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Large Animal Medicine > Protozoal, Nutritional, & Toxic Neurological Diseases of Ruminants > Flashcards

Protozoal, Nutritional, & Toxic Neurological Diseases of Ruminants Flashcards

1
Q

What is the most common protozoal cause of neurological disease in ruminants? What 3 signs are seen?

A

Coccidiosis

  1. seizures with opisthotonos and tonic-clonic movements
  2. medial strabismus
  3. eyelid snapping

(all with periods of normalcy!)

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2
Q

What risk factors are associated with nervous coccidiosis? How is it treated?

A

feedlot, winter

  • Sulfonamides
  • Amprolium
  • TLC - protection during seizures
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3
Q

What is polioencephalomalacia?

A

blindness in young ruminants with thiamine deficiency (B1)

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4
Q

What is characteristic of polio in ruminants? What other signs are seen? What is not affected?

A

central blindness (+ PLR) with dorsomedial strabismus

  • ataxia, tremor
  • opisthotonos
  • convulsions
  • recumbency

rumen, no fever, normal CN

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5
Q

How is polio diagnosed? What is seen on necropsy?

A
  • clinical signs and history
  • response to thiamine (blindness may take a while to recover)
  • CSF - mononuclear, mild protein elevation, xanthochromia

swollen, yellow cerebrum, autofluorescence of cortex under UV light

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6
Q

How is polio treated?

A
  • thiamine (B1) - should have a response in 1-2 days
  • control convulsions with Diazepam
  • TLC
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7
Q

What ruminants are most commonly affected by polio? What is it most commonly secondary to?

A

younger —> 6-12 months

  • ruminal acidosis (high sulfate diet) —> increases thiaminase production, which breaks down thiamine responsible for water balance in the brain
  • competitive thiamine analogs - Amprolium overdose with treatment of Coccidiosis
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8
Q

How is polio prevented?

A
  • supply moderate carbohydrate diet with increased roughage
  • decrease sulfates in diet
  • supplement diet with thiamine

excellent progosis when therapy is induced before incumbency —> neurologic changes may be permanent

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9
Q

What provides the most evidence for diagnosing polio?

A

necropsy

  • swollen, slightly yellow cerebrum
  • cerebellar and/or cerebral herniations (acute)
  • autofluorescence of freshly cut surface of cerebral cortex under UV light (may not be present with acute death)
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10
Q

How can the rumen be used for diagnosing polio?

A

fluid evaluation —> sequela to grain overload, most common in calves on creep feeders —> rare for pH to be acidic, but the normal protozoal flora will not be present

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11
Q

What is the pathogenesis of polio?

A

BRAIN SWELLING

  • gray matter necrosis due to lack of glycolysis with resulting brain edema and dysfunction of ATPase (Na, K) causes cellular swelling
  • swelling causes pressure necrosis of the gray matter
  • decreased thiamin limits transketolase activity
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12
Q

What is salt poisoning? What diagnostic history is associated?

A

overload of salt or lack of water intake results in hypernatremia with resultant neurological signs of cerebral edema —> aggressiveness, recumbency, coma

  • distance to water
  • frozen water source
  • lack of water
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13
Q

How is salt poisoning diagnosed?

A
  • serum and CSF Na markedly increased (>160 mEq/L)
  • brain edema and cerebrocortical necrosis on histopath

(more common in pigs)

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14
Q

What is characteristic of vitamin A deficiency in cattle? When is this most common?

A

irreversible central blindness

when stock do not have access to succulent plants

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15
Q

What are the most common signs of lead poisoning?

A
  • aggression, convulsions
  • central blindness
  • wandering, head pressing
  • opisthotonos, odontoprisis
  • bellowing
  • eventual death
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16
Q

How is lead poisoning diagnosed? 3 options for treatment?

A
  • CBC = basophilic stippling and nucleated RBCs
  • lead levels in serum or urine following chelation
  • junk pile in field - lead paint, linoleum, caulking compounds, batteries, machinery, oil/grease
  • busy roads with heavy pollution near
  1. Ca EDTA - urinary lead excretion via chelation
  2. thiamine
  3. magnesium sulfate - laxative forms insoluble lead sulfides
17
Q

What signs are indicative of Scrapie? How is it spread?

A

signs of BSE (insidious apprehension, hyperesthesia, incoordination) + itching

placental tissue and fluids (NOT ZOONOTIC)

18
Q

How is Scrapie diagnosed? Eradicated?

A

lymphoid tissue of 3rd eyelid or necropsy

keep resistant (RR) or less susceptible (QR) sheep and goats in breeding programs

(1/500 culled sheep are positive!)

19
Q

Blindness is a common sign of which of the listed diseases?

a. rabies
b. BSE
c. lead toxicity
d. listeriosis
e. TEME
f. polio
g. brain abscess
h. tetanus

A

C, E, F, G

20
Q

How does BVD affect calves when infected in utero?

A

cerebellar hypoplasia —> sawhorse stance, intention tremor

21
Q

What is indicative of hydrocephalus?

A

depressed newborns with dome-shaped heads

22
Q

What is the difference between hydrocephalus and hydranencephaly?

A

HYDRO = thinning brain due to fluid accumulation associated with vitamin A deficiency in dams and inherited in Herefords, Charlolais, Dexter, Holstein, and Jersey

HYDRA = congenital anscence of brain due to failure of growth or cellular necrosis (VIRAL)

23
Q

What infection is associated with hydranencephaly?

A
  • BVD
  • Bluetongue

typically come in waves as herds build immunity and lose it overtime —> calves commonly walk around normally until they bump into something

24
Q

What plant is associated with neurological disease in cattle? Where is it most commonly found?

A

Locoweed

western US

25
Q

What toxicity is a common differential for rear end weakness and flaccid paralysis in ruminants?

A

organophosphates —> check for grease or oil in the field

r/o spinal abscess, botulism, and rabies

26
Q

What meningeal worm causes neurologic signs? How does it cause disease? How are ruminants infected?

A

Parelaphostrongylus tenuis —> SR > cattle

aberrant parasite migration through CNS = downer status

white-tailed deer serve as DH and sheds it in feces —> worms are taken up by snails that host the second larval stage, which can be ingested by ruminants

27
Q

Where is meningeal worm infection most common? What does it cause?

A

eastern US —> follows WTD distribution

downer small ruminants —> head tilt, incoordination, progressive weakness in the rear

28
Q

What signs of meningeal worm infections are most common in camelids, sheep, and goats?

A

CAMELIDS - neck and head lesions

SHEEP/GOATS - alert downers

29
Q

What is the most reliable diagnostic for meningeal worm infection? What treatments are recommended?

A
  • fecal detection of larvae (aberrant hosts rarely shed)
  • CSF tap - eosinophilia

Fenbendazole and Ivermectin + anti-inflammatories + TLC —> full recovery possible if caught early

30
Q

What are 3 ways of controlling meningeal worm infection?

A
  1. keep deer away from ruminants
  2. drain wet areas to eliminate snails
  3. routine deworming to kill larvae before they reach CNS
31
Q

When treated in a timely manner, the disease with the best prognosis is…

a. Listeriosis
b. meningitis
c. vitamin A deficiency

A

A

vitamin A deficiency results are permanent (blindness)

32
Q

Regarding TEME, which of the following is true?

a. cranial nerves may be affected
b. tends to occur mostly in the summer
c. primarily a disease of adult cattle

A

A

more common in 1-2 y/o feedlot cattle in the winter

33
Q

In regards to meningitis, which of the following is true?

a. affected cattle are usually alert and hyperesthetic
b. drug of choice is Penicillin
c. signs usually have an acute onset

A

C

NOT alert, tends to be caused by E. coli

34
Q

Which of the following is true regarding tetanus?

a. if left untreated, animals live only around 14 days
b. there are no reliable clinical tests for diagnosis
c. tetanus toxoid should not be given at the same time as the tetanus anti-toxin

A

B

Large Animal Medicine (34 decks)

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