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Neuro > Farm Animal Neuro > Flashcards

Farm Animal Neuro Flashcards

1
Q

What are the viral causes of cerebral disease?

A

Maedi visna

caprine arthritis encephalitis

Border disease

BVD

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2
Q

What are the parasitic causes of cerebral disease?

A

Luoping ill

Coeneurosis/Gid

Sarcosystis

Coccidiosis

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3
Q

What are the possible TSE causes of cortical disease?

A

Scrapie

BSE

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4
Q

What are the two other causes of cerebral disease (not parasitic, viral or TSE)

A

Trauma/abscess/neoplasia

Cerebrocortical necrosis

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5
Q

What is the main cause of cerebellar disease?

A

BVD

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6
Q

What are the causes of Brainstem and cranial nerve disease?

A

Listeriosis

Otitis (media/interna)

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7
Q

What are the causes of spinal/peripheral nerve disease?

A

Enzootic neonatal ataxia (swayback)

Fractures/abscesses/luxations

Spastic paresis

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8
Q

What are the metabolic causes of FA neuro disease?

A

ketosis

hypocal

hypomag

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9
Q

What are the neuromuscular causes of FA neuro disease?

A

Botulism

Tetanus

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10
Q

What is the proper name for cerebrocortical necrosis?

A

polioencephalomalacia

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11
Q

What part of the brain becomes necrotic in cerebrocortical necrosis?

A

The grey matter

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12
Q

What species does cerebrocortical necrosis occur in?

A

Ruminants and pseudo ruminants

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13
Q

How does altered thiamine metabolism lead to cerebrocortical necrosis?

A

Thiamine is co-factor for transketolase, provides glucose for the brain.

Loss of ketolase due to lack of thiamine (vit B1) –> increased lactate, pyruvate and oxoglutarate –> intraneuronal swelling –> increased cranial pressure –> neuronal necrosis –> oedema and cortical necrosis

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14
Q

Which conditions can cause cerebrocortical necrosis due to thiamine alteration?

A

Any that reduces thiamine activity e.g. excessive grain intake/sudden feed change (–> thiaminase producing bacteria)

Deficient pastures

Thiaminase producing plant E.G. BRACKEN

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15
Q

How is sulphur found in beef feed?

A

As sulphur, sulphates, gypsum, cruciferous vegetables, molasses

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16
Q

Why is excess sulphur bad for the cow?

A

Sulphur turned into sulphide in the body.

Sulphide neurotoxic, prevent ATP production by inhibiting cytochrome C oxidase

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17
Q

What are the clinical signs of polioencephalomalacia/CCN?

A

May be found dead, sudden death, or found recumbent or comatose, convulsions, seizures - Grave prognosis

Or may develop over hours/days:

Appear blind (cortical blindness),

Opisthotonous (severe arching of back)

Hypermetric gait

Hyperaesthetic

depressed

Miosis

Strabismus

Head tilt

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18
Q

What is the treatment for CCN?

A

Thiamine IM or SQ

Maybe dexamethasone for cerebral oedema?

Control seizures - diazepam NB licensing

Usually respond within 24hrs

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19
Q

What clin path findings would you exepct to see with CCN?

A

Erythrocyte transketolase activity (sens & spec but expensive)

Mild pleiocytosis on CSF & increased CSF protein

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20
Q

What would you expect to find on PM of an animal with CCN?

A

Cortical swelling, softening and flattening of gyri

Areas of cortical necrosis which will autofluoresce under UV

Severe cases-herniation of cerebellum

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21
Q

Which species is affected by maedi visna virus?

A

Sheep

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22
Q

What are the clinical signs of maedi visna?

A

May show ataxia, proprioceptive deficits, convulsions, circling, blindness, coma

May just show emaciation

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23
Q

What is the typical time of onset to death in maedi visna?

A

1-2 years

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24
Q

Why do animals with maedi visna often get mastitis, pneumonia/other infections?

A

Causes immunosuppression

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25
Q

How is maedi visna spread?

A

Aerosol, milk, transplacental, colostrum

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26
Q

How do you test for Maedi visna?

A

Antibody ELISA

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27
Q

What kind of inflammation do you get with maedi visna?

A

Diffuse non suppurative inflammation

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28
Q

What species is affected by caprine arthritis encephalitis?

A

Goats

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29
Q

What are the clinical signs of CAE?

A

ataxia, paresis, head tilt, nystagmus, opisthotonous, decreased PLR, paralysis

May have enlarged joints, shifting lameness, weight loss, mistitis, ill thrift

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30
Q

How is CAE spread?

A

Aerosol, colostrum, milk, transplacental

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31
Q

How do you test for CAE?

A

Ab ELISA

Test and cull

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32
Q

What is the coloquial name for border disease virus?

A

Hairy shakers

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33
Q

What is the pathogenesis of border disease

A

Affects naive ewes in pregnancy, lambs are aborted or infertile or have deformities

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34
Q

What happens if the ewe (and therefore lamb) are infected in the first half of pregnancy?

A

Become immunotolerant and persistently infected

Adult sheep have short asymptomatic viraemia then become resistant

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35
Q

How is Border disease spread?

A

Vertical and horizontal transmission

36
Q

What systems are affected in lambs infected <60 days in gestation?

A

Skin (steel wool coat, hyperpigmented), CNS (tremors, ataxia, hopping) and skeletal (short legs, deformed head, small orbits, arthrogryposis (joints stuck)

37
Q

At what age do CNS signs disappear in border disease lambs?

A

20 weeks but still small lambs

38
Q

How do you test for border disease?

A

Antibody testing of young sheep to determine flock status

Virus testing to identify PIs

39
Q

What does BVD do to the brain?

A

Hydrocephalus

Cerebellar hypoplasia

40
Q

What are the clinical signs of BVD?

A

tremors

weakness

proprioceptive deficits

ataxia

blindness

strabismus/nystagmus

Often die shortly after birth

41
Q

What stage in gestation are BVD calves infected?

A

100-150 days

42
Q

What do persistently infected BVD calves often die of?

A

They become immunotolerant to BVD when infected in utero with the less pathogenic strain. When encounter more pathogenic strain do not mount response and die

43
Q

What is the proper name for louping ill?

A

ovine encephalomyelitis

44
Q

What is louping ill/OEM spread by?

A

Ticks - ixodes ricinus

45
Q

What is the epidemiology of louping ill?

A

Yearling sheep affected when on infected pasture, mortality rate low, recover in around 12 days.

Supportive treatment

46
Q

What is the pathogen in Coenurosis?

A

Intermediate stage of taenia multiceps

47
Q

What is the epidemiology of coenurosis?

A

Adult worms shed in dog/cat faeces

Ingested on pasture

Eggs hatch in SI, migrate to CNS via blood

48
Q

What is the treatment for coenurosis?

A

Praziquantal

Prevent dog/cat access

Worm dogs and cats

49
Q

Which species are affected by nervous coccidiosis?

A

Feedlot calves

Sheep and goats

50
Q
A
51
Q

What is the pathogen in nervous coccidiosis?

A

Eimeria spp

52
Q

What are the clinical signs of coccidiosis?

A

GI signs then depression, anorexia, hyperaesthesia, opisthotonous, seizures

53
Q

What is the epidemiology of nervous coccidiosis?

A

Clincal signs caused by toxin from parasite, high mortality

54
Q

How do you treat nervous coccidiosis?

A

Diclazuril/Toltrazuril

55
Q

What is the epidemiology of sarcocystis?

A

Large numbers of sarcocytes ingested, normally asymptomatic

56
Q

What is the treatment of sarcocystis?

A

Doclazuril

Toltrazuril

Sulfa drugs

Control access to carnivore crap

57
Q

Are TSEs notifiable?

A

hell yes

58
Q

What is the epidemiology of TSE infections?

A

Accumulation of abnormal prion proteins –> deposition as amyloid plaques in the CNS and lymphoreticular tissue

There is post translational modification of PRPc to PRPsc which has different protein structure and is resistant to degradation

59
Q

What are the clincical signs of scrapie?

A

Different bhaviour-separate from flock, restless

Weight loss

Pruritis (wool loss, dermatitis, excoriation, nibble reflex)

Ataxia, weakness, tremors, ptyalism (excess salivation), seizures, collapse

60
Q

Under the TSE testing program, all fallen stock sheep over the age of **** are tested

A

18 months

61
Q

How is scrapie spread?

A

Colostrum, milk, placenta, faeces, urine, can survive in soil

62
Q

How is susceptibility to scrapie controlled?

A

Via 3 codons on chromosome 13

Breed for resistance

63
Q

How do you diagnose scrapie?

A

Immunohistochemistry and western immunoblot

64
Q

What are of cows are affected by BSE?

A

4-6 years old

65
Q

What are the clinical signs of BSE?

A

Separation from herd, fearful, excited, hyperaesthesia, aggression, ataxia, tremors

66
Q

What does BSE cause in humans?

A

nvCJD

(creudzvelt-jakob disease)

67
Q

How is BSE spread?

A

Feeding of meat and bone marrow to cattle (no genetic component)

68
Q

What are the 3 main steps to stop BSE coming into the human food chain?

A

Control of risk materials: brain, spinal cord, caudal ileum, eyes tonsils (these do not enter food chain)

Cattle > 30 months must be tested before sold for food

No mechanically recovered meat

69
Q

What type of bacteria is lysteria?

A

Listeria monoytogenes - gram positive anaerobic bacteria

70
Q

What does listeria cause (neurologically)?

A

Acute meningoencephalitis

multifocal microabscesses

71
Q

Which species does listeriosis affect?

A

Sheep goats and cattle but more acute and severe in sheep and goats

72
Q

How does listeria get spread?

A

Contaminated feed, faeces, rotting vegetation

SURVIVES IN ENVIRONMENT for long periods of time

73
Q

How does listeria get to the brain?

A

Haematogenous spread via cranial nerve rootlets

74
Q

What are the clinical signs of listeriosis?

A

Fever-early in disease

anorexia

depression

proprioceptive deficits

head pressing

compulsive circling

75
Q

Which cranial nerves are often dysfunctional in listeriosis?

A

V to XII

Signs associated with these nerves same as in small animals

76
Q

What would you see on a CSF tap with listeriosis?

A

Increased protein and white blood cells

77
Q

How do you treat listeriosis?

A

High dose penicillin

NSAIDs

Fluid support

78
Q

Why is listeriosis a public health concern?

A

Can be spread in milk products

79
Q

What is the other name for spastic paresis?

A

Elso Heel

80
Q

What age group tend to get spastic paresis?

A

Young animals age 3 weeks to 1 year

Seems to possible be genetic

81
Q

What is the main clinical sign of spastic paresis?

A

Progressive hyperextension of the hindlimbs

Progressive contraction of gastrocnemius

Unable to flex hock during hindlimb protraction

82
Q

What is the cause of spastic paresis?

A

Overstimulation of gamma motorneurons in spinal cord

83
Q

What are the differentials for spastic paresis?

A

Patella luxation

Fractures

84
Q

What is the treatment for spastic paresis?

A

Surgical - partial tenectomy of medial and lateral heads of gastrocnemius or tibial neurectomy

This is a salvage procedure to allow them to reach slaughter weight without discomfort. Do not keep in the herd - genetic

85
Q

What species are affected by enzootic neonatal ataxia?

A

Sheep and goats

86
Q

What is the cause of enzootic neonatal ataxia?

A

Copper deficiency

87
Q

What are the clinical signs of sway back?

A

Progressive incoordination - starts hind limbs progresses to foremlimbs

Weight loss, diarrhoea, coat changes

Neuro (13 decks)

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