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Neurology > Farm animal neurology > Flashcards

Farm animal neurology Flashcards

1
Q

2 main types of cortical disease

A
  • cerebrocortical necrosis (CCN)

- viral (MV, CAE, BDV, BVD)

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2
Q

Most important brainstem and CN disease

A

listeriosis

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3
Q

Name 3 metabolic diseases with neuro effects

A
  • nervous ketosis
  • hypoclacaemia
  • hypomagnasaemia
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4
Q

List spinal cord and peripheral nn disorders

A
  • spastic paresis (Elso heel)
  • enzootic neonatal ataxia (swayback)
  • fractures, luxations, spinal abscesses
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5
Q

Name 2 neuromuscular disease

A
  • tetanus

- botulism

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6
Q

Which parasites can cause neuro disease?

A
  • louping ill
  • coenurosis / gid
  • sarcocystis
  • nervous coccidiosis
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7
Q

Another name for cerebrocortical necrosis (CCN)

A

polioencephalomalacia (PCN)

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8
Q

aetiology - CCN

A
  • multiple, all lead to necrosis of grey matter:
  • THIAMINE metabolsim
  • SULPHUR metabolism
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9
Q

Species - CCN

A

all ruminants and pseudo-ruminants

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10
Q

Occurence of CCN

A

worldwide, common

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11
Q

Pathogenesis - CCN - altered thiamine metabolism

A
  • thiamine is co-factor for transketolase in pentose phosphate pathway (–> glucose for brain), loss –> increased lactate, pyruvate and oxoglutarate –> intraneuronal swelling (decreased ATP Na/H2O transport) –> increased ICP adn neuronal necrosis –> oedema and cortical necrosis
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12
Q

Outline ruminant thiamine storage

A

poor - daily requirement only marginally less than production in rumen

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13
Q

Cause - altered thiamine metabolism which leads to CCN

A

any condition that inactivates thiamine in rumen OR its synthesis –> rapidly causes thiamine deficiency:

  • exessive grain intake or sudden feed change (promotes thiaminase producing bacteria)
  • deficient pastures, unsupplemented
  • thiaminase producing plant spp (bracken)
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14
Q

Explain how altered sulphur metabolism –> CCN

A
  • sulphur found in beef cattle fed as sulphur, sulphates, gypsum, cruciferous vegetables, molassess
  • sulphate reduced to SULPHIDES and ultimately incoorporated into CP and energy is released. Sulphide are NEUROTOIXC (inhibit cytochrome C oxidase thus preventing ATP production) –> neuronal swelling –> increased ICP (as for altered thiamine metabolism)
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15
Q

CCN - CS

A
  • sudden death or found recumbent, comatose, convulsions, hypertonic between seizuers (GRAVE prognosis)
  • or can develop over hours to days: cortical blindness, opisthotonus, hypermetric gait, hyperaesthetic progresses to depreession, miosis, strabismus, head tilt
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16
Q

Tx - CCN

A
  • THIAMINE - IM or SQ, NOT multivit (–> toxicity), Iv –> anapphylaxis
  • DEXAMETHASONE ? to reduce CE
  • DIAZEPAM - control seziures
  • usually respond within 24 hours, can be dramatic
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17
Q

Dx - CCN

A
  • response to tx, hx and CS
  • Erythrocyte transketolase activity (sensitive, specific, expensive, hard to find lab which runs it)
  • CSF (mild pleiocytosis and increased [protein])
  • PME: cortical swelling, softening, flattening of gyri, necrotic areas of cerebral cortex autofluoresce under UV, severe cases can herniate the cerebellum (indicated by constant seizuring)
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18
Q

Name viral diseases which affect neuro system

A
  • Maedi visna (MV(
  • CAprine arthritis encephalitis (CAE)
  • Border disease
  • BVDV
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19
Q

CS - MV

A
  • DIFFUSE ENCEPHALITIS: ataxia, proprioceptive deficits, circling, blindness, coma, convulsions.
  • Can show just emaciation
  • Time from onset - death: 1-2 years
  • immunosuppression
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20
Q

Pathology - MV

A

diffuse non-suppurative inflammation

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21
Q

Spread - MV

A
  • aerosol*

- colostrum, milk, transplacental

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22
Q

Is there an accreditation testing scheme for MV?

A

Yes - Premium Sheep and Goat Health Scheme

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23
Q

Dx - MV

A

Ab ELISA

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24
Q

Define CAE

A

Caprine Arthritis Encephalitis virus

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25
Q

CS - CAE

A
  • LEUKOENCEPHALOMYELITIS: ataxia, paresis, head tilt, nystagmus, opisthotonus, reduced PLR, parallysis
  • symmetric or asymmetric
  • usually young goats (neuro form)
  • (adults: enlarged joints, shifting lameness, weight losss, mastitis, ill thrift)
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26
Q

Spread - CAE

A

aerosol and colostrum, milk, transplacental

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27
Q

IS there a CAE accreditation testing scheme?

A

Yes - Premium Sheep and Goat Health Scheme

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28
Q

Dx - CAE

A

Ab ELISA

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29
Q

Tx - CAE

A

Test and cull OR make 2 herds (dirty and clean, keep at least 6m b/w the two)

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30
Q

Outline Border disease virus infection

A
  • infects naive ewes in pregnancy
  • abortion, infertility, deformities
  • lambs infected in utero in first half of gesttation become immunotolerant and remain viraemic –> PI
  • adult sheep develop short, inapparent viraemia, develop immunity to reinfection
  • similar to BVDV
  • vertical and horizontal
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31
Q

What happens if a lamb is infected in utero before 60 dyas?

A
  • foetal survival - hairy shakeer
  • weak or normal lambs which are PI with virus
  • no Ab detectable
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32
Q

When does a lamb foetus gain immunological competence?

A

between 60 and 85 days gestation

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33
Q

CS - border disease virus

A
  • lambs infected
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34
Q

Dx - border disease virus

A
  • AB testing young sheep for flock status

- Virus/Ag testing to find PIs

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35
Q

BVDV - CS

A
  • weak
  • head tremors
  • proprioceptive deficits
  • ataxia
  • blindness
  • stabismus/ nystagmus
  • often die shortly after birth
36
Q

Brain abnormalities

A
  • hydrocephalus

- cerebellar hypoplasia

37
Q

What is another name for ovine encephalomyelitis?

A

Louping ill in sheep

38
Q

Transmission - ovine encephalomyelitis

A

Tick - Ixodes ricinus

39
Q

What are the 2 commonest parasitic diseases in farm animals that cause CNS problems?

A
  • ovine encephalomyelitis / louping ill

- coenurosis

40
Q

What is coenurosis?

A

= Coenurus cerebralis

  • intermediate stage of Taenia multiceps (tapeworm)
  • causes cranium SOL: ataxia, unilateral vision loss, head tilt, circling hypermetria, coma
  • adult worms shed in dog/cat faeces, infested on pasture, eggs hatch in SI and migrate to CNS via blood
41
Q

Tx - coenurosis

A

PRAZIQUANTEL - to worm dog/cat.

- prevent dog/cat access.

42
Q

What are nervous coccidiosis and sarcocystis?

A

other parasites which can cause neuro signs

43
Q

What causes TSEs?

A

accumulation of abnormal prion proteins (PrPsc) in CNS, deposited as amyloid plaque within lymphoreticular and nervous tissue. PrPc post-translational modification to abnormal PrPsc which has a different protein structure, resistant to degradation

44
Q

Which species does Scrapie affect?

A

sheep and goats

45
Q

Is scrapie notifiable?

A

yes - like all TSEs

46
Q

Age of animals with scrapie

47
Q

CS - scrapie

A
  • BEHAVIOURAL: separate from flock, restlessnes, nervous
  • WEIGHT LOSS
  • PRURITUS: wool loss, dermatitis, excoriation, nibble reflex (lip smacking)
48
Q

What is the TSE testing programme?

A

all fallen stock (sheep, goats) > 18 mo need testing for scrapie

49
Q

Transmission - scrapie

A

spread by colostrum, milk, dam to offspring, placenta, faeces/urine
* can survive in soil

50
Q

Can you breed for genetic resistance to scrapie?

A

Yes - there a 3 codons on chromosome 13 to control susceptibility

51
Q

Dx - scrapie

A

IHC and western immunoblot

52
Q

BSE - age

53
Q

CS - BSE

A
  • BEHAVIOUR: separate from herd, fear, panic or excited

- Hyperaesthesisa, aggression, ataxia, tremors

54
Q

What does BSE cause in humans?

55
Q

Is there a genetic component to BSE?

A

No - unlike sheep scrapie

56
Q

How can BSE risk be prevented in food chain?

A
  • Specific RIsk Material COntrol (brain, eyes, SC, distal ileum, tonsils don’t enter food chain)
  • cattle> 30 months not sold for food unless tested and born after 1996
  • no mechanically recovered meat
57
Q

What is Listeria monocytogenes?

A

gram positive anaerobic bacteria

58
Q

How does listeriosis affect brain?

A

acute meningoencephalitis and multifocal brain abscesses in brain tissue

59
Q

How many animals does listeriosis affect?

A

usually individuals, may be more

60
Q

How does fatality rate of listeriosis vary between sheep/goats and cows?

A

Sheep/goats - more acute disease so higher fatality than cattle

61
Q

Source - listeria

A

COntaminated forage (e.g. spoiled silage) but occasionally seen on animals not on silage. Faeces carrier animals (end pregnancy and lambing time). rotting veg.

62
Q

How does environment affect L monocytogenes?

A

survives long periods in environment, multiplies in low temps

63
Q

How does listeria infect brain?

A

infects brain by haematogenous spread or by ascent from CN (trigeminal) rootlets. later exposed in younger animals when permanent teeth erupt or break in mucosa.

64
Q

CS - listeriosis

A
  • FEVER (early in disease): anorexia, depression, proprioceptive deficits, head pressing, compulsive circling
  • CN 5-12 dysfunctional- progresses to unconsciousness, coma and seizures
65
Q

How does listeria affect CN 5 (trigeminal)?

A

dropped, asymmetric jaw, facial analgesia

66
Q

How does listeria affect CN 6(abducens)?

A

medial strabismus on lesion side

67
Q

How does listeria affect CN 7 (facial)?

A

ptosis, loss of menace response, absent palpebral reflex, drooped ear, deviated philtrum (loss of tone), drooling saliva from ipsilateral side, exposure keratitis

68
Q

How does listeria affect CN 8 (vestibulocochlear)?

A

nystagmus, head tilt toward lesion, circle to lesion side

69
Q

How does listeria affect CN 9, 10 , 12 (glossopharyngeal, vagus, hypoglossal)?

A

stertor, dysphagia, paresis of tongue, tongue may protrude from ipsilateral side

70
Q

Dx - listeriosis

A
  • clinical suspiciion

- CSF tap: increased protein and WBCs

71
Q

Tx - listeriosis

A
  • high doses of penicillin (above label limit), BIM if IM or QID if IV
  • (oxytetracycline is alternative but penicillin better)
  • NSAIDs
  • fluids
72
Q

How is listeria a public health concern?

A

contamination of milk products (raw milk and cheese)

73
Q

Name 3 spinal cord and peripheral nn disorders

A
  • spastic paresis
  • peripheral nn disorders (e.g. sciatic, obturator nn paralysis)
  • enzootic ataxia (swayback)
74
Q

Another name for spastic paresis

A

= Elso heel

75
Q

Which animals are affected by spastic paresis?

A

Cattle - genetic basis (Holstein, Angus, Charolais, Shorthorn, Herefords)

76
Q

Age of animals affected by spastic paresis

A

young animals (3wks - 1 year)

77
Q

What does spastic paresis cause?

A

progressive hyperextension of HL

  • excessive extensor tone when standing (gastrocnemius and superficial extensor mm)
  • progressive contraction of gastroc mm –> non-weight bearing of affected limb
  • unable to flex hock during HL protraction
  • overstimulation of gamma motorneurons of spinal cord
78
Q

Ddx - spastic paresis/ Elso heel

A
  • patella luxation

- fractures

79
Q

Tx - spastic paresis

A
  • SURGICAL: tibial neurectomy (if in early stages) OR partial tenectomy of medial and lateral heads of gastrocnemius tendon (later stages)
  • these are salvage procedures to enable continued growth and comfort before culling
  • don’t keep in herd (genetic basis)
80
Q

What is another name for swayback?

A

enzootic neonatal ataxia

81
Q

What does swayback affect?

A

lambs and kids

82
Q

What cuasees enzootic neonatal ataxia/ swaybakc?

A

copper deficiency

83
Q

What does enzootic neonatal ataxia cause?

A

progressive incoordination and recumbency, starting in HLs and progressing to TLs

84
Q

CS - swayback

A
  • progressive incoordination and recumbency, starting in HLs and progressing to TLs
  • weight loss
  • diarrhoea
  • coat changes
85
Q

Tx - swayback

A
  • usually cull animals affected with CS
  • Cu supplements at level needed–> toxicity,
  • tx aim = prevent is rest of herd

Neurology (26 decks)

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