostrongylus axei infections, exsheathed L3s penetrate between the gastric glands and their subsequent growth and development cause nodular lesions similar to those produced by Ostertagia in sheep and cattle. Erosion of glandular epithelium with replacement by immature undifferentiated cells results in changes similar to ostertagiosis - a rise in the pH of abomasal contents and increased permeability of the mucosa. T. axei infections in horses may produce a hyperemic gastritis . In the case of infections with intestinal species, exsheathed L3s penetrate between the epithelial glands with formation of tunnels between the epithelium and the lamina propria. emergence of immature adults some 10-12 days later cause erosions of mucosal surfaces accompanied by hemorrhage and loss of plasma proteins into the intestinal tract. In the duodenum, villi are distorted and stunted thereby reducing the intestinal surface area for absorption. In the stomach/abomasum nodular lesions containing developing worms may be seen.
Clinical signs
Light infections are usually asymptomatic but but may contribute to poor appetites, diminished growth rates and soft feces. However, heavy infections (10,000+ worms) will produce a diarrhea that is serious and can be debilitating, especially in ruminants. The term "black scours" is sometimes used to describe the diarrhea because it is often watery and dark green (almost black) in color. The accompanying image shows a dead sheep which succumbed to trichostrongylosis. The fecal lumps attached to the hind quarters typically result from diarrhea due to Trichostrongylus infections and can be a source of attraction for blowflies producing a myiasis.
Trichostrongylus species
Epidemiology
Trichostrongylus species are not usually primary pathogens in temperate regions of the world. Their role is usually contributory to parasitic gastroenteritis in which Ostertagia or Haemonchus are the primary pathogens in ruminants. However, in warmer subtropical areas Trichostrongylus species are important pathogens in grazing ruminants and counts of 10,000 or more worms per animal are not unusual in clinical outbreaks. Hypobiosis occurs at the L3 stage and is an important controlling feature of life cycles in temperate areas of the world. Survival of preparasitic stages - Eggs and infective L3s are able to survive both heat and cold. In temperate zones of both hemispheres enough L3s may survive winter and produce clinical outbreaks of trichostrongylosis in grazing ruminants in early spring. In Australia and Brazil, clinical outbreaks of trichostrongylosis have occurred when rain followed a dry period. In these cases, large numbers of L3s survive drought by becoming desiccated and are re-hydrated by subsequent rains. The ability of T. axei to cross-infect between horses and ruminants may lead to amplification of T. axei infections in horses when mixed grazing of pastures with horses and ruminants is used as a parasite control measure.
Diagnosis
A diagnosis of trichostrongylosis is made on the basis of a combination of factors Clinical signs Seasonal occurrence of disease Necropsy findings Presence of Strongyle-type eggs in the feces of infected animals Fecal cultures to identify Trichostronglyus L3s In herds or flocks with heavy infections, clinical signs of a watery diarrhea and weight loss will be present in a variable number of animals, although these signs are only suggestive of a diagnosis since other g.i. nematodes may also be the cause of diarrhea and weight loss. In temperate areas, infections will be seen only during the grazing season, from early spring through to late autumn (fall). L3s may survive winter in sufficient numbers to produce clinical infections soon after the start of the grazing season. In subtropical areas, clinical infections may be seen after the dry season or a period of drought. Trichostrongylus adults are too small to be readily observed in situ at necropsy. They are readily identified with a microscope with males having uniquely shaped spicules. Trichostrongylus eggs are "strongyle-type" and, as such, are not distinguishable from other g.i. nematodes that produce similar eggs.
Haemonchus species
Haemonchus species are the largest of the nematodes found in the abomasum of ruminants (10-30mm). They range from 10-30mm in length and are reddish when fresh because they are blood suckers. They achieve this by using a tiny lancet in their small buccal capsule. Because they feed on blood, the female has a striking appearance, looking like a barber pole because the white ovaries wind around the red blood filled intestine.
The copulatory bursa (A) of the male is distinct because it has an asymmetrical dorsal lobe with a Y-shaped dorsal ray (B), which is sometimes confused with the spicules (C). Within the genus Haemonchus there are two important species: Nematode Species Host Species Predilection site
Haemonchus contortus sheep and goats Abomasum Haemonchus placei cattle Abomasum
The Nematodes
Haemonchus - pathogenesis
Haemonchosis is characterized by a hemorrhagic anemia attributable to blood loss via the blood-sucking activities of worms in the abomasum. Fourth stage larvae as well as adults are blood suckers which means that blood losses, sufficient to cause a clinically obvious anemia, may occur before an infection is patent. The actual mechanism of blood sucking involves the worm attaching to the mucosa and extruding its oral lancet to slit capillaries in the abomasal mucosa. They ingest blood flowing from these slit capillaries. Worms also secrete an anticoagulant into the bleeding lesion ensuring that these lesions will continue to bleed after the worm is replete and has moved away.
In hyperacute haemonchosis, sudden deaths in a flock of previously healthy sheep are seen. This syndrome results from ingestion of large numbers of infective larvae by sheep grazing on a heavily contaminated pasture. It often follows a period of warm, wet weather during which massive numbers of Haemonchus eggs develop rapidly to infective stages. At necropsy, large numbers of worms are found in the abomasum - anywhere from 20,000 to as many as 50,000 have been reported. In acute haemonchosis, grazing sheep develop a sudden onset anemia. In the absence of treatment, and if grazing continues, these animals will progressively worsen. The PCV drops initially, plateaus, then falls even further, signaling exhaustion of the erythropoietic system. Without treatment, death is the usual outcome. At necropsy, these animals will be pale and edematous and longitudinal sections of the long bones will show expansion of red marrow into the medullary cavity. Anywhere from 2,000 to 20,000 worms may be found and the abomasal contents will be brown due to the presence of blood. Hemorrhagic lesions will usually be present on the abomasal mucosa . Chronic haemonchosis in a sheep flock usually results from a combination of infections with small numbers of worms and poor nutrition that persist for a prolonged period of time (several weeks or months). Infected sheep suffer a chronic daily loss of small amounts of blood but this loss is exacerbated by a diet poor in protein. As a result, these animals are unable to replace all their lost serum proteins fom their deficient diet. Consequently, they lose weight as they mobilize muscle proteins to provide the amino acids necessary to synthesize vitally important proteins such as plasma proteins and hemoglobin.
Another form of chronic haemonchosis may also be seen in sheep flocks where mild to moderate infections occur and where nutrition is good. The accompanying image shows how body weights and growth rates of sheep are affected by chronic haemonchosis. After 16 weeks of infection, these animals appear to be clinically healthy but their weight gains are approximately half those of controls. These reduced growth rates cannot be accounted for by loss of appetite since nitrogen (N) intake values show that infected sheep were consuming more protein than the control sheep. It is clearly important that infected sheep maintain physiological levels of important plasma proteins and Hb, in the face of blood losses due to the infecting worms. They do this by diverting available dietary proteins away from muscle synthesis and towards vital organs such as the liver and bone marrow where plasma proteins are synthesized and red cells are produced. chronic haemonchosis of this type will clearly have financial consequences due to poor weight gains combined with increased feed intake.
The Nematodes
Clinical signs
Sudden death from hemorrhagic gastritis in the hyperacute form. Acute haemonchosis - anemia (pale mucous membranes), severe edema (ascites and submandibular edema "bottle jaw"), weakness, loss of wool, dark feces. Chronic haemonchosis - weight loss, lethargy, mild anemia, edema may or may not be present.
Diagnosis
Clinical signs. Fecal egg counts Necropsy - worms in the abomasum, expansion of red bone marrow in the long bones, edema, pale mucous membranes.
Ostertagia
Species
These are small (~10mm) reddish brown worms found in the abomasum of ruminants. On a global basis they are the major cause of parasitic gastritis (Ostertagiosis) of ruminants in temperate climates. The following table lists the three major species.
Nematode Species Host Species Predilection site Ostertagia ostertagi cattle Abomasum Ostertagia circumcincta sheep and goats Abomasum (Teladorsagia) Ostertagia trifurcata sheep and goats Abomasum
Other, less common species include O. lyrata, and O. kolchida in cattle plus O. leptospicularis found in cattle, sheep and goats. Ostertagia species are found throughout temperate and subtropical areas of the world. The cattle species, Ostertagia ostertagi is particularly important in temperate areas wherever cattle are raised.
Morphology
Adult worms are small (approximately 1 cm long) and brownish in color. They are difficult to see at necropsy unless they are present in large numbers (thousands). All parasitic larval stages are found in the gastric glands of the abomasum which must be digested in order to release the larvae for observation with a microscope. A buccal cavity is present, although tiny, as shown by the linked images from light microscopy and scanning electron microscopy. The spicules of males are fairly similar in size and shape but are quite distinguishable from spicules of males in other abomasal nematodes (Trichostrongylus axei and Haemonchus).
Trichostrongyles of the abomasum Male spicules
Haemonchus placei - tail end of male showing paired spicules (A)
Ostertagia ostertagi- tail end of male showing paired spicules (B)
Trichostrongylus axei - tail end of male showing paired spicules (C)
Ostertagia
Epidemiology (for US only)
The epidemiological patterns of ostertagiosis have been well defined in most areas of the world. There are also four common features that influence these epidemiological patterns despite the wide range of climates and management conditions under which cattle are raised. 1. The influence of temperature and moisture on the survival and development of preparasitic stages of the life cycle. 2. The different ways in which pasture is used to raise dairy replacement heifers and beef calves. 3. The influence of seasonal arrested development (hypobiosis) on the parasitic phase of the life cycle. 4. The influence of the immune response on infection and disease. 1. Temperature and moisture The most important factors controlling the preparasitic phase of the life cycle of Ostertagia species are temperature and moisture. Temperature determines the rate of development and moisture is essential for development to occur in the first place. Although the climate in the continental United States is predominantly temperate there are significant variations ranging from cool and wet in the pacific Northwest to hot and dry in the southwest and a warm, wet, almost subtropical climate in the southeast. 2. Arrested development In the United States, as in other temperate areas of the world, seasonal arrested development or hypobiosis is the most significant factor controlling transmission patterns of Ostertagia ostertagi because it occurs regularly from year to year.
In the northern states, hypobiosis begins in autumn, enabling Ostertagia to survive the long, cold (sometimes harsh), winters characteristic of the north. The stimulus for larvae to arrest is falling temperatures in early autumn, signaling the approach of winter. L3s so stimulated will arrest if they are ingested by grazing cattle and will remain arrested throughout the subsequent winter. The image shows the approximate lines of demarcation between the geographical areas where Ostertagia arrests over winter and where it arrests over summer. (Source US Veterinary Services, 2005). Although there are two distinct patterns to hypobiosis and transmission of Ostertagia ostertagi the divisions are not entirely absolute because weather patterns do not fall readily into two distinctive northern and southern regions and also because weather
conditions vary from year to year in many localities. In the transition zone, which lies approximately between the two broken white lines, hypobiosis may begin in autumn, in spring or not at all depending on the locality. The influence of climate on the epidemiology of Ostertagia and other nematodes of the gi tract will be discussed more extensively in a later chapter. Southern areas of the United Sates are characterized by a warm spring and autumn, a hot summer and a mild winter. Here, hypobiosis begins in the spring and lasts over the hot summers with resumption of development of arrested larvae in late summer and early fall. The stimulus for larvae to arrest in these areas is not precisely known but is thought to be either rising temperatures or possibly declining moisture levels that are usually seen in late winter-early spring.
Ostertagiosis is seen as two distinct clinical entities, Type I and Type II. Type I disease occurs most commonly in young cattle grazing contaminated pastures for their first time. In these cases the pathological insults and clinical signs are always due to immature adults leaving gastric glands after developing from L3s ingested approximately 3 weeks before. Type II disease always results from arrested L4's resuming their development to immature adults and leaving the gastric glands approximately 7-10 days after development resumes, but weeks or months after first being ingested as L3s. The table below summarizes the major influences on transmission of Ostertagia ostertagi and the times of year when the disease and hypobiosis generally occur in the two major regions of the United States.
Southern United States Mild and warm, occasional cool Winter or cold periods of short duration. Precipitation mostly rain with very occasional sleet or snow showers. Very hot and humid with variable Summer Warm, sometimes very humid with variable amounts amounts of rain usually as of rain usually as thunder thunderstorms. storms. Pasture A minor wave is seen in April Pasture levels of L3s usually and May. This dips in June peak from March through mid L3s and July but rises to peak May. This is followed by a steady again in August through decline through the hot summer October. Pasture levels of months to low levels . These L3s begin to decline in late begin to rise again slowly in October and reaches low November and a more rapid rise levels in December through to peak levels begins in March. February. Type I Outbreaks may be seen in Outbreaks may be seen anytime late spring but occur more from mid December through the disease commonly between late end of May but the most severe summer and mid autumn outbreaks usually occur in the due to the peak levels of months of January, February pasture L3s at this time. and March.
Feature
Northern United States Cold, often severely so. Precipitation most often as snow, sleet and freezing rain.
Hypobiosis Significant numbers of arrested larvae may be found anytime between mid October and the end of March with peak numbers between mid December and mid February. Type II Outbreaks of Type II ostertagiosis may be seen disease anytime between early February and early May.
Significant numbers of arrested larvae may be found between early April and the end of September with peak numbers in the months of May, June, July and August. Type II ostertagiosis may be seen in the months of September, October, November and December.
3. Pasture use in cattle management In the United States there are wide regional variations in the methods by which dairy cattle are raised. These variations depend to a large extent on the prevailing regional climate which, in turn determines the seasonal availability of pastures for grazing. In general adult lactating dairy cattle are kept in confinement housing with access to dry lots or pastures only for exercise during mild weather periods. Dry cows and replacement heifers are usually turned out to pasture during the growing season in northern but may be pastured year for most of the year in some southeastern states and the Pacific northwest. There are fewer variations in the management and grazing of beef cow herds. Cow herds and their calves tend to be on pastures for most of the year in all regions of the United States with supplementary feeding only when pastures are limited due to weather that is either too hot or too cold. After weaning, calves are often sent directly to feed lots for finishing or are kept at their herd of origin as replacements or as "stocker cattle" raised on pasture for several more months before being sent to feed lots for finishing. In general, most beef calves are born either in the spring or autumn. Clearly the epidemiology of ostertagiosis in beef calves will differ depending on whether they are spring-born or autumn-born and also in which region of the United States they are raised. These regional and climatic influences on the epidemiology of Ostertagia infections will be considered in more detail along with other gastrointestinal nematodes in the later chapter on Parasites of Cattle. 4. Immunity Significant immunity does not develop in grazing cattle until after a full grazing season and that immunity will decline when animals are not exposed to infective L3s for several months during their first winter housing. Immunity tends to be strong in adult cattle and clinical ostertagiosis tends to be uncommon in cattle over two years old. Their is some evidence that a periparturient relaxation of immunity may occur in first calving heifers and this may lead to significant infections and disease outbreaks in these animals. It is speculated that these animals are probably harboring large numbers of Ostertagia larvae in arrested development because of the host's immune response. The periparturient relaxation of immunity allows these larvae to resume development and cause severe enough pathological changes in gastric glands to result in clinical disease. Management practices that limit the acquisition of immunity will also affect the the patterns of ostertagiosis. For example dairy calves raised in confinement housing will have limited exposure to Ostertagia infections and will not develop a strong immune response. These animals will be susceptible to infection and disease throughout their lives if they are ever exposed to pastures contaminated with Ostertagia infective larvae.
Ostertagia in sheep and goats

Ostertagiosis in small ruminants appears to be much less important in the United States
than in cooler parts of the world such as Northern Europe and the British Isles. In the northern and central United States, Ostertagia circumcincta is quite prevalent in sheep and goats along with Haemonchus contortus and Trichostrongylus colubriformis but its significance in disease is considerably less than Haemonchus even though it is often found in greater numbers at necropsies. This is because small numbers of Haemonchus may cause significant problems as a result of its propensity for sucking blood. In the southern United States, Ostertagia circumcincta is of no real significance in small ruminants because the hot and often dry summers are hostile to the survival of its preparasitic stages and it would appear that O. circumcinta, unlike its bovine counterpart, has not developed hypobiosis as a mechanism for survival. In the western U.S. particularly the cooler, wetter, coastal areas of Washington, Oregon and Northern California, Ostertagia circumcincta is the dominant nematode of sheep and goats. However, it is not usually cited as a major cause of disease probably because it is present in relatively small numbers. In Europe, the more temperate climate allows Ostertagia circumcincta and Ostertagia trifurcata to thrive more readily than the United States and clinical outbreaks of diarrhea may be seen in late summer and early autumn in grazing lambs. Hypobiosis is a generally recognized phenomenon in Ostertagia species of sheep and allows survival of the nematode over winter. Type II ostertagiosis has been reported in yearling sheep that grazed pastures the previous years.
Ostertagia ostertagi
Clinical signs
The range of recorded clinical signs in bovine ostertagiosis is as follows. Diarrhea Anorexia or reduced appetite Dehydration Thirst Weight loss Submandibular edema Anemia
The primary clinical sign in bovine ostertagiosis is diarrhea which is often described as "profuse and watery" and is usually accompanied by anorexia, dehydration and thirst. Affected animals are usually depressed with dull, rough coats and their hindquartes are always soiled with feces as a result of the profuse diarrhea. Weight loss may be significant and, in heavy infections with severe diarrhea and anorexia, animals may become rapidly emaciated, losing up to 20% of their body weight in 10 days or less. Submandibular edema (commonly called "bottle jaw") may also be seen and this directly results from a hypoproteinemia that is, in turn, a reflection of the severe protein loss through the damaged gastric glands. A more substantial description and explanation of hypoproteinemia and edema is given in the later chapter on pathophysiology. A low grade anemia may be seen, especially in Type II ostertagiosis, but its significance and cause is unknown. Ostertagiosis can be a serious disease especially in young cattle and unless sick animals are removed from contaminated pastures and treated with appropriate anthelmintics they will likely die. Animals infected with fewer worms may still show clinical signs, especially diarrhea, but with appropriate treatment they will recover quickly and resume their normal growth patterns. Animals with lighter Ostertagia infections may not show any clinical signs but, in the absence of adequate treatment and control measures, their growth rates will be retarded and the costs of rearing such animals will increase substantially. The results will be significant economic penalties to affected farms or ranches whether ostertagiosis manifests as subclinical or clinical disease.
Ostertagiosis in lactating adults

Although grazing animals remain susceptible to O. ostertagi throughout their lives, infections in mature animals are usually light in terms of worm burdens. Reports in the literature have provided evidence that anthelmintic treatments of adults cows at or near parturition will produce increases in milk yields with attendant financial
benefits to the producer. Other reports have denied such benefits and still others have shown substantial increases only in the milk yields of lactating heifers following treatment at their first parturition but not in adult cows in later lactations.
The effects of these suggested benefits are shown in the accompanying image. The red line represents the milk production curve of a cow that is untreated with any anthelmintics at all during its production life beginning with the first parturition. The green line represents the production curve of a cow that is treated with an anthelmintic approximately 3-4 months after parturition. The presumption is that this anthelmintic would be one with a zero withdrawal time so that milk from treated cows would not have to be discarded or otherwise kept from the human food supply. The blue line represents the production curve following treatment, at or near parturition, with a drug whose withdrawal time does not exceed 96 hours - the time of colostrum production when such milk would be kept from the human food supply anyway. The presumption and the claim is that anthelmintic treatment at parturition offers substantial benefits in terms of increased milk production during the subsequent lactation and this will be translated directly into significant economic benefits to the milk producer.
Although adult cows harbor substantially lower worm burdens than growing calves and heifers, it is theorized that even low burdens of Ostertagia ostertagi will produce pathological changes in the abomasum and severe enough derangements in protein metabolism that milk production will be affected. It has been postulated that hypersensitivity reactions to even small numbers of developing larvae will produce changes in the gastric glands that are significant enough to result in mucosal permeability of the kind usually seen only in heavy infections.
Diagnosis
A diagnosis of ostertagiosis is usually made on the basis of several characteristics. In severe Type I disease, the clinical sign of diarrhea accompanied by losses of appetite and weight in calves that are currently grazing known contaminated pastures is highly suggestive of a diagnosis of ostertagiosis. Treating these animals with an anthelmintic effective against O. ostertagi and removing them from pastures will confirm the diagnosis if the clinical signs subside. Under field conditions such action is often warranted even before a diagnosis is confirmed because in seriously ill cattle, time is of the essence. In severe Type II disease the same clinical signs in older animals with a previous history of grazing contaminated pastures is also highly suggestive of ostertagiosis. In these animals clinical signs will only subside if they are treated with an anthelmintic effective against arrested larvae as well as adult worms. In this event, time is also important and for this reason treatment is sometimes implemented before ostertagioisis is confirmed as a definitive diagnosis. The presence of strongyle-type eggs in the feces of affected animals will merely confirm the presence of adult strongyle nematodes in the g.i. tract. In Type I disease, egg counts greater than 1,000 epg are usually seen but counts are much more variable in Type II disease.
Nematodirus
These are slender, relatively long worms (up to 2.5 cm long). As the accompanying image shows, t are distinguished morphologically by an inflated cuticle around the anterior end which may also sho transverse striations. Large numbers of these long slender worms are usually seen at necropsy, in small intestine, as clumps resembling cotton wool.
The image above shows the tail end of a Nematodirus battus female. The black arrow shows the long, pointed tail which in other Nematodirus species ends bluntly and has a small spine attached.
The image above shows the tail end of a Nematodirus battus male. Spicules of all species are paired and long and the tips are fused (A). In N. battus, each bursal lobe has one pair of parallel rays (B) while all the other species have two.
The species occurring in North America are listed in the table below
Nematode Species Nematodirus battus Nematodirus spathiger Nematodirus filicollis Nematodirus helvetianus Nematodirus abnormalis
Host Species Predilection site sheep small intestine sheep and goats small intestine sheep and goats small intestine cattle small intestine sheep and goats small intestine
N. spathiger and N. filicollis are commonly seen in sheep throughout the United State. N. battus was first recorded in the U.S. in Oregon in 1985 and has since been identified in Washington and several New England and Mid Atlantic States (Vermont, New York, Maryland)
As the accompanying image shows, the eggs (B) of Nematodirus are approximately twice as large as the typical strongyle-type egg (A).
Life-cycle
The most important feature of the life cycle is that L3's develop within the protective egg shell. Development is slow, taking as long as 2 months in temperate climates. There is no migration within the definitive host and the prepatent period is approximately 15 days.
Pathogenesis and clinical signs

Nematodirus is not usually a primary pathogen in ruminants in North America. Its importance therefore is as an additive affect in mixed infections of nematodes causing parasitic gastroenteritis. However, Nematodirus battus does cause significant disease in lambs in Britain because its unusual hatching requirements may result in heavy contamination of pastures with newly hatched L3s just as lambs are close to weaning and are beginning to graze pastures more in late spring (May and early June in Britain). Diarrhea followed rapidly by dehydration are the primary clinical signs. Adult ewes have developed a strong immunity to Nematodirus and are usually unaffected.
Epidemiology
The most important factor influencing transmission of Nematodirus species is the ability of L3s to survive from year to year enclosed inside their protective egg shells. In N. battus infections in Britain the special hatching requirements ensure that lambs will be invariably exposed to heavily contaminated pastures in late spring. Combined with the short prepatent period this will lead to sudden outbreaks of diarrhea in young lambs during the period before and after weaning. Arrested development has been recorded in sheep in Canada and the northern United States and has been attributed to hypobiosis at the L4 stage as a mechanism for survival over winter. However, it is also claimed that larval arrest in Nematodirus species is entirely due to host resistance since in Britain there appears to be no obvious seasonal pattern to its occurrence.
Diagnosis
In acute outbreaks of disease in lambs (in Britain), diarrhea will often occur before patency and eggs will often be absent in feces. However, Nematodirus infections in North America are usually subclinical and the presence of the nematode is diagnosed by detecting the characteristic eggs (A) in fecal floats along with strongyle-type eggs (B) of other trichostrongylid nematodes.
Cooperia
Cooperia species are nematodes of the small intestine of ruminants. Species in domestic animals are usually 5-9mm long and males have a prominent bursa in relation to their size. Cooperia curticei is easily recognized on microscopic examination by its coiled appearance that has been described as like a "watch spring", as shown in the accompanying image of a female. The most distinguishing morphological feature of the genus is the cephalic vesicle, found in all the species, giving the head end a slightly bulbous appearance when worms are examined under a dissecting microscope or under the low power of a compound microscope. In addition the anterior cuticle has transverse striations and these can be seen by clicking on the image or here. Male spicules are short and their shapes may be used to identify the different species. The image on the right shows the tail end of Cooperia oncophora with a prominent bursa typical of the genus and paired spicules whose shape is characteristic of the species..
There are five important species in ruminants.

Nematode Species Cooperia curticei Cooperia oncophora Cooperia pectinata Host Species sheep and goats cattle cattle
Predilection small intestine small intestine small intestine
Cooperia punctata Cooperia surnabada
cattle cattle and sheep
small intestine small intestine
Life cycle
The life cycle is direct and similar to the other Trichostrongyles. Arrested development is an important feature of the life cycle.
Pathogenesis
Cooperia are generally considered to be mild pathogens. They contribute secondary effects to the primary pathogens Ostertagia and Haemonchus in parasitic gastroenteritis. However, Cooperia punctata, pectinata and suranabada are believed to be more pathogenic since they penetrate the mucosa during larval development causing changes similar to those of intestinal species of Trichostrongylus.
Epidemiology
Patterns of transmission are different depending on the species. In temperate climates the patterns follow Ostertagia with winter hypobiosis at the L4 stage in the northern hemisphere. In subtropical areas the patterns of transmission follow those of Haemonchus with hypobiosis during the dry seasons.
Clinical signs
A variety of clinical signs have been attributed to Cooperia species and these include diarrhea, weight loss, anorexia and poor weight gains.
Diagnosis
Cooperia infections are usually secondary contributors to parasitic gastroenteritis caused by the more important nematodes, Ostertagia and Haemonchus. Therefore, they are rarely diagnosed as monospecific infections. However, like most other trichostrongyles, females pass strongyle-type eggs that may be found in host feces. The image to the right shows strongyle-type eggs (including Cooperia) and a Nematodirus egg (A) in a fecal sample.
Hyostrongylus
The only species of importance in domestic animals is Hyostrongylus rubidus , commonly called the "red stomach worm" of pigs. It is a slender worm, 5-10mm in length. The image on the right shows fresh specimens in the stomach at necropsy. Its reddish color when fresh has led to the assumption that the worm is an active blood feeder although this claim is disputed because its parasitic phase in the host is very similar to Ostertagia species. It is a common nematode of adult swine, with access to pasture and has a world wide distribution in areas with temperate climates.
Life cycle
The life cycle is similar to other members of the family Trichostrongylidae. The prepatent period is approximately 3 weeks. Infected animals pass "strongyle type eggs" which cannot be distinguished morphologically from Oesophagostomum dentatum and Trichostrongylus axei except by larval cultivation. Seasonal hypobiosis is an important feature of the life cycle in temperate areas of the world. Because of the free-living larval requirements, infection is mostly seen in pigs with access to pasture. However, transmission has been recorded in pigs raised totally in confinement.
Pathogenesis
and clinical signs
Pathogenic effects of Hyostrongylus infections are similar to Ostertagia in cattle. It causes a hemorrhagic gastritis and usually presents as a chronic wasting disease with anemia, loss of condition, anorexia and sometimes diarrhea. Since L3s invade the gastric glands and emerge as immature adults as in ostertagiosis, parietal cells are replaced by proliferating immature cells that produce nodules (as shown in the accompanying image) similar to those in ostertagiosis. Heavy infections may produce ulceration of the gastric mucosa with excessive bleeding from ruptured blood vessels giving rise to a hemorrhagic gastritis. It seems likely that the reddish appearance of the worms may be due to passive ingestion of hemorrhagic stomach contents during feeding by adults.
Dictyocaulus
Members of the family Dictyocaulidae are unusual among the Trichostrongyloidea in that they parasitize the lungs, especially the bronchi of the diaphragmatic lobes and the trachea. They are found throughout the world but are more common and clinically important in temperate areas particularly when summer rainfall is above average. They are thin, thread-like worms, from 3 to 8 cm long. The mouth is surrounded by 4 lips and the mouth opening leads into a small buccal capsule. The males have a prominent copulatory bursa.
Dictyocaulus head end showing the small mouth opening (arrow).
Scanning electron Dictyocaulus male bursa micrograph of showing the short, fat, Dictyocaulus showing the dark spicules and one mouth opening surrounded dorsal ray with a trilobed by lips. tip(arrow)
There are three Dictyocaulus species of importance in domestic anmials.
Nematode Species
Dictyocaulus filaria Dictyocaulus viviparus Dictyocaulus arnfeldi
Host Species
sheep and goats cattle and deer donkeys and horses
Predilection site
trachea and bronchi trachea and bronchi trachea and bronchi
Dictyocaulus viviparus
Dictyocaulus viviparus is the most pathogenic and will be discussed in detail.
Life cycle
A fuller description of the life cycle may be viewed by clicking here. A summary will be given on this page. Females are ovoviviparus which means that they lay eggs that are already embryonated. These hatch immediately, L1s migrate up the trachea, are coughed up, swallowed and pass out from infected cattle in their feces.
The preparasitic phase of the life cycle is similar to the other Trichostrongyles, with one exception. Because the L3's are not particularly motile, they have evolved a method of facilitating their dispersal from the fecal pad to the surrounding grass where they can be ingested by susceptible grazing animals. Larvae migrate onto the sporangia of the fungus Pilobolus that commonly grows in cattle feces, as shown in the image to the right.
Image courtesy of Merial Inc
When the sporangia explode, releasing their spores into the surrounding environment, the larvae of Dictyocaulus are also released. This is shown in the image cartoon on the right.
Ingested L3s migrate through the intestinal wall to the mesenteric lymph nodes, molt to L4, then continue via the lymphatics and blood to the lungs where they migrate through the capillary walls into the alveoli. The final molt occurs and the immature adults move up the bronchioles to the bronchi. The prepatent period is 3 to 4 weeks.
Pathogenesis
Severe pathological changes can occur before patency due to larvae and immature adults migrating through the alveoli, bronchioles and bronchi and inducing an inflammatory response. Bronchiolar passages become clogged with inflammatory cells, including eosinophils, macrophages and neutrophils and if severe enough may result in collapse of alveoli distal to these cellular infiltrates because air cannot pass through these plugs. Air present in the alveoli is absorbed into the blood and the alveoli collapse because new air cannot pass the eosinophilic plug. The severity of these lesions is directly related to the degree of infection such that heavy infections may lead to interstitial emphysema and pulmonary edema that is often fatal. Patent disease is associated with adult worms in the bronchi and manifests as a bronchitis with a mucus exudate followed by pneumonia due to aspiration of eggs and L1's into the alveoli where they are surrounded by inflammatory cells, including macrophages and giant cells, and ingested. The bronchial epithelium is infiltrated by inflammatory cells and becomes hyperplastic. Heavy infections may progress to emphysema and edema. In lightly infected animals, recovery will occur following expulsion of the adult worm population. In moderate to heavy infections, the bronchial lesions may take several weeks or months to recover. However, during this recovery phase a small number of animals may succumb to a postpatent parasitic bronchitis or a secondary bacterial pneumonia. The etiology of the syndrome, postpatent parasitic bronchitis, is unknown but is due to a proliferation of alveolar epithelial cells converting the thin, permeable alveolar epithelium into a thickened layer of cells that is much less permeable to the passage of oxygen and carbon dioxide, thereby compromising gaseous exchange at the alveolar surfaces. Interstitial emphysema and pulmonary edema are common complications of this syndrome and when this stage is reached, death is almost certain. Pulmonary edema results from the onset of cardiac failure in animals with dyspnea. Alveoli fill with transuded fluid and the alveolar walls become lined with protein "hyaline membranes" as water in the transuded fluid evaporates or is reaborbed. These membranes further compromise gas exchange at the alveolar epithelial surfaces and lead to a significant deterioration in clinical condition.
Images showing the development of parasitic bronchitis in cattle due to Dictyocaulus viviparus Dictyocaulus viviparus
1. Larva migrating up a bronchus.
2. Eosinophilic plug in a small bronchiole and collapse of surrounding alveoli.
3. Adults in a bronchus with exudation and intense cellular infiltration surrounding the bronchus.
4. Adult worms in the diaphragmatic bronchi.
5. Distribution of lung worm lesions in the diaphragmatic lobes.
6. Parasitic pneumonia with giant cells and macrophages engulfing aspirated eggs and newly hatched larvae
7. High power - parasitic pneumonia with giant cells and macrophages engulfing aspirated eggs and newly hatched larvae
8. Post patent parasitic bronchitis - diffuse epithelialization (swelling and proliferation of type II pneumocytes). Many macrophages are present in the lumen of these epithelialized alveoli
9. Reinfection lesion dead worm surrounded by an eosinophilic necrotic area and proliferating lymphoid tissue.
10. Gross picture of emphysema
11. Microscopic picture of 12. Pulmonary edema emphysema
13. Hyaline membranes lining the alveolar surfaces
Epidemiology
Calves and yearlings turned out to pasture for the first time are highly susceptible to infections with Dictyocaulus viviparus since their lack of previous exposure means they have not developed an immune response. In areas of the world where cattle are primarily raised on pasture, adult animals will have been already exposed to the parasite during their growing phase and will therefore have a strong acquired immunity. D. viviparus is endemic in temperate areas of the northern hemisphere with mild summers and high rainfall. It is common in cattle-raising areas with permanent pastures used for seasonal grazing. These areas are mostly in northern Europe including the British Isles. In the United States, D. viviparus is less common than in Europe and often goes undiagnosed because veterinarians are generally unfamiliar with the nematode and the methods used to diagnose infections. In a number of cases reported in the literature, parasitic bronchitis went undiagnosed and untreated for several weeks after the initial reporting of clinical signs (usually sporadic coughing in animals on pasture) because sick animals were usually treated initially for pneumonia of either viral or bacterial origin. Parasitic bronchitis due to D. viviparus has been reported sporadically in North America during the last 50 years. Cases have been consistently reported from the northeast United States, the mid west, the Pacific northwest and Eastern Canada. Many of these more recent cases were reported in adult lactating dairy cows and all occurred in animals managed on intensive grazing systems. These animals clearly lacked immunity to D. viviparus and we can safely conclude that they received little or no exposure to the parasite during their growing phase and so were still susceptible to infections as adults. Epidemiological investigations in Britain have concluded that survival of Dictyocaulus and its transmission are dependent on two conditions 1. Third stage larvae(L3s) may survive over winter on pasture in enough numbers to cause infections and perhaps disease in susceptible animals turned out to pasture in early spring. 2. Older animals (yearlings and adults) may serve as carriers over winter in that some adult worms - either as fully mature or hypobiotic immature adults - will survive in the bronchi. Hypobiosis at the immature adult stage (L5) as been documented in mainland Europe, Britain and eastern Canada, although its precise role in transmission has not been determined as yet. The recent increases in cases of parasitic bronchitis in adult cattle, in Britain may be attributed to several factors 1. Use of the lungworm vaccine (Dictol) in Britain was high in the early years after its introduction in 1965. However, vaccinated animals are still susceptible to infection at a low level even though they are protected against disease. These animals often had small numbers of adult Dictyocaulus in their lungs and passed small numbers of L1s - sufficient to maintain low level contamination of pastures. Over time the annual use-levels of the vaccine in susceptible calves tapered off. Some of these unvaccinated animals would not be exposed to sufficient levels of infections to initiate a protective immune response and would therefore remain susceptible to infections even as adults. Contamination levels of L3s eventually build up, on pasture, to the point where disease outbreaks may be seen in susceptible unvaccinated cattle (of all ages). These observations reinforce the point that calfhood vaccination programs must be continued every year with every new group of susceptible calves. The small numbers of L3s on pasture serve to boost the immune response of vaccinated calves throughout their lives but may produce clinical parasitic bronchitis in susceptible animals. 2. Weather patterns in Britain seem to have changed during the last 10-15 years with dry, warmer summers being more frequent. These conditions have resulted
in fewer larvae on pasture so that grazing calves have not only experienced fewer outbreaks of parasitic bronchitis but also have not developed strong immune responses to the parasite. As a result they remain susceptible to the parasite through to their lives as adults. In areas of the United States where Dictyocaulus is prevalent, summers are not consistently cool and wet leading to variable levels of pasture contamination with L3s depending on temperature and moisture. In warm or hot and dry summers, Dictyocaulus infections and disease will rarely be seen. However, when summers are cooler and wetter than normal, outbreaks of parasitic bronchitis will be seen more frequently. These kinds of changeable weather patterns make it more likely that calves will grow to adults without significant exposure to D. viviparus and will therefore remain susceptible to infections. There is some evidence that Dictyocaulus larvae may burrow into the soil where it is cooler than on the surface pasture. This behavior may allow larvae to survive periods of inclement weather that would be hostile to their survival and return to the surface pasture when conditions are more favorable. The vaccine used in western Europe consists of third stage larvae partly attenuated by irradiation and administered orally to calves at least two months old and before they are exposed to infection by turning them out to pasture. Two doses of the vaccine are given 4 weeks apart and vaccinated animals should not be placed on pasture until two weeks after the second dose. There is also evidence that deer may serve as reservoirs of infection, maintaining L3s on pasture at sufficient levels to produce clinical disease in grazing cattle.
Clinical signs
In herd outbreaks of parasitic bronchitis, a spectrum of clinical signs may be seen as illustrated in the following table.
Mild Moderate Severe infections infections infections Intermittent. Frequent even A deep, harsh More at rest. cough pronounced on exercise Respiratory Often normal Tachypnea 40- Severe tachypnea rate 60/minute >80/minute Lung Often normal, Diaphragmatic Diaphragmatic auscultation sometimes lobes lobes - pronounced occasional pronounced squeaks and squeaks squeaks and crackles. crackles. Other signs None Usually none Respiratory distress (dyspnea), gasping for air with head and neck outstretched. Salivation, loss of appetite, fever.
Clinical signs in parasitic bronchitis are associated with a progressively developing bronchitis and pneumonia - coughing, tachypnea, fever, anorexia, loss of weight and dyspnea. In adult cattle milk production will be affected. Respiratory distress is characterized by animals assuming the "air hunger" position - head and neck held straight out horizontally with tongue protruded.
Clinical sign Coughing
Diagnosis
The clinical signs of coughing in cattle either on pasture or with a recent history of grazing is usually strongly indicative of parasitic bronchitis due to Dictyocaulus viviparus.
Confirmation of the diagnosis comes from finding characteristic first stage larvae(L1s) in the feces of animals with patent infections by using a Baerman apparatus. The image on the right shows such a larva. They are 310-360 microns long and 16-19 microns wide and the latter two thirds of the body contains prominent dark brown food granules present in the intestinal cells. Since D.
viviparus is the only lungworm of cattle, finding these L1s in cattle feces is diagnostic. In a herd outbreak of suspected parasitic bronchitis repeat fecal samples should be taken and examined for L1s since clinical signs in heavy infections are usually first seen during the prepatent period. This is particularly true in cooler, temperate areas where heavily contaminated pastures with Dictyocaulus L3s may produce severe outbreaks in calves soon after turnout to pasture in the spring. At necropsy, adult worms may be easily seen in the bronchi of infected lungs. The absence of L1s in the feces of animals with severe clinical signs of parasitic bronchitis usually means that these cattle are strongly immune but are undergoing a severe challenge infection, with large numbers of developing larvae being destroyed by the immune response.
The Strongyloidea
Strongylida
The order Strongylida includes many of the important nematodes found in the gastrointestinal tracts of ruminants, horses, and swine, as well as the lungworms of ruminants and the hookworms of dogs and cats. The following table gives an overview of the classification of this order with an emphasis on the superfamily Strongyloidea.
Order Superfamily Family Subfamily Genus - examples
Strongylida
Trichostrongyloidea
Trichostrongylidae Dictyocaulidae
Strongyloidea
Strongylidae
Strongylinae
Strongylus Triodontophorus
Cyathostominae
Cyathostomum Cylicostephanus Cylicocyclus Cylicodontophorus Poteriostomum Gyalocephalus
Chabertiidae
Chabertiinae Oesophagostominae
Chabertia Oesophagostomum Stephanurus Syngamus
Syngamidae
Stephanurinae Syngaminae
Ancylostomatoidea Metastrongyloidea
Ancylostomatidae Metastrongylidae Protostrongylidae Filaroididae
Their distinguishing features include a copulatory bursa (in males) and a buccal capsule of variable shape and size. Examples of direct (free living larvae) and indirect (intermediate host) life cycles can be found among the members of this order. There are four superfamilies of importance in domestic animals:
Trichostrongyloidea Strongyloidea Ancylostomatoidea Metastrongyloidea
Females belonging to the superfamilies Trichostrongyloidea, Strongyloidea and Ancylostomatoidea produce smooth, thin-shelled, ellipsoidal "strongyle-type" eggs (A), approximately 80-100 microns long and 40-50 microns wide. One exception to this rule is Nematodirus, whose species produce eggs that are approximately twice the size of "strongyle-type eggs (B). Notice the difference between these eggs and the whipworm (Trichuris) egg (C).
A fifth (minor) superfamily, the Diaphanocephaloidea, are bursate nematodes found in
the digestive tracts of terrestrial snakes and occasionally lizards. There are two genera and thirty three species in this superfamily. Females pass a "strongyle-type" egg and their life cycles are direct and similar to the Trichostrongyloidea but it is also believed that paratenic hosts (snails and slugs) may play a role in their life cycles.
The Strongyloidea
Members of this superfamily are widespread throughout the world. They are primarily parasites of herbivores such as ruminants and horses although a few species are found in ratite birds and marsupials. They have the following general features They are large-bodied worms and are easily seen in situ at necropsy of infected hosts. Males have a copulatory bursa Most have large mouth openings and prominent buccal capsules which may contain teeth in some species. They use their buccal capsules in feeding, either by grazing the mucosal surface or by attaching to a plug of mucosa, drawing it into the buccal capsule and digesting it. Leaf crowns may be present as accessory cuticular structures around the opening of the buccal capsule. Most females of this group pass strongyle-type eggs. Some species have life cycles that include extensive migrations through the bodies of their hosts. They include the large strongyles of equines (e.g. Strongylus vulgaris), the gape worm of birds (Syngamus trachea) and the kidney worm of swine (Stephanurus dentatus). Most have direct life cycles with infection by ingestion of infective third stage larvae but a few such as Stephanurus dentatus (the swine kidney worm) and Syngamus trachea (the gapeworm of fowl) may include earthworms as transport hosts. Most are found in the large intestine but a few species occur in the respiratory and urinary tracts. Three families are important in domestic animals - Strongylidae, Chabertiidae and Syngamidae
Strongylidae
Members of this family are common in equines but they are also found in elephants, ostriches, rhinoceros, tapirs, tortoises, warthogs and marsupials. Their predilection sites include primarily the cecum and colon. The preparasitic phases of the life cycles are similar with strongyle-type eggs passing in the feces of infected hosts. Development to the infective, ensheathed third stage larvae may take as little as 7-10 days in a warm, moist environment. Equine strongylids are usually divided into the large strongyles, belonging to the subfamily Strongylinae and the small strongyles which are members of the subfamily Cyathostominae.
Chabertiidae
This family has been further subdivided into two subfamilies - the Chabertiinae and the Oesophagostominae. The Chabertiinae are often called the bowel worms because of their location in the
colon of their hosts. They have a prominent bell-shaped buccal capsule. The Oesophagostominae are often called the nodular worms because their parasitic larvae provoke nodule formation in the intestines of their definitive hosts. Adults are found in the colon and are common in pigs, ruminants, primates and rodents. The table below lists the species of this family commonly found in domestic and wild animals.
Family
Subfamily
Species
Castorstrongylus castoris
Hosts
Chabertiidae Chabertiinae
North American beaver Chabertia ovina Camels, cattle, chamois, deer, gazelles, goats, sheep Ternidens African and deminutus Asian non-human primates Oesophagostominae Oesophagostomum Sheep, columbianum goats, alpaca, antelope (African) Oesophagostomum Pigs
dentatum Oesophagostomum radiatum
Cattle, zebra, water buffalo Oesophagostomum Ruminants venulosum primarily sheep and goats Oesophagostomum Pigs
quadrispinulatum
Syngamidae
The syngamids are found mainly in the respiratory systems of birds and mammals but one species occurs in the urinary tract of swine and another occurs in the intestines of porcupines. There are two subfamilies, the Stephanurinae and the Syngaminae. Examples of species occurring in domestic and wild animals and birds are given in the following table.
Family Subfamily
Species
Hosts
Syngamidae Stephanurinae Stephanurus dentatus Syngaminae. Cyathostoma bronchialis
Swine
Ducks, geese, swans Mammomonogamus Cattle, sheep, spp goats, deer, felids and elephants in the tropics Syngamus trachea Birds primarily quail, pheasants, guinea fowl
This is the kidney worm of swine, so-called because its predilection sites include the kidneys and associated tissues - more specifically the walls of the ureter and in capsules in the peri-renal fat. It is the only known species in the genus and is found throughout the world but is more common in warm temperate, subtropical and tropical areas. It is of particular importance where pigs are raised outdoors because its preparasitic larvae are free living and may also utilize earthworms as transport hosts. In the United States it is more prevalent in the South, particularly the southeastern states, where it is also common in feral swine.
Morphology
It is a large-bodied worm with a mottled appearance because its transparent cuticle shows its internal organs. It is 2-4 cm long, has a prominent buccal capsule with teeth and males have a copulatory bursa.
Stephanurus dentatus adult worms in situ in the perirenal fat
Stephanurus dentatus Stephanurus dentatus adult worms male (upper) adult worms protruding and female (lower) from a ureter
Pathogenesis
The extensive migrations of S. dentatus during its parasitic phase results in considerable damage to host organs. Skin penetration by infecting L3s may cause cutaneous lesions and swelling of superficial lymph nodes. Liver migrations produce a marked inflammatory reaction with eosinophilia. Repair of these lesions will result in liver scarring and cirrhosis. Migration of immature adults through other organs such as the pancreas may result in abscesses, fibrosis and adhesions.
Images showing liver lesions due to migrating Stephanurus dentatus
Normal pig liver for Stephanurus dentatus comparison with the other liver lesions caused by images in this table migrating larvae and Image courtesy of Dr. Edward immature adults.
Batte Image courtesy of Merial Inc
Stephanurus dentatus fibrotic tracks resulting from migrations of larvae and immature adults
Stephanurus dentatus extensive fibrosis resulting from migrations of larvae and immature adults
Image courtesy of Dr Edward Batte
Epidemiology
Free living larvae cannot survive the cold temperatures encountered during winters in the northern U.S. As a result, kidney worm infections are more common in the southern United States. Infected older sows and boars are the usual source of infection for younger animals and the longevity of adult worms in their host (2-3 years) means that adult infected pigs may be constant sources of infections for young animals. Batte and his colleagues demonstrated transplacental transmission in pregnant gilts but it is uncertain how important this is as a factor in transmission. The dependency of the life cycle on free living preparasitic larvae and earthworms as transport hosts means that this is a parasite primarily seen in pigs raised outdoors. Raising pigs indoors will significantly reduce the prevalence of kidney worms. The "gilts only" system of breeding and rearing pigs was devised as an effective method to control swine kidney worms. In this system, breeding is confined to gilts which are then marketed immediately after weaning their first litters. The long prepatent period of 9-16 months means that pigs are raised , bred and marketed before infections become patent and this system was shown to be an effective method of controlling transmission of Stephanurus dentatus. The problem is that the system fails economically since gilts have smaller litters than older sows and the economic return from these smaller litters is not enough for the system to be viable.
Clinical signs
Overt clinical signs are unusual in Stephanurus infections. Aberrant migrations of larvae to the spinal cord may cause a posterior paralysis but these cases are not common. The usual picture is one of failure to thrive with the primary effects on weight gains. Heavy infections in pigs raised outdoors may cause enough liver damage to result in emaciation and death. The image to the right is of a pig showing chronic effects of Stephanurus dentatus infections. Strongyle-type eggs were present in the urine and at necropsy there were extensive liver lesions and adult worms in the perirenal areas.
Diagnosis
The long prepatent period of Stephanurus means that patent infections are unusual in pigs less than two years old. Infections in adult sows and boars are easily diagnosed by finding the distinctive strongyle-type egg in urine of infected animals - as shown in the accompanying image. Infections often go undiagnosed in live animals, especially in pigs less than a year old. Therefore infections are more often diagnosed at necropsies or at meat inspections when the characteristic liver lesions are found.
Syngamus trachea
This is the gapeworm of poultry, found in the trachea of chickens, turkeys, guinea fowl and many species of wild birds. It is of particular importance in farm-raised pheasants. Although Syngamus is found throughout the world, conversion of domestic poultry raising from outdoors to indoors has significantly reduced its prevalence in the United States.
Morphology
The most distinctive feature of this nematode is that males and females are joined together in a state of permanent copulation forming a Y shape as seen in the image on the right. Females are much larger (up to 20mm long) than males (up to 6mm long).
Life cycle
The life cycle is complicated in both its preparasitic and parasitic phases. In the preparasitic phase L3s develop inside the eggs at which time they may hatch. Earthworms play an important role in the life cycle, serving as transport (paratenic) hosts. Larvae have been shown to remain viable for more than three years encapsulated in earthworm muscles. Other invertebrates may also serve as paratenic hosts and these include terrestrial snails and slugs as well as the larvae of Musca domestica (the common house fly) and Lucilia sericata (the greenbottle fly responsible for cutaneous myiasis). The parasitic phase involves substantial migration in the definitive host to reach the predilection site.
Pathogenesis
Young birds are most severely affected with migration of larvae and adults through the lungs causing a severe pneumonia. Lymphoid nodules form at the point of attachment of the worms in the bronchi and trachea. Adult worms appear also to be blood suckers. Worms in the bronchi and trachea provoke a hemorrhagic tracheitis and bronchitis with formation of large quantities of mucus, plugging the air passages and, in severe cases, causing asphyxiation. Pheasants appear to be particularly susceptible to Syngamus infections resulting in mortality rates as high as 25% during outbreaks.
Epidemiology
Earthworm transport hosts are important factors in the transmission of Syngamus trachea where poultry and game birds are reared on soil. The longevity of L3s in earthworms (up to 3 years) is particularly important in perpetuating the infection from year to year. Wild birds may serve as reservoirs of infection and have been implicated as the sources
of infections in outbreaks on game-bird farms as well as poultry farms. Wild reservoir hosts may include pheasants, ruffed grouse, partridges, turkeys, magpies, meadowlarks, robins, grackles, jays, jackdaws, rooks, starlings and crows. There is also evidence to suggest that strains of Syngamus trachea from wild bird reservoir hosts may be more infective for domestic birds if they first pass through an earthworm transport host rather than by direct infections via ingestion of L3s or eggs containing L3s.
Clinical signs
Blockage of the bronchi and trachea with worms and mucus will cause infected birds to gasp for air. They stretch out their necks, open their mouths and gasp for air producing a hissing noise as they do so. This "gaping" posture has given rise to the common term "gapeworm" to describe Syngamus trachea. These clinical signs first appear approximately 1-2 weeks after infection. Severely affected birds, particularly young ones, will deteriorate rapidly; they stop drinking and become anorexic. At this stage, death is the usual outcome. Adult birds are usually less severely affected and may only show an occasional cough or even no obvious clinical signs.
Diagnosis
A diagnosis is usually made on the basis of the classical clinical signs of "gaping". Subclinical infections with few worms may be confirmed at necropsy by finding copulating worms in the trachea and also by finding the characteristic eggs in the feces of infected birds.
Syngamus trachea bioperculate egg
Syngamus trachea - adult worms in the trachea of an infected turkey
Chabertia ovina
Chabertia ovina is commonly called the large-mouthed bowel worm. In domestic animals, its predilection site is the colon of sheep and goats and it is occasionally seen in cattle. It has a worldwide distribution but it tends to be more common in temperate areas of the world. In the United States, Chabertia ovina is relatively uncommon but is found primarily in more temperate areas of the north. Chabertia ovina is one of the easiest ruminant nematodes to identify because of its size (1-2cm long), location (colon) and its prominent, curved, bell-shaped buccal capsule which lacks teeth. The image on the right shows the head end of Chabertia ovina with its buccal capsule curved anteriorly and ventrally.
Life cycle
The life cycle is direct with the preparasitic phase similar to the Trichostrongyles. After ingestion by the final host, L3s exsheath in the small intestine, penetrate the mucosa and molt to L4s. These emerge, gather in the cecum, molt to immature adults (L5s) and pass on the colon to mature. The prepatent period is approximately 6 weeks.
Pathogenesis
Pathogenic effects are caused by the feeding adults which become attached to the mucosa and draw a plug of mucosa into the buccal capsule which is then digested. This results in area of mucosal ulceration and local hemorrhage with protein loss into the gut through these lesions. In heavy infections, the feeding effects of 200-300 adult worms results in a colon that is edematous and thickened with local areas of hemorrhage where the worms were attached. Some reports claim that larvae and immature adults are blood suckers.
Epidemiology
Infective third stage larvae will survive mild winters on pasture. Hypobiosis is also an important winter survival mechanism in the life cycle of this nematode with L4s being the hypobiotic stage in the mucosa of the small intestine or the cecum. In most parts of the world, Chabertia is not a primary parasite in terms of disease. Its effects are usually additive to more important pathogens such as Ostertagia and Haemonchus. However, in Australia and South Africa it has been recorded as a primary pathogen in sheep.
Clinical signs
Diarrhea is the usual clinical sign in Chabertia infections where it is seen as a primary pathogen. Otherwise, infected sheep may lose weight and condition and may become
anemic. In heavy infections, clinical signs may occur during the prepatent period since immature adults are aggressive feeders. In these cases eggs will be absent from feces but since these are strongyle-type, they cannot be distinguished from the eggs of many other trichostrongyle and strongyle nematodes infecting the guts of ruminants.
Diagnosis
A specific diagnosis is not usually possible in live animals for the reasons mentioned above. At necropsy the worms are readily identified from their location, size and shape of the buccal capsule.
Oesophagostomum species
Morphology and species
Members of this genus are known as the "nodular worms" because they are associated with nodule formation in the intestines of their hosts. They are common parasites of ruminants, pigs, primates and rodents. The species found in domestic animals are often of pathogenic importance:
Nematode Species Oesophagostomum radiatum Oesophagostomum columbianum Oesophagostomum venulosum Oesophagostomum dentatum Oesophagostomum quadrispinulatum
Host Species cattle cattle sheep and goats swine swine
Adults are 1-2cm long. The buccal capsule is relatively shallow and the head end is distinctive because of the cephalic inflations of the cuticle. Males have a bursa and the egg passed by the female worms is a strongyle-type egg
Oesophagostomum Oesophagostomum Oesophagostomum columbianum - the dentatum - adult radiatum with posterior end worms with a pin to cuticular show comparative modifications at the showing the copulatory bursa (A) sizes. The female anterior end: (left of the pin) is the A = cephalic vesicle containing bursal thicker of the two. rays. B = cervical vesicle Image courtesy of The specimen to the C = cervical alae right of the pin is a Merial Inc male L4 with a dorsally curved tail.
Pathogenesis
The most serious problems seen in Oesophagostomum infections arise from larvae penetrating the musosa of the intestine. After initial infections, small nodules about 1mm in diameter form around larvae in the mucosa. When larvae move back into the intestinal lumen the remaining nodules may be hemorrhagic particularly in acute infections but often they fill with pus, in which cases they are more properly described as small abscesses. In heavy infections, the mucosa becomes inflamed and edematous and regional lymph nodes are often much enlarged. Chronic infections will produce an intestinal mucosa that is filled with nodules particularly if these repeat infections have been heavy. In these chronic cases tissue reactions are more severe and the nodules are much larger (up to 6mm in diameter) and creamy in color due to the development of connective tissue around them. In chronic infections, most infecting larvae will be killed by host reactions. Therefore older animals will usually show extensively nodular intestines but with few, if any, adult worms in the colon.
Acute infection with Oesophagostomum radiatum in cattle. Hemorrhagic nodules in the small intestine.
Chronic infection with Oesophagostomum dentatum in pigs. Fibrous nodules in the small intestine.
In sheep, Oesophagostomum venulosum is much less pathogenic than Oesophagostomum columbianum, apparently because it does not stimulate nodule formation. infections with 500 L3s have been reported to produce a transient diarrhea accompanied by petechiae and small ulcers in the small intestine.
Epidemiology
All domestic animals are infected by grazing pastures contaminated with L3s. Oesophagostomum radiatum in cattle is common throughout the world especially in tropical and subtropical areas and is also common in North America. In tropical areas with seasonal rainfall (such as Queensland in Australia) heavy infections with high mortalities may be seen in calves under natural grazing conditions during the rainy season. In sheep and goats, Oesophagostomum columbianum is seen throughout North America except for the west coast. The climatic requirements for survival of preparasitic larvae are similar to Haemonchus contortus therefore O. columbianum is more commonly seen in tropical and subropical areas. However, the requirements for survival of O. venulosum preparasitic larvae are similar to those for Ostertagia and Trichostrongylus and therfore it is more common in temperate areas. Hypobiosis at the L4 stage is the primary method of survival of O. venulosum during
winters in temperate areas of the world. O. dentatum and O. quadrispinulatum also undergo hypobiosis at the L4 stage in pigs but L3s are also known to survive winters on pasture. The resumption of development of these two species in spring can give rise to a periparturient rise in egg counts(PPR) in pregnant and lactating sows. It is speculated that hypobiois may occur in O. columbianum although definite experimental confirmation of this is still awaited. Transmission of Oesophagostomum in housed pigs has been explained by the possibility of percutaneous infections, the easy development of infective larvae in feces and pen to pen transmission by dipteran flies carrying infective L3s on their legs.
Clinical signs
Acute infections are the result of larval penetrations of the intestinal mucosa during the prepatent period. Diarrhea is the usual clinical sign in these cases and may be accompanied by weight loss and submandibular edema ("bottle jaw") in ruminants. Chronic oesophagostomosis is most common in sheep and is due to repeated infections. Intermittent diarrhea accompanied by loss of appetite are the usual clinical signs and in more severe chronic cases sheep may become emaciated and anemic. Infections in pigs may produce a range of clinical signs including acute diarrhea and a syndrome in adult females called the "thin sow syndrome" - a chronic infection with periodic acute flare-ups due to the resumption of development of hypobiotic larvae during spring farrowing. This syndrome shows as weight loss after farrowing and reduced milk production with adverse effects on the growth of litters.
Diagnosis
In acute infections clinical signs will occur during the prepatent period and diarrhea will occur without strongyle-type eggs being seen in the feces of infected animals. In chronic infections, strongyle-type eggs will be commonly seen but are indistinguishable from eggs produced by other strongyle nematodes. Necropsies will show the classic nodular lesions throughout the small and large intestines
Growing pigs (4-5 months old) with acute diarrhea due to a prepatent infection with Oesophagostomum dentatum
Strongyle-type eggs from a patent experimental infection with Oesophagostomum dentatum in pigs.
Strongyles of Horses
The intestinal strongyles of horses are members of the superfamily Strongyloidea and the family Strongylidae. Members of the family are abundant in equines, including horses and donkeys, but are also found in diverse hosts including elephants, ostriches, rhinoceros, tapirs, tortoises, warthogs and marsupials in Australia. The strongylidae are further divided into two subfamilies, the Strongylinae ( the large strongyles) and the cythostominae ( the small strongyles) as shown in the table below.
Superfamily
Family
Subfamily
Genus - examples Strongylus Triodontophorus Cyathostomum Cylicostephanus Cylicocyclus Cylicodontophorus Poteriostomum Gyalocephalus
Strongyloidea Strongylidae Strongylinae (large strongyles) Cyathostominae (small strongyles)
The strongylinae are commonly called the "large strongyles" because of their larger size relative to the cyathostominae which in turn are called the "small strongyles". Both groups are among the most important nematodes of domestic equines throughout the world because of their high degree of pathogenicity and they are certainly so in North America.
Large Strongyles of Horses

Species and morphology
The large strongyles are members of the subfamily strongylinae which includes two genera in domestic horses and donkeys, the genus Strongylus and the genus Triodontophorus.
Strongylus species are commonly found throughout the world and they are of particular importance in horses in North America. The predilection site for all species is the cecum and colon and because of their size they are readily visible at necropsy as seen in the image on the right. The three species are Strongylus vulgaris, Strongylus edentatus and Strongylus equinus. All three species are important pathogens of horses. Adult worms are destructive feeders on the mucosa of the cecum and colon and parasitic larvae undergo extensive migrations in their equine hosts causing significant damage to organs during their migratory routes. They are especially pathogenic in susceptible foals and yearlings.
Mature adults of these species can usually be identified by their relative sizes but more precise identification, especially immature adults and L4s, is based on microscopic features such as the shape of the buccal cavity and the presence or absence of teeth. These features of strongylus species are illustrated in the table below.
Strongylus vulgaris. The buccal cavity contains 2 ear-shaped teeth. Mature adult worms are about 2cm long.
Strongylus edentatus. The buccal cavity is devoid of teeth. Mature adult worms are 4-5cm long.
Strongylus equinus The buccal cavity contains 3 teeth - 1 large and 2 small. Mature adult worms are 5cm long.
Several Triodontophorus species are found in horses but they appear to be less pathogenic than Strongylus because no migrations occur in the host although the buccal cavities of adults contain teeth so damage does occur in the large intestine due to their feeding activities. Triodontophorus appears to be the more common species and it is usually seen at necropsy gathered in clusters around ulcers in the colon.
Triodontophorus adults feeding at an ulcer in the colon of a horse.
Head end of Triodontophorus showing its large buccal cavity with teeth at the base and fringed by a prominent leaf crown around the opening.

Strongylus equinus - life cycle
The preparasitic phase of this life cycle is virtually identical to that of Strongylus vulgaris described previously. Of the three large strongyles, we know the least about the parasitic phase of the life cycle of Strongylus equinus because it is less common than the others and so has been little studied. Infection is by ingestion of third stage larvae and exsheathment occurs in the small intestine. Exhseathed L3s invade the wall of the small intestine, cecum and colon and become encapsulated in nodules in which they molt to L4s by 12-14 days after infection. L4s leave their nodules and cross the peritoneal cavity to the liver, the right lobe of which is in close aposition to the cecum. Most L4s will have reached the liver by 19-20 days after infection and will remain there for at least 12 weeks. Finally, they begin to migrate back to the large intestine by leaving the liver and crossing the abdominal cavity directly or by first passing through the pancreas ( which is closely associated with the right lobe of the liver) and then the abdominal cavity. The final molt to immature adults (L5s) occurs about 15 weeks after infection during their migration back to the large intestine. L5s penetrate the gut wall and enter the lumen of the large intestine via the formation of nodules. Reproduction takes place and the prepatent period is approximately 9 months.
Strongylus edentatus - life cycle

Again, the preparastitc phase of this life cycle is virtually identical to that of Strongylus vulgaris described previously. Ingested L3s exsheath in the terminal portion of the small intestine as well as the cecum and right ventral colon, invade the gut wall, penetrate blood vessels and migrate to the liver via the hepatic portal vein. Molting to L4s occurs in two weeks (range from 11 to 18 days), after which larvae wander throughout the liver before they leave beginning about 42 days after infection. Larvae escape from the liver by migrating under the liver capsule, through the hepatic ligament and underneath the parietal peritoneum to the right flank. Here they molt to immature adults between 13 and 15 weeks after infection and finally return to the large intestine via the mesentery bertween 3 and 5 months after infection. They migrate through the wall of the cecum and colon via formation of nodules. Maturation takes place in the large intestine and the prepatent period is generally acknowledged to be approximately 11 months although it is claimed by some authors that this may be as short as 6 months.
Strongylus edentatus - immature Strongylus edentatus - an adults under the peritoneum of immature adult dissected out of a subperitoneal cyst on the right the right flank. flank.
Strongylus edentatus - an immature adult (arrow) having returned to the large intestine via the nodule (N).

Pathogenesis of adult worms in the large intestine
The pathogenic effects due to large strongyle infections in horses can be divided into those caused by adult worms in the large intestine and those caused by larvae and immature adults during their extensive migrations in other organs. The pathogenic effects due to adults in the cecum and colon of infected horses are similar in all three species of large strongyles because they all provoke the formation of nodules in the gut wall as they pass through in completing their parasitic migrations and their methods of feeding are similar. The formation of nodules in the gut wall appears to be a mechanism to allow immature adults to migrate from the serosal to the mucosal side without the leakage of gut contents into the peritoneal cavity. After the worms have escaped into the lumen of the gut, they leave behind ulcerated nodules that appear to heal quickly. It is generally accepted that although these nodules may each be several centimeters in diameter, they are of of minor clinical consequences in horses with large intestines that measure 12 feet or more in length depending on the size of the horse.
Large nodule (N) caused by an immature adult of Strongylus edentatus (arrow) migrating through the wall of the large intestine onto the mucosal surface.
Nodules casued by immature adults of Strongylus vulgaris migrating through the wall of the cecum onto the mucosal surface
All three strongylus species have large buccal cavities and are aggressive feeders. They attach to the mucosa of the large intestine by their mouth openings and draw a plug of mucosa into the buccal cavity where it is ground up by teeth, if present, digested by secreted enzymes then drawn into the intestine by the sucking action of the muscular esophagus. Adult worms then move to a fresh site leaving behind small bleeding ulcers that may be seen as red spots at necropsy. Although these worms do not appear to be actual blood suckers, damage to mucosal blood vessels during feeding may cause significant blood loss particularly if the damage extends to the level of the muscularis mucosa. Pathophysiological studies by Duncan and Dargie have shown that 30ml of blood may be lost per day by foals infected with 75-100 Strongylus vulgaris adults. These ulcers appear to heal readily after the feeding worms move on. However, if the damage is deep into the muscularis, as is often the case with the largest of the three strongyles (Strongylus edentatus), granulation tissue will be formed and healing will result in a circular scar at each feeding site.
Strongylus vulgaris feeding by

drawing a plug of mucosa into its buccal cavity.
Strongylus edentatus feeding by Large strongyles attached to the drawing a plug of mucosa into mucosa. Red dots are sites of its buccal cavity. previous attachments.
Strongylus vulgaris
Pathogenesis due to larval migrations
Strongylus vulgaris is the most pathogenic of the large strongyles because of the prolonged (at least 4 months) and extensive migrations through the mesenteric arterial system and its branches before returning to mature in the cecum and colon. Larval migrations cause damage to the smooth endothelial surfaces of arteries, providing a focus for clot formation. These clots (thrombi) are accompanied by inflammation and a progressive thickening of the arterial walls. The time sequence of lesions caused by migrating larvae following experimental infections are summarized in the table below and have been gleaned from many reports in the literature. A summary of these reports has been given by Ogbourne and Duncan in a 1985 publication from the Commonwealth Institute of Parasitology entitled "Strongylus vulgaris in the horse: its biology and importance.
Time sequence of lesions caused by infections with Strongylus vulgaris 0-48 hours Mucosal hemorrhages in the ileum, cecum and after colon. infection 0-7 days Inflammation of small intestinal arteries in the after submucosa and formation of thrombi along the infection tracks of migrating larvae. Significant infiltration of neutrophils in the submucosa. 8-10 days Arteritis extends through the muscularis mucosa to after the serosa. infection 11-21 days Arteritis extends along all the branches of the after ileo-cecal colic artery (supplying the ileum, the dorsal infection and ventral colon and the cecum) to the cranial mesenteric artery. Arterial walls become thickened and histological sections show a marked cellular infiltration including neutrophils, macrophages, lymphocytes and plasma cells. 3 weeks-4 The wall of the cranial mesenteric artery is thickened months and fibrous and thrombi are associated with the after presence of 4th stage larvae and immature adults. infection Fibrin tracks in teh aorta associated with some larvae migrating beyond the cranial mesenteric artery. 4-9 months In the absence of reinfection, arterial lesions heal. after By 9 months after infection, the endothelial lining of infection affected arteries is smooth again and there are few indications of damage other than histological evidence of fibrosis in arterial walls and the presence of macrophages.
In naturally infected animals, arterial lesions are most commonly seen in the cranial mesenteric artery and its branches. However, lesions have also been found less commonly in other arteries including the abdominal aorta, the renal arteries and the celiac axis. The walls of the cranial mesenteric and the ileo-ceco-colic arteries are invariably thickened and contain large amounts of thrombus material in which are found S. vulgaris larvae. This lesion is properly called verminous arteritis. The lumen of the cranial mesenteric artery is usually constricted in its diameter due to the thickening of the wall and the presence of thrombi. The lumen of smaller arteries may be entirely occluded. Some reports in the literature describe aneurysms of the cranial mesenteric artery and its branches. True aneurysms with dilation and thinning of the arterial wall due to a loss of elastic fibres are unusual and may result from penetration of the elastic layer of the arterial wall by larvae. In horses that have died of an acute clinical syndrome, infarction and necrosis of areas of the intestine are usually found at necropsy. These areas of infarction invariably coincide with occlusions (due to thrombi and emboli) in arteries supplying blood to the affected region(s) of the intestine.
Images illustrating the pathogenesis of Strongylus vulgaris infections in horses
The celiac axis and its branches and the cranial mesenteric artery and its branches showing thrombosis and thickening of arterial walls due to Strongylus vulgaris larval migrations.
Necrosis of the cecum and ventral colon of a horse resulting from ischemis and infarctions due to lesions produced by migrating larvae of Strongylus vulgaris.
The dorsal aorta of a horse showing fibrin tracks due to migrations of Strongylus vulgaris larvae beyond the root of the cranial mesenteric artery.
Arteriographic picture of the abdomen of a foal 30 days after infection with 50 third stage larvae of Strongylus vulgaris.
Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris.
Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris and treatment at 30 days with a larvicidal anthelmintic.
Strongylus equinus and Strongylus edentatus

Pathogenesis of migrating stages
Migrating larvae of Strongylus equinus and edentatus do not appear to cause pathological changes of enough severity to translate into recognizable clinical signs. However, migrations of larvae through the liver may produce nodules and formation of fibrous tissue that are readily seen at necropsies of infected horses. The early migrations of Strongylus equinus larvae into the intestinal mucosa produce hemorrhagic nodules that are easily recognized at necropsy or during abdominal surgery in horses with colic. Whether or not these nodules may themselves produce colic in horses is debatable. However, their presence certainly indicates recent infections and it is safe to assume that such horses will also be infected with other large and small strongyles and these may be primary contributors to the observed signs of colic. The life cycle of Strongylus edentatus includes migration to the flanks where immature adults and L4s may be found at necropsy enclosed in subperitoneal cysts. Although these lesions have no clinical significance, they do indicate the presence of strongyle infections and a poor parasite control program in the farm of origin.
Abdominal surgery in a horse with chronic colic showing hemorrhagic nodules in the small intestine caused by larvae of Strongylus equinus
Necropsy of a horse showing Cross section of a larvae of hemorrhagic nodules in the Strongylus edentatus in the liver intestine due to migrating larvae of a foal 62 days post infection. of Strongylus equinus.
Acute reaction in the liver of a Extensive fibrosis in the liver of Strongylus edentatus - an foal 2 months after infection with a foal 5 months after infection immature adult dissected out of a subperitoneal cyst on the right Strongylus edentatus. with Strongylus edentatus. flank.
The Small Strongyles

Species and morphology
The small strongyles include 40 or so species that commonly infect the cecum and colon of horses and donkeys. Approximately 30 of these have been assigned to the subfamily cyathostominae. Thus they are commonly called the Cyathostomes. They vary in size from 6 to 22mm in length with a reasonably well developed buccal capsule that is also much smaller than those seen in the large strongyles. Species are differentiated on the basis of size, characteristics of the buccal capsule and, in particular, the arrangement of internal and external leaf crowns. The image to the right shows the head end of a cyathostomum species with its obvious buccal capsule and with a prominent external leaf crown at its apex..
Superfamily
Family
Subfamily
Genus - examples Strongylus Triodontophorus Cyathostomum Cylicostephanus Cylicocyclus Cylicodontophorus Poteriostomum Gyalocephalus
Strongyloidea Strongylidae Strongylinae (large strongyles) Cyathostominae (small strongyles)
Small strongyles
Pathogenesis - larval stages
The larvae of most cyathostome species penetrate the gut wall as far as the mucosa but no further, but a few species will go as far as the muscularis mucosa. However deep the penetration, all larvae become encapsulated in small nodules in which they continue their development. These nodules are readily visible at necropsy and may be quite numerous - Poynter has recorded as many as 60 nodules per square centimeter of mucosa in work published in 1970 and others have recorded similar numbers. However, with the use of more effective anthelmintics in parasite control programs far fewer nodules have been seen at necropsies in more recent times. The size and location of nodules appears to depend on the species involved. For example Cylicostephanus species appear to develop in the mucosa producing small red to blackish nodules 2-3mm in diameter. Cylicocyclus and Gyalocephalus species penetrate to the submucosa and provoke larger nodules anywhere from 3-6mm in diameter. Mucosal dwelling larvae become surrounded by fibroblasts. Histological sections will show goblet cell hypertrophy and hyperplasia around the capsule with an accompanying infiltration of lymphocytes and eosinophils. The latter becomes particularly intense as the larvae emerge from their capsules to reenter the gut lumen. Larvae in the submucosa provoke a similar but more intense reaction and the capsule is usually thicker. In horses with light infections, pathological changes tend to be restricted to the encapsulated larvae and the immediately surrounding areas. In heavy infections the pathological changes are correspondingly more serious - lesions become coalesced and result in a generalized disruption of the mucosa, a more intense cellular infiltration, edema and copious production of mucus. Surface ulcerations may be common and result from larvae escaping from their nodules.
Encapsulated small strongyle Encapsulated small strongyle larvae in the cecal wall as seen larvae shown via trans-mucosal at necropsy. illumination.
A close-up view of encapsulated Histological section of the large small strongyle larvae in the intestine showing an cecal wall. encapsulated small strongyle larva in the mucosa
Pathological changes tend to be more severe in equines less than two years old. In these animals, heavy infections tend to produce gross changes in the cecum and colon that are characterized by hemorrhagic, catarrhal and fibrinous enteritis. The mucosa tends to be thickened and edematous with varying numbers of ulcers produced by larvae escaping from their nodules. The color of the mucosa varies from a normal greyish pink with varying numbers of small hemorrhages to a dark red in severe infections. Mucus production tends to be significant and some areas of the mucosa may have fibrinous deposits.
Pathogenesis - adult stages

Pathological changes due to adult small strongyles tend to be less severe than those due to either their larval stages or adult large strongyles. Their shallow buccal capsules mean that they feed mainly by grazing on surface areas of the mucosa in contrast to the larger bites taken by the large strongyles. However, small strongyles tend to be present in much greater numbers than large strongyles so their cumulative effects can be more serious especially where parasite control programs are poorly implemented or ineffective. However, larval migrations of Strongylus vulgaris are potentially more pathogenic because of their migrations through the mesenteric arterial system.
Epidemiology of Equine Strongyle Infections (US predominantly)

The large and small strongyles are cosmopolitan parasites. They appear to have adapted to a wide range of climatic conditions and, in the absence of good parasite control programs, are common in horses, donkeys and mules throughout the world. The biological characteristics of the preparasitic stages of the small strongyles and of Strongylus vulgaris are well known and are presumed to be similar for the other two important species of large strongyles in equines, Strongylus equinus and Strongylus edentatus. Most of our current information comes from studies conducted in temperate climate zones in the Northern Hemisphere with pronounced seasonal changes in weather conditions.
Hatching and development

Eggs of equine strongyles will only hatch between 8'C (46'F) and 38'C(100'F). This means that in most temperate areas of the Northern Hemisphere eggs will hatch only from March through October. However, within this temperature range there are constraints on the number of hatched larvae that will develop through to infective third stages (L3s). Laboratory studies have shown that few hatched larvae will survive at the upper and lower extremes of this temperature range and within this range, the number of hatched larvae that will reach the L3 stage is also directly dependent on the prevailing temperature. The table below illustrates this point.
Effects of temperature on development of strongyle larvae from hatching to infective L3s

Temperature % hatched larvae developing to L3s 0% 3% 17% 35% 55% 65% 68% 44% 32% 10% 0% Time for hatched larvae to develop to L3s ------->35days 26days 16days 8 days 6 days 5 days 4 days 3 days 2 days --------
<8'C (46'F) 10'C (50'F) 12'C (54'F) 15'C (59'F) 20'C (68'F) 22'C (72'F) 25'C (77'F) 28'C (82'F) 30'C (86'F) 35'C (95'F) >38'C (100'F)
The highlighted row in the table shows the optimum temperature(25'C/77'F) at which the maximum number of hatched L1s(68%) develop to L3s within the shortest time (5
days). These figures suggest that in the United States transmission of equine strongyles will occur in most regions from mid April through mid November. In the northeast, mid west and mid atlantic states, transmission of equine strongyles will generally follow that pattern. However, in the hot summer months of July and August when temperatures often exceed 85'F and may sometimes reach 100'F, transmission will decline. Temperature patterns in this region suggest that transmission will be optimal in May and June will fall off in July and August and will rise to optimal levels again in September and October. Minimal transmission will occur from November through March. In the southeast states, temperature patterns suggest that transmission of equine strongyles may be significant throughout the year except for the very hot summer months of July and August when transmission will be minimal because prevailing temperatures often exceed 90'F and few larvae will survive for long on pastures at these temperatures. In northern New England, the Pacific Northwest (especially the coastal areas of Washington and Oregon) and northern California, transmission of equine strongyles is likely to follow the European pattern with transmission occurring from May through mid October and maximum transmission during the summer months of June, July and August. There will be negligible transmission in the winter months of December, January and February.
Arrested development
Some species of cyathostomes are able to undergo hypobiosis (arrested development) as exsheathed, encysted early third stage larvae (EL3s) in the intestinal mucosa of infected horses. As with Ostertagia, Haemonchus and other ruminant nematodes hypobiosis in the cyathostomes stops the life cycle in the host at a time when prevailing environmental conditions are hostile to the survival of eggs and preparasitic larvae. In north temperate areas of the world this occurs in winter and hypobiosis is clearly a mechanism of survival for these nematodes. Little is known about the biology of hypobiosis in cyathostomes but it is presumed that the signal for arrest is received by pasture L3s and that the signal is a falling prevailing temperature in fall and early winter. L3s thus stimulated will undergo hypobiosis if they are subsequently ingested by grazing equines before winter ensues. Synchronous emergence of large numbers of previously arrested L4s occurs in early spring and is the cause of the clinical syndrome known as larval cyathostomosis. However, it is also known that larval emergence from hypobiosis may occur throughout the year and it is theorized that hypobiosis may be used by the cyathostomes as a mechanism of controlling the numbers of adult worms in the gut. This hypothesis is supported by the observation that treating horses with an anthelmintic to eliminate adult cyathostomes from the gut will stimulate the development of hypobiotic EL3s to repopulate the cecum and colon with adult worms. Hypobiois in cyathostomes is an important consideration in developing parasite control programs because these arrested larvae are refractory to treatment with many of the anthelmintics used in horses, including Ivermectin and Moxidectin.
Epidemiology of equine strongyles

Seasonal changes in strongyle egg counts
Field observations of strongyle egg counts in mares and other adult horses throughout the Northern Hemisphere show a distinct seasonal pattern. They begin to rise in March, peak anywhere from July to October and decline over winter to a low level in February and March before beginning to rise again. Differential larval counts have shown that more than 90% of these strongyle eggs come from small strongyles with only a small percentage (4-10%) coming from large strongyles. This is because under natural grazing conditions horses are infected with tens of thousands and sometimes even hundreds of thousands of adult small strongyles and only several hundred or at most a few thousand adult large strongyles. Necropsies of horses with high strongyle fecal egg counts in March, April and May show large numbers of cyathostomes in the cecum and colon. Clearly these infections could not have come from ingested larvae that had over-wintered on pasture because, in fact, so few L3s survive this way. The rise in strongyle egg counts in grazing horses in spring comes primarily from adult cyathostomes that survived winter as hypobiotic EL3s in the intestinal mucosa and resumed their development to adults in late winter and early spring. As environmental temperatures rise these eggs hatch and develop rapidly to infective L3s providing a source for constant reinfection of grazing horses and, more importantly, infections of newly weaned foals in spring and early summer.
Several studies in the southeast and midwest have shown a pattern of strongyle egg counts and pasture L3 levels, similar to that in the image to the right. An initial wave of strongyle egg output in horse feces occurs in May and this is presumably due to the emergence of arrested larvae from the mucosa in early spring followed by their development to egg-laying adults. Strongyle eggs on pasture develop rapidly to infective L3s and their ingestion by grazing horses in June result in patent infections 6-8 weeks later as shown by the second smaller peak in egg counts. Pasture levels of L3s fall off rapidly in July and August because hot summer temperatures are quickly lethal to all preparasitic stages. Eggs passed onto pasture in the second wave of egg counts in August are readily translated into rising levels of L3s. Since rainfall is more abundant and temperatures are lower than they were in July and August these L3s survive longer. Infections in grazing horses from this second wave of pasture L3s, will be seen as arrested EL3s in the mucosa over the subsequent winter. However, in certain parts of the southern United States where winters are exceptionally mild (e.g. Florida) high levels of pasture L3s may persist over winter and present problems to grazing horses during this time. In these areas, grazing horses may be at risk during spring, fall and winter. In the hot summer months, minimal transmission of small strongyles occurs because pasture L3s die off rapidly in the hot temperatures and, it is also postulated by some that small strongyles may undergo hypobiosis during the hot summers prevalent in the southeast.
Epidemiology of Equine Strongyle Infections

Development of strongyle infections in foals
Foals will be infected with strongyle larvae as soon as they begin to graze while on pastures with their dams. Initial infections in early spring result primarily from ingestion of L3s that have successfully overwintered on pasture. However, overwintered pasture larvae that fail to be ingested by a host will die off rapidly in spring as temperatures rise and their food reserves are quickly used up. The primary source of infections in foals will therefore be L3s that have developed from eggs passed by their dams and other horses on the same pasture. These eggs will develop rapidly to infective L3s as temperatures rise in spring and summer, producing dangerous levels of L3s on pastures during late spring, summer and fall.
Several studies have shown that strongyle eggs may appear in the feces of foals, on pasture, as early as 4 weeks of age. The majority of these eggs are small strongyles but fecal cultures show that as many as 25% may be eggs of Strongylus vulgaris and Strongylus edentatus. Clearly these eggs cannot be from adult worms because the prepatent periods of these species are 6 months and 11 months respectively and also because prenatal infections with equine strongyles do not occur. In fact Strongylus eggs may be found in the feces of foals up to 12 weeks of age and it is believed that their presence results from ingestion of maternal and other adult feces by foals to populate the large intestine with microorganisms necessary for cellulose digestion.
In the absence of an effective parasite control program, the strongyle egg counts of foals will increase steadily during the first 12 months of life and this is shown in the accompanying graph. Patent infections of Strongylus vulgaris are detected by the time foals are 7-8 months old and eggs from Strongylus edentatus appear at 11-12 months of age consistent with the prepatent periods of these species. However, it should be remembered that during their first 6 months of life, foals are at risk from migrating larvae of Strongylus vulgaris. It is therefore important that foals are introduced to a parasite control program that includes larvicidal anthelmintics by the time they are 2 months old. Depending on when they are born, the initial source of infective larvae for foals will be either L3s that have successfully over-wintered, or larvae that have developed from eggs passed in spring by their dams and other adult horses on the same pasture. Whatever the source of their strongyle infections it is clear that this epidemiological picture shows clear evidence that foals are at risk from strongyle infections early in life and certainly by the time they are 2-3 months old.
Treatment and Control of Equine Strongyle Infections

The large and small strongyles are considered to be the "bread and butter" parasites of control programs because of their widespread occurrence throughout the world and potential for causing serious disease. In North America, control of equine strongyles forms the foundation of all parasite control programs and effective measures against other internal parasites such as bots, lungworms and stomach worms are built on this initial foundation.
The use of anthelmintics to control strongyle infections
The first safe and effective anthelmintics against adult large and small strongyles (benzimidazoles) were first introduced in the mid 1960s. Following this, it was widely recommended that horses should be treated year-round with anthelmintics at 4-6 week intervals. This recommendation was based not only on the known prepatent periods of 4-8 weeks (depending on the species) for the small strongyles, but also that strongyle eggs could be
detected year-round in the feces of horses. This recommendation was reflected in the advertising campaigns mounted by the drug manufacturers during the 1960s and 1970s as reflected in this print advertisement ( use your browser back button to return to this page). The accompanying graph illustrates the rebound of strongyle eggs in the feces of grazing horses 4-6 weeks after treatment with Pyrantel pamoate (PRT). More modern anthelmintics such as the macrocyclic lactones, Ivermectin and Moxidectin are much more effective against the equine strongyles because they kill larval stages of large and small strongyles as well as the lumen-dwelling adults. As a result it takes longer for egg counts of grazing horses to rebound following treatment and this is shown in the graphs below. This graph shows the effects of treating horses with strongyle infections using Ivermectin at a dose of 0.2mg/kg. This dose is highly effective and eliminates not only cyathostome larvae and adults in the lumen of the large intestine but also the mucosal dwelling L4s. The result is a longer interval for the gut to be repopulated by adults developing from unaffected encysted L3s and
newly ingested L3s. In addition, Ivermectin has a two week residual effect from drug residues that are sequestered in body fat. If Ivermectin is used in a year-round control program its frequency of use can be reduced to once every 10-12 weeks. One significant advantage to using Ivermectin is that it is also highly effective against adult Strongylus equinus plus migrating stages and adults of Strongylus vulgaris and Strongylus edentatus. However, Ivermectin is not effective against cyathostome L3s (hypobiotic early L3s or developing L3s) in the mucosa.
A similar result is obtained when horses are treated orally with Moxidectin at a dose of 0.3 mg/kg. It is effective against all stages of cyathostomes except for encysted hypobiotic early L3s. It has the same range of activity as Ivermectin against the large strongyles and appears to have a longer residual effect (of 12-16 weeks) than Ivermectin.
Treatment and Control of Equine Strongyle Infections

Control of small strongyle infections with anthelmintics
The table, below, shows a sampling of the drugs used in practice against the small strongyles. There are, in fact, many more drugs that are approved for use against the small strongyles in the United States but the marketplace of horse-owners and veterinarians has selected those in the table as the most widely accepted drugs for use in parasite control programs. As a result, some manufacturers have withdrawn a number of other drugs from the market even though they remain on the approved list by the Food and Drug Administration (FDA)
ANTHELMINTICS EFFECTIVE AGAINST THE SMALL STRONGYLES Drug Dose EL3s LL3s Mucosal L4s (hypobiotic) oral Oxibendazole ------------10 mg/kg
Fenbendazole Oxfendazole Febantel Pyrantel pamoate Pyrantel tartrate Ivermectin Moxidectin
oral 10 mg/kg daily for 5 days oral 10 mg/kg oral 6 mg/kg oral 6.6 mg/kg oral continuous feeding @14.4 mg/kg oral 0.2 mg.kg oral 0.3 mg/kg
++++ -------------------------
++++ --------------------++++
++++ ------------++++ ----++++
* Benzimidazole resistance, ++ = partial activity, ++++ = highly effective, ---- = minimal activity
Fenbendazole given orally at a dose of 10mg/kg daily for five days has the broadest spectrum of activity against parasitic stages of the small strongyles. It is generally recommended that larvicidal doses of Fenbendazole should be incorporated into parasite control programs at least once and possibly twice during the calendar year. The single yearly treatment is usually given in November or December and the twice yearly treatments are recommended for April and October. The problem of anthelmintic resistance among the small strongyles is particularly prevalent in the benzimidazoles. Oxibendazole and larvicidal doses of Fenbendazole are effective against adult small strongyles but veterinarians and horse-owners should be particularly vigilant for the
emergence of anthelmintic resistance to these two drugs. The use of larvicidal doses of Fenbendazole is becoming popular and this increased use could hasten the emergence of drug resistance.
The Ascaridoidea
Nematodes in the order Ascaridida are relatively large nematodes found in a wide variety of aquatic and terrestrial vertebrates. In domestic animals there is only one important superfamily, the Ascaridoidea.
Biological and structural characteristics

Large nematodes with a predilection for the small intestine. Lumen dwellers feeding on gut contents Three lips surround the mouth opening Serrated ridge or denticle on the inner surface of each lip adjacent to the mouth opening Extremely small buccal capsule Tail end of male coiled, lacks a copulatory bursa but may have caudal papillae Females lay thick-shelled eggs containing a single cell when passed in host feces Direct infection of hosts by ingestion of eggs containing infective second stage larvae(L2s) Life cycles may be direct or indirect and may involve transport hosts in some species The parasitic phases of the life cycles usually involve extensive migrations in definitive hosts Includes species infecting dogs, cats, swine and horses
ASCARIDOIDEA
Species, hosts and importance
The superfamily is divided into 5 families only one of which, the Acarididae is of major importance in domestic animals. One other family, the Anisakidae, is a large group of nematodes widely distributed in marine mammals, birds, fishes and reptiles as definitive hosts. The anisakids require water for transmission and usually involve fish and aquatic invertebrates as paratenic or intermediate hosts. Anisakis simplex is of medical importance because its larvae can cause a severe enteritis in humans after eating undercooked marine fish and squid that serve as paratenic hosts for Anisakis simplex. Pseudoterranova decipiens is economically important because its intermediate and paratenic hosts include fish that are of commercial importance such as the Atlantic cod and American plaice.
Anisakids of marine mammals

Species Definitive hosts Transmission
Ingestion of L3s in marine crustaceans such as shrimps (intermediate hosts) or paratenic hosts such as fish (herring, cod, salmon, mackerel and halibut) and squid.
Comments
Anisakis simplex Marine mammals primarily cetaceans (dolphin, porpoise, whales) but also pinnipeds (seals)
Humans may become infected by eating fish or squid that is raw, undercooked, pickled, smoked or salted. Other Anisakis species may also be involved. Pseudoterranova Pinnipeds Ingestion of larvae in fish May also be seals, sea lions intermediate hosts implicated in enteritis decipiens and walruses in humans.
Ascarids of domestic animals

Species Definitive hosts Transmission Comments
Ascaris suum Pigs
Parascaris equorum
Horses and donkeys
1. Ingestion of eggs Global distribution containing second stage larvae. 1. Ingestion of eggs Global distribution containing second stage larva.
Toxocara canis
1. Ingestion of eggs containing second stage larvae. 2. Ingestion of mice paratenic hosts. 3. Prenatal transmission. 4. Transmammary transmission. Toxocara cati Cats 1. Ingestion of eggs containing second stage larvae. 2. Ingestion of mice paratenic hosts. 3. Transmammary transmission. Toxascaris Dogs and cats 1. Ingestion of eggs leonina containing second stage larvae. 2. Ingestion of mice intermediate hosts. Toxocara Mainly cattle 1. Ingestion of eggs vitulorum but also sheep containing second and goats stage larvae. 2. transmammary transmission. Baylisascaris Raccoons 1. Ingestion of eggs procyonis primarily but containing second occasionally in stage larvae. dogs. 2. Ingestion of intermediate hosts.
Dogs
Global distribution
Global distribution
Global distribution
Global distribution. In North America, mainly in the southern U.S. Implicated in serious neurologic disease (larval migrans) in domestic animals and humans
Ascaris suum
Pathogenesis
Migrating larvae in the liver cause an inflammatory reaction, intralobular tissue destruction and hemorrhage. This is followed by an intense infiltration of eosiniphils and collagen production. These lesions are visible at necropsy on liver surfaces as whitish areas and are commonly called "milk spots" since they resemble splashes of milk. In the absence of reinfection these lesions will begin to regress after larvae migrate beyond the liver and will be healed completely after 4 to 6 weeks: therefore their presence at necropsy is an indication of recent infections. In pigs that experience multiple reinfections during their lifetimes, livers become markedly fibrotic .
Pig liver - normal
Pig liver - "milk spot" lesions
Pig liver - fibrosis
Migration of larvae in the lungs also produces hemorrhagic lesions and intense infiltrations of eosinophils around alveoli into which larvae are migrating on their way up the bronchial tree. Repeated infections will produce more widespread hemorrhages, edema and emphysema. The image to the left shows significant hemorrhagic lesions in the apical and cardiac lobes of Ascarisinfected lungs. Damage to lungs by migrating A. suum larvae may also exacerbate enzootic pneumonia and enhance latent infections with swine influenza virus.
Ascaris suum
Epidemiology
Female worms may produce as many as 2 million eggs daily during her lifetime in the definitive host which can be a year or more. These thick-shelled eggs are resistant to freezing and drying and can therefore survive for as long as five years under most farm environments. However, exposure to sunlight and prologed exposure to drying will destroy them. Overall, these factors ensure that the normal swine environment will be well contaminated with Ascaris eggs, ensuring that all young pigs, especially those raised on soil, will become infected.
Ascaris suum egg
Embryonation and development to the infective second stage larva takes between 13 and 18 days at temperatures between 30 and 33 'C provided the humidity is high and oxygenation is adequate. In temperate climates, with clearly defined seasonal changes, development will be minimal in winter and only one generation of Ascaris will occur each year. In heated confinement operations and in warm temperate climates found in the Southeast United States, development will be year round and several generations of A. suum may occur each year. Ascaris suum egg containing an infective L2.
A. suum eggs will hatch in a number of animal species including ruminants, rodents and humans. However, larvae usually do not migrate beyond the lungs. In ruminants, "milk spot" lesions and an asthma-like syndrome have been recorded in sheep and cattle grazing on pasture previously occupied by swine. In humans, clinical signs of asthma accompanied by an eosinophilia will develop 10 to 14 days after exposure to infective eggs.
Diagnosis
In young pigs significant respiratory disease may occur during the prepatent period in response to migrating larvae. In these cases, clincial signs may be present without finding the characteristic eggs in feces of infected pigs. In older animals infections are usually patent, in which cases a clear diagnosis can be made on finding the characteristic eggs ( small, ovoid, and thick-shelled with a mammillated outer coat) by fecal flotation.
Parascaris equorum
Pathogenesis
Pathological changes in P. equorum infections in foals are similar to those seen in pigs infected with Ascaris suum and closely follow the pathway of migrating larvae. Focal hemorrhages are first seen in the liver 24 hours after an intial infection and are followed by the infiltration of eosinophils into tracks produced by larvae during their wandering through the liver parenchyma. As larvae move on to the lungs, these hemorrhagic lesions resolve and are replaced by fibrous tissue eosinopils and lymphocytes which appear grossly similar to "milk spot" lesions in livers of pigs infected with A. suum. Larval migrations through the lungs are associated first with the apearance of petechial hemorrhages followed by intense infiltrations of eosinophils around alveoli, bronchioles and small blood vessels. These are later replaced by lymphocytes. Beginning approximately four weeks after infection, lymphocytic nodules begin to appear under the pleura. They are raised, greyish-green in color and contain dying larvae and lymphocytes surrounded by a fibrous capsule. These nodules are more common in older foals that have experienced multiple natural reinfections and may indicate a strong immune response to migrating larvae.
Disease
A wide array of clinical signs have been attributed to P. equorum infections in foals and they include: coughing nasal discharges death (following impaction and intestinal rupture) reduced weight gains/weight loss reduced food intake In foals up to 6 months old, coughing and greyish-white nasal discharges are seen during larval migrations through the lungs. Endoscopic examinations of the trachea, at this time, show a frothy mucus in the upper air passages. Rapidly developing worms in the small intestine may be associated with a reduction in food intake and poor weight gains compared with worm-free animals. Infected foals have low levels of serum albumin that is attributed to a reduced appetite combined with the ingestion of amino acids(such as methionine) in the small intestine by feeding worms.
Heavy infections may result in gut impactions and death following rupture of the small intestine. Although this is not a common outcome of Parascaris infections, it's possibility emphasizes the necessity for good parasite control in growing foals. P. equorum - rupture of the small intestine
Parascaris equorum
Epidemiology
Female worms are prolific egg layers and as a result infected foals may pass millions of eggs daily in their feces. These thick-shelled eggs are resistant to freezing and drying and can therefore survive for long periods in the environment. The outer layer is sticky and ensures that eggs will be present almost everywhere in a foal's environment. Optimal temperatures for development of eggs to the infective stage(25'c to 35'C) ensure that transmission of Parascaris will be maximum during the summer months in most temperate areas of the world. Infection rates in foals begin to decline significantly by the time they are six months old. This is due to a combination of an age-dependent resistance and a potent immune response. By the time foals are 12 months old, patent infections are relatively uncommon and and when they are found, worm numbers and egg counts are usually low. This state of solid immunity, combined with infrequent patent infections usually lasts throughout the adult lives of equines. Experimental studies have shown that the immune response acts in the liver and lungs since infections of mature horses with large numbers of eggs produce significant lesions in livers and lungs but few larvae reach the small intestine. P. equorum eggs may hatch in rodents and undergo a limited migration but the nematode seems not to be a cause of visceral larva migrans in humans.
Diagnosis
A coughing foal with a nasal discharge is a likely indication of a prepatent infection with P. equorum. Otherwise a diagnosis is dependent on finding the distinctive thick-shelled egg in the feces of horses with patent infections.
Parascaris equorum egg on fecal floation
Oxyuroidea
Introduction
Nematodes in the order Oxyurida are classified into two superfamilies. members of the Superfamily Oxyuroidea are found in vertebrates and the Thelastomatoidea in herbivorous arthropods such as cockroaches. The Oxyurida is the only significant group of nematodes with adult members in both vertebrates and invertebrates. The only oxyurid of significance in domestic animals is Oxyuris equifound in the cecum and colon of horses. However, a number of species are of importance in humans and laboratory animals.
Species
Enterobius vermicularis Passalurus ambiguus
Hosts
Predilection sites
Humans & other primates (gibbons, Cecum & chimpanzees & marmosets) appendix Rabbits & hares Cecum & colon Colon Cecum Small & large intestines Cecum & colon
Skrjabinema ovis Sheep & goats Syphacia obvelata Aspiculuris tetraptera Oxyuris equi Mice(laboratory & wild) Mice (laboratory & wild) & rats Horses & donkeys
Oxyuris equi
O. equi is found worldwide in horses and donkeys. The esophagus has a prominent posterior bulb. They are commonly called pinworms because of their pointed tails and the single pin-shaped spicule of males. Females are larger than males, measuring from 5 to 15 cm in length while males are approximately 1 cm long. The female vulva is situated anteriorly.
Oxyuris equi - male
Oxyuris equi
Pathogenesis
Fourth stage larvae have a relatively large buccal capsule and they feed by ingesting plugs of intestinal mucosa to which they are attached. This causes mucoal erosions which appear to produce little in the way of clinical signs. Adult worms live freely in the intestinal lumen feeding on gut contents. However, the main pathogenic effects appear to be related to the egg laying habits of the female worms. Fertilized females travel down to the rectum and extrude their anterior end through the host's anal opening. They lay eggs on the peritoneum in clumps contained in a greyish-yellow gelatinous material. This causes an irritation resulting in anal and perineal pruritis.
Clinical signs
Infected animals rub their hind ends frequently in attempts to relieve the pruritis and irritation caused by the egg-laying females. Rubbing causes broken hairs, bare patches and inflamed skin over the rump and tail head causing the tail to assume an ungroomed "rat-tailed" appearance as shown in the acompanying two images. Animals are also restless causing them to feed less producing a loss of condition and often a dull staring coat.
Horse with O. equi infection Horse with O. equi infection
Diagnosis
Diagnosis of O. equi infections is straightforward. The clinical signs described above are clearly indicative and combined with observing egg masses on the peritoneum, make this an infection that is easy to recognise. Sometimes owners will notice the long-tailed female worms in the feces of infected animals. The egg laying habits of female worms means that Oxyuris eggs are rarely found in feces taken directly from the rectum. They must be looked for in the perineal clumps or in fecal samples taken from the ground. Oxyuris eggs are diagnostic. They are ovoid, yellow, slightly flattened on one side and with a mucoid plug at one pole.
Egg of Oxyuris equi
Treatment and control

O. equi is susceptible to a wide range of available anti-parasitic drugs. The hind quarters of clinically affected animals should be washed to remove egg masses before treatment to avoid further contamination of the host's environment and to reduce the likelihood of reinfections.
Fasciola hepatica
Fasciola hepatica can infect a wide variety of mammalian hosts, particularly sheep and cattle. It requires snails of the genus Lymnaea as intermediate hosts. The most common is L. truncatula, an amphibious snail with a world-wide distribution.
Life Cycle
Mature adults live in the bile ducts of livers in their mammalian hosts. Eggs are laid in the bile ducts, pass to the small intestine then out in the feces of the host. The first stage, a miracidium (A), develops within each egg, which hatches and releases the mature, motile, ciliated miracidium. Hatching of eggs takes less than two weeks at optimal temperatures between 220C and 260C. Development is negligible below 100C. Hatched miracidia are short-lived because they do not feed . They must find a suitable snail intermediate host within twenty four hours of hatching or they die. Miracidia swim, using their cilia, and seek out snails by chemotaxis. They adhere to snails and penetrate their soft tissues using an enzyme and a cone-shaped papilla at the anterior end. The miracidium loses its cilia and continues to develop into the sporocyst stage (B), which is a sac containing germinal cells. Each germinal cell grows and divides eventually becoming a redia (C). These first generation rediae burst through the wall of the sporocyst and migrate to the hepato-pancreas of the snail. A second generation of "daughter" rediae may develop from germinal cells in the first, parent generation. Germinal cells in these daughter rediae develop into the final cercarial stages(D). Cercariae are, in fact, immature flukes with tails used for swimming. They attach to plants such as grass blades, lose their tails and encyst as metacercariae (E) the infective stages for their final mammalian hosts. ( ) Following ingestion of metacercariae by the final host, they excyst in the small intestine (F), migrate through the gut wall, cross the peritoneum and penetrate the liver capsule (G). The immature flukes tunnel through the liver parenchyma for 6 to 8 weeks, then enter the small bile ducts, then migrate to the larger ducts and occasionally the gall bladder. ( ) Eggs laid by adult flukes pass down the bile ducts through the gastrointestinal tract and exit the host in feces, completing the cycle. The prepatent period is 10 to 12 weeks, and the minimal period for completion of one entire life cycle of Fasciola hepatica is 17 to 18 weeks.

Terminology
The umbrella term Parasiticide is used to describe a drug that is effective in killing parasites of one form or another. It does not mean that the drug kills all parasites, merely that it will kill at least one species of parasite Most antiparasitic drugs are usually effective in killing several related species of parasites while others may have broad spectrum properties in that they are effective against a wide range of parasites. A good example of such a compound is Selamectin with activity against several species of nematodes of dogs and cats including heartworm as well as fleas, ticks and some mites. In the early years of drug development, the compounds discovered were usually effective only against some of the parasites in one of the major groups such as the helminths. In this case, the drugs were collectively called anthelmintics. Similarly those compounds active only against insects were called insecticides and those effective only against ticks and mites (the acarina) were called acaricides. In the mid to late 1950's some of the organophosphates were discovered to have activity against a wider range of parasites including nematodes and insects. Therefore those particular organophosphates were classified as both anthelmintics and insecticides. More recently the avermectins and the milbemycins (collectively called the macrocyclic lactones) have been marketed as broad spectrum parasiticides with most of them having activity against nematodes, insects, mites and ticks. Therefore they can be classified as anthelmintics, insecticides and acaricides.
Introduction
Control programs for parasites in all our domestic animals rely heavily on the use of antiparasitic drugs. large numbers of anthelmintics are approved for use in the United States but many of the narrower spectrum compounds, with activity limited to a small number of nematodes, have been discontinued by the manufacturers because their profitability has declined to the point where it is uneconomical to manufacture and market them.In the United States, Development of anthelmintics and registration through the Food and Drug Administration (FDA) takes on average 15 years and an investment of close to $400 million. Of all the compounds screened initially and having activity against parasites, only one in five thousand will make it to the market. Clearly for this kind of investment the drug companies expect a substantial return with annual sales of at least $500 million and hopefully as much as $1 billion. Information on FDA-approved drugs for domestic animals can be obtained at the following
web site www.fda.gov/cvm which also has a useful search engine
Properties
In developing anthelmintics, the pharmaceutical companies measure newly discovered and promising compounds against an ideal standard. While no anthelmintic yet discovered has met all the criteria of an "ideal anthelmintic", some of the more recently developed drugs have come quite close. The properties of an ideal anthelmintic are listed below. Broad spectrum of activity. Non toxic to treated animals at the therapeutic dose Should possess a wide margin of safety fro treated animals as well as the user.. Metabolism and excretion should be rapid. There should be no residues in milk or meat going into the human food chain. Administration should be easy. The drug should be cost effective.
This image shows how the potency of discovered anthelmintics has increased with time. The earliest of the modern anthelmintics was phenothiazine. This drug was primarily used against nematodes in ruminants. It was a drug that not only had a narrow spectrum of activity but also a high therapeutic dose of more than 600 mg/kg as well as a narrow margin of safety. As other groups of anthelmintics were discovered, their effective dosages were found to be less than previous compounds and their spectra of activity were broader. Each of the most recently discovered macrocyclic lactones (Ivermectin, Abamectin, Moxidectin, Doramectin and Eprinomectin) have a broad spectrum of activity in all our domestic animals and also have a very small therapeutic dose of less than 200 ug/kg. In addition, they are extremely safe to use in most domestic animals.

Spectrum of activity
In terms of the usefulness of anthelmintics against nematodes, it is important that they have as broad a spectrum of activity as possible. Ideally they should be effective against a wide range of different nematodes infecting domestic animals and also in killing all parasitic stages of those nematodes. An added bonus would include effectiveness in killing other parasitic helminths and arthropods. The table below shows the spectrum of activity of two macrocyclic lactones and Fenbendazole used in horses. It includes manufacturers' label claims against a range of species of nematodes and bots as well as a range of different larval stages.
Spectrum of Activity of Macrocylic Lactones in Horses Parasite

Strongylus vulgaris adults, L4s, L5s Strongylus edentatus adults & migrating larvae Strongylus equinus adults Triodontophorus adults brevicauda, serratus spp Triodontophorus adults minor, tenuicollis spp Small strongyles - adults Cyathostomum, Cylicostephanus,Cylicocyclus, Cylicodontophorus, Small strongyles - adults Gyalocephalus capitatus Small strongyles L4s in lumen Small strongyles Encysted L3s and L4s Small strongyles Hypobiotic L3s Parascaris equorum adults & L4s Parascaris equorum L3s Oxyuris equi - adults & L4s Trichostrongylus axei - adults Habronema muscae - adults Gastrophilus intestinalis 1st instar
Moxidectin Ivermectin Fenbendazole

++++ ++++ ++++ ++++ ---++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++* adults only ++++ ++++ ------++**
++++ ++++ ++++ ---++++ ---++++ ++++ ++++ ----
---++++ ------++++ ++++ ++++ ++++ ++++ ++++
++** ---++++ ++++ ++++ ---++++ adults only ----------
Gastrophilus intestinalis 2nd & 3rd instars Gastrophilus nasalis 1st, 2nd & 3rd instars Dictyocaulus arnfieldi adults & L4s Strongyloides westeri - adults Habronema - cutaneous L3s Draschia - cutaneous L3s Onchocerca spp - microfilariae
++++ -------------------
++++ ++++ ++++ ++++ ++++ ++++ ++++
----------------------
++++ = highly effective. ---- = no label claim/no activity. * daily for 5 days. ** daily for 5 days, no label claim for individual species just "small strongyles" and problems with fenbendazole-resistant species reducing its effectiveness against adults of some small strongyle species.
These comparisons clearly show that Ivermectin has the broadest spectrum of activity against parasites in horses. However, label claims do not always convey the complete picture. For example, although Fenbendazole has no claim for activity against Dictyocaulus arnfieldi and Trichostrongylous axei, it is likely to be effective against both of these nematodes since the drug has good activity and label claims against their counterparts in cattle namely T. axei and D. viviparus. In addition, fenbendazole's effectiveness against hypobiotic larvae of the small strongyles is an important property lacking by both Moxidectin and Ivermectin. However, the problem of benzimidazole resistance in many species of small strongyles is a critical factor limiting its use against adult popoulations. The usual recommendation is to use a drug such as Moxidectin and Ivermectin at strategic times of the year and to supplement this regimen with one or two annual treatments with Fenbendazole to kill hypobiotic early third stage larvae.

Safety considerations
Anthelmintics are basically poisons and their safe use in animals is directly dependent on the therapeutic dose against the parasite being very much lower than the toxic dose in treated animals. As a result we can place a safety factor on each anthelmintic that readily identifies how safe/unsafe it is. Ideally, the toxic dose will be several orders of magnitude greater than the therapeutic dose. Clearly, the closer these two numbers are the riskier it is to use a drug since there is little margin for error in computing dosages based on an animal's weight particularly if weights are estimated rather than measured accurately with a scale.
ANTHELMINTICS AVAILABLE FOR HORSES

DRUG Strongyloides Parascaris Strongylus spp Small Oxyuris Bot strongyles larvae Safety Factor
Oxibendazole Fenbendazole Oxfendazole Febantel Pyrantel Ivermectin Moxidectin Oxfendazole +Trichlorfon Piperazine
++++ ++++ ---++++ ---++++ ++++ -------
++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++
++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++
++++* ++++ N/A 60X +++* ++++ N/A 100X ++* ++* ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ N/A N/A N/A ++++ ++++ 10X 40X 20X 60X 60X 1X 1X
++++ ++++ ++ N/A
* Benzimidazole resistance, ++ = partial activity, ++++ = highly effective, ---- = minimal activity N/A = no activity
Looking a the above table it can be seen that anthelmintics available for use in horses vary widely in their safety factors. The benzimidazoles are extremely safe - it requires dose rates from10-100 times before these drugs pose safety problems in horses. The avermectins, Ivermectin and Moxidectin, are generally considered to be very safe drugs not only in horses but also in other domestic animals. However, it is well established that collies as a breed-type are sensitive to the avemectins and its is generally advised to avoid their use in those particular breeds. Before the discovery of the avermectins, the benzimidazoles, such as Oxfendazole, were often combined with an organophosphate like Trichlorfon to broaden the spectrum of activity to include the bots. In doing so it had to be remembered that the safety factor of the combination equaled that of the most toxic component namely Trichlorfon: a property that seems obvious but easily forgotten in the whirl of a busy practice. The problem with
the organophosphates is that they are acetylcholinesterase inhibitors in mammalian as well as parasite neuromuscular junctions. This, of course, is their mode of action against the nematodes and insects. Since neuromuscular transmission is cholinergic in mammals, insects and nematodes - acetylcholinesterase is required for post synaptic inactivation of acetylcholine - the organophosphates will prolong muscle depolarization and contraction. Therefore their mode of action is also the reason why they have a narrow margin of safety when used in mammals. The use of organophosphates as boticides in horses has fallen considerably in the last five years because they have been replaced by the avermectins, compounds that are not only very effective against bots but also much safer than the organophosphates such as Trichlorfon. Piperazine, a compound often used in the past against benzimidazole resistant small strongyles, also has a narrow safety margin. However, it is now little used having been superseded by the more effective and safer avermectins. It is particularly important to use anthelmintics with wide safety margins in horses, ruminants and pigs because weights in these animals for computing doses are usually estimated for convenience and speed. The use of drugs with narrow safety margins becomes problematical if weights are overestimated because animals will be given a dose that is not only greater than the therapeutic dose but also may be close to or at the toxic dose.

Residues
Anthelmintics should be rapidly metabolized and excreted from the bodies of treated animals so that any residues left after treatment will be minimal or zero. This is particular important in milk and meat producing animals. If drugs are used in these animals and leave residues for prolonged periods of time, producers are legally required not to place meat and milk products into the human food chain for a pre-defined number of days. The latter is called the "withdrawal period" and is fixed for each drug/anthelmintic used in food animals. The table below gives some examples of withdrawal periods for anthelmintics used in cattle and swine.
Withdrawal TImes for a Selection of Anthelmintics in Food Animals

Dairy Cattle
Fenbendazole Eprinomectin
Beef Cattle
Swine
Sheep
Moxidectin
Doramectin
Zero Zero Zero NA NA
8 days Zero Zero
Zero NA NA
NA NA NA
35/45 days 24 days NA Ivermectin 24 days (Oral 5 days (feed 11 days paste) premix) (Oral 35 days (SQ 18 days (SQ liquid) injection) injection) 48 days (Topical) 184 days (SR bolus) SR bolus = slow release bolus implanted in the rumen. SQ= subcutaneous. Topical = liquid applied as a pour-on product to the animal's back. NA= no FDA-approved use in these animal groups.
From this table, it is clear that Eprinomectin and Moxidectin have significant advantages over the others, at least from the consideration of withdrawal times in meat and milk . However, withdrawal times are not the only consideration. Spectrum of activity is also important and the following table details the activities of four macrocyclic lactones against a wide range of internal and external parasites when used as their topical formulations in cattle. These compounds are applied to the backs of cattle as pour-on products. They are becoming increasingly popular because they are easily administered
to cattle. [anthel_T7.htm] At first glance these compounds would seem to have considerable differences in their effectiveness. However, these differences are minor in practice since all four have significant activities against most of the economically important parasites of cattle. In any case, the effective use of the macrocyclic lactones in routine parasite control programs can be increased by rotating among the members of the group during a grazing season or from year to year.
Costs
The cost of anthelmintics should be reasonable. They must be considered an investment in food and fibre producing animals where return on investment is a major consideration. However, two factors should also be remembered. 1. First, veterinary services are one of the smallest components of the total cost of production. Therefore the impact of anthelmintic treatments on total production costs will be minimal. 2. Second, the positive impact on productivity of broad spectrum anthelmintics in parasite control programs is considerable. Therefore the return on investment is significant.

Routes of administration
Anthelmintics are administered to animals by a variety of methods and formulations. The three routes of administration are oral, injection and topical. Oral formulations are marketed in a variety of forms - liquids, pastes, hard pills, boluses (large pills), chewable soft pills, medicated salt blocks for licking and premedicated feed or salt mixtures. Horses are often treated individually and common formulations include pastes, gels and liquid suspensions. These are usually administered orally using a syringe or may be given via stomach tube in the case of liquid suspensions. Palatability is very important in orally administered products particularly to horses and cats which can be difficult animals to treat with drugs that have unpleasant tastes. Tablets in their various forms are most commonly used in dogs and cats because they are clearly single dose preparations and are relatively easy to give. A more recent innovation in oral administration is the use of intraruminal sustained release devices in cattle and sheep. They allow a slow release of active drug over a period of time, usually the complete grazing season. The aim is to prevent establishment of nematode populations in hosts during periods of maximum availability of third stage infective larvae. Injectables are most commonly given to cattle and swine which can be easily crowded into restricted spaces or run-through shutes (in the case of cattle) and treated with multiple dose syringes. They are given as sterile solutions and the subcutaneous route is the most favored because of the risks of hurting carcass quality when the intramuscular route is used. Topical pour-on macrocyclic lactones, absorbed through the skin, are also available for treatment of internal and external parasites in cattle. This formulation is clearly preferred by producers and veterinarians because of the ease of use which markedly reduces stress for treated animals. The active compound is absorbed via the sebaceous glands and hair follicles. Their presence in the skin makes them valuable and effective drugs for controlling a variety of external parasites in cattle. Feed additives are particularly useful and popular in controlling parasites in swine raised intensively. These compounds allow the stress-free, economical treatment of large numbers of animals. They are also useful in treating range cattle as additives to mineral mixes and salt blocks. Using them avoids the stress and expense of rounding up cattle to pass them through shutes for oral and injectable treatments. The table below illustrates the wide variety of formulations commonly available for
domestic animals.
Anthelmintic Formulations
Horses Cattle Ivermectin Eprinomectin Doramectin Moxidectin Milbemycin Albendazole Febantel Fenbendazole Oxfendazole Oxibendazole Levamisole
O - paste O - liquid O - paste O - liquid O - feed mix O - paste O- paste O - liquid O - liquid O - bolus O - gel O - feed mix I - liquid SC T-? O - paste O - liquid O - feed mix O - feed mix O - water additive O - liquid O - feed mix O - salt block O - mineral mix O - liquid O - feed mix O - liquid O -tablets O - feed mix O - tablet O- gel O - paste O - liquid O - paste O - SR bolus I - liquid SC T - pour on T - pour on I - liquid SC T - pour on O-? I - liquid SC T - pour on I - liquid SC O-?
Swine
O - feed mix I - liquid SC
Dogs
O - tablets O - chewables I - liquid SC
Cats
O - tablet
O - tablets
Pyrantel Diethylcarbamazine Dichlorvos Praziquantel Clorsulon
O - feed mix
O - tablet O - chewable O - liquid O - tablet O - chewable O- syrup
O - feed mix
O - gel cap O - tablet I - liquid SC O - tablet I - liquid SC
O - liquid
O = oral, I = injection, SC = subcutaneous, T = topical, SR = slow release

Major groups
The following table includes the major anthelmintic groups commonly available for use in livestock.
Anthelmintic Group
Examples
Mode of Action Bind to glutamated chlorine channels causing paralysis
Macrocyclic Lactones Ivermectin (Macrolides) Eprinomectin Doramectin Moxidectin Milbemycin oxime Selamectin Benzimidazoles Thiabendazole Mebendazole Fenbendazole Oxfendazole Oxibendazole Albendazole Febantel Tetramisole Levamisole
Interfere with energy metabolism by inhibition of polymerization of microtubules Same as benzimidazoles Cholinergic agonists Cholinergic agonists Inhibitors of cholinesterase Anticholinergic action - block neuromuscular transmission
Pr0-benzimidazoles Imidazothiazoles
Tetrahydropyrimidines Morantel Pyrantel Organophosphates Dichlorvos Haloxon Trichlorfon Piperazine salts
Piperazines
Their modes of action are not fully understood in every detail but their lethal effects on parasites result from one of two mechanisms 1. They interfere with energy-generating metabolism causing death by starvation. 2. They interfere with neuromuscular transmission in nematodes causing paralysis.

The Macrocyclic Lactones
The macrocyclic lactones are natural fermentation products of Streptomycetes bacteria. They consist of two sub groups, the avermectins and the milbemycins. Their basic chemical structure consists of a cyclic lactone and a spiroketal addition constructed of two 6-membered rings. The avermectins also include a sugar (disaccharide oxy) linked at position 13.
The macrocyclic lactones come closest to our concept of the "ideal anthelmintic" and, as a result have become the "gold standard" in parasite control programs. They have broad spectrum activities against a range of nematodes and arthropods. As a group, they are highly effective at low doses (micrograms per kilogram of body weight) against most of the economically important nematodes of food-producing livestock and have a wide margin of safety. Some of them have zero meat and milk withdrawal times. In the United States, there are, currently, six commercially available macrocyclic lactones: Ivermectin, Eprinomectin, Moxidectin, Selamectin, Doramectin and Milbemycin. They have been so successful in the market place that production of a number of other useful anthelmintics has been discontinued by their manufacturers. However, despite their obvious advantages the macrocyclic lactones are expensive. Despite this they have gained wide acceptance by veterinarians, horse owners, farmers and the dog and cat owning public. The obvious conclusion from this is that they are cost effective in terms of parasite control, despite their high cost. This conclusion is supported by the results of studies of their use in food animals. As their patents expire and generic alternatives begin to compete with them, their cost effectiveness will increase significantly. The macrocyclic lactones are not effective against trematodes and cestodes. To compensate for this, some manufacturers have combined them with other drugs to broaden their spectrum of activity. For example, Ivermectin has been combined with Clorsulon to add liver fluke efficacy in cattle. This product is marketed in areas of the United Sates where liver flukes are an important problem in grazing cattle.

Ivermectin
Ivermectin was the first macrocyclic lactone to be developed for commercial use. It is a mixture of two avermectins that are first produced naturally from fermentation of Streptomycetes avermitilis and then modified chemically at certain positions - position 5 on the benzenefuran component and positions 22, 23 and 26 on the spiroketal system.
The two components of Ivermectin are the 22, 23 - dihydroxyavermectin B1a and 22, 23 dihydroxyavermectin B1b. Both have three hydrogens added, one each at positions 22 and 23 and one added to the oxygen at position 5. In addition, avermectin B1a has a C2H5 added at position 26 while avermectin B1b has a CH3 added at position 26.
Ivermectin is available in a variety of formulations as shown in the following table.
Ivermectin Formulations Commonly Available Dogs

Oral liquid paste tablets chewable SR* bolus feed premix Topical Pour-on liquid Injection Subcutaneous No No Yes Yes No No No No
Cats
No No Yes No No No No No
Horses
Yes Yes No No No No No No
Cattle
No Yes1 No No Yes2 No Yes3 Yes4
Sheep
Yes5 No No No No No No No
Swine
No No No No No Yes6 No Yes7
* SR = intraruminal sustained release. Withdrawal times: 1=24 days, 2=184 days, 3=48 days, 4=35 days, 5= 11 days, 6=5 days, 7=18 days Withdrawal times in cattle apply only to meat, therefore Ivermectin should not be used in pregnant or lactating dairy cattle.
One formulation for use in cattle is an intraruminal sustained release device (IVOMEC SR Bolus). This is implanted orally in the rumen of cattle, at least 12 weeks old (i.e. certain to be ruminating) at the beginning of the grazing season. The device is osmotically driven, pulling in water from the rumen that flows on through a permeable barrier into a chamber containing the active drug. Ivermectin dissolved in water in water flows out to the rumen through a port screen. The device is calibrated so that a predetermined amount of Ivermectin (12 mg per day) is carried out to the rumen and on through the gastrointestinal tract where it is effective in killing parasitic stages of all the economically important g.i. nematodes infecting cattle.

Heartworm - Host Range
Host Species
In addition to the domestic dog, many other species can act as alternate hosts for Dirofilaria immitis. These species, known as alternate hosts, will also maintain blood levels of circulating microfilaria sufficiently high to act as reservoirs of infections for mosquito intermediate hosts. Examples of alternate hosts include:
Alternate Hosts for Dirofilaria immitis
red coyote wolf grey wolverine* fox red ferret* fox
California sea lion* domestic and wild felids*
*Although these species may constitute microfilaremic reservoirs, the length of the microfilaremia is brief compared to the other species.
Other vertebrates may act as aberrant or dead end hosts. These species may become infected from the bite of a vector mosquito. However, they do not develop a microfilaremia because migrating Dirofilaria fail to reach sexual maturity. Examples of these include:
Aberrant Hosts for Dirofilaria immitis
humans bears raccoons beavers
Heartworm
Epidemiology of Canine Heartworm Disease
The accompanying map shows the distribution of canine heartworm disease. It is an international problem, occurring on every continent except Antarctica. Please click on the map to see an enlarged version
In order for this infection to be maintained in any one location, four factors must be present: a susceptible host population a stable reservoir of the disease a stable population of susceptible mosquito-vector species a climate supportive of the development of the parasite
The climate must be sufficiently warm in order for the larval stages to develop into the L3 infective stages in the mosquito vector. For D. immitis , the larvae require approximately two weeks of temperatures at or above 27C (80F), and no development will occur if the temperature goes beneath 14C (57F). As a result, heartworm is not only geographically limited, but also seasonally limited. These are important considerations when screening for heartworm infections, or when advising clients on the use of chemical prophylaxis. For example, with a prepatent period of 6-7 months, patent D. immitis infections may not be detected for a significant time after after the end of the heartworm season.
The accompanying map shows the distribution of heartworm disease in the United States which is controlled primarily by climatic factors favoring not only the presence of suitable mosquito vectors but also the development of the life cycle of D. immitis in these mosquito intermediate hosts. The Southeast and the Mississippi river valleys (shaded red) have the highest prevalence of canine heartworm disease because the climate in those regions is best suited for the vector species. The rest of the U.S. shows a lesser prevalence because there may not be a large enough population of reservoir hosts in some areas, or the vector may not be well enough adapted to survive or to serve as a suitable intermediate host for the larval stages.
The nematode D. immitis is, in fact, quite cosmopolitan, adapting to life in a number of mosquito species, including members of the genera Aedes , Culex, Anopheles , and Mansonia . In the U.S., the main vectors are Aedes taeniorhynchus , Ae. solicitans , Culex. salinarius , Cx. quinqefasciatus , and Anopheles. quadrimaculatus . They are found in many regions of the country, and feed on domestic canines, wild canines (the reservoir host in many endemic areas of heartworm disease), as well as other species which may contract heartworm disease.
There has been a significant increase in the prevalence of heartworm disease in the United States during the last 30-40 years. The accompanying map shows that during the 1960's, D. immitis was found mostly in the Southeast (red shaded area). The nematode and its accompanying disease is now found in all 50 states, although the prevalence in Alaska is still lower than elsewhere.
There are several factors to explain the spread of D. immitis and heartworm disease. 1. The increasing urbanization of the U.S. has resulted in the movement of the human population, acompanied by their pet dogs and cats, into areas that were previously sparsely populated.
2. This population movement, especially into rural and coastal areas (natural habitats for mosquitos) has increased the potential for contact among vector species, reservoir hosts and domestic pets. 3. Increased dog density. The dog population in the United States has grown significantly during the last 30 years and is now a large potential reservoir for D. immitis infections. More than a third of all U.S. households own dogs and the current dog population has been estimated as more than 40 million. 4. D. immitis shows a preference for certain species of mosquito. However, during its spread throughout the United States it has adapted well to using other mosquito species as vectors. 5. Adaptation by D. immitis to a wider temperature range for development of larval stages in the mosquito. There are some factors s which place some dogs at higher risk than others for heartworm disease. For example, a higher risk of infection occurs with increasing age and exposure of dogs to the outdoors. In addition, sporting breeds and large dogs tend to be at higher risk than other dogs, since they are more likely to be outdoors during the transmission season. However, there seems to be no increased risk associated with gender or hair coat length.
Heartworm
Pathogenesis - Cardiopulmonary Disease
Several disease entities can result from a D. immitis infection. Of paramount concern is cardiopulmonary disease, where one finds narrowing and occlusion of the pulmonary arteries due to proliferation of intima, not direct blockage by the adult worms. The distribution and severity of the lesions does depend on both the number and location of adult worms, but caudal lobar arteries are the most heavily infected. If there is a high worm burden, worms may be found in the right atrium and ventricles, and the vena cavae may be involved as well.
Pulmonary hypertension is the major consequence of intimal proliferation, and one can see right ventricular dilation and hypertrophy, as well as ischemia and right ventricular failure as a result.
It has been proposed that heartworms disrupt the intima of the pulmonary arteries, attracting platelets, and stimulating release of Platelet Derived Growth Factor (PDGF). PDGF triggers proliferation of medial smooth muscle cells and fibroblasts. Endothelial cells also secrete PDGF, which may help maintain plaque growth. Changes to the lung parenchyma can be seen upon necropsy, with edema around the arteries, thromboemboli containing dead adults, and areas of inflammation near dead adults, microfilariae, and thrombi. Individuals with cardiopulmonary disease may show exercise intolerance, and this can lead to right-sided heart failure. Heart failure in these individuals can be acute or gradual, and can lead to ascites, hydrothorax, and hydroperitoneum.
Clinical signs of cardiopulmonary disease can vary from no signs at all, to chronic coughing, dyspnea, hemoptysis, and syncope. Exercise intolerance can be present, increasing in severity with increasing resistance to pulmonary blood flow. Heartworm infections of a given size will be less well tolerated by working or sporting dogs than by sedentary dogs. These signs may resolve completely following successful adulticide treatment. Pulmonary thromboembolism can occur, and is often a response to dying adult worms, whether the death of the worms be spontaneous or due to treatment with adulticidal drugs. Thrombi form around a degenerating parasite, and a periarterial granuloma can develop in the lung parenchyma.
Heartworm
Caval Syndrome
Caval syndrome is an acute disease due to large numbers of adult heartworms accumulating in the right atrium, tricuspid valve area, and posterior vena cava. Worms can literally pack these areas, increasing venous pressure Worms from a caval syndrome dog in the liver, and causing damage to beneath a sample of the parenchyma. Liver dysfunction hemoglobinuria and normal urine. causes decreased esterification of serum cholesterol, increases cholesterol content of the red blood cell membranes, resulting in red blood cell fragility. This leads to hemolysis, anemia, and hemoglobinuria and bilirubinemia.
Common in younger individuals, from 3-5 years of age, clinical signs include an acute onset of weakness and anorexia, dyspnea, collapse, pale mucous membranes and/or jaundice, bilirubinemia, bilirubinuria, and hemoglobinuria, which is pathognomonic for this syndrome. Although there may not be time to evaluate these cases radiographically (see radiographic signs below), there is a 100% occurrence of the 'classic' radiographic signs seen with dirofilariasis. Most dogs (88%) with caval syndrome are microfilaremic as well. This syndrome is a clinical emergency. Death may occur within 24-48 hours.
Heartworm
Renal Disease
It is debated as to whether heartworm can cause renal disease, as the evidence as yet is indirect. There has been an association noted between heartworm infection and renal disease, and the renal problems have been alleviated following heartworm therapy. Most infected dogs have no renal damage. The immune response of the infected individual may also affect the probability of renal disease. There are three proposed mechanisms as to how the renal disease may progress. The disease may be immune complex mediated, causing damage to the glomerular basement membrane. Fluorescent antibody tests have demonstrated Ig deposition on the basement membrane. Secondly, microfialria induced trauma to the glomerular epithelium may cause glomerulosclerosis. Thirdly, some heartworm dogs have been observed to have amyloidosis. Following adulticide treatment against the worms, microgranulomas may occur, and any renal problems that already existed may worsen. Laboratory analysis of the dogs with renal problems will reveal a proteinuria, hematuria, microfilariae in the urine, as well as a hypoalbuminemia. Treatment consists of adulticidal heartworm therapy and supplementation with fluids, bicarbonate, and vitamins B and C.
Hepatic Disease
With hepatic complications, the dog may exhibit phlebitis of hepatic veins, dilatation of central veins due to pressure necrosis of hepatocytes, and dilatation of capsular lymph nodes. There are several ways that the liver may become damaged. Organoarsenical adulticide thiacetarsemide and microfilaricidal drugs, may have direct hepatotoxicity. Passive congestion of liver vessels can occur. However, elevated liver enzymes do not preclude aldulticide treatment.
Heartworm
Ectopic Infections
Occasionally, adult worms may go to sites other than the large veins and heart, and cause ec infection. If they go to the eye, an individual may show conjunctival discharge, photophobia, o Treatment is by surgical removal of the worm, and adulticide treatment is contraindicated.
If the worms migrate to the CNS, they are usually found in the cerebral arteries or the lateral v Signs vary, but may include convulsions, blindness, ataxia, excess salivation, prostration, and Treatment is by surgical removal.
Systemic arteries may also be involved in heartworm infection. The rear legs are most commo affected. Cases usually present on an emergency basis, and surgical removal of the worms is recommended treatment.
Heartworm
Microfilarial Hypersensitivity and Allergic Pneumonitis
Serving as the basis for immune-mediated occult heartworm infection, hypersensitivity results in antibody mediated leukocyte adherence to the microfilariae. This adherence decreases the motility of these embryonic worms, and facilitates their adherence to reticuloendothelial (RE) cells in the microvasculature, particularly in the lung. Allergic Pneumonitis results from an interstitial infiltration of eosinophils and development of microgranulomas and interstitial fibrosis.
Occult Heartworm Infection

In an occult infection, there is either a prepatent infection, or there are adult worms present, but no detectable microfilariae. This can confound parasitological diagnostic techniques, so radiographic tools and immunodiagnostics become much more important in these cases. There are several ways that an individual can maintain such an infection. There may be an immune mediated response, such that the microfilariae are removed from the circulation. Chemosterilization of adult worms can occur with the macrolide endectocide prophylactic treatments (see below). There may be single-sex infections, or the infections exist where single worms are isolated in ectopic sites. If there is a build-up of dead microfilariae, as may occur with an immune mediated response, they may become trapped in the lung and cause interstitial lung disease. The overall incidence of occult infections is approximately 20% but may be much higher, 10 to 60%, depending on the composition of clinical syndromes in the population.
Heartworm
Clinical and Laboratory Diagnosis
There are several approaches to take when attempting to make a diagnosis of heartworm infection -- clinical, parasitological, and immunological. Clinically, a history demonstrating exposure to mosquitoes in an enzootic area is sufficient grounds to test for Dirofilaria infection. There are, however, NO pathognomonic clinical signs for heartworm disease, with the exception of the signs of caval syndrome, but in the appropriate context, clinical signs may raise a high index of suspicion. Signs that may give clues as to the presence of infection include rapid breathing and coughing during early disease stages. In advanced stages, animals can show syncope, hemoptysis, and chronic weight loss with good appetite. A decreased exercise tolerance will also develop, and is more common than either the syncope or hemoptysis. By the time heart failure develops, ascites and hepatomegaly will be present. Clinical laboratory tests will very often reveal an eosinophilia and basophilia in the early stage of infection. but this finding lacks specificity. Serum chemistry will change based on secondary organ involvement. As a result, a laboratory database is insufficient to make an etiological diagnosis.
Heartworm
Radiographic Diagnosis
In using radiographs to look for evidence of heartworm, one should take both DV and lateral views. One should see several characteristic lesions in the canine infection, including: Heart enlarged right ventricle Arteries enlarged main pulmonary artery enlarged peripheral pulmonary arteries decreased peripheral pulmonary artery taper (i.e. truncation) tortuous peripheral pulmonary arteries saccular dilation of the peripheral pulmonary arteries Lungs interstitial/alveolar pulmonary pattern with a caudal lobar distribution Differential diagnoses for this can include a possible pulmonary fibrosis, bronchopneumonia, infarction, granulomas, and eosinophilic pneumonia.
Lateral radiographs of a normal canine thorax (left) and one infected with heartworm (right).
DV radiographs of a normal canine thorax (left) and one infected with heartworm (right).
Echocardiography is recommended if the right ventricle appears enlarged on a radiograph or signs of congestive heart failure are present. Echocardiography cannot
visualize the adult worms in the peripheral pulmonary arteries, but with a high worm burden, they may be seen in the right heart and main pulmonary artery. Other abnormalities which may be observed are dilatation of the right ventricle, a thickened right ventricular free wall and intraventricular septum, or a decrease in right ventricle to left ventricle chamber size ratio.
Heartworm
Parasitological and Immunological Diagnostics
Traditionally, the first line of diagnosis for heartworm infection has been a parasitological examination, looking for microfilariae in the peripheral blood. A direct examination of the blood in a wet mount with 1-2 drops is a quick, easy method of doing this. However, this type of test is relatively insensitive, and microfilariae cannot be examined morphologically.
In order to deal with shortcomings of the direct smear, concentration methods can be used. The Knott method is a sensitive technique allowing for morphological examination, but a centrifugation step is required. Filtration methods are quick, easy, and sensitive, but precise morphological Three D. immitis microfilariae as examination is difficult. These methods allow seen with a Knott technique. for easy quantification, but the number of microfilaria DO NOT correlate well with either number of adult worms or with disease severity. In addition, dogs with naturally occurring occult infections and most dogs receiving macrolide chemoprophylactics cannot be tested with any of these parasitologic methods. Therefore examinations for microfilariae are no longer the primary method of testing for heartworm infection.
The earliest that heartworm microfilariae and antigenemia can be detected is 6.5 months after infection. As a result, no puppy needs to be tested before the age of 7 months. Even in areas where prevalence of heartworm infection is high, many animals do not have detectable microfilaremia, and an immunodiagnostic test is a much more specific way for identifying occult infections with at least one female.Microfilaria testing may be much more useful as a conformation method, and should be done each time DEC prophylaxis is restarted, and the species of microfilariae should be identified in order to insure that any microfilariae found are truly D. immitis, and not another species which may be nonpathogenic. Identification of microfilarial species is made easier by several methods. The now-outdated Indirect Fluorescent Antibody (IFA) test was specific to antibodies produced against microfilaria. The current methodology, ELISA tests, utilizes a monoclanal antibody to detect circulating worm antigen. These antigen tests all have a high degree of specificity for the detection of adult female heartworms, and are the standard for diagnosis of canine heartworm. Different tests exist, and although all are highly accurate, they differ in the amount of technical expertise needed to run them, the
ease of running batch or individual tests, unit cost, and ability to quantitate the amount of circulating antigen.
Heartworm
Dipetalonema reconditum
This nematode is common, found throughout the mid-Atlantic United States, but its transmission is not limited to warm months. The microfilariae are much smaller and narrower than D. immitis (270 x 4.5 vs. 300 x 6.5 um), and the body is more curved. They live within the dog's subcutaneous connective tissues. The microfilariae have a distinguishing cephalic hook, a blunt anterior end, and, in formalin fixed specimens, a 'button hook' tail. They are carried by vector fleas of the genus Ctenocephalides. Development requires about ten days. These ARE NOT clinically significant, although they may give elevated eosinophil and leukocyte counts. Its importance, however is its tendency to cause false positives in tests for circulating D. immitis microfilariae. They are easily distinguished by their staining patterns with acid phosphatase. While Dipetalonema stains realatively evenly, Dirofilaria concentrates the acid phosphatase in two regions.
Acid phosphatase-stained microfilaria of Dipetalonema reconditum.
Acid phosphatase-stained microfilaria of Dirofilaria immitis.
Heartworm
Drug Treatment and Chemoprophylaxis
Adulticidal Treatment
Drug treatment involves a three pronged approach, in order to account for varying drug susceptibility and drug safety. First, the adults must be killed, and there are two main classes of adulticides used. Melarsomine dihydrochloride, "Immiticide", is a new arsenical adulticide which is given intramuscularly into the lumbar muscles. The standard protocol is two doses of the drug twenty-four hours apart, however there is a modified protocol where a single dose is given, followed by paired doses 4-6 weeks later. The latter regimen is especially useful in treating very sick dogs, or dogs with high worm burdens at risk of thromboembolic complications. The other adulticide used is thiacetarsemide ('Caparsolate'), the predecessor to Immiticide. Caparsolate must be administered intravenously, and tissue sloughing can occur if the drug goes perivascularly. This drug is contraindicated when some liver and kidney diseases are present. With either of these drugs, if treatment with adulticides is successful, antigenemia and microfilaremia should be gone by sixteen weeks post-treatment.
Microfilaricidal Treatment
Microfilaricides are the next major type of drugs used when treating for heartworm. Ivermectin, not approved as a microfilaricide, has been used at fairly low doses, although microfilaricides are usually not given until after recovery from any side effects due to the arsenicals, not earlier than 3-4 weeks after this treatment had been administered. Milbemycin oxime at 500-999mcg/kg is an effective microfilaricide, and ivermectin given on an off-label basis, at 50 mcg/kg, will kill circulating microfilariae. Careful observation is required after an initial dose in order to treat potential systemic side effects. There have been some CNS side effects in rough coated collies (and other pure breeds) at high doses of Ivermectin outside the recommended dosage range.
Chemoprophylactic Treatment
Finally, prophylaxis is the major component of heartworm chemotherapy for any animal that could potentially become infected. Three main drugs exist for this purpose. All dogs should be tested for microfilariae before medication begins, particularly when using DEC, because microfilaremic dogs may progress to hypovolemic shock and death if DEC is administered. Macrolide endectocides, such as ivermectin (6-12 mcg/kg) and milbemycin oxime (500-999 mcg/kg) are completely effective in preventing adult maturation. Ivermectin (Heartguard) is administered orally, and has a low potential for shock reaction relative to
DEC. Milbemycin oxime (Interceptor) is also administered orally, and acts as both a microfilaricide and a larvicide. CNS effects have not been shown with this drug. Either of these drugs should be given once monthly per os from within one month following the onset of the transmission season to one month after transmission is considered unlikely. If a dose is missed, there is some afforded protection from residual amounts of drug remaining in the circulation. As a result, delayed administration may not lead to an adult infection. Diethylcarbamazine (DEC) is given orally once per day, and is highly effective, but is only safe in amicrofilaremic dogs. However, missed doses are significant if the elapsed time is longer than 2 months. If the omission time is under six weeks, readministration should establish full protection in the dog again. Other than the potential for shock reaction in microfilaremic dogs, no significant direct side effects have been seen with DEC, even at elevated doses.
Heartworm
Surgical Removal of Heartworm
Rather than destroy heartworms in situ, it is sometimes better to physically remove them from the right heart and pulmonary arteries. This mode of treatment allows for removal of most of the worms without risking complications due to thromboembolism. As a result, individuals with severe cor pulmonale or caval syndrome may be benefitted most.
During this surgery, the patient is under local anaesthesia. Flexible alligator forceps are inserted into the arteries to remove the worms. It should be performed as rapidly as possible to alleviate the obstruction to blood flow. Within 2 weeks after recovery from surgery, adulticide therapy is recommended to eliminate any worms that remain in the circulation.
While a very popular procedure in Japan, the forceps technique requires anaesthesia and fluoroscopic imaging, and offers no practical advantage over the use of adulticide administration, with the exception of heavily infected cases, such as those with caval syndrome, in which it is the treatment of choice.
The results of a successul surgery!
Heartworm
Heartworm Disease in Cats
Although the life cycle of Dirofilaria immitis remains similar whether the worms enter a dog or cat, felids often react to infection differently than the dogs. Adult worms mature in the feline host, but are much more short-lived, usually 2-3 years. In addition, most cases of feline heartworm do not show microfilaria in the peripheral blood. Those that are positive exhibit a low, transient microfilaremia, lasting only 2-3 weeks. Infection rates are generally much lower than the surrounding dog populations, ranging from 5-20% of the surrounding prevalence of canine infection, and the feline infection tends to exhibit a lower worm burden than in dogs. The prepatent period is also longer for the cat, at about 242 days.
When a cat is infected, it may show the same type of cardiopulmonary disease seen in the dog, but it is very often more severe with a smaller number of worms than seen with canine infections. Ectopic infections are more commonly seen in cats than in dogs, suggesting that the parasite is not as well adapted to these feline hosts. Sudden deaths may occur from acute circulatory and respiratory failure. Cats may also show thromboembolism more often than dogs, and this can be exacerbated by adulticide treatment. Cats with heartworm disease are more likely to be 3-6 years old and male. Common presenting signs are coughing dyspnea, vomiting, weight loss and lethargy.
Radiographically, one observes an interstitial lung pattern, enlarged lobar pulmonary arteries, and occasionally right sided heart enlargement. Lab analysis of the blood may show a transient eosinophilia during the early stages of infection and may be absent thereafter.
Treatment of feline heartworm should be watched carefully. If an individual is infected without clinical signs of disease, the cat may be able to clear the worms without any treatment, but with monitoring to watch for complications every 6 to 12 months. If there are radiographic signs of pulmonary disease, prednisone may be used. Supportive therapy is indicated in the case of acute collapse, and parenteral fluids may be appropriate. Adulticide therapy is usually reserved for those cats which cannot be helped by other therapies, but there is a very high risk of thromboembolism with adulticides such as Caparsolate. Prevention of feline heartworm is best done with monthly chemoprophylaxis, using extralabel doses of ivermectin (24 ug/kg) or milbemycin oxime (500ug/kg). Diagnosis of feline heartworm disease is difficult. When looking for microfilariae in the blood, if there is a microfilaremia, it usually is not very high, and a concentration method may be of help; however, there is no guarantee that they will be found. Many other heartworm infections are missed because many of these cats die suddenly without preceding clinical signs. If clinical signs are present, they often do not reflect pulmonary disease (e.g. vomiting). Often heartworm cases are misdiagnosed as feline asthma, or other pulmonary diseases. If heartworm is suspected, there is a higher incidence of false negatives with the existing antigen tests than seen when used with dogs due to the low levels of antigen seen in these feline infections. Because of the difficulties seen with the parasiological and antigen-based tests, the best way to find a case of feline heartworm is with an antibody-based ELISA. If heartworm was suspected, a necropsy may provide the best confirmation of infection. Examination of the systemic veins, right side of the heart, and pulmonary veins should be performed. Ectopic sites, such as systemic arteries and body cavities may contain the worms. If neurologic signs were present, the central nervous system should be checked thoroughly.
LAB 1 DEMO Quiz Answer

A. Given the dorso-ventral compressed shape, the oral and ventral sucker:
Kingdom:
Phylum:
Class:
B. Trematode eggs do not always float in a salt solution (they are too heavy, i.e. specific gravity greater than 1.2). A direct smear may find them if they are numerous, however, the best answer (the correct answer) is to use a sedimentation technique which provides some concentration of the eggs, thus, use the ETHYL ACETATE SEDIMENTATION TECHNIQUE.
RETURN TO LAB 1
Nematode Taxonomy
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Class: Nematoda
Superfamily: Trichostrongyloidea
Genera:
Trichostrongylus Haemonchus Ostertagia Cooperia
Nematodirus Dictyocaulus
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Nematode Taxonomy
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Class: Nematoda
Superfamily: Family: Genera: Strongyloidea Strongylidiae Strongylus Cyathostoma Oesophagostomum Stephanurus
Family: Genera:
Ancylostomatidae Ancylostoma Uncinaria Bunostomum
Nematode Taxonomy
Class: Nematoda
Superfamily: Genera: Metastrongyloidea Metastrongylus Muellerius Oslerus (Filaroides) Aelurostrongylus
Nematode Taxonomy
Class: Nematoda
Superfamily: Genus: Rhabditoidea Strongyloides
Nematode Taxonomy
Class: Nematoda
Superfamily: Genus: Oxyuroidea Oxyuris
Nematode Taxonomy
Class: Nematoda
Superfamily: Genera: Ascaridoidea Ascaris Parascaris Toxocara Toxascaris Baylisascaris Anisakis
Nematode Taxonomy
Class: Nematoda
Superfamily: Genera: Subuluroidea Heterakis Ascaridia
Nematode Taxonomy
Class: Nematoda
Superfamily: Genera: Spiruoidea Spirocerca Habronema Draschia Thelazia
Nematode Taxonomy
Class: Nematoda
Superfamily: Genera: Filarioidea Dirofilaria Dipetalonema Onchocerca Setaria Stephanofilaria
Nematode Taxonomy
Class: Nematoda
Superfamily: Genera: Trichuroidea Trichuris Trichinella Capillaria
Nematode Taxonomy
Class: Nematoda
Superfamily: Genus:
Dioctophymatoidea Dioctophyma
LAB 2 DEMOS QUIZ ANSWERS

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A. Small strongyles (Cyathostomum spp., etc.) and Strongylus vulgaris (the smallest of the large strongyles, compare it to the penny in the picture).
B. Strongylus vulgaris would be the more important pathogen.

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A. Ancylostoma caninum (Canine small intestinal location and size.) This identification is supported by the clinical signs: anemia.
B. Given the age of the dog, the most likely route of transmission was transmammary.
LAB 4 DEMO Answer to Quiz Question

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A.
Given that the puppy was from Philadelphia:
Left egg is Ancylostoma caninum Right egg is Toxocara canis
B. Toxocara canis entered the puppy in utero. The larvae crossed the placenta and arrested in the liver of the fetus. After the pup was born the larvae resumed their migration from the liver, through the heart to the lungs where they broke out of the capillaries and into the alveoli, causing the symptoms of pneumonia. Ancylostoma caninum would have entered this young pup through the milk (transmammary). Orally ingested hookworm larvae do not undergo a somatic migration. So, the answer to "B" is Toxocara canis.
RETURN TO LAB 4

Back to Lab 5 Demos
A. The microfilaria seen in the photo is that of Dipetalonema reconditum (based on the bent body, blunt anterior end and button-hook tail). The antigen tests for heartworm do not cross react with this skin dwelling filarid. B. The acid phosphatase staining technique would confirm that this microfilaria is Dipetalonema reconditum .
C. Dipetalonema reconditum is considered non-pathogenic to the dog.
PARASITOLOGY 4001 Lab Practical 1 - 1995
Question 1
Question 1. A. A local dairy farmer has just acquired some livestock from Louisiana and is concerned that they may have liver flukes (the trematode Fasciola hepatica). What fecal examination method will give you the best chance of finding the eggs of this parasite? (3 pts.) B. A 3-week-old puppy has watery diarrhea. Given its age and clinical signs you suspect a Giardia infection. What fecal examination method will give you the best chance of detecting this parasite? (3 pts.) C. A 4-year-old dog has a chronic cough and you have included the nematodes that live in the lungs on your list of possible causes. What fecal examination method(s) will give you enough information to rule out (or in) the presence of these "lungworms"? (3 pts.) Look at the answers to this question.
Lab Exam Question 2
Question 2. A. The fecal sample in the device at your place came from a 4-year-old male Rottweiler as part of his yearly check-up. Examine the sample and identify the eggs of the parasite (give Genus and species). (7 pts.)
B. What other similar looking egg could appear in dog feces and how could You tell it apart from the egg you identified in part A? (3 pts.) Look at the answers to this question.
Lab Exam Question 3
Question 3. A. The sample of meat in the dish at your place is beef hamburger that is thought to have been contaminated with pork. Is it likely that the hamburger has pork in it (yes, no, can't tell)? (4 pts.)
B. Explain your answer to part A. (3 pts.) Look at the answers to this question.
Lab Exam Question 4
Question 4. A. A saturated salt flotation was done on a fecal sample from a 4 month old Puppy which has been brought to you for its first check-up. The results of this test are shown under the microscope at Station #4. Identify the parasite egg (give Genus and species). (7 pts.)
B. What other similar looking egg may be found the feces of a dog and how could you tell it apart from the egg you identified in part A? (3 pts.) Look at the answers to this question.
Lab Exam Question 5
Question 5. A. A 6-year-old male mixbreed dog was brought in to your practice with the complaint that it had chronic vomiting. The results of a saturated salt flotation fecal examination is shown under the microscope at Station #5. Identify the egg (give Genus and species). (6 pts.)
B. What pathologic changes may have been caused by this parasite and what other procedures would you do to determine if this dog had these pathologic conditions? (3 pts.) Look at the answers to this question.
Lab Exam Question 6
Question 6. A. The egg seen under the microscope at Station #6 was recovered from the feces of a 1 month old foal which has diarrhea. Many of these eggs are present on the slide. Identify the parasite (give Genus and species). (6 pts.)
B. Why would you expect to see eggs of this parasite in a young foal rather than in a mature horse? (3 pts.) Look at the answers to this question.
Lab Exam Question 7
Question 7. A. The egg seen under the microscope at Station #7 was recovered during a urine analysis of a pig. Identify the parasite (give Genus and species). (6 pts.)
B. In what organ does the adult worm reside? (3 pts.) Look at the answers to this question.
Lab Exam Question 8
Question 8. A. The worms seen under the microscope at Station #8 were recovered from the small intestine of a sheep which died of bacterial pneumonia. Identify the parasite (give Genus only). (6 pts.)
B. Describe the egg you would expect to find in the feces. (3 pts.) Look at the answers to this question.
Lab Exam Question 9
Question 9. A. A number of adult nematodes, each about 1.5cm long, were recovered from the large intestine of a horse which died suddenly. The anterior end of the worm is shown on the kodachromes at Station #9. Identify the parasite (give Genus and species). (6 pts.)
B. Where in the horse would the fourth-stage larvae (L4) of this worm be found? (3 pts.) Look at the answers to this question.
Lab Exam Question 10
Question 10. A. The dish under the microscope at Station #10 contains a skin biopsy in saline. The biopsy was taken from the ventral midline of a horse with itching dermatitis in this area. Identify the parasite (give Genus only). (6 pts.)
B. How is this parasite transmitted? (3 pts.) Look at the answers to this question.
ANSWER TO THE LAB 6 REVIEW QUESTION
A. Dicrocoelium dendriticum B. The deer ate an ant infected with the metacercariae.
Answer to Lab 7 Review Question
A. Family Anoplocephalidea B. Triangular or diamond shaped, with a pyriform apparatus around the oncosphere.

A. Dermacentor B. Rocky Mountian Spotted Fever
A. A sucking louse (suborder Anoplura) [Linognathus setosus]

B. No, Dipylidium caninum is carried by fleas and chewing lice.
Answer to Lab 10 Review Question A. Toxoplasma B. Yes, the oocyst is sporulated and therefore infectious. The dog, like many mammals, can be an intermedate host of this parasite and thus can be infected.
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Cat Homepage Parasites of the Cat
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Aelurostrongylus abstrusus - uncommon Alaria marcianae - rare Ancylostoma braziliense - uncommon Ancylostoma tubaeforme - common Capillaria aerophilia - uncommon Capillaria plica - uncommon Cryptospiridium parvum - uncommon Cuterebra spp. - common Cytauxzoon felis - rare Diphylobothrium latum - rare Dipylidium caninum - common Dirofilaria immitus - common Echinococcus multilocularis - rare Eurytrema procyonis - rare Giardia lamblia - common Hammondia hammondi - uncommon Isospora felis - common Isospora rivolta - common Mesocestoides spp. - uncommon Ollulanus tricuspids - rare Paragonimus kellicotti - uncommon Parametorchius complexus - rare Platynosomum fastosum - rare Physaloptera spp. - uncommon Sarcocystis spp. - uncommon Spirometra mansonoides - rare Strongyloides spp. - rare Taenia taeniaeformis - common Toxascaris leonina - common Toxocara cati - common Toxoplasma gondii - uncommon Trichinella spiralis - not looked for Trichuris spp. - rare
Diagnostic Stages of Feline Endoparasites
Below is a list and where possible images of parasite diagnostic stages.

Nematode eggs and larvae that are found in fecal samples. Nematode larvae that are found in muscle Nematode adults and larvae found in skin or eye Nematode eggs and larvae found in tracheal and nasal washes Nematode larvae found in blood Tapeworm Eggs (found in feces) Trematode Eggs (found in feces) Protozoans - found in feces Protozoans - found in blood Protozoans - found in biopsy Artifacts - frequently found in feces Acanthocephalan eggs (feces)
Quiz Case #1
Case 1
The egg shown in the photo was found during a zinc sulphate fecal examination of a 6 year old, indoor/outdoor (70%/30%) male cat. This was a routine exam done as part of the cat's yearly examination. Identify the egg shown: A. Toxocara cati B. Toxascaris leonina C. Paragonimus kellicotti D. Trichuris felis E. Physaloptera rara
Quiz Case #1
Case 2
An 8 week old kitten was brought into the clinic for its first check-up. The kitten looks normal on the physical exam, but the owner states that it has had diarrhea for the past 3 days. A fecal exam is run and many objects shown above were found (it measures about 40 um long). Identify the parasite: A. Ancylostoma tubaeformae B. Ancylostoma braziliense C. Isospora felis D. Isosporsa rivolta E. Plant cell
Quiz Case #3
A 7 year old, indoor/outdoor (50%/50%) female cat is showing difficulty in breathing. The owner also reports that the pet has been vomiting recently. You have radiographed the cat and the result is shown here.
Click on image for full size representation and help to identify pathology Which of the following parasites should be considered as a cause for the clinical signs and the damage seen in the radiograph? A. Capillaria aerophilia B. Aelurostrongylus abstrusus C. Filaroides osleri D. Dirofilaria immitis E. Toxocara cati
Quiz Case #4
A 6 year old male indoor/outdoor (50%/50%) cat is brought in to your center city Philadelphia practice for a yearly check-up. A fecal flotation was performed and the result is shown in the photo below. The cat is healthy and showing no clinical signs.
Identify the egg to genus: A. Trichuris B. Capillaria C. Toxocara D. Physaloptera E. Dipylidium
Quiz Case #5
A 4 year old female, spayed, cat was brought in to it's local veterinarian in Massachusetts becuase it was not doing well. It had lost a fair amount of weight over the last 2 months. Blood work indicated elevated liver enzymes (Alk phos, GGT). A biopsy of the liver was taken and sent out for pathology. A H&E stained slide of the biopsy is presented below (1A). The specimen shown in figure 1B was recovered from the bottom of the container in which the biopsy had been shipped to the lab.
1A
1B
Note: You can click on image 1A to see the cross-section of the adult parasite highlighted. To what class does this parasite belong? A. Cestoda B. Trematoda C. Nematoda D. Insecta E. Pentastomida
Eggs, larvae and cysts of Cat Parasites: A QUIZ Click on photo to see answer.
NOTE: Photos are not to scale !
Eggs and cysts found in feces or expressed from tapeworm proglottids:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
In urine:
15.
Answers:
1. Toxocara cati 2. Toxascaris leonina 3. Ancylostoma tubaeforme 4. Taenia taeniaeformis 5. Dipylidium caninum 6. Spirometra mansonoides 7. Aelurostrongylus abstrusus 8. Capillaria aerophilia 9. Isospora felis 10. Isospora rivolta (sporulated) 11. Trichomonas sp. 12. Giardia 13. Toxoplasma gondii (sporulated and unsporulated) 14. Fungal spore (artifact, not a parasite of cats) 15. Capillaria plica
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Parasites of the Dog
Ancylostoma brazilensis - rare Anclystoma caninum - common Babesia canis - uncommon Babesia gibsoni - rare Balantidium coli - rare Baylisacaris procyonis - uncommon Capillaria aerophila - uncommon Capillaria boehmi - uncommon Capillaria plica - uncommon Crenosoma vulpis - uncommon Cryptosporidium parvum - uncommon Cuterebra spp. - common Dioctophyme renale - rare Dipetalonema reconditum - uncommon Dipylidium caninum - common Diphyllobothrium latum - uncommon Dirofilaria immitis - common Dracunculus insignis - rare Echinococcus granulosus - rare Echinococcus multilocularis - rare Entamoeba histolytica - rare Filaroides hirthi - rare Oslerus(Filaroides) osleri - rare Giardia duodenalis - common Heterobilharzia americana - rare Isospora canis - common Isospora ohionensis - common Leishmania spp. - uncommon Macracanthorhynchus ingens - rare Mesocestoides corti - rare Nanophyetus samincola - rare Neospora caninum - uncommon Paragonomus kellicotti - uncommon Parametorchius complexus - rare Platynosomum fastosum - rare Physaloptera spp. - uncommon Sarcocystis cruzi - uncommon Spirocerca lupi - rare Spriometra mansonoides - rare Strongyloides stercoralis - uncommon Taenia hydatigena - rare Taenia ovis - rare
Taenia pisiformis- common Taenia multiceps - rare Taenia serialis - rare Thelazia californiensis - rare Toxascaris leonina - common Toxocara canis - common Trichinella spiralis - rare Trichomonas spp. - uncommon Trichuris vulpis - common Trypanosoma cruzi - rare Uncinaria stenocephala - uncommon
Diagnostic Stages of Canine Endoparasites
Below are pages with images of parasite diagnostic stages.

Nematode eggs ands larvae that are found in fecal samples. Nematode larvae that are found in muscle Nematode adults and larvae found in skin or eye Nematode eggs and larvae found in tracheal and nasal washes Nematode larvae found in blood Tapeworm Eggs (found in feces) Trematode Eggs (found in feces) Protozoans - found in feces Protozoans - found in blood Protozoans - found in biopsy Artifacts - frequently found in feces Acanthocephalan eggs (feces)
Quiz Case #1
Case 1
A 10 week old, male German Shepard, "Bailey", is brought to your practice. The owner states that Bailey just lays around and appears sick (ain't doin' right). Upon examination you note that Bailey is underweight for his age and breed and he has pale gums. Based upon your examination and Bailey's history you suspect a parasitic infection. Which of the following tests should you run? Knott test Fecal flotation Urine Sedimentation Tracheal wash
Canine Quiz Case #2
A 10 week old, female mixed breed puppy, "Ariel", is brought to your practice. The owner has brought Ariel in for her first examination and vaccinations. A fecal sample was also brought in for a routine examination. Upon gross examination of the fecal sample, you note that the feces are normal in color but semi-formed (mushy). No tapeworm segments are noted. Based upon your gross examination of the feces and Ariel's history, which of the following tests should you run? Saturated salt fecal flotation ZnSO4 fecal flotation Direct examination of a fecal smear Ethyl acetate fecal sedimentation
Quiz Case #3
Case 3
A six year old male Rottweiler (Cirus) has been brought in because it has bloody diarrhea. The owner first noticed the diarrhea yesterday, although it may have been going on for awhile. You see bright red blood on the stool, which also appears to have mucus in it. Cirus is allowed to run loose in the large wooded area behind the owner's house and is known to catch and eat rabbits and rodents. Other neighborhood dogs are also allowed loose in this same area. Raccoons, opossums, and deer are common in the woods. Which one of the following tests should you run on the fecal sample? ZnSO4 fecal flotation Saturated salt fecal flotation Fecal occult -blood test fecal-starch test
Quiz Case #4
A six year old male Labrador Retriever, Mackenzie, has been presented to you for his yearly check-up. Mackenzie spends a lot of time outdoors and goes camping with his owners every summer. You performed a fecal flotation, and the two eggs shown below were found.
Identify the parasites whose eggs are shown in "A" and "B". 1. A= Taenia taeniaeformis and B= Toxocara canis 2. A= a taenid tapeworm and B= Toxascaris leonina 3. A= a taenid tapeworm and B= Toxocara canis 4. A= Taenia pisiformis and B= Toxocara canis 5. A= a unknown tapeworm and B= Toxascaris leonina.
Eggs, larvae and cysts of Dog Parasites: A QUIZ Click on photo to see answer.
NOTE: Photos are not to scale !
IN FECES (or from proglottids found in feces)
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IN URINE
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Answers: 1. Toxocara canis 2. Baylisascaris 3. Toxascaris leonina Return to Quiz Return to Quiz
4. Taenia or Echinococcus 5. Spirometra 6. Dipylidium caninum 7. Spirocerca lupi 8. Ancylostoma 9. Uncinaria 10. Trichuris vulpis 11. Filaroides 12. Strongyloides stercoralis 13. Heterobilharzia americana 14. Paragonimus kellicotti 15. Capillaria aerophilia 16. Capillaria bhmi 17. Giardia 18. Isospora canis 19. Isospora ohionensis 20. Cryptosporidium parvum 21. Sarcocystis 22. Trichomonas 23. Pine pollen 24. Plant cells 25. Dioctophyma renale 26. Capillaria plica Return to Quiz To TOP OF PAGE Return to Quiz Return to Quiz Return to Quiz Return to Quiz
Parasites of Cattle
Bunostomum phlebotmum Capillaria bovis Cooperia punctata Cryptospordium Dictyocaulus viviparus Eimeria bovis Fasciola hepatica Giardia Gongylonema pulchrum Haemonchus contortus Moniezia benedeni Moniezia expansa Nematodirus spathiger Onchocerca lienalis Ostertagia ostertagi Strongyloides papillosus Toxocara vitulorum Toxoplasma gondii
Trichostrongylus axei Trichostrongylus colubriformis Trichuris ovis Tritrichomonas foetus
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Parasites of the Ferret

Eimeria furonis Eimeria vison Eimeria ictidea Isospora laidlawi Sarcocystis putorii Cryptosporidium parvum Giardia sp. Dirofilaria immitis Toxoplasma gondii Dipylidium caninum
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Parasites of Goats
Bunostomum trigonocephalum Capillaria longipes Capillaria bovis
Chabertia ovina
Cooperia punctata, Cooperia spp. Cryptosporidium

Dictyocaulus filaria Dicrocoelium dendriticum Echinococcus granulosus
Eimeria spp.
Entamoeba spp. (E. ovis, E. dilimani, E. wenyoni)
Fasciola hepatica Giardia Gongylonema pulchrum Haemonchus contortus Moniezia benedeni Moniezia expansa
Muellerius capillaris
Nematodirus spp. (N. spathiger, N. filicollis, N. battus)
Oesophagostomum spp. (O. venulosum, O. columbianum)
Ostertagia circumcincta
Protostrongylus rufescens Sarcocystis spp.
Strongyloides papillosus
Taenia hydatigena (larval stage only) Taenia multiceps (Multiceps multiceps) (larval stage only) Taenia ovis(larval stage only)
Toxoplasma gondii Trichostrongylus spp. Trichostrongylus colubriformis Trichuris ovis Trichuris globulosa
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PARASITES OF HORSES
Anoplocephala magna Anoplocephala perfoliata Paranoplocephala mamillana Parascaris equorum Habronema muscae Draschia megastoma Gongylonema pulchrum Halicephalobus gingivalis Strongyloides westeri Strongylus equinus Strongylus edentatus Strongylus vulgaris Triodontophorus spp. Cyathostomum spp. and other small strongyles Trichostrongylus axei Cooperia oncophora Oxyuris equi
Gasterophilus spp. Trichomonas spp. Giardia sp. Entamoeba spp. Eimeria spp. Fasciola hepatica Echinococcus granulosus Trypanosoma equiperdum Babesia equi Dictyocaulus arnfieldi Onchocerca cervicalis Sarcocystis spp. Setaria equina Return to top of page
Parasites of Llamas
Fasciola hepatica Fascioloides magna Parelaphostrongylus tenuis Marshallagia Camelostrongylus Haemonchus Ostertagia Trichostrongylus Strongyloides papillosus Cooperia Nematodirus battus, N. helvetianus Capillaria Trichuris tenuis Oesophagostomum Dictyocaulus Eimeria lamae Cryptosporidium
Sarcocystis
(The llama is an intermediate host) (The llama is an intermediate host)
Toxoplasma gondii Giardia
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Parasites of the Pig
Ascaris suum Strongyloides ransomi Trichinella spiralis Oesphagostomum dentatum Macracanthorynchus hirudinaceus Trichuris suis Metastrongylus elongatus Stephanurus dentatus Taenia solium Swine are the intermediate host (They have the larval
stage of this parasite)
Hyostrongylus rubidus Giardia lamblia Eimeria suis Isospora suis
Balantidium coli Cryptosporidium parvum Fasciola hepatica
Parasites of the Robin
Parasite List for Turdus migratorius (Most of this list is from C.L. Cooper and J.L. Crites, 1976. The American Midland Naturalist 95:194-198) To jump to a parasite section: Cestodes, Trematodes, Nematodes, Acanthocephalans, Protozoa Cestodes: Anomotaenia constricta Aploparaksis dujardini neoarcticus Aploparaksis turdi Choanotaenia iola Dilepis undula Hymenolepis fariminosa Hymenolepis microcirrosa Hymenolepis planestici Hymenolepis serpentulus Hymenolepis turdi Southwellia sp Tatria decacantha
To TOP of PAGE Nematodes: Capillaria obsignata Capillaria quiscali Capillaria caudinflata Capillaria contorta Capillaria exilis Capillaria ovopunctatum Cardiofilaria inornata Dispharynx nasuta Habronema sp Microfilaria sp Microtetrameres sp Oxyspirura petrowi Porocaecum brevispiculum Porocaecum ensicaudatum Splendidofilaria caperata Syngamus trachea To TOP of PAGE Acanthocephala Luehia adluehia Luehia boreotis
Mediorhynchus grandis Mediorhynchus robustus Plagiorhynchus formosus To TOP of PAGE Trematodes Brachylaemus pellucidum Brachylecithum mosquensis Collyriclum faba Leucochloridium variae Lutztrema monenteron Plagiorchis noblei Posthodiplostomum minimum To TOP of PAGE Protozoa Isospora robini Plasmodium spp Leucocytozoon dubreuili
Sulcascaris sulcata Homepage
Common name: Loggerhead stomach worm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascaridoidea Genus: Sulcascaris Species: sulcata
Click on the text below to jump down to the desired section of this page. Adult Parasite Hosts Life cycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment
Adult Parasite:
Males measure 9 cm long. Females are 11 cm long.
Adult worms recovered from the stomach of a Loggerhead Turtle.
Hosts:
Definitive: Marine turtles Intermediate: Scallops and other mollusks
Life Cycle:
Eggs pass out in the feces and fall to the sea floor. The larva develops in the egg and under goes 2 molts to the L3 stage. The L3 hatch from the eggs beginning at 7 days after the egg was laid. L3 are taken up by mollusks (Scallops and possibly others) and go to the tissues. The L3 will molt to the L4 in the scallop in 3 to 4 months. When the infected mollusk is eaten by the loggerhead turtle the L4 attach to the stomach wall (at the esophago-gastric junction) and will molt to the adult in 7 days. Adults will become gravid in 5 to 6 months. (G.N. Berry and L.R.G. Cannon, 1981. International Journal for Parasitology 11:43-54.)
Site where adult parasite is found in host:

Stomach
Diagnostic Stage:
Egg: Ovoid or triangular 61 - 75 by 86 - 100 m. Thin shelled with a rough surface.
Common Diagnostic Test:

Fecal float Identification of the adult worm recovered from the feces. Return to top of page
Clinical Signs:
Worms may aggregate and cause ulceration of the stomach with almost complete destruction of the upper layer of mucosa.
Treatment:
No Data
Ozobranchus margoi Homepage
Common name: Marine turtle leech Kingdom: Animalia Phylum: Annelida Class: Hirudinea Order: Rhynchobdellidae Family: Ozobranchidae Genus: Ozobranchus Species: margoi
Adult Parasite:
Adult leeches recovered from the skin of a Loggerhead Turtle.
Hosts:
Definitive: Marine turtles
Life Cycle:
Eggs are laid in sheets on the plastron of the turtle. Adults feed on areas of exposed skin.

Skin of the ventral surface of flippers, the neck, external cloaca, around the mouth and in the area between the carapace and the plastron. Return to top of page
Diagnostic Stage:
Adult leech from skin or eggs attached to turtle shell.

Identification of the adult leech. Return to top of page
Clinical Signs: Turtles with heavy infections will stop feeding. Leeches will eat away skin and eyes, exposing bone. Turtles will die of heavy infestations.
(F. J. Schwartz, 1974. Journal of Parasitology 60(5):889-890.)
Treatment:
1.35 kg of cupric sulfate was added to tank water (125,070 liter tank) and water circulation stopped. Within 14 hrs all adult leeches were dead. Turtles were kept in the tank for an additional 46 hrs with no water circulation. No new infestation occurred after circulation was resumed, so apparently the eggs were also killed by this treatment. (F. J. Schwartz, 1974. Journal of Parasitology 60(5):889-890.)
Ancylostoma caninum
Ancylostoma caninum
Ancylostoma caninum
Ancylostoma caninum
Dirofilaria immitis
Dirofilaria immitis
Dirofilaria immitis
Dirofilaria immitis
Echinococcus granulosus (Instructions)
The Nematodes
Cuticle modifications - anterior end
The following six images illustrate nematodes with anterior cuticular modifications. Click on each image with a blue border to show an enlarged, labeled version of the same image.
Fig. 1.
Fig. 2.
Fig. 3.
Anterior end of an equine strongyle showing a leaf crown (A) surrounding the opening to the buccal cavity.
Oesophagostomum with cuticular modifications at the anterior end: A = cephalic vesicle B = cervical vesicle C = Cervical alae
Anterior end of Ostertagia showing a pair of spine-like cervical papillae (A) in the esophageal region
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Fig. 6.
Scanning electron micrograph of Haemonchus contortus showing cervical papillae, cuticular striations and the buccal lancet used for slitting capillaries during blood feeding
Scanning electron micrograph of Ostertagia ostertagi showing circular(B) and longitudinal cuticular striations( C). The small mouth opening or stoma is labeled A.
Anterior end of Toxocara canis, the roundworm of dogs, showing the tapering lance-shaped cervical alae (A)
The Nematodes
Cuticle modifications - posterior end
The following six images illustrate nematodes with posterior cuticular modifications. Click on each image to show an enlarged, labelled version of the same image.
Fig.1. Cooperia.Tail end of male showing copulatory bursa, spicules and bursal rays.
Fig. 2. Heterakis. Tail end of male showing Spicule (A), caudal ala (B) and pre-cloacal sucker (C). Vas deferens = D.
Fig. 3. Oesophagostomum. Tail end of a female showing caudal ala (A) and a tapering tail with a blunt end.
Fig. 4. Bunostomum. Tail end of a male showing spicules (A), and a pronounced copulatory bursa with lateral lobes (B) and bursal rays (C).
Fig. 5. Equine strongyles.Two males (A) competing to copulate with a female (B). Copulatory bursae are labeled (C).
Fig. 6. Oesophagostomum. Copulating male (A) and female (B). Copulatory bursa is labeled (C).

The Nematodes
Internal Morphology
The basic nematode body consists of an outer tube (the body wall) enclosing an inner tube (the digestive tract). The fluid-filled body cavity lies between these two tubes and contains the reproductive tract. This body cavity is a pseudocoelom because, unlike a true coelom, it does not possess a cellular lining or peritoneum. There is no vascular system in the nematodes, instead the circulation of nutrients in the pseudocoelom is assisted by body movements and locomotion. The body wall has three layers: cuticle, hypodermis and an inner layer of muscle cells. The hypodermis, lying beneath the cuticle, is relatively thin and is a syncytium of cells in the majority of nematodes of veterinary importance. The primary function of the hypodermis is to secrete the cuticle. The hypodermis has four longitudinally thickened areas or cords that protrude into the body cavity in the mid-dorsal, mid-ventral and lateral regions.The dorsal and ventral cords contain longitudinal nerve trunks while the lateral cords contain excretory canals. Internal to the hypodermis are one or more layers of longitudinally arranged striated (somatic) muscles. These are closely associated with the hypodermis and also connect to the cuticle by fibers passing from the contractile part of each muscle cell. Each muscle cell consists of a contractile part with muscle fibers and a non-contractile part or cell body containing the nucleus, mitochondria and other organelles in addition to glycogen and lipid stores. Muscle cells of nematodes are unusual because they are not innervated by nerve fibers as is the case with muscles of other animals. Instead, processes from muscle cell bodies link muscle cells to the nerve trunks.
Movement of Nematodes
Nematodes are covered by an outer cuticle that is structured so as to maintain the body at a constant diameter while allowing longitudinal flexibility. Since nematodes have longitudinally arranged but no circular muscles, contraction of muscles bend the body dorsally or ventrally.Since the cuticle prevents radial swelling, contraction of one muscle group will stretch another. This situation ensures that the dorsal and ventral muscles will act antagonistically to each other, allowing nematodes to move in a sinusoidal manner by undulating waves of muscle contractions. These movements allow nematodes to move among soil particles and swim in body fluids of a host. Click here to view a cross sectional drawing of a female nematode at the level of the intestine. Click here to return to the drawing of a nematode at the level of the esophagus
The Nematodes
Digestive System
The digestive system of nematodes is usually a simple tube with the majority of variations occurring in the sizes of the mouth opening, buccal capsule (syn = buccal cavity) and esophagus. The mouth may be a simple opening with a tiny buccal cavity leading directly to the esophagus as shown in the accompanying image of Nematodirus ( a small nematode found in the small intestine of ruminants). At the other extreme, the mouth opening may be quite large leading to a prominent buccal cavity with thick walls and often containing teeth ( e.g. Strongylus vulgaris). The type of mouth opening and accompanying buccal cavity appears to be related to diet. A large mouth opening and prominent buccal cavity is found in those nematodes that feed by taking a bite of mucosa, and drawing it into the buccal cavity where it is digested (e.g the large strongyles of horses). These nematodes are often called "plug feeders". In nematodes that feed by simple ingestion of host fluids the mouth opening and accompanying buccal cavity are generally quite small.(e.g. Ostertagia in which the mouth opening and buccal cavity are so small they can only be viewed effectively by scanning electron microscopy and, Nematodirus spp). In nematodes that are described as mucosal grazers, rather then plug feeders, the mouth opening and its buccal cavity are usually intermediate in size (e.g. Oesophagostomum radiatum a nematode found in the large intestine of swine). In most nematodes, the esophagus is muscular and is used to pass food into the intestine by a pumping action. The shape of the esophagus may be used as an initial screening characteristic for identification. For example, adult nematodes belonging to the Superfamily Strongyloidea have a club-shaped (strongyliform) esophagus which, as the name suggests, is shaped like a club. Adult members of the Superfamily Oxyuroidea have an esophagus which has a prominent posterior bulb separated from the rest of the esophagus by a narrow isthmus. The intestine is a straight tube roughly circular in cross section and with a wall consisting of a single layer of columnar (rectangular-shaped) cells. The lumen surfaces of these cells consist of multitudes of projecting microvilli used in absorption and because of their vast numbers provide an immense absorptive capacity. The intestine terminates in a rectum in females and a cloaca in males. The cloaca is a common termination for the intestinal tract and the vas deferens in adult males. In either case, the cloaca (males) and rectum (females) leads to an anus which usually opens to the outside at the posterior end of the body.
The Nematodes
Reproductive System
The sexes are separate in most species of nematodes and males are almost always smaller than females since females need to accommodate the production of large quantities of eggs. This disparity in size between male and female nematodes in shown in the accompanying image of Syngamus trachea in copulation: the smaller, pale blue, male (0.5 cm long) is dwarfed by the larger female (2.0 cm long) whose body is packed with coils of its yellowish-white reproductive tract. The female reproductive system is tubular and in most nematodes of veterinary importance consists of two ovaries, each of which connects to an oviduct, and a uterus. The two uteri end in a common vagina which opens to the outside by a vulva which is often covered by a protective flap of cuticle, the vulva flap. In female members of the order Strongylida a muscular structure called an ovejector controls the exit of eggs from the uterus. The male reproductive system in nematodes of veterinary importance is a single tube differentiated into testis, seminal vesicle and vas deferens and terminating in a muscular ejaculatory duct which empties into the cloaca. In most nematode species there are two accessory male organs, spicules and a gubernaculum as shown in the accompanying image of Haemonchus contortus. Spicules (A) are made of cuticle, are often paired and used in copulation to dilate the female vulva. The gubernaculum (B) is a cuticular modification of the dorsal wall of the cloaca and is used to guide the spicules down through the cloaca so as to penetrate the female vulva. In this particular species, the spicules normally protrude from the cloaca even at rest. In members of the order Strongylida a copulatory bursa is used to grasp the female at the level of the vulva, the rigid spicules are then extruded and inserted into the vagina to keep it open so that amoeboid sperm can be transferred for fertilization to occur.
The Nematodes
Infective stages
Click here to view a table showing examples of nematode infective stages. In the majority of nematodes of veterinary importance, the third larval stage (L3) is the infective stage for the definitive host. In some species this L3 develops as a completely free-living stage from a hatched L1 while in others the L1 does not hatch and develops to an L3 inside the protective egg shell. Therefore, the infective stage may be either a free-living L3 or an egg containing an L3 (Egg+L3). In nematodes where a larvated (embryonated) egg is is the infective stage, transmission to the definitive host is invariably via the oral route. However, where a hatched L3 is the infective stage, transmission to the definitive host may be via the oral route or by skin penetration and in some nematode species, such as the hookworms, either route is possible. Whichever nematode stage is infective for the definitive host, it is usually quiescent, does not grow and does not feed because its mouth is sealed. In these respects, it is different from all other larval and adult stages. Infective larvae, whether they are entirely free living or inside an egg, are usually also environmentally resistant and are often enclosed in a sheath - the loose-fitting cuticle of the preceding stage. The infective stage is, in fact, the nematode stage that provides a link between a free living and a parasitic way of life. Even in nematodes where intermediate hosts play a critical role in the life cycle, the infective stage is still the link to the definitive host. In these cases the intermediate host serves as a "bridge" for the infective stage to link up with its definitive host. A good example of this concept is found in the nematode Dirofilaria immitis ( the heartworm of dogs), belonging to the family onchocercidae. Blood-sucking mosquitos serve as intermediate hosts: they ingest circulating first stage larvae, called microfilariae. These grow through two molts, in the mosquito intermediate host, to the infective third stage and are transferred back to a definitive host when the mosquito takes a blood meal. Although this is still an example of transmission via skin penetration it is the intermediate host that bridges the skin barrier of the definitive host rather than the L3 directly as is seen in the hookworms.
Diagnostic stages
Click here to view a table showing examples of nematode diagnostic stages. The diagnostic stage of nematodes is the stage which leaves the definitive host in order to continue its development and which can be detected by sampling appropriate tissues in a live, infected animal. In gut dwelling nematodes such as the Trichostrongylidae of grazing ruminants, the diagnostic stage is an egg and is found in the host's feces. In Dirofilaria immitis, the dog heartworm, the diagnostic stage is a microfilaria (L1), circulating in the peripheral blood, where it is available for ingestion by an intermediate host. Since the diagnostic stage is the life cycle stage leaving the definitive host, it is the stage that links the parasitic way of life with either the free-living phase of the life cycle or the phase of development that occurs in an intermediate host. The diagnostic stages of most nematodes are found in the feces of the definitive host since this is the easiest route of exit from the host. This is obviously true for nematodes found in the alimentary tract but is also true for nematodes found in the lungs and other organs remote from the gut. For example, the adults of Parelaphostrongylus tenuis , a nematode of white-tailed deer are found in the venous sinuses and the subdural space of the cranium. (A) Eggs laid by female are deposited into the venous circulation, carried to the heart (B) then lungs (C) where they lodge in the capillaries. First stage larvae (L1s) break out into the alveoli, migrate up the bronchial tree (D) to the pharynx where they are
coughed up, swallowed and pass out with host feces (E). In summary, the diagnostic stage is that stage of the life cycle that leaves the definitive host and thus links the parasitic phase in the definitive host with the preparasitic phase occurring either as free-living developing stages or as stages developing inside an intermediate host. The infective stage is that stage of the life cycle that enters the definitive host and thus provides the link between the preparasitic and parasitic phases of the life cycle.
Example
Infective stage
Route(s) of infection Oral Oral, Skin Oral
Intermediate host
Paratenic host
Family: Trichostrongylidae Family: Ancylostomatidae - the "hookworms" Families: Metastrongylidae Protostrongylidae - the "lungworms" The ascarids Fam: Ascaridae Ascaris Parascaris Toxocara
L3 L3
No No
No Yes, in some species No
L3
Yes
(Egg+L2) (Egg+L2) (Egg+L2) hatched L2 L3 (Egg+L3) L3
Oral Oral Oral Oral Oral Oral Skin
No No No No No No Yes
Yes No No Yes No No No
Family: Oxyuridae Family: Onchocercidae
PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Trichostrongyloidea
Trichostrongylidae - life cycles

Nematodes belonging to the family Trichostrongylidae have life cycles that are closely similar. Predilection sites include the abomasum, stomach or small intestine of ruminants, horses or swine depending on the species. Some examples are given in the following table.
Nematode Host Predilection site Abomasum
Ostertagia Cattle ostertagi Trichostrongylus Ruminants, Abomasum, axei horses, or stomach pigs Cooperia Sheep, Small curticei goats intestine
Pre-parasitic phase
The pre-parasitic phase of larval development is entirely free living. Eggs are passed in the feces of infected hosts. Contained embryos will develop into first stage larvae and hatch if temperature and humidity are optimal (22-26'C and 100% humidity). First (L1) and second (L2) larval stages feed on fecal and soil bacteria but the third stage(L3) cannot feed because it is enclosed by a protective, impermeable sheath (the retained L2 cuticle). These ensheathed L3's survive by utilizing nutrients stored by the actively feeding L1 and L2 stages. Development of all preparasitic stages - from eggs through to infective 3s is also controlled by temperature and humidity. Optimal development occurs at 100% humidity and between a temperature range of 22'-26'C. At higher temperatures, the rate of development may be faster but metabolic activity of L3s is also increased and food reserves may be used up more quickly leading to larval death unless larvae readily find and infect a host. At lower temperatures, development slows and metabolic activity is reduced. At temperatures less than 10'C larval development, movement and metabolism are minimal. At temperatures below freezing preparasitic stages are vulnerable and few will survive. Similarly with humidity: the optimal humidity for development is 100% and little development occurs below 80%. However, even when atmospheric humidity is low, larvae may survive and develop because the microclimate within their environment on pasture may be sufficiently humid to allow
survival and some development. Prolonged dry spells and seasonal dry periods open larvae to death by desiccation.
Parasitic phase
The trichostongylid infective stage is an L3 enclosed in its protective sheath and hosts are infected, by ingesting L3s, as they graze on pasture. Exsheathment is the next event in the parasitic phase of these life cycles. Exsheathment sites are species-specific and are always proximal to the predilection site of each particular trichostrongylid species. As examples, Ostertagia ostertagi, an abomasal nematode, exsheaths in the rumen, while Cooperia curticei, with its predilection site in the small intestine, exsheaths in the abomasum. Exsheathment is immediately followed by movement of parasitic L3's to the predilection site where growth and development to adults occurs (L3--> L4-->Adults). Following sexual reproduction, mature females lay eggs approximately 2-3 weeks after infection. The time from infection to egg-laying by adult females is specific for each nematode species and is called the prepatent period. The following table gives some prepatent periods for several members of this family.
Nematode Ostertagia species Haemonchus species Cooperia species Trichostrongylus species
Prepatent period 17-21 days 2-3 weeks 15-18 days 7-25 days
Hypobiosis or seasonal arrested development is an important feature of the life cycles of members of this family. It occurs where the prevailing seasonal temperature and humidity fall to levels that threaten their survival. Hypobiosis is therefore a mechanism to ensure survival whereby the nematode halts its development in a host when prevailing environmental conditions might jeopardize the survival of any progeny.
Trichostrongylus species - life cycles
Predilection sites are the abomasum/stomach (A) for T. axei or the small intestine (B) forT. colubriformis and T. vitrinus).
Preparasitic phase
The preparasitic phase is entirely free living. Eggs (C) laid by female worms pass to the external environment in host feces. These eggs are "strongyle-type", with thin, smooth shells and ellipsoidal in shape. Under warm, moist conditions, these eggs will develop to first stage larvae (L1), hatch within 48 hours and develop through L2 to the L3 infective stage in 7-14 days. Infective larvae of ruminant species tend to migrate onto vegetation, enclosed in a film of moisture, where they are available for ingestion by grazing animals.
Parasitic phase
The parasitic phase is non-migratory. In ruminant species, exsheathment of ingested L3's takes place in the rumen (D) forT. axei or the abomasum (A) forT. colubriformis and T. vitrinus. Further development to adults occurs in the mucosa of the abomasum (A) or small intestine (B), depending on the species. The prepatent period is 2-3 weeks in ruminants and 25 days in horses (T. axei).
The Nematodes
Haemonchus contortus - life cycle
The predilection site is the abomasum (A) of sheep and goats. Females are prolific layers of "strongyle-type" eggs (B) which pass to the external environment in host feces.
Preparasitic phase
The preparasitic phase consists of free living eggs and larvae and is similar to other species in the family Trichostrongylidae. Development of eggs to L1's, hatching and further development through L2's to infective ensheathed larvae (L3's) takes place on pasture and will occur in as little time as 5 days at an optimum temperature of 22'C and high humidity. At temperatures from 16-20'C, almost all Haemonchus eggs wil reach the ensheathed infective stage in 10-14 days.
Parasitic phase
(----)Following ingestion by grazing sheep, L3's exsheath in the rumen (C), pass to the abomasum, settle close to the abomasal glands where they molt twice and mature to adult females and males. the prepatent period is 2-3 weeks in sheep. The cattle species, H. placei, has a similar life cycle but its prepatent period is 4 weeks.
The Nematodes
Haemonchus contortus - Epidemiology
The following factors are important determinants that influence transmission of Haemonchus contortus in sheep. Warm climates: Optimal larval development takes place at relatively high temperatures (22C = 72F). High humidity is also important, so high rainfall will trigger rapid development to L3, leading to disease outbreaks. High egg output: This parasite has a high biotic potential. Females are prolific egg producers so that even moderate infections (1-2,000 worms) may result in counts of 2,000 epg (eggs per gram of feces) or ten million eggs per day passed by the animal in the feces! Large populations of L3's may appear quite suddenly especially when prevailing weather conditions are conducive to rapid development of free-living preparasitic stages. Arrested development: Survival of this parasite is also associated with its ability to undergo arrested development at the L4 stage. In tropical areas this occurs at the beginning of the dry season, and development resumes just prior to the onset of the rainy season. In warm temperate areas it begins at the onset of fall in mid to late September and early October. Development resumes at the end of winter and early spring (end of February to mid March). Field evidence also suggests that arrested development in H. contortus may have an immunological component. Self cure: Significant acquired immunity to H. contortus can be seen in sheep older than 6 months, but this immunity is not absolute, and sheep in endemic areas may remain susceptible throughout their lives. Periodic natural expulsion of adult haemonchus from sheep is known as "Self-cure" and in some cases appears to have an immunological basis - an immediate type hypersensitivity reaction provoked by antigens secreted by developing larvae. However, self-cure induced by a challenge infection is not always followed by protection since larvae in the challenge infection may develop to maturity.
Periparturient Rise (PPR): Ewes that are not treated with an anthelmintic effective against arrested larvae are susceptible to disease in the late spring after arrested larvae resume development. Untreated ewes will shed eggs onto pasture and these, in turn, will develop to L3's during the grazing season and be responsible for disease outbreaks in grazing sheep especially when pasture contamination is high.
Genetic resistance: there is some evidence that resistance to Haemonchus contortus may be controlled genetically, and may be related to breed differences as well as to hemoglobin differences within breeds. The accompanying graph shows Haemonchus egg counts in two groups of lambs grazing a contaminated pasture. Lambs homozygous for Hemoglobin type A showed negligible egg counts and worm counts. Lambs heterozygous for Hemoglobin type A and B showed much higher egg and worm counts indicating that heterozygous (AB) lambs were more susceptible to infection with H contortus than were homozygous lambs (AA). In tropical and subtropical areas, the severity of Haemonchosis in any specific area is determined by rainfall. In the rainy seasons, acute Haemonchosis may be common and results from ingestion of large numbers of infective larvae from heavily contaminated pastures. Hypobiois during the dry season allows Haemonchus to survive inside the host as arrested L4's and resumption of development begins at the end of the dry season just as the rainy season begins. However, in tropical areas where a prolonged dry season does not occur e.g. East Africa, hypobiois does not occur.
Haemonchosis in cattle
Haemonchus placei is the species infecting cattle.
Common in tropical, subtropical and warm temperate areas of the world. Clinical signs similar to sheep. Hypobiosis occurs in areas where a prolonged dry season occurs. Immune responses are good so that the disease is more common in animals <2 years old. Outbreaks of Haemonchosis in adult cattle are usually associated with poor nutrition or unusually heavy challenge infections, for example when range cattle congregate around watering holes.
Haemonchosis in goats
Haemonchus contortus is the species infecting goats.
Pathogenesis and epidemiology is similar to sheep. Goats on pasture are highly susceptible to infection. Clinical signs similar to sheep
Ostertagia ostertagi
Life Cycle
The predilection site is the abomasum (A) of cattle. The life cycle is direct - preparasitic larval development is entirely free living. No migration occurs inside the definitive host.
Preparasitic phase
"Strongyle-type" eggs (B ) are passed in host feces and development through to infective L3's takes place inside host feces, on pasture. Under optimal temperatures, prevailing during late spring and early summer in most temperate zones, development from eggs to L3's will take two weeks or less. larval development is favored by cool (55-75'F), moist conditions. In the presence of moisture, usually after a rainfall, infective L3's, in large numbers, will migrate away from the fecal pad, in which they have developed, onto pasture where they will be more available for ingestion by grazing hosts. These L3's accumulate in drops of water on blades of grass. Hot, dry weather will cause fecal deposits to crust over, although the interiors may still be moist enough to allow survival of free-living eggs and larval stages.
Parasitic phase
(-----) Infection is by ingestion of ensheathed L3's by grazing hosts. Exsheathment takes place in the rumen ( C ) and larvae pass on to the abomasum (A) where they burrow into the gastric glands, mainly in the pyloric and fundic regions. They undergo two molts then emerge from the gastric glands as immature adults (L5's) approximately 18 days (17-21) after infection. Maturation takes place on the mucosal surface and eggs are produced soon after. Therefore the prepatent period is approximately 21 days (3 weeks) when development proceeds normally. However, arrested development (hypobiosis) is an important feature of the Ostertagia life cycle. It occurs at the early fourth larval stage (EL4) within the gastric glands and may last for as long as 6 months. Clearly, when arrested development occurs the prepatent period will be prolonged.
Ostertagia
Pathogenesis
Ostertagia ostertagi is the commonest cause of parasitic gastritis in grazing cattle. Unlike infections with other nematodes such as the blood-sucking Haemonchus, the pathogenic effects of Ostertagia are not due to its feeding behavior but rather to the growth of developing larvae in gastric glands and the emergence of immature adults from these glands. Click here for a picture of a developing L4 larva 7-10 days after infection. Click here for a picture of a developing L4 larva 15 days after infection During its time in a gastric gland the nematode grows and develops from a tiny third stage larva (approximately 1mm long) to an immature adult (approximately 1cm long) which leaves the gastric gland and returns to the surface of the abomasal mucosa. This ten-fold growth, taking place within the small, confined gastric gland, initially causes erosion of the mature secreting cells lining the gland and these are replaced by immature cells. Continued growth of the nematode results in constant erosion and replacement of the gland epithelium. These changes are at their maximal severity as the immature adults struggle, twist and turn to leave their glands. Grossly each parasitised gland is swollen giving it a nodular appearance on postmortem inspection. These swollen glands impinge on neighboring glands causing a pressure necrosis of their epithelial lining cells. In a heavily parasitised abomasum the mucosa is a sea of nodules, some parasitised, some not. The effect has been described as akin to "morocco leather". Click here to see a closer view of the nodular appearance of a parasitised abomasum. In addition, the folds of the abomasum may be edematous and reddened and in some cases necrosis and sloughing of the mucosa will be seen. The normal histological architecture of a normal gastric gland is shown in this image Mature cells in a gastric gland epithelium have two features. 1. They secrete specific components important in protein digestion. Mature parietal cells secrete hydrochloric acid and chief (zymogen/peptic) cells secrete pepsinogen which is converted by hydrochloric acid to pepsin, the functional hydrolytic enzyme of the abomasum. 2. They form "tight junctions" with adjacent epithelial cells. Specifically these junctions are areas of fusion between the lipo-protein layers of the plasma membranes of adjacent cells. The proper term for a tight junction is zonula occludens (plural = zonula occludentes). The function of these tight junctions is to maintain the integrity of the epithelial sheet and prevent the passage of small protein molecules across the mucosa. The frame image is an electron micrograph of a tight junction. The white arrows point to the cell borders between which is the tight junction. This image clearly shows no leaking of material between these cells. Click here to show an electron micrograph image of a "leaky" tight junction. The white arrow points to electron dense material leaking between adjacent gland cells. Immature cells in parasitised gastric glands lack both these features - they are non-secretory and lack tight junctions. Thus the number of functional gastric glands will be reduced in an Ostertagia-infected abomasum and the amount of that reduction will be directly related to the severity of infections i.e. the number of infected glands. The lack of tight junctions means that the epithelium in a parasitised gland has lost its integrity and become permeable. These structural changes will produce three significant outcomes. 1. A reduction in the number of secreting parietal cells means that less hydrochloric acid will be produced and this will result in a rise in the pH of abomasal contents from 2 to7. This changed pH will prevent the conversion of pepsinogen to pepsin and allow multiplication of bacteria
because the bacteriostatic effect of an acid pH is lost. 2. A reduction in the number of secreting chief cells will result in a corresponding reduction in the amount of pepsinogen produced. Whatever pepsinogen is produced will not be converted to pepsin and the consequence of this is that protein digestion will cease. 3. The lack of tight junctions will allow the passage of small protein molecules across the epithelial sheet. Albumin will pass from mucosal capillaries into the abomasum and pepsinogen will pass from the abomasum into the blood stream. Such a mucosa is usually described as permeable and the effects are illustated in this drawing. The net clinical effect of all these changes is that large amounts of osmotically active substances bacteria, undigested proteins and plasma proteins (especially albumin) - congregate in the intestine and these will promote the passage of water into the gut producing a (watery) diarrhea. Clinically, ostertagiosis presents as two forms, Type I and Type II, even though the pathogenic mechanisms are the same in both. Type I disease occurs in young cattle grazing contaminated pastures for their first time. In these cases the pathological insults and clinical signs are always due to immature adults leaving gastric glands after developing from L3s ingested approximately 3 weeks before. Type II disease always results from arrested L4's resuming their development to immature adults and leaving the gastric glands approximately 7-10 days after development resumes, but weeks or months after being ingested as L3s. The pathophysiology of Ostertagia-induced clinical and subclinical disease will be described in more detail in a later chapter.
Nematodirus
Nematodirus is of special importance as a parasite of lambs in temperate regions. Its hosts are ruminants, and its predilection site is the small intestine. Nematodirus species are distributed worldwide, but more commonly in temperate zones.
Life Cycle
The preparasitic phase of Nematodirus is almost unique in the trichostrongyloids in that development to the L3 takes place within the egg shell. This development is generally very slow and in temperate climates takes at least two months. In N. battus, hatching requires a prolonged period of chill followed by a mean day/night temperature of more than 100C. This means that eggs deposited on pasture in summer will undergo development through to L3's but will not hatch until the following spring after the necessary conditioning by the cold temperatures of winter. The eggs of other species (e.g. N. spathiger, N helvetianus, N spathiger and N. fillicollis) develop and hatch like other Trichostrongylids, during spring and summer, when environmental conditions are warm and moist. In the United States, strains of N. battus do not appear to require cold conditioning for hatching and are therefore transmitted throughout the entire grazing season as opposed to the single yearly transmission cycle during spring in Northern England and Scotland. During hatching, L3's cast off the L1 cuticle, leaving it in the egg shell but they retain the L2 cuticle as a sheath which is lost after infection of the definitive host ( ) Following ingestion of L3's, exsheathment occurs in the abomasum and subsequent developing stages are found on the mucosal surface of the small intestine (A). The parasitic phase is non-migratory and the pre-patent period is 15 days.
Cooperia
Cooperia species usually play a secondary role in the pathogenesis of parasitic gastroenteritis of ruminants although they may be the most numerous trichostrongyle present.
Life Cycle
Cooperia has a direct life cycle and there is no migration in the definitive host. ( ) Following ingestion of infective L3s, the larvae reach the small intestine and develop into adults (A). The prepatent period varies from 15 to 18 days.
Life Cycle
The predilection sites for this nematode are the lungs (L) of cattle, more specifically the bronchi and traches. Females lay eggs that are already embryonated with fully developed first stage larvae (L1s) and these hatch almost immediately. ( ) Migration route of L1s from the bronchi to the external environment.
The location of adults in the bronchi means that hatched L1s must undergo an extensive migration through the respiratory and intestinal tracts, of the host, to reach the external environment. L1s migrate up the bronchial tree and trachea, are coughed up, swallowed and passed from infected hosts in feces (A). Therefore the diagnostic stage for Dictyocaulus is an L1 found in freshly passed feces.
Preparasitic phase
The preparasitic larval stages of Dictyocaulus do not feed: they rely on food stores already present in the L1 when it is laid by the female worm. As a result, the preparasitic larvae are not actively motile since they do not have to search for food and complete their development to infective L3s within the host's feces on pasture. This lack of motility has forced Dictyocaulus to develop a method of facilitating dispersal of L3s from host feces onto surrounding pastures where they are more readily ingested by grazing cattle hosts. They utilize Pilobolus ( P), a fungus that grows readily in cattle feces and can be seen approximately 7 days after feces are deposited on the ground. L3s migrate up the stalks and onto the sporangia of Pilobolus. When these sporangia explode, releasing their spores, they also disperse Dictyocaulus L3s into the surrounding environment. Larvae can be propelled at least ten feet beyond the fecal pad and perhaps more with the aid of any prevailing breezes.
Parasitic phase
( ) Migration route of L3s from the pharynx to the lungs (L).
Grazing cattle are infected by ingesting L3s on pasture. Ingested L3s are swallowed and migrate through the intestinal wall to the mesenteric lymph nodes (M) where they molt to L4s. From there they travel to the via the lympatic and venous sytems to the lungs and migrate throught capillary walls to the alveoli. Migration thus far takes approximately 7 days. L4s migrate up the bronchial tree to the bronchioles where the final molt occurs. Immature adults (L5s) continue to the bronchi where they mature and reproduce. The prepatent period is between 3 and 4 weeks.
Dictyocaulus in horses,donkeys and sheep

Dictyocaulus arnfieldi
This nematode is seen in the trachea and bronchi of horses and donkeys. It appears to be is a relatively benign infection in donkeys since it is rarely associated with clinically obvious disease. In horses, because the worm rarely reaches maturity, infections are usually not patent.
Life cycle - the life cycle is similar to D. viviparus except for the following:
The stage passed in feces is an egg containing an L1 which hatches soon after leaving the host. The prepatent period ranges from 2 to 4 months.Patent infections may be seen in donkeys of all ages but in horses are usually only seen in foals and yearlings.
Pathogenesis - The lung lesions seen in both horses and donkeys consists of raised
areas in the caudal lobes each of which contain lungworms inside a small bronchus and a mucopurulent exudate. The bronchial epithelium is usually hyperplastic, has an increased number of mucus cells and is infiltrated with lymphocytes.
Clinical signs - Infections in donkeys may produce mild clinical signs of harsh lung
sounds on auscultation and a slight increase in respiratory rate. In horses clinical signs are uncommon in foals and yearlings and in adult horses may be present as a persistent cough and increased respiratory rate.
Epidemiology - It is believed that horses acquire their infections from pastures

contaminated by donkeys with patent infections. Donkeys are usually infected first as foals and through re-exposure remain infected throughout their lives.
Diagnosis - First stage larvae are easily recovered from feces of infected donkeys.
These larvae are similar to the L1s of D. viviparus but are slightly larger and have a sharply pointed tail.
PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Stephanurus dentatus

Life Cycle
Preparasitic development from egg to L3 is typically strongyloid, though earthworms may intervene as transport hosts. There are three modes of infection: by ingestion of the free L3s (A), ingestion of earthworms carrying L3s (B), and skin penetration by L3s (C). ( ) Ingested larvae exsheath in the intestine (D), enter lymphatic vessels and pass to the mesenteric lymph nodes where the first molt occurs. Molting larvae can be found in the nodes anywhere from 1 to 9 days after infection. They continue on to the liver (E), where the final molt takes place. Following ingestion of infected earthworm transport hosts, L3s are released in the gut as the earthworm is digested. The released L3s migrate to the liver as described above. Click anywhere on the S. dentatus life cycle image to see the percutaneous migration route. ( ) Larvae infecting pigs via skin penetration probably molt to L4s in subcutaneous tissues and reach the liver via the lungs (H) and systemic circulation (I). Click anywhere on the life cycle to return to the first image. In the liver young adults wander in the parenchyma for three months or more before piercing the capsule and migrating through the peritoneal cavity to the perirenal region (F). There they become enclosed in a cyst by host reaction, and complete their development. The cyst communicates with the ureter either directly or, if it is more distant, by a fine connecting canal, allowing the worm eggs to be excreted in the urine via the bladder (J). Occasionally, abberrant migration occurs with worms ending up in the pancreas (G), muscle, and other organs of the host where they are trapped by encapsulation and never reach the perirenal area. The prepatent period ranges from 6 to 19 months and adult worms have a longevity of about two years . There are reports in the literature supporting a case for transmission of this nematode to piglets in utero.
PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Syngamus trachea

Syngamus trachea is a parasite of the upper respiratory tract of non-aquatic birds. It is commonly known as the "gapeworm" and may be responsible for respiratory distress and death in domestic fowl and game birds such as pheasants and partridges.
Life Cycle
Eggs are passed in the feces of infected birds. Unlike other strongyloids, S. trachea larva develops within the egg until it reaches the L3 stage. Infection may occur in one of three ways. 1. By ingestion of an egg containing an L3 (A). 2. By ingestion of the hatched L3 (B). 3. By ingestion of a transport host containing encapsulated L3s (C). ( ) Following ingestion, the L3s exsheath in the duodenum (D) of the final host, moult, and pair off. They penetrate the intestine and travel first to the liver and then to the lungs (E) via the bloodstreamd. Two parasitic moults take place in the lungs within 4-7 days after infection. Adult males and females pair off move up to the trachea and begin copulation in the bronchi and trachea (F). ( ) Eggs escape from the vulva under the bursa of the permanently attached male and are carried up the trachea in the excess mucus produced in response to infection. They are then swallowed and passed in the feces, completing the cycle. The prepatent period is approximately two weeks with a range of 12-17 days. Various reports have shown that adults may survive for 23-147 days in chickens, 48-224 days in turkeys and approximately 98 days in guinea fowl.
Life Cycle
The preparasitic phase of Oesophagostomum is typically strongyloid, and infection is by ingestion of L3s. ( ) The L3s exsheath in the small intestine then enter the mucosa of any part of the small or large intestines. In some species (Oe. columbianum, Oe. quadrispinulatum and Oe. radiatum) L3s become enclosed in obvious nodules in which they moult to L4s . These L4s then emerge on to the mucosal surface, migrate to the colon (A), and develop to the adult stage. The prepatent period is 32 to 45 days, depending on the species. On reinfection with most species, the larvae may remain arrested as L4s, in nodules, for up to one year.
Strongylus vulgaris
Life Cycle
The life cycles of all three large strongyles have similar preparasitic phases. Adults are found in the cecum and colon of infected horses and donkeys. Strongyle-type eggs are laid by mature females and pass to the outside in host feces. Hatching and larval development to infective L3s will occur within a temperature range of 8-38 C. Development from egg to the L3 will take about one week in mid summer in temperate climates. Infection is by ingestion of the ensheathed L3s. Click on the image of the gastrointestinal track (A) to get a close up diagram of larval migrations inside host. ( ) After ingestion, S. vulgaris L3s exsheath in the small intestine, penetrate the intestinal mucosa and moult to L4s by 7 days after infection(B). These L4s penetrate submucosal arteries and migrate along the endothelium to the cecal and colic arteries (by 14 days post infection) and then to the root of the cranial mesenteric artery and its main branches (C) which they reach by day 21 after infection. After a period of development of 3-4 months, the larvae have molted to immature adults (L5s) but retain the fourth-stage cuticle as an external sheath. They return to the intestinal wall via the lumen of arteries. Nodules are formed around the L5s mainly in the wall of the cecum and colon (D) Subsequent rupture of these nodules releases the young adult parasites into the lumen of the intestine where they mature in another 6 to 8 weeks. ( ) Adult male and females copulate and females lay eggs which reach the external environment in host feces. The prepatent period is 6 to 7 months. Click anywhere on the image to return to the S. vulgaris life cycle.
The Large Strongyles

Clinical signs - patent infections
It is generally accepted that mucosal feeding adults of all three Strongylus species can have significant effects on infected horses although there appear not to be any clinical signs that can be specifically attributed to them.
General clinical signs of pale mucous membranes, poor weight gains and even weight loss combined with dull, staring coats are seen in horses infected with large strongyles. However, these clinical signs are generally seen in most parasitic infections of the g.i. tract. The "wormy horse" (as shown in the image on the right), is generally a poor performer and poor looking, a description that is often described as "unthrifty". Horses like this are now relatively uncommon in the United States because of the wide use (some would say the overuse) of anthelmintics and the acceptance of parasite control programs by veterinarians and the horse-owning public.
These clinical signs are related to the feeding habits of adult worms which grasp a piece of mucosa with their large mouths and digest it, a process that produces considerable bleeding at the bite site and results in formation of an ulcer. Necropsies show that there are many more ulcers than adult large strongyles in the cecum and colon, a finding that suggests these worms feed, then move to a fresh site . It also implies that their primary source of food is mucosal tissues and that blood is ingested only as part of the mucosal meal. This means that the large strongyles are more accurately described as mucosal feeders than blood suckers. However, their method of feeding, which can reach deep into the muscularis with significant damage to blood vessels, can produce significant blood loss and result in a clinically apparent anemia. Radio-active isotope studies comparing infected with worm-free foals have shown significant protein and red cell losses into the g.i. tracts of infected animals. These findings are not surprising but give a pathophysiological foundation for the clinical picture we see in patent infections with large strongyles. Click here to see a picture of a feeding Strongylus edentatus adult but remember to use the "back" button of your browser to return to this page.
Clinical signs - prepatent disease
PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Cyathostomes
(Small strongyles)
Life cycles
Cyathostome species have similar life cycles. The cecum and colon of horses are the predilection sites for all species and all life cycles are direct. Pre-parasitic phase "Strongyle-type" eggs are laid by female worms and are passed in the feces of infected horses (---> A). A first stage larvae (L1) develops inside each egg, then hatches. This L1 develops and molts into a second stage larva (L2) which, in turn, develops and molts into a third stage larva (L3) but retains the L2 cuticle as a protective sheath. Ensheathed L3's are the infective stages for the definitive hosts (equines) of these nematodes and they are non-feeding stages surviving on food granules accumulated by the feeding first and second stage larvae. Temperature and moisture control both development and survival of these free living stages, with optimal development taking place at approximately 25'C and 80% humidity. Under optimal conditions development of eggs through to infective third stage larvae may take as little time as 2 or 3 days. L3s actively migrate from their host feces (in which they have developed) onto the surrounding pasture thereby increasing the chances of being ingested by grazing horses.
Parasitic phase
(--->) Horses are infected by ingesting sheathed L3's while grazing(B). These pass through the stomach (C ) and exsheath in the small intestine (D ). Parasitic third stage larvae pass on to the cecum and colon(E) where they pass into the crypts of Lieberkuhn and penetrate the mucosa and, in some species, the submucosa. Here, larvae become encysted by host fibroblasts and molt to L4's. The majority (98%) of encysted larvae are found in the walls of the cecum and ventral colon. L4's emerge from their tissue cysts and resume development in the lumen of the large intestine with the majority(about 95%) of mature adult cyathostomes being found in the lumen of the ventral and dorsal colon. The prepatent period (depending on the species) is from 6-14 weeks but may be greatly prolonged when emergence of larvae from the mucosa is delayed due to arrested development(hypobiosis) at the early third stage(EL3).
Toxocara canis
Life Cycle
Toxocara canis has a complex ascarid life cycle. Like most other nematodes, T. canis is not immediately infectious when it leaves the definitive host. It must grow and develop into the infective stage, ensheathed L2, in order for it to infect the definitive host. Dogs may become infected by four routes: 1. 2. 3. 4. Direct transmission, by ingesting infective eggs. Paratenic host transmission, by ingesting infected mice. Transmammary transmission in which nursing pups ingest L3s in their mother's milk. Prenatal transmission where pups are born infected as a result of L2s migrating from tissue reservoirs in the pregnant bitch - across the placenta and through the umbilical vein to the fetal liver, where they remain until birth. They then resume migration to the lungs of the newborn pups.
The life cycle patterns of T. canis in puppies and in dogs over six months of age are different. Nursing pups are mainly infected by prenatal transmission of larvae from their mothers (A). Larvae reach the small intestine after migrating from the lungs of newborns and move up the bronchial tree and trachea to the pharynx, where they are swallowed and develop to maturity in the small intestine. If pups are infected by direct ingestion of infective eggs (B ), hatched larvae will also follow a tracheal migration. The third, and least common method of transmission in nursing pups - transmammary transmission of L3s (C ) - does not involve tracheal migration. Instead, ingested larvae develop directly to adults in the small intestine. In dogs over six months old, infections occur either by direct ingestion of infective eggs (D ) or by ingesting infected mouse paratenic hosts (E). In the case of paratenic host transmission, no further migration takes place in dogs since the requirement for lifecycle migration is satisfied in the mouse hosts. In direct transmission, only a small proportion of larvae undergo tracheal migration, while the majority continue migrating through the lungs and the pulmonary veins to the heart, where they are distributed to somatic tissues via the peripheral circulation. This somatic migration sets up the conditions for prenatal and transmammary transmission to pups since latent somatic larvae are reactivated during each pregnancy and migrate either across the placenta to the fetal liver after the 42nd day of gestation or to the mammary gland.
Toxocara cati
Life Cycle
The lifecycle of T. cati, while complex, is different from that of T. canis in five important ways: 1. Paratenic hosts, such as mice, play a more significant role in the lifecycle of T. cati because of the more aggressive predatory nature of cats. 2. Prenatal infection does not occur in the lifecycle of T. cati. 3. A high percentage of larvae (hatching from ingested infective eggs) undefgo tracheal migration, even in older, mature cats. 4. Transmammary transmission is the major route of infection for T cati in kittens. Tissue larvae and larvae acquired during pregnancy will migrate to the mammary glands of lactating queens and be available for nursing kittens throughout the entire lactiation. 5. A wide range of other animals, in addition to mice, may also serve as paratenic hosts. These include chickens, earthorms, and cockroaches.
Toxascaris leonina
Life Cycle
Toxascaris leonina has the most straightforward lifecycle of the dog and cat ascarids. Dog and cat definitive hosts may become infected in two ways: 1. Ingestion of infective eggs containing second-stage larvae. 2. Ingestion of intermediate hosts containing encysted third-stage larvae. Since there is no somatic migration in dogs and cats, there are no prenatal or transmammary infections. Mice, and to a lesser extent, other rodents and chickens, may serve as paratenic hosts for T. leonina.
Ascaris suum
Introduction
A. suum is one of the commonest nematodes of pigs and is also the largest with female worms ranging from 25 to 40 cm in length and 5 mm in diameter. Males are smaller, ranging from 15 to 25 cm long and 3 mm in diameter. The image shows mature Ascaris suum from a pig at necropsy. The small intestine is opened to show the mass of adult worms present. The mouth opening is surrounded by three lips as shown in this scanning electron micrograph. There is one dorsal lip (A) and two ventro-lateral lips (B) The yellow arrows point to rows of tiny denticles on the inner surface of each lip.
The Nematodes
Ascaris suum- life cycle
The predilection site for Ascaris suum is the small intestine of swine.
Pre-parasitic phase
Eggs laid by female worms pass to the external environment in host feces (A). These eggs are oval and thick-shelled with a rough mammillated, sticky external coat and are laid in the one-celled stage. Development to the infective stage takes place inside the egg and consiss of one molt only. Therefore the infective stage for Ascaris suum is an egg containing a second stage (L2) larvae (C). Earthworms (D) and dung beetles may ingest ascarid eggs while feeding on soil and feces. When that happens eggs will hatch and L2s will migrate to tissues and encyst giving rise to the possibility that these invertebrates may serve as paratenic hosts for Ascaris suum.
Parasitic phase
Pigs are infected by ingesting (E) eggs or paratenic hosts containing second stage larvae. Following hatching in the small intestine (F), L2s burrow into the intestinal wall, enter the hepatic portal system and are carried to the liver (G) within 24 hours of infection. Here the first parasitic molt (L2 to L3) takes place. (If infected paratenic hosts (D) are ingested by pigs, L2s are released during digestion in the stomach and small intestine. Their migratory route and parasitic development are the same as infective larvae from eggs). Third stage larvae (L3s) continue their migration from the liver to the lungs via the venous system, right heart and pulmonary arteries, reaching the lungs (H) by 4 to 6 days after infection. They break out of the alveolar capillaries and migrate up the bronchial tree to the pharynx (I) where they are swallowed. The final two parasitic molts (L3 to L4 to immature adults) are completed in the small intestine (F) by 3-4 weeks after infection. Mature, gravid females begin to lay eggs approximately 6 to 8 weeks after infection.
Parascaris equorum
Introduction
Parascaris equorum is a large conspicuous worm. The females may be as large as 50 cm in length and 8 mm in diameter. Males are smaller, ranging from 15 to 28 cm long. The mouth opening is typically ascarid with three prominent lips. Each lip is divided into two parts, anterior(A) and posterior(B) by a groove(G) along the medial surface. Its predilection site is the small intestine of equines, including zebra. In heavy infections Parascaris may be responsible for gut impactions and ruptures leading to a fatal peritonitis. The black arrow points to a hole in the small intestine resulting from a rupture along the line of the mesenteric attachment caused by pressure from the mass of worms. Infections are found mainly in nursing and weaned foals less than a year old.
Parascaris equorum
Life cycle
The predilection site for adult worms is the small intestine of equines.
Preparasitic phase
The life cycle is direct. Eggs are passed in the feces of infected animals and at temperatures of 25'C to 35'C will be infective within 10 days. The infective stage is an egg containing a second stage larva (Egg+L2).
Parasitic phase
Infection and migration to the lungs Foals become infected by ingesting eggs containing L2s. These hatch in the gut and, L2s migrate through the wall of the small intestine (A) to the liver (B ) via the hepatic portal system. Most L2s reach the liver within 24 hours after infection. The molt from L2 to L3 appears to occur between the mucosa of the small intestine and the liver Within 7-14 days after infection, the majority of larvae have migrated on to the lungs (C ) via the heart and pulmonary arteries. Migration from lungs to the gut L3s break out of the alveolar capillaries into the alveoli and migrate up the bronchial tree to the trachea and pharynx. They are coughed up and swallowed. The final two parasitic molts (L3--> L4 --> immature adults) take place in the small intestine. The prepatent period ranges from 12-16 weeks.
Oxyuris equi
Life cycle
Preparasitic phase
Oxyuris equi has a direct life cycle and its predilection site is the large intestine (B). After fertilization, the gravid female migrates to the anus of the definitive host, emerges head first and lays her eggs in clumps (C) in a yellowish-grey gelatinous material on the perineal skin. After completing their egg laying, the females pass outof the anus and die. Development to the infective third stage larva takes place inside the egg and is quite rapid, taking only 3 to 5 days. Parasitic phase The infective stage of Oxyuris equi is an egg containing a third stage larva (Egg + L3) and the definitive host is infected by ingestion. Larvae (L3s) hatch in the small intestine (A), pass into the large intestine and enter the mucosal crypts of the cecum and colon. Here they molt to the fourth stage (L4) about 8 to 10 days after infection. The final molt to immature adults takes place between 45 and 60 days after infection and this is followed by a lengthy maturation phase of about 100 days until gravid females lay their eggs anywhere from 139 to 156 days after infection. The prepatent period is approximately 5 months.
PARASITES AND PARASITIC DISEASES OF DOMETIC ANIMALS
Siphonaptera(Fleas)
Life Cycles
The life cycles of all fleas are basically the same. They consist of six stages - egg, 3 larval stages, pupa and adult (male or female). The general cycle is illustrated here using the specific life cycle of Ctenocephalides, which contains the two species (C. canis and C. felis) of importance in dogs and cats. Adults are the only flea stages spending most of their time on a host. They leave the host occasionally and usually only when one host makes contact with another. All other flea stages - eggs, larvae and pupae - are found in the immediate environment of the host. In dogs and cats this would primarily include places in the home and kennel used for resting and sleeping. Therefore by far the greatest majority of fleas are found concentrated in the host's environment as eggs, larvae, pupae and newly emergent adults and only a small proportion of the total flea population is found on a host as feeding, reproducing adults plus newly laid eggs and hatched larvae that have not dropped off. Adult Ctenocephalides lay eggs on their hosts. These are approximateley 0.5mm long and white in color. At optimal conditions of temperature and humidity, first stage larvae will hatch about four days later. A mixture of eggs, L1s and adult flea feces drop off the host into the environment where most of the cycle develops. Larvae feed on feces from adult stages and this largely consists of dried host blood and tissue ingested by these feeding adults. Larval stages molt twice and will reach the third stage (L3) in two weeks when their environment is warm and moist. L3s which are about 5mm long now spin a cocoon and inside each pupal case transform (metamorphose) into an adult. Adults emerge from the pupa and seek a host to feed and reproduce. Females will lay eggs within 48 hours of feeding on their new host Under optimal conditions of a warm, moist environment the whole flea life cycle may be completed in three weeks. Temperature and moisture are the primary factors controlling the flea life cycle. Studies have shown that the Ctenocephalides life cycle stages will develop within a range of temperatures from 13'C to 32'C and a range of relative humidity from 50% to 92%. The life cycle will be completed in 2 to 3 weeks at the high ends of these ranges and may take as long as 3-4 months at the low ends. Temperatures greater than 35'C will kill developing larvae and pupae. Adult fleas may survive from 2 to 6 months in the absence of a host for feeding. However, when hosts are present, adult fleas will spend the majority of their time feeding and reproducing on their hosts. Adults fleas are fairly long-lived. Most will live up to one year and some can live as long as two years under natural conditions if they are unthreatened by chemical control products.
Heartworm Dirofilaria immitis

Dirofilaria immitis, the dog heartworm, is a nematode classified as a member of the superfamily Filarioidea and the family Onchocercidae. It is a large, whitish worm. The females are approximately 30cm long, while the males are 23cm long with a spirally coiled tail. Adults are primarily found in the right ventricle and pulmonary arteries of dogs. After reproduction, the females produce small, vermiform embryos called microfilariae. They can cross the capillary beds and so are found throughout the vascular circulation.
Return to view life cycle
The Life Cycle:

Circulating microfilariae are ingested by a female mosquito while taking a bloodmeal from an infected host (A). Over 60 species of mosquito are capable of functioning as intermediate hosts. These prelarval stages migrate to the Malpighian tubules of the mosquito vector where development, involving two molts after the microfilariae differentiate into first stage larvae, will continue to the third stage (L3) larva (B). These infective L3's migrate from the tubules to the lumen of the labial sheath in the vector's mouthparts. Development in the mosquito is temperature dependent, requiring approximately two weeks of temperature at or above 27C (80F). Below a threshold temperature of 14c (57F), development cannot occur, and the cycle will be halted. As a result, transmission is limited to warm months, and duration of the transmission season varies geographically. During a later bloodmeal on an appropriate host (C), the L3 will exit the labium, enter the bite wound, and penetrate local connective tissues. Molting to the L4 ensues within seven days of infection (D). L4 stages undertake extensive migration through the subcutis, which continues for some 60-90 days until the final molt to the immature adult (E). The juvenile worms migrate to the right heart within a few days of their final molt (F), presumably carried by the venous circulation. Final maturation and mating occur in the pulmonary arteries, and the adult worms live in the right heart and pulmonary arteries, where they may survive for up to seven years. Production of microfilariae by inseminated female worms begins approximately six and a half months (192 days) after infection. Microfilariae are then released into the circulation, for a mosquito to ingest during a subsequent blood meal.
Return to view life cycle
PARASITOLOGY 4001 Lab Practical 1 - 1995

Answer to Question 1
Question 1. A. A local dairy farmer has just acquired some livestock from Louisiana and is concerned that they may have liver flukes (the trematode Fasciola hepatica). What fecal examination method will give you the best chance of finding the eggs of this parasite? (3 pts.) Ethyl acetate sedimentation B. A 3-week-old puppy has watery diarrhea. Given its age and clinical signs you suspect a Giardia infection. What fecal examination method will give you the best chance of detecting this parasite? (3 pts.) Zinc Sulfate Flotation (Partial credit -- 2 points -- given for direct smear) C. A 4-year-old dog has a chronic cough and you have included the nematodes that live in the lungs on your list of possible causes. What fecal examination method(s) will give you enough information to rule out (or in) the presence of these "lungworms"? (3 pts.) Baermann (Filaroides) and float (Capillaria) BACK TO QUIZ
Lab Exam Answer to Question 2
Question 2. A.The fecal sample in the device at your place came from a 4-year-old male Rottweiler as part of his yearly check-up. Examine the sample and identify the eggs of the parasite (give Genus and species). (7 pts.)
Trichuris (5 pts.) vulpis (2 pts.) B. What other similar looking egg could appear in dog feces and how could You tell it apart from the egg you identified in part A? (3 pts.)
These eggs may be confused with the eggs of Capillaria spp. (1 pt). They may be distinguished because Trichuris spp. have a smooth, lemon-shaped egg with symmetrically placed plugs, while Capillaria spp. have a rough shell with parallel sides and asymmetric plugs. (2 pts.)
BACK TO QUIZ
Question 3. A. The sample of meat in the dish at your place is beef hamburger that is thought to have been contaminated with pork. Is it likely that the hamburger has pork in it (yes, no, can't tell)? (4 pts.)
yes (4 pts.) B. Explain your answer to part A. (3 pts.) Found Trichinella spp., which is highly unlikely to be in beef.(3 pts.) If answer = Can't tell, no Trichinella found, or Trichinella can be in beef, -1 point
BACK TO QUIZ
Question 4. A. A saturated salt flotation was done on a fecal sample from a 4 month old Puppy which has been brought to you for its first check-up. The results of this test are shown under the microscope at Station #4. Identify the parasite egg (give Genus and species). (7 pts.)
Toxocara (5 pts.) canis (2pts.)
B. What other similar looking egg may be found the feces of a dog and how could you tell it apart from the egg you identified in part A? (3 pts.)
A similar egg is Toxascaris leonina (1 pt.). T. canis has a rough shell, and the center mass takes up most of the egg, which is round. T. leonina, in contrast, has a smooth shell, is oval, and there is more space around the central mass (2pts.).
BACK TO QUIZ
Question 5. A. A 6-year-old male mixbreed dog was brought in to your practice with the complaint that it had chronic vomiting. The results of a saturated salt flotation fecal examination is shown under the microscope at Station #5. Identify the egg (give Genus and species). (6 pts.)
Spirocerca (4 pts.) lupi (2 pts.)
B. What pathologic changes may have been caused by this parasite and what other procedures would you do to determine if this dog had these pathologic conditions? (3 pts.) One would find a mass around the esophagus, and the body of nearby vertabrae would be increased in size (2 pts.). Radiology would be used to best detect these changes (1 pt.).
BACK TO QUIZ
Question 6. A. The egg seen under the microscope at Station #6 was recovered from the feces of a 1 month old foal which has diarrhea. Many of these eggs are present on the slide. Identify the parasite (give Genus and species). (6 pts.)
Strongyloides (4 pts.) westeri (2 pts.)
B. Why would you expect to see eggs of this parasite in a young foal rather than in a mature horse? (3 pts.) There is transmammary transmission of this parasite (3 pts.). (-2 if only immunity mentioned)
BACK TO QUIZ
Question 7. A. The egg seen under the microscope at Station #7 was recovered during a urine analysis of a pig. Identify the parasite (give Genus and species). (6 pts.)
Stephanurus (4 pts.) dentatus (2 pts.)
B. In what organ does the adult worm reside? (3 pts.) Kidney BACK TO QUIZ
Question 8. A. The worms seen under the microscope at Station #8 were recovered from the small intestine of a sheep which died of bacterial pneumonia. Identify the parasite (give Genus only). (6 pts.)
Cooperia spp.
B. Describe the egg you would expect to find in the feces. (3 pts.)
One would expect to see a strongyle -type egg -- clear shelled, oval egg with embryo in the 8 to 32 cell stage. BACK TO QUIZ
Question 9. A. A number of adult nematodes, each about 1.5 cm long, were recovered from the large intestine of a horse which died suddenly. The anterior end of the worm is shown on the kodachromes at Station #9. Identify the parasite (give Genus and species). (6 pts.)
Strongylus (3 pts.) vulgaris (3 pts.)
B. Where in the horse would the fourth-stage larvae (L4) of this worm be found? (3 pts.) Mesenteric artery BACK TO QUIZ
Question 10. A. The dish under the microscope at Station #10 contains a skin biopsy in saline. The biopsy was taken from the ventral midline of a horse with itching dermatitis in this area. Identify the parasite (give Genus only). (6 pts.)
Onchocerca
B. How is this parasite transmitted? (3 pts.)
By biting flies (3pts.), such as the black fly seen above (Simulium spp.)
BACK TO QUIZ
Aelurostrongylus abstrusus Homepage

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Common name: Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Filaroididae Genus : Aelurostrongylus Species: abstrusus
Bookmarks Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment
Adult Parasite:
The male measures 7.5 mm and the female 9.9 mm. Males have a short bursa and the vulva of the female opens near the posterior end.
Histological section of Aelurostrongylus in lung tissue, cross section of one parasite is shown highlighted. top of page
Hosts:
Definitive: Cats Intermediate: Snails and slugs Paratenic: mice, voles, birds, frogs, and lizards. top of page
Life Cycle:
Adult female worms lay their eggs in the alveoli of the cat's lung. The eggs hatch and the first stage larvae (L1) are carried up the trachea, swallowed and pass out with the feces. The L1 can live for about 2 weeks in the environment. If the L1 find a snail or slug they enter the "foot" where they grow to the infectious third-stage (L3). If a paratenic host eats the snail, the L3 migrate into the tissues of the new host and arrest. Cats are more likely to be infected by eating the paratenic hosts as snails and slugs are usually not part of their diet. The L3 will penetrate the gut wall and migrate through the peritoneal and thoracic cavities to the lung. The larvae will develop to the adult stage and egg laying will begin 5 to 6 weeks after the cat ingested the L3. top of page

Terminal bronchioles and alveolar ducts of the lung. top of page
Diagnostic Stage:
The first-stage larvae (L1) in the feces.
top of page

Baermann Technique A ZnSO4 flotation may recover L1 that can be identified. Eggs or L1 can be found in the sputum or in a tracheal wash top of page
Clinical Signs: Light infections may be asymptomatic. In moderate infections you may see coughing and anorexia. In heavy infections there may be a chronic cough, dyspnea and polypnea, diarrhea, and wasting.
top of page
Treatment:
Drug: Fenbendazole (for an extend period of time), Ivermectin (at a dose of 0.4 mg/kg, may have to be repeated). top of page
Alaria marcianae Homepage

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Common name: Alaria Kingdom: Animalia Phylum: Platyhelminths Class: Trematoda Order: Strigeatida Family: Diplostomatidae Genus: Alaria Species: marcianae
Adult Parasite:
The adult has a spoon-shaped forebody (containing the oral and ventral suckers) and a cylindrical hindbody.
Left: Alaria adult attached to the small intestine mucosa. Photo and illustration adapted from Bowman, D.D., Georgis' Parasitology for Veterinarians, sixth edition, 1995. Page 126 - 127. top of page
Hosts:
Definitive: Raccoons, Cats Intermediate: First: snails (Helisoma spp.) Second: tadpole (Rana pipiens) Paratenic: frogs, snakes, birds, mammals (other than raccoon or cat) top of page
Life Cycle:
Eggs leave the cat in the feces and hatch in fresh water. The miracidium enter snails of the genus Helisoma and develop to sporocysts, daughter sporocysts and finally to cercariae. The cercariae leave the snail and penetrate the skin of a leopard frog tadpole where they develop into mesocercariae. If a frog, snake, bird, or any mammal, other than the raccoon or cat, eats the infected tadpole, the mesocercaria invade the tissues of this paratenic host and remains as a mesocercaria. If a cat eats an infected tadpole or paratenic host the mesocercariae will penetrate into the body cavity
and migrate through the diaphragm to the lungs where some of them develop into metacercariae. The metacercaria is carried up the trachea and is swallowed. It develops into the adult worm in the small intestine. If a female cat which has mesocercariae in her tissues begins to lactate the larvae can enter the kittens through the milk. In the kittens the larvae will develop into adults. In the raccoon there is no development past the mesocercarial stage unless the female raccoon gives birth. In this case the offspring are infected transmammary and the larvae continue their development to the metacercaria and eventually to the adult stage. top of page

Small intestine. top of page
Diagnostic Stage:
Egg 98-134 X 62-68 m
Photo from Foreyt, W. J., Veterinary Parasitology Reference Manual, third edition, 1994. Page 27. top of page

Ethyl Acetate Concentration Eggs may sometimes float with ZnSO4 top of page
Clinical Signs: Adults cause little damage. However, the migrating mesocerariae may cause pulmonary hemorrhage, as well as damage to other organs they may migrate through. top of page
Treatment:
Drug: Praziquantel
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Ancylostoma braziliense Homepage

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Common name: Hookworm Kingdom: Animalia Phylum: Nematoda Class: Secernentea Order: Strongylida Superfamily: Ancylostomatoidea Genus : Ancylostoma Species: braziliense
Adult Parasite:
Males measure 7.5 to 8.5 mm. Females measure 9 to 10.5 mm. The buccal capsule has one pair of small medium teeth and one of larger outer teeth.
Hosts:
Definitive: dog (Canis Familiaris), Cat (Felis catus). Return to top of page
Life Cycle:
Anclystoma braziliense follows the same developmental pattern of human and canine hookworms. Separate strains occur in cats and dogs. Eggs are passed in feces. Larvae develop in soil to the L3 infective stage and then are ingested by the host or they enter the host through cutaneous contact and then the larvae migrate to the lungs, and then on to the intestinal tract of the host. In the intestinal tract, the larvae develop into adults. Eggs are then expelled in feces and the cycle continues. NOTE: The canine and feline strains of A. braziliense are unable to to penetrate the subdermal layers of the skin of man. When man is exposed to the infective larvae, the larvae tunnel through the skin creating a lesion that is at first inflamed and then elevated and vesicular, and finally dry and crusted. The larvae may tunnel through the skin for weeks but rarely reach the circulation, thus humans are a "dead end host" of A. braziliense.

Small intestine Return to top of page
Diagnostic Stage:
Eggs are found in fecal flotation. Eggs are 60 x 40 um. L1 larvae are occasionally found in older feces (over 24 hours old) and are diagnostic of infection.
Ancylostoma braziliense eggs (left), L1 larvae (middle), diagram of L1 larvae (right). Return to top of page
Common Diagnostic Test

Fecal float to recover eggs.
Clinical Signs: Puppies and kittens: Anemia, diarrhea, weight loss, weakness, poor growth, occasionally death. Adults: Usually asymptomatic but any of the above symptoms may be present. Return to top of page
Treatment:
Drug: Febantel, Febantel/Pyrantel embonate, Fenbendazole, Ivermectin, Mebendazole, Milbemycin oxime, Pyrantel Pamoate
Ancylostoma tubaeforme Homepage

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Common name: Cat Hookworm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Ancylostomatidae Genus: Ancylostoma Species: tubaeforme
Adult Parasite:
Males are 9.5 to 11 mm long and have a well developed bursa, females are 12 to 15 mm. The mouth has three pairs of ventral teeth.
Hosts:
Definitive: Cats. Return to top of page
Life Cycle:
The egg leaves the host in the feces and hatches in one or two days. The larvae grow and molt, reaching the infective third stage (L3) in under a week. The L3 are enclosed in the cuticle of the previous stage and thus are protected from the environment. Under good conditions they may survive for months. The L3 are ingested by the cat and they take up residence in the small intestine without undergoing a somatic migration. The adult worm feeds on blood. Return to top of page

Small Intestine Return to top of page
Diagnostic Stage:
Egg: 64 X 41 m Return to top of page

Fecal flotation Return to top of page
Clinical Signs: In heavy infections anemia will develop and may be fatal. Low to moderate levels of infection produce a mild enteritis. Return to top of page
Treatment:
Drug: Febantel, Fenbendazole, Ivermectin, Milbemycin oxime, Pyrantel Pamoate, Selamectin, Febantel/Pyrantel embonate
Eucoleus (Capillaria) aerophilia Homepage
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Common name: Lungworm of dogs and cats Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Trichuroidea Genus: Eucoleus (previously: Capillaria) Species: aerophilia
Bookamrk Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment
Adult Parasite:
The adult worms measure 25 mm (male) to 32 mm (female).
Illustration C. aerophilia. A - adult worm. B - vulva. C - posterior end of female . D, E, F - posterior end of male. G , H - eggs. From: Levine, 1998. Nematode parasites of domestic animals and man. Burgess Publishing Co., Minneapolis, MN. Return to top of page
Hosts:
Dogs, cats, foxes, coyotes, wolves (definitive). Earthworms (paratenic). Return to top of page
Life Cycle:
The host ingests an infective egg or an earthworm which contains an infective larva in its tissues. The infective larva leaves the egg or earthworm in the small intestine of the host and penetrates the intestinal wall. The larva is carried by the blood to the lungs where it develops to the adult stage in the mucosa of the trachea and bronchi. Eggs are laid into the lumen of these organs, coughed up, swallowed and eventually pass out with the feces. The prepatent period is about 6 weeks. The egg will reach the infective stage in 5 to 7 weeks. If an earthworm ingests an infective egg, the egg will hatch in the gut of the worm and the larva will migrate to the worm's tissues where it will
wait for a definitive host to eat the worm. Return to top of page
Site in host where adult parasite is found:

Mucosa of the trachea and bronchi Return to top of page
Diagnostic Stage:
Egg with bipolar plugs (asymmetrical) and a rough surface ("netted" in appearance). The egg measures 70 um X 35 um.

Fecal float Tracheal wash Return to top of page
Clinical Signs: Usually asymptomatic in dogs and cats, sometimes causing a slight cough. In heavily infected foxes may show rattling and wheezy breathing and some coughing. Return to top of page
Treatment
:
Ivermectin 0.2 mg/kg, SQ or PO, one dose, repeat if needed. Fenbendazole 50 mg/kg, PO, SID, for 7 to 10 days
Pearsonema (Capillaria) plica Homepage
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Common name: Bladder worm of dogs and cats. Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Trichuroidea Genus: Pearsonema (previously: Capillaria) Species: plica
Bookmarks Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment
Adult Parasite:
The adult worms measure 30 mm to 60 mm long.
Illustration C. aerophilia. A - adult worm. B - vulva. C - posterior end of female . D, E, F - posterior end of male. G , H - eggs. From: Levine, 1998. Nematode parasites of domestic animals and man. Burgess Publishing Co., Minneapolis, MN.
Hosts:
Dogs, cats, foxes, wolves and probably other canids (definitive). Earthworms (intermediate) . Return to top of page
Life Cycle:
The earthworm ingests an infective egg, which will hatch in the gut of the worm and the larva will migrate to the worm's tissues where it will wait for a definitive host to eat the worm. The first stage-larvae leaves the earthworm in the small intestine of the definitive host, molts, and invades the intestinal wall, where it will molt again in 7 days. The third stage-larva will make its way to the wall of the urinary bladder via the blood to the kidney and then migrate down the ureter. The prepatent
period is about 60 days. Eggs are laid into the lumen of the bladder, and pass out with the urine. Return to top of page

Mucus membrane of the urinary bladder Sometimes seen in the pelvis of the kidney or other areas of the urinary tract. Return to top of page
Diagnostic Stage:
Egg with bipolar plugs (asymmetrical) and a rough surface. The egg measures 65 um X 25 um.

Urine sedimentation. Return to top of page
Clinical Signs: Usually asymptomatic in dogs and cats Sometimes causing cystitis. Return to top of page
Treatment:
Treatment: Ivermectin 0.2 mg/kg, SQ or PO, one dose, repeat if needed. Fenbendazole 50 mg/kg, PO, SID, for 10 to 14 days. Return to top of page
Cryptosporidium parvum Homepage

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Common name: Cryptosporidium . Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiida Family: Cryptosporidiidae Genus: Cryptosporidium Species: parvum
Bookmarks Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment
Adult Parasite:
The schizonts live in the epithelial cells of the small intestine. Return to top of page
Hosts:
Definitive: Many mammals, including humans, cattle, dogs, cats. Return to top of page
Life Cycle:
Life Cycle: The oocyst is ingested by the host. It excysts in the small intestine and the sporozoites (4 per cyst) invade the microvillus border of intestinal epithelial cells. The parasite undergoes two types of schizogony and one round of gametogony. The type I schizont produces zoites that can produce either type I or type II schizonts, thus the parasite can undergo continuous asexual reproduction as type I schizonts. Type II schizonts produce zoites which develop into gametocytes. Sporulated (infective) oocysts leave the cells and most of them pass out with the feces. However, some of the oocysts will excyst in the intestine, invade cells and begin the life cycle over (autoinfection).
Lifecycle illustration adapted from: Georgi's' Parasitology for Veterinarians, 6th edition, D.D. Bowman, 1995. W.B. Saunders Co., Philadelphia, PA
Site in host where adult parasite is
found:
Cells of the small intestine. Return to top of page
Diagnostic Stage:
Oocyst 4 um to 8 um

Fecal flotation . It may be very difficult to identify the oocysts. Acid Fast Stain of a Direct Smear to identify oocysts. Return to top of page
Clinical Signs: Many times asymptomatic Profuse watery diarrhea. Return to top of page
Treatment:
None known. Treat symptoms. Supportive therapy to prevent
dehydration. Return to top of page
Cuterebra spp. Homepage

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Common name: Rodent Bot Fly Kingdom: Animalia Phylum: Arthropoda Class: Insecta Order: Diptera Family: Cuterebridae Genus: Cuterebra Species: buccata, americana, lepivora, emasculator, and others.
Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment
Adult Parasite:
The adult fly measures 20 mm or more in length.
Hosts:
Larvae are found in rabbits, mice, rats, squirrels, chipmunks, cats and dogs. Return to top of page
Life Cycle:
The adult female lays her eggs near the entrance of a rodent burrow. The eggs hatch and the first instar larvae wait for a host. When a host passes by they attach to the hair and move to the skin. Once on the skin they move to natural body openings such as the nares. Inside the nose they penetrate the mucosa and migrate to a subcutaneous position. The larva then cuts a hole in the skin in order to breath. The larva grows and molts until it has become a third instar and about 25 mm long, this takes 3 to 4 weeks. The larva will then emerge through its breathing hole and drop to the ground where it will pupate under the soil. The fly may over winter as a pupa. In the spring the fly will emerge from the pupal case. Adult flies do not feed and will live for about 2 weeks. Return to top of page
Site where adult parasite is found in
host:
Under the skin, in cats the larvae have also been found in the brain, and throat (trachea). Return to top of page
Diagnostic Stage:
Larva:
Histological section of Cutebra in cat brain (0.75 mm long) - click on image to highlight parasite. Return to top of page

Gross examination Return to top of page
Clinical Signs: Depends on where the larva is located: In the skin the larva causes few problems. In the trachea the larva may block the air supply In the brain will cause neurological symptoms consistent with the area of the brain in which it is located. Return to top of page
Treatment:
Surgical removal of the intact larva. Return to top of page
Cytauxzoon felis Homepage

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Common name: Cytauxzoon Kingdom: Animalia Phylum: Apicomplexa Class: Sporozoea Order: Piroplasmida Family: Theileriidae Genus: Cytauxzoon Species: felis
Adult Parasite:
The schizont is found in mononuclear phagocytes. Ring forms can be found in red blood cells.
Hosts:
Definitive: Bobcat, cats Vector: Dermacentor variabilis Return to top of page
Life Cycle:
The cat is infected via the bite of the tick Dermacentor variabilis. Schizonts are found in the reticuloendothelial cells in the liver, lung, spleen and lymph nodes. Piroplasms (ring forms) are found in the erythrocytes. A nymphal tick will pick up the parasite while feeding on an infected cat (bobcats show no clinical signs and thus may act as a reservoir host) and transmit it to another cat when it feeds again as an adult (thus acting as a transstadial vector).

In macrophages lining the blood vessels of the spleen, liver, lungs, in the bone marrow and lymph nodes. Piroplasms are found in the erythrocytes. Return to top of page
Diagnostic Stage:
Schizonts or piroplasms.
Image adapted from JAVMA, 1994, 205(#3):455-460. Fig 1 and 3. Right: Intraerythrocytic piroplasms (arrows) seen in cat blood smear, Left: Schizonts of C. felis seen in mononuclear cell from a bone marrow aspirate smear (arrow). Return to top of page

Cytological examination of blood smears, bone marrow or spleenic aspirates. Return to top of page
Clinical Signs: Lethargy, depression, dehydration, icteric, prolonged capillary re-fill time, anemia. Return to top of page
Treatment:
No known treatment. Supportive treatment may help temporarily. Rapidly fatal. Return to top of page
Diphyllobothrium latum Homepage

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Common name: Broad Fish Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Pseudophyllidea Family: Diphyllobothriidae Genus : Diphyllobothrium Species: latum
Bookmark. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment
Adult Parasite
The adult worms are up to 2 m in length and gravid proglottids have a tightly coiled uterus full of brown eggs.
Adult D. latum
Proglottid of D. latum Return to top of page
Hosts:
Mink, humans, dogs, cats, bears and other fish eating mammals(definitive). Copepod (first intermediate). Freshwater fish (2nd intermediate or paratenic). Return to top of page
Life Cycle:
The egg hatches in water releasing a ciliated, free-swimming coracidium. A copepod ingests the coracidium and it develops into a procercoid in the body cavity. When a fish ingests the infected copepod, the procercoid will migrate to the muscles or viscera and
develop to the pleurocercoid stage. If the second intermediate host is eaten by another fish the pleurocercoid will migrate to the muscles or viscera of the new (paratenic) host. When the host containing the pleurocercoid is ingested by a definitive host the worm attaches to the small intestine wall and begins to develop proglottids. The prepatent period is 3 to 4 weeks. Eggs are released from the gravid proglottids and pass out in the feces. Return to top of page

The small intestine Return to top of page
Diagnostic Stage:
Egg, or examination of the proglottid if they happen to pass in the feces. Eggs are 75 - 45 um.

Eggs can sometimes be seen on Fecal flotation, although they
don't always float. Eggs can be found in a fecal sedimentation. Return to top of page
Clinical Signs: Usually asymptomatic in the dog and cat. In humans may cause pernicious anemia due to vitamin B12 uptake by the worm. Return to top of page
Treatment:
Epsiprantel, Praziquantel
Dipylidium caninum Homepage

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Common name: Double-pore Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Dipylidiidae Genus : Dipylidium Species: caninum
Bookmark. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment
Adult Parasite
The adult worms measure up to 50 cm long.
Adult Dipylidium caninum (left), gravid proglottid (middle), scolex (right).
Schematic illustration of Dipylidium caninum Return to top of page
Hosts:
Dogs, cats, fox, humans (definitive). Fleas [Ctenocephalides felis], lice [Trichodectes canis] (intermediate). Return to top of page
Life Cycle:
The larval flea ingests the egg. The cysticercoid develops in the flea, reaching infectivity in the adult flea about 1 day after the flea has found a host. When the dog ingests an infected flea while grooming,
the cysticercoid is digested out, the protoscolex attaches to the small intestinal wall and the worms begin to form proglottids. Gravid proglottids, containing the eggs, detach from the end of the worm and pass out in the feces. The prepatent period is about 2 weeks. Return to top of page

The small intestine. Return to top of page
Diagnostic Stage:
Proglottid (seen on feces, the peri-anal area, or left behind where the pet was sitting) and/or egg packets. Eggs are 25 to 30 um in oblong packets of 20 or less eggs.
Egg packets expressed from a Dipylidium caninum proglottid.
Dipylidium caninum proglottids on cat feces. The proglottids are the cream colored objects on the surface of the sample. 4 proglottids are near the kitty-litter and 3 others are seen on the parts of the sample free of kitty-litter.

Examination of the proglottid. Egg packets can sometimes be seen on Fecal flotation - if a proglottid has broken and spilled its eggs into the feces. Return to top of page
Clinical Signs: Usually asymptomatic in the dog and cat. Return to top of page
Treatment:
Dirofilaria immitis Homepage

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Common name: Canine heartworm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Family: Filariidae Genus : Dirofilaria Species: immitis
Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment
Adult Parasite:
The adult worms measure 15 cm (male) to 30 cm (female). Adult worms: male and female (left), worms in situ (right) Return to top of page
Hosts:
Dogs, cats, ferrets, seals (definitive). Mosquitoes (intermediate) . Return to top of page
Life Cycle:
The mosquito ingests a microfilaria when feeding on an infected dog. The microfilaria develops into an infective larva in about 14 days. When the mosquito again feeds on a dog the infective third stage-larva is injected into the skin. The third stage-larva moults to the fourth stage within 48 hours. The fourth stage-larva migrates through the dog's tissues, eventually reaching the pulmonary artery where it matures to the adult stage.. The female worm lays micro-filariae into the blood. The pre-patent period is about 6 months. Return to top of page
Site in host where adult parasite is found :

The pulmonary arteries and sometimes the right atrium. Return to top of page
Diagnostic Stage:
The only stage of the parasite which can be recovered for diagnosis is the microfilaria (a free swimming embryo found in the blood). However, microfilaria will be missing from about 30% of infected dogs and most of the infected cats. Therefore serological techniques are usually used to make a diagnosis. In dogs and cats we can look for Antigen produced by mature female worms (over 6 months of age). In cats we can look for Antibody produced against heartworm larvae and adults which have been in the cat for more than 60 days (thus the antibody test tells us the cat was exposed, but not if there are adult worms present). In cats ultrasound of the heart and the base of the pulmonary arteries can show the presence of heartworm adults. Microfilariae are 270 to 325 um in length, and are 6.7 to 7.0 um wide. Microfilariae are found in blood smear using the Knott technique:
Micro-filariae are found in blood smear :
Microfilariae are found in blood smear using acid phosphatase stain:
Common Diagnostic Tests

Antigen Tests Antibody Test (cats) Blood smear Modified Knott Method . Filter test Ultrasound (cats) This is a real time movie of an ultrasound of an infected cat. Ultrasound (ferrets) This is a real time movie of an ultrasound of an infected ferret.
Clinical Signs: Asymptomatic in dogs with low worm burdens. With greater worm burdens exercise intolerance, hypertension, right heart failure may be seen. Sudden death may be the only clinical feature seen in some cases of feline heartworm. Return to top of page
Treatment:
Pharmacueticals or surgery to remove worms.
Adulticides Thiacetarsamide sodium Melarsomine dihydrochloride - Tradename: Immiticide
Prophylactics
Ivermectin - Trade names: Heartgard Plus, Heartgard 30, Iverhart

Plus, Advantage Duo, Tri-Heart Plus Chewable Tablets, Heartgard for Cats
Moxidectin - Trade names: ProHeart, ProHeart 6 Milbemycin oxime - Trade names: Interceptor, Sentinel
SELAMECTIN - Trade name: Revolution
DIETHYLCARBAMIZINE - Trade name: Filaribits Return to top of page
Also see the Dirofilaria immitis life cycle page
Echinococcus multilocularis Homepage

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Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus : Echinococcus Species: multilocularis
Adult Parasite:
The adult worms measure 1 to 5 mm long.
E. multilocularis adult
E. multilocularis adults from coyote Return to top of page
Hosts:
Foxes, dogs, cats, coyotes, wolves and other wild canids (definitive). Microtine rodents (voles, shrews, field mice, etc.) (intermediate). Return to top of page
Life Cycle:
The vole ingests an egg. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travels to the liver via the blood. The alveolar hydatid cyst develops in (in order of likelihood) the liver, lungs, brain or other organ. When the dog eats the vole and ingests the hydatid cyst, the protoscolices attach to the small intestinal wall and the worms begin to form proglottids. Gravid proglottids, containing the eggs, detach from the end of the worm and spill their eggs into the lumen of the intestine. The eggs pass out in
the feces. The prepatent period is less than 40 days. Return to top of page

Diagnostic Stage:
Eggs are found in fecal flotation

Fecal float to recover eggs . Eggs are 38 - 32 um. Return to top of page
Clinical Signs: Usually asymptomatic in the dog. Clinical signs in the intermediate host depend on where the hydatid
cyst is located and how old (large) it is. E. multilocularis produces a more serious condition than E. granulosus as the hydatid cyst becomes more irregular, filled with connective tissue and gelatinous masses, and grows like a malignant tumor with metastasis Return to top of page
Treatment:
Epsiprantel, Praziquantel, Fenbendazole

Eurytrema procyonis Homepage

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Common name: Pancreatic Fluke Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Plagiorchiida Family: Dicrocoeliidae Genus: Eurytrema Species: procyonis
Adult Parasite:
The adult measures 2.9 mm long by 1.2 mm wide.
The above image is adapted from Fig 1-10, pg 28, Soulsby, Helminths, arthropods, and Protozoa of Domesticated Animals, 7th ed., 1982, Lea & Fabiger, Philadelphia, PA. Return to top of page
Hosts:
Definitive: Cats, red and grey foxes, and raccoons. Intermediate: First: Snails (Mesodon thyroidus) Second: arthropod (grasshopper?) Return to top of page
Life Cycle:
Eggs are ingested by snails. The trematode develops in the hemocoel of the snail. Two generations of sporocysts are produced. The cercariae develop and remain in the daughter sporocysts. Masses of sporocysts, covered in mucus, are expelled form the snail's respiratory pore and deposited on vegetation. These masses are eaten by grasshoppers, or some other second intermediate host. When the metacercariae in the grasshopper are eaten by the definitive host, the worm excysts in the gut and migrates to the pancreatic duct where it matures to the adult stage. Eggs pass down the pancreatic duct, make their way to the intestine, and exit in the feces.

Pancreatic duct Return to top of page
Diagnostic Stage:
Egg in feces: 56 by 36 m . Adult worm surgically removed from bile duct. Return to top of page

Ethyl acetate sedimentation Return to top of page
Clinical Signs: Usually none, however, it has been noted that in some cats with hundreds of worms, the pancreatic duct becomes hardened and thickened and this may lead to pancreatic insufficiency. Return to top of page
Treatment:
Drug: Praziquantel Return to top of page
Giardia duodenalis Homepage
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Common name: Giardiasis (also known as G.lambia, G. intestinalis and G. doudenalis) Kingdom: Protista Phylum: Protozoa Class: Sarcomastigophora Order: Diplomonadida Family: Hexamitidae Genus: Giardia Species: duodenale
Adult Parasite:
Trophozoite: The feeding stage of this flagellate measures about 18 um long X 5 -10 um wide. It has 8 flagella and the ventral side is modified as a sucking disk.
Left Panel: Giardia trophozoite. Right Panel: Giardiatrophozoite (lower right).
Illustration of Giardia trophozoites and cysts. Return to top of page
Hosts:
Most mammals, including dogs, cats, cattle, sheep, pigs, horses and primates. Return to top of page
Life Cycle:
The cyst is ingested (usually in fecally contaminated water or food) and encysts in the small intestine. The trophozoite attaches to the mucosa of the small intestine, where it absorbs nutrients across its surface. The trophozoite divides by binary fission. The trophozoites will either continue to divide or they (some, but not all, of them)
encyst. The cysts will pass out of the host in the feces. The prepatent period can be variable, but it is usually given as 1 week. Return to top of page

Small intestine (usually the duodenum or jejunum). Return to top of page
Diagnostic Stage:
Cyst: Measures about 14 um X 8 um.
Giardia cysts Return to top of page

ZnSO4 centrifugational flotation ELISA for fecal antigen Note: Cyst shedding is inconsistent and several samples taken on different days may need to be examined.
Clinical Signs: In young animals: Soft stools, diarrhea (which may be chronic). The stools may have a large fat content due to malabsorption and appear mucoid. In adult animals: Usually asymptomatic Return to top of page
Treatment:
Drug: Fenbendazole Dose: Dog and Cat: 50 mg/kg PO SID, for 5 days. Drug: Metronidazole Dose: Dog and Cat: 30 mg/kg. SID, for 5 days , PO. Drug: Febantel Dose: Dog: 25 mg/kg (PO) (Drontal Plus) for 5 days. Return to top of page
Hammondia hammondiHomepage
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Common name: Kingdom: Animalia Phylum: Apicomplexa Class: Sporozoea Order: Eucoccidiida Family: Sarcocystidae Genus: Hammondia Species: hammondi
Adult Parasite:
Schizonts and gametocytes are intracellular in the intestine of the cat. The photo below is of Toxoplasma gondii, but the appearance of H. hammondi and Toxoplasma are so similar that differentiation of the
two can only be accomplished through study of the parasite lifecycle.
Photo from Dubey, J.P., An Atlas of Protozoan Parasites in Animal Tissues, 1988. Page 53. Return to top of page
Hosts:
Definitive: Cats Intermediate: Rodents Return to top of page
Life Cycle:
The unsporulated oocyst leaves the cat in the feces. It takes 3 days in the environment to develop to the infective, sporulated stage (which contains 8 zoites). When a rodent ingests the infective oocyst, the zoites invade intestinal cells and multiply as tachyzoites. In about 10 days some of the tachyzoites, after invading a skeletal muscle cell, become bradyzoites, a slowly multiplying cyst stage. The bradyzoite is infectious to the cat. When the cat eats a rodent with bradyzoites in its tissues, the zoites from the cyst invade the intestinal cells and develop to the schizont stage. The schizonts release more zoites which invade new cells and give rise to either more schizonts, or to gametocytes. The male gametocyte releases gametes which fuse with the female gametocytes and form oocysts. The oocysts rupture out of the cells and are voided with the feces. It is 5 or 6 days between the initial infection of the cat and the release of oocysts.

Small intestinal cells Return to top of page
Diagnostic Stage:
The oocyst: 11 X 12 m (easily confused with the oocyst of Toxoplasma gondii).
Coccidia of the cat. H. hammondi oocyst (#5) is highlighted. Drawing adapted from Soulsby, pg. 627. Helminths, Arthropods and Protozoa of Domesticated Animals, 7th Edition, EJL Soulsby, 1982, Lea & Febiger, Philadelphia. Return to top of page

Fecal flotation
Clinical Signs: None, Hammondia hammondi is not pathogenic to the immunocompetent cat. Return to top of page
Treatment:
None known. Try treating as for Toxoplasma: Clindamycin.
Drug: Clindamycin
Isospora felis Homepage

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Common name: Coccidia Kingdom: Animalia Phylum: Apicomplexa Class: Sporozoea Order: Eucoccidiida Family: Sarcocystidae Genus: Isospora Species: felis
Adult Parasite:
Schizonts and gametocytes are intracellular in the intestine of the cat.
Top photo from Dubey, J.P., An Atlas of Protozoan Parasites in Animal Tissues, 1988. Page 33. Return to top of page
Hosts:
Definitive: Cats Paratenic: Mice Return to top of page
Life Cycle:
The unsporulated oocyst leaves the cat in the feces. It takes 3 days in the environment to develop to the infective, sporulated stage (which contains 4 sporozoites in each of 2 sporocysts). The cat can become infected by ingesting a sporulated oocyst or a mouse which has ingested an infective oocyst. When a rodent ingests the infective oocyst, the sporozoites invade intestinal cells and encyst as bradyzoites. The bradyzoite is infectious to the cat. When the cat eats an infective oocyst or a rodent with bradyzoites in its tissues, the
zoites invade the intestinal cells and develop to the schizont stage. The schizonts release more zoites which invade new cells and give rise to the next generation of schizonts. There are 3 generations of schizonts. Zoites released from the last generation of schizonts invade cells and form gametocytes. The male gametocyte releases gametes which fuse with the female gametocytes and form oocysts. The oocysts rupture out of the cells and are voided with the feces. It is 7 or 8 days between the initial infection of the cat and the release of oocysts. During its first infection a cat will shed oocysts for 10 to 11 days. Return to top of page

Diagnostic Stage:
The oocyst: 42 X 28 m
Right: Isospora felis sporulated (infectious) oocyst, Left: unsporulated Return to top of page

Clinical Signs: Usually no signs. In young cats with a heavy infection and stress (due to numerous causes, especially infection with other intestinal pathogens) chronic diarrhea, sometimes with blood in the stool, is seen. Return to top of page
Treatment:
Drug: Sulfadimethoxine
Isospora rivolta Homepage

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Common name: Coccidia Kingdom: Animalia Phylum: Apicomplexa Class: Sporozoea Order: Eucoccidiida Family: Sarcocystidae Genus: Isospora Species: rivolta
Adult Parasite:
Schizonts and gametocytes are intracellular in the intestine of the cat.
Top photo from Dubey, J.P., An Atlas of Protozoan Parasites in Animal Tissues, 1988. Page 33. Return to top of page
Hosts:
Definitive: Cats Paratenic: Mice Return to top of page
Life Cycle:
The unsporulated oocyst leaves the cat in the feces. It takes 3 days in the environment to develop to the infective, sporulated stage (which contains 4 sporozoites in each of 2 sporocysts). The cat can become infected by ingesting a sporulated oocyst or a mouse which has ingested an infective oocyst. When a rodent ingests the infective oocyst, the sporozoites invade intestinal cells and encyst as bradyzoites. The bradyzoite is infectious to the cat. When the cat eats an infective oocyst or a rodent with bradyzoites in its tissues, the
zoites invade the intestinal cells and develop to the schizont stage. The schizonts release more zoites which invade new cells. Zoites released from the last generation of schizonts invade cells and form gametocytes. The male gametocyte releases gametes which fuse with the female gametocytes and form oocysts. The oocysts rupture out of the cells and are voided with the feces. It is 4 to 7 days between the initial infection of the cat and the release of oocysts. During its first infection a cat will shed oocysts for greater than 14 days. Return to top of page

Diagnostic Stage:
Oocyst: 25 X 20 m
This oocyst is sporulated (infectious). Return to top of page
Clinical Signs: Usually no signs. In young cats with a heavy infection and stress (due to numerous causes, especially infection with other intestinal pathogens) chronic diarrhea, sometimes with blood in the stool, is seen. Return to top of page
Treatment:
Mesocestoides corti Homepage

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Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Order: Mesocestoididea Family: Mesocestoididae Genus: Mesocestoides Species: corti
Adult Parasite:
The gravid proglottid of the adult contains a paruterine organ in which the eggs are stored.
From left to right: Schematic illustration and photomicrograph of Mesocestoides scolex, Mesocestoides adult segments.

Hosts:
Carnivores (including dogs), birds and humans (definitive). Free-living mites (first intermediate). Amphibians, reptiles, birds, and mammals (2nd intermediate) Return to top of page
Life Cycle:
The life cycle is not completely known. Probably an orbatid mite or a coprophillic insect ingests the egg. A cysticercoid develops in the arthropod. When the 2nd intermediate host (amphibians, reptiles, birds, and mammals) ingests an infected arthropod, the cysticercoid is digested out and develops to a tetrathyridium in the peritoneal cavity. This larval form will multiply asexually. When the second intermediate host is eaten by a dog or other carnivore the tetrathyridium is digested out, the protoscolex attaches to the small intestinal wall and the worms begin to form proglottids. Gravid proglottids, containing the eggs, detach from the end of the worm and pass out in the feces. The prepatent period is about 16 to 20 days. The adult worms may multiply asexually in the definitive host's intestine. Also, the tetrathyridium, upon entering the definitive host, may go to the peritoneal cavity and multiply asexually. Return to top of page

Diagnostic Stage:
Gross examination of the proglottid in feces.

Examination of the proglottid in feces. Return to top of page
Clinical Signs: Usually asymptomatic in the dog when infected with the adult. When infected with the tetrathyridium, peritonitis and ascites may develop. Return to top of page
Treatment:
For adult tapeworms:
For treatment of tetrathyridia in peritoneal cavity*:

Lavage the peritoneal cavity to remove fluid and tetrathyridia, then give:
Fenbendazole: 100 mg/kg, PO, q 12 h, for 1 or 2 months.

*(Crosbie, P.R., et al. 1998. J. Am. Vet. Med. Assoc. 213:1578-1583.)
Ollulanus tricuspis Homepage

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Common name: Stomach worm of cats Kingdom: Animalia Phylum: Nemathelmintes Class: Nematoda Order: Strongylida Family: Ollulanidae Genus: Ollulanus Species: tricuspis
Adult Parasite:
The male worm measures 0.7 to 0.8 mm long and has a well developed bursa. The female worm measures 0.8 to 1 mm long, the
vulva is in the posterior part of the body and the tail has 5 cusps.
Line drawing adapted from from Soulsby pg. 261. Helminths, Arthropods and Protozoa of Domesticated Animals, 7th Edition, EJL Soulsby, 1982, Lea & Febiger, Philadelphia. . Return to top of page
Hosts:
Definitive: Cats (wild and domestic), foxes, pigs, and dogs (rarely). Return to top of page
Life Cycle:
Adult worms live in the stomach and may burrow into the gastric mucosa. The eggs hatch while in the female and develop to the infectious third-stage larvae (L3), which is released into the lumen of the stomach. The L3 may continue its development to the L4 and adult stage in the same cat or it may be carried into the environment in parasite-induced vomitus. The L3s may live in the vomitus for up to 12 days. If the L3s in the vomitus are ingested by a suitable host they will develop to adults in the stomach. The prepatent period (the time from when the L3s enter the host till the next generation of L3s is born) is about 33 to 37 days. Larvae which pass into the intestine die and are digested.

Stomach Return to top of page
Diagnostic Stage:
The L3, L4 or adults in the vomitus.
Image from Fig 3 pg 23 M.A. Hasslinger, 1984. Ollulanus tricuspis, the stomach worm of the cat, Feline Practice 14 (5): 22 - 35. Return to top of page

Diagnosis can be made by finding larvae or adults after inducing the cat to vomit or after stomach irrigation (described in: M.A. Hasslinger, 1984. Ollulanus tricuspis, the stomach worm of the cat, Feline Practice 14 (5): 22 - 35). The larvae may be concentrated from the vomitus by use of the Baermann technique
Clinical Signs: Vomiting chronic gastritis Return to top of page
Treatment:
Drug: Fenbendazole Return to top of page
Paragonimus kellicotti Homepage || Root || Main ||
Common name: Lung fluke Kingdom: Animalia Phylum: Platyhelminthes Class: Tramatoda Order: Digenea Family: Troglotrematidae Genus: Paragonimus Species: kellicotti
Adult Parasite:
Adult fluke
Cross section of a pair of adult flukes Return to top of page
Hosts:
Mink, muskrat, dogs, cat, raccoons, fox and other carnivores (definitive). Snails [Melania, Ampullaria, and other genera] (first intermediate). Fresh-water crabs and crayfish (second intermediate). Return to top of page
Life Cycle:
The egg matures (2 to 3 weeks) and hatches in water. The
miracidium finds and penetrates a snail. Sporocysts, and then redia develop in the snail. Cercariae develop in the redia, and when mature emerge from the snail. The cercariae swim around until they find a crustacean which they penetrate and encyst in the heart, liver, or muscles as metacercaria. When the definitive host eats the crayfish the metacercaria excyst in the host's small intestine. The young fluke penetrates the gut wall and wanders in the peritoneal cavity for 1 to 14 days before penetrating the diaphragm and then the lungs. The adult flukes are normally found in pairs within cysts in the lung. The cyst has an opening to a bronchiole. Eggs are laid in the cyst and pass out to the bronchiole. They are passed up with the lung mucus and are swallowed. The eggs then pass out with the feces. The prepatent period is about 3 to 36 days. Return to top of page

The lungs Return to top of page
Diagnostic Stage:
Egg 90 X 50 m

Ethyl-acetate sedimentation. Tracheal wash. Return to top of page
Clinical Signs: Intermittent cough, lethargy, chronic bronchiolitis, chronic eosinophilic granulomatous pneumonia. Return to top of page
Treatment:
Praziquantel at a high dose, Fenbendazole for 10 to 14 days. Return to top of page
Parametorchis complexus Homepage

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Common name: Bile duct fluke of cats and dogs Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Opisthorchiida Family: Opisthorchiidae Genus: Parametorchis Species: complexus
Adult Parasite:
The adult measures 5 to 10 mm long by 1.5 to 2 mm wide.
Hosts:
Definitive: cats and dogs Intermediate: First: Snails, Second: Fish Return to top of page
Life Cycle:
Egg hatches in water. The miracidium invades a snail. Cercariae leave the snail and invade the skin of a fish. In the fish the parasite encysts as a metacercaria. When the infected fish is eaten by the cat the metacercaria excysts and the worm makes its way to the bile duct where it matures. Eggs in the bile make their way to the intestine and exit in the feces. Return to top of page

Bile duct Return to top of page
Diagnostic Stage:
Egg in feces: 24 by 12 um. Adult worm surgically removed from bile duct. Return to top of page

Ethyl acetate sedimentation Return to top of page
Clinical Signs: Range from none to obstruction of the bile duct and hepatic insufficiency. Return to top of page
Praziquantel, Fenbendazole
Treatment:
Platynosomum fastosum Homepage

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Common name: Bile duct fluke of cats and dogs Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Plagiorchiida Family: Dicrocoeliidae Genus: Platynosomum Species: fastosum
Adult Parasite:
The adult measures 4 to 8 mm long by 1.5 to 2.5 mm wide.
Photo adapted from Bowman, D.D., Georgis' Parasitology for Veterinarians, sixth edition, 1995. Return to top of page
Hosts:
Definitive: Cats Intermediate: First: Snails Sublima octona, Second: Lizards, toads, geckos, and skinks. Return to top of page
Life Cycle:
Eggs are ingested by snails. Cercariae encyst in lizards and other second intermediate hosts. The metacercaria is found in the bile ducts of the lizard. When the infected lizard is eaten by the cat the metacercaria excysts and the worm makes its way up the common bile duct to the bile ducts and gall bladder where it matures. Eggs in the bile make their way to the intestine and exit in the feces. Return to top of page
Site where adult parasite is found in
host:
Bile ducts and gall bladder Return to top of page
Diagnostic Stage:
Egg in feces: 34 to 50 by 20 to 35 um Adult worm surgically removed from bile duct. (cross-section shown below).

Ethyl acetate sedimentation Note: if the bile duct is occluded eggs will not be able to make their way into the feces. Return to top of page
Clinical Signs: Range from none to obstruction of the bile duct and hepatic insufficiency, and possibly death.
Treatment:
Drug: Praziquantel
Physaloptera Homepage
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Common name: Stomach worm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Family: Physalopteridae Genus: Physaloptera Species: rara
Adult Parasite:
Anterior end of worm Return to top of page
Hosts:
Dogs and cats - other species occur in wildlife (definitive). Coprophagous beetles (intermediate) - larval stages. Return to top of page
Life Cycle:
The egg, containing the infective first stage-larva, is passed in the feces and eaten by a beetle larva. The larva develops to the infective third stage larva. The dog eats the beetle and the worm develops to the adult stage in the stomach. Eggs are laid in the stomach and pass out with the feces. Return to top of page

Attached to the mucosa of the stomach.
Diagnostic Stage:
Thick walled egg with a larva inside it. The egg measures 55 um X 32 um.

These eggs do not usually float on a standard fecal flotation (they have a specific gravity > 1.2) Fecal sedimentation Direct fecal smear Return to top of page
Clinical Signs: Usually asymptomatic Sometimes causing chronic vomiting. Return to top of page
Treatment:
Mebendazole, Pyrantel pamoate, Fenbendazole and Ivermectin.
Sarcocystis cruzi Homepage || Root || Main ||

Common name: Sarcocystis Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiida Family: Sarcocystiidae Genus: Sarcocystis Species: cruzi
Adult Parasite:
The sarcocysts are found in the striated muscles of the intermediate host. Sexual stages are found
in the intestine of the definitive host.
Hosts:
Dogs, foxes, wolves, coyotes, and raccoons (definitive) Cattle (intermediate). Other species of Sarcocystis use horses, rodents, llamas and other mammals. Return to top of page
Life Cycle:
Prepatent period in dogs is 9 to 10 days.
Lifecycle illustration from : Georges' Parsitology for Veterinarians, 6th edition, D.D. Bowman, 1995. W.B. Saunders Co., Philadelphia, PA

Lamina propria of the small intestine. Return to top of page
Diagnostic Stage:
Sporocyst (16 X 11 um).

Biopsy to screen for cysts and adults Fecal flotation Return to top of page
Clinical Signs:
Asymptomatic (unless the dog is immunosuppressed). Return to top of page
Treatment:
None usually given. Drug: Clindamycin may be tried in the dog. Return to top of page
Spirometra mansonoides Homepage
Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Pseudophyllidea Family: Diphyllobothriidae Genus: Spriometra Species: mansonoides
Adult Parasite
The adult worms are pinkish in color and gravid proglottids have a tightly coiled uterus full of brown eggs.
Hosts:
Dogs, raccoons, cats, bobcat (definitive). Copepod (first intermediate). Amphibians, reptiles [esp. the water snake Natrix], birds, and mammals (2nd intermediate or paratenic). Return to top of page
Life Cycle:
The egg hatches in water releasing a ciliated, free-swimming coracidium. A copepod ingests the coracidium and it develops into a procercoid in the body cavity. When a vertebrate other than a fish ingests the infected copepod, the procercoid will migrate to the muscles or connective tissue and develop to the pleurocercoid stage. If the second intermediate host is eaten by another animal the pleurocercoid will migrate to the muscles or connective tissue of the new (paratenic) host. When the host containing the pleurocercoid is ingested by a definitive host the worm attaches to the small intestine wall and begins to develop proglottids. The prepatent period is 10 to 30 days. Eggs are released from the gravid proglottids and pass out in the feces. Return to top of page

Diagnostic Stage:
Egg (~ 57 X 39 m), or examination of the proglottid if they happen to pass in the feces.

Eggs can sometimes be seen on fecal flotation , although they don't always float. Eggs can be found in a fecal sedimentation. Return to top of page
Clinical Signs: Usually asymptomatic in the dog and cat. Return to top of page
Treatment:
Strongyloides stercoralis Homepage

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Common name: None. Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Rhabditida Family: Strongyloididae Genus: Strongyloides Species: stercoralis
Adult Parasite:
The adult worms measure 2 mm long.
Adult female Return to top of page
Hosts:
Dogs, humans, and other higher primates (definitive). Return to top of page
Life Cycle:
The first stage larva passes out with the feces. The larva has a choice of developmental directions: it can develop to the infective third stage-larva or it can develop to the free living adult. There are both male and female free-living adults, they mate, the female lays eggs which hatch releasing first stage-larvae. These larvae will all develop to an infective third stage-larva. The infective third-stage larva will penetrate the skin of the host, migrate through the tissues by a variety of routes and eventually end up in the small intestine where it will molt twice and become an adult parthenogenic female. The adult lays eggs in the crypts of the small intestine where they hatch, the first stage-larvae make their way to the lumen of the intestine and pass down the intestine. While in the lumen of the intestine the larva can make a developmental choice: it can remain as a first stage-larva and pass out with the feces, or it can molt twice and become an autoinfective third stage-larva while still in the
intestine. Generally autoinfective larvae develop only in young or immunosuppressed hosts. Autoinfective larvae will penetrate the intestinal wall (usually the wall of the large intestine). Many of these penetrating autoinfective larvae will get into a lymph vessel or vein and be carried to the lungs where they break out into the air spaces. From here they are carried up the trachea, swallowed and eventually reach the small intestine where they molt twice and mature to the adult stage. If the bitch has either infective or autoinfective third-stage larvae migrating through her body, they may end up in the mammary glands and be passed to the pups in the milk (transmammary transmission). Return to top of page

crypts of the small intestine Return to top of page
Diagnostic Stage:
First stage-larva in the feces
L1 larvae (left), L3 larvae (middle), and L1 larvae (right) of Strongyloides stercoralis

Baermann Technique. Sometimes the ZnSO4 flotation technique will bring up a larva in good enough shape that it can be identified. Return to top of page
Clinical Signs: Light infections are usually asymptomatic In heavier infections you may see diarrhea. In cases with massive autoinfection, the host may have trouble breathing as a verminous pneumonia develops. Return to top of page
Treatment: Ivermectin 2 doses a week apart. Fenbendazole, SID,

for 14 days. Return to top of page
Taenia taeniaeformis Homepage

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Common name: Cat Tapeworm Kingdom: Animalia Phylum: Platyhelminthes Class: Cestoda Order: Taeniidea Family: Taeniidae Genus: Taenia Species: taeniaeformis
Adult Parasite:
Measures up to 60 cm long, lacks a neck and has a large scolex with 2 rows of hooks on the rostellum.
Hosts:
Definitive: Cats. Intermediate: Rodents Return to top of page
Life Cycle:
Eggs are ingested by a rodent and hatch in its gut. The hexacanth larva makes its way through the gut wall to the liver where it matures to the infectious strobilocercus stage. This portion of the life cycle takes about 60 days. When the cat eats the infected rodent the larval tapeworm attaches to the cat's gut wall by its protoscolex. The rest of the larva is digested away and the tapeworm begins to grow. The pre-patent period is between 36 and 42 days. Return to top of page

Small intestine.
Diagnostic Stage:
Proglottid with taenia-type eggs (31 to 36 um).

Gross visualization of the proglottid on the feces or attached to the perianal region. Crushing the proglottid between two slides releases the taenia-type eggs. Return to top of page
Clinical Signs: Usually none. Return to top of page
Treatment:
Toxascaris leonina Homepage

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Common name: Roundworm (Ascarid) Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascarididae Genus : Toxascaris Species: leonina
Adult Parasite:
The adult worms measure between 7 cm (males) and 10 cm (females) long.
Anterior end of adult Return to top of page
Hosts:
Dogs, cats and other canids and felids (definitive). Rodents (paratenic). Return to top of page
Life Cycle:
Life cycle illustration from : Georges' Parsitology for Veterinarians, 6th edition, D.D. Bowman, 1995. W.B. Saunders Co., Philadelphia, PA
Larvae may be a cause of visceral larval migrans (VLM) in humans.

The prepatent period is between 48 and 72 days with most of the dogs becoming patent between 56 and 65 days.
Pre patent period from: J.C. Parsons. 1987. Ascarid infections of cats and dogs. The Veterinary Clinics of North America. 17(6):1307-1340. WB Saunders Co. Philadelphia.

Lumen of the small intestine. Return to top of page
Diagnostic Stage:
Eggs are found in fecal flotation. The egg measures 80 um X 67 um. Eggs are colorless, mostly smooth and they possess a prominent vitelline membrane.

Fecal float to recover eggs. Return to top of page
Clinical Signs: Adults in the small intestine: Asymptomatic in light infections. In heavy infections the dog may appear unthrifty, may be pot-bellied, and have diarrhea. Return to top of page
Treatment:
Febantel, Febantel/Pyrantel embonate, Fenbendazole, Ivermectin, Milbemycin oxime, Piperazine, Pyrantel Pamoate
Toxocara cati Homepage

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Common name: Ascarid (Roundworm) of Cats Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascaridoidea Genus: Toxocara Species: cati
Adult Parasite:
Males measure 3 to 6 cm and females 4 to 10 cm. There are large cervical alae which end abruptly, giving the anterior end an
arrow-head shape.
Hosts:
Definitive: Cats and wild felines. Paratenic: Rodents and other mammals, earthworms, birds. Return to top of page
Life Cycle:
The egg is passed in feces and develops in the environment to the infectious stage. The infectious egg contains a second-stage larva. The cat can be infected in 3 ways. First, if a cat ingests an infective egg, the egg hatches in the stomach, the larvae migrate through the gut wall, pass through the liver to the lungs. In the lungs the larvae breakout into the air spaces, are carried up the trachea and are swallowed. They develop through the 3rd and 4th stages to the adults, which live in the small intestinal lumen. The prepatent period
for this route of transmission is 56 days, although the adult worms are present in the small intestine by day 28. The second route of infection is via a paratenic host. If a mouse eats an infective egg the larva hatches and migrates to the tissues (liver) where it arrests. When the cat eats the mouse the larvae are freed and develop in the gut to adults. There is no extra-intestinal migration in this case. The final route of infection is transmammary. The second stage larvae acquired in the milk by the nursing kitten develop in the intestine to adults. Like the case with a paratenic host, no extra-intestinal migration takes place after transmammary transmission. The prepatent period is about 3 weeks when the transmammary or paratenic host routes are utilized.
Pre patent periods from: J.C. Parsons. 1987. Ascarid infections of cats and dogs. The Veterinary Clinics of North America. 17(6):1307-1340. WB Saunders Co. Philadelphia.

Diagnostic Stage:
Egg: 65 to 75 m in diameter and it has a pitted shell. (Slides of egg in cross-section and surface pitting)

Fecal float Identification of the adult worm recovered from the feces or vomitus. Return to top of page
Clinical Signs: The kitten may appear unthrifty, pot-bellied, and have intermittent diarrhea. Return to top of page
Treatment:
Fenbendazole, Ivermectin,Milbemycin oxime, Piperazine, Pyrantel Pamoate, Pyrantel embonate
Toxoplasma gondii Homepage

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Common name: Toxoplasma Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiida Family: Sarcocystiidae Genus: Toxoplasma Species: gondii
Adult Parasite:
The schizonts are found in the small intestinal cells of cats.
Photo from Dubey, J.P., An Atlas of Protozoan Parasites in Animal Tissues, 1988. Page 53 Return to top of page
Hosts:
Cat and other felids (definitive) . Dogs, rodents, humans, many other mammals and birds (intermediate). Return to top of page
Life Cycle:
The cat is infected either by ingesting a sporulated oocyst or an infected intermediate host. In the cat the parasite can exist in a number of forms in a number of different tissues. In the cat's intestine the parasite will undergo schizogony and gametogony, resulting in the release of unsporulated oocysts which pass out in the feces. The oocysts will sporulate in about 2 days in the environment. When an intermediate host ingests a sporulated oocyst the parasite excysts in the small intestine, the tachyzoites invade cells and multiply. They then break out of these cells and invade new cells, until the immune response of the host kills them. The tachyzoites can be carried by the blood to any tissue of the body. Some of the tachyzoites will form bradyzoites (tissue cysts) which are slow growing and can evade the immune response. Tachyzoites and bradyzoites can also be found in the cat.
Illustration from: Georges' Parasitology for Veterinarians, 6th edition, D.D. Bowman, 1995. W.B. Saunders Co., Philadelphia, PA

Small intestinal cells. Return to top of page
Diagnostic Stage:
In cat: oocyst. In intermediate hosts: Tissue cysts.
Sporulated and unsporulated oocysts
Tachyzoites in peritoneal macrophage. Return to top of page

Cat: Fecal flotation or serology In all animals: Cyst in Necropsy specimen or Serology (if available) Return to top of page
Clinical Signs: In cats with an intestinal infection: usually asymptomatic. In animals with tissue infection: light infections are usually asymptomatic. Heavier infections, such as those seen in immunocompromised hosts will have symptoms that depend on the tissue infected. Infections of the CNS are most likely to show clinical signs. Toxoplasma gondii may cause abortion in sheep, goats and humans. Return to top of page
Treatment:
Drug: Clindamycin
Trichinella spiralis Homepage

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Common name: Trichina Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Genus: Trichinella Species: spiralis
Adult Parasite:
The adult worms measure 1.5 mm (male) to 3.5 mm (female) long
T. spiralis adults. Female (left) and male (right). Note: pictures are not comparable in size. The male is 1.5 mm long, and the female is 3 to 4 mm long.
T. spiralis in tissue
Tail of male Trichinella spiralis Return to top of page
Hosts:
Mammals, especially carnivores and omnivores (definitive). Mammals, especially carnivores and omnivores (intermediate) Return to top of page
Life Cycle:
The host ingests the first stage larvae which are encysted in the muscles of the intermediate host. The larvae develop to the adult stage in the small intestine of the host. The adult female will penetrate the mucosa of the intestine and lay live pre-larvae into lymph vessels. The pre-larvae are carried by the blood throughout the body. The pre-larva enters a muscle fiber and changes it into a "nurse cell". The pre-larva in the nurse cell develops to the infective first stage-larva in about 3 weeks. Thus, the definitive host is also the intermediate host. Return to top of page

Small intestine and mucosa of small intestine Return to top of page
Diagnostic Stage:
First stage-larva (arrows) in the nurse cell. Larval cysts can get up to 3 mm in diameter.

Muscle biopsy Antibody ELISA Return to top of page
Clinical Signs: Usually asymptomatic. Heavy infections have been reported to cause a hemorrhagic enteritis, muscle pain and stiffness. Return to top of page
Treatment:
Treatment against the adults in the gut: Ivermectin 0.2 mg/kg, SQ or PO, one dose, repeat if needed. Fenbendazole 50 mg/kg, PO, SID, for 7 to 10 days Treatment for the muscle phase may not be very effective, but the above drugs can be tried.
Trichuris vulpis Homepage

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Common name: The whipworm of dogs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Trichuridae Genus: Trichuris Species: vulpis
Adult Parasite:
Trichuris adults - male (coiled) and female (straight).
Hosts:
Dogs and foxes, cats (very rare) (definitive). Return to top of page
Life Cycle:
The egg containing an infective larva is ingested by the dog. The egg hatches in the small intestine, and the infective third stage-larva penetrates into the intestinal wall. The larva stays here for 2 to 10 days, then re-enters the lumen. It passes down to the cecum and large intestine where it matures to the adult stage. The adults burrow their narrow anterior ends into the mucosa, leaving the posterior ends in the lumen. Eggs are laid into the lumen and pass out with the feces. The eggs develop to the infectious stage in about 3 weeks. The prepatent period is about 90 days. Return to top of page

Embedded in the wall of the cecum and large intestine. Return to top of page
Diagnostic Stage:
Egg which measures 80 um long by 40 um wide (smooth= shell).

Clinical Signs: Light infections are asymptomatic. Bouts of diarrhea, often with large amounts of mucus and some frank blood on the stool, are seen in heavy infections.
Treatment:
Drug: Butamisole Hyrdochloride, Febantel, Febantel and Pyrantel embonate, Fenbendazole, Mebendazole, Milbemycin oxime
Nematode Eggs and Larvae Found in Feces
Click on the images to see full sized copies.
Toxocara cati egg (90 um X 75um).
Toxascaris leonina egg (80 um X 67 um).
Ancylostoma species egg (60 um X 40 um).
Capillaria aerophilia egg (70 um X 35 um).
Physolaoptera species eggs (40 um X 48 um).
Strongyloides stercoralis L1 (55 um X 32 um).
Trichuris vulpis egg (80 um X 40 um). Note: very very rare in cats in the United States but probably more common than the whipworms of tropical cats.
Nematode Larvae Found in Muscle
Trichinella spiralis L1 (cysts may reach up to 3 mm long).
Trichinella spiralis L1. Stained with H+E.
Nematode Eggs and Larvae Found in Tracheal or Nasal Washes
Aelurostrongylus abstrusus L1
Nematode Larvae Found in Blood
Click on the images to see full sized copies. Dirofilaria immitis (270 X 325 um by 6.7- 7.0 um).
Tapeworm Eggs and Proglottids
Taeniaand Echinococcus species egg (38 X 32 um).
Taeniaspecies proglottid.
Dipylidium caninum egg (25 X 30 um in oblong packets of 20 or less eggs).
Dipylidium caninum proglottid.
Diphyllobothrium latum egg (75 X 45 um).
Diphyllobothrium latum proglottid.
Mesocestoides proglottid. Spirometra mansonoides egg (60 um). Photo from Foreyt, W. J., Veterinary Parasitology Reference Manual, third edition, 1994. Page 51.
Trematode Eggs
Paragonimus kellicotti egg (90 X 50 um). Alaria marciannae egg (98-134 X 62-68 m). Photo from Foreyt, W. J., Veterinary Parasitology Reference Manual, third edition, 1994. Page 27.
Eurytrema Procyonis egg (56 X 36 m).
Parametorchis complexus
egg (24 X 12 um).
Protozoan Trophozoites and Cysts Found in Feces
Cryptosporidium parvum oocyst (4 X 8 um).
Giardia species cyst (14 X 8 um).
Isospora felis oocyst (sporulated). (30 X 38 um).
Isospora felis oocyst (unsporulated). (30 X 38
um).
Isospora rivolta oocyst (sporulated). (25 X 20 um).
Sarcocystis cruzi sporocysts (16 X 11 um).
Toxoplasma gondii oocysts (16 X 11 um).
Protozoans Found in Feline Blood
Click on the images to see full sized copies. Cytauxzoon felis schizonts and piroplasms. Image adapted from JAVMA, 1994, 205(#3):455-460. Fig 1 and 3. Right: Intraerythrocytic piroplasms (arrows) seen in cat blood smear, Left: Schizonts of C. felis seen in mononuclear cell from a bone marrow aspirate smear (arrow).
Protozoan Trophozoites and Cysts Found by Tissue Biopsy
Toxoplasma gondii - tachyzoites in peritoneal macrophage. (From peritoneal lavage).
Quiz Case #1
You chose: Toxocara cati
Correct!
It is an ascarid egg that is round, with a center-filling mass, and has a rough surface. How did this cat most likely acquire this parasite? A. Transmammary B. Transplacental C. Ingested an egg D. Ingested a rodent or a bird E. All of the Above are equally likely
Quiz Case #1
You chose: Toxascaris leonina
Wrong.
You are right in thinking that it is an ascarid egg, but the egg shown has a rough surface, not a smooth surface like Toxascaris leonina. Return to the previous page and try again Go to a review of Toxascaris leonina
Quiz Case #1
You chose: Paragonimus kellicotti
Wrong.
Paragonimus kellicotti is a trematode and it's egg has an operculum (cap). Return to the previous page and try again Go to a review of Paragonimus kellicotti
Quiz Case #1
You chose: Trichuris felis
Wrong.
Trichuris felis is a very rare parasite of cats and it has a football-shaped egg with a plug at either end, much like that of Trichuris vulpis. Return to the previous page and try again
Quiz Case #1
You chose: Physaloptera rara
Wrong.
Physaloptera rara , the stomach worm, is a spirurid and has a thick-walled egg which contains a larva when it passes in the feces. (Note: the bar at the top of this page depicts many Physaloptera eggs). Return to the previous page and try again
Quiz Case #2
You chose: Ancylostoma tubaeforme
Wrong.
A hookworm egg would be larger (about 62um long for A. tubaeforme) and have an early embryo at the 8 or 16 cell stage. This object has only one cell and is a different shape and size. Return to the previous page and try again Go to a review of Ancylostoma tubaeforme
Quiz Case #2
You chose: Ancylostoma braziliense
Wrong.
A hookworm egg would be larger (about 55um long for A. braziliense) and have an early embryo at the 8 or 16 cell stage. This object has only one cell and is a different shape and size. Return to the previous page and try again Go to a review of Ancylostoma braziliense
Quiz Case #2
You chose: Isospora felis.
Right!
You have the owner treat the cat for five days with sulfadimethoxine. A week later the owner calls and tells you that the cat has diarrhea, and this time there is blood in the stool. You request that a fecal exam be brought in. The fecal exam is repeated and many objects like the object shown below were found (it measures about 20 um long).
What is going on? A. Drug resistence, the coccidia is resistant to sulfadimethoxine. B. The owner did not comply with treatment instructions. C. The cat was re-infected with Isospora felis. D. The cat is infected with another coccidian E. The cat ingested a mouse and is just passing oocysts of that host's coccidia. Click here if you wish to go to a review of Isospora felis
Quiz Case #2
You chose: Isospora rivolta

Close, but you are wrong. The object shown is too large to be Isospora rivolta,and it is the wrong shape. Return to the previous page and try again Go to a review of Isospora rivolta
Quiz Case #2
You chose: Plant cell.
Wrong.
Although plant cells seen in the feces come in all shapes and sizes, they are rarely as regularly shaped as this object and usually have a clear lipid-like drop in the center. Return to the previous page and try again Go to a review of artifacts
Click here to highlight pathology Click here to return to quiz
Quiz Case #3
You chose: Capillaria aerophilia

Capillaria is a lung parasite and should be initially considered, however, Capillaria aerophilia would not produce the enlarged pulmonary artery seen in this radiograph. Return to the previous page and try again Go to a review of Capillaria aerophilia
Quiz Case #3
You chose: Aelurostrongylus abstrusus

Aelurostrongylus is a lung parasite and should be initially considered, however, Aelurostrongylus abstrusus would not produce the enlarged pulmonary artery seen in this radiograph. Return to the previous page and try again Go to a review of Aelurostrongylus abstrusus
Quiz Case #3
You chose: Filaroides osleri
Wrong.
Filaroides does not infect cats. Return to the previous page and try again Go to a review of Filaroides osleri
Quiz Case #3
You chose: Dirofilaria immitis
Right!
The presence of adult heartworms in the pulmonary arteries of the cat will cause an enlargement of the arteries. Breathing difficulty and vomiting have both been associated with heartworm in cats. To confirm your tentative diagnosis, which of the following tests should you run? A. Knott Test (microfilaria test). B. Heartworm Antibody Test C. Heartworm Antigen Test D. Ultrasound E. All of the above Return to the previous page and try again
Quiz Case #3
You chose: Toxocara cati

You might consider it, but even though T. cati larvae may migrate through the lungs, the type of damage seen in the radiograph (enlarged pulmonary artery) is not consistent with the transient migration of ascarid larvae. Return to the previous page and try again Go to a review of Toxocara cati
Quiz Case #4
You chose: Trichuris
Wrong.
Trichuris eggs do have bipolar plugs, but the shape is not entirely consistent with the egg shown, and the surface is not smooth as seen in Trichuris spp. eggs. Return to the previous page and try again Go to a review of Trichuris vulpis
Quiz Case #4
You chose: Capillaria
Correct!
The bipolar plugs, parallel sides and rough surface identify this as a Capillaria spp. egg. The egg in the photo measures 54 X 20 um. Four of this type of egg were found upon a complete examination of the cover slip from the fecal float. Identify this egg to species: A. Capillaria aerophilia B. Capillaria bohemi C. Capillaria plica D. Capillaria hepatica E. Capillaria tomentosa
Quiz Case #4
You chose: Toxocara
Wrong.
You are way off track. Return to the previous page and try again Go to a review of Toxocara cati
Quiz Case #4
You chose: Physaloptera
Wrong.
Physaloptera eggs ususally do not float in a typical fecal flotation, and the ova shown does not have a larvae inside of it like a spirurid egg, and also, it just doesn't look anything like a Physaloptera egg. Return to the previous page and try again Go to a review of Physaloptera
Quiz Case #4
You chose: Dipylidium
Wrong.
A tapeworm egg would have 6 "hooks" inside of it. Return to the previous page and try again Go to a review of Dipylidium caninum
Quiz Case #5
You chose: Cestoda
Wrong!
The cestodes do not have a mouth and gut as can be seen in figure B Return to the previous page and try again
Quiz Case #5
You chose: Trematoda
Correct!
The predilection site of a parasite is a clue which can be used to idenify it. The liver biopsy slide (figure 2A) shows the adult trematode in its predilection site. Identify the predlection site.
2A
Click hereto magnify image. A. Liver parenchyma B. Vein C. Artery D. Bile duct
Quiz Case #5
You chose: Nematoda
Wrong!
You can see in figure 1A that there is no body cavity in this parasite. Return to the previous page and try again
Quiz Case #5
You chose: Insecta
Wrong!
Quiz Case #5
You chose: Pentastomida
Wrong!
Ancylostoma caninum Homepage
Common name: Canine Hookworm Kingdom: Animalia Phylum: Nematoda Class: Secernenttea Order: Strongylida Superfamily: Ancylostomatoidea Genus : Anclystoma Species: caninum
Click on the text below to jump down to the desired section of this page. Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment
Adult Parasite:
Adult worms in petri dish (left), and anterior of an adult worm (right). Return to top of page
Bursa of Male Return to top of page
Hosts:
Definitive: Dog (Canis familiaris) Paratenic: Rodents Return to top of page
Life Cycle:
Eggs are passed in feces. Larvae develop in soil to the infective L3 stage and then are either ingested by the host or they enter the host through cutaneous contact. The larvae migrate to the lungs, and then on to the intestinal tract of the host. In the small intestine, the larvae develop into adults. Eggs are then expelled with the feces and the cycle continues. Alternatively, larvae may migrate in the host to subcutaneous fat, and in females, to the skeletal muscles and mammary glands. Once in these tissues, the larvae become inactive. When infected females begin to nurse offspring, the larvae are activated and passed to the young who become infected. This "trans-mammary route "of infection is of primary importance as younger animals are more susceptible to infection. Older animals often develop resistance to repeated exposures of the parasite. Thus, it is much more likely that young animals will be infected with the parasite than the older animals. Finally, if a rodent ingests the L3 larvae, the larvae will migrate to the tissues and become dormant. If the rodent is eaten by a dog, the larvae will mature to adulthood in the small intestine. The pre-patent period is two weeks.
Site where adult parasite occurs:

Small intestine
Diagnostic Stage:
Eggs are found in fecal flotation. Eggs are 60 x 40 um. L1 larvae are occasionally found in feces and are diagnostic of infection.
Ancylostoma eggs (left), L1 larvae (middle), diagram of L1 larvae (right). Return to top of page

Clinical Signs: Puppies: Anemia, pale membranes, diarrhea, weight loss, weakness, poor growth, occasionally death. Adults: Usually asymptomatic but any of the above symptoms may be present.
Treatment:
Drug: Febantel, Febantel/Pyrantel embonate, Fenbendazole, Ivermectin, Mebendazole, Milbemycin oxime, Pyrantel Pamoate, Selamectin
Babesia canis Homepage
Common name: Babesiosis Kingdom: Protista Phylum: Apicomplexa Class: Piroplasmia Order: Babesiidae Family: Babesia Genus: canis
Adult Parasite:
Trophozoites can be round or pear shaped, 2-5 um long, and several may be seen in the same red blood cell.
Babesia canis trophozoites in red blood cells Return to top of page
Hosts:
Dog (Canis Familiaris) Return to top of page
Life Cycle:
Vector is the brown dog tick, Rhipicephalus sanguineus. Sporozoites of the parasite are carried in the alveoles of the ticks salivary gland. Upon biting the host, the sporozoites enter the dog and infect erthyrocytes. The parasite feeds on the cytoplasm of the erythrocyte and undergoes merozoite formation. Then, when another tick bites the host and obtains a blood meal, the parasite is taken up by the vector where it forms gametes and produces sporozoites.

erythrocytes (red blood cells) Return to top of page
Diagnostic Stage:
Babesia canis is most often seen in blood obtained from cutaneous capillaries than from systemic venous blood. The trophozoite in the red blood cell is the diagnostic stage (see pictures above). Return to top of page

Examination of Blood smear (wrights stain) Serology Return to top of page
Clinical Signs: Weakness Hemolytic anemia Depression Anorexia Pyrexia Weight loss Increased pulse and respiration rate Death Return to top of page
Treatment:
Imidocarb dipropionate - 6.6
mg/kg, 2 doses, 14 days
apart, IM
Clindamycin - Babesia spp. in dogs: 25 mg/kg (PO) divided BID until cured (extra label use). Supportive therapy should also be provided. Return to top of page
Babesia gibsoni Homepage
Common name: Babesiosis Kingdom: Protista Phylum: Apicomplexa Class: Piroplasmasida Order: Piroplasmorida Family: babesiidae Genus: Babesia Species: gibsoni
Adult Parasite:
Trophozoites can be round or pear shaped, 2-5 um long, and several may be seen in the same red blood cell.
Babesia trophozoites in red blood cells Return to top of page
Hosts:
Dog (Canis Familiaris) Return to top of page
Life Cycle:
Vector is the brown dog tick, Rhipicephalus sanguineus. Sporozoites of the parasite are carried in the alveoles of the ticks salivary gland. Upon biting the host, the sporozoites enter the dog and infect erythrocytes. The parasite feeds on the cytoplasm of the erythrocyte and undergoes merozoite formation. Then, when another tick bites the host and obtains a blood meal, the parasite is taken up by the vector where it forms gametes and produces sporozoites.

erythrocytes Return to top of page
Diagnostic Stage:
Babesia gibsoni is most often seen in blood obtained from cutaneous capillaries than from systemic venous blood. The trophozoite in the red blood cell is the diagnostic stage (see pictures above). Return to top of page

Examination of Blood smear (wrights stain) Serology Return to top of page
Clinical Signs: Weakness Hemolytic anemia Depression Anorexia Pyrexia Weight loss Increased pulse Respiration rate Death. Return to top of page
Treatment:
Drug: Clindamycin, Imidocarb dipropionate but relapses (incomplete cures) are common.
Balantidium coli Homepage
Common name: Balantidiasis Kingdom: Protista Phylum: Protozoa Class: Ciliata Order: Heterotrichida Family: Bursaridae Genus: Balantidium Species: coli
Adult Parasite:
The trophozoite is oval in shape and averages 75 x 50 um in size, but varies from 30 to 100 um in width, and 30 to 300 um in length. Return to top of page
Hosts:
Pig (Sus scrofa), Guinea pig, Dog (Canis familiaris) (rarely), Man (Homo sapiens), Monkey (various species). Return to top of page
Life Cycle:
Balantidium coli is widely epidemic among the pig population of the world. The adult resides in the large intestine and cecum. Cysts are expelled in feces and reinfect host via accidental ingestion. The parasite excysts in the host intestine. The parasite normally feeds upon fecal material, starch granules, and cell fragments. The ciliates often invade the mucosa and submucosa of the intestines and produce severe ulcers, that are often flask like in shape.
NOTE: Trichuris suis, whipworm infection, often occurs in conjunction with Balantidium coli infection in pigs. Return to top of page

Large intestine Return to top of page
Diagnostic Stage:
Adult ciliated organisms Cysts are sometimes found. Return to top of page

Clinical Signs:
Diarrhea Weight loss Nausea Vomiting Abdominal pain Dysentery Weakness Poor growth Bloody and mucusoid stools Return to top of page
Treatment:
Drug: Metronidazole
Dose: Dog and Cat: 30 mg/kg. SID, for 5 days , PO. Return to top of page
Baylisascaris procyonis Homepage
Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascarididae Genus : Baylisascaris Species: procyonis
Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment
Adult Parasite:
The adult worms measure between 7 and 13 cm long. Return to top of page
Hosts:
Raccoons and dogs (definitive). Many mammals (including dogs and humans) and birds (paratenic). Return to top of page
Life Cycle:
Life Cycle: The definitive host ingests an infective egg or a paratenic host which contains an infective larva in its tissues. The infective larva penetrates the intestinal wall. The larva is carried by the blood to the lungs where it breaks out into the air space, migrates up the trachea and is swallowed. The larva develops to the adult stage in the lumen of the small intestine. The pre patent period is about 5 weeks. Eggs are laid into the lumen of the intestine and pass out with the feces. The eggs take about 30 days to develop to the infectious stage. If paratenic host ingests an infective egg, the egg will hatch in the gut and the larva will migrate to various tissues, including the host's central nervous system, where they will wait for a definitive host to eat the paratenic host. The larva will grow during its migration in the paratenic host and by the time it reaches the brain it may be large enough (1.5 to 2 mm) to cause problems. Humans can be infected with the larval stage by ingesting infectious eggs. Return to top of page

Lumen of the small intestine. Return to top of page
Diagnostic Stage:
Egg looks like a Toxocara egg, but the Baylisascaris egg is smaller and the surface pitting is finer. Eggs measure 76 X 60 m (range: 63 - 88 X 50 - 70 m).
Left: egg at 40X magnification, Right: surface of egg

Clinical Signs: Adults in the small intestine: Asymptomatic in light infections, in heavy infections one might expect to see the same signs as in a dog infected with Toxocara. Larvae in the brain: Neurological signs. Return to top of page
Treatment:
No drug is labeled for the treatment of Baylisascaris procyonis but drugs
which are used to treat Toxocara infections should work against the adult stage of this ascarid. Some of these are:
Piperazine, Pyrantel Pamoate, Febantel, Fenbendazole, Ivermectin
Eucoleus (Capillaria) bohmi Homepage
Common name: Nasal worm of dogs and foxes. Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Trichuroidea Genus: Eucoleus (previously: Capillaria) Species: boehmi
Adult Parasite:
Illustration C. aerophilia. A - adult worm. B - vulva. C - posterior end of female . D, E, F - posterior end of male. G , H - eggs. From: Levine, 1998. Nematode parasites of domestic animals and man. Burgess Publishing Co., Minneapolis, MN.
Hosts:
Dogs, foxes, wolves and probably other canids (definitive). Earthworms (paratenic). Return to top of page
Life Cycle:
The life cycle of this parasite is not well known, probably it is similar to that of C. aerophilia. The definitive host ingests an infective egg or an earthworm which contains an infective larva in its tissues. The infective larva leaves the egg or earthworm in the small intestine of the host and penetrates the intestinal wall. The larva is carried by the blood to the lungs where it
develops to the adult stage in the mucosa of the nasal cavity, frontal and paranasal sinuses. Eggs are laid into the lumen of these organs, carried to the back of the throat with the mucus, swallowed and eventually pass out with the feces. If an earthworm ingests an infective egg, the egg will hatch in the gut of the worm and the larva will migrate to the worm's tissues where it will wait for a definitive host to eat the worm. Return to top of page
Site in host where adult parasite is found

Mucosa of the nasal cavity, frontal and paranasal sinuses. Return to top of page
Diagnostic Stage:
Egg with bipolar plugs (asymmetrical) and a rough surface ("pitted" in appearance). The egg measures 60 um X 30 um.

Fecal flotation
Nasal wash (if the dog has a nasal discharge) Return to top of page
Clinical Signs: Usually asymptomatic in dogs Sometimes causing sneezing and a mucopurulent (sometimes bloody) discharge. Return to top of page
Treatment:
Ivermectin 0.2 mg/kg, SQ or PO, one dose, repeat if needed. Fenbendazole 50 mg/kg, PO, SID, for 10 to 14 days Return to top of page
Crenosoma vulpis Homepage
Common name: Fox lungworm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Crenosomatidae Genus: Crenosoma Species: vulpis
Adult Parasite:
The adult worm measures less than 16 mm long. The cuticle of the anterior end of the this worm is thrown into crenated folds as seen in this photomicrograph of a portion of the worm recovered by a tracheal
wash.
Hosts:
Foxes, wolves, raccoons and dogs (definitive). Snails and slugs (intermediate). Return to top of page
Life Cycle:
The first stage-larva penetrates the intermediate host (a snail or slug). The larva molts twice and by 17 days post-infection becomes a third stage-larva. The third stage-larva remains in the snail's tissues until the snail is eaten by a definitive host. The third stage-larva makes its way to the lungs and develops to the adult stage in the bronchi and bronchioles. The female worm lays live first stage-larvae, which are carried up the trachea, are swallowed and pass out with the feces. The prepatent period is about 19 days. Return to top of page
found:
The bronchi and bronchioles Return to top of page
Diagnostic Stage:
First stage-larva in the feces
Photomicrographs of L1 from tracheal wash

Baermann Technique Tracheal wash Sometimes a ZnSO4 fecal flotationwill bring up a larva that can be identified. Return to top of page
Clinical Signs: Rhinotracheitis Bronchitis
Nasal discharge. Return to top of page
Treatment:
Ivermectin, Fenbendazole for 7 to 10 days, Febantel for 7 to 10 days Return to top of page
Dioctophyme renale Homepage
Common name: The Giant Kidney Worm of Carnivores Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Dioctophymidae Genus : Dioctophyme Species: renale
Adult Parasite:
The adult worms measure 35 cm (male) to 103 cm (female) and are blood red in color.
Hosts:
Mink, dogs, foxes, and other carnivores (definitive). Oligochaete annelids (intermediate) fish and frogs (paratenic) Return to top of page
Life Cycle:
The eggs pass out in the urine and develop in water to the infective stage (1 to 7 months). When the infective egg is swallowed by an oligochaete annelid it hatches and develops over a period of about 100 days to the third stage larva. If the worm is eaten by a frog or fish the third stage-larva will encyst in the predator (paratenic host) where they may live for years. Most paratenic hosts will have only a few larvae. When the worm or paratenic host is eaten by the definitive host the larva penetrates the stomach wall, the molt takes place here in about 5 days. The worms then penetrate into the peritoneal cavity where they develop for a while. Apparently the molt to the adult stage takes place in the body cavity and the adults enter the kidney. In mink the worms tend to enter the right kidney due to its position in relationship to the stomach. In the dog it is also the right kidney that is most likely infected, but adult worms free in the peritoneal cavity have been reported. Adult worm have also been found in the peritoneal cavity of seals (Phoca spp.). The parasite grows in the kidney destroying the parenchyma of this organ. Eggs are laid in the kidney and pass out with the urine. The prepatent period is about 135 days in the dog and 154 days in the mink and the adult worms may
live 3 to 5 years. For more information see: Lena N. Measures, 2001. Chap. 13, Dioctophymatosis (pp. 357 - 364). In: "Parasitic diseases of wild mammals". Iowa State University Press, Ames. Edited by W. Samuel, M.J. Pybus and A.A. Kocan.

The right kidney.
The peritoneal cavity
Diagnostic Stage:
Egg in urine. Eggs are 65 - 42 um.

Urine sedimentation Return to top of page
Clinical Signs:
Usually the left kidney is able to serve the entire body and the infection is asymptomatic. Sometimes the host shows signs of kidney trouble.
Vomiting often occurs when the L3 penetrate into the wall of the stomach.
Treatment:
Surgical removal prevention: do not feed animal raw fish. Return to top of page
Dipetalonema reconditum Homepage
Common name: None Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Family: Setariidae Genus: Dipetalonema Species: reconditum
Adult Parasite:
Hosts:
Dogs (definitive). Fleas [Ctenocephalides felis] and lice [Heterodoxus spiniger] (intermediate). Return to top of page
Life Cycle:
The flea ingests a microfilaria when feeding on an infected dog. The microfilaria develops into an infective larva in 7 to 14 days. When the flea again feeds on a dog the infective larva is injected into the skin. The larva develops to the adult stage in the connective tissue of the dog's skin. The female worm lays microfilariae which find their way into the blood. The prepatent period is about 61 to 65 days. Return to top of page

The connective tissue of the skin. Return to top of page
Diagnostic Stage:
Microfilariae are 215 to 270 um in length, and are 4.7 to 5.8 um wide. Microfilaria are found in blood.
Above left: Knott test, Above right: Acid phosphate stain Return to top of page

Microfilariae are found by blood smears and using the modified knott method. Return to top of page
Clinical Signs: Asymptomatic. Return to top of page
Treatment:
No treatment is necessary - infection is non-pathogenic.
Drug: Ivermectin
Dracunculus insignis Homepage
Common name: "Guinea-Worm" of North American wildlife. Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Superfamily: Dracunculoidea Genus : Dracunculus Species: insignis
Adult Parasite:
The adult worms measure 4 cm (male) to 120 cm (female).
Adult female Guinea worm manipulated into shedding L1 into a tube of water.
Adult worm Both photos courtesy of ML Eberhard (CDC) Return to top of page
Hosts:
Raccoons, Dogs, cats, mink and other carnivores (definitive). Cyclops, a copepod (intermediate) Return to top of page
Life Cycle:
A copepod of the genus Cyclops ingests the first stage-larva and the parasite develops to the infective third stage-larva in about 3 weeks. It has been shown experimentally that if a tadpole ingests the infected copepod, the L3 will go to the somatic tissues and persist there throughout the development of the frog (Eberhard and Brandt, 1995, J. Parasitology 81:792-793). Thus frogs may be paratenic hosts. When the definitive host ingests the infected copepod in
drinking water, the larva invades the intestinal wall and gets into the body cavity where it develops to the fourth stage-larva. Adult female worms are usually found under the skin of the extremities. The worm causes a shallow ulcer to form in the skin over the anterior end of the worm. When this ulcer comes in contact with water, the female worm extrudes her anterior end, prolapses a length of uterus, which bursts releasing first stage-larvae into the water. The prepatent period is about 309 to 410 days. Return to top of page

The subcutaneous tissues of the limbs Occasionally found in other areas of the body (i.e. heart, vertebral column, conjunctiva, etc.) Return to top of page
Diagnostic Stage:
L1 from the extruded worm or the adult worm. L1 measures 500 - 750 um.

When the ulcer and inflamed area around the worm is noticed, a tube of water is placed over the ulcer. The adult female will then shed larvae into the water. The water in the tube can then be examined for the larvae. Return to top of page
Clinical Signs: The site where the adult worm lies painful and itchy. An ulcer will be apparent in the skin. Return to top of page
Treatment:
If possible surgically remove the worm. Also treat with an anthelmintic to kill undeveloped worms: Ivermectin or Fenbendazole for 7 to 10 days. Anthelmintics seem to work only if given before 90 days of infection.
Drug: Fenbendazole Drug: Ivermectin

Echinococcus granulosus Homepage
Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminthes Class: Eucestoda Class: Cestoda Order: Cyclophyllidea Genus : Echinococcus Species: granulosus
Adult Parasite:
Echinococcus granulosus adult (left), Echinococcus granulosus adults in situ - intestine of dog (right).
Hydatid cyst in human (above)
Schematic illustration of hydatid cyst Return to top of page
Hosts:
Dogs, coyotes, wolves and other wild canids (definitive). Sheep, horses, camels, pigs, and other ungulates (intermediate). Return to top of page
Life Cycle:
The sheep ingests an egg. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travels to the liver via the blood. The hydatid cyst develops in (in order of likelihood) the liver, lungs, brain or other organ. When the dog eats the sheep viscera and ingests the hydatid cyst, the protoscolices attach to the small intestinal wall and the worms begin to form proglottids. Gravid proglottids, containing the eggs, detach from the end of the worm and spill their eggs into the lumen of the intestine. The eggs pass out in the feces. The prepatent period is about 47 days. Return to top of page

Diagnostic Stage:
Eggs are found in fecal flotation

Fecal float to recover eggs. Eggs are 38 - 32 um. Return to top of page
Clinical Signs: Usually asymptomatic in the dog. Clinical signs in the intermediate host depend on where the hydatid cyst is located and how old (large) it is. Return to top of page
Treatment:
Epsiprantel, Praziquantel,
Fenbendazole
Entamoeba histolytica Homepage
Common name: Ameba Kingdom: Protista Phylum: Protozoa Class: Lobosea Order: Amoebida Family: Entamoebidae Genus: Entamoeba Species: histolytica
Adult Parasite:
The trophozoites are found in the lumen of the large intestine and occasionally in the wall of the intestine, the liver, or other organs.
Adult trophozoites (above)
Illustration of E. histolytica trophozoite and cyst

Hosts:
Dogs, primates, including humans (definitive). Return to top of page
Life Cycle:
Infective cysts are ingested by the host and excyst in the intestine. The trophozoite feeds on bacteria and sometimes host cells. It divides by binary fission. Under some circumstances the trophozoite can round up and form a cyst wall around itself. This cyst will then pass out with the feces. In dogs the trophozoites rarely form cysts.

Lumen of the large intestine sometimes will invade the intestinal wall, liver or other organs. Return to top of page
Diagnostic Stage:
Trophozoite (10 to 70 um in length) in fresh feces. In other animals: Cyst (8 - 20 um in diameter).
E. histolytica cyst

Fecal float Return to top of page
Clinical Signs: Usually asymptomatic Diarrhea. Return to top of page
Treatment:
Drug: Metronidazole ?
Filaroides hirthi Homepage
Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Superfamily: Filariodea Genus: Filaroides Species: hirthi
Adult Parasite:
Filaroides osleri in tracheal nodes. Left - nodes are uncut, right - nodes are cut open.
Hosts:
Dogs (definitive). Return to top of page
Life Cycle:
The first stage-larvae pass in the feces or in vomitus. The dog eats the feces or vomitus containing the first stage-larvae. The larvae make their way to the lung where they develop to adults in the lung parenchyma. The females lay thin walled eggs which hatch in the lung. The larvae are carried up the trachea and are swallowed. The prepatent period is about 32 to 35 days. Return to top of page

Parenchyma of the lung.
Diagnostic Stage:
First stage-larva in feces or tracheal wash. L1 are 325 - 378 um.
L1 larvae (left), and histological cross section of several parasites (right). Highlighted area indicates the cross section of a single parasite.

Baermann Technique Tracheal wash Sometimes larvae can be recovered in identifiable shape by the ZnSO4 flotation method. Return to top of page
Clinical Signs: Usually asymptomatic Severe infections in immunocompromised dogs have been fatal.
Treatment:
Drug: Fenbendazole, Ivermectin
Oslerus (Filaroides) osleri Homepage
Common name: Lungworm of dogs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Filaroididae Genus: Filaroides Species: osleri
Adult Parasite:
Filaroides osleri in tracheal nodes. Left - nodes are uncut, right - nodes are cut open.
Hosts:
Dogs, dingo (definitive) Return to top of page
Life Cycle:
The first stage-larvae pass in the feces or in vomitus. The dog eats the feces or vomitus containing the first stage-larvae. The larvae make their way to the lung where they develop to adults in nodules in the trachea and bronchi. The females lay thin walled eggs which hatch in the lung. The larvae are carried up the trachea and are swallowed. The prepatent period is about 10 weeks. Return to top of page

Nodules in the trachea and bronchi.
Diagnostic Stage:
First stage-larva in feces or tracheal wash. L1 are 325 - 378 um.
L1 larvae (left), and histological cross section of several parasites (right). Highlighted area indicates the cross section of a single parasite.

Baermann Technique Tracheal wash Sometimes larvae can be recovered in identifiable shape by the ZnSO4 flotation method. Return to top of page
Clinical Signs: Spasmodic attacks of a dry, hard cough (can be started by exercise or exposure to cold air).
Treatment:
Ivermectin, Fenbendazole (SID, 7 to 10 days). Return to top of page
Heterobilharzia americana Homepage
Common name: Dog Shistosome Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Digenea Family: Schistsomatidae Genus: Heterobilharzia Species: americana
Click on the text below to jump down to the desired section of this page Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment
Adult Parasites:
The adult worms measure 2 to 4 mm long. There are two sexes in this trematode.
Adult male and female schistosomes Return to top of page
Hosts:
Dogs, raccoons, bobcats, nutria, rabbit (definitive) Snails [Lymnaea cubenisis] (intermediate). Return to top of page
Life Cycle:
The egg hatches in water and the miracidium finds and penetrates a snail. Sporocysts and then daughter sporocysts develop in the snail. Cercariae develop in the daughter sporocysts, and when mature emerge from the snail. The cercariae swim around until they find a definitive host, whose skin they will penetrate. They migrate to the liver where they mature and then make their way to the mesenteric veins where the male and female worms join together. The female spends the rest of her life in the gynecophoric groove of the male. Eggs are laid in the mesenteric vein and make their way through the intestinal wall into the lumen of the intestine. Eggs pass out in the feces. Return to top of page

The mesenteric veins. Return to top of page
Diagnostic Stage:
Schistosome egg
Illustration from Slaughter, J.B., Billups, L.H., Acor, G. K., Compendum Small Animal, Vol 10, No. 5, page 607, May 1988.

Ethyl-acetate sedimentation (use saline instead of water) Return to top of page
Clinical Signs: Usually asymptomatic in the dog and cat.
Treatment:
Praziquantel or Fenbendazole for 10 days Return to top of page
Isospora canis Homepage
Common name: Coccidia Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiorida Family: Eimeriidae Genus: Isospora Species: caninum
Adult Parasite:
Tissue stages: The schizonts are found in the epithelial cells of the small intestine.
Hosts:
Dogs (definitive). Rodents (paratenic). Return to top of page
Life Cycle:
The dog ingests a sporulated oocyst which excysts in the small intestine releasing 8 sporozoites. The sporozoites invade intestinal epithelial cells. The sporozoites develop into a schizont which undergoes an asexual internal multiplication known as schizogony. There are 3 generations of schizonts, the last round of schizogony leads to the formation of gametes. The gametes which invade other cells, the male gamete will divide, then break out of its host cell, invade the host cell containing the female gamete and fuse with the female gamete forming a zygote. The zygote develops into an oocyst which breaks out of its host cell and passes out in the feces. The prepatent period for this parasite is about 9 to 11 days. The oocyst will sporulate in 4 days and then is infectious for the next host. The dog may also become infected by ingesting a rodent which has the asexual stages in its tissues. Return to top of page

Small intestinal epithelium Return to top of page
Diagnostic Stage:
Diagnostic stage: unsporulated oocyst which measures 38 um X 30 um.

Clinical Signs: Usually asymptomatic In young puppies a heavy infection may be accompanied by severe watery diarrhea, but Isospora canis may not be the sole pathogen in these cases.
Treatment:
Drug: Sulfadimethoxine, Amprolium

Isospora ohioensis Homepage
Common name: Coccidia Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiorida Family: Eimeriidae Genus: Isospora Species: ohioensis
Adult Parasite:
Tissue stages: The schizonts are found in the epithelial cells of the small intestine:
Hosts:
Dogs, and maybe other canids. Return to top of page
Life Cycle:
The dog ingests a sporulated oocyst which excysts in the small intestine releasing 8 sporozoites. The sporozoites invade intestinal epithelial cells. The sporozoites develop into a schizont which undergoes an asexual internal multiplication known as schizogony. There are 2 generations of schizonts, the last round of schizogony leads to the formation of gametes. The gametes which invade other cells, the male gamete will divide, then break out of its host cell, invade the host cell containing the female gamete and fuse with the female gamete forming a zygote. The zygote develops into an oocyst which breaks out of its host cell and passes out in the feces. The prepatent period for this parasite is about 4 to 6 days. The oocyst will sporulate in 4 days and then is infectious for the next host. Return to top of page

Small and large intestinal epithelium. Return to top of page
Diagnostic Stage:
Unsporulated oocyst which measures 25 m X 20 m. Note: There are a number of Isospora spp. which infect the dog and produce cysts almost identical to that of I. ohioensis. For purposes of treatment, many veterinarians will consider all these parasites to be I. ohioensis.
Isospora oocyst. Return to top of page

Fecal float Return to top of page
Clinical Signs: Usually asymptomatic In young puppies a heavy infection may be accompanied by severe watery diarrhea, but Isospora ohioensis may not be the sole pathogen in these cases. Return to top of page
Treatment:
Drug: Sulfadimethoxine, Amprolium

Leishmania donovani , Leishmania infantum Homepage
Common name: Visceral Leishmaniasis Kingdom: Protista Phylum: Protozoa Class: Zoomastigophorea Order: Kinetoplastida Family: Trypanosomatidae Genus: Leishmania Species: donovani and infantum
Adult Parasite:
The amastigotes are found in the macrophages of the internal organs.
Amastigotes in bone marrow macrophages.
Hosts:
Hosts: Dogs, rodents and humans (definitive). Sandflies (intermediate). . Return to top of page
Life Cycle:
Infective promastigotes are injected when a sandfly bites a host. The promastigotes are taken up by macrophages in which they transform to the amastigote form. Amastigotes multiply within the macrophages, eventually breaking out and infecting new macrophages. When a sandfly feeds on an infected host it takes up amastigotes (in macrophages). In the gut of the sandfly the amastigote transforms to the reproductive stage promastigote in the midgut. These promastigotes multiply in the midgut and, after an indeterminate number of divisions, they migrate to the pharynx of the fly where they mature to the infective promastigote form.
Original illustration from: Parasitic Diseases, 1982. Katz, Despommier, Gwadz, Springer-Verlag. New York.

Liver Spleen Bone marrow Lymph nodes Return to top of page
Diagnostic Stage:
Amastigote in tissue smear. Promastigote in culture of blood, ascites or tissue.
Amastigotes in tissue smear

Serology Stained biopsy smear culture of biopsy, blood or ascites PCR of lymph node or spleen biopsy. Return to top of page
Clinical Signs: Asymptomatic initially, eventually hepatoslenomegly, ascites, alopecia. Return to top of page
Treatment:
Treatment not always successful. Dogs may not be worth treating as they are acting as reservoirs for human infections. Trivalent sodium antimonyl gluconate and/or allopurinol for dogs. Pentavalent sodium stibogluconate in other hosts. For a review of treatment options for dogs see:
G. Baneth and S. E. Shaw. 2002. Chemotherapy of canine leishmaniosis. Veterinary Parasitology 106:315-324.
For L. infantum in dogs the following has been reported: "...orally

15mg/kg of allopurinol every 12h until the clinical signs improved, in the following 1 month period allopurinol at same dose and subcutaneously 30mg/kg of sodium stibogluconate combination were given daily and at the end of the combined treatment, allopurinol was continued alone at the same dose till the end of 8 months." PASA, S., et al. 2005. Clinical and serological follow-up in dogs with visceral
leishmaniosis treated with allopurinol and sodium stibogluconate. Veterinary Parasitology 128:243-249.
Macracanthorhynchus ingens Homepage
Common name: Thorny headed worm Kingdom: Animalia Phylum: Acanthocephala Class: Acanthocephalae Order: Archiacanthocephala Family: Oligacanthorhynchidae Genus : Macracanthorhynchus Species: ingens
Adult Parasite:
The adult males are 10 cm and the females are up to 35 cm long.
Hosts:
Raccoons, dogs, foxes (definitive). Millipedes (intermediate). Return to top of page
Life Cycle:
The millipede ingests an egg. The egg hatches and the larva develops to the cystacanth stage. When the raccoon eats the infected millipede the larva is digested out and attaches to the wall of the small intestine and grow to the adult stage. Return to top of page

Diagnostic Stage:
Eggs. Return to top of page

Clinical Signs: Usually asymptomatic in the dog, On rare occasions the worm may perforate the gut and peritonitis may result. Return to top of page
Treatment:
Drug: Ivermectin
Ivermectin is an "extra label use". 200 ug/kg, once a day for 7 days, removed M. hirudinaceus from pigs (Alva Valdes, et al., 1989. Am. J. Vet. Res. 50:1392-1395). Return to top of page
Nanophyetus samincola Homepage
Common name: Salmon fever fluke Kingdom: Animalia Phylum: Platyhelminthes Class: Tramatoda Order: Digenea Family: Troglotrematidae Genus: Nanophyetus Species: samincola
Adult Parasite:
Hosts:
Dogs, cat, raccoons, fox bear, mink, coyote (definitive). Snails [Oxytrema silicula] (first intermediate). Salmonid fishes (second intermediate). Return to top of page
Life Cycle:
The egg matures (3 months) and hatches in water. The miracidium finds and penetrates a snail. Redia develop in the snail. Cercariae develop in the redia, and when mature emerge from the snail. The cercariae swim around until they find a trout or salmon whose skin they penetrate and encyst as metacercaria in various tissues. When the definitive host eats the fish the metacercaria excyst and develop to the adult stage in the host's small intestine. Eggs are laid in the small intestine and pass out with the feces. Return to top of page

Diagnostic Stage:
Egg Return to top of page

Ethyl-acetate sedimentation Return to top of page
Clinical Signs: Usually asymptomatic in the dog and cat, unless the agent of salmon poisoning (Neorickettsia helminthoeca) is present in the parasite. This rickettsia produces a hemorrhagic enteritis and lymph node enlargement. Return to top of page
Treatment:
Praziquantel or Fenbendazole for 10 days (Neorickettsia helminthoeca can be treated with broad spectrum antibiotics.) Return to top of page
Neospora caninum Homepage
Common name: Neospora Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiida Family: Sarcocystiidae Genus: Neospora Species: caninum
Adult Parasite:
The cysts have been found in the CNS tissues of several mammals.
Hosts:
The definitive host is probably dogs. Dogs, rodents and cattle are known to be infected with the tissue cyst stage (intermediate hosts?). Return to top of page
Life Cycle:
Unknown Return to top of page

Unknown. Return to top of page
Diagnostic Stage:
Tissue cyst Return to top of page

Cyst in Necropsy specimen
Serology Return to top of page
Clinical Signs: In neonatal puppies: polyradiculitis, death. In cattle: abortion. Return to top of page
Treatment:
Clindamycin for 4 or more weeks.

Spirocerca lupi Homepage
Common name: Esophageal worm of Dogs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Family: Thelaziidae Genus: Spirocerca Species: lupi
Adult Parasite:
The adult worms measure 40 mm (male) to 80 mm (female) long.
Hosts:
Dogs, foxes, other canids and wild felids (definitive). Coprophagous beetles (intermediate). Lizards, birds, rodents (paratenic). Return to top of page
Life Cycle:
The egg, containing the infective first stage-larva, is passed in the feces and eaten by a beetle. The larva develops to the infective third stage larva in the beetle. If a paratenic host eats the beetle the larva will encyst in some organ of this host. When the dog eats the beetle or paratenic host the larva penetrates through the stomach wall, and migrates in the arteries, eventually reaching the thoracic aorta in about 3 weeks. After about 10 to 12 weeks in the aorta the larva will migrate to the esophagus where it forms a cystic nodule which is connected by a fistula to the lumen of the esophagus. Here it develops to the adult stage. Eggs are laid in the cyst, pass out to the lumen of the esophagus and pass out with the feces. The prepatent period is between 5 and 6 months. With time a granuloma forms around the cyst and eventually develops into a sarcoma of the
esophagus. Return to top of page

In cysts connected to the esophagus or stomach.
The picture to the right shows the esophagus of a dog infected with Spirocerca lupi. Note the nodules/granulomas which form around the worms in the wall of the esophagus. A worm can be seen emerging from the larger nodule. The picture to the right shows the esophagus of a dog infected with Spirocerca lupi. A sarcoma has developed around the site where the worms resided in the wall of the esophagus.
Diagnostic Stage:
Thick walled egg with a larva inside it. The egg measures 34 um X 13 um. Note: If the granuloma does not have an opening to the lumen of the esophagus, eggs will not be found in the feces.

Fecal float
, however because the egg has a high specific gravity a flotation medium with a specific gravity of about 1.36 (add more ZnSO4 salt to the normal ZnSO4 solution until the higher spG is achieved). If there is no opening between the worms in the granuloma and the lumen of the esophagus, eggs will not be present in the feces. In these cases radiographs or direct visualization of the granulomas by endoscopy may be useful.
Clinical Signs: Dysphagia. Vomiting. Esophageal neoplasia. Aortic aneurysm or rupture. Secondary pulmonary osteoarthropathy. Return to top of page
Treatment:
Disophenol sodium 10 mg/kg; 2 doses, a week apart, (no longer
available in the United States). Ivermectin 0.2 mg/kg, may have to be repeated OR 0.6 mg/kg, SQ, twice, 14 days apart along with prednisolone, orally, 0.5 mg/kg BW, every 12 h, for a total of 3 weeks, tapering the dose
accordingly. ( Mylonakis, M. E., Rallis, T. S., Koutinas, A. F., Ververidis, H. N., Fytianou, A.. 2004. A comparison between ethanol-induced chemical ablation and ivermectin plus prednisolone in the treatment of symptomatic esophageal spirocercosis in the dog: a prospective study on 14 natural cases. Veterinary Parasitology 120:131-138.)
Doramectin 0.4 mg/kg, SQ, every 2 weeks for 6 doses then monthly until granuloma disappears. (Lavy E. Aroch I. Bark H. Markovics A. Aizenberg I. Mazaki-Tovi M. Hagag A. Harrus S. 2002. Evaluation of doramectin for the treatment of experimental canine spirocercosis. Veterinary Parasitology. 109(1-2):65-73.)
Taenia hydatigena Homepage
Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: hydatigena
Adult Parasite:
The adult worms measure up to 500 cm.
Taenia sp. proglottid Return to top of page
Hosts:
Dogs, foxes, and other canids (definitive). Sheep, other domestic and wild ruminants (intermediate). Return to top of page
Life Cycle:
The sheep ingests an egg. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travel to the liver via the blood. The cysticercus migrates in the liver for 18 to 30 days then burrows out into the peritoneal cavity where it attaches to the viscera. When the dog eats the sheep viscera and ingests the cysticercus the protoscolex attaches to the small intestinal wall and the worm begins to form proglottids. Gravid proglottids, containing the eggs, detach from the end of the worm and pass out in the feces. The prepatent period is about 51 days. Return to top of page
Diagnostic Stage:
Proglottid or eggs . Eggs are 38 - 32 um.

Gross examination of the proglottid. Fecal flotation may bring up eggs if a gravid proglottid has been broken in the feces. Cysticerci may be found in the abdominal cavity of sheep and goats on necropsy. Return to top of page
Clinical Signs: Usually asymptomatic. Extremely heavy worm burdens in small dogs may cause blockage of the intestine. Cysticerci in sheep and goats normally cause no problems. A very heavy infection may cause damage to the liver as the larvae
migrate through, leading to signs of hepatitis. Return to top of page
Treatment:
Taenia ovis Homepage
Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: ovis
Adult Parasite:
Hosts:
Dogs, foxes, and other canids (definitive). Sheep and goats (intermediate). Return to top of page
Life Cycle:
The sheep ingests an egg. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travel to the heart and muscles via the blood. The cysticercus develop in the cardiac and skeletal muscles, reaching the infecitive stage in about 46 days. When the dog eats the sheep and ingests the cysticercus, the protoscolex attaches to the small intestinal wall and the worm begins to form proglottids. Gravid proglottids , containing the eggs, detach from the end of the worm and pass out in the feces. The prepatent period is about 60 days. Return to top of page
Diagnostic Stage:
Proglottid or eggs Eggs are 38 - 32 um.

Gross examination of the proglottid Fecal flotation may bring up eggs if a gravid proglottid has been broken in the feces. Upon necropsy the cysticerci can be found in the muscles of sheep and goats. Return to top of page
Clinical Signs: Usually asymptomatic. Extremely heavy worm burdens in small dogs may cause blockage of the intestine. In sheep and goats clinical signs are not usually seen.
Treatment:
Taenia pisiformis Homepage
Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: pisiformis
Adult Parasite:
T. pisiformis scolex - scanning electron micrograph (left), adult T. pisiformis (right).
Taenia species causing intestinal blockage Return to top of page
Hosts:
Dogs, foxes, and other canids (definitive). Rabbits and hares (intermediate). Return to top of page
Life Cycle:
The rabbit ingests an egg. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travel to the liver via the blood. The cysticercus develops in the liver for 2 to 4
weeks then burrows out into the peritoneal cavity where it attaches to the viscera. When the dog eats the rabbit and ingests the cysticercus the protoscolex attaches to the small intestinal wall and the worm begins to form proglottids. Gravid proglottids , containing the eggs, detach from the end of the worm and pass out in the feces. Return to top of page

Diagnostic Stage:
Proglottid or eggs. Eggs are 38 - 32 um.
Taenia species eggs.
T. pisiformis proglottids Return to top of page

Gross examination of the proglottid. Fecal flotation may bring up eggs if a gravid proglottid has been broken in the feces. Return to top of page
Clinical Signs: Usually asymptomatic. Extremely heavy worm burdens in small dogs may cause blockage of the intestine. . Return to top of page
Treatment:
Taenia multiceps Homepage
Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: multiceps
Adult Parasite:
Hosts:
Dogs, foxes, and other canids (definitive). Sheep and other ungulates (intermediate). Return to top of page
Life Cycle:
The sheep ingests an egg. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travel to the brain and spinal cord via the blood. The coenurus develops in the brain, reaching the infective stage in about 6 to 8 months. (In goats the coenurus can develop in a variety of tissues.) When the dog eats the sheep and ingests the coenurus, the protoscolices attach to the small intestinal wall and the worms begin to form proglottids. Gravid proglottids, containing the eggs, detach from the end of the worm and pass out in the feces. Return to top of page
Diagnostic Stage:

Gross examination of the proglottid Fecal float may bring up eggs if a gravid proglottid has been broken in the feces.
The coenurus may be found upon necropsy in the brain of sheep and goats.
Clinical Signs: Usually asymptomatic. Extremely heavy worm burdens in small dogs may cause blockage of the intestine.
In infected sheep or goats, the coenurus in the brain may cause ataxia, blindness, a stumbling gait, and paralysis.
Treatment:
Taenia serialis Homepage
Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: serialis
Adult Parasite:
Hosts:
Dogs, foxes (definitive). Rabbits (intermediate). Return to top of page
Life Cycle:
The rabbit ingests an egg. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travels to the subcutanenous and intramuscular connective tissue via the blood. The coenurus develops in the connective tissue. When the dog eats the rabbit and ingests the coenurus, the protoscolices attach to the small intestinal wall and the worms begin to form proglottids. Gravid proglottids, containing the eggs, detach from the end of the worm and pass out in the feces. Return to top of page
Diagnostic Stage:

Gross examination of the proglottid. Fecal flotation may bring up eggs if a gravid proglottid has been broken in the feces. Return to top of page
Clinical Signs: Usually asymptomatic. Extremely heavy worm burdens in small dogs may cause blockage of the intestine. Return to top of page
Treatment:
Thelazia californiansis Homepage
Common name: Eye worm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Superfamily: Thelaziodea Genus: Thelazia Species: californiensis
Adult Parasite:
The adult worms measure 10 mm (male) to 15 mm (female) long.
Hosts:
Hosts: dogs, cats, sheep, deer, man (definitive). Face flies (intermediate). Return to top of page
Life Cycle:
The eggs are laid and hatch in the conjunctival and lacrimal sacs. The first stage-larva is picked up by a face fly (Musca spp. or Fannia spp.) when it feeds on the secretions from the infected eye. The larva develops to the infective third-stage in the fly and then migrates to the mouthparts of the fly (this takes 2 to 4 weeks). When the fly feeds on the next host's eye the infective larva leaves the mouthparts. In the conjunctival and lacrimal sacs the larva develops to the adult stage. Return to top of page
found :
Conjunctival and lacrimal sacs of the eye. Return to top of page
Diagnostic Stage:
Adult stage in the conjunctival and lacrimal sacs (see photograph of adult parasite above). Return to top of page

Direct observation of the worm. Return to top of page
Clinical Signs: Usually asymptomatic, in heavier infections a mild conjunctivitis may develop Return to top of page
Treatment:
If possible remove the adult worms with a fine forceps.
Drug: Ivermectin
Toxocara canis Homepage
Common name: Common Roundworm (Ascarid) of Dogs Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida family: Ascaridida Genus : Toxocara Species: canis
Adult Parasite:
The adult worms measure between 10 cm (males) and 18 cm (females) long.
Hosts:
Dogs and foxes (definitive). Many mammals (paratenic) Return to top of page
Life Cycle:
Animals are infected either by ingestion of embryonated eggs, paratenic hosts or they are infected in utero via transmission from an infected bitch. Pre-patent period is 30 to 34 days after ingestion of an egg, 21 to 40 days after prenatal infection, and 19 days after ingestion of a paratenic host. When an older dog ingests an infective egg, the larva that hatches from the egg will arrest in the dog's tissue as L3. These L3 will come out of arrestment after day 45 of pregnancy and migrate to the fetus (through the placenta and into the fetal liver). After birth the L3 migrate from the liver, through the lungs, up the trachea and eventually reach the small intestine where they develop to adult worms. In dogs younger then 6 months the larva that hatches from the egg (L2) invades the intestinal wall, gets into the vascular system and is carried to the lungs. It will molt to the L3 in the lungs or the trachea. It is then carried up the trachea, swallowed, and in the small intestine it will molt twice becoming an adult. The adults live in the lumen of the small intestine. The L3 that
is in the paratenic host's tissue will develop in the dog's small intestine to the adult stage without undergoing a tissue migration. The egg, after it is passed with the feces, needs about 4 weeks in the environment to reach the infective stage. Larvae can be a cause of visceral larval migrans (VLM) and ocular larval migrans (OLM) in humans.
Life cycle illustration from : Georges' Parsitology for Veterinarians, 6th edition, D.D. Bowman, 1995. W.B. Saunders Co., Philadelphia, PA
Pre patent periods from: J.C. Parsons. 1987. Ascarid infections of cats and dogs. The Veterinary Clinics of North America. 17(6):1307-1340. WB Saunders Co. Philadelphia.

Lumen of the small intestine.
Diagnostic Stage:
Eggs are found in fecal flotation. Eggs are light brown with a thick protein coat that is pitted. The egg measures 90 um X 75 um.

Clinical Signs: Adults: Asymptomatic in light infections. Puppies: In heavy infections, the puppy may appear unthrifty, pot-bellied, have abdominal pain, diarrhea and vomiting. Visceral larval migration in puppies. Uncommonly leads to pneumonia. Return to top of page
Treatment:
Dichlorvos, Febantel, Febantel/Pyrantel embonate, Fenbendazole, Ivermectin, Mebendazole, Milbemycin oxime, Piperazine, Pyrantel Pamoate
Trichomonas spp. Homepage
Common name: Trichomonas Kingdom: Protista Phylum: Protozoa Class: Zoomastigophorea Order: Trichomonadida Family: Trichomonadidae Genus: Tritrichomonas, Trichomitus, Tetratrichomonas, and Pentatrichomonas Species: Various
Adult Parasite:
The trophozoite is the only stage in the life cycle. The various species range in length from 3 to 10 um.
Adult trophozoites of Trichomonas
Illustration of Trichomonas trophozoite Return to top of page
Hosts:
Vertebrates (definitive). Return to top of page
Life Cycle:
Trophozoites live in the cecum and large intestines of their hosts.
There is no cyst stage in the life cycle. Transmission is via fresh fecal contamination, usually mother to offspring. Return to top of page

Cecum and large intestine Return to top of page
Diagnostic Stage:
Trophozoite.

Direct smearof liquid diarrhea. Return to top of page
Clinical Signs: Usually asymptomatic Sometimes found associated with severe diarrhea. Return to top of page
Treatment:
Drug: Metronidazole
Trypanosoma cruziHomepage
Common name: None Kingdom: Protista Phylum: Protozoa Class: Zoomastigophorea Order: Kinetoplastida Family: Trypanosomatidae Genus: Trypanosoma Species: cruzi
Adult Parasite:
The amastigotes are found in various cells of the definitive host. Below - amastigotes in lung of dog.
Infective trypomastigote form:
Hosts:
Dogs, cats, armadillos, raccoons, opossums, rodents and humans (definitive). Triatomin bugs [Reduviidae] (intermediate). Return to top of page
Life Cycle:
Infective trypomastigotes are present in the bug's feces. The bug
defecates while it feeds and the feces (including the parasite) are rubbed into the wound left by the bug. Also the feces may be rubbed into the eye and the parasites gain entry that way. The trypomastigotes enter cells ( almost any cell, including reticuloendothelial, neural, glila cells, smooth and cardiac muscle cells). In the cell the parasite transforms to an amastigote which divides by binary fission. Eventually the cell ruptures and the amastigotes are freed. They change to trypomastigotes and circulate in the blood until they find another cell to invade or are picked up by a feeding triatomin bug. In the hindgut of the bug the trypomastigote multiplies and eventually transforms to the metacylic trypomastigote which passes out with the feces. Return to top of page

Lymph nodes, smooth and cardiac muscle, as well as other sites. Return to top of page
Diagnostic Stage:
amastigote in tissue biopsy.
. Return to top of page

Serology, Stained biopsy Return to top of page
Clinical Signs: Clinical signs: Asymptomatic initially, lyphadenopathy, acute myocarditis. Return to top of page
Treatment:
Treatment not always successful. Dogs may not be worth treating.
Drug: Quinapyramine sulphate

Tradename: Suramin Return to top of page
Uncinaria stenocephala Homepage
Common name: The Northern hookworm of dogs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Ancylostomatidae Genus: Uncinaria Species: stenocephala
Adult Parasite:
The adult worms measure 7 mm (males) to 10 mm (females) long.
Anterior end of adult Uncinaria stenocephala. Return to top of page
Hosts:
Dogs, cats, and foxes (definitive). Return to top of page
Life Cycle:
The host ingests an infective third stage-larva. The larva matures to the adult in the small intestine. Eggs are laid in the small intestine and pass out with the feces. The pre-patent period is about 15 to 17 days. The eggs hatch in the soil and the larvae molt twice to reach the infective third-stage. Return to top of page

Diagnostic Stage:
Eggs are found in fecal flotation. Egg measures 75 um long by 45 um wide.

Clinical Signs: Light infections are asymptomatic. Diarrhea and hypoproteinemia occur in heavier infections.
Treatment:
Febantel, Febantel/Pyrantel embonate, Fenbendazole, Ivermectin, Mebendazole, Pyrantel Pamoate

Nematode Eggs and Larvae Found in Feces
Toxocara canis egg (90 um X 75um).
Toxascaris leonina egg (80 um X 67 um).
Spirocerca lupi egg (34 um X 13 um).
Ancylostoma sp. egg (60 um X 40 um).
Ancylostoma caninum L1
Capillaria bhmi egg (70 um X 35 um).
Crenosoma vulpis L1
Filaroides osleri L1 (325 um X 378 um).
Physolaoptera sp. eggs (40 um X 48 um).
Strongyloides stercoralis L1 (55 um X 32 um).
Trichuris vulpis egg (80 um X 40 um).
Uncinaria stenocephala egg (75 um X 45 um).
Baylisacaris procyonis egg (80 um X 60 um).
Nematode Larvae Found in Muscle
Trichinella spiralis L1 (cysts may reach up to 3 mm long).
Trichinella spiralis L1. Stained with H+E.
Nematodes Found in Skin or Eye
Thelazia californiansis. Diagnosis is by direct observation of adult worm in eye.
L1 of Dracunculus insignis . (500 um X 750 um). Adult female worms are usually found under the skin of the extremities. The adult female worm causes a shallow ulcer to form in the skin over the anterior end of the worm. When this ulcer comes in contact with water, the female worm extrudes her anterior end, prolapses a length of uterus, which bursts releasing first stage-larvae into the water.
Nematode Eggs and Larvae Found in Tracheal or Nasal Washes
Capillaria bhmi egg (70 um X 35 um).
Filiroides osleri and Filiroides hirthi L1 (237 um X 267 um).
Crenosoma vulpis larvae
Crenosoma vulpis Adult (less than 16 mm long).
Nematode Larvae Found in Blood
Dipetalonema reconditum L1 (215 X 270 um by 4.7 - 5.8 um).
Dirofilaria immitis (270 X 325 um by 6.7- 7.0 um).
Tapeworm Eggs and Proglottides
Taeniaand Echinococcus species egg (38 X 32 um).
Taeniaspecies proglottid.
Dipylidium caninum egg (25 X 30 um in oblong packets of 20 or less eggs).
Dipylidium caninum proglottid.
Diphyllobothrium latum egg (75 X 45 um).
Diphyllobothrium latum proglottid.
Mesocestoides proglottid.
Trematode Eggs
Heterobilharzia americana egg
Paragonimus kellicotti egg (90 X 50 um).
Nanophyetus samincola egg (70 X 40 um).
Protozoan Trophozoites and Cysts Found in Feces
Balantidium coli Trophozoite (30 X 150 um).
Cryptosporidium parvum oocyst (4 X 8 um).
Entamoeba histolytica cyst (18 X 5 -10 um).
Entamoeba histolytica trophozoite (10 to 60 um in length).
Giardia species cyst (14 X 8 um).
Isospora canis oocyst (30 X 38 um).
Isospora ohionensis oocyst (sporulated). (25 X 20 um).
Sarcocystis cruzi sporocysts (16 X 11 um).
Protozoans Found in Blood
Babesiatrophozoites in a red blood cell.
Leishmania amastigote in bone marrow macrophage.
Protozoan Trophozoites and Cysts Found by Tissue Biopsy
Neospora caninum cyst
Trypanosome cruzi amastigotes (in lung tissue).
Toxoplasma gondii - tachyzoites in peritoneal
macrophage. (From peritoneal lavage).
Acanthocephalan Eggs
Macracanthorhynchus ingens egg
Quiz Case #1
Wrong: The Knott test is used to look for heartworm. Dogs

have a 6 month pre-patent period. You would be wasting your time doing a heartworm test on a 10 week old puppy. Return to the Quiz and try again Heartworm review Knott test review
Quiz Case #1
Correct!
Reason: Based on the history and the physical exam, a fecal
flotation is the most logical test to run.
Findings: The feces appeared dark and tarry, and when

examined by fecal flotation, many objects like the one pictured below were seen. This object measures 60u X 40u.
Identify the parasite:

A) Toxocara canis B) Uncinaria stenocephala C) Ancylostoma caninum D) Trichuris vulpis
Quiz Case #1
Wrong: Parasites of the urinary bladder or kidney (C. plica

and D. renale) would not be causing the clinical signs seen in a dog of this age. Return to the quiz and try again Review Capillaria plica Review Dioctophyme renale
Quiz Case #1
Wrong: While you might get lucky and find a migrating larvae
of the parasite that is causing the puppy's problems, given the clinical signs and the dog's age there is another test that is much more likely to provide the diagnostic stage of the larvae. Return to the quiz and try again
Quiz Case #2
Saturated salt fecal flotation

Results: Nothing seen. This is the test most often used to
examine canine fecal specimens, however, this does not mean the puppy is free of parasites. Another test should be employed. Go to a comparison of the various methods for examining feces. Return to the quiz and try again.
Quiz Case #2
ZnSO4 fecal flotation

Results: The objects shown below in the photomicrograph below were
several of the many similar objects seen on the ZnSO4 flotation. They measure about 12 um long.
What are they?

Coccidia oocyst (Isospora sp.) Giardia cyst fungal spore Toxoplasma gondii cyst
Quiz Case #2
Direct examination of a fecal smear

Results: Nothing seen. This test is useful when looking for
protozoal trophozoites (the motile, reproductive form of the parasite). Since trophozoites are normally killed by the removal of water from the feces in the large intestine, it doesn't pay to examine formed or semi-formed stool by the direct smear. However, you should examine any watery stool by this method, as well as by a concentration method. Go to a comparison of various methods of examining feces Return to the quiz and try again
Quiz Case #2
Ethyl acetate fecal sedimentation

Results: The fecal sample contained only a normal amount
of fat. Nothing was seen on your first slide, however you have enough material left in the tube to make about 10 more slides! Good luck! (You may eventually find something, but if you want to save time, try another method.) Return to the quiz and try again Go to a comparison of the various methods of examining feces
Quiz Case #3
Correct!
Test: ZnSO4 flotation. You could use this test or you could
also use a Saturated sugar/salt flotation.
Results: Upon examination of the float you find many of the

eggs shown in the photomicrograph labeled "A". These eggs measure about 80 um long. You also find a few of the objects shown in the micrograph labeled "B" (they measure about 40 um long).
B
Which one of the answers below correctly identifies : "A" and "B"? Capillaria aerophilaandIsospora canis Capillaria aerophilaand Paragonimus kellicotti Trichuris vulpisand Eimeria sp.
Trichuris vulpisand Paragonimus kellicotti
Quiz Case #3
Correct!
Test: Saturated sugar/salt flotation. You could use this test or
you could also use a ZnSO4 flotation.
Results: Upon examination of the float you find many of the

eggs shown in the photomicrograph labeled "A". These eggs measure about 80 um long. You also find a few of the objects shown in the micrograph labeled "B" (they measure about 40 um long).
B
Which one of the answers below correctly identifies : "A" and "B" ? Capillaria aerophila and Isospora canis Capillaria aerophila and Paragonimus kellicotti Trichuris vulpis and Eimeria sp. Trichuris vulpis and Paragonimus kellicotti
Quiz Case #3
Test: Fecal occult-blood test Result: There is blood present in the feces.
This test is unnecessary as you already have noted blood in the feces upon gross examination. Return to previous page and try again
Quiz Case #3
Test: Fecal-starch test. Result: Negative.

The presence of starch in the feces would indicate a lack of amylase in the digestive tract, thus suggesting pancreatitis. Since there was no mention of abdominal discomfort, there is no reason to believe Cirus has pancreatitis. Return to previous page and try again
Quiz Case #4
You choose: Taenia taeniaeformis and Toxocara canis Answer: Partially right, but Taenia taeniaeformis is found in cats, not dogs. Return to previous page and try again
Quiz Case #4
You choose: a taenid tapeworm and Toxascaris leonina Answer: Partially right, but Toxascaris leonina eggs are smooth shelled. Return to previous page and try again Review Toxascaris leonina
Quiz Case #4
You chose: a taenid tapeworm and Toxocara canis Answer: Right. However, several questions remain. You could, of course, treat Mackenzie (you have enough information at this point to give the proper anthelminthics) and send the dog home, but you still would not know why an older dogs such as this had a patent Toxocara infection and which taenid tapeworm was present. Which of the following reasons may explain the patent Toxocara canis infection? A. Mackenzie is pregnant and arrested larvae have "woken" up and some made their way to the small intestine and matured. B. Mackenzie ate an infected paratenic host. C. Mackenzie is immunocompromised due to some problem, thus allowing arrested larvae to migrate to the gut and develop. 1. A 2. B 3. C 4. A and B 5. B and C
Quiz Case #4
You chose: Taenia pisiformis and Toxocara canis Answer: Maybe, but how can you be sure "A" is the egg of Taenia pisiformis? Don't guess at this stage. Return to previous page and try again
Quiz Case #4
You chose: an unknown tapeworm and Toxascaris leonina Answer: No, You can make a more specific identification of the tapeworm egg and Toxascaris leonina eggs are smooth shelled. Review Toxascaris leonina Return to previous page and try again
Dictyocaulus viviparus Homepage
Common name: Lung Worm of Cattle Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Dictyocaulidae Genus: Dictyocaulus Species: viviparus
Adult Parasite:
Adults in the lung of a 3 year old cow.
Hosts:
Cattle, deer, reindeer, buffalo and camel Return to top of page
Life Cycle:
The adult worms live in the bronchi of the lungs. Eggs are laid in the lungs and may hatch there or in the intestine (after being coughed up and swallowed). First stage larva emerge from the cow in the feces. The larvae reach the ensheathed infectious third-stage (L3) by about 4 days. L3 are either washed out of the fecal pads or expelled from the fecal pad when they happen to be on a sporangium of the fungus Pilobolus which explodes to release its spores. On pasture the L3 will migrate up grass blades and be eaten by the cow. The L3 exsheath in the small intestine, penetrate the bowel wall and molt to L4 in the mesenteric lymph nodes. They then migrate to the lungs via the thoracic duct. They reach the lungs about 2 weeks after they were ingested. They molt to the adult stage at about 15 days of infection and begin laying eggs around 22 days post-infection (PI). The adult worms begin to be expelled at about 50 days PI, and most are gone by 70 days PI. A few adults or late stage larvae may over winter in the lungs of an infected animal and L3 may over winter on pasture by migrating down into the root mat and soil.
Bronchi of the lungs.

Diagnostic Stage:
The first stage larva (0.3 to 0.36 mm) is found in the fresh feces.
Common Diagnostic Tests Fecal flotation (zinc sulfate centrifugation) Baermann technique Return to top of page
Clinical Signs:
In heavy infections: During the first 25 days of infection there may be tachypnea and coughing. During days 25 to 55 the lung signs increase in intensity with harsh lung sounds (ronchi and emphysematous crackling) being heard. In mild infections the disease may be asymptomatic.
Treatment:
Ivermectin Doramectin
Fasciola hepatica Homepage
Common name: Liver Fluke Kingdom: Animalia Phylum: Platythelminthes Class: Trematoda Order: Digenea Family: Fasciolidae Genus: Fasciola Species: hepatica
Adult Parasite:
The adult worm may reach 30 X 13 mm. It is leaf shape with a cone-shaped projection at the anterior end. Living specimens are a grayish-brown in color.
Hosts:
Infects swine, sheep, goats, cattle and other ruminants, horses, humans and other mammals that eat the vegetation on which the metacercaria encysts. Return to top of page
Life Cycle:
The eggs leave the host in the feces and if the
egg gets into fresh water the embryo will develop into a miracidium. It takes 2 to 4 weeks for the miracidium to develop after which the operculum of the egg is pushed off and the miracidium uses its cilia to swim out of the egg. The miracidium finds a snail (Lymnaea truncatula) and bores into it. (If the miracidium fails to find a snail within 24 hours, it runs out of energy and dies.) In the snail, the trematode takes up residence in the digestive gland and develops into a sporocyst. Germinal cells within the sporocyst develop into rediae, which when fully developed burst out of the sporocyst. Each redia has a mouth and digestive system and will feed on the snail's tissue. Within the redia germinal cells will develop into a second generation of rediae (daughter rediae). The germinal cells within the daughter redia will develop into cercariae. The time from sporocyst to cercaria is about 1 to 2 months depending on the temperature. The cercaria will burrow out of the snail, swim around until it finds a plant and then will climb a short distance out of the water and encyst on the plant as a metacercaria. When the plant and metacercaria is eaten by a mammal, the larval trematode will emerge from the metacercarial cyst and burrow through the intestinal wall and migrate to the liver which it will also burrow into. After a few weeks of migrating through the liver parenchyma (growing all the time) the young fluke will penetrate into a bile duct where it will mature to the adult stage. Adult liver flukes will feed on the epithelium of the bile duct. Eggs are laid in the bile duct and carried out into the intestine by the bile. The complete life cycle may be completed in 3 to
5 months, the pre-patent period is 10 to 12 weeks.

Bile ducts and occasionally the gall bladder. Return to top of page
Diagnostic Stage:
Egg: Measures 130 - 150 by 63 - 90 m They have an operculum at one end.

Fecal flotation May distort the egg. Sedimentation Recovers eggs undistorted. Return to top of page
Clinical Signs:
The clinical signs depend on the host the fluke has infected.
Acute disease in sheep (due to a large initial infection) appears while the young fluke are migrating through the liver. The bleeding into the damaged liver may result in weakness, pale mucus membranes, and enlarged livers. Chronic disease results in anemia and hypoalbuminaemia as blood is lost into the bile ducts. The sheep show a loss of condition and sometimes edema. In cattle the chronic form of the disease is more common and there is the added feature of calcification of the bile ducts over time.
Treatment:
Albendazole
Sheep: 7.5 milligrams per kilogram of body weight (3.4 milligrams per pound). Administer as a single oral dose using dosing gun or dosing syringe. Cattle: 4.54 milligrams per pound of body weight (10 milligrams per kilogram). Administer as a single oral dose using dosing gun or dosing syringe. Withdrawal times: slaughter. Cattle: 27 days before slaughter, Sheep: 7 days before
Clorsulon Cattle: 7 milligrams per kilogram or 3.2 milligrams per pound of body
weight. Withdrawal time: 8 days before slaughter.
More information on the use of these products can be found by searching the "FDA Approved Animal Drug Products Online Database System" : http://dil.vetmed.vt.edu/NadaFIrst/NADA.cfm
Eimeria vison Homepage
Common name: Coccidia Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiorida Family: Eimeriidae Genus: Eimeria Species: vison
Adult Parasite:
Tissue stages: The schizonts are found in the epithelial cells of the small
intestine. Return to top of page
Hosts:
Mustela putorius (syn. M. putorius furo - ferret); Mustela vison (Mink)
Life Cycle:
The first schizonts were observed in the epithelial cells of the duodenal villi of minks 72 h after infection with sporulated oocysts of E. vison, a 2nd generation of schizonts appeared 140 h after infection and a 3rd generation was observed 221 h after infection, i.e. after the end of the prepatent period. The 3 generations of schizonts differed in size, number of merozoites and localization. The first generation of schizonts (S1) measured 5.6 to 9.8 x 5.6 m and contained 8 to 12 merozoites, S2 were 10 to 17 x 8.9 to 13 m and contained 23 to 30 merozoites and S 3 were 12.2 to 15.4 x 8 to 11.2 m and contained 18 to 26 merozoites. The 3 generations of schizonts developed in the epithelial cells of the villi of the duodenum, jejunum and ileum, and in heavy infection some sexual stages penetrated the connective tissue. The average lengths of the prepatent and patent periods were 7 and 11 days respectively. From: Umurzakov, M. D. Nukerbaeva, K. K. The life cycle of Eimeria vison in minks. [Russian]. Izvestiya Akademii Nauk Kazakhskoi SSR, Biologicheskaya. 1985. No.2, 48-53.
Small intestinal epithelium Return to top of page
Diagnostic Stage:
Diagnostic stage: unsporulated oocyst which measures .

Clinical Signs:
Treatment:
Ascaris suum Homepage
Common name: Ascarid (Roundworm) of Pigs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascaridoidea Genus: Ascaris Species: suum
Adult Parasite:
Males measure 15 to 25 cm long and 3 mm thick. Females are 15 to 41 cm and 5 mm thick.
Adult Ascaris suum in the small intestine of a pig.
Hosts:
Definitive: Swine and sometimes humans Paratenic: Birds and rodents are suspected
Life Cycle:
The egg is passed in feces and develops in the environment to the infectious stage in about 3 to 6 weeks (longer at lower temperatures). The larva within the egg appears as an L1 around 17 days, molts to the L2 between 22 and 27 days and finally molts to the L3 (infectious stage) between 27 and 60 days. When the egg is ingested, it hatches in the intestine and the L3 invade the wall of the cecum and colon. It has been shown that the viscera of birds that have ingested A. suum eggs contain L3 which are infectious for pigs, therefore there is the possibility of paratenic hosts in this life cycle. From the colon the L3 migrate within 24 hours to the liver of the pig via the portal veins. They pass through the liver (the immune response to their passage damages the tissue which heals with fibrosis, leaving white
"milk spots" in the liver) and are carried via the blood to the lungs. They penetrate into the air spaces (if many move through at one time they will cause coughing ("thumps") and in some cases may cause the death of the pig) and are carried up the trachea and swallowed arriving in the small intestine about a week after the eggs were ingested. They molt to the L4 in the small intestine and to the adult stage by 3 to 4 weeks post-egg ingestion. Eggs are laid 60 days after the initial infection. Return to top of page

Diagnostic Stage:
Egg: Oval 50 - 70 by 40 -50 m. Thick shelled, the outer layer has prominent projections. They are a yellow - brown in color.
Ascaris suum egg as recovered from the feces of a pig.
Ascaris suum egg containing an infectious larva.

Fecal float Identification of the adult worm recovered from the feces. Return to top of page
Clinical Signs:
An infected neonatal pig with a heavy infection may have pneumonia, lighter infections in these pigs usually produce a cough ("thumps") and stunted growth. Older pigs with a heavy infection will have diarrhea and slowed growth rate. The livers of pigs exposed to migrating larvae several times will show white areas of fibrosis ("milk spots").
Pig infected with Ascaris suum
Liver from Pig infected with Ascaris suum. The white "milk spots" are a fibrous response to the larvae which have migrated through the liver.
Treatment:
Ivermectin
Levamisole 8mg / kg body wt. Fenbendazole Pyrantel tartrate Return to top of page
Strongyloides ransomi Homepage
Common name: Threadworm of Pigs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Rhabditida Family: Strongyloididae Genus: Strongyloides Species: ransomi
Adult Parasite:
The adult worms measure 3.5 to 4.5 mm long.
Adult female of pig
Histology of female in sm. intestine Return to top of page
Hosts:
Swine Return to top of page
Life Cycle:
The third-stage larva (L3) is the infectious stage of this nematode. Infections are initiated in one of 3 ways: 1) transmammary (with the majority of the L3 being found in the colostrum during the first day of lactation, but L3 are still being passed in the milk for at least 20 days). 2) Skin penetration. 3) prenatal (rare). L3 entering a neonatal pig via the skin will migrate through the body to the lungs (arriving there about 72 hours post-infection), penetrate the air spaces and carried up the trachea, swallowed and arrive in the small intestine by about 96 hrs post-infection. Adult worms (all female) live in the small intestine and eggs begin to be passed in the feces on the 6th day post-infection. L3 entering an older pig via the skin will migrate to adipose tissue, especially the fat tissue around the mammary glands. L3 will remain in the adipose tissue for a long time (in experimentally infected sows, L3 were passed in the colostrum for at least the first 3 farrowings). In the last 10 days prior to parturition the L3 will move from the adipose tissue into the mammary glands and thus many will be in the colostrum the first time a piglet suckles. L3 entering the neonatal pig in the
colostrum or milk will mature to adults in the small intestine without a migration through the tissues of the piglet. Eggs will appear in the feces of the piglet at 4 days of age (4 days post-infection). Eggs will be shed in the feces of piglets for 10 to 20 weeks. Eggs hatch on the ground and the larva derived from eggs produced during the first few weeks will develop homogonicly to L3, insuring the susceptible neonatal pig will become heavily infected. Larvae hatching from eggs after the first few weeks of infection will develop either to L3 or to free-living male and female worms. Eggs from these free living adult worms will normally develop to L3, thus insuring a source of infection as stored L3 in the fat tissue of older pigs. (Moncol, 1975 Proc Helminthol Soc Wash 42:86-92.)

crypts of the small intestine Return to top of page
Diagnostic Stage:
Egg containing a larva is found in the feces. The egg measures 45 to 55 by 26 to 35 m.
Egg stained with iodine
Clinical Signs: Light infections and infections in adult pigs are usually asymptomatic In heavier infections in young pigs bloody diarrhea is seen. Anorexia, rapid weight loss, anemia and stunting are also seen in infected piglets.
These pigs are littermates. The one on the right was infected 3 months ago. The one on the left is uninfected.
Treatment:
Fenbendazole
Ivermectin
Levamisole
Oesphagostomum dentatum Homepage
Common name: Nodular worm of Pigs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Family: Genus: Oesphagostomum Species: dentatum
Adult Parasite:
The adult males measure 8 - 10 mm long and the females measure 11 -
14 mm.. Return to top of page
Hosts:
Swine Return to top of page
Life Cycle:
Eggs leave the pig in the feces and hatch in a couple of days at summer temperatures. The larvae reach the infectious L3 (ensheathed in the L2 cuticle) 2 to 3 days after hatching. The pig ingests the larvae, which exsheath in the small intestine. The L3 then enter the mucosa of the large intestine causing small nodules to form. They molt to the L4 within the nodule and then return to the lumen of the large intestine (this takes about 1 week). They will molt to the adult stage and eggs will first pass in the feces in 21 to 49 days depending on the strain of parasite.

Large intestine
Diagnostic Stage:
Egg (strongyle-type) is found in the feces. The egg measures 40 X 70 m.
Egg stained with iodine

Clinical Signs: Light infections and infections in adult pigs are usually asymptomatic In heavy infections anorexia, enteritis and blood stained feces can be seen. Death may occur.
Treatment:
Fenbendazole
Ivermectin
Levamisole
Thiabendazole
Macracanthorhynchus hirudinaceus Homepage
Common name: Thorny headed worm Kingdom: Animalia Phylum: Acanthocephala Class: Acanthocephalae Order: Archiacanthocephala Family: Oligacanthorhynchidae Genus : Macracanthorhynchus Species: hirudinaceus
Adult Parasite:
The body is flattened and has transverse grooves. The adult males are 10 cm and the females are up to 35 cm long.
Adults attached to small intestine of pig Proboscis of Adult
Hosts:
Pigs and wild boars (definitive). Dung beetles, May bugs, June beetles (intermediate). Return to top of page
Life Cycle:
The beetle ingests an egg. The egg hatches and the larva develops to the cystacanth stage which encysts in the body cavity of the insect. When the pig eats the infected beetle the larva is digested out and attaches to the wall of the small intestine and grows to the
adult stage. Return to top of page

Diagnostic Stage:
Eggs 67 - 110 by 40 - 65 m. The eggs have 4 shells, and is dark brown.

Clinical Signs:
Mild infections will be asymptomatic, severe infections will cause slow growth and even emaciation.
There will be inflammation and a granuloma in the intestinal wall around the site of attachment. On rare occasions the worm may perforate the gut and peritonitis may result. Return to top of page
Treatment:
Drug: Loperamid
Loperamid is an "extra label use". 1.5 mg/kg, PO, twice daily for 3 consecutive days (Mehlhorn. et al. 1990. Parasitology Research 76:624-626.)
Drug: Ivermectin
Ivermectin is an "extra label use". 200 g/kg, once a day for 7 days, removed M. hirudinaceus from pigs (Alva Valdes, et al., 1989. Am. J. Vet. Res. 50:1392-1395). However, another report suggested variable results (13 to 77% removal) (Primm, et al. 1992. Am. J. Vet. Res. 53:508-512.) Return to top of page
Homepage
Common name: Kidney-worm of swine Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Stephanuridae Genus: Stephanurus Species: dentatus
Adult Parasite:
The male measures 2 to 3 cm long and the female measures 3 to 4.5 cm long. Internal organs may be visible through the cuticle.
Hosts:
Pigs
Life Cycle:
Eggs pass out in the urine and hatch in the environment in about 30 hrs. Larvae will reach the infectious third-stage in about 4 days and in moist, warm environments they will live for 2 or 3 months (some may survive up to 5 months). Larvae will infect a pig either through the skin or by being ingested. Larvae ingested by earthworms can use the worm as a transport host, infecting the pig when the earthworm is eaten. The larvae will molt to the fourth-stage 70 hours post-infection (PI), this molt will be in the wall of the stomach if the larva was eaten or in the skin or muscles if the larva penetrated the skin. Larvae reach the liver via the portal veins (if eaten) or via the systemic circulation (after penetrating the skin). They will remain in the liver, wandering under the capsule, for 3 or more months before penetrating into the peritoneal cavity. They will then migrate to the kidney and either enter the kidney or encyst next to the kidney or ureter, which they connect to via a small canal. The per-patent period varies from 6 to 9 months and the adults may live for up to 2 years.

Generally found in the pelvis of the kidney, or in the perirenal fat or the walls of the ureters.
Diagnostic Stage: Eggs are found in the urine, they measure about 56 X 105 m.

Seen in urine sedimentation
Clinical Signs:
General signs include depressed growth rate, loss of appetite and, in severe cases, emaciation. Larval migration in the liver may lead to cirrhosis and ascites may be present.
Treatment:
Ivermectin benzimidazoles: fenbendazole,
Isospora robini Homepage
Common name: Coccidia Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiorida Family: Eimeriidae Genus: Isospora Species: robini
Adult Parasite:
No information.
Hosts:
Robin (Turdus migratorius)
Life Cycle:
Little data. The oocysts are found in the feces of the robin. Both adult and fledgling birds have been seen infected. Life cycle is assumed to be direct.

Schizonts are probably found in the cells of the small intestine epithelium.
Diagnostic Stage:
Oocysts are ovoid to ellipsoidal, measure 20 X 23 m and are brownish in color. They have no micropyle. The sporulated oocyst has no residuum, but does contain
a large prominent polar granule. (T.E. McQuistion and B.B. Holmes, 1988. Proc. Helminthol. Soc. Washington 55:324-325.)

Clinical Signs:
None reported.
Treatment:
None
Heartworm Dirofilaria immitis

Life Cycle
Dirofilaria immitis adults are primarily found in the right ventricle and pulmonary arteries of dogs. After reproduction, the females produce small, vermiform embryos called microfilariae. They can cross the capillary beds and so are found throughout the vascular circulation.
Preparasitic phase
Circulating microfilariae are ingested by a female mosquito while taking a bloodmeal from an infected host (A). These prelarval stages migrate to the Malpighian tubules of the mosquito vector where development through to third stage larvae takes place (B). These infective L3's migrate from the tubules to the lumen of the labial sheath in the mosquito's mouthparts.
Parasitic stage
During a later bloodmeal on an appropriate host (C) - primarily dogs but also cats and ferrets, the L3's will exit the labium, enter the bite wound, and penetrate local connective tissues. Molting to the next stage (L4) occurs within seven days of infection (D). L4 stages undertake extensive migration through the subcutis, which continues for some 60-90 days until the final molt to the immature adult (E). The juvenile worms migrate to the right heart within a few days of their final molt (F), carried there by the venous circulation. Final maturation and mating occur in the pulmonary arteries, and the adult worms live in the right heart and pulmonary arteries, where they may survive for up to seven years. Production of microfilariae by inseminated female worms begins approximately six and a half months (192 days) after infection. Microfilariae are then released into the circulation, for a mosquito to ingest during a subsequent blood meal.
Eimeria bovis
Life Cycle
Eimeria bovis is one of the many bovine gastrointestinal parasites, and it is ubiquitous in the environment. It has a general form of coccidian life cycle, including both asexual multiplication and sexual multiplication. Sexual multiplication culminates in the formation of oocysts, which are discharged with the feces (A). Four sporoblasts develop within each oocyst (B), and two infective sporozoites develop within each sporocyst (C). ( ) Following the ingestion of sporulated oocysts by calf (D), the sporozoites invade the epithelial cells (E) or the lamina propria of the host's small intestine. Click on the small intestine to get a closer view of Eimeria life cycle or click anywhere on the closeup diagram to return to the over view. Sporozoites inside host cells can round up as a trophozoite (F), grow larger, and become a first generation schizont, or a megaschizont (G). The megaschizont then releases many merozoites which further infect fresh host cells (H). There may be several more schizogonic generations for other Eimeria, but two or three is usually the limit for may of the important species. Click on the large intestine to get a closer view of Eimeria life cycle or click anywhere on the closeup diagram to return to the over view. A merozoite produced by the final schizogony is a telomerozoite (I). Telomerozoites can enter a fresh host cell and develop into either a male or a female gametocyte or developing sex cell (J). The female gametocyte enlarges, stores food materials, and induces hypertrophy of both cytoplasm and nucleus of its host cell. When mature, it is called a macrogamete or female sex cell. The male gametocyte undergoes repeated nuclear division nd becomes multinucleate. Each nucleus is finally incorporated into a biflagellate microgamete or male sex cell. Only a small fraction will find and fertilize macrogametes to form oocysts. The oocyst is released by rupture of the host cell and passes out with the feces to undergo sporulation, provided that the environment is adequate.
PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Nematodes

Trichostrongyles - life cycles Nematodes belonging to the family Trichostrongylidae have life cycles that are closely similar. Predilection sites include the abomasum, stomach or small intestine of ruminants, horses or swine depending on the species. Some examples are given in the following table. Nematode Ostertagia ostertagi Trichostrongylus axei Cooperia curticei Host Cattle Ruminants, horses, pigs Sheep, goats Predilection site Abomasum Abomasum, or stomach Small intestine
Pre-parasitic phase
The pre-parasitic phase of larval development is entirely free living. Eggs are passed in the feces of infected hosts. Contained embryos will develop into first stage larvae if temperature and humidity are optimal (22-26'C and 100% humidity). First (L1) and second (L2) larval stages feed on fecal and soil bacteria but the third stage(L3) cannot feed because it is enclosed by a protective, impermeable sheath (the retained L2 cuticle). These ensheathed L3's survive by utilizing nutrients stored by the actively feeding L1 and L2 stages.
Parasitic phase
The trichostongylid infective stage is an L3 enclosed in its protective sheath and hosts are infected, by ingesting L3's, as they graze on pasture. Exsheathment is the next event in the parasitic phase of these life cycles. Exsheathment sites are species-specific and are always proximal to the predilection site of each particular trichostrongylid species. As examples, Ostertagia ostertagi, an abomasal nematode, exsheaths in the rumen, while Cooperia curticei, with its predilection site in the small intestine, exsheaths in the abomasum. Exsheathment is immediately followed by movement of parasitic L3's to the predilection site where growth and development to adults occurs (L3--> L4-->Adults). Following sexual reproduction, mature females lay eggs approximately 2-3 weeks after infection. The time from infection to egg-laying by adult females is specific for each nematode species and is called the prepatent period. The following table gives some prepatent periods for several members of this family.
Nematode
Ostertagia species Haemonchus species Cooperia species
Prepatent period
17-21 days 2-3 weeks 15-18 days
Ascaris suum
Life cycle
The predilection site for Ascaris suum is the small intestine of swine.
Pre-parasitic phase
Eggs laid by female worms pass to the external environment in host feces (A). These eggs are oval and thick-shelled with a rough mammillated, sticky external coat and are laid in the one-celled stage. Development to the infective stage takes place inside the egg and consists of one molt only. Therefore the infective stage for Ascaris suum is an egg containing a second stage (L2) larva (C). Earthworms (D) and dung beetles may ingest ascarid eggs while feeding on soil and feces. When that happens eggs will hatch and L2s will migrate to tissues and encyst giving rise to the possibility that these invertebrates may serve as paratenic hosts for Ascaris suum.
Parasitic phase
Pigs are infected by ingesting (E) eggs or paratenic hosts containing second stage larvae. Following hatching in the small intestine (F), L2s burrow into the intestinal wall, enter the hepatic portal system and are carried to the liver (G) within 24 hours of infection. Here the first parasitic molt (L2 to L3) takes place. (If infected paratenic hosts (D) are ingested by pigs, L2s are released during digestion in the stomach and small intestine. Their migratory route and parasitic development are the same as infective larvae from eggs). Third stage larvae (L3s) continue their migration from the liver to the lungs via the venous system, right heart and pulmonary arteries, reaching the lungs (H) by 4 to 6 days after infection. They break out of the alveolar capillaries and migrate up the bronchial tree to the pharynx (I) where they are swallowed. The final two parasitic molts (L3 to L4 to immature adults) are completed in the small intestine (F) by 3-4 weeks after infection. Mature, gravid females begin to lay eggs approximately 6 to 8 weeks after infection.
The Nematodes
Paralephostrongylus tenuis - life cycle
The predilection site for this nematode is the brain (A) of white-tailed deer, specifically the subdural space and meningeal venous sinuses.
Pre-parasitic phase
The pre-parasitic phase of larval development takes place entirely inside an intermediate host. Development of fre-living stages does not does not occur in this life cycle. The location of adults in the brain means that eggs and hatched first stage larvae must undergo a tortuous path through the body of a host in order to reach the external environment where they will encounter required intermediate hosts. -----> Migration route of eggs and first stage larvae(L1s) from the brain to the external environment. Eggs are deposited in the venous sinuses by female worms. These eggs are carried via venous blood flow to the right heart (B) and then via the pulmonary arteries to the lungs(C) where they lodge in the alveolar capillary beds. First stage larvae(L1s) develop, hatch, escape into the alveoli and migrate up the bronchial tree(D) - aided by the upward flow of epithelial cilia - to the pharynx where they are swallowed. They pass through the gastrointestinal tract and out to the external environment with the hosts feces.(E) Terrestrial gastropods (slugs and snails) serve as intermediate hosts. They are infected when L1s penetrate the gastropod foot, as the snails and slugs travel across deer feces. The infective third larval stage (L3) is reached in gastropods following two molts (L1 to L2 to L3).
Parasitic phase
-----> Migration route of ingested L3s to the brain. Deer are infected by ingesting (F) infected slugs and snails as they browse and graze on low vegetation. Third-stage larvae are released from snail and slug tissues during digestion in the abomasum and small intestine. They penetrate the gut wall, migrate across the peritoneal cavity to the lumbar vertebrae, follow the lumbar nerves, and reach the vertebral canal approximately ten days after infection. Growing, developing larvae migrate anteriorly in the neural parenchyma, specifically the dorsal horns of the gray matter. Approximately forty days after infection, immature adults can be found in the subdural space of the spinal cord in which they continue their migration to the predilection site the subdural space and meningeal venous sinuses of the brain. Immature adult worms complete their development to sexual maturity, copulation takes place, and adult female worms complete the cycle by laying their eggs in the meningeal blood vessels. The prepatent period is approximately 7weeks (range = 82-91 days).
Example Ostertagia Strongylus Dirofilaria
Diagnostic Location Definitive stage host(s) egg egg host feces host feces ruminants horses
Predilection site abomasum cecum & colon heart brain subcutaneous tissues lungs
L1 peripheral Dogs (microfilaria) blood host feces deer horses ruminants, horses
Parelaphostrongylus L1 Onchocerca Dictyocaulus
L1 skin (microfilaria) L1 host feces
PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Trichostrongyloidea
Trichostrongylidae - life cycles

Nematodes belonging to the family Trichostrongylidae have life cycles that are closely similar. Predilection sites include the abomasum, stomach or small intestine of ruminants, horses or swine depending on the species. Some examples are given in the following table. Nematode Host Predilection site Abomasum
Ostertagia Cattle ostertagi Trichostrongylus Ruminants, Abomasum, axei horses, or stomach pigs Cooperia Sheep, Small curticei goats intestine
Pre-parasitic phase
The pre-parasitic phase of larval development is entirely free living. Eggs are passed in the feces of infected hosts. Contained embryos will develop into first stage larvae and hatch if temperature and humidity are optimal (22-26'C and 100% humidity). First (L1) and second (L2) larval stages feed on fecal and soil bacteria but the third stage(L3) cannot feed because it is enclosed by a protective, impermeable sheath (the retained L2 cuticle). These ensheathed L3's survive by utilizing nutrients stored by the actively feeding L1 and L2 stages. Development of all preparasitic stages - from eggs through to infective 3s is also controlled by temperature and humidity. optimal development occurs at 100% humidity and between a temperature range of 22'-26'C. At higher temperatures, the rate of development may be faster but metabolic activity of L3s is also increased and food reserves may be used up more quickly leading to larval death unless larvae readily find and infect a host. At lower temperatures, development slows and metabolic activity is reduced. At temperatures less than 10'C larval development, movement and metabolism are minimal. At temperatures below freezing preparasitic stages are vulnerable and few will survive. Similarly with humidity: the optimal humidity for development is 100% and little development occurs below 80%. However, even when atmospheric humidity is low, larvae may survive and develop because the microclimate within their environment on pasture may be sufficiently high. Prolonged dry spells and seasonal dry periods open larvae to death by desiccation.
Parasitic phase
The trichostongylid infective stage is an L3 enclosed in its protective sheath and hosts are infected, by ingesting L3's, as they graze on pasture. Exsheathment is the next event in the parasitic phase of these life cycles. Exsheathment sites are species-specific and are always proximal to the predilection site of each particular trichostrongylid species. As examples, Ostertagia ostertagi, an abomasal nematode, exsheaths in the rumen, while Cooperia curticei, with its predilection site in the small intestine, exsheaths in the abomasum. Exsheathment is immediately followed by movement of parasitic L3's to the predilection site where growth and development to adults occurs (L3--> L4-->Adults). Following sexual reproduction, mature females lay eggs approximately 2-3 weeks after infection. The
time from infection to egg-laying by adult females is specific for each nematode species and is called the prepatent period. The following table gives some prepatent periods for several members of this family.
Nematode Ostertagia species Haemonchus species Cooperia species Trichostrongylus species
Prepatent period 17-21 days 2-3 weeks 15-18 days 7-25 days
Hypobiosis or seasonal arrested development is an important feature of the life cycles of members of this family. It occurs where the prevailing seasonal temperature and humidity fall to levels that threaten their survival. Hypobiosis is therefore a mechanism to ensure survival whereby the nematode halts its development in a host when prevailing environmental conditions might jeopardize the survival of any progeny.
Hyostrongylus rubidus
The predilection site of this nematode is the stomach of swine.
Life Cycle
Hyostrongylus rubidus has a typical life cycle of the family Trichostrongylidae. The free-living and parasitic phases of the life cycle are similar to those of Ostertagia. ( )Following the ingestion of infective L3s, the larvae migrate to the stomach (A) and penetrate the gastric glands. There they grow and develop through two molts, emerging as immature adults approximately 17 days after infection to mature and reproduce on the surface of the stomach mucosa. The prepatent period is 3 weeks unless hypobiosis intervenes in which case the prepatent period may be delayed by several months until the arrested L4s resume their development . The free living stages, particularly L3s are susceptible to cold and drying which means that transmission is minimal in winter and when summers are dryer than usual. Under warm, moist conditions development from eggs through to L3s will take place in 7-14 days.
Strongylus vulgaris - pathogenesis

The image shows an arteriographic picture of the mesenteric arterial system of a foal 30 days after oral infection with 50 third stage larvae of Strongylus vulgaris. At this stage most of the larvae will have reached the cranial mesenteric artery and the image shows some of the early effects of their migratory pathway. The ventral colic (vc) branch of the ileo-ceco-colic artery (icc) is blocked by thrombi since only a small portion is visible from contrast material that has perfused via anastomoses with the dorsal colic artery (dc) artery. The medial cecal artery (m) is also blocked along most of its length. Most other arteries branching off the abdominal aorta (a) are dilated and irregular in their outline because of inflammation and the presence of mural thrombi. Other labels: c - celiac artery, s = splenic artery h = hepatic artery, g = gastric artery cm = cranial mesenteric artery pm = posterior (caudal) mesenteric artery l = lateral cecal artery
Arteriographic picture of the mesenteric arterial system of a foal 30 days after infection with 50 Strongylus vulgaris third stage larvae. Image courtesy of Dr. Jay Georgi.
Strongylus vulgaris - pathogenesis

The image shows an arteriographic picture of the mesenteric arterial system of a foal 60 days after oral infection with 50 third stage larvae of Strongylus vulgaris adn treatmetn at 30 dasy with a larvicidal dose of an anthelmintic. This arteriograph shows that significant healing has occurred in this foal and it is clear that the larvicidal treatment at 30 days after infection was successful in killing most if not all migrating fourth stage larvae and allowed the natural healing process to take place. The cranial mesenteric artery is reduced in size and thrombotic occlusions have resolved. All major branches from the cranial mesenteric artery contain contrast material and are therefore now open. The fan of grey lines extending from the ileo-ceco-colic artery (icc) are jejunal and iliac arteries supplying blood to the small intestine. Although there is irregularity in the walls of some arteries, it is clear that the lesions caused by migrating S. vulgaris larvae are well on the way to complete resolution and healing. Labels: a = abdominal aorta cm = cranial mesenteric artery icc = ileo-ceco-colic artery dc = dorsal colic artery vc = ventral colic artery m = medial cecal artery l = lateral cecal artery c - celiac artery g = gastric artery h = hepatic artery s = splenic artery pm = posterior mesenteric artery
Arteriographic picture of the mesenteric arterial system of a foal 60 days after infection with 50 Strongylus vulgaris third stage larvae and treatment at 30 days with a larvicidal dose of an anthelmintic. Image courtesy of Dr. Jay Georgi.
Ultrasound Detection of Feline Heartworm Infection

Back to Dirofilaria immitis homepage The following video shows an ultrasound of the base of the pulmonary arteries of a cat with adult heartworm(s) present. When using ultrasound to examine a cat for heartworm, care (and time) must be taken to get a good view of the bases of the pulmonary arteries. Worms will appear as a pair of bright parallel lines (some of which have are marked by an arrow in the video). It is not possible to count the number of worms using ultrasound as different loops of the same worm may be showing up as separate reflections of the beam. The video will loop until the "Back to D. immitis" is clicked.
Back to Dirofilaria immitis homepage
Ultrasound Detection of Heartworm Infection in a Ferret

Back to Dirofilaria immitis homepage The following video shows an ultrasound of the apex of a ferret's heart ("4-chamber" view) with adult heartworm(s) present in the right atrium. When using ultrasound to examine a ferret for heartworm, care (and time) must be taken to get a good view of the bases of the pulmonary arteries and the right atrium. In this ultrasound clip, worms appear as a pair of bright parallel lines in the right atrium (which will be located to the lower left-center of the ultrasound). It is not possible to count the number of worms using ultrasound as different loops of the same worm may be showing up as separate reflections of the beam. The video will loop until the "Back to D. immitis" is clicked.
Back to Dirofilaria immitis homepage
Quiz Case #1
You chose: Transmammary
Not likely,
for a 6 year old cat and transmmary infection is only a minor infection route for Toxocara cati. Return to the previous page and try again Go to a review of Toxocara cati
Quiz Case #1
You chose: Transplacental

Toxocara cati is not known to use the transplacental route, and in a 6 year old cat it is unlikely that any worms that were passed to it from its mother would still be present. Return to the previous page and try again Go to a review of Toxocara cati
Quiz Case #1
You chose: Ingested an egg

Ingesting an egg that has reached the infectious stage may be the route by which this cat was infected. However, there is another route of infection that may have been more likely for this cat. Return to the previous page and try again
Quiz Case #1
You chose: Ate a rodent or bird.
Correct!
Yes, this is the most likely route of infection. Rodents and birds accidentally ingest eggs as they feed, and, over time, these paratenic hosts accumulate a store of arrested larvae in their tissues. When the cat is outdoors, it hunts and ingests infected paratenic hosts. Ingestion of one or more of these hosts is likely to give the cat a greater infection at one time than the occasional ingestion of an egg. Given that this is an older, male cat, does this infection have to be treated (there are no clinical signs present)? A. Yes B. No
Quiz Case #1
You chose: All of the above are equally likely.
Wrong.
Although A, B, C and D are all routes of infection for this parasite, they are not all equally likely at all stages of the cat's life. Return to the previous page and try again
Quiz Case #2
You chose: Drug resistance.
Not likely.
The fact that the diarrhea went away (and then came back) suggests that the drug worked, also the object pictured is not Isospora felis. Return to the previous page and try again Go to a review of Isospora felis.
Quiz Case #2
You chose: The owner did not comply with treatment

instructions.
Not likely.
The diarrhea went away (and then came back) and the object pictured is not Isospora felis. Return to the previous page and try again Go to a review of Isospora felis.
Quiz Case #2
You chose: The cat was re-infected with Isospora felis.
Not likely.
The object pictured is not Isospora felis. Immunity to a particular Isospora spp. is very strong, therefore it is unlikely you would see a re-infection of the same Isospora spp. causing disease. Return to the previous page and try again Go to a review of Isospora felis.
Quiz Case #2
You chose: The cat is infectedwith another coccidian.
Correct!
The object pictured is not Isospora felis, but it is a coccidian oocyst. Identify the parasite found in the second fecal exam.
A. Isospora felis B. Isospora rivolta C. Isospora ohionensis D. Toxoplasma gondii E. Hammondia hammondi
Quiz Case #2
You chose: The cat ingested a mouse and is just passing

oocysts of that host's coccidia.
Unlikely.
If a cat eats a mouse infected with coccidia and is passing oocysts, the oocysts in the mouse gut will pass through the cat. However, the number of these oocysts you would find on a fecal exam is going to be small, not the "many" found in this case. Also, would a 9 week old cat be hunting mice? Ask the owner to find out. Return to the previous page and try again
The pulmonary arteries, highlited in red are enlarged. Also note that the lungs (large black triangle) are not as radiolucent as they should be. This indicates damage to the lungs. Click here to return to quiz
Quiz Case #3
You chose: Knott Test
Not a good choice.

You might want to know if there are microfilariae present in order to determine a course of therapy. However, microfilariae are only transiently found during a heartworm infection in cats. Therefore the Knott Test is not the best test to run in order to diagnose an infection in cats. Return to the previous page and try again
Quiz Case #3
You chose: Heartworm Antibody Test

Antibodies to heartworm are found as early as 2 months post infection, which is well before larvae reach the pulmonary arteries. In fact, many of the larvae present at 2 months post infection will die before maturing to the adult stage. Thus, this test tells you if the cat has been exposed and therefore might be infected, but it does not tell you if adult heartworms are present. Results of the Heartworm antibody test on this cat:Positive Return to the previous page and try another test to help you confirm your diagnosis
Quiz Case #3
You chose: Heartworm Antigen Test

Antigens detected by the Heartworm Antigen Tests currently available are produced by the adult female worm. Thus, they may be absent in infections where only male worms are present. However, if present the positive antigen test conforms the diagnosis. Results of the Heartworm Antigen Test: Negative Return to the previous page and choose another test to help you confirm your diagnosis
Quiz Case #3
You chose: Ultrasound.

If done properly and care is taken to visualize the pulmonary arteries, ultrasound can be a definitive test. The ultrasound on this cat showed the following: characteristic parallel lines produced by the echo from a worm in the pulmonary artery.
Click on image to see full size pictures
(left: short view, Right: long pasternal view)
Quiz Case #3
You chose: All of the above
Not a bad choice.

With the exception of the Knott Test, which is unlikely to provide you with a diagnosis, any of the above tests would be a good start. Both the antigen test and ultrasound, if positive, would provide a definitive diagnosis. However, a negative result does not rule out heartworm. The antibody test is usually positive if the cat is infected, but may also be positive if the cat was exposed to migrating L4 which died off before reaching the vasculature. If the cat is immunocompromised the antibody test may be negative even if an adult worm is present. The test results on this cat: 1. Knott Test: Negative 2. Feline heartworm antibody test: Positive 3. Heartworm antigen test: Negative 4. Ultrasound: Shows parallel lines in the pulmonary artery.
Click on image to see full size pictures
(left: short view, Right: long pasternal view) What do these test results tell you? A. The cat is infected with Dirofilaria immitis B. The cat might be infected with heartworm C. The cat is probably not infected with heartworm
Quiz Case #4
You chose: Capillaria aerophila
Wrong.
Although the surface of the ova shown is similiar to Capillaria aerophila, the egg is too small. Return to the previous page and try again Go to a review of Capillaria aerophila
Quiz Case #4
You chose: Capillaria bohemi.
Wrong.
The surface is not that of Capillaria bohemi. Return to the previous page and try again Go to a review of Capillaria bohemi
Quiz Case #4
You chose: Capillaria plica
Wrong.
Although the surface of the ova shown is similiar to Capillaria plica, the size is wrong and Capillaria plica eggs are found in the urine (although contamination of the feces is possible). Return to the previous page and try again Go to a review of Capillaria plica
Quiz Case #4
You chose: Capillaria hepatica
You may be Right.

The size and surface of the ova shown are consistent with Capillaria hepatica. How did the cat get these eggs in its feces, and is it likely this parsite will cause problems forthe cat? A. Fecal contamination of the cat's paws (eggs just passing through)/ No. B. Fecal contamination of the cat's paws (eggs just passing through)/ Yes. C. Hunting (eggs just pasing through)/ No. D. Hunting (eggs just passing through)/ Yes. E. Hunting (cat is infected) Yes.
Quiz Case #4
You chose: Capillaria tomentosa
Wrong.
Capillaria tomentosa infects fish in Europe. Return to the previous page and try again
Click here to magnify image. Click here to return to quiz
Quiz Case #5
You chose: Liver parenchyma

No. The worm is in a vessel of some sort. Return to the previous page and try again
Quiz Case #5
You chose: Vein

No. The structure of the vessel wall is not that of a vein. Return to the previous page and try again
Quiz Case #5
You chose: Artery

No. The structure of the vessel wall is not that of an artery. Return to the previous page and try again
Quiz Case #5
You chose: Bile duct.
Yes!
The parasite in question is thus a bile duct fluke of cats. However, there are several species of bile duct flukes that infect cats. A parasitologist could identify the species of the fluke by examining the adult shown in figure 1B. However, you can make an educated guess based on the life histories of the cat bile duct flukes. The two bile duct flukes listed on the "Cat ParasiteList" are Parametorchis complexis and Platynosum fastosum. Both use a snail as a first intermediate host, but they differ in the second intermediate host. What are the second intermediate hosts for these two worms? A. Rodents and birds B. Rodents and fish C. Birds and snakes D. Fish and lizards E. White footed mice and palmetto bugs
Doramectin
Chemical group: Macrocyclic lactone Trade names: Dectomax Mode of action: Probably works like other macrocyclic lactones and opens glutamate-gated chloride channels in the nerve cells, causing paralysis Pharmacokinetics: The plasma pharmacokinetics of doramectin in young beef cattle after topical administration of 500 :g/kg: Cmax :12.2+/-4.8 ng/ml; Tmax : 4.3+/-1.6 days . The mean residence time (MRT) was 12.8+/-1.9 days (Vet Parasitol. 1999 Feb 1;81(1):47-55). The drug can be excreted in the milk. Dose: Swine: 300 :g/kg SQ, Cattle: 200 :g/kg SQ. Toxicity: Fatalities in dogs have been seen. In dogs given 4 mg/kg/day for a month ataxia, mydriasis, decreased food consumption, weight loss and tremors were seen. The LD50 for rats given the compound orally in sesame oil was between 50 and 200 mg/kg. Parasite Targets: Ascaris suum, Oesophagostomum dentatum, Oesophagostomum quadrispinulatum, Strongyloides ransomi, Hyostrongylus rubidus, Metastrongylusspp., Stephanurus dentatus, Sarcoptes scabiei var. suis, Haematopinus suis, Haemonchus contortus, Trichostrongylus axei, Trichostrongylus colubriformis, Ostertagia ostertagi, Ostertagia circuncicta, Cooperia oncophora, Cooperia punctata, Nematodirus spathiger, Oesophagostomum venulosum, Trichuris ovis, Bunostomun phlebotomum, Strongyloides papillosus, Oesophagostomum radiatum, Dictyocaulus viviparus, Dermatobia hominis, Linognathus vituli, Haematopinus eurysternus, Solenopotes capillatus, Cochliomyia hominivorax, Psoroptes bovis.
Quiz Case #1
Wrong
Although T. canis can be found in young puppies, it does not cause the anemia and intestinal bleeding that you noticed in this dog. Also, the egg of T. canis does not look like the egg that was shown.
T. canis egg
Review Toxocara canis Return to the previous page and try again
Quiz Case #1
Wrong
Although U. stenocephala looks like the object shown, it is slightly larger. More importantly, the clinical signs seen (anemia and bleeding into the intestine) are not typical of an U. stenocephala infection. Review U. stenocephala Return to the previous page and try again
Quiz Case #1
Correct!
A. caninum is passed to the nursing puppies in the milk, so it is common in puppies. Also the anemia (pale membranes) and bleeding into the small intestines (black tarry stools) are classical clinical symptoms of a heavy canine hookworm infection. Go to a review of A . caninum Return to the dog homepage and try another quiz case
Quiz Case #1
Wrong
The egg of T. vulpis does not look anything like the egg shown. Also, T. vulpis has a 3 month pre-patent period, so you would not see eggs in the stool of a 10 week old dog. Finally, the disease caused by the whipworm has different clinical signs from those that seen in this puppy.
Trichuris eggs
Go to a review of T. vulpis Return to the previous page and try again
Quiz Case #2
Wrong
The smallest Isospora sp. oocyst is about twice the size of the object shown and looks quite different. Review Isospora canis Return to the previous page and try again
Quiz Case #2
Correct: The age of the dog and the condition of the stool
would suggest you pay attention to this finding. While Giardia infections are usually asymptomatic and will eventually be cleared by the dog's immune response, this dog is probably experiencing its first infection with this parasite. Ariel is already showing mild symptoms (the mushy stool) and since the parasite can increase in numbers within the host, the disease may get worse before it gets better. You should probably treat Ariel. Go to Giardia Homepage Return to canine homepage to try another quiz
Quiz Case #2
Close, but wrong. The size and shape are correct for many
fungal spores, but spores usually have no internal details. The object in the previous photomicrograph shows several internal structures, while the one below does not.
Fungal spore
Return to the previous page and try again
Quiz Case #2
Wrong
Remember that dogs do not shed oocysts of Toxoplasma gondii. Return to the previous page and try again Go to Toxoplasma gondii homepage
Quiz Case #3
You chose: Capillaria aerophila and Isospora canis : WRONG: The egg in "A" is the wrong shape and color for Capillaria
sp. and the object in "B" is the wrong shape and color for Isospora canis. Return to previous page and try again Go to a review of Capillaria aerophila Go to a review of Isospora canis
Quiz Case #3
You chose: Capillaria aerophila and Paragonimus kellicotti WRONG: The egg in "A" is the wrong shape and color for Capillaria
sp. and the object in "B" is the wrong size and color for Paragonimus kellicotti. Return to previous page and try again Go to a review of Capillaria aerophila Go to a review of Paragonimus kellicotti
Quiz Case #3
You chose: Trichuris vulpis and Eimeria sp.
Correct!
Which of the parasites you just identified is most likely causing the dog's problem? Trichuris vulpis Eimeria sp. Both are likely to be contributing
Quiz Case #3
You chose: Trichurisvulpis and Paragonimus kellicotti Wrong: The object in "A" is Trichuris vulpis, but the object in "B" is
the wrong size and color for Paragonimus kellicotti. Return to previous page and try again Go to a review of Paragonimus kellicotti
Quiz Case #4
You chose: "A" - Mackenzie is pregnant and arrested larvae have "woken" up and some made their way to the small intestine and matured. Answer: Wrong, Mackenzie is a male dog. Return to previous page and try again
Quiz Case #4
You chose: "B" - Mackenzie ate an infected paratenic host. Answer: Very likely, but there may be another reason Return to previous page and try again
Quiz Case #4
You chose: "C" - Mackenzie is immunocompromised due to some problem, thus allowing arrested larvae to migrate to the gut and develop. Answer: Could be, but there may be a better explanation. Return to previous page and try again
Quiz Case #4
You chose: "A" and "B" - Mackenzie is pregnant and arrested larvae have "woken" up and some made their way to the small intestine and matured, and Mackenzie ate an infected paratenic host. Answer: Wrong, Mackenzie is a male dog. Return to previous page and try again
Quiz Case #4
You Chose: "B" and "C" - Mackenzie ate an infected paratenic host, and Mackenzie is immunocompromised due to some problem, thus allowing arrested larvae to migrate to the gut and develop. Answer: Both these explanations are possible. What do you do to determine which is the likely explanation? A. Perform a complete blood work up, including antibody levels and T and B cell ratios. B. Ask the owners if Mackenzie has ever been known to eat rodents or birds.
Quiz Case #1
You chose: Yes, the cat should be treated.
Right.
Although this infection is unlikely to cause this cat any problems, and will be eliminated quickly by the immune system, Toxocara cati is zoonotic. Therefore, you should treat the cat to prevent this pet from contaminating areas where children may come in contact with the eggs. Return to Cat Homepage and try another quiz
Quiz Case #1
You chose: No, the cat does not need to be treated
Wrong!
Although this infection is unlikely to cause this cat any problems, and probably will be eliminated quickly by the immune system, Toxocara cati is zoonotic. Therefore, you should treat the cat to prevent this pet from contaminating areas where children may come in contact with the eggs. Return to the Cat Homepage and try another quiz
Quiz Case #2
You chose: Isospora felis.
Wrong.
The object pictured is not Isospora felis. Immunity to a particular Isospora spp. is very strong, therefore it is unlikely you would see a re-infection of the same Isospora spp. causing shedding of "many" oocysts. Return to the previous page and try again Go to a review of Isospora felis.
Quiz Case #2
You chose: Isospora revolta
Correct!
This oocyst is that of Isospora revolta.. Clickhere to review the particulars of Isospora revolta, or continue with the quiz below. You again have the owner treat the cat for 5 days with sulfadimethoxine. A few days later the owner calls and tells you that the cat still has bloody diarrhea. You request that another fecal sample be brought in. The fecal exam is repeated and no parasites are seen. What is going on?? A. Drug failure. B. Not enough time has elapsed for the drug to have cured the infection. C. Pre-patent infection with another coccidia. D. The cat has a Campylobacter infection E. Pre-patent hookworm infection
Quiz Case #2
You chose: Isospora ohionensis.
Wrong.
Isospora ohionensis is a dog parasite and will not infect cats. Return to the previous page and try again Go to a review of Isospora ohionensis
Quiz Case #2
You chose: Toxoplasma gondii
Wrong.
The oocyst pictured is too large to be that of Toxoplasma gondii. Return to the previous page and try again Go to a review of Toxoplasma gondii.
Quiz Case #2
You chose: Hammondia hammondi
Wrong.
The oocyst pictured is too large to be that of Hammondia hammondi Return to the previous page and try again Go to a review of Hammondia hammondi
Quiz Case #3
You chose: Results indicate that the cat is infected with

Dirofilaria immitis.
Yes !!!
The positive antibody titer and the presence of a worm detected by Ultrasound indicate that the cat is infected. The initial radiograph indicates that the worm(s) has produced pathology in the cat that may be responsible for the clinical signs. Return to the Cat Homepage and try another quiz Go to a review of Dirofilaria immitis.
Quiz Case #3
You chose: The cat might be infected with heartworm.
No.
The test results indicate that the catis infected Return to the previous page and try again
Quiz Case #3
You chose: The cat is probably not infected with heartworm.
No.
The test results indicate that the cat isinfected Return to the previous page and try again
Quiz Case #4
You chose: Fecal contamination of the cat's paws (eggs just

passing through)/ No.
Wrong.
Capillaria hepatica eggs are found only in the liver of mice so you would not find them in fecal material. Return to the previous page and try again
Quiz Case #4
You chose: Fecal contamination of the cat's paws (eggs just

passing through)/ Yes.
Wrong.
Capillaria hepatica eggs are found only in the liver of mice so you would not find them in fecal material. Return to the previous page and try again
Quiz Case #4
You chose: Hunting (eggs just pasing through)/ No.
Correct!!
Capillaria hepatica eggs are found only in the liver of mice, so you would expect to see them in cats that eat mice. The eggs are freed from the liver in the cat's intestine and just pass out in the cat's feces. They would not infect the cat. Return to the feline page and try another quiz
Quiz Case #4
You chose: Hunting (eggs just passing through)/ Yes.
Almost right.
Capillaria hepatica eggs are found only in the liver of mice, so you would expect to see them in cats that eat mice. The eggs are freed from the liver in the cat's intestine and just pass out in the cat's feces. They would not infect the cat. Return to the previous page and try again
Quiz Case #4
You chose: Hunting (cat is infected)/ Yes.
Almost right.
Capillaria hepatica eggs are found only in the liver of mice, so you would expect to see them in cats that eat mice. The eggs are freed from the liver in the cat's intestine and just pass out in the cat's feces. They would not infect the cat. Return to the previous page and try again
Click here to return to quiz Click here to shrink image down one size
Quiz Case #5
You chose: Rodents and birds
Wrong.
Click here to continue
Quiz Case #5
You chose: Rodents and fish
Wrong.
Quiz Case #5
You chose: Birds and snakes
Wrong.
Quiz Case #5
You chose: Fish and lizards
Right!!!
Given that the cat was from Massachusetts, which intermediate host was the cat more likely to come across? A. Minnows B. Geckos
Quiz Case #5
You chose: White footed mice and palmetto bugs
Wrong.
Quiz Case #3
Right!
You chose Trichuris vulpis. Go to a review of Trichuris vulpis. Given the following points from the dog's history: A. Cirus runs loose in the woods B. Other dogs run loose in the woods C. Raccoons, opossums and deer are common in the woods. D. Cirus eats wildlife. What part of the history explains the presence of Eimeria oocysts in the dog's feces? A A and B C D
Quiz Case #3
You chose: Eimeria sp. Wrong. No species of Eimeria infects the dog.
Return to previous page and try again
Quiz Case #3
You chose: Eimeria sp. and Trichuris vulpis Wrong. No species of Eimeria infects the dog.
Return to previous page and try again
Quiz Case #4
You Chose: "A" - perform a complete blood work up, including antibody levels and T and B cell ratios. Answer: This answer is correct only if you have gotten a negative response to question B and have seen some other indication during the Mackenzie's PE to suggest that such a complete work up is necessary. Go to previous page and try again
Quiz Case #4
You chose: "B" - ask the owner if Mackenzie has ever been
known to eat rodents or birds.
Answer: This is the easiest (and least expensive) place to

start. In fact Mackenzie enjoys hunting rabbits and rodents. Given this response, could you conclude that the tapeworm egg you found belongs to Taenia pisiformis? 1. Yes 2. No
Quiz Case #2
You chose: Drug failure.
Wrong.
The drug appears to have worked - there are no oocyst in the feces. Return to the previous page and try again
Quiz Case #2
You chose: Not enough time has elapsed for the drug to
have cured the infection.
Wrong.
The drug should stop the symptoms in a few days and it seems to have worked (there are no oocysts in the feces). And, to be picky, sulfadimethoxine is a coccidiostat, that is, it does not kill the coccidia. Rather, it halts the replication of the organism in a non-pathogenic stage and keeps it at that stage until the immune response "cures" the infection. Return to the previous page and try again
Quiz Case #2
You chose: Pre-patent infection with another coccidia.
Wrong.
Pathogenic coccidia cause problems during the formation of the oocyst, therefore pre-patent disease would be measured in hours and not days. Also, the drug should prevent other coccidia from maturing to the pathogenic stage. Return to the previous page and try again
Quiz Case #2
You chose: The cat has a Campylobacter infection.
Correct!
Campylobacter infection is a good bet. Coccidia rarely cause disease in cats when they are the only pathogen present, and in this case there is no indication that the Isospora is still present. Very likely the coccidia were adding to the symptoms of another pathogen, and the bloody diarrhea is typical of a Campylobacter infection. Return to The Feline Page and try another quiz
Quiz Case #2
You chose: Pre-patent hookworm infection.
Wrong.
Symptomatic pre-patent hookworm infections wouldn't last for a few days. One day is more likely, and it would be symptomatic only if the cat received a very big dose of larvae all at once. Return to the previous page and try again
Platynosomum fastosum Hosts Definitive: Cats

Intermediate: First: Snails Sublima octona, Second: Lizards, toads, geckos, and skinks. Eggs are ingested by Life Cycle snails. Cercariae encyst
Parametorchis complexis
Definitive: cats and dogs Intermediate: First: Snails, Second: Fish
Egg hatches in water. The miracidium invades in lizards and other a snail. Cercariae leave second intermediate the snail and invade the hosts. The metacercaria skin of a fish. In the fish is found in the bile ducts the parasite encysts as of the lizard. When the a metacercaria. When infected lizard is eaten the infected fish is eaten by the cat the by the cat the metacercaria excysts metacercaria excysts and the worm makes its and the worm makes its way up the common bile way to the bile duct duct to the bile ducts and where it matures. Eggs gall bladder where it in the bile make their matures. Eggs in the bile way to the intestine and make their way to the exit in the feces. intestine and exit in the feces. Continue with quiz
Quiz Case #5
You chose: Minnows
Right!!!!
The morphological identification of the recovered adult indicated that it was Parametorchis complexis which has been found in cats from the Northeast USA. Return to the Cat Homepage
Quiz Case #5
You chose: Geckos
Wrong.
Geckos are not common in Massachusetts. The morphological identification of the recovered adult indicated that it was Parametorchis complexis which has been found in cats from the Northeast USA. Return to the previous page and try again
Quiz Case #3
Wrong.
You chose "A" - Cirus runs loose in the woods. Return to previous page and try again.
Quiz Case #3
Wrong.
You chose "A and B" - Cirus and other dogs both run loose in the woods. Though incorrect, this would explain where the whipworm probably came from. Return to previous page and try again.
Quiz Case #3
Wrong.
You chose "C" - Raccoons, opossums and deer are common in the woods. Though incorrect, this might explain where the Eimeria originally came from. Return to previous page and try again.
Quiz Case #3
Correct!
You chose "D" - Cirus eats wildlife. This could be why Cirus has oocysts in his feces of a species of coccidia that does not infect canines. The oocyst, which would have been present in the large intestine of wildlife (which the dog consumed), would just pass through Cirus after he ingested them. As dogs are coprophagic, the oocysts may also have been in wildlife feces that Cirus ingested. Return to canine page and try another quiz.
Quiz Case #4
You chose: Yes, you can conclude that the tapeworm egg is Taenia pisiformis. Answer: Wrong. The egg might be from Taenia pisiformis, but you can not be sure. Go to previous page and try again
Quiz Case #4
You chose: No, you can notconclude that the tapeworm egg is from Taenia pisiformis. Answer: Right, you need some more information. Which of the following will allow you to identify the parasite? A. Ask the client if they have noticed proglottids on the dog's stools B. Look in the left-over fecal sample for proglottids C. Look around the perianal area for dried up proglottids D. All of the above
Quiz Case #4
You chose: "A" - Ask the client if they have noticed proglottids on the dog's stool. Answer: This would help if they said they saw some, but they haven't. What else can be done from the list? Return to previous page and choose another option
Quiz Case #4
You chose: Look in the left-over fecal sample for proglottids. Answer: This would help if you found one (actually you should have your tech do this, and it is the first thing the tech should do when the sample is processed). However, no proglottids were found in the fecal sample. What else can you do? Return to previous page and choose another option
Quiz Case #4
You chose: Look around the perianal region of the dog for dried up proglottids. Answer: This would help if you found one (you could put it in a little water to soften it and allow it to return to its original shape). However, you do not see any proglottids stuck to the skin. What else could you do? Return to previous page and choose another option
Quiz Case #4
You chose: All of the above - Ask the client if they have noticed proglottids on the dog's stool, look in the left-over fecal sample for proglottids, and look around the perianal area for dried up proglottids. Answer: Right, all three of these things can be done, however no proglottids were ever seen. Would asking the owners if Mackenzie ever ate raw sheep help in identifying this tapeworm? 1. Yes 2. No
Quiz Case #4
You chose: "Yes" - asking the owners if Mackenzie ever ate raw sheep would help in identifying the tapeworm Answer: It might help, since most of the Taenia species found in dogs are carried by sheep. Mackenzie was never feed raw sheep. Can you conclude that the taenid egg was that of Taenia pisiformis? A. Yes B. No
Quiz Case #4
You chose: "No" - asking the owners if the dog ever ate any raw sheep would not help in identifying the tapeworm. Answer: Wrong. Go to previous page and try again
Quiz Case #4
You chose: "Yes" - You can conclude that the taenid egg was that of Taenia pisiformis. Answer: No you can't. Even though Taenia pisiformis is the only likely member of Genus Taenia to be found in dogs in North America, taenid type eggs can also be found in tapeworms of the genus Echinococcus. Go to previous page and try again Review Taenia pisiformis Review Echinococcus granulosus Review E. multilocularis
Quiz Case #4
You chose: "No" - You can not conclude that the taenid egg was that of Taenia pisiformis. Answer: Right. Even though Taenia pisiformis is the only likely member of Genus Taenia to be found in dogs in North America who has not been fed raw sheep, taenid type eggs can also be found in tapeworms of the genus Echinococcus. What might lead you to seriously consider that Mackenzie might be infected with Echinococcus multilocularis? A. The dog hunts rodents and rabbits B. No proglottids were found C. The dog was allowed to hunt rodents in Wisconsin D. The dog was never feed raw sheep. E. All of the above. Review Taenia pisiformis Review Echinococcus granulosus Review E. multilocularis
Quiz Case #4
You chose: "A" - Mackenzie hunts rodents and rabbits. Answer: Partially Correct. This fact also points towards an infection with T. pisiformis. Return to the previous page and try again Review Echinococcus multilocularis
Quiz Case #4
You chose: "B" - No proglottids were found. Answer: Partially Correct. This fact doesn't say much, as small numbers of proglottids are easily over looked. Return to the previous page and try again Review Echinococcus multilocularis
Quiz Case #4
You chose: "C" - Mackenzie was allowed to hunt rodents in Wisconsin. Answer: Partially Correct. This fact also points towards an infection with T. pisiformis. Return to the previous page and try again Review Echinococcus multilocularis
Quiz Case #4
You chose: "D" - Mackenzie was never fed raw sheep. Answer: No, this fact may rule out infections with the taenids carried by sheep, but it does not rule out T. pisiformis. Return to the previous page and try again Review Echinococcus multilocularis
Quiz Case #4
You chose: "E" - Mackenzie hunts rodents and rabbits, no proglottids were found, Mackenzie was allowed to hunt rodents in Wisconsin, and Mackenzie was never feed raw sheep. Answer: Taken together all these facts would suggest that E. multilocularis should be considered, especially because of its zoonotic potential. (E. multilocularis endemic in Wisconsin (and the surrounding states), it uses a meadow vole as the intermediate host, the eggs of this tapeworm are freed from the gravid proglottid as it passes down the intestinal tract, and the only other member of this genus in the United States, E. granulosus, uses large animals such as sheep, horses, deer, elk, etc. as intermediate hosts.) The owners should be told of the possibility of becoming infected via the eggs that are found in the feces. Given the vast numbers of eggs which may be simultaneously released when you treat the dog, you should also warn them on how to dispose of the feces. End of Quiz Section Return to Canine Page Review Echinococcus multilocularis
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Veterinary Parasitology by Valsoriml

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Veterinary Parasitology by Valsoriml

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E-LEARNING RESOURCES IN VETERINARY PARASITOLOGY

1. DIAGNOSIS OF VETERINARY ENDOPARASITIC INFECTIONS

2.LIFE CYCLES OF SOME IMPORTANT PARASITES

3. Parasites and Parasitism in Livestock

4. Laboratory Demonstrations in Parasitology Useful Biological Prefixes and Suffixes

Diagnosis of Veterinary Endo-parasitic Infections

As per Diagnostic Techniques Click on the procedure for further details:

Techniques for Blood Samples

Filtration Method Smears Procedure for concentration of blood (Knott's Test)

This section is intended to reinforce important principles

Parasites and Parasitism in Livestock

Veterinary Parasitology Laboratory Demonstrations

Useful Biological Prefixes and Suffixes

erythro-fer-fract-gastro-gen-glossoglyc-gnath-gnosis -graph -helminth hemoheterohomohydrohyperhypo-iasis interintrairischn or ischno -itis kata-, cata-

parapathoperiphago-phil-plasmplaty-pnea pneumo-ped polypostpropropriopseudopsychopulmo-renal -rrhea sarco-

body body mouth

somatic cell chromosome ancylostoma

Index of Commonly Used Pharmaceuticals in the Treatment of Veterinary Parasitic Infections

Amprolium Butamisole Hyrdochloride Clindamycin Dichlorvos

Corid Styquin Antirobe Task

Ivomec, Heartgard, Heartgard

Pipa-tabs, Tasty Paste, WRM Rid, etc.

Droncit, Drontal, Drontal Plus

Drontal, Drontal Plus Revolution Albon, Bactrovet

Diagnosis of Veterinary Endoparasitic Infections

Loggerhead turtle - Caretta caretta

Comparison of Fecal Examination Techniques

Saturated Sucrose or Salt

Zinc Sulfate Flotation

Ethyl Acetate Sedimentation

Free living mite and mite egg (dog feces)

Above: Stained with iodine Below: unstained and at a higher magnification

Free living mites and mite egg (dog feces)

Monocystis sp. sporocyst and plant nematode in dog feces (10X).

Monocystis sp. sporocyst (40X)

Pollen in dog feces

Pine pollen in dog feces

Plant spine Fiber

Direct Fecal Smear Examination

Direct Smear Fecal Exam

Fecal Examination Using the Zinc Sulfate Centrifugal Flotation Method

Note: If the sample contains a large amount of fat or other

gravity of the solution).

Fecal Examination Using the Ethyl Acetate Sedimentation Method

NOTE:When removed from the centrifuge, your tube

NOTE: If you did this technique just to remove fat,

Fecal Examination Using The Baermannization Method

Fecal Examination Using the Stoll Egg Counting Method

Fecal Examination Using the McMaster Egg Method

Above: McMaster slide

Sources for McMaster slides are:

Fecal Examination Using the Saturated Salt Flotation Method

Saturated Salt Flotation

Filtration Method to Detect Microfilariae in Blood

Procedure for Making Blood Smears

Modified Knott Method

Directions for site us

-FReturn to top of page

-JReturn to top of page

-KReturn to top of page

-NReturn to top of page

-QReturn to top of page