Exam 1 - FA Diffuse Brain Disease Flashcards
what 8 diseases/conditions are on your differential list for diffuse intracranial signs?
- polioencephalomalacia
- lead toxicity
- rabies
- water deprivation/salt water toxicity
- nervous coccidiosis
- urea toxicosis
- bacterial meningitis
- thrombotic meningoencephalitis (TEME)
what are the 2 most common causes of polioencephalomalacia?
thiamine deficiency & excess sulfates in feed/water
what animals are primarily affected by the thiamine deficiency form of polioencephalomalacia?
young cattle, sheep, goats, antelope, & deer
typically on a high concentrate low roughage diet
what is the mechanism of the thiamine deficient polioencephalomalacia?
decreased activity of transketolase enzyme in RBCs which decreases utilization of glucose in the tissue
decreases ATP
decreases utilization of glucose by the brain
end result - intracellular edema of the brain
what are the 5 main factors causing thiamine deficiency?
disturbances in metabolism
decreased synthesis rate
increased excretion
thiamine antimetabolites
feeds - DDG, corn gluten, kocia, & turnips
how does molasses cause a decreased rate of thiamine synthesis?
decreases propionate (glucose precursor) production
what are some examples of processes that cause disturbances in thiamine metabolism?
low intake & increased demand
clostridium - thiaminase I
bacillus - thiaminase II (excessive grain intake)
what is the mechanism of high sulfates causing polioencephalomalacia?
too much sulfur in the diet that preferentially selects for one particular population of bacteria - sulfates are used for respiration & then the bacteria release H2S gas
the H2S gas inhibits cytochrome oxidase activity
what animals are predisposed to developing polioencephalomalacia as a result of high sulfates?
animals with high sulfates in their diet
what is the first stage of disease seen in polioencephalomalacia?
spastic, uncoordinated movement/convulsions when excited/may or may not be blind, & hyperesthesia
what is the second phase seen of polioencephalomalacia?
blind/opisthotonus/star gazing (4th CN)/circles/head press/diarrhea
what is the 3rd phase of polioencephalomalacia?
lateral recumbency/paddling/death/head tilt/nystagmus
what is the hallmark sign of polioencephalomalacia?
acute onset of CNS signs with cortical blindness (PLR intact) & small ruminants that ‘act funny’
what can you look at in the blood diagnostically for polioencephalomalacia?
transketolase activity - giving thiamine may help you diagnostically
what is the treatment for polioencephalomalacia caused by thiamine deficiency?
thiamine 10-15mg/kg QID IM/SQ on day 1
TID for 2 more days
BID fpr 2 days
SID for 2 days
IV needs to be given in 5% dextrose
what is the post-mortem diagnosis of polioencephalomalacia?
moist, swollen, yellow, cortical gyri, & cerebral coning
may fluoresce under UV light due to lipofuscin
what are some ways to prevent polioencephalomalacia caused by thiamine deficiency or high sulfates?
brewer’s yeast - extra thiamine source
increase roughage in diet - selects for favorable rumen bacteria
check sulfate levels in diet/water!!
when trying to diagnose polioencephalomalacia from excess sulfates, what should you do?
check water as a potential source!!!
on a herd basis - levels of sulfates can be measured chute side using a rumen gas cap test
what is the pathophysiology of lead toxicity?
lead binds to RBC & increase fragility of cells
this inhibits enzymes in heme synthesis
leads to poryphrin build up
inhibits the utilization of iron
what are common sources of lead toxicity?
BATTERIES!!
lead arsenate
grease/used motor oil/lead based paints
what is the most common presentation of lead toxicity?
encephalopathy
T/F: signs of acute lead toxicity should put rabies on your differential list
true
what are the acute clinical signs of lead toxicity?
12-24 hours to develop
CNS/GI
cortical blindness with intact PLR
rumen atony/dead protozoa
cerebral signs
seizures
what are the clinical signs of chronic lead toxicity?
normocytic normochromic anemia
basophilic stippling
weight loss
lead stored in bone
how is lead toxicity diagnosed in most acute cases?
in a purple top - whole blood lead is > or = to 0.35ppm
how is lead toxicity diagnosed in most chronic cases?
blood levels may be normal - assess blood ALA levels/poryphrins
most will have a normal hemogram, but you may see an inappropriately responsive anemia with basophilic stippling
what lesion would you expect to see on necropsy for an animal with suspected lead toxicity?
polioencephalomalacia
what is the treatment for lead toxicity?
oral magnesium sulfate!!
Ca disodium EDTA 6.6% solution - 73mg/kg IV SID for 5 days, rest for 2 days, then repeat
thiamine 5-10mg/kg SID - decreases lead deposition & counters lead inhibition of thiamine synthesis
rumenotomy
what is the cause of rabies?
rhabdovirus
what is the pathophysiology of rabies?
saliva contamination or CNS fluids enter through a break in skin
migrates up neurons to the CNS where it replicates & goes to the salivary glands & nasal secretion
what is the incubation period of rabies?
3 weeks to 3 months
what animals serve as reservoirs for rabies virus?
foxes, skunks, raccoons, & bats
what are the 3 forms of rabies?
furious
dumb
paralytic
what clinical signs are associated with the furious form of rabies?
tenesmus, hypersexuality, aggressive behavior, bellowing, paraphimosis, excitability, fear, & rage
what clinical signs are associated with the dumb form of rabies?
depression, anorexia, febrile, can’t drink, excessive salivation, flaccid tongue/anus/tail/bladder, circling, head pressing, strabismus, nystagmus, base wide stance, ptosis, dropped head & neck
what clinical signs are associated with the paralytic form of rabies?
1st sign often unexplained astaxia & shifting leg lameness, decreased spinal reflexes, recumbency/flaccidity, & down 3-5 days & die at day 10
what is the most common way that rabies is transmitted?
bites from an infected animal
other than bites, how is rabies transmitted?
nervous tissue/CNS fluid, aerosol (bat caves), & milk
how is rabies diagnosed?
post mortem only
FA stained hippocampus & cerebellum, negri bodies with a non-supperative encephalitis, & mouse inoculation
how is rabies prevented?
vaccinate animals!! pest control!
what is the common name for pseudorabies?
mad itch
in what environments is pseudorabies seen?
where livestock come into contact with pigs
what clinical signs of pseudorabies are seen in cattle, sheep, & goats?
ataxia, circling, GP deficits, nystagmus, excoriation, depression/aggression, & looks like rabies!!!
how is pseudorabies diagnosed?
VI from nasal swabs, saliva, or nervous tissue & serology
what is the pathophysiology of pseudorabies?
virus enters the skin or respiratory epithelium & travels to the CNS via axonal migration
what clinical signs are seen in neonatal pigs with pseudorabies?
convulsions, tremors, ataxia, & possible acute death
what is the pathophysiology of water deprivation causing salt toxicity?
Na ion concentration becomes higher in the brain than the CSF & blood due to the hyperosmolar CSF & brain tissue created during the time of water deprivation - this inhibits the pump to get Na out
idiogenic osmoles are created
when water is offered, the sodium content of the water is lower than the ion content of the CSF/tissues
water moves from area of greater concentration to lesser concentration (from blood to CSF & brain)
causes cerebral swelling!!!
what clinical signs are seen with water deprivation/salt toxicity?
cerebral - from brain swelling
can get GI signs from high salt intake - severe diarrhea
how is water deprivation/salt toxicity diagnosed post mortem?
inflammation of omasum, abomasal, & omasal surfaces (may be hemorrhagic & dark)
cerebral edema (coning)
in swine only - eosinophilic meningoencephalitis
how is water deprivation/salt toxicity diagnosed antemortem?
clinical signs - pigs, sit & spin
history
CSF Na > than serum Na or serum & CSF Na > than 160 mEq/L
cerebral Na 1800 ppm or greater
histopathology
how is water deprivation/salt toxicity prevented?
access to fresh water at all times
check salt levels in water & feed
what is the treatment for water deprivation/salt toxicity?
frequent small amounts of water
IV mannitol to decrease edema
diazepam for seizures
hypertonic saline - helps lessen the gradient
if giving a scouring calf fluids & CNS signs develop - give IV fluids high in sodium to slow the movement of water into the brain
what animals are at risk for developing water deprivation/salt toxicity?
show pigs held off water, scouring calves, calves fed exclusively milk without access to fresh water that are weaned & offered water, animals on automatic feeders that freeze
what is the maximum tolerable salt level in feed for cows?
4% for lactating cows & 6% for non-lactating cows
what is the maximum tolerable salt level in water for all livestock species?
5,000 PPM
what lesion would you expect to see on necropsy of an animal with water deprivation/salt toxicity?
polioencephalomalacia
what is the suggested pathophysiology of nervous coccidiosis?
seen most commonly following or during outbreaks of bloody diarrhea in weaning age calves (eimeria)
toxin liberated from the GI tract during coccidia infection
what is the progression of disease of nervous coccidiosis?
intermittent in the beginning then frequency between normalcy decreases
what are the clinical signs seen with nervous coccidiosis?
convulsions, paddling, opisthotonus, muscle tremors, tetanic spasms, & strabismus
how is nervous coccidiosis diagnosed?
clinical signs & fecal float
how is nervous coccidiosis prevented?
coccidiostats
what is the treatment for nervous coccidiosis?
albon & vitamin A 1 time & then put in a quiet place, use diazepam for seizures
amprolium 50mg/kg SID 5 days
2-4mg/kg of calcium gluconate with magnesium SQ
what animals are most commonly affected by urea toxicosis?
animals that aren’t accustomed to consuming urea
what are the common sources/causes of urea toxicosis?
improper mixed
soybeans fed with urea
screw up - wrong bag in the feeder
what is the pathophysiology of urea toxicity?
excessive amounts of NH3 are produced which causes the pH in the rumen to go up
this causes NH4 to be converted back to NH3
the high load of NH3 going to the liver overwhelms the ability of the liver to convert NH3 to urea to be excreted
NH3 is rapidly absorbed in the blood
what are the clinical signs seen with urea toxicity?
salivation, bruxism, abdominal pain, dull/weak, hyperirritability, tetany, muscle tremors, & prostration/death (1-4 hours)
how is urea toxicity diagnosed?
check sources/feeding history
rumen content pH > 8 rumenocentesis
freeze blood & rumen contents
NH3 content > 2mg/dl blood
>80mg/dl rumen content
how is urea toxicity treated?
1/2 gallon vinegar in cold water - sheep gets 1 quart
rumenotomy
what animals are typically at risk for bacterial meningitis?
young calves, lambs, kids, & piglets
what is the suggested pathophysiology of bacterial meningitis?
failure of passive transfer, omphalitis, & likely e. coli is involved in the etiology
what are the clinical signs of bacterial meningitis?
omphalitis, hypopyon, swollen joints, stiff/extended neck, hyperesthesia, opisthotonus, exaggerated spinal reflexes, & abnormal vocalization
if I have a calf with suspected bacterial meningitis, what are my differentials for a calf that is dull without a suckle reflex?
hypoglycemia, hypothermia, septic, dehydrated, or acidotic
how do you treat bacterial meningitis?
antibiotics/supportive fluids/nsaids
whole blood? - consider failure of passive transfer
what is the suggested pathophysiology of thrombotic meningoencephalitis?
histophilus somni - vasculitis with thrombus formation & septic infarcts in various organs
causes endothelial cells to slough
what are the clinical signs of thrombotic meningoencephalitis?
high fever, blind, GP deficits, very depressed/obtunded, nervous signs, ataxia, paralysis, & coma
how is thrombotic meningoencephalitis?
hemorrhages in the retina
CSF - xanthochromia, neutrophils, total protein > 100mg/dl
CBC - neutropenia initially
what is the toxic dose for urea in cattle?
1-1.5g/kg
what is the toxic dose for urea in sheep?
2g/kg bw
how is urea toxicity prevented?
adding urea slowly to diets so animals get accustomed to change
avoid screw ups with mixing & feeding
how is bacterial meningitis prevented?
ensure passive transfer
how is thrombotic meningoencephalitis treated?
oxytetracycline 5mg/lb IV BID
florfenicol 20mg/kg IV SID
ceftiofur
NSAIDS
how is thrombotic meningoencephalitis prevented?
vaccine may reduce severity & incidence of CNS disease
need new vaccine
mass medicate LA 200 or aureomycin in feed (5-10mg/lb/cow/day)
lower stress
what is the typical history of a cow presenting with nervous ketosis?
post partum dairy cow - negative energy balance
what are the clinical signs of nervous ketosis?
excessive licking of themselves/inanimate objects, ataxia, blind, circling, & aggressive
what is the treatment for nervous ketosis?
nervous signs will decrease as ketosis is addressed
treat the primary problem
IV dextrose 50%
transfaunate
T/F: nervous ketosis is usually secondary to other diseases or conditions such as mastitis, metritis, etc
true
