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LA DX & TX I > Exam 1 - FA Diffuse Brain Disease > Flashcards

Exam 1 - FA Diffuse Brain Disease Flashcards

1
Q

what 8 diseases/conditions are on your differential list for diffuse intracranial signs?

A
  1. polioencephalomalacia
  2. lead toxicity
  3. rabies
  4. water deprivation/salt water toxicity
  5. nervous coccidiosis
  6. urea toxicosis
  7. bacterial meningitis
  8. thrombotic meningoencephalitis (TEME)
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2
Q

what are the 2 most common causes of polioencephalomalacia?

A

thiamine deficiency & excess sulfates in feed/water

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3
Q

what animals are primarily affected by the thiamine deficiency form of polioencephalomalacia?

A

young cattle, sheep, goats, antelope, & deer

typically on a high concentrate low roughage diet

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4
Q

what is the mechanism of the thiamine deficient polioencephalomalacia?

A

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

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5
Q

what are the 5 main factors causing thiamine deficiency?

A

disturbances in metabolism

decreased synthesis rate

increased excretion

thiamine antimetabolites

feeds - DDG, corn gluten, kocia, & turnips

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6
Q

how does molasses cause a decreased rate of thiamine synthesis?

A

decreases propionate (glucose precursor) production

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7
Q

what are some examples of processes that cause disturbances in thiamine metabolism?

A

low intake & increased demand

clostridium - thiaminase I

bacillus - thiaminase II (excessive grain intake)

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8
Q

what is the mechanism of high sulfates causing polioencephalomalacia?

A

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

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9
Q

what animals are predisposed to developing polioencephalomalacia as a result of high sulfates?

A

animals with high sulfates in their diet

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10
Q

what is the first stage of disease seen in polioencephalomalacia?

A

spastic, uncoordinated movement/convulsions when excited/may or may not be blind, & hyperesthesia

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11
Q

what is the second phase seen of polioencephalomalacia?

A

blind/opisthotonus/star gazing (4th CN)/circles/head press/diarrhea

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12
Q

what is the 3rd phase of polioencephalomalacia?

A

lateral recumbency/paddling/death/head tilt/nystagmus

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13
Q

what is the hallmark sign of polioencephalomalacia?

A

acute onset of CNS signs with cortical blindness (PLR intact) & small ruminants that ‘act funny’

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14
Q

what can you look at in the blood diagnostically for polioencephalomalacia?

A

transketolase activity - giving thiamine may help you diagnostically

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15
Q

what is the treatment for polioencephalomalacia caused by thiamine deficiency?

A

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

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16
Q

what is the post-mortem diagnosis of polioencephalomalacia?

A

moist, swollen, yellow, cortical gyri, & cerebral coning

may fluoresce under UV light due to lipofuscin

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17
Q

what are some ways to prevent polioencephalomalacia caused by thiamine deficiency or high sulfates?

A

brewer’s yeast - extra thiamine source

increase roughage in diet - selects for favorable rumen bacteria

check sulfate levels in diet/water!!

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18
Q

when trying to diagnose polioencephalomalacia from excess sulfates, what should you do?

A

check water as a potential source!!!

on a herd basis - levels of sulfates can be measured chute side using a rumen gas cap test

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19
Q

what is the pathophysiology of lead toxicity?

A

lead binds to RBC & increase fragility of cells

this inhibits enzymes in heme synthesis

leads to poryphrin build up

inhibits the utilization of iron

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20
Q

what are common sources of lead toxicity?

A

BATTERIES!!

lead arsenate

grease/used motor oil/lead based paints

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21
Q

what is the most common presentation of lead toxicity?

A

encephalopathy

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22
Q

T/F: signs of acute lead toxicity should put rabies on your differential list

A

true

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23
Q

what are the acute clinical signs of lead toxicity?

A

12-24 hours to develop

CNS/GI
cortical blindness with intact PLR
rumen atony/dead protozoa
cerebral signs
seizures

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24
Q

what are the clinical signs of chronic lead toxicity?

A

normocytic normochromic anemia
basophilic stippling
weight loss
lead stored in bone

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25
how is lead toxicity diagnosed in most acute cases?
in a purple top - whole blood lead is > or = to 0.35ppm
26
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
27
what lesion would you expect to see on necropsy for an animal with suspected lead toxicity?
polioencephalomalacia
28
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
29
what is the cause of rabies?
rhabdovirus
30
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
31
what is the incubation period of rabies?
3 weeks to 3 months
32
what animals serve as reservoirs for rabies virus?
foxes, skunks, raccoons, & bats
33
what are the 3 forms of rabies?
furious dumb paralytic
34
what clinical signs are associated with the furious form of rabies?
tenesmus, hypersexuality, aggressive behavior, bellowing, paraphimosis, excitability, fear, & rage
35
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
36
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
37
what is the most common way that rabies is transmitted?
bites from an infected animal
38
other than bites, how is rabies transmitted?
nervous tissue/CNS fluid, aerosol (bat caves), & milk
39
how is rabies diagnosed?
post mortem only FA stained hippocampus & cerebellum, negri bodies with a non-supperative encephalitis, & mouse inoculation
40
how is rabies prevented?
vaccinate animals!! pest control!
41
what is the common name for pseudorabies?
mad itch
42
in what environments is pseudorabies seen?
where livestock come into contact with pigs
43
what clinical signs of pseudorabies are seen in cattle, sheep, & goats?
ataxia, circling, GP deficits, nystagmus, excoriation, depression/aggression, & looks like rabies!!!
44
how is pseudorabies diagnosed?
VI from nasal swabs, saliva, or nervous tissue & serology
45
what is the pathophysiology of pseudorabies?
virus enters the skin or respiratory epithelium & travels to the CNS via axonal migration
46
what clinical signs are seen in neonatal pigs with pseudorabies?
convulsions, tremors, ataxia, & possible acute death
47
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!!!
48
what clinical signs are seen with water deprivation/salt toxicity?
cerebral - from brain swelling can get GI signs from high salt intake - severe diarrhea
49
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
50
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
51
how is water deprivation/salt toxicity prevented?
access to fresh water at all times check salt levels in water & feed
52
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
53
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
54
what is the maximum tolerable salt level in feed for cows?
4% for lactating cows & 6% for non-lactating cows
55
what is the maximum tolerable salt level in water for all livestock species?
5,000 PPM
56
what lesion would you expect to see on necropsy of an animal with water deprivation/salt toxicity?
polioencephalomalacia
57
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
58
what is the progression of disease of nervous coccidiosis?
intermittent in the beginning then frequency between normalcy decreases
59
what are the clinical signs seen with nervous coccidiosis?
convulsions, paddling, opisthotonus, muscle tremors, tetanic spasms, & strabismus
60
how is nervous coccidiosis diagnosed?
clinical signs & fecal float
61
how is nervous coccidiosis prevented?
coccidiostats
62
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
63
what animals are most commonly affected by urea toxicosis?
animals that aren't accustomed to consuming urea
64
what are the common sources/causes of urea toxicosis?
improper mixed soybeans fed with urea screw up - wrong bag in the feeder
65
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
66
what are the clinical signs seen with urea toxicity?
salivation, bruxism, abdominal pain, dull/weak, hyperirritability, tetany, muscle tremors, & prostration/death (1-4 hours)
67
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
68
how is urea toxicity treated?
1/2 gallon vinegar in cold water - sheep gets 1 quart rumenotomy
69
what animals are typically at risk for bacterial meningitis?
young calves, lambs, kids, & piglets
70
what is the suggested pathophysiology of bacterial meningitis?
failure of passive transfer, omphalitis, & likely e. coli is involved in the etiology
71
what are the clinical signs of bacterial meningitis?
omphalitis, hypopyon, swollen joints, stiff/extended neck, hyperesthesia, opisthotonus, exaggerated spinal reflexes, & abnormal vocalization
72
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
73
how do you treat bacterial meningitis?
antibiotics/supportive fluids/nsaids whole blood? - consider failure of passive transfer
74
what is the suggested pathophysiology of thrombotic meningoencephalitis?
histophilus somni - vasculitis with thrombus formation & septic infarcts in various organs causes endothelial cells to slough
75
what are the clinical signs of thrombotic meningoencephalitis?
high fever, blind, GP deficits, very depressed/obtunded, nervous signs, ataxia, paralysis, & coma
76
how is thrombotic meningoencephalitis?
hemorrhages in the retina CSF - xanthochromia, neutrophils, total protein > 100mg/dl CBC - neutropenia initially
77
what is the toxic dose for urea in cattle?
1-1.5g/kg
78
what is the toxic dose for urea in sheep?
2g/kg bw
79
how is urea toxicity prevented?
adding urea slowly to diets so animals get accustomed to change avoid screw ups with mixing & feeding
80
how is bacterial meningitis prevented?
ensure passive transfer
81
how is thrombotic meningoencephalitis treated?
oxytetracycline 5mg/lb IV BID florfenicol 20mg/kg IV SID ceftiofur NSAIDS
82
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
83
what is the typical history of a cow presenting with nervous ketosis?
post partum dairy cow - negative energy balance
84
what are the clinical signs of nervous ketosis?
excessive licking of themselves/inanimate objects, ataxia, blind, circling, & aggressive
85
what is the treatment for nervous ketosis?
nervous signs will decrease as ketosis is addressed treat the primary problem IV dextrose 50% transfaunate
86
T/F: nervous ketosis is usually secondary to other diseases or conditions such as mastitis, metritis, etc
true

LA DX & TX I (45 decks)

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