Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/38

Click to flip

38 Cards in this Set

  • Front
  • Back
what are clostridial bacteria?

anaerobic


spore forming


toxin producing


normally present in soil, faeces and intestinal contents.

with exception of botulism, what do clostridial diseases result from?

toxin production following opportunistic rapid multiplication of bacteria in animal.


management factors

what do clostridial diseases usually cause?
sudden death
what are two important enterotoxaemias due to clostridial perfringens?

lamb dysentry


pulpy kidney

what management factors can cause enterotoxaemias due to clostridium perfringens?

c. perfringens= saccharolytic


can multiply rapidly when anaerobic conditions in abomasum and SI are combined with present of large quantities of fermentable carbohydrate.


these conditions occur when sudden changes made in diet- overflow of undigested material enters SI.


gut stasis- insufficient fibre.


severe GI parasitism


C.perfingens produces non toxic protoxins which are converted to toxins by digestive enzymes.

which lambs does dysentery most commonly cause sporadic sudden death in?

1-3days old


stronger single lambs- ingest most milk - spills over from abomasum into SI= substrate for C perfringens multiplication.




unhygienic conditions

what PM findings do you usually see with lamb dysentery?
dark red and distended intestines.
ulceration of intestinal mucosa.
blood stained peritoneal fluid.
liver may be pale and friable.
kidneys may be enlarged.

dark red and distended intestines.


ulceration of intestinal mucosa.


blood stained peritoneal fluid.


liver may be pale and friable.


kidneys may be enlarged.



how else can you diagnose lamb dysentery?

intestinal scrapings- gram stained smears.


anaerobic bacterial culture from intestinal contents.

toxin ELISA from intestinal contents and peritoneal fluid.= however don't confirm as immune animals can have.


in what aged lambs is pulpy kidney commonly seen in?

well grown lambs 4-10 wks old.


fattening lambs 6m-1yr

what is pulpy kidney associated with, management wise?

change in diet


CHO rich

what signs might you see in lambs with pulpy kidney before they die?

hyperaesthesia and ataxia


neuro signs associated with focal symmetrical encephalomalacia.

what are the gross PM findings of pulpy kidney?
excess pericardial fluid
endorcardial haemorrhages
swollen viscera
congested and friable liver
pale and swollen kidneys- autolysed

excess pericardial fluid


endorcardial haemorrhages


swollen viscera


congested and friable liver


pale and swollen kidneys- autolysed



what will you find on urinalysis of bladder at PM, to confirm that kidney disease occurred before death and not due to a PM change?
glucose
what could you do to look for focal symmetrical encephalomalacia?
brain histopath

what are two differentials for sudden death in lambs that have been moved onto better pasture?

systemic pasteurellosis


red gut

how can you prevent enterotoxaemias caused by clostridium perfringens?

vaccination:


initial course 4-6 weeks apart before entering breeding flock.


annual booster 6 weeks before lambing


ensures passive protection of lambs for 8-12 weeks so can give lambs vaccination here then booster 4 weeks later.




good stock husbandry:


hygiene at lambing


colostrum intake


careful intro to improved nutrition.

which lambs does clostrium sordelli abomasitis commonly affect?

intensively reared creep feed lambs


3-10 weeks old

what do the toxins that cause blackleg cause?

cellulitis


necrotising myositis


toxaemia


gas production

what do outbreaks of blackleg follow?

docking


castration


shearing under dirty conditions


using dirty needles


wintering hogs on root crops


poor lambing hygiene and dystocia

what are the clinical signs of blackleg?

depend on site infected:


limbs= stiff and unable to move, subcut odema, gas production.


parturition injury= vulval and perineal odema and necrosis.


fighting rams= odema of the head




rapid progression to recumbency, coma and death.





what are the PM findings of blackleg?

carcase swells and bloats rapidly after death.


affected muscle oedematous, dark red, crepitus, rancid smell.


overlying fascia oozes oedema.


other signs associated with toxaemia:


pericarditis


lung congestion


pale swollen liver

how can you confirm diagnosis of blackleg?

histopathology of formalin fixed sections from edge of lesions.


positive fluorescent antibody tests on smears of unfixed tissue from periphery of lesions.

how can you control blackleg?

vaccination


hygiene at castration, docking, shearing and lambing.

what can trigger black disease?
migrating liver fluke larvae
how can you diagnose black disease?
hx and knowledge of migrating liver fluke larvae.


PM- engorged subcut vessels= black appearance to carcase. (caused by haemolysis).
dark liver with distinct paler necrotic areas
ecchymotic haemorrhages
fluorescent antibody test on fresh air drie...

hx and knowledge of migrating liver fluke larvae.




PM- engorged subcut vessels= black appearance to carcase. (caused by haemolysis).


dark liver with distinct paler necrotic areas


ecchymotic haemorrhages


fluorescent antibody test on fresh air dried smears of liver tissue

what is another ddx for haemolysis in sheep?
copper toxicity

how can black disease be controlled?

vaccination


control liver fluke will reduce incidence

what is malignant oedema of sheep?

non specific


massive facial swelling with pitting oedema and gas production.

what are some ddx for malignant oedema of sheep?

photosensitisation


dog bite

where is clostridium tetani ubiquitous?
soil
when does tetanus occur?

when spores enter deep wounds with devitalised tissue.


eg docking wound

what are the clinical signs of tetanus?
neurotoxin reaches brain via peripheral nerves and spinal cord
causes state of  sustained spasm and rigidity of voluntary muscles
unable to swallow or eructate.
become laterally recumbent.
'saw horse' appearance.
eventual death from asphyxiation ...

neurotoxin reaches brain via peripheral nerves and spinal cord


causes state of sustained spasm and rigidity of voluntary muscles


unable to swallow or eructate.


become laterally recumbent.


'saw horse' appearance.


eventual death from asphyxiation due to resp muscle paralysis.

how can you diagnose tetanus?

hx


clinical signs


no PM signs

how can tetanus be treated?

tetanus antitoxin


antibiotics


anti- inflammatories




however prognosis always guarded and treatment expensive.

how can tetanus be prevented?

vaccination


change method of docking


routine use of tetanus antitoxin (expensive)

where are two potential sources of botulism toxin?

poultry litter- spread on fields


carcase contamination of silage

what are the clinical signs of botulism?

flaccid paralysis and incoordination


starts with pelvic limbs


progression to lateral recumbency

how can botulism be diagnosed?

hx


clinical signs


no specific PM findings