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Neuro > Farm Neuro (McSloy) > Flashcards

Farm Neuro (McSloy) Flashcards

1
Q

What brain stem diseases affect FA?

A
  • Listeriosis

- Otitis media-interna (bacterial)

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2
Q

What cerebellar diseases affect FA?

A

BVD

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3
Q

Which metabolic diseases cause neuro signs?

A
  • nervous ketosis
  • hypocalcaemia
  • hypomagnesaemia
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4
Q

Which spinal cord and peripheral nerve disorders affect FA?

A
  • spastic paresis (Elso heel)
  • enzootic neonatal ataxia (swayback)
  • Fx, luxation and spinal abscesses
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5
Q

Which neuromuscular diseases affect FA?

A
  • tetanus

- botulism

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6
Q

Wha this cerebrocortical necrosis also known as?

A

Polioencephalomalacia (polio= grey matter, encephalo = Brain, malaria = softening)

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7
Q

Is cerebrocortical necrosis common? Where is it seen and what causes it? Is it treatable?

A
  • worldwide
  • common
  • treatable
    > multiple aetiologies
  • necrosis of the grey matter of the brain d/t THIAMINE or SULPHUR metabolism
  • seen all ruminants and pseudo ruminants
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8
Q

How does thiamine metabolism link to cerebrocortical necrosis?

A
  • altered thiamine (vit B1) metabolism
  • thiamine cofactors for glucose production
  • brain obligate glucose metaboliser
    -> ^ lactate, pyruvate and oxoglutarate
    -> intraneuronal sweeping d/t v activity ATP Na/H2O pumps
  • ^ ICP, neuronal necrosis, oedema and cortical necrosis
  • Thaimine storage very poor in ruminants so absolute requirement daily of thiamine
  • Any condition that Inactivates thiamine or v synthesis -> deficiency.
    > eg. Excessive grain intake suddenly or chronically (promotes thaminase producing bacteria)
    > eg. Deficiency of pasture with no supplements
    > eg. Thaminase producing plants like bracken
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9
Q

Now can sulphur link to cerebrocortical necrosis?

A
  • sulphur found in beef cattle feed
    > sulphur, sulphates and gypsum.
    > found in cruciferous vegetables and molasses
  • sulphates reduced to sulphides, encore orated into crude protein and released
  • sulphides are neurotoxic (inhibit cytochrome C oxidase, prevent ATP production)
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10
Q

Clinical signs of CCN?

A
  • sudden death/recumbent and comatose/convulsions/hypertonic between seizures (GRAVE PROG)
  • hours/days onset
  • cortical blindness
  • opisthotonos (star gazing)
  • hypermetric gait
  • hyperaesthesia -> depression
  • miosis
  • strabismus
  • head tilt
    > if caught early PROG GOOD
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11
Q

Tx CCN? How quick does recovery occour?

A

= response within 24hours, very rewarding!
> thiamine vit b1
- NOT multivitamin (will cause toxicity of other vitamins)
- IM or SC (10mg/kg TID initially)
> dexamethosone to v cerebral oedema?
> diazepam to control seizures? (NOT LIC, use pets only)

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12
Q

Clinical path findings for dx of CCN?

A
  • response to Tx after suspicion d/t hx and clinical signs
  • erythrocyte transketolasek activity (??££££ and usually has to go abroad)
  • CSF tap to r/o meningitis etc. - will see MILD pleiocytosis only and ^ protein conc
  • PME: cortical swelling, softening and flattening of gyri; necrotic areas of cerebral cortex fluorescence under UV; severe cases cerebellum may herniate -> constant seizuring
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13
Q

4 main viruses affected neuro FA

A

> maedi visna
- retrovirus affects sheep (can cross species infect goats)
- also known as ovine progressive pneumonia
caprine arthritis encephalitis virus
- retrovirus affects goats (can cross species infect sheep)
- also known as infectious leukoencephalomyeloitis.
border disease virus
= BVDV
- pestivirus
- sheep and goats
- hairy shaker
- may infect cattle -> BVDV
BVDV
- pestivirus
- cattle

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14
Q

Clinical signs of maedi visna

A
  • diffuse encephalitis: ataxia, proprioceptive deficits, circling, blindness, coma, convulsions
  • or just emaciation
  • time from onset - death 1-2years
  • immunosuppressive - 2* infection (mastitis, pneumonia)
  • spread: aerosol, colostrum, milk, transplacental
  • diffuse non supparative inflam
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15
Q

How is the incidence of maedi visna changing over time?

A

Increasing in UK

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16
Q

How can maedi visna be controlled ?

A
  • ab ELISA

- accreditation testing scheme (Premium sheep and goat health scheme) for maedi visna free status

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17
Q

Clinical signs of caprine arthritis encephalitis virus

A
  • Leukoencephalomyeltitis: ataxia, paresis, head tilt, nystagmus, opisthotonos, v PLR, paralysis
  • symmetric or asymmetric
  • usually young goats
  • enlarged joints, shifting lameness, weight loss, mastitis, Ill thrift
  • spread: aerosol and colostrum, milk, transplacental
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18
Q

How can caprine arthritis encephalitis virus be controlled?

A
  • ab ELISA
  • test and cull (easiest)
  • can form 2 herds clean and dirty to try and phase out but £££ and effort (need 6m apart and no fomite transfer)
  • accreditation (Premium sheep and goat health scheme)
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19
Q

Outline pathogenesis of Border Disease virus

A

= BVDV

  • infect naive ewes in pregnancy
  • abortion, infertility, deformities
  • lambs infected in utero in first half either resorb/abort or closer to 60d become immunotolerant and develop a persistent viraemia -> PI lambs (hairy shaker) no Ab de table look for virus Ag
  • adults develop short inapparent viraemia and develop immunity to re infection (not big problem)
  • spread vertical and horizontal transmission
  • immunological competence around d60-85
  • if infection occurs 2nd half pregnancy :death in utero ~85d or closer to parturition- weak/normal lambs with Ab for virus but no virus present
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20
Q

Clinical signs of Border Disease Virus

A

> lambs affected

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21
Q

Testing for border disease virus

A

Antibody young sheep for flock status

Virus. Testing to find PIs

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22
Q

Clinical signs of BVDV

A 
> hydrocephalus 
> cerebellar hypoplasia 
- head tremors 
- weak 
- proprioceptive deficits
- ataxia 
- blindness 
- strabismus / nystagmus 
- often due shortly after birth 
> if infected at 100-150d gestation
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23
Q

4 parasitic diseases that can affect CNS

A 
> ovine encephalo-myelitis 
- Louping ill in sheep 
- transmitted by ixides ricinus tick 
> coenuresis
- sheep gid  
- coenuresis cerebralis and intermediate stage of Taenia multiceps
> nervous coccidiosis 
- feedlot calves mainly +- sheep/goats
- eimeria species (coccidia)
> sarcocystis
- sporozoan infection ruminants 
- sarcocystis cruzi and hirsuta
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24
Q

Clinical signs of ovine ecaphalomyelitis

A

Fever, depression, mm tremors, ataxia, hypermetria, bunny hopping, convulsions, coma

  • yearling sheep grazing contaminated pastures (spring) weeks after put on pasture
  • mortality low, recover ~2 weeks
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25
Q

Tx of ovine encephalo-myelitis

A

Supportive

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26
Q

Which regions of the UK is ovine encephalomyelitis seen in?

A

~SW and North

27
Q

Clinical signs of coenuresis. How is it spread? Pathogenesis ?

A

Space occupying cranial lesion so depends where lesion is

  • ataxia, unilateral vision loss, head tilt, circling, hypermetria, coma
  • adult worms shed in dog/cat, ingested on pasture, eggs hatch in SI migrate to CNS via blood and mature into c. Cerebralis.
28
Q

Tx coenuresis

A

Praziquantel

  • Tx cats and dogs
  • prevent access cats and dogs
29
Q

Intermediate host of ovine encephalo myelitis

A

Grouse

30
Q

Where is nervous coccidiosis more commonly seen? Clinical signs? Pathogenesis? Mortality?

A
  • US/New Zealand
  • GI signs then depression, ataxia, hyperaesthesia, opisthotonos, seizures
  • neurotoxin from parasite
  • mortality rate high
31
Q

Tx nervous coccidiosis

A

Tx coccidiosis - diclazuril, toltrazuril

32
Q

Clinical signs of sarcocystis. Common? Pathogenesis?

A
  • rare
  • usually abattoir issue d/t muscular form of disease
  • ataxia, weakness, tremors, hyperexcitability, seizures
  • if ^ number sport cysts ingested (mostly asymptomatically)
33
Q

Tx sarcocystis

A
  • Diclazuril/toltrazuril
  • Sulfa drugs
  • control access to carnivore fences
34
Q

What are TSEs?

A
  • NOTIFIABLE
  • Slowly progressing fatal infectious neurodegenerative diseases
  • accumulation of abnormal prion proteins (PrPsc) in CNS
  • deposition as amyloid plaques in lymphoreticular and nervous tissue
  • PrPc post translational modification to abnormal PrPsc which has different protein structure and is resistant to degradation
35
Q

What are the main categories of cortical disease in fa?

A 
>cerebrocortical necrosis 
> viral 
- maedi visna 
- caprine arthritis encephalitis 
- border disease 
- BVD 
> parasitic 
- Louping ill
- coenuresis/gid
- sarcocycstis
- nervous coccidiosis 
> TSE 
- scrapie 
- BSE 
> trauma/abscess/meningitis/tumour
36
Q

What TSE is seen in sheep and goats?

A

Scrapie

37
Q

Clinical signs of scrapie

A

> aged 1-5yrs
behavioural
- separate from flock, restless and nervous
weight loss
pruritis
- wool loss, dermatitis, excoriation, nibble reflex
ataxia, weak, tremors, ptyalism, seizures, collapse

38
Q

What testing or legislation is in place around scrapie?

A
  • notifiable

- TSE testing programme: all fallen stock (goats and sheep) aged >18months tested

39
Q

How is scrapie spread?

A
  • colostrum/milk
  • dam-offspring
  • placenta
  • feaces/urine
  • can survive in soil
40
Q

Diagnosis and prevention?

A
  • dx: IHC and western immunoblot
  • brred for genetic resistnace: NSP1 type 1 (ARR) codons control susceptibility
    > native rare breeds more likely susceptible d/t less breeding for resistnace
41
Q

What TSE is seen in cattle?

A
  • BSE (mad cow dz)
42
Q

Clinicla signs of BSE

A 
> 4-6yo 
> behaviour 
- separate from herd
- fear/panic/excitement 
> NO pruritis cf. sheep 
> hyperaesthesia, aggression, ataxia and tremors
43
Q

Cause of BSE

A

feeding meat and bone meal to cattle
- banned and ban tightened -> v incidence
NO genetic component (unlike scrapie)

44
Q

What may BSE cause in humans?

A

nvCJD

45
Q

Prevention of BSE risk in food chain

A
  • specified risk material control: brain, eyes, SC30 months cannot be sold for food unless tested
  • no mechanically recovered meat (stripping carcasses to get all tiny bits off of SC etc.)
46
Q

What is listeria? What does listeria cuase?

A

> Listeria monocytongenes, G+ anaerobe
found in spoiled silage, soil, rotting vegetation, feaces carrier animals (end pregnancy and lambing time), environment etc. (not necessarily just silage)
muiltiplies at low temperatures
- acute meningoencephalitis
- usually individual (not herd) problem
- infects brain by haematogenous spread or ascent from CN 5 rootlets
-> multifocal microabscesses in brain tissue

47
Q

Which species more severely affected by listeria/

A

sheep and goats - more acute and higher fatality rates cf cattle

48
Q

When is trigem rootlet exposed and susceptible to listeria infection?

A

younger animals when permenant teeth erupting or breaks in mucosa

49
Q

CLinical signs of listeriosis?

A
  • fever (early disease)
  • anorexia
  • depression
  • proprioceptive deficits
  • head pressing
  • compulsive circling
    > CN V-XII deficits
  • 5: dropped/asymmetric jaw, facial analgesia
  • 6: medial strabismus on lesion side
    7: ptosis, loss menace response, absent palpebral, drooped ear, deviated philtrum (loss tone), drooling slaiva from ipsilateral side, exposure keratitis
    8: nystagmus, head tilt towards lesion, circle towards lesion
    9,10,11: stertor, dysphagia, paresis of tongue, tongue may protrude from ipsilateral side
    > progressive to seizures, unconsciousness, coma
50
Q

Dx of listeriosis

A
  • clinical suspicion

- CSF tap: ^ protein and WBC

51
Q

Tx listeriosis

A
  • ^ dose penicillin (off label, double the dose 44,000IU instead of 22, if IM BID, if IV QID
  • try to maintain peak concentration
    ~ oxytetracycline 10mg/kg not as good as penicillin
  • NSAIDs
  • fluids
52
Q

Why is listeriosis a concern?

A

Public health

- contamination of raw milk products and cheese etc.

53
Q

When should you consider euthanasia with Listeriosis?

A

If down for 12-24hrs, try tx then PTS if no up.

- if still standing prognosis not too bad

54
Q

3 main metabolic diseases causing neruo signs?

A

> nervous ketosis (Van Windens NEB lect)
hypmagnesaemia (grass staggers/grass tetany)
hypocalcaemia (milk fever)
- Van Windens Macromineral lect

55
Q

Top 3 spinal cord and peripheral nerve disorders

A
  • spastic paresis (elso heel)
  • peripheral nerve disorders (Van windens down cow lect) Sciatic n. etc. usually diary cows
  • enzootic ataxia (swayback)
56
Q

2 main neuromuscular disorders of FA?

A
  • tetanus (clostridium tetani)
  • botulism (clostridium botulinum)
    === horses (vax tet, not bot) see Richard peirceys neuromuscular lect
57
Q

What is spastic paresis?

A
  • elso heel
  • commonish
  • cattle: genetic component?
  • young animals 3weeks - 1 year
  • progressive hyperextension of the hindlimb/s
  • excessive extensor tone when standing (gastrocnemius and superifical extensor mm.)
  • progressive contraction of gastrocnemius muscle -> unable to flex hock during HL protraction, cranial ‘flick’ to gait
  • still able to flex manually and CAN KICK!!
  • overstimulation of gamma motor neurons of SC
58
Q

Ddx for Elso heel?

A
  • patella luxation (r/o as cant physically flex the limb with this condition)
  • fx
  • joint infection
59
Q

Tx elso heel

A

> surgical
- partial tenectomy of medial and lateral head of gastrocnemius tendon
- tibial neurectomy (more minor surgery, likely less effective)
- this is a salvage procedure to allow comfort and growth before culling
DO NOT BREED!!!
not good for showing aniamls either

60
Q

How much will a diary cow go for meat|? Beef bull? How much would a parital tenectomy cost to carry out?

A

dairy cow £800
beef bull £1500
- sx: £200

61
Q

Aetiology of swayback?

A

= enzootic neonatal ataxia

  • lambs and kids born to Cu deficient dams
  • sheep and goats have ^ requirement for copper cf. cattle etc.
62
Q

Clinicla signs of swayback?

A
  • progressive incordination and recumbency
  • starts HLs progresses to forelimbs
  • weight loss
  • D+
  • coat changes
63
Q

Tx swayback?

A
  • usually cannot tx clinically affected individual

- prompt prophylactic tx of whole flock

Neuro (30 decks)

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