Food Animal - CNS Dz Flashcards

1
Q

List differential diagnoses for ruminants with an elevated white blood cell count in their CSF.

A
  • Neutrophils: bacterial meningitis.
  • Lymphocytes: viral encephalitis, listeriosis.
  • Macrophages: trauma, polioencephalomyelitis.
  • Eosinophils: parasite migration.
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2
Q

List clinical signs of cerebral disease in ruminants.

A
  • Excitement, mania.
  • Seizures.
  • Compulsive behaviour.
  • Stupor.
  • Coma.
  • Abnormal vocalisation.
  • Central blindness.
  • Hyperaesthesia.
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3
Q

What is the most common cause of symmetric cerebral disease in ruminants?

A

Metabolic abnormalities incl dehydration, acid-base abnormalities, electrolyte disturbances.

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4
Q

Outline aetiologic agents of polioencephalomalacia (PEM) in ruminants.

A
  • Thiamine deficiency.
  • Sulphur toxicity.
  • Lead toxicity.
  • Salt toxicity.
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5
Q

Describe the pathophysiology of thiamine deficiency in PEM of ruminants.

A
  • Thiamine is produced by rumen microflora; production meets daily requirements; not stored.
  • Thiamine essential for cerebral glucose metabolism; it is a co-enzyme of the pentose-phosphate pathway.
  • Thiamine deficiency can be caused by rumen acidosis/disruption, thiamine inhibition or ingestion of plants containing thiaminases e.g. bracken fern, horsetail.
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6
Q

Describe the pathophysiology of suphur toxicity in PEM of ruminants.

A
  • Sulphur in the rumen is either assimilated into microbial protein or combines with H to form H2S.
  • H2S is detoxified by the liver.
  • Excess H2S prod –> overwhelms liver, or eructated and excess H2S inhaled.
  • H2S inhibits cytochrome C oxidase –> no ATP –> neuronal swelling –> PEM.
  • Source of S: feed intake limiters e.g. gypsum, by-products of corn, beet and sugar cane extraction e.g. molasses, water sources, S-accum plants incl rape, kale, turnips. Lamb’s quarters, Burning bush.
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7
Q

Describe the pathophysiology of lead toxicity in PEM of ruminants.

A
  • Lead has a profound effect on sulfhydryl-containing enzymes, the thiol content of erythrocytes, antioxidant defenses, and tissues rich in mitochondria –> cerebellar hemorrhage and edema associated w capillary damage.
  • Industrial pollution from smelting.
  • Junk piles: lead paint, gasoline and motor oil, insecticides, herbicides, lead batteries, shotgun pellets.
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8
Q

Describe the pathophysiology of salt toxicity in PEM of ruminants.

A
  • May be due to true salt poisoning e.g. ingestion of salt-licks, but usually due to water restriction.
  • Alteration of cerebral energy metabolism –> dec pentose phosphate pathway activity –> dec ATP prod –> accum of Na –> oedematous swelling.
  • Brain’s immediate response to hypertonic state is to lose water; rapid correction occurs through accum of electrolytes then idiogenic osmoles and water.
  • RISK OF TX!! If you rapidly correct the hypertonic state cerebral oedema will occur due to the idiogenic osmoles.
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9
Q

List clinical signs of PEM in ruminants.

A
  • Depression/stupor.
  • Central blindness.
  • Convulsions.
  • Head pressing.
  • Aimless wandering.
  • Inco-ordination.
  • Ataxia.
  • Muscle tremors.
  • Opisthotonos.
  • Dorsomedial strabismus.
  • Nystagmus.
  • Bruxism.
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10
Q

Outline test results for diagnosis of PEM in ruminants.

A
  • CSx and Hx.
  • CBC/MBA/CSF cytology: rarely useful.
  • CSF may have subjectively inc pressure on collection.
  • Thiamine defic: blood thiamine (160mmol/L or CSF:serum >1.
  • Sulphur tox: rumen H2S, sulfur content of feed and water
  • Lead tox: blood or tissue lead, or if chronic and blood Pb no measure RBC δ‐aminolevulinic acid dehydratase; RBCs may show basophilic stippling.
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11
Q

Describe necropsy findings in ruminants with PEM.

A
  • Gross lesions: brain swelling with gyral flattening and coning of the cerebellum due to herniation into the foramen magnum, slight yellowish discoloration of the affected cortical tissue, autofluorescent bands of necrotic cerebral cortex when viewed with ultraviolet illumination –> macroscopically evident cavitation of cerebrocortical tissue. - Histo: necrosis of cerebrocortical neurons; neurons are shrunken and have homogeneous, eosinophilic cytoplasm, nuclei are pyknotic, faded, or absent, vessel cells undergo hypertrophy and hyperplasia; later stages –> cortical tissue undergoes cavitation as macrophages infiltrate and necrotic tissue is removed.
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12
Q

Outline treatment options for PEM in ruminants.

A
  • Thiamine: 10mg/kg IV q6h.
  • Diuretics: 20% mannitol.
  • Dexamethsone: 1-2mg/kg IV.
  • Chelation therapy for Pb: EDTA IV, oral MgSO4 forms insoluble lead sulphides.
  • IVFT as needed.
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13
Q

Describe the rabies virus.

A
  • Family: Rhabdoviridae; bullet-shaped viruses.
  • Genus: Lyssavirus.
  • Non-segmented, negative-stranded RNA virus.
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14
Q

Describe transmission and incidence of rabies in the US.

A
  • Distinct strains in raccoons (most common), skunk, bat, coyote, fox, canine.
  • Transmission by exposure to saliva containing rabies virus (bite or non-bite); possible all warm-blooded animals.
  • US 2012 cases: 5,669 wildlife, 115 cattle, 47 equids, 13 small ruminants, 1 human.
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15
Q

Describe clinical manifestations of rabies in cattle.

A
  • Multiple forms: dumb, paralytic, furious; not mutually exclusive.
  • Rapidly progressive and uniformly fatal.
  • Odontopharyngeal paralysis.
  • Ptyalism.
  • Hindlimb ataxia.
  • Perineal analgesia.
  • Yawning.
  • Tenesmus.
  • Hyperaesthesia.
  • Paraphimosis.
  • Hypersexuality.
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16
Q

Describe the pathophysiology of rabies in ruminants.

A
  • Ruminant bitten by infected animal.
  • Virus uptake into peripheral nerves.
  • Retrograde axoplasmic flow to the CNS.
  • Incubation for 30-90 days.
  • Virus replicates then invades innervated sites (salivary glands and nasal planum).
  • Behaviour change enhances perpetuation.
  • Shedding before clinical signs in possible.
  • Causes a non-suppurative encephalitis.
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17
Q

Describe diagnosis of rabies in infected ruminants.

A
  • Examine whole brain.
  • Histology: non-suppurative encephalitis; negri bodies are pathognomonic lesion but not seen in all cases.
  • Fluorescent antibody test on brain tissue; highly specific; gold standard by public health departments.
  • Notifiable!!
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18
Q

What should be done with livestock potentially exposed to a rabid animal?

A
  • Unvaccinated livestock: slaughter or sacrifice immediately:
  • If within 7 days post‐bite: ok to eat cooked meat.
  • Federal inspectors will reject if within 8 mo of known
    exposure
  • Unvaccinated livestock, owner unwilling to slaughter: keep under close observation for 6 months.
  • Currently vaccinated livestock (reg for cattle and sheep): revaccinate immediately and 45 day quarantine.
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19
Q

What is the aetiologic agent of Bovine Spongiform Encephalopathy (BSE)?

A
  • Transmissible spongiform encephalopathy of cattle.
  • A prion i.e. infectious protein that replicates without the need for nucleic acid.
  • Induces conformation change in normal cell membrane protein (PrPc) to form the abnormal prion (PrP-BSE).
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20
Q

Describe the pathophysiology of BSE.

A
  • Long incubation period; CSx most in 4-6yo cattle therefore higher incidence in dairy than beef breeds.
  • Ingested in cattle by-products e.g. bone meal.
  • Propogates in distal ileum, moves through GIT-associated lymphoid tissue to peripheral nerves –> brain, optic nerve, cervical, thoracic and trigeminal ganglia, facial and sciatic nerves.
  • Accumulation of PrP-BSE in the CNS –> progressive and irreversible neuro dysfunction (exact mech unknown).
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21
Q

List the clinical signs of BSE.

A
  • Early subtle behaviour changes may be missed.
  • Apart from herdmates.
  • Apprehensive, fearful.
  • Unprovoked aggression.
  • Hyperaesthesia.
  • Headshaking.
  • Ptyalism.
  • Head rubbing.
  • Muscle fasciculations.
  • Excessive vocalisations.
  • Freq/repetitive head tossing, licking nostrils, yawning, flehmen, head butting and restlessness.
  • Relative bradycardia given level of excitement.
  • Wt loss and dec mild prod.
  • Ataxia and tremors.
  • Recumbency.
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22
Q

Outline diagnosis of BSE in cattle.

A
  • No in vivo test, only post-mortem.
  • Histo: neuronal degeneration and intraneuronal vacuolation in specific brain areas; obex of medulla.
  • Tests to ID prion in brain or SC tissue: Western blot, paraffin-embedded tissue blot, ELISAs.
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23
Q

Outline treatment and prognosis for BSE in cattle.

A
  • No tx.

- Always fatal.

24
Q

Describe the aetiology of scrapie.

A
  • Oldest known TSE.
  • Infects sheep, goats and mouflons.
  • Prion (PrP-Sc) is distinct from BSE prion.
25
Q

Describe the pathophysiology of scrapie.

A
  • Unlike BSE, can infect a variety of non-neural tissues incl lymphoreticular system, kidney and placenta.
  • Majority of transmission during birthing season –> oral intake of prior in birthing fluids/placenta.
  • PrP-Sc trans to CNS along vagus n from the GIT.
  • Dysfunction of CNS appears to roughly correlate w accum of PrP-Sc in the brain.
26
Q

List the clinical signs of scrapie.

A
  • 1-5yo sheep.
  • Typically dz course slow; lasts several months,
  • Wt loss.
  • Stay apart from the herd, restless, nervous.
  • Pruritis of inc intensity –> secondary wool loss, dermatitis, skin infections or excortiations on head, withers, flanks, back, rump, base of tail and lower limbs.
  • Head and fact rubbing and shaking –> ocular lesions or aural haematomas.
  • Bruxism.
  • Ptyalism.
  • Regurgitation.
  • Head to generalised tremors.
  • Apathy, exercise intol, hypermetria and ataxia.
  • May progress to stupor, episodic collapse and convulsions.
27
Q

Outline diagnosis of scrapie in sheep.

A
  • IHC may show PrP-Sc in biopsies of lymphoid tissue of tonsils, nictitating membrane, retropharyngeal LNs and rectoanal junction; limited sensitivity.
  • PM collect brainstem (partic obex), tonsillar tissue and medial retropharyngeal LNs.
  • Histo: neuronal vacuolations and PrP-Sc deposits in specific brain nuclei.
  • IHC, Western blot, ELISA in autolysed tissue.
28
Q

Outline treatment and prognosis for scrapie.

A
  • No treatment.

- Invariably fatal.

29
Q

Describe the aetiology of pseudorabies (Aujeszky Dz) in cattle.

A
  • Suid hervesvirus type 1; alphaherpesvirus of pigs.

- Causes acute, severe and usually fatal encephalitis in cattle, sheep, goats, cats, dogs, wildlife, rarely horses.

30
Q

Describe the pathophysiology of pseudorabies in cattle.

A
  • Incubation period 90-156h; illness lasts 8-72h.
  • Sudden death.
  • Paraesthesia w severe pruritis, self-trauma.
  • Fever.
  • Bellowing.
  • Bloat.
  • Foot stamping.
  • Ptyalism.
  • Twitching.
  • Chewing of the tongue.
  • Ataxia, circling, nystagmus, strabismus.
  • Agression may be seen but depression more common.
  • Tenesmus.
  • Hyperaesthesia.
  • Excessive licking of nostrils.
  • Continuous mastication.
  • Coma.
  • Convulsions.
  • Opisthotonus.
31
Q

List the clinical signs of pseudorabies in cattle.

A
  • Exposure can be intradermal, subcutaneous, intranasal or oral –> virus spreads to CNS by axonoplasmic transport.
  • Eliminated from domestic swine herds in US but still present in feral pigs.
32
Q

Outline diagnosis of pseudorabies in cattle.

A
  • Virus can be isolated from pharyngeal or nasal swabs or infected neural tissue (sensory ganglia or dorsal horn SC).
  • ABs to IBR may cross-neutralise the pseudorabies virus, founding serologic tests.
  • Necropsy: non-suppurative encephalitis, neuronal degeneration, eosinophilic intranuclear inclusion bodies; lesions most pronounced in dorsal nerve rootlets and the dorsal horn of the SC.
33
Q

Outline treatment and prognosis for pseudorabies in cattle.

A
  • No treatment.

- Most cases are fatal.

34
Q

Which two bovine herpesviruses have been associated with encephalitic disease in cattle?

A
  • BoHV-1 - CNS dz rare.
  • BoHV-5 - neurotropic, more common CNS dz than than BoHV-1; more common in Sth America than USA.
  • Both alpha-herpesviruses.
35
Q

List the clinical signs of encephalitic bovine herpesvirus infection.

A
  • Depression.
  • Mild nasal and ocular discharge (URT dz before/during).
  • Conscious proprioceptive deficits.
  • Pyrexia (esp. BoHV‐1).
  • Lethargy, inappetence, apathy.
  • Muscle trembling, circling, ptyalism, jaw chomping, tongue protrusion, head pressing, ataxia.
  • No blindness noted in natural and experimental cases.
  • Recumbency and seizures, opisthotonos.
  • Frequently fatal.
36
Q

Describe the pathophysiology of encephalitic bovine herpesvirus infection.

A
  • Transmission via direct contact or aerosole.
  • Infection of upper respiratory tract NB respiratory signs uncommon with BoHV‐5.
  • Spread to CNS via trigeminal and olfactory nerves
  • Establishment of persistent infection in trigeminal ganglion
37
Q

Outline diagnosis of encephalitic bovine herpesvirus infection in cattle.

A
  • Indistinguishable from other viral encephalitides.
  • Seroconversion in survivors.
  • Histopath: Nonsuppurative encephalitis.
  • VI, IHC, PCR on brain tissues.
38
Q

Outline treatment and prevention of encephalitic bovine herpesvirus infection in cattle.

A
  • Treatment is supportive care only.
  • Vaccination; no BoHV‐5 vaccines available but cross‐protection gained from BHV‐1 vaccine.
  • MLV is protective against disease.
  • Vaccines do not prevent infection and latency.
  • Eradication in some EU countries:
    – Test and cull
    – Use of marker vaccines (gE‐negative vaccines).
39
Q

List the aetiologic agent of nervous coccidiosis and the signalment of affected animals.

A
  • Eimeria spp.
  • Calves and yearling cattle.
  • Sheep and goats.
  • Most common in Winter.
40
Q

Describe the pathophysiology of nervous coccidiosis.

A
  • Unknown.
  • Abnormal electrolyte status?
  • Abnormal glucose status?
  • Neurotoxin elaborated by coccidia and absorbed from abnormal intestines?
41
Q

List the clinical signs of nervous coccidiosis in ruminants.

A
  • Dxa, tenesmus, haematochezia prior to neuro signs.
  • Depression, inco-ordination, twitching, hyperaesthesia.
  • Progresses to recumbency, opisthotonus, periodic tremors, horizontal nystagmus, frothing at mouth, bellowing, snapping eyelids.
  • Blindness rarely seen.
  • Stimulation may precipitate tonic-clonic seizures.
42
Q

How is coccidiosis diagnosed?

A
  • Faecal flotation shows high burden of coccidial oocysts (5000-4 million epg).
  • CBC, chem, CSF, measure vit A, Pb to rule out other dz.
  • Necropsy: no macroscopic lesions in CNS; microscopic brain lesions are mild and non-specific incl oedema, occ shrunken neurons; parasitic invasaion of ileum, caecum and colon seen.
43
Q

Outline the treatment and prognosis for nervous coccidiosis in ruminants.

A
  • Sulphonamides or amprolium.
  • IVFT, electrolytes as needed.
  • Diazepam, phenobarbital if needed for convulsions.
  • Response to tx poor; high mortality (70%).
44
Q

What protozoal organisms is capable of causing neurologic disease in newborn calves following infection of the pregnant cow?

A
  • Neospora (closely resembles neospora caninum).
  • NB mainly causes abortions at 3-8mo gestation w foetal lesions consisting of non-suppurative encephalitis, non-suppurative myocarditis and myositis.
45
Q

What clinical signs are seen in calves with neosporosis?

A
  • Vary due to variable location of parasite in CNS.
  • Often unable to stand and suckle w abnormal spinal reflexes.
  • Flexural contracture of FLs, domed skull, torticolis have been reported.
  • Signs often progress after birth.
46
Q

Describe necropsy findings in calves with neosporosis.

A
  • Focal areas of brain discolouration.
  • Focal cavitation with cyst formation.
  • Reduction of grey matter.
  • Histo: non-suppurative inflamm of grey and white matter, focal lymphocytic meningitis, neuronal necrosis.
  • May also see myocarditis, hepatitis and myositis.
  • Protozoa can be seen in stained tissues.
47
Q

Which tick-bourne parasites can cause of encephalitis in cattle?

A
  • Babesia bovis, bigemina or argentina:
    • Usually cause intravascular and extravascular haemolysis and liver and kidney failure but occ cause encephalitis.
  • Erhlichia ruminantium (Africa and W. Indies) –> fatal encephalitis in goats, sheep and cattle.
  • Theileria spp. - exotic dz; T. mutans found in US is relatively non-pathogenic.
  • Trypanosoma: dz of African cattle.
48
Q

What are the risk factors for development of urea toxicity in cattle?

A
  • Exposure to either: feedstuff containing urea or ammonia, contaminated water sources or ingestion of fertilizers.
  • Plus lack of adaptation, high rumen pH, lack of fermentable carbohydrates.
  • NB study in JVIM 2012 reported 1% BWt soybean meal –> mild elevations in blood ammonia but no CSx; 2% BWt soybean meal –> nervous signs, hyperlgycaemia, hyperinsulinaemia, hyperammonaemia 12-22h post-admin.
49
Q

Describe the pathophysiology of urea toxicity in cattle.

A

• Rumen catabolizes urea to ammonia:
- Normally assimilated to bacterial proteins.
- Too much ammonia can overwhelm system.
• CSx develop rapidly w/in 10 – 30 min after feeding
• Alkaline rumen content favour non‐ionized ammonia
• Ammonia rapidly absorbed –> effect on intermediary metabolism, systemic lactic acidosis, hyperkalemia, ammonia accumulation in blood –> metabolic alkalosis.

50
Q

List the clinical signs of urea toxicity in cattle.

A
  • Abdominal pain (bruxism), bloat, frothing
  • Muscle tremors, weakness, ataxia
  • Hyperesthesia, violent struggling, convulsions
51
Q

Outline treatment of urea toxicity in cattle.

A
  • Ruminal infusion with cold water and 5% vinegar.
  • IV fluids.
  • Rumenotomy.
52
Q

Describe the aetiology of vitamin A deficiency in cattle.

A
  • Vitamin A is found in green plants and vit A precursors can be fed in cattle rations as b-carotene or retinoids.
  • Growing feedlot cattle have high vit req and are fed little green plants; can also occur w prolonged dry lot.
  • Feeds low in vit A: cereal grains other than corn, beet pulp, cottonseed hulls.
  • Can also occur w grains stored for a prolonged time in high temp/humidity or prolonged feeding of mineral oil.
53
Q

Describe the pathophysiology of vitamin A deficiency in cattle.

A
  • Vit A is resp for regeneration of rhodopsin in the retina, normal function of osteoblasts and osteoclasts, epi tissues, choroid plexus and repro tissues.
  • Vit A defic –> thickened dura mater –> diminished CSF absorption from the arachnoid granulations and nerve rootlets PLUS in young animals remodelling of bony foramina –> inc CSF pressure (–> papilledema).
  • Three forms of blindness:
    • Nyctalopia (night blindness) from dec regen of retinal pigment rhodopsin; reversible.
    • Degen in outer retinal layers; reversible if early.
    • Stenosis of optic foramen and compression of optic n; not reversible.
54
Q

List the clinical signs of vitamin A deficiency in cattle.

A
  • Calves: ill-thrift, anorexia, blindness, diarrhoea, pneumonia, intermittent fevers.
  • Adults: star-gazing posture, blindness, diarrhoea, anasarca, nystagmus, strabismus, exophthalmus, loss of PLR, intermittent tonic-clonic convulsions; coma, death; in good BCS if other nutrients in diet not lacking.
  • Characteristic ocular changes: papilledema –> pale optic disk w indistinct borders, may become atrophic (dull, flattened, small), retinal blood veseels become tortuous or appear occluded; retinal detachment may occur.
  • Repro disturbances: malformed foetuses, abortion, testicular degen, dec sperm counts.
  • Low vit A and carotene conc in feed and plasma.
55
Q

List diagnostic test findings in cattle with vitamin A deficiency.

A
  • Blindness w absent PLRs (vs blindness w normal PLRs in PEM) due to constrictions of optic n at optic foramen.
  • Low vit A and beta-carotene conc in feed, plasma (200mmHg) in some cases, inc protein, mononuclear pleocytosis.
56
Q

Outline treatment and prognosis for cattle with vitamin A deficiency.

A
  • Acute encephalopathy and simple papilledema: may respons to short course of Vit A supplementation; must give high dose oral therapy as can’t get enough into inj.
  • If severe vision loss vision will not be returned.
  • Supplement diet in all an animals off green feed: leafy, freshly cured hay, green pasture, alfalfa meal or stablised supplements.
57
Q

List viral agents which are capable of inducing hydrocephalus or hydrancephaly in developing calves via in utero infection.

A
  • Akabane virus.
  • BVDV.
  • Bluetongue.
  • Cache valley virus.
  • Border disease.
  • Aino.
  • Schmallenberg virus.