Flashcards in Farm Neuro (McSloy) Deck (63):
What brain stem diseases affect FA?
-Otitis media-interna (bacterial)
What cerebellar diseases affect FA?
Which metabolic diseases cause neuro signs?
- nervous ketosis
Which spinal cord and peripheral nerve disorders affect FA?
- spastic paresis (Elso heel)
- enzootic neonatal ataxia (swayback)
- Fx, luxation and spinal abscesses
Which neuromuscular diseases affect FA?
Wha this cerebrocortical necrosis also known as?
Polioencephalomalacia (polio= grey matter, encephalo = Brain, malaria = softening)
Is cerebrocortical necrosis common? Where is it seen and what causes it? Is it treatable?
> multiple aetiologies
- necrosis of the grey matter of the brain d/t THIAMINE or SULPHUR metabolism
- seen all ruminants and pseudo ruminants
How does thiamine metabolism link to cerebrocortical necrosis?
- 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
Now can sulphur link to cerebrocortical necrosis?
- 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)
Clinical signs of CCN?
- sudden death/recumbent and comatose/convulsions/hypertonic between seizures (GRAVE PROG)
- hours/days onset
- cortical blindness
- opisthotonos (star gazing)
- hypermetric gait
- hyperaesthesia -> depression
- head tilt
> if caught early PROG GOOD
Tx CCN? How quick does recovery occour?
= 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)
Clinical path findings for dx of CCN?
- 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
4 main viruses affected neuro FA
> 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
- sheep and goats
- hairy shaker
- may infect cattle -> BVDV
Clinical signs of maedi visna
- 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
How is the incidence of maedi visna changing over time?
Increasing in UK
How can maedi visna be controlled ?
- ab ELISA
- accreditation testing scheme (Premium sheep and goat health scheme) for maedi visna free status
Clinical signs of caprine arthritis encephalitis virus
- 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
How can caprine arthritis encephalitis virus be controlled?
- 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)
Outline pathogenesis of Border Disease virus
- 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
Clinical signs of Border Disease Virus
> lambs affected
Testing for border disease virus
Antibody young sheep for flock status
Virus. Testing to find PIs
Clinical signs of BVDV
> cerebellar hypoplasia
- head tremors
- proprioceptive deficits
- strabismus / nystagmus
- often due shortly after birth
> if infected at 100-150d gestation
4 parasitic diseases that can affect CNS
> ovine encephalo-myelitis
- Louping ill in sheep
- transmitted by ixides ricinus tick
- sheep gid
- coenuresis cerebralis and intermediate stage of Taenia multiceps
> nervous coccidiosis
- feedlot calves mainly +- sheep/goats
- eimeria species (coccidia)
- sporozoan infection ruminants
- sarcocystis cruzi and hirsuta
Clinical signs of ovine ecaphalomyelitis
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
Tx of ovine encephalo-myelitis
Which regions of the UK is ovine encephalomyelitis seen in?
~SW and North
Clinical signs of coenuresis. How is it spread? Pathogenesis ?
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.
- Tx cats and dogs
- prevent access cats and dogs
Intermediate host of ovine encephalo myelitis
Where is nervous coccidiosis more commonly seen? Clinical signs? Pathogenesis? Mortality?
- US/New Zealand
- GI signs then depression, ataxia, hyperaesthesia, opisthotonos, seizures
- neurotoxin from parasite
- mortality rate high
Tx nervous coccidiosis
Tx coccidiosis - diclazuril, toltrazuril
Clinical signs of sarcocystis. Common? Pathogenesis?
- usually abattoir issue d/t muscular form of disease
- ataxia, weakness, tremors, hyperexcitability, seizures
- if ^ number sport cysts ingested (mostly asymptomatically)
- Sulfa drugs
- control access to carnivore fences
What are TSEs?
- 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
What are the main categories of cortical disease in fa?
- maedi visna
- caprine arthritis encephalitis
- border disease
- Louping ill
- nervous coccidiosis
What TSE is seen in sheep and goats?
Clinical signs of scrapie
> aged 1-5yrs
- separate from flock, restless and nervous
> weight loss
- wool loss, dermatitis, excoriation, nibble reflex
> ataxia, weak, tremors, ptyalism, seizures, collapse
What testing or legislation is in place around scrapie?
- TSE testing programme: all fallen stock (goats and sheep) aged >18months tested
How is scrapie spread?
- can survive in soil
Diagnosis and prevention?
- 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
What TSE is seen in cattle?
- BSE (mad cow dz)
Clinicla signs of BSE
- separate from herd
> NO pruritis cf. sheep
> hyperaesthesia, aggression, ataxia and tremors
Cause of BSE
feeding meat and bone meal to cattle
- banned and ban tightened -> v incidence
NO genetic component (unlike scrapie)
What may BSE cause in humans?
Prevention of BSE risk in food chain
- 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.)
What is listeria? What does listeria cuase?
> 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
Which species more severely affected by listeria/
sheep and goats - more acute and higher fatality rates cf cattle
When is trigem rootlet exposed and susceptible to listeria infection?
younger animals when permenant teeth erupting or breaks in mucosa
CLinical signs of listeriosis?
- fever (early disease)
- 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
Dx of listeriosis
- clinical suspicion
- CSF tap: ^ protein and WBC
- ^ 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
Why is listeriosis a concern?
- contamination of raw milk products and cheese etc.
When should you consider euthanasia with Listeriosis?
If down for 12-24hrs, try tx then PTS if no up.
- if still standing prognosis not too bad
3 main metabolic diseases causing neruo signs?
> nervous ketosis (Van Windens NEB lect)
> hypmagnesaemia (grass staggers/grass tetany)
> hypocalcaemia (milk fever)
- Van Windens Macromineral lect
Top 3 spinal cord and peripheral nerve disorders
- spastic paresis (elso heel)
- peripheral nerve disorders (Van windens down cow lect) Sciatic n. etc. usually diary cows
- enzootic ataxia (swayback)
2 main neuromuscular disorders of FA?
- tetanus (clostridium tetani)
- botulism (clostridium botulinum)
=== horses (vax tet, not bot) see Richard peirceys neuromuscular lect
What is spastic paresis?
- elso heel
- 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
Ddx for Elso heel?
- patella luxation (r/o as cant physically flex the limb with this condition)
- joint infection
Tx elso heel
- 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
How much will a diary cow go for meat|? Beef bull? How much would a parital tenectomy cost to carry out?
dairy cow £800
beef bull £1500
- sx: £200
Aetiology of swayback?
= enzootic neonatal ataxia
- lambs and kids born to Cu deficient dams
- sheep and goats have ^ requirement for copper cf. cattle etc.
Clinicla signs of swayback?
- progressive incordination and recumbency
- starts HLs progresses to forelimbs
- weight loss
- coat changes