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38 Cards in this Set
- Front
- Back
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what are clostridial bacteria?
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anaerobic spore forming toxin producing normally present in soil, faeces and intestinal contents. |
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with exception of botulism, what do clostridial diseases result from?
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toxin production following opportunistic rapid multiplication of bacteria in animal. management factors |
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what do clostridial diseases usually cause?
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sudden death
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what are two important enterotoxaemias due to clostridial perfringens?
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lamb dysentry pulpy kidney |
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what management factors can cause enterotoxaemias due to clostridium perfringens?
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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. |
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which lambs does dysentery most commonly cause sporadic sudden death in?
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1-3days old stronger single lambs- ingest most milk - spills over from abomasum into SI= substrate for C perfringens multiplication. unhygienic conditions |
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what PM findings do you usually see with lamb dysentery?
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dark red and distended intestines. ulceration of intestinal mucosa. blood stained peritoneal fluid. liver may be pale and friable. kidneys may be enlarged. |
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how else can you diagnose lamb dysentery?
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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. |
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in what aged lambs is pulpy kidney commonly seen in?
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well grown lambs 4-10 wks old. fattening lambs 6m-1yr |
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what is pulpy kidney associated with, management wise?
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change in diet CHO rich |
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what signs might you see in lambs with pulpy kidney before they die?
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hyperaesthesia and ataxia neuro signs associated with focal symmetrical encephalomalacia. |
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what are the gross PM findings of pulpy kidney?
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excess pericardial fluid endorcardial haemorrhages swollen viscera congested and friable liver pale and swollen kidneys- autolysed |
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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?
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glucose
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what could you do to look for focal symmetrical encephalomalacia?
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brain histopath
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what are two differentials for sudden death in lambs that have been moved onto better pasture?
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systemic pasteurellosis red gut |
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how can you prevent enterotoxaemias caused by clostridium perfringens?
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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. |
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which lambs does clostrium sordelli abomasitis commonly affect?
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intensively reared creep feed lambs 3-10 weeks old |
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what do the toxins that cause blackleg cause?
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cellulitis necrotising myositis toxaemia gas production |
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what do outbreaks of blackleg follow?
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docking castration shearing under dirty conditions using dirty needles wintering hogs on root crops poor lambing hygiene and dystocia |
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what are the clinical signs of blackleg?
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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. |
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what are the PM findings of blackleg?
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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 |
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how can you confirm diagnosis of blackleg?
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histopathology of formalin fixed sections from edge of lesions. positive fluorescent antibody tests on smears of unfixed tissue from periphery of lesions. |
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how can you control blackleg?
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vaccination hygiene at castration, docking, shearing and lambing. |
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what can trigger black disease?
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migrating liver fluke larvae
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how can you diagnose black disease?
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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 |
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what is another ddx for haemolysis in sheep?
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copper toxicity
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how can black disease be controlled?
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vaccination control liver fluke will reduce incidence |
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what is malignant oedema of sheep?
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non specific massive facial swelling with pitting oedema and gas production. |
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what are some ddx for malignant oedema of sheep?
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photosensitisation dog bite |
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where is clostridium tetani ubiquitous?
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soil
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when does tetanus occur?
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when spores enter deep wounds with devitalised tissue. eg docking wound |
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what are the clinical signs of tetanus?
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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. |
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how can you diagnose tetanus?
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hx clinical signs no PM signs |
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how can tetanus be treated?
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tetanus antitoxin antibiotics anti- inflammatories however prognosis always guarded and treatment expensive. |
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how can tetanus be prevented?
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vaccination change method of docking routine use of tetanus antitoxin (expensive) |
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where are two potential sources of botulism toxin?
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poultry litter- spread on fields carcase contamination of silage |
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what are the clinical signs of botulism?
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flaccid paralysis and incoordination starts with pelvic limbs progression to lateral recumbency |
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how can botulism be diagnosed?
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hx clinical signs no specific PM findings |
