1-year-old male Rocky Mountain Horse, Equus caballus.This colt from northern Indiana was euthanized along with a 2-year-old filly, and presented
for necropsy in September 2007, after two days of weakness, depression, and neurologic signs including
head pressing. Both horses had been reared on the premises and had received no vaccinations.
Ascarids were in the small intestine.Â Verminous arteritis with serpiginous intimal
tracts was noted in the cranial mesenteric artery.Â Cerebral leptomeninges were congested and wet.Â The
lateral ventricles of the brain were slightly dilated.Â
In this section of cerebrum, cortical gray matter is more
severely affected than white matter by inflammatory
changes and necrosis.Â Thin cuffs (1 or 2 cell layers) of
lymphocytes, plasma cells, macrophages and neutrophils surround venules in the cerebral cortex.
These perivascular cuffs are thicker (4 or 5 layers) in the cerebral white matter.Â The leptomeninges,
especially in sulci, also have perivascular to diffuse infiltration by the same types of leukocytes.Â Some
venules, especially in the cerebral cortex, have fibrinoid material in their walls or in surrounding
tissue; a few have microscopic perivascular hemorrhage.Â There is widespread, predominantly
neutrophilic infiltration of the cortical gray matter.Â Increased numbers of macroglia and microglia
accompany the leukocytes.Â Focally, heavy neutrophil infiltration is noted in foci of parenchymal necrosis.
Many neuronal soma are shrunken with intense cytoplasmic eosinophilia and pyknosis
or karyolysis.Â Some of these dead neurons are surrounded by numerous
neutrophils; others are not.Â A few are undergoing neuronophagia.Â Similar,
but less severe neutrophilic inflammation is evident in the cerebral white matter.
Cerebrum, neutrophilic poliomeningoencephalitis.
Brain tissue from both horses
was positive by PCR for Eastern equine encephalitis
(EEE) virus, negative by fluorescent antibody test for
rabies virus, and negative by RT-PCR for West Nile
virus; EEE virus was also isolated in cell culture.
Eastern Equine Encephalitis
Eastern equine encephalitis (EEE) was suspected because of the clinical
signs in two young unvaccinated horses in late summer, so tissues
were shipped to the National Veterinary Services Laboratories
(NVSL) for diagnostic testing.Â Histologic changes of severe
neutrophilic polio encephalitis supported the tentative diagnosis,
which was confirmed by PCR and subsequent virus isolation in both
horses.Â This colt proved to be the sentinel case in an EEE outbreak in
northern Indiana.Â By late October 2007, 17 horses in 24 Indiana
counties had tested positive for EEE.Â This outbreak was considered the widest dispersion of
EEE in Indiana in the past 10-15 years.Â The fact that the first cases were not detected until September was
attributed to dry weather in early and mid-summer followed by rainy weather in late summer to support
the mosquito population.Â Horses are considered accidental hosts for EEE virus, which is maintained in
birds and transmitted to horses, people and other animals by mosquito vectors.1 After the development
of viremia, the virus invades the brain hematogenously and replicates in neurons, glial cells and vessels.
Histologic lesions target the cerebral cortex, sparing white matter and ganglia, resulting in neuronal
degeneration and death, typically with prominent neutrophil infiltration, especially in acute fatal cases.
Spinal cord: Meningoencephalitis, neutrophilic and lymphocytic, diffuse, moderate, with
neuronal necrosis and neuronophagia.
In some sections, there is rare
vasculitis and thrombosis, with large areas of
hemorrhage and necrosis.Â In horses with Eastern
equine encephalitis (EEE), gross lesions are
asymmetrical in the gray matter and include
congestion, hemorrhage, malacia, cerebral hyperemia,
edema, petechiation and focal necrosis.(2) Gray matter
lesions are more severe in the frontal, rhinencephalic,
and occipital areas of the cerebral cortex, as well as the
thalamus and hypothalamus, and the intensity of
inflammation diminishes as lesions progress caudally.
Eastern equine encephalitis virus may cause small
intestinal lesions that include multifocal myonecrosis,
lymphomonocytic myositis and focal mild perivascular
lymphocytic infiltration in the submucosa.Â Pigs
typically develop myocarditis from EEE virus, and
Guinea pigs and white mice are highly susceptible.(1)
Other new-world alphaviruses in the Togaviridae family include Western equine encephalitis (WEE) virus and Venezuelan equine encephalitis (VEE) virus. The three basic phases of alphavirus encephalitis, common to EEE, WEE, and VEE, are virus replication in peripheral tissue and subsequent spread, neuroinvasion, and viral spread within the CNS with primary infection of neurons and fatal neurodegeneration.(2) Western equine encephalitis is typically the least virulent of the three viruses, although lesions and pathogenesis are similar to EEE and VEE.Â In horses, VEE often presents as a purely nonsuppurative encephalomyelitis, sometimes accompanied by myeloid depletion of the bone marrow and lymphocytolysis in the spleen and lymph nodes. Necrotizing vasculitis, thrombosis and cerebrocortical necrosis are particularly prominent in VEE, but are also reported in EEE, as demonstrated in this case.(3) VEE has been shown to enter the CNS directly via olfactory neuroepithelium to the olfactory bulbs.(2)
1.Â Maxie MG, Youssef S.Â Nervous system.Â In: Maxie MG, ed.Â Jubb, Kennedy and Palmers Pathology of Domestic Animals. 5th ed.Â Vol 1.Â New York, NY: Elsevier Saunders; 2007:423-425.
2.Â Steele KE, Twenhafel NA.Â REVIEW PAPER: pathology of animal models of alphavirus encephalitis.Â Vet Pathol. 2010;47(5):790-805.
3.Â Zachary JF.Â Nervous system.Â In: McGavin MD, Zachary JF, eds.Â Pathologic Basis of Veterinary Disease.Â 5th ed.Â St.Â Louis, MO: Mosby; 2011:839-40.