CLOSTRIDIAL DISEASES

Clostridial Diseases
Bacterium
Clostridium Difficile
Clostridium Haemolyticum
Clostridium Novyi type B
Clostridium Perfringens type B & C
Clostridium Perfringens type D
Clostridium Chauvoei
Clostridium Botulinum A – G
Clostridium Tetani
Clostridium Piliforme
Clostridium Septicum
Disease
Enteritis in piglets
Bacillary hemoglobinuria (Red water disease)
- Infectious necrotic hepatitis (Black disease) in cattle
- Big head (swollen head) in rams
Enterotoxemia
- Lamb dysentery (type B).
- Calf enterotoxemia (type B & C).
- Necrotic enteritis in pigs (type C).
- Foal enterotoxemia (type B).
- Acute enterotoxemia “Struck” in sheep (type C).
- Goat enterotoxemia (type C).
Pulpy Kidney Disease or Overeating Disease
(Type D enterotoxemia)
Blackleg disease
Botulism (Lamziekte) lame sickness
- Shaker Foal Disease (type B toxin).
- Equine Dysautonomia (type B toxin).
- Limberneck in birds (type C toxin).
Tetanus (Lock Jaw)
Tyzzer’s disease (Dead Foal Disease)
[Enterohepatic disease]
Edema disease

1- Enteritis in piglets
Most common cause of diarrhea in neonatal swine (1 – 7 days old).
 Causative agent
Clostridium Difficile [anaerobic, gram positive, spore forming rod].
 Pathogenesis
C. Difficile produces “large clostridial toxins” A and B toxin A is enterotoxin that causes
fluid secretion into gut lumen, and toxin B is a cytotoxin.
 Clinical presentation
- Diarrhea (may not be present in all pigs affected).
- Dyspnea.
- Abdominal distention.
- Scrotal edema.
 Necropsy
- Mesocolon edema (edema of the ascending colon) [the colon is primarily affected with
multifocal exudation of mucous and fibrin plus submucosal edema].
- Pasty to watery colonic contents (pasty watery yellowish feces).
- Ascites and hydrothorax.
 Treatment

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- Antibacterials (Erythromycin, Tetracycline and Tylosin) may be useful for treatment of
suckling piglets.

2- Bacillary Hemoglobinuria (Red water disease)

- Acute, infectious toxemic disease affects primarily cattle but has also been found in sheep.
- The name “Red water disease” comes from the classic red color of the urine in the affected
animals due to the presence of hemoglobin from lysed RBCs.
 Causative agent
Clostridium Haemolyticum
 Pathogenesis
- It is found naturally in the GIT of cattle and survives for long in soil cattle ingest the
organism and latent spores settle in the liver.
- Any cause of localized hepatic necrosis [like migration of liver fluke (Fasciola hepatica),
accidental liver puncture, liver biopsy and rarely by high nitrate content of the diet]
Can become a site of spore germination.
- When condition for anaerobiosis are favorable, the spores germinate and the resulting
vegetative cells multiply and produce β toxin (Phospholipase C) intravascular hemolysis
resulting in hemolytic anemia and hemoglobinuria.
 Clinical presentation
- Cattle may be found dead without previous signs.
- Sudden onset of severe depression, fever, abdominal pain, dyspnea, dysentery
hemoglobinuria and dark feces.
- Anemia, jaundice are present in varying degrees.
- Edema of brisket may occur.
- Mortality in untreated animals is about 95%.
 Necropsy
- Dehydration, anemia and sometimes S/C edema.
- Bloody fluid in abdominal and thoracic cavities.
- Lungs are not affected and trachea contains bloody froth with hemorrhages in the mucosa.
- Large and small intestine contain free or clotted blood.
- The bladder contains purplish red urine.
 Treatment
- Early treatment with Penicillin or Tetracyclines at high doses is essential.
- Blood transfusion and fluid therapy.
 Vaccination
- Clostridium Haemolyticum inactivated bacterin prepared from whole culturs confers
immunity for about 6 months.
- It is recommended to vaccinate every 6 months where constant exposure is likely.

3- Infectious Necrotic Hepatitis (Black disease)

- Acute toxemia of sheep that is sometimes seen in cattle and rare in pigs and horses.

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 Clostridial Diseases
 Causative agent
Clostridium Novyi type B (The bacterium is soilborne and present in the intestine and liver of
herbivores).
 Pathogenesis
- Fecal contamination of pasture by carrier animals is the most important source of infection.
- The organism multiplies in areas of liver necrosis caused by migration of liver flukes and
produces a powerful necrotizing toxin (α toxin).
- The lethal and necrotizing toxin damages hepatic parenchyma, thereby permitting the
bacteria to multiply and produce a lethal amount of toxin.
 Clinical presentation
- Sudden death without previous signs.
- Affected animals often are 2 – 4 years old.
- The disease is most prevalent in well-nourished adult sheep and seems to be eliminated to
animals infected with liver flukes most cases occur in the summer and early fall when
liver fluke infection is at its peak.
 Necropsy
- Greyish, yellow necrotic foci in the liver along migratory tracks of the liver flukes.
- Enlarged pericardial sac filled with straw colored fluid and excess fluid in peritoneal and
thoracic cavity.
- Extensive rupture of S/C capillaries adjacent skin turn to black (Black disease).
 Control
Incidence may be lowered by reducing the numbers of Lymnea spp. snails, the intermediate
host of the liver fluke or by otherwise reducing the fluke infection of sheep.

4- Type B and C Enterotoxemia

Infection with C. Perfringens Type B and C causes severe enteritis, dysentery, toxemia and
high mortality in young lambs, calves, pigs and foals.
 Causative agent
Clostridium Perfringens type B and C.
 Pathogenesis
C.Perfringens type B and C produce highly necrotizing and lethal β toxin responsible for
severe intestinal damage.
 Resulted diseases
- Lamb dysentery (type B).
- Calf enterotoxemia (type B & C).
- Necrotic enteritis in pigs (type C).
- Foal enterotoxemia (type B).
- Acute enterotoxemia “Struck” in sheep (type C).
- Goat enterotoxemia (type C) in adult goats.
 Clinical presentation

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- Lamb dysentery
 May die before clinical signs are seen, some lambs stop nursing, become listless and
remain recumbent.
 A fetid, blood-tinged diarrhea and death occurs within a few days.
- Calf Enterotoxemia
 Acute diarrhea, dysentery, abdominal pain, convulsions and opisthotonus.
 Death may occur in a few hours.
- Necrotic Enteritis in pigs
 Diarrhea, dysentery, reddening of the anus, and a high fatality rate (death within 12
hours).
- Foals Enterotoxemia
 Acute dysentery, toxemia and death.
- Struck in adult sheep
 Death without premonitory signs.
 Necropsy
Hemorrhagic enteritis with ulceration of the mucosa is the major lesion in all species.
 Treatment
Treatment is usually ineffective because of the severity of the disease but if attempted, it
includes specific hyperimmune sera and oral antibiotics.
 Vaccination
The disease is best controlled by vaccination of the pregnant dam during the last third of
pregnancy, initially 2 vaccination 1 month apart and annually thereafter.

5- Type D Enterotoxemia (Pulpy Kidney disease) or

(Overeating disease)
- It is the classic endotoxemia of sheep and is seen less frequently in goats and rarely in
cattle.
- It affects all ages but it is most common in lambs either ≤ 2 weeks old or weaned (4 – 10
weeks of age) in feedlots and on a high carbohydrate diet or less often on lush green
pastures.
 Causative agent
Clostridium Perfringens type D.
 Pathogenesis (predisposing factors are essential)
- Ingestion of excessive amounts of feed or milk in the very young lamb the disease is
restricted to ewes with single lambs.
- In the feedlot, the disease usually is seen in lambs switched rapidly to high grain diets.
- Under natural conditions, the ingestion of feed contaminated by infected feces introduces
the organism into the alimentary tract but the disease does not occur unless other factors
intercede.

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- As starch intake increases suitable medium for growth of C. Perfringens D, producing
Epsilon toxin.
- The epsilon toxin causes vascular damage (capillary damage in kidney, lungs and
particularly capillaries of brain).
 Clinical presentation
- Lambs
 Sudden death in the best-conditioned lambs (excitement, incoordination and convulsions
occur before death).
 Common neurologic signs include circling, opisthotonus and head pressing.
 Diarrhea may or may not develop (green or pasty diarrhea) and frothy salivation.
- Adult sheep
 Often lag behind the rest of the flock and show nervous signs as (weakness,
incoordination, and convulsions) and death within 24 hours.
- Calves
 Calves that are not found dead show mania, convulsions, blindness and death within few
hours.
- Goat
 Watery diarrhea with or without blood to sudden death.
N.B.
 Glucosuria is a considered a hallmark of type D enterotoxemia in sheep and cattle.
 Necropsy
- Lambs
 Patchy congestion and hyperemic areas of the abomasal and intestinal mucosa.
 Clear straw colored fluid in the pericardial sac.
 Rapid postmortem autolysis of kidneys always found in affected young lambs and
seldom found in affected goat or cattle [the kidney has a mottled appearance, soft
consistency and the cortex is jelly-like or semi-fluid Pulpy kidney].
 Edema and leukoencephalomalacia detected microscopically in the basal ganglia,
cerebellum and thalamus of lambs (also known as focal symmetrical encephalomalacia).
- In Older animals
 Hemorrhagic areas on the myocardium, petechiae and ecchymoses of the abdominal and
serosa of the intestines.
 Treatment
Treatment is ineffective due to rapid progression of the disease.

 Control
- Breeding ewes should be given two injections of type D toxoid in their first year, a booster
injection 4 – 6 weeks before lambing and on each year thereafter.

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- Enterotoxemia in feedlot lambs can be controlled by reducing the amount of concentrate in
diet.

6- Blackleg disease
Acute, febrile, highly fatal disease of cattle and sheep and characterized by emphysematous
swelling commonly affecting heavy muscles (Clostridial myositis).
 Causative agent
Clostridium Chauvoei
 Pathogenesis
- C. Chauvoei spores remain viable in the soil and are purported to be a source of infection.
- Bacterial spores are ingested in contaminated feed or soil, pass through the wall of the GIT
and gain access to the blood stream, are deposited in muscles and other tissues(spleen,
liver and alimentary tract) and may remain dormant indefinitely.
- In cattle, blackleg infection is endogenous. Lesions develop without any history of wounds,
although bruising or excessive exercise may precipitate disease in some cases.
- In sheep, the disease is almost always the result of a wound infection and often follows
some form of injury such as shearing cuts, docking, crutching or castration.
- The injury reduces blood flow to the area, thereby reducing the supply of oxygen, the
spores germinate and multiply. As they grow, the bacteria produce toxin which destroy
surrounding tissues.
- The toxins are absorbed into animal’s blood stream which makes the animal acutely
diseased and cause rapid death.
- Most cases are seen in cattle 6 – 24 months old, but thrifty calves as young as 6 weeks and
cattle as old as 10 – 12 years may be affected.
 Clinical presentation
- Onset is sudden and a few cattle may be found dead without premonitory signs.
- Acute severe lameness with swelling of muscles.
- Characteristic edematous and crepitant swelling develop in the hip, shoulder, chest, back,
neck:
 At first, the swelling is small,, hot and painful.
 As the disease rapidly progresses, the swelling enlarge, there is a crepitation on palpation
and the skin becomes cold and insensitive with decreased blood supply to affected areas.
- Death occurs within 12 – 48 hours.
- In some cattle, the lesions are restricted to the myocardium and the diaphragm.
 Necropsy
- The rapid accumulation of gas under the skin and the body cavity gives the carcass a
bloated appearance.
- There may be a frothy, blood discharge from the mouth, nostrils and anus.
- If the skin over the affected area is removed excess bubbly blood stained fluid can
be seen and the muscle immediately will be dark in color.

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 Clostridial Diseases
 Control
- A multivalent vaccine containing C. Chauvoei, C. Septicum and C. Novyi is safe and reliable
for cattle and sheep.
- Calves 3 – 6 months of age should be vaccinated twice 4 weeks apart followed by annual
boosters.
- Naïve ewes should be vaccinated 1 month before lambing and then with yearly boosters.
- In outbreaks, prophylactic Penicillin and antiserum treatment are recommended.

7- Botulism (Lamziekte) [Lamziekte = lame sickness]

Botulism is a rapidly fatal motor paralysis caused by ingestion of the toxin produced by
Clostridium botulinum types A – G.
 Causative agent
Clostridium Botulinum A – G.
 Pathogenesis
- Botulism results from ingestion of toxins of C. Botulinum types A – G in food.
- The botulinum toxin is a zinc-binding metalloprotease that cleaves specific proteins in
synaptic vesicle. Motor neuron surface receptors vary for the different botulinum toxins,
explaining some of the species differences in susceptibility to the different toxins.
- Toxicoinfection Botulism is the name given to the disease in which C. Botulinum grows
in tissues of a living animal and produce toxins there.
- Gastric ulcers foci of necrosis in the liver, abscesses in the naval and lungs, wounds of the
skin and muscle, and necrotic lesions of the GIT are predisposing sites for development of
toxicoinfection botulism.
 Resulted diseases
- Shaker foal disease in foals type B toxin.
- Equine grass sickness (Equine Dysautonomia) in adult horses Type B toxin.
- Limberneck in birds Type C toxin.
 Clinical presentation and necropsy
- The signs of Botulism are caused by flaccid muscle paralysis and include progressive motor
paralysis, disturbed vision, difficulty in chewing and swallowing and generalized progressive
paresis the toxin prevents release of Acetylcholine at motor endplates.
- Shaker foal syndrome [foals are usually < 4 weeks old]
 Necropsy of Shaker foal disease
 They may be found dead without premonitory signs; most often they exhibit signs of
progressive symmetric motor paralysis.
 Silted gait, muscular tremors and inability to stand for 4 – 5 mins.
 Other clinical signs include dysphagia, constipation, mydriasis and frequent urination.
 As the disease progresses, dyspnea with extension of head and neck, tachycardia and
respiratory arrest.
 Death (24 – 72 hours after onset of clinical signs) due top respiratory failure.

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 Necropsy of Shaker foal disease
- Pulmonary edema and congestion and excessive pericardial fluid which contains free-floating
strands of fibrin.
- Limberneck [Western Duck sickness] (Botulism in birds)
 Pathogenesis of Limberneck
Invertebrates especially fly larvae (maggots) feed on carcasses that have died from
Botulism and thus consume botulinum toxin they are resistant to toxin and
concentrate them in their bodies outbreaks in waterfowl and other water birds result
from consumption of toxin-laden invertebrates.

 Clinical presentation of Limberneck

- Leg weakness and paresis that progress to flaccid paralysis of the legs, wings, eyelids and
neck (“Limberneck” the common name of Botulism in birds comes from the neck paralysis).
- Affected birds may have their legs extended behind them because they are unable to pull
them into a normal sitting position.
- Severely affected birds are in ventral recumbency on the floor with their eyes partially or
completely closed and neck overstretched.
- Waterfowl weakness, reluctant to fly, stumbling gaits and eventually paralysis. They
can drown in water as they cannot keep their heads above the water.

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 Necropsy of Limberneck
No lesions in affected birds except maggots or other invertebrates may be found in the crop.
- Equine Dysautonomia [Grass Sickness]
 Marked reduction of GIT motility due to widespread degeneration within the autonomic
nervous system.
 Incidence at any age but highest in horses (2 – 7 years old) and mainly in spring.
 The exact etiology is unknown but the causal agent is thought to be associated with
grazing (C. Botulinum toxin may be involved).
 Clinical presentation of Grass Sickness
- Fever, tachycardia, ileus and colic.
- Patchy sweating and fine muscular fasciculations are seen over the shoulder and flanks and
penile prolapse may develop.
- Horses adapt a “tucked up” stance.
- Ptosis with droopy eyelashes is prominent.
- Dysphagia and esophageal dysfunction which cause drooling, difficulty passing a stomach
tube, nasal reflux of gastric contents
- On rectal palpation, mucosa is dry, hard and scant feces.
- Distended loops of small intestines and impaction of large colon.
- Cachexia and Rhinitis Sicca (dry nose) in chronic cases.

 Necropsy of Grass Sickness

- Stomach and small intestines with fluid, impaction of large intestines.

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- Neuronal degeneration of pre- and postganglionic sympathetic and parasympathetic neurons
is characteristic.
 Treatment and Control
- Shaker Foal Disease
 Early administration of Antitoxin Type B specific or polyvalent to foals before recumbency is
successful. Prognosis is poor in recumbent animals.
- Equine Dysautonomia [Grass Sickness]
 Mildly affected (chronic) cases can survive with dedicated nursing care, acute and subacute
cases have not survived and should be euthanized.
- Limberneck
 Affected birds may recover without treatment.
 Antibiotics effective against Clostridia may be useful if the disease is toxicoinfection.
 Fly control may reduce the risk of toxic maggots in the environment.
 Active immunization with Inactivated Type C bacterin –toxoid has been successful in
pheasant operations but is not cost-effective or feasible in commercial chickens and wild
ducks.

8- Tetanus
Tetanus toxemia is caused by specific neurotoxin produced by C. Tetani in necrotic tissue.
 Causative agent
Clostridium Tetani (anaerobe with terminal spherical spores).
 Pathogenesis
- Almost all mammals are susceptible, horses and lambs seen to be the most sensitive of all
species, birds are quite resistant.
- C. Tetani is introduced into the tissues through wounds, particularly deep wounds that
provide a suitable anaerobic environment.
- The spores of C. Tetani are unable to grow in normal tissue but the suitable conditions for
multiplication in necrotic tissues.
- The bacterium remains localized in necrotic tissues at the original site of infection and
multiply bacterial cell undergo autolysis potent neurotoxin is released
the neurotoxin a zinc-binding protease that cleaves Synaptobrevin, a vesicle-associated
membrane protein toxin absorbed by motor nerve travels retrograde up the
nerve tract to the spinal cord where it causes Ascending Tetanus.
- The toxin causes spasmodic, tonic contractions of the voluntary muscles by interfering with
the release of inhibitory neurotransmitters from presynaptic nerve endings.
- If more toxin release carried off by the lymph to the blood stream CNS
(Descending Tetanus).
- The spasms may be severe enough to cause bone fracture.
- Spasms affecting larynx, diaphragm and intercostal muscles respiratory failure.
- Involvement of autonomic nervous system arrythmia, tachycardia and hypertension.

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 Clinical presentation
- First, localized stiffness involving the masseter muscles, muscles of neck and the hind
limbs.
- 1 day later, general stiffness, tonic spasms and hyperesthesia.
- The reflexes increase in intensity and the animal is easily excited into more virulent,
general spasms by sudden movement or noise.
- Spasms of head muscles cause difficulty in prehension and mastication of food “Lock Jaw”.
- Horses
 Erection of ears, stiff and extended tail, anterior nares dilated and prolapse of third eyelid.
 Spasms of the neck and back muscles cause extension of head and neck.
 Stiffness of leg muscles cause “Sawhorse” stance.

 Sweating is common.
 General spasms disturb circulation and respiration increased heart rate, rapid
breathing and congestion of m.m.
- Sheep, goat and pigs
 Fall to ground and opisthotonus when startled.
 Treatment
- In early stage, Curariform agents, tranquilizers, barbiturates in conjunction with Tetanus
antitoxin have been effective in treatment of horses.
- Injection of tetanus antitoxin into the subarachnoid space through the cisterna magna.
- Draining and cleaning the wounds and administration of Penicillin.
- The horse should be placed in quiet, darkened box stall.
 Vaccination
- Active immunization can be accomplished with Tetanus Toxoid.
- If a dangerous wound occurs after immunization, another injection of toxoid to increase the
circulating antibody should be given.
9- Tyzzer’s disease (Dead Foal Disease)
- Is an enterohepatic syndrome of wide range of animals.

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- It is highly fatal disease of young foals.
- The disease primarily affects young well-nourished animals especially those fed high-protein
diets during period of stress.
 Causative agent
Clostridium Piliforme (motile, spore-forming rod-shaped flagellated intracellular bacterium).
 Predisposing factors
- 2 factors increase Tyzzer’s disease incidence:
• Immunosuppression immunosuppressive drugs or sulphonamide.
 Stress shipping, overcrowding and poor sanitation.
 Pathogenesis
- The feces of infected and carrier animals are the primary source of spores that contaminate
the environment.
- The primary site of infection is the lower intestinal tract with subsequent dissemination via
the blood or lymphatics to the liver and heart.
- The disease in foals occurs most often between 1 – 6 weeks of age with most cases
occurring between 1 – 2 weeks of age.
- The disease is more common during spring when nursing mares are exposed to lush, high-
protein pastures overgrowth of C. Piliforme in gut of nursing mares feces of
dams contain massive numbers of the bacterium foals consume the feces of their
dams soon after birth as a mechanism to establish their normal intestinal flora
immature gut is more permeable to pathogens like C. Piliforme [older foals up to 6 weeks
old and adults are more resistant to disease because gut becomes more mature and
immune factors may be involved).
- The disease in young foals primary affects liver massive multifocal necrosis and
hepatitis (death from acute liver failure).
 Clinical presentation
- Affects apparently healthy, fast-growing foals and most foals are found in a coma or dead.
- Signs if seen (short duration from few hours – 2 days) are depression, pyrexia, jaundice,
diarrhea and recumbency.
- Terminally, convulsions and death.
 Necropsy
- Lesions are seen in liver, GIT and myocardium:
- Liver
 White, grey or yellowish foci of necrosis in the liver.
 Hepatomegaly, edema and hyperplasia of hepatic lymph nodes.
- GIT
 Diffuse “Paint brush” hemorrhage seen on serosa of cecum.
 Patchy areas of mucosal necrosis in cecum and colon and edema of wall of cecum.
 Mesentric lymph nodes may be enlarged and edematous.
- Myocardium
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 White streaks in the myocardium especially near the apex
 Treatment
- The disease seems to be nearly 100% fatal in neonatal foals.
- Older foals that are less severely affected may survive.
- Animals affected have been treated with 50% dextrose, followed by 10% dextrose and
antibiotics.
- C. Piliforme is sensitive to Tetracycline, partially sensitive to Streptomycin, Erythromycin
and Penicillin.
 Control
- Reducing the nitrogen dietary compounds and reducing factors that cause stress and
immunosuppression.

10- Malignant Edema

- Malignant edema is an acute , generally fatal toxemia affecting all species and ages of
animals.
- It is marked by painful gangrenous swelling and severely toxic symptoms.
 Causative agent
Clostridium Septicum (found in soil and intestinal contents of animals).
 Pathogenesis
- Infection ordinarily occurs through contamination of wounds containing devitalized tissue,
soil or some other tissue debilitant.
- Potent local exotoxins cause excessive inflammation, resulting in severe edema, necrosis and
gangrene.
 Risk factors
- Include IM injections in horse, shearing and docking in sheep, traumatic parturation and
castration in cattle.
 Clinical presentation
- General signs as anorexia and high fever.
- Local lesions are soft swelling that pit on pressure and extend rapidly because of the
formation of large quantities of exudate that infiltrates S/C and IM CT of affected areas.
- Muscles in such areas are dark brown to black.
- Accumulation of gas in S/C tissue and along muscle fascias may be present or not.
- Extensive local sloughing of skin and tissue in progressive state.
- Malignant edema associated with lacerations of the vulva at parturition is characterized by
marked edema of vulva.

 Treatment
- High doses of parental Penicillin, Tetracyclines is indicated early in the disease.
 Control
- Multivalent vaccine (C .Septicum with C. Chauvoei) are used for immunization.

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- In endemic areas, animals should be vaccinated before they are castrated, dehorned or
docked.
- Calves should be vaccinated at 2 month of age.

11- Big Head (Swollen Head) Disease

- Acute, infectious disease characterized by a nongaseous, non-hemorrhagic, edematous
swelling of the head, neck, face of young rams.
 Causative agent
Clostridium Novyi
 Pathogenesis
- The infection is initiated in young rams by fighting or continual butting of one another.
- The bruise and buttered S/C tissues provide conditions suitable for growth of pathogenic
Clostridia.
 Clinical presentation
- Edematous swelling of head, face and neck of young rams.
 Treatment
- Broad-spectrum antibiotics or Penicillin.

Clostridial Vaccines
- A wide variety of vaccines is available. Singly or in combinations that consists of Bacterins,
Toxoids, or mixture of Bacterins and Toxoids.

- Single vaccination with most clostridial vaccines doesn’t provide adequate levels of
protection and must be followed by booster dose within 3 – 6 weeks.

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- Vaccination of young animals doesn’t yield adequate protective immunity until they are at
least 1 – 2 months age. Therefore, most vaccination strategies target the pregnant dam so
that maximal immunity is transferred to the neonate via colostrum.
- Most commercial vaccines are inactivated usually contain 2-, 4-, 7-, 8-way combinations of
clostridial organisms/toxoids.
- Tetanus is used as single vaccine in horse but used in combination (Tetanus toxoid plus C.
Perfringens types C and D) in sheep, goats and cattle.

- In cattle, a combination frequently used in feedlot is a 4-way vaccines (killed cultures of C.

chauvoei, C. Septicum, C. Novyi, C. Sordellii) to protect against Blackleg and Malignant
Edema.

- The clostridial vaccines often cause tissue reactions and swelling and should therefore be
administered to cattle in the neck and by the S/C rather than the IM route.

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