Clostridial Disease in Ruminants Flashcards
What type of organism is clostridia?
Ubiquitous organisms
- Gram+, anaerobic bacilli
- Produce spores
Where is clostridia found? (3)
•Soil, rotting vegetation, decomposing matter
Where is clostridia a commensal?
The gut of livestock
What are the trigger factors of clostridia? (4)
- Management: diet change (especially in sheep)
- , handling (handling the mucosa allowing the bacteria in)
- Parasites : e.g. fluke
- Injury – allows the spores in and produce toxins
Why is it hard to know the incidence/prevalence of clostridia?
•Sudden and sporadic death; carcasses disposed of without investigation – we would look for anthrax but then if we don’t find this we don’t look for much more! (Hard to look for prevalence and incidence- see lecture later)
What are the 3 different types of clostridia?
Lamb dysentery (B) – Middle common
Struck (C) – Least common
Pulpy kidney (D) – Most common
What are the predisposing factors for clostridia (5)
- Low proteolytic activity in neonatal intestine (trypsin inhibitors in colostrum)
- Certain types are predisposed to different ages due to this
- Incomplete establishment of normal flora in neonates
- Dietary influences
- Frosty paddocks – thought might trigger clostridium?
- Increased concentrate?
- Change from milk to roughage?
- Abrupt diet change, gorging energy rich diet
- Struggle to deal with this
- Intestinal hypomotility, consequence of overeating
Which is the most common enterotoxaemia?
Pulpy kidney (C. perfringens type D)
Pulpy kidney (C. perfringens type D):
A) Which animals are affected?
B) What toxin is present?
C) What is found on PM?
D) What are the clinical signs?
A) Growing (4-10 weeks) & Finishing (>6 months)
B) ε toxins (specific)
C) Rapid (kidney) autolysis
D) Often found dead, neurological signs
Lamb dysentery (C. perfringens, type B):
A) Where is it seen?
B) What are the clinical signs?
A) Lambs <1-2 weeks of age
B) Haemorrhagic enteritis with ulceration in small intestine
- Usually found dead
- Abdominal pain, Collapse, Blood-stained scour, CNS signs
- Severe picture
Struck (C. perfringens, type C):
A) What is seen on PM?
B) Who is affected?
C) What season is it associated with?
A) Necrotic enteritis, jejunal ulceration (on PM – quite typical)
•Usually found dead
B) Neonates & adult sheep
C) Spring grass?
•Frosty in the morning? No evidence yet but thought to be to do with the diet change.
How can we diagnose clostrdia peringens?
Diagnosis from acutely affected (euth/dead)
Post mortem (NEED THIS ideally from recent death or euthanise a very ill one and PM – a dead animal will overgrow in any dead sheep (Normal GI tract commensal)):
Carcass or gut contents asap
Isolation of C. perfringens means nothing
Culture on its own not useful
Get relevant suspect history!
•Crucial to have this with the PM results
What is seen on PM with pulpy kidney?
cerebral lesions (focal encephalomalacia)
What is seen on PM with lamb dysentry?
ulcerations intestinal mucosa
How can we use ELISA for diagnosis?
3 toxins (α, β, ε) of C. perfringens
What is seen histologically with clostridia?
Gross pathology, confirmed by histopathology with IFAT on tissue
Discuss the prevalance of enterotoxamia in cattle
- Uncommon cause of sudden death cf. sheep
- Described in pre-weaned calves and yearling replacement heifers most of the time
- Adult cattle – less likely unless there is an underlying (calving may get a lesions and cause)
- Enterotoxaemia – very rare!
- Similar clinical signs and sudden death
- Haemorrhagic bowel syndrome?
Braxy, C. septicum:
A) When is it seen?
B) What is the onset?
C) What are the signs?
A) Seen in autumn and winter; Frosted feeds, microclimate
B) Sudden onset
C) Pyrexia and colic, coma and death
•Abomasitis
Black disease, infectious necrotic hepatitis, C. novyi type B:
A) Where is it seen?
B) What is the trigger?
C) What is characteristic on PM?
D) What is seen on impression smears?
A) Sporadic deaths; older sheep, rarely cattle
B) Trigger: Fluke larvae migration
C) Hepatic necrosis; characteristic lesions at PM (sharply delineated yellow necrotic areas of liver) / evidence of migratory fluke
D) IFAT on impression smears
Discuss the association of fluke with black disease
•Fluke = liver damage = anaerobic damage = clostridia takes opportunity
Where does botulism come from?
Poultry litter – probably has some dead chickens in too
Silage with dead rat
What is the difference between tetanus and botulism?
Tetnus – spasms, third eyelid protusion
Botulism – Flaccid, tongue hanging out
How can you treat clostridia?
- EARLY!! antibiotics (penicillin), NSAIDs
- Most of the time it is too late and they are dead anyway
- Keep an eye and if there is malignant oedema – need to have at least 5 days AB!
What iis the prognosis of clostridia?
depends on how early treatment starts, generally poor
How can you prevent clostridia?
- Vaccination – all but black disease are toxins for produce vaccine! (most others have questionable efficacy) But as there are toxins this means these are very effective and they are very consistent –with low antigenic variability
- Management:
- Don’t change the diet suddenlt
- Low stress environment
- Stocking density
- Reduce the chances of lesions
- Good quality feed – reduce mucosa damage
- Good quality equipment to prevent skin damage
Why are vaccines so good?
- Vaccines are readily available! AND CHEAP!!
- Breeding ewes and cows vaccinated prior to lambing
- AB transfer in the colostrum is good!
- E.g. Lamb dysentry really affects them in the first few weeks of life!
- all but black disease are toxins for produce vaccine! (most others have questionable efficacy) But as there are toxins this means these are very effective and they are very consistent –with low antigenic variability
Which 3 animals should we vaccinate?
- Breeding ewes and cows vaccinated prior to lambing
- Also camelids! Quite likely to get clostridia disease
- Vaccines are not registered but there is not hesitation in using these
Why may vaccination efficacy not be as good as it could be? (8)
- Improper storage
- Clostridia vaccine has to be stored 2-8 degrees
- Administration
–Incorrect route
–We don’t know yet if going neck or body for example makes a difference
–MUST VACCINATE IM OR SC IF IT SAYS
–Not given at all!
–Timing
–No booster
–Wrong product!
–Other products given concurrently
•Unfit, poor condition animals – the animal immune system is going to need to work
What is a common sequel to infection?
Sudden death..
