CNS disease in cattle Flashcards

1
Q

What does hyperaethetic mean

A

Hyper responsive to stimuli

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2
Q

What does obtundation mean

A

No response to normal stimuli levels

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3
Q

What does stupor mean

A

Respond only to painful stimuli

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4
Q

What does coma mean

A

No reponse to ANY stimuli

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5
Q

Two spots where we can take a CSF tap

A

Cisterna magna and lumbosacral space

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6
Q

How does lesion affect limb responses based on position

A

When cranial to limb get hyperactive reflexes (+ataxia and weakness)

When level with limb = depressed reflexes + ataxia and weakness

When caudal to limb = no effect on limb

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7
Q

What clinical signs do forebrain lesions give

A

seizures, behavioural changes, propulsive pacing, circling, aggression, charging, mania, excessive licking

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8
Q

What clinical sign does cerebral disorders give

A

apparent blindness; but still have normal pupillary light reflex

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9
Q

What is hydrocephalus and what might the cause be

A

Congenital condition where calves are born with domed forehead
- May relate to VIt A deficiency, Schmallenberg

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10
Q

What is hydrancephaly; and what might have caused it

A

‘Dummy syndrome’ in calves; born without brain hemispheres in skull
- Due to viral infection in utero; BVDv, bluetongue, Schmallenberg

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11
Q

What in utero viral infection is most associated with cerebellar hypoplasia (intention tremors, ataxia, dymetria)

A

Bovine viral diarrhoea virus
[Also bluetongue]

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12
Q

What brain inflammatory condition can bull rings be associated with

A

Pituitary infections

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13
Q

When we get embolic spread of from distant abscesses/septicaemia to brain what form abscesses; what organism do we commonly isolate from it

A

Trueperella

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14
Q

What does listeriosis in calves look like

A

Facial cranial nerve deficits; drooped ear/eyelids, strabismus, nystagmus, loss of sensation

> On PM see microabscesses in pons and medulla

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15
Q

What might be a common route of brain infection with listeria in calves

A

Via oral route (from low quality silage); via cuts in mouth e.g due to cheek teeth

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16
Q

What are notifiable neurological diseases

A

Rabies (classical)
Aujesky’s diseases = pseudorabies/mad itch = a pig herpes virus
BSE
Bluetongue

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17
Q

What is the causative agent in thromboembolic meningoencephalitis

A

Histophilus somni
> NB respiratory disease more common than neurological

18
Q

What brain condition can lack of thiamine cause in cattle

A

Cerebrocortical necrosis

19
Q

What is an unusual finding in cerebrocortical necrosis (from thiamine deficiency)

A

Cut surface of the brain fluoresces

20
Q

How might we treat lead poisoning

A

Rumenotomy to remove lead material
Chelation therapy i.e using calcium EDTA

21
Q

What brain condition can salt poisoning cause

A

Cerebral oedema

22
Q

How might a cow suffering from cerebrocortical necrosis present

A

Recumbant and comatose
Cortical blindness, paddling movements, head pressing, nystagmus etc

23
Q

What is nervous ketosis

A

= neurological manifestation of ketosis; see high excitability, apparent blindness, head pressing

Treat via IV glucose

24
Q

What is ‘night blindness’ a sign of

A

Vitamin A deficiency

25
Q

In what vitamin deficiency might we see retinal bleeding

A

Vitamin A

26
Q

What is hepatic encephalopathy

A

Where we see changes in behaviour and seizures in cows; because diffuse liver damage has cause hyperammonaemia and other toxic factor accumulation

27
Q

Signs of botulism in cattle; and what is common source of contamination

A

> Flaccid paralysis, sternal recumbency, hind limb ataxia, loss of tail tone

Associated with contamination of feed with dead rodents or the use of poultry with chicken carcasses in it as manure

28
Q

In what situations might we see tetanus in cattle

A

With deep, anaerobic puncture wounds e.g from castration or dehorning
Or ruminal damage from fibrous feeds

29
Q

Which viral diseases can cause cerebellar hypoplasia in neonates

A

Bovine viral diarrhoea virus
Bluetongue virus
Schmallenberg virus

30
Q

What diet change would encourage more thiaminase producing ruminal bacteria and therefore more risk of cerebrocoritcal necrosis

A

High carbohydrate diet

31
Q

Why does thiamine deficiency lead to cerebrocortical necrosis

A

Because it is a co-enzyme in carbohydrate metabolism
- SO deficiency leads to lower glucose
-> NEURONS NEED GLUCOSE

Without energy in brain: get failure of Na+ and H2O transport; get cerebrocortical oedema, raised intracranial pressure, lower blood flow and necrosis

32
Q

How does lead poisoning cause cerebral lesions

A

Because lead binds to sulfhydryl groups on enzymes, including those involved in carbohydrate metabolism
- Get fall in energy metabolism + effects on endothelial cells

Oedema and raised ICP –> lower blood flow and ischaemia

33
Q

Why do we see cerebro-cortical necrosis (distribution) in thiamine deficiency

A

Because these are the neurons which are most susceptible to energy impairment so die first

34
Q

Which bacteria is classically associated with haematogenous spread to brain and infectious thrombo-embolic meningoencephalitis

A

Histophilus somni

35
Q

How does listeria reach the brain

A

Ascneding infection via nerves

36
Q

What is typical histopathology for viral encephalitis

A

Perivascular cuffing with lymphocytes
Vasculitis
Cell death
Lesions usually diffuse

37
Q

What rare CNS condition can neospora caninum cause in cattle

A

Degeneration of the spinal cord; following in utero infection

38
Q

Why might cattle get a thiamine (B1) deficiency

A
  • Low intake
  • Rumen producing thiaminases; high carb diet causes overgrowth of gram +ve bacteria so more thiaminase producing ones
  • Ingestion of thiaminases e.g bracken
  • anti-thiamine drugs
    Risk factors: sudden diet change, high grain intake, excess sulfur
39
Q

What mechanism does thiamine deficiency cause CCN

A

Thiamine is a co-enzyme in carbohydrate metabolism; so defieicny causes failure in glucose metabolism which neurons rely on

Therefore low energy in neurons; failure of Na+ and water transport causing intracellular oedema and raised ICP

40
Q

What mechanism does lead toxicity cause neurological signs

A

Lead binds to and stops enzymes in carbohydrate metabolism working properly

Get failure of energy metabolism + impact on endothelial cells in BBB
So get oedema and raised ICP similar to with CCN causing decreased blood flow and ischaemia

41
Q

Which different agents cause which type of inflammatory response

A

Bacteria; mostly neutrophils
Viruses; lymphocytes
Parasites; eosinophils

42
Q
A