Food animal neurology 3 Flashcards
Verminous Meningoencephalitis
- causes in various species?
Hypoderma lineatum & bovis (cattle, horse, deer)
Paralophastrongylus tenuis (sm. ruminants, camelids, cervids (& horses)) – meningeal worm white-tailed deer)
Strongylus vulgaris (horse)
Halicephalobus gingivalis (formerly - Micronema deletrix) (horse)
Sorghum (Sudan Grass) Toxicity
- geography
- signs
- who is affected?
- toxin?
Southwestern USA, Australia
Ataxia, cystitis
Horses (cattle, sheep)
Toxin – unknown; may be chronic cyanide toxicity.
Sorghum Toxicity - more signs
– ataxia – hind limbs followed by urinary
incontinence. Swaying pelvic limb gait, knuckle at fetlocks. Horse may “bunny hop,” have difficulty backing & may fall.
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Genitalia
Vulva – laxity
Penis – dropped, lax
<><>tail weakness
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Loss of skin sensation of hindquarters.
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- Cystitis – secondary to urine retention
- Urine scalding of skin
- (pyelonephritis – rare)
Sorghum Toxicity - signs in sheep
Sheep – head shaking, ataxia, weakness, recumbency, opisthotonus, death (mortality <50%)
Sorghum Toxicity - additional signs in mares, foals, and lambs
– abortion in mares, arthrogryposis (foals & lambs), neurologic abnormalities (lambs)
Tetanus
- agent
- found where
- resistance?
- toxins?
- species sensitivity?
- signs
Clostidium tetani – anaerobic, spore-forming, Gram-positive bacterium
Bacteria are ubiquitous in environment
Spores are very resistant to disinfectants
Toxins: exotoxins: tetanospasmin (TeNT), tetanolysin
Sensitivity to the toxins: Horse > small ruminant > cattle
Signs: muscle rigidity & spasm
Death common – convulsions, respiratory failure
Tetanus
Horses - common ways to get infected
Wounds – esp. lower legs
Surgical wounds
Post partum uterus
Umbilicus
Injection site abscesses
Tetanus
Ruminants - common ways to getinfected
Post partum uterus
Elastrator bands, sharp castration sites
Tail docking, dehorning, disbudding
Bull rings, ear tags, shearing
IM injections
Umbilicus
Idiopathic tetanus
– rough feed causes mouth trauma.
> Toxicoinfectious, ingest toxin??
Tetanus
Pathogenesis
Tetanolysin causes tissue necrosis
Tetanospasmin – hematogenous spread to somatic neuromuscular
junctions and autonomic ganglia.
Binds to neuron, is internalized, moves by reverse axon transport
Reaches neuronal cell body, goes across synaptic cleft and binds to presynaptic junction, irreversibly binds, prevents release of inhibitory
neurotransmitters (glycine, GABA)
> Disinhibition of motor neurons
Botulism
- agent
- result of infection, signs
Clostridium botulinum
Anaerobic, spore-forming bacterium
Gram-positive
Highly fatal
Progressive, paralysis – generalized
Death – respiratory failure, euthanasia
Botulism - toxins, where found
– 8 types; A-G
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In general:
Soil contamination – A & B
Carcass contamination – C & D
Type B – mid-Atlantic States, Kentucky
Type A – western states
Type C – sporadic identification
Type D – rarely identified in North America
Botulism
- ways to get infected? most common?
- who is most susceptible? epidemiology?
Ingest preformed toxin – forage poisoning (most common)
Toxicoinfectious – gastrointestinal growth, very young animals (foals;
shaker foals)
Wound-associated (includes surgical sites)
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Horses much more susceptible than cattle
Usually 1 to a few horses in a herd but can have outbreaks
Cattle – may occur as outbreaks (increased incidence of poultry litter-associated)
Botulism - Pathogenesis
Toxin absorbed into blood stream
Travels to neuromuscular end plates
Attaches to the presynaptic nerve terminus
Receptor-mediated internalization
Light chain → prevention of attachment & release of acetylcholine vesicles
Paralysis – motor neurons, parasympathetic smooth muscle
Irreversible binding. Recovery - need to sprout new motor end- plates (takes weeks)
Feed Sources of botulism
Ensiled feed
> Small grains, hay
> Corn silage
Hay, grains
Carcasses
Poultry litter!!
botulism diagnosis?
Based solely on clinical signs
Identification of toxin, bacteria, spore detection: very difficult to do
> Mouse lethality assay – not available anymore
> Antibody detection in convalescent animal
Routine blood analysis, necropsy – may help to rule-out other diseases.
Diagnosis – Clinical Signs of botulism
Slow, ambling gait
Dysphagia – slow eating, drop feed, pharyngeal dysfunction,
fluid/feed material out of nose
Decreased gut sounds, colic
Weakness, muscle fasciculations, recumbency
Facial nerve paresis, paralysis
Weakness – tongue, eyelid, iris, tail tone
> flaccid paresis → flaccid paralysis
Botulism
Treatment
Remove source
Specific anti-toxin - obtain from commercial plasma sources
High-dose penicillin especially if wound-associated or gastrointestinal growth of bacteria.
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Caution – do not use gentamicin, oxytetracycline or procaine penicillin G as these will have a detrimental affect on neural conduction.
> always true but only really relevant in botulism cases!
Supportive care
Botulism
Prognosis –
Very poor if untreated, esp. if recumbent
With treatment – may be favorable if early, not severe
Requires intensive nursing care (fluid therapy, nutritional therapy);
> recumbent animals prone to secondary muscle damage & necrosis due to the weight.
CFIA – Rabies Cases 2023
- province with greatest prevalence?
- strain / species most prevalent?
- Ontario! >5x Sk, Nu… ~50% of all cases in canada
- mostly bat strain (far second is skunk)
Botulism Prevention
Do not feed ensiled feed to horses unless vaccinated against botulism
Vaccinate – Type B vaccine labelled for horses
