Bovine Flash Notes - Polioencephalomalacia Flashcards

1
Q

what is the classic presentation of a ruminant with polioencephalomalacia?

A

fast growing calf or lamb, neurologic signs, blind/staggering/down

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2
Q

what is the presumed pathogenesis of polioencephalomalacia?

A

poorly understood nutritional disease of ruminants - thought to be associated with altered thiamine status and/or high sulfur intake

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3
Q

what clinical signs are often seen in ruminants with polioencephalomalacia?

A

bilaterally symmetric clinical signs of cerebral dysfunction especially in calves/kids/lambs - staggering, recumbent, opisthotnos, cortical blindness, & pathognomic dorsomedial strabismus

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4
Q

how is polioencephalomalacia diagnosed?

A

clinical signs & history of diet change, poor pasture, or other disease causing anorexia, dorsomedial strabismus, rotten egg smell in rumen gases with high sulfur, & response to treatment with vitamin B1

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5
Q

response to treatment with what is suggestive of a diagnosis of polioencephalomalacia?

A

B1 (thiamine) treatment

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6
Q

what neurologic sign is pathognomic for polioencephalomalacia in ruminants?

A

dorsomedial strabismus

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7
Q

how is polioencephalomalacia treated?

A

THIAMINE!!!! vitamin B1: 10-20mg/kg TID dosing, first IV, then IM, then SQ - continue for days past improvement

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8
Q

what is the prognosis of early stage polioencephalomalacia? what is the last clinical sign to disappear?

A

reversible with early treatment - blindness is the last sign to disappear

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9
Q

what is the prognosis of advanced/prolonged cases of polioencephalomalacia? why?

A

grave prognosis - permanent brain damage is possible

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10
Q

what is the treatment of choice for an afebrile, recumbent, blind, sheep suspected of having polioencephalomalacia? what route is the treatment given? how long do you give it?

A

thiamine (vitamine B1): 10-20mg/kg TID dosing - initial dose IV, then IM, then SC - continue vitamin B1 for days past improvement!!!

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11
Q

what are two key etiologies thought to be most commonly associated with development of polioencephalomalacia in ruminants?

A

altered thiamine status and/or high sulfur intake

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