Neurological Disease Flashcards
characteristics of polioencephalomalacia and pathogenesis?
usually YOUNG ruminants affected, can be sporadic individuals or group outbreaks
thiamine is needed for cell energy, sudden change to high carb diet and the rumen does not respond well to the change, sometimes high sulfate in ration or water can play a role too, end result is altered neuron metabolism causing cerebral edema and necrosis
CS of PEM?
SYMMETRICAL usually
blindness, ataxia, stargazing, tremors, coma, death
what diagnostics can help you with PEM?
clinical signs suggestive + history (sudden diet change)
testing the feed or water for high sulfur, necropsy lesions and testing–>will glow in the dark
you go see a cow named MARGE and she is star gazing, head pressing, and is walking into walls. how will you treat her? prevention of this happening again?
PEM–>thiamine IV or IM BID to QID first day, could also add dexamethasone
prevention: dont change diet too suddenly, provide good water not too high in sulfur
who is most susceptible to lead posisoning?
cattle/ruminants>horses>pigs
you go on to a farm that has one cow found dead and another cow that is very sensitive to stimuli and is showing aggressive behavior with some head pressing. On PE you see the cow is bloated and is having trouble passing manure. When you walk the property you find an old car at the very back of the property. The farmer asks you “doc what da heck wron wi ma cow? how did this happen?” and you tell him…
this is likely lead toxicity. the cows likely chewed or swallowed a piece of metal. the metal deposits into tissues like the liver, kidney, bone, and in the brain. It is slowly released from the organs over time. At high doses it causes ischemic damage to the brain and brain swelling, similar to how polio looks.
the farmer with the possible lead toxicity cows wants to do diagnotistc testing. you tell him
we can check the feed and mixers to make sure there arent pieces of metal going to all the cows. we can also do a blood test of the live cow (toxic is >0.35ppm), can do urine testing as well. On the dead cow we can submit liver, kidney, and bone for lead testing (>10ppm is diagnostic)
if you diagnose lead toxicity in a cow that is still alive, how can you treat it?
remove it from the GI (rumenotomy, give epsom salts orally to create an insoluble precipitate), lead chelation
treatments need to be repeated and often go on for a looooong time
why is lead poisoning reportable?
because these animals cannot enter the food chain or be sent to market
in order to sent the cow for slaughter, blood values need to come down to 0.11ppm
how does salt toxicity happen?
when there is not free access to good water, a feed mix error, or if there’s water deprevation like int the winter
you go out to a farm to see a herd of animals in the middle of january. the cows have diarrhea and are showing neurologic signs such as blindness, ataxia, and seizures. When you investigate, you find out the water bunks have been frozen over and the heating system to keep the water from freezing has malfunctioned OH NO! what is this? pathogenesis?
salt intoxication/water deprevation
sudden change in osmolarity: go from hyperosmolar state to a hypo-osmolar state (i dont understand this)
brain edema–>water follows the salt in the brain causing it to swell
how do you treat salt toxicity
diurectics to get rid of the fluid in the brain
if cows have not started to drink water again make sure they do this slowly!give them controlled access to small amounts of water to minimize the fluid that moves into the brain
which form of rabies is more common in cows
the dumb form: ataxia, drool, cranial nerve deficits, tenesmus, *unable to swallow or drink water–>progress to recumbency/paralysis and death
not the furious form like in carnivores.
thromboembolic meningoencephalitis is caused by what bacteria? what other body systems does this bacteria infect?
histophilus somni
joints, lungs, myocardium
CS and pathogenesis of thromboembolic meningoencephalitis?
anorexia, staggering, coma, sudden death–>animals can look sleepy
can also have a fever, be coughing, and be lame
septic–>thrombosis of small vessels in the nervous system
