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
Course of rabies disease
Sudden onset of signs
Signs are rapidly progressive
Signs often change
Affected horse becomes recumbent
Invariably fatal disease (<14d)
Diagnostic testing for rabies
CBC
Biochem profile
CSF analysis
ALL NORMAL ^#&$^$#$
Postmortem rabies
Wear gloves***
Remove brain, send to state lab and place in formalin. Tests are conclusive and within 24-48 hrs
Pathology for rabies
Postmortem exam - could have diffuse edema, congestion, hemorrhage
Lymphocytic perivascular cuffing
Neuronal degeneration
Negri bodies in horses w signs >4 days
West Nile viral encephalomyelitis
Inflammatory disease of brain and spinal cord of horse caused by West Nile virus
Flava virus that resides in wild birds, transmitted via mosquitos
WNVE epidemiology
Reported frequently in horses in Africa Middle East, Asia, southern Europe during 1900’s
WNVE history /physical exam
Sudden onset of dullness and inappetence
Fever in 50% of cases
Neurologic signs = weakness, ataxia, muscle fasiculations, hyperesthsia, blindness
May progress to recumbency
WNVE diagnostic tests
Antemortem - serum antibodies IgM ELISA
CSF analysis: mononuclear pleocytosis
Increased protein
Xanthochromia
Post mortem diagnosis by RT-PCR of tissues of CSF
WNVE treatment
Supportive care - fluid therapy, enteral or parenteral nutrition, deep bedding
Anti inflammatory medications: flunixin, dexamethazone, dimethylosulfoxide
