Clostridial Diseases Of Sheep And Cattle

Front 1

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

Back 1

Sudden death.

Front 2

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

Back 2

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.

Front 3

What is the general disease state produced by clostridum perfringens?

Back 3

Enterotoxaemia.

Front 4

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

Back 4

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

Front 5

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

Back 5

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.

Front 6

What toxin causes lamb dysentry?

Back 6

Beta and epsilon toxin of C perfringens type B.

Front 7

What age of lambs are usually affected by lamb dysentry?

Back 7

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

Usually the stronger single lambs.

Front 8

Post mortem findings with lamb dysentry?

Back 8

Dark red and distended loops of bowel.

Ulceration of intestinal mucosa.

Serous, blood stained peritoneal fluid.

Pale and friable liver.

Enlarge kidneys.

Front 9

What is needed for a diagnosis of lamb dysentry?

Back 9

1) Gram stained smears of the organisms.

2) Anaerobic culture from intestines.

3) Elisa for the epsilon toxins and beta.

4) PM findings.

Front 10

Why do single lambs tend to get lamb dysentry?

Back 10

They ingest large volumes of milk.

This overspills into the intestine.

Feeds clostridium.

They rapidly multiply and cause disease.

Front 11

What is the aetiology of pulpy kidney?

Back 11

Epsilon toxin made by C. Perfringens type D.

Front 12

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

Back 12

Diet changes.

Front 13

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

Back 13

Well grown lambs between 4-10 weeks.

Fattening lambs between 6 months and 1 year.

Front 14

Signs of pulpy kidney?

Back 14

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.

Front 15

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

Back 15

Systemic pasteurellosis.

Red gut.

Front 16

How do we confirm a diagnosis of pulpy kidney?

Back 16

History of sudden death in well grown unvaccinated lambs.

PM findings.

Glucose in the urine.

Positive elipson toxins ELISA.

Brain histopathology.

Front 17

What are post mortem findings with pulpy kidney?

Back 17

Excess pericardial fluid.

Endocardial haemorrhages.

Swollen viscera.

Congested friable liver.

Pale and swollen autolysed liver.

Front 18

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

Back 18

Struck is caused by clostridium perfringens type C beta toxin.

Causes enteritis, peritonitis and sudden death.

Front 19

How do we prevent enterotaxaemia?

Back 19

Vaccination.

7+ 1 vaccine containing lamb dysentry.

Combined with good husbandry.

Good hygiene.

Adequate colostrum.

Careful introduction to a new plane of nutrition.

Front 20

What is the protocol for vaccinating sheep for enterotoxaemias?

Back 20

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.

Front 21

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

Back 21

Vaccination.

Restrict feeding.

Front 22

What is the history associated with clostridium sordelli ?

Back 22

Sudden death in unvaccinated and vaccinated ewes.

Usually effects 3-10 week intensively creep fed lambs.

Housing and creep feeding.

Front 23

What are signs of clostridium sordelli in live sheep?

Back 23

Depressed and bloated.

Front 24

How can we come to a diagnosis of clostridium sordelli?

Back 24

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.

Front 25

How do we prevent C. sordelli outbreaks?

Back 25

Vaccination.

Avoid rapid changes in dietary fermentable carbs.

Front 26

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

Back 26

Sudden death of hoggs.

Severe abomasitis.

Ingestion of frosted foods.

Front 27

How do we prevent braxy in sheep?

Back 27

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.

Front 28

What causes braxy?

Back 28

Clostridium Septicum

Front 29

What is the causative agent of black leg?

Back 29

Clostridium Chauvoei.

Front 30

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

Back 30

Docking.

Castration.

Shearing under dirty conditions.

Using dirty needles to vaccinate.

Wintering hoggs on root crops.

Front 31

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

Back 31

Depend on site affected.

If the limbs:

Stiffness.

Unable to move.

Subcutaenous oedema and gas.

Front 32

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

Back 32

Erosion of vulval mucosa.

Vulval/perineal oedema.

Dark red and gassy necrosis extending to adjacent muscle.

Blood stained droplets oozing from skin.

Front 33

What factor predisposes to blackquarter metritis?

Back 33

Poor skilled lambing.

Oedematous uterus with foetus dead and anasarcous.

Front 34

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

Back 34

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

Front 35

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

Back 35

Recumbency, coma and death.

Front 36

What are post mortem findings with sheep black leg?

Back 36

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.

Front 37

How does visceral black leg manifest?

Back 37

Heart muscle.

Pleurisy.

Meningitis.

Pericarditis.

Front 38

How do we come to a diagnosis of black leg?

Back 38

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.

Front 39

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

Back 39

Rough handling in a dirty yard.

Front 40

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

Back 40

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.

Front 41

Which muscles are usually affected by black leg in cattle?

Back 41

Spinal muscles

Upper limbs.

Front 42

What is early treatment of black leg?

Back 42

Debride the necrotic lesion and clean.

High doses of penicillin.

Supportive fluids.

High doses of corticosteroid.

Front 43

How do we prevent black leg?

Back 43

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.

Front 44

What clostridium causes blacks disease?

Back 44

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

Front 45

What triggers blacks disease?

Back 45

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

Front 46

What colour is the liver lesion causing blacks disease?

Back 46

White necrotic lesion.

Front 47

Post mortem findings with blacks disease?

Back 47

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.

Front 48

How do we diagnose blacks disease?

Back 48

History and knowledge of migrating fluke.

PM findings.

FAT.

Gram stained smears.

Front 49

How do we control blacks disease?

Back 49

Control liver fluke.

Vaccination.

Front 50

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

Back 50

Clostridium novyi Type D.

Role of migrating fluke.

Front 51

CLinical signs of red water?

Back 51

Fever.

Ruminal stasis.

Abdominal pain.

Anaemia and jaundice.

Dark red urine.

Death in 2-3 days.

Front 52

PM findings with bacillary haemoglobinuria?

Back 52

Jaundice.

Generalised subcutaenous gelatinous oedema.

Myocardial haemorrhage.

Blood tinged pleural, pericardial and peritoneal fluid.

Pale necrotic focus on liver.

Front 53

How do we diagnose bacillary haemoglobinuria?

Back 53

History.

Signs.

PM findings.

Gram stain.

FAT.

Front 54

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

Back 54

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

Usually seen in rams.

Front 55

Main differentials for malignant oedema?

Back 55

Photosensitisation- Primary or secondary.

Dog bite!!!

Front 56

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

Back 56

Clostridium tetani- ubiquitous in the soil.

Fatal paralyzing disease due to the neurotoxin produced.

Front 57

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

Back 57

Via deep puncture wounds.

Around docking etc.

Front 58

Signs of tetanus?

Back 58

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.

Front 59

Pathogenesis of tetanus?

Back 59

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

Front 60

How do we diagnose tetanus and how is it different?

Back 60

No gross PM findingd!!

Depends on history.

Clinical signs.

Front 61

How do we treat an early case of tetanus?

Back 61

Tetanus antitoxin.

Antibiotics.

Anti-inflammatory.

Front 62

How do we prevent tetanus?

Back 62

Antitoxin administered to lambs in face of outbreak.

Vaccination.

Antitoxin at docking.

Hygiene at docking!!!

Front 63

What causes botulism?

Back 63

Ingestion of C. botulism toxins!

Type C + D : Poultry litter.

Type B: carcass contamination of silage.

Associated with big bale sileage and poultry litter.

Front 64

Signs of Botulism?

Back 64

Flaccid paralysis and incoordination.

Starts with pelvic limbs.

Progresses to recumbency and death within 24 hours.

Front 65

What is the protocol for administering a clostridial vaccine?

Back 65

S/C in neck.

Clean needle.

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

Use before expiry