Toxocara canis

Life cycle: direct (paratenic host possible), L3 infective stage (right image) Host: dogs and wild canids (small intestine) Transmission: Ingestion tracheal (usual) or somatic migration. Ingestion of paratenic host Transplacental most important (tracheal migration in pup) Transmammory least important PPP: 3-6 weeks Diagnosis: fecal float (preferred), worms in vomit/feces, post mortem Morphology: thick pitted shell wall, subspherical single dark cell 85-90 x 75 m Pathogenesis: usually nonpath., ill thrift syndrome (pot belly), obstruction (rare), death (neonate to 2-3weeks old). Zoonotic potential: visceral larva migrans Control: Sanitation, antihelmintics, preventative (2,4,6,8 weeks)

Toxocara cati
Life cycle: direct (paratenic host possible), L3 infective stage Host: cats and wild felids (small intestine) Transmission: Ingestion tracheal (usual) or somatic migration. Ingestion of paratenic host Transmammory mucosal migration PPP: 5-8 weeks Diagnosis: fecal float (preferred), worms in vomit/feces, post mortem Morphology: thick pitted shell wall subspherical single dark cell 65-75 m Pathogenesis: usually nonpath., ill thrift syndrome (pot belly) Zoonotic potential: visceral larva migrans (potentially) Control: Sanitation, antihelmintics, no hunting, preventative (3,5,7,9 weeks)

Toxocara leonina
Life cycle: direct (paratenic host possible), L3 infective stage Host: dogs and cats (small intestine) Transmission: Ingestion mucosal migration. Ingestion of paratenic host mucosal migration PPP: 8-9 weeks Diagnosis: fecal float (preferred), worms in vomit/feces, post mortem Morphology: thick smooth shell wall elliptical single light cell 75-85 x 60-75 m Pathogenesis: usually nonpath., fatal in puppies (extremely rare) Zoonotic potential: none Control: Sanitation, antihelmintics

Baylisascaris procyonis (left) Toxocara canis (right)

Life cycle: direct (paratenic host possible) Host: raccoon and sometimes dogs (small intestine) Transmission: Ingestion of paratenic host neuro-tropic migration Diagnosis: fecal float (preferred), worms in vomit/feces, post mortem Morphology: thick smooth shell wall elliptical brown coat may be present 62-79 x 52-68 m Pathogenesis: severe central nervous system disease Zoonotic potential: visceral and ocular larva migrans Control: Sanitation, antihelmintics, avoid raccoon latrine areas

Ancylostoma caninum / Uncinaria stenocephala (bigger)

Life cycle: direct (paratenic host possible), L3 infective stage (in 2-8 days) Host: small intestine of dogs, cats (A. braziliense), dog & cat (A. tubaeforme) Transmission: Ingestion of L3 mature in gut or somatic migration (dominant) L3 skin penetration tracheal or somatic migration. Transmammory A. caninum only (dominant for A. c.) Ingestion of paratenic host accumulate in lungs of rodents. PPP: 2-3 weeks Diagnosis: fecal float (preferred), clinical signs (peracute hookworm disease) Morphology: thin smooth barrel shaped wall, ellipsoidal, clustered cells 64 x 40 m (A. c.), 70-90 x 40-50 m (U. s.) Pathogenesis: chronic (anemia), acute & peracute (can be fatal), cutaneous larva migrans Zoonotic potential: cutaneous larva migrans, eosinophilic enteritis Control: Sanitation, antihelmintics (2-12 wks e.o.w., then monthly to 6mths)

Taenia spp / Echinococcus spp.

Life cycle: indirect (intermediate needed), eggs immediately infective Host: dogs, cats, humans (small intestine) Transmission: Carnivorism predator (definitive host), prey (intermediate) Diagnosis: Morphology: segments in feces, fecal float (if eggs free, but usually in segments), meat inspection (ruminants and swine) adult scolex w/ 4 suckers & rostellum +/- hooks egg thick wall w/ radial striations, hooks present internally

Pathogenesis: carcass condemnation, coernurus cerebralis (space occupying lesion in brain of ruminants), pressure atrophy & allergic reactions (E. spp.) Zoonotic potential: cysticercosis (often in CNS) Control: 3 steps cestocide, stop hunting, prevent carnivore fecal contamination

Trichuris spp. (whipworm)

Life cycle: direct, L1 infective Host: dogs (T. vulpis), cats (T. campanula), ruminants (T. ovis), pigs (T. suis) Transmission: Ingestion of eggs very resistant. Larvae enter wall of sm. intestine. Emerge and mature in cecum of colon. PPP: 11-12 weeks (T. vulpis), 7-9 (T. ovis), 6-7 (T. suis) Diagnosis: Morphology: centrifugal fecal float (preferred), clinical signs (shedding sporadic), endoscope, necropsy/slaughter. thick smooth shell wall, lemon shaped bipolar plugs w/ threading

Pathogenesis: usually nonpath., severe disease rare, young pigs (diarrhea, anemia), dogs diarrhea and death (heavy infections) Zoonotic potential: Trichuriasis (T. suis) Control: Sanitation, antihelmintics, difficult to rid in dogs

Capillaria spp.
Life cycle: direct or indirect, L1 infective Host: dogs, cats, ruminants, rodents, and birds Transmission: Indirect earthworm (intermediate) Direct Ingestion of egg Diagnosis: Morphology: fecal float (preferred), nasal secretions, sputum or urine (spp. dependent), thick smooth shell wall, ovoid to barrel shaped recessed bipolar plugs w/out threading

Pathogenesis: rhinitis, tracheitis, bronchitis, cough, can be fatal in young foxes, cystitis, hepatitis, enteritis. Zoonotic potential: none Control: Sanitation, antihelmintics, no hunting

Dipylidium caninum (flea tapeworm)

Life cycle: indirect, flea/chewing louse (intermediate host) Host: small intestine of dogs, cats, foxes and humans Transmission: Flea/louse larva ingests egg from eating segment. cystecircoid develops. dog/cat ingests flea. PPP: 14-21 days Diagnosis: Morphology: Segments in feces (rice grains), fecal float (less common) Segments bilateral genital pores Scolex 4 suckers, armed rostellum Eggs packets of 5-30

Pathogenesis: usually nonpath. Zoonotic potential: children infected if they ingest flea. Control: Treat for flea or louse infestation.

Diphyllobothrium spp. / Spirometra spp. (tapeworms)

Life cycle: indirect, copepod (1 intermediate), fish (2 intermediate nd Diphy.), reptile/amphibian (2 Spiro.) Host: small intestine fish eating mammals and birds Transmission: coracidium hatches (ciliated), procercoid develops in copepod copepod ingested by fish, plerocercoid develops in muscles eaten by definitive host and matures. PPP: 21-28 days Diagnosis: Morphology: Sedimentation technique, occasionally segments in feces. Segments genital and uterine (ventral) pores (Diphy.) Scolex unarmed wi 2 bothria (slit like grooves) (Diphy.) Eggs operculate, grey-green to brown
st nd

Pathogenesis: usually nonpath., enteritis, can be severe in fish (Diphy.). Sparganosis rare, fatal if proliferative (Spiro.) Zoonotic potential: infection with ingestion Control: Avoid raw fish, cestocides

Nanophyetus salmincola / Paragonimus kellicotti (flukes)

Life cycle: indirect, snail (1 ), crayfish (2 Para.), salmonid (2 Host: small intestine fish/crayfish eating mammals Transmission: Eating intermediate PPP: 5-8 days (dogs Nano.), 30-36 days (Para.) Diagnosis: Morphology:
st nd nd

Nano.)

Sedimantation technique (operculate eggs in feces), Radiology cysts in lungs (Para.) Eggs operculate

Pathogenesis: Para. chronic bronchiolitis, fatal pneumothorax (cyst rupture) Nano. salmon poisoning disease (rickettsia) Control: Avoid raw fish/crayfish, anthelminitcs (little use)

Fasciola hepatica (Liver Fluke)

Life cycle: indirect, snail (intermediate Host: bile duct of ruminants Transmission: ciliated miracidia infect snail metacercaria encyst on vegetation eaten by definitive host, penetrate gut & migrate to bile duct via the liver (6-8 weeks) PPP: 2-3 months Diagnosis: Morphology: Sedimentation technique, find flukes postmortem. Operculate eggs

Pathogenesis: Cattle chronic disease Sheep acute to chronic. Secondary clostridial infections. Control: Pasture management (snails), flukicides (strategic deworming)

Giardia spp.
Life cycle: direct Host: duodenum and upper small intestine of mammals and birds Transmission: Cyst (left) ingested and excyst after exposure to stomach acid and alkaline duodenum. Trophozoite (right) asexual repro., colonize sm. intestine. encyst with increasing bile, passed in feces. PPP: 7-10 days Diagnosis: Morphology: ZnSO4 fecal float (gold standard cyst cytoplasm collapses), direct smear (trophs falling leaf), ELISA. Cyst oval, 4 nuclei (2 trophs/cyst), axostyle, median bodies. Troph. bilateral symmetry, pyriform, venral disk, axostyle, 2 median bodies, 4 pair of flagella, binucleate.

Pathogenesis: Variable (host and parasite dependent), dose dependent, malabsorption, increased intestinal motility. Control: Sanitation and hygiene, reduce stress, no licensed treatments.

Isospora spp.
Life cycle: direct, host specific Host: intestinal epithelial cell of host (varies with species) Transmission: sporolated oocysts ingested, invade cell become trophzoite. Grows into meront asexual repro (merogony) merozoites nd Burst out to infect other cells (2 generation). Last generation micro & macrogametocyte (gametogony) Sexual repro. zygote oocyst (w/in thick wall) Cell bursts passed in feces sporolates (right conditions) Diagnosis: Morphology: fecal float, Hx & clinical signs, lesions at necropsy. oocyst round, unsporolated is single celled (A), sporolated has 2 sporocysts (B).

Pathogenesis: Variable (host and parasite dependent), dose dependent, malabsorption, villus atrophy, crypt hyperplasia, hemorrhage. Control: Supportive care, environ. management, prophylactic drugs.

B A

Toxoplasma gondii (B)

Life cycle: indirect, any warm blooded mammal (intermediate) Host: epithelial cells of small intestine of felids Transmission: Host ingests bradyzoite (tissue cyst) or sporolated oocyst. excyst merogony in epithelial cells merozoites invade other cells gametocytes fuse into oocyst (zygote w/ capsule) into feces sporolate (viable 12-18 mths). PPP: 3-10 days (bradyzoite), >18 days (oocyst) Diagnosis: Morphology: Centrifugal fecal float (sugar or ZnSO4), serology (humans), ELISA. oocyst small round 10-12 m (A = Isospora sp.)

Pathogenesis: Variable. No signs (intestinal phase), clinical signs to death (extra-intestinal phase). Zoonotic potential: flu-like symptoms to severe disease (immunocomp.) Control: No hunting, no raw meat, drugs to reduce shedding.

Neospora caninum
Life cycle: indirect, any warm blooded mammal (intermediate) Host: small intestine of canids Transmission: Congenital predominant route. Ingestion of cysts oocyst and tissue cysts (as in Toxoplasma) Diagnosis: Morphology: fecal float (rare because sporadic), gross lesions, immunohistochemistry, ELISA. oocyst small round 10-12 m

Pathogenesis: focal areas of necrosis (tachyzoites), non-suppurative inflammation. Subclinical common (dog), abortion (cattle). Control: No hunting, no raw meat, drugs to reduce shedding, treat all littermates. Cattle cull abortive cows, protect feed and water, no dogs eating fetuses etc.

Sarcocystis spp.
Life cycle: indirect, prey animal (intermediate) Host: goblet cells of small intestine of canids and felids Transmission: Asexual stages in intermediate host, sexual in definitive host. oocysts sporolate in lamina propria, pass in feces. Ingested by intermediate vascular endothelium (merogony) myocytes invaded by merozoites transform into metrocytes bradyzoites. PPP: 75 days (for sarcocyst to be infectious to definitive host) Diagnosis: Morphology: Clinical signs, histology (sarcocysts), fecal float (definitive host) sporocyst small, ellipsoid, 7-22 m, thin wall (A), 4 sporozoites (B), residual bodies (C).

Pathogenesis: Most pathogenic to intermediate only. Variable disease Control: no fecal contamination, no raw meat (definitive), anticoccidials (intermediate).

Trichostrongyle type egg

Life cycle: direct, Host: small intestine, abomasums, gastri glands of ruminants Transmission: Eggs shed in feces develop into L3 in environment (retain sheath) ingested. PPP: varies w/ species and host Genuses: Cooperia spp., Haemonchus spp., Ostertagia spp., Trichostrongylus spp. Diagnosis: Morphology: fecal float. thin smooth shell light brown segmented cluster of cells. 50 x 80 m

Pathogenesis: anemia (Haemonchus), green diarrhea, anorexia, weight loss. Control: Strategic deworming, pasture management.

Nematodirus spp.
Life cycle: direct, L3 infective. Host: Ruminants Transmission: Ingestion L3 larvated egg. Hypobiosis resistant to desiccation (overwinter) PPP: 14-21 days Diagnosis: fecal float, clinical signs, herd flock history. Morphology: Thin smooth shell w/ thickened ends, ellipsoidal. Segmented brown nucleus (2-8 cells), wide clear area around. 200 x 95 m (larger than trichostrongyles) Pathogenesis: Mixed. Diarrhea, anorexia, poor hair coat, etc. Control: Strategic deworming, pasture management.

Monezia spp. (tapeworm)

Life cycle: indirect, orbatid mite (intermediate) Host: small intestine of ruminants Transmission: Ingestion of mite PPP: 28-42 days Diagnosis: fecal float (eggs), segments in feces, trailing from anus. Morphology: bicyle seat (M. expansa [both images]), square (M. benedeni) Embryo w/ hooks and pyriform apparatus. 56-75 m Pathogenesis: usually nonpath., ill thrift in young lambs w/ heavy infections Zoonotic potential: none Control: cestocides (not economically worth it)

Dictyocaulus viviparous / filarial (lungworm)

Life cycle: direct Host: bronchi of ruminants Transmission: L1 hatches from egg in lungs or intestines, passes in feces. Ingest L3 while grazing migrate to alveolar space via lymph/blood PPP: 4-5 weeks Diagnosis: Morphology: Baermann technique (L1 in feces), nasal secretions, adult worms in bronchi. tail straight, pointed or blunted intestinal granules.

Pathogenesis: sheep well tolerated to bronchitis or secondary infections. cattle significant pathogen in young, atelectasis, emphysema Control: Anthelmintics

Strongyloides papillosus
Life cycle: two cycles homogonic and heterogonic (L3 infective) Host: small intestines of ruminants Transmission: Homogonic occurs in host, autoinfection or eggs passed in feces and ingested by new host. Tracheal and somatic migration of L3. Heterogonic in environment, eggs develop into male and female. female produces larvated eggs. Routes transmammory, skin penetration, ingestion Diagnosis: Morphology: fecal float (larvated eggs in feces), Baermann technique (larva in feces) smooth thin membrane, ellipsoidal Colorless fully developed larva inside

Pathogenesis: subclinical, foot rot w/ skin penetration Control: rarely needed, anthelmintics

Cryptosporidium spp.
Life cycle: direct, immediately infective (sporolated) Host: microvilli of epithelial cells (GI & resp.) of ruminants (C. bovis), pigs (C. suis), dogs/cats/cattle/horses/humans (C. parvum) Transmission: sporozoites merontsmerozoitesgamontsoocysts. thick walled oocysts passed in feces, ingested by new host. thin walled oocysts autoinfection cycle (same host). PPP: 4-6 days Diagnosis: Histopathology (microvilli), fecal float w/ sugar (eggs in feces) Morphology: smooth, round, small 4-8 m., colorless to pinkish hue granular nuclei. Staining to differentiate from yeast. Pathogenesis: Cryptosporidiosis villous atrophy/fusion, malabsorptive diarrhea. Zoonotic potential: Cryptosporidiosis Control: Sanitation, good management, no treatment available

Eimeria spp.
Life cycle: direct (often mixed infections) Host: intestinal epithelial cell of host (varies with species) (not in dogs/cats) Transmission: sporolated oocysts ingested, invade cell become trophzoite. Grows into meront asexual repro (merogony) merozoites nd Burst out to infect other cells (2 generation). Last generation micro & macrogametocyte (gametogony) Sexual repro. zygote oocyst (w/in thick wall) Cell bursts passed in feces sporolates (right conditions) Diagnosis: Morphology: fecal float, Hx & clinical signs, lesions at necropsy. oocyst round, unsporolated is single celled, sporolated has 4 sporocysts. Micropyle cap may be visible (operculum)

Pathogenesis: Variable (host and parasite dependent), dose dependent, Summer/winter/nervous coccidiosis Control: Supportive care, environ. management, prophylactic drugs.

Strongyle type egg

Life cycle: direct, Host: cecum and large colon of equids Transmission: Eggs shed in feces develop into L3 in environment (retain sheath) ingested. PPP: varies w/ species and host Genuses: Small strongyles Cyathostomum sp., Petrovinema sp. Large strongyles Strongylus vulgaris, S. edentatus Diagnosis: Morphology: fecal float, clinical signs, deworming history. thin smooth shell, ellipsoidal light brown segmented cluster of cells. 60-120 x 35-60 m

Pathogenesis: Larval Cyathostominosis, L4 emergence causes inflammation Control: Strategic deworming (timing), pasture management, choice of anthelmintics.

Parascaris equorum
Life cycle: direct, L3 infective stage Host: small intestine of equids Transmission: Ingestion of L3 in egg tracheal migration. Viable in soil months to years. PPP: 72-110 days Diagnosis: fecal float. Morphology: thick pitted shell wall, subspherical single or binucleate granular nucleus Protein coat may or may not be present (dark brown) 90-100 m Pathogenesis: foals susceptible (pot belly, enteritis) age immunity after 6 months. Coughing from larva migration through lungs. Control: Sanitation, antihelmintics 6 week intervals (6 weeks 6 months).

Strongyloides westeri (threadworm)

Life cycle: two cycles homogonic and heterogonic (L3 infective) Host: small intestines of equids Transmission: Homogonic occurs in host, autoinfection or eggs passed in feces and ingested by new host. Tracheal and somatic migration of L3. Heterogonic in environment, eggs develop into male and female. female produces larvated eggs. Routes transmammory, skin penetration, ingestion Diagnosis: Morphology: fecal float (larvated eggs in feces), Baermann technique (larva in feces) smooth thin membrane, ellipsoidal Colorless fully developed larva inside

Pathogenesis: common in foals mild diarrhea. Immunity after 15-35 weeks. Control: rarely needed, anthelmintics

Oxyuris equi (pinworm)

Life cycle: direct Host: cecum and large colon of equids Transmission: Female deposits eggs on perineal area, infective in 3-5 days. Ingested, hatch in gut, mature in mucosal crypts of large intestine. PPP: 4-6 months Diagnosis: Morphology: Acetate tape technique, clinical signs (damaged tail), Hx, fecal float usually negative (eggs not in feces). Operculate, thick, smooth shell. One side flattened. Embryonated or not. 90 x 42 m

Pathogenesis: Stabled animal problem. Anal pruritis (itchy) Control: Sanitation, anthelmintics effective.

Anoplocephala spp.
Life cycle: indirect, orbatid mite (intermediate) Host: Large and small intestine of equids Transmission: Adulteggscysticercoid ingesting free living pasture mites. A. perfoliata common, A. magna - rare PPP: 28-42 days Diagnosis: Morphology: fecal float (although eggs commonly not found), adults at necropsy. Thick grayish multilayered shell. Hooked embryo amid pyriform apparatus. D shaped 90 x 42 m

Pathogenesis: mucosal erosions, spasmodic colic, mild enteritis. Control: Sanitation, Cestocides.

Eimeria leukarti
Life cycle: direct Host: intestinal epithelial cell of equids Transmission: sporolated oocysts ingested, invade cell become trophzoite. Grows into meront asexual repro (merogony) merozoites nd Burst out to infect other cells (2 generation). Last generation micro & macrogametocyte (gametogony) Sexual repro. zygote oocyst (w/in thick wall) Cell bursts passed in feces sporolates (right conditions) Diagnosis: Morphology: fecal float, sedimentation technique, Hx & clinical signs. oocyst tear drop shaped, thick brown shell, granular nucleus. Micropyle opening at one end (B).

Pathogenesis: Rare diarrhea and weight loss Control: Supportive care, environ. management, prophylactic drugs.

Strongyle/Trichostrongyle type eggs

Life cycle: direct, Host: large intestine (Oesaphogostomum dentatum) and stomach (Hyostrongylus rubidus) of pigs Transmission: L3 Ingested encysts in intestinal wall. PPP: 41 days Diagnosis: Morphology: fecal float, caseated nodular lesions (O. dentatum). Blood red worms in stomach (H. rubidus). thin smooth shell, ellipsoidal light brown segmented cluster of cells. 60-120 x 35-60 m

Pathogenesis: O. dentatum Serious (breeding stock), enteritis, diarrhea. H. rubidus suck blood, anemia, death loss (by gastric ulcers). Control: Sanitation, pasture management, anthelmintics.

Ascaris suum
Life cycle: direct, L3 infective stage Host: small intestine of pigs Transmission: Ingestion of L3 in egg tracheal migration. Viable in soil months to years. PPP: 60-620 days Diagnosis: fecal float, milk spots on necropsy. Morphology: thick pitted shell wall, subspherical, granular nucleus fills ova. Protein coat may or may not be present (dark brown). 88-90 x 66-68 m Pathogenesis: Young pigs milk spot liver, thumps or heaves in lungs (predispose for secondary infection), intestinal obstruction. Zoonotic potential: Ascariasis Control: Sanitation, antihelmintics 2 weeks prior to farrowing & piglets at 5-6weeks/repeat in 30 days.

Coccidial oocyst
Life cycle: direct Host: intestinal epithelial cell of pigs (Isospora spp. or Eimeria spp.) Transmission: sporolated oocysts ingested, invade cell become trophzoite. Grows into meront asexual repro (merogony) merozoites nd Burst out to infect other cells (2 generation). Last generation micro & macrogametocyte (gametogony) Sexual repro. zygote oocyst (w/in thick wall) Cell bursts passed in feces sporolates (right conditions) Diagnosis: Morphology: fecal float, Hx & clinical signs. oocyst round, smooth refractile shell. pale granular nuclei.

Pathogenesis: Severe in nursing piglets. Sour milk diarrhea. Control: Sanitation, supportive care, environ. management, drugs ineffective.

Balantidium coli (ciliate)

Life cycle: direct Host: G.I. tract of pigs Transmission: Trophozoite binary fission (asexual) or conjugation (sexual) reproduction in large intestine. Encyst in response to dehydrated feces. shed in feces. Ubiquitous in pigs. Diagnosis: Trophs wet mount. Cysts wet mount, fixed smear, or fecal float Morphology: Troph (A) Thick ovoid ciliated shell, central macronucleus and micronucleus, funnel shaped cytosome (mouth). Cyst (B) spherical, thick, refractile shell, no cilia. Pathogenesis: most asymptomatic, secondary infection from lesions. mild colitis, occasional severe dysentery. Zoonotic potential: Amoebic dysentery. Control: Pigs Sanitation, hygiene, no drugs. Humans tetracyclines

Leucocytozoon spp.
Life cycle: indirect, intermediate vector black fly (Simulium spp.) Host: various tissues of wild and domestic birds Transmission: Sporozoite transmitted when fly feeds. enter cellsschizogonymerozoites emergeinfect circulatory cells and endotheliumdevelop into gametocytes and megaloschizontsmerozoites from megaloschizont releaseddevelop into elongate gametocytes (image) ingested by flyfusion and sporogony in gut & salivary gland of fly. Diagnosis: gametocyte in blood smear, schizonts in tissue, clinical signs, Hx. Morphology: elongate, w/in leukocyte, cytoplasmic horns. Pathogenesis: anemia, leukocytosis, splenomegaly, hepatomegaly, obstruction. Young most susceptible death w/in 24 hrs. Control: Control fly, separate domestic and wild birds, preventative medicine.

Babesia spp.
Life cycle: indirect, intermediate vector tick (host/tick specific [see notes for details]) Host: bovine, equine, canine, feline, vole/mouse (human) Transmission: transmitted as tick feeds. Infect erythrocytes. Merogony & gametogony I occur in vertebrate. Gametogony II & sporogony in tick. Diagnosis: blood smear (trophs in erythrocytes), use capillary blood ( #s), Hx, clinical signs. Morphology: piriform shaped merozoite/trophozoites within the erythrocytes. Wright-Geimsa stain. Pathogenesis: rare disease hemolytic anemia, capillary obstruction, anoxia, organ failure. Control: tick control, diaminazene IM or phenamide SC.

Trypanosoma spp.
Life cycle: indirect, intermediate vector tsetse fly or triatomine bugs Host: dogs, humans Transmission: transmitted in feces of arthropod. Trypomastigotes enter body through bite or scratch. Enter blood, then organs and muscle cellsamastigotebinary fissionrelease from cellback into trypomastigoteingested by bug with blood mealepimastigote in gut of bug. Diagnosis: blood smear or lymph (w/in 5 weeks), culture, IFA, xenodiagnosis. Morphology: slender, pointed posterior. kinetoplast at posterior (A), flagellum at anterior (B), narrow undulating membrane (C), central nucleus (D). Pathogenesis: cell distruction, necrosis. Chronic or acute disease. Control: control arthropod, avoid reservoir animals, drugs kill only extracellular form.