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65 Cards in this Set

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What are clostridial diseases often associated with in terms of disease?

What are clostridial diseases often associated with in terms of disease?

Sudden death.

What type of organism is the clostridial organisms implicated in disease and cattle? Name an exception?

Anaerobic, spore forming, toxin producing organism normally present in soil, faeces and intestinal contents.




Botulism being an exception which is production of toxin by the bacteria in the environment.

What is the general disease state produced by clostridum perfringens?

Enterotoxaemia.

What conditions lead to rapid multipication of C. perfringens and enterotoxaemia?
What conditions lead to rapid multipication of C. perfringens and enterotoxaemia?

Anaerobic conditions in the abomasum and small intestine are combined with large amounts of ferment-able carbohydrate.

What type of substrate does c perfringens prefer? When does disease usually occur with c perfringens?

What type of substrate does c perfringens prefer? When does disease usually occur with c perfringens?

Saccharolytic- sugars




Sudden diet change- overflow of undigested feed into the small intestine.




Also diseases causing gut stasis allow build up of toxin.




Severe GIT parasitism.

What toxin causes lamb dysentry?

What toxin causes lamb dysentry?

Beta and epsilon toxin of C perfringens type B.

What age of lambs are usually affected by lamb dysentry?

1-3 days commonly but can get disease from 1-3 weeks.




Usually the stronger single lambs.

Post mortem findings with lamb dysentry?

Dark red and distended loops of bowel.


Ulceration of intestinal mucosa.


Serous, blood stained peritoneal fluid.


Pale and friable liver.


Enlarge kidneys.

Dark red and distended loops of bowel.




Ulceration of intestinal mucosa.




Serous, blood stained peritoneal fluid.




Pale and friable liver.




Enlarge kidneys.

What is needed for a diagnosis of lamb dysentry?

1) Gram stained smears of the organisms.




2) Anaerobic culture from intestines.




3) Elisa for the epsilon toxins and beta.




4) PM findings.

Why do single lambs tend to get lamb dysentry?

They ingest large volumes of milk.




This overspills into the intestine.




Feeds clostridium.




They rapidly multiply and cause disease.

What is the aetiology of pulpy kidney?

What is the aetiology of pulpy kidney?

Epsilon toxin made by C. Perfringens type D.





What is pulpy kidney disease associated with in terms of management?

What is pulpy kidney disease associated with in terms of management?

Diet changes.

What age of sheep are most commonly effected by pulpy kidney?

What age of sheep are most commonly effected by pulpy kidney?

Well grown lambs between 4-10 weeks.




Fattening lambs between 6 months and 1 year.

Signs of pulpy kidney?

Signs of pulpy kidney?

Sudden death.




Occasionally seen alive with hyperaesthesia and ataxia, progressing to recumbency, opistotonuss, convulsions and death.




Signs associated with focal symmetrical encephalomalacia and diarrhoea seen in lambs who live longer.

What are other differentials for sudden death of lambs at pasture in late summer?

Systemic pasteurellosis.




Red gut.

How do we confirm a diagnosis of pulpy kidney?

History of sudden death in well grown unvaccinated lambs.




PM findings.




Glucose in the urine.




Positive elipson toxins ELISA.




Brain histopathology.

What are post mortem findings with pulpy kidney?

Excess pericardial fluid.




Endocardial haemorrhages.




Swollen viscera.




Congested friable liver.




Pale and swollen autolysed liver.

What causes struck? What type of disease does it cause?

Struck is caused by clostridium perfringens type C beta toxin.




Causes enteritis, peritonitis and sudden death.

How do we prevent enterotaxaemia?

How do we prevent enterotaxaemia?

Vaccination.




7+ 1 vaccine containing lamb dysentry.




Combined with good husbandry.




Good hygiene.




Adequate colostrum.




Careful introduction to a new plane of nutrition.

What is the protocol for vaccinating sheep for enterotoxaemias?

Initial course of two vaccines 4-6 weeks apart when they enter breeding flock.




Annual booster 6 weeks prior to lambing which provides passive protection of lambs up to 16 weeks.




Lambs born to vaccinated ewes should recieve a sensitiser dose at 8-12 weeks then second booster at 4 weeks later.

How do we manage animals in the face of an outbreak of enterotoxaemia?

Vaccination.




Restrict feeding.

What is the history associated with clostridium sordelli ?

What is the history associated with clostridium sordelli ?

Sudden death in unvaccinated and vaccinated ewes.




Usually effects 3-10 week intensively creep fed lambs.




Housing and creep feeding.

What are signs of clostridium sordelli in live sheep?

What are signs of clostridium sordelli in live sheep?

Depressed and bloated.

How can we come to a diagnosis of clostridium sordelli?

How can we come to a diagnosis of clostridium sordelli?

History of sudden death.




Gross pathology findings:


Abdominal distension.


Pale to congested mucous membranes.


Enlargement and haemorrhage of anterior LN.


S/C oedema and congestion of blood vessels.


Abomasum distended and displaced.


Thickened abomasal wall, emphysematous and oedematous.




Gram stained smears from necrotic lesions in abomasal folds.




Indirect IFAT on air dried smears.

How do we prevent C. sordelli outbreaks?

Vaccination.




Avoid rapid changes in dietary fermentable carbs.

What is the classic signalment history of sheep found dead due to Braxy?

What is the classic signalment history of sheep found dead due to Braxy?

Sudden death of hoggs.

Severe abomasitis.

Ingestion of frosted foods.

Sudden death of hoggs.




Severe abomasitis.




Ingestion of frosted foods.

How do we prevent braxy in sheep?

How do we prevent braxy in sheep?

History of unvaccinated hoggs grazing frosted food during the autumn.




PM findings:


Oedematous abomasum with mucosal and submucosal haemorrhages.


Oedema of adjacent tissues.


Excess of serous pericardial and peritoneal fluid.




Gram stained smears from abomasum.




Fluorescent antibody technique.

What causes braxy?

Clostridium Septicum

What is the causative agent of black leg?

What is the causative agent of black leg?

Clostridium Chauvoei.

In association with what management events do outbreaks of black leg usually occur around in sheep?

In association with what management events do outbreaks of black leg usually occur around in sheep?

Docking.




Castration.




Shearing under dirty conditions.




Using dirty needles to vaccinate.




Wintering hoggs on root crops.

What do clinical signs of black leg depend on in the sheep sheep?

Depend on site affected.




If the limbs:


Stiffness.


Unable to move.


Subcutaenous oedema and gas.

If the clostridial chauveoi infection (blackleg) is associated with a birthing injury what would be signs?

If the clostridial chauveoi infection (blackleg) is associated with a birthing injury what would be signs?

Erosion of vulval mucosa.




Vulval/perineal oedema.




Dark red and gassy necrosis extending to adjacent muscle.




Blood stained droplets oozing from skin.

What factor predisposes to blackquarter metritis?

Poor skilled lambing.




Oedematous uterus with foetus dead and anasarcous.

What are signs of black leg of the head in sheep?

What are signs of black leg of the head in sheep?

Swelling of the entire head usually associated with rams fighting in the autumn.

With all cases of black leg what is the final clinical signs?

Recumbency, coma and death.

What are post mortem findings with sheep black leg?

What are post mortem findings with sheep black leg?

Carcass swells and bloats rapidly.




Affected muscles are oedematous,dark red creipitous and rancid smell.




Overlying fascia oozes oedema.




Other signs associated with toxaemia:


Pericarditis.


Lung congestion.


Pale swollen liver.

How does visceral black leg manifest?

How does visceral black leg manifest?

Heart muscle.




Pleurisy.




Meningitis.




Pericarditis.

How do we come to a diagnosis of black leg? 

How do we come to a diagnosis of black leg?

History of sudden death and related management factors.




Gross PM findings.




Gram positive rods in smears of oedema fluid or margins of the muscle lesions.




Histopath.




FAT of C. Chauvoei.




Bone marrow smears.

What is blackleg in cattle often associated with in terms of management?

What is blackleg in cattle often associated with in terms of management?

Rough handling in a dirty yard.

If cattle are seen alive with blackleg what are signs of the disease?

If cattle are seen alive with blackleg what are signs of the disease?

Pyrexic.


Depressed.


Tachypnoiea.


Anorexia.


Stiff and lame on affected limb.


Swelling at site and creipitus.


Wounds may discharge a rancid smelling serosanguinous dischgarge.




Progresses to tremors, ataxia, recumbency comma and death.

Which muscles are usually affected by black leg in cattle?

Which muscles are usually affected by black leg in cattle?

Spinal muscles




Upper limbs.



What is early treatment of black leg?

What is early treatment of black leg?

Debride the necrotic lesion and clean.




High doses of penicillin.




Supportive fluids.




High doses of corticosteroid.



How do we prevent black leg?

How do we prevent black leg?

Vaccination- formalin killed bacteria and toxoid.




Single vaccine for cows and multicomponent for sheep.




Hygienic precautions- clean needles, hygiene at docking, castration and lambing.




On high risk farms use long acting penicillin at docking and lambing.





What clostridium causes blacks disease?

What clostridium causes blacks disease?

Fatal peracute infection of sheep of all ages.




Alpha and beta toxins of Clostridium novyi type B.




A normal commensal of sheep gut and soil

What triggers blacks disease?

What triggers blacks disease?

Liver fluke migrating through the liver parenchyma.




These liver fluke cause tracts of necrotic debris and inflammatory exudate perfect for the germination of C. Novyi

What colour is the liver lesion causing blacks disease?

What colour is the liver lesion causing blacks disease?

White necrotic lesion.

Post mortem findings with blacks disease?

Post mortem findings with blacks disease?

Engorged subcutaenous vessels.


Dark liver with distinct paler necrotic areas.


Evidence of recent liver fluke migration.


Blood tinged fluid in pericardium and peritoneum.


Myocardial petechial haemorrhage.

How do we diagnose blacks disease?

History and knowledge of migrating fluke.




PM findings.




FAT.




Gram stained smears.

How do we control blacks disease?

Control liver fluke.




Vaccination.

What is the causative agent of bacillary haemoglobinuria (Red water)?

Clostridium novyi Type D.




Role of migrating fluke.

CLinical signs of red water?

Fever.




Ruminal stasis.




Abdominal pain.




Anaemia and jaundice.




Dark red urine.




Death in 2-3 days.

PM findings with bacillary haemoglobinuria?

PM findings with bacillary haemoglobinuria?

Jaundice.




Generalised subcutaenous gelatinous oedema.




Myocardial haemorrhage.




Blood tinged pleural, pericardial and peritoneal fluid.




Pale necrotic focus on liver.





How do we diagnose bacillary haemoglobinuria?

History.




Signs.




PM findings.




Gram stain.




FAT.

What clostridial disease causes massive facial swelling? What sheep are mainly effected?

What clostridial disease causes massive facial swelling? What sheep are mainly effected?

Malignant oedema caused by C. Chauvoie, C. septicum, C.novyi.




Usually seen in rams.

Main differentials for malignant oedema?

Main differentials for malignant oedema?

Photosensitisation- Primary or secondary.




Dog bite!!!

What is the causative agent of tetanus? What sort of disease does it produce?

What is the causative agent of tetanus? What sort of disease does it produce?

Clostridium tetani- ubiquitous in the soil.




Fatal paralyzing disease due to the neurotoxin produced.

How does C. tetani get into the animal to cause disease?

Via deep puncture wounds.




Around docking etc.

Signs of tetanus?

Signs of tetanus?

Sustained spasm and rigidity of voluntary muscle.




Unable to swallow/eructate.




Laterally recumbent.




Characteristic saw horse appearance- extension of neck, thoraci limbs and pelvic limbs.




Asphyxiation and death.

Pathogenesis of tetanus?

Incubation of 1-3 weeks the neurotoxin travels up peripheral nerves to the brain and spinal cord.







How do we diagnose tetanus and how is it different?

No gross PM findingd!!




Depends on history.




Clinical signs.

How do we treat an early case of tetanus?

Tetanus antitoxin.




Antibiotics.




Anti-inflammatory.





How do we prevent tetanus?

Antitoxin administered to lambs in face of outbreak.




Vaccination.




Antitoxin at docking.




Hygiene at docking!!!

What causes botulism?

What causes botulism?

Ingestion of C. botulism toxins!




Type C + D : Poultry litter.




Type B: carcass contamination of silage.




Associated with big bale sileage and poultry litter.

Signs of Botulism?

Flaccid paralysis and incoordination.




Starts with pelvic limbs.


Progresses to recumbency and death within 24 hours.

What is the protocol for administering a clostridial vaccine? 

What is the protocol for administering a clostridial vaccine?

S/C in neck.




Clean needle.




Correct storage of vaccine in a dark place at 5 degrees.




Use before expiry