Equine Behaviroal Disorders Flashcards
Lesion location
Neural
Cerebrum
Brainstem
Extra neural
Liver failure
Renal failure
Cerebrum
Dull, blind, seizures
Brainstem
Dull, weakness/ataxia, cranial nerve dysfunction
Adult differentials
Equine viral encephalomyelitis
Rabies
West Nile virus
Hepatic encephalopathy
Bacterial meningitis
Equine leukoencephalomalacia (moldy corn) rare
Foal differentials
Neonatal encephalopathy
Bacterial meningitis
Equine viral encephalomyelitis
3 different strains of virus
Eastern, western and Venezuelan
Virus persists in environment by asymptomatic infection of reservoir hosts (birds, reptiles, rodents)
Mosquitos are transfer hosts
Risk of EVE
Peak season
Temperate climate: June-November
Subtropical: year round
Horses are sentinel animal for human risk * good idea to report
presenting signs of EVE
Sudden onset of dullness, inappetence, fever, stiff
Hyperesthsia, aggressive, compulsive walking, blind, headpressing, circling, ataxia, head tilt, paralysis of pharynx, larynx or tongue
Diagnosing EVEM
CBC: leukopenia
CSF: increased protein/leukocytes
PCR - antibody titer
Serology: four fold increase in antibody titer, high terminal titer
Treating EVEM
No specific antiviral meds
Treat w anti inflammatories
Fluid therapy, nutritional support
Prognosis for EVEM
Depends on strain of virus
EEE: 75-90% fatality
WEE: 25-50% fatality
VEE: 40-90% fatality
Survivors retain permanent deficits
Prevention for EVEM
Monovalent bivalve t or trivalent killed vaccines
Initial 2 doses followed by annual vaccination
Protection for 6 months
Equine rabies
Neurotrophic rhabdovirus
Transmitted by bite from infected animal
Long incubation period (3w-3m)
Neurological exam findings for rabies
Dumb form: dullness, ataxia, weakness, Dysphagia, dysphonia
Furious form: aggression, hyperesthsia, seizures, tremors
Paralytic form: progressive ascending paresis/paralysis, flaccid tail
Common findings with rabies
Paraparesis
Hyperesthsia
Aggression
Caudal hypotonia
Pharyngeal paralysis
Seizures
Self mutilation