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Topic:Encephalomyelitis
Encephalomyelitis in horses refers to inflammation of the brain and spinal cord, often caused by viral infections such as Eastern, Western, and Venezuelan equine encephalomyelitis viruses. These conditions can lead to neurological symptoms including fever, ataxia, and behavioral changes. The disease can be transmitted through mosquito vectors, with horses serving as dead-end hosts. Diagnosis typically involves serological testing and clinical evaluation. This page aggregates peer-reviewed research studies and scholarly articles that explore the etiology, pathogenesis, clinical presentation, and management strategies for encephalomyelitis in equine populations.
Meningoencephalomyelitis in horses associated with equine herpesvirus 1 infection. During an outbreak of abortion caused by equine herpesvirus 1, a neurologic disease characterized clinically by dullness and ataxia occurred in several mares. Equine herpesvirus 1 was isolated from brain and lung of two severely affected mares. Histologically, both mares had disseminated meningoencephalomyelitis characterized by necrotizing arteritis, focal malacia in grey and white matter of brain and spinal cord, and accumulation of lymphocytes and neutrophils in paravertebral ganglia. Eosinophilic intranuclear inclusion bodies occurred in foci of necrosis in thyroid adenomas of both mares.
Disseminated necrotizing myeloencephalitis: a herpes-associated neurological disease of horses. Equine viral rhinopneumonitis type I virus was isolated from spinal cord and brain of a paraparetic horse with disseminated necrotizing myeloencephalitis. Necrotic arteriolitis,nonsuppurative necrotizing myeloencephalitis and Gasserian ganglioneuritis were present. On record were 12 more cases of horses with similar lesions. The horses had been ataxic or paretic for up to several weeks. A field survey indicated that 14 of 24 horses with acute myelitic signs developed them after recent exposure to respiratory disease.
A field study of persistence of antibodies in California horses vaccinated against western, eastern, and Venezuelan equine encephalomyelitis. As a result of the continuing threat of Venezuelan equine encephalomyelitis (VEE), a study was made to determine if revaccination against VEE (TC-83 vaccine) was feasible and if revaccination could be incorporated into other routine vaccination practices. Of the horses given annual vaccination with bivalent western equine encephalomyelitis (WEE) and eastern equine encephalomyelitis (EEE) vaccine, 57% retained detectable serum-neutralizing (SN) antiboyd titers for VEE 18 months after the initial VEE vaccination was given. Of horses with no record of WEE-EEE vacinnation, 100% retained detectable...
Immunoglobulins produced by the antigenized equine fetus. The foal is born without detectable antibody and except for small amounts of IgM is devoid of immunoglobulins. Intrafetal administration of either Venezuelan equine encephalomyelitis virus (VEE-TC83) or ovine erythrocytes elicited IgGa, IgGb and a trace of IgG(T). The fetal blood VEE-TC83 neutralization titre was higher than the neutralization titre elicited by the same preparation in older horses.
Laboratory studies of Venezuelan equine encephalitis virus in equines, Texas, 1971. During the summer and fall of 1971, epizootic and epidemic Venezuelan equine encephalitis was detected in Texas. Isolates of epizootic (IB) and vaccine (TC-83) strains were distinguished by virulence of the former for guinea pigs. Vaccine virus was isolated from 1 to 14 days after vaccination and neutralization tests demonstrated the appearance of antibody about a week after vaccination. Viremia titers of subtype IB in horses ranged from 2.2 to 8.3 log10 suckling mouse intracranial 50% lethal doses per ml. Of 101 equines from which Venezuelan equine encephalitis virus (IB or TC-83) strains wer...
A serologic survey of pronghorns in Alberta and Saskatchewan, 1970-1972. To determine the exposure of free-ranging pronghorns (Antilocapra americana Ord) to selected pathogens, serum samples were obtained from 33 live-trapped animals from southwestern Saskatchewan in 1970, and from 26 and 51 animals from southeastern Alberta, in 1971 and 1972, respectively. Antibodies were found to the agents of parainfluenza 3, bovine virus diarrhea, eastern and western encephalomyelitis, infectious bovine rhinotracheitis and the chlamydial group. No serologic reactors were found to the agents of bluetongue, epizootic hemorrhagic disease, brucellosis, or leptospirosis (4 serotypes...
Comparative analyses of members of the Venezuelan equine encephalomyelitis virus complex. Polyacrylamide gel electrophoretic examination of viruses selected from the Venezuelan equine encephalomyelitis (VEE) complex revealed distinct strain to strain differences in profiles of the two virion envelope proteins. The core protein was identical in all viruses tested. We detected five electrophoretic patterns into which the virus strains could be classified and these were designated alpha (alpha), beta (beta), gamma (gamma), delta (delta), and episolon (episolon). Isolates representing variant E of subtype I exhibited a profile characterized by only one apparent envelope band. The epizo...
A microprecipitation test for rapid detection and identification of Venezuelan, eastern and western equine encephalomyelitis viruses. The development of a new diagnostic procedure for the identification of Venezvelan, eastern and western equine encephalomyelitis (VEE, EEE, WEE) viruses is described. The procedure utilizes virus precipitation with reference fluorescein-conjugated gamma globulin, followed by cellulose acetate electrophoresis. Clinical specimens containing varying concentrations of virus yielded, in primary duck embryo cell culture, sufficient virus for detection within 22 to 44 hours. Identification of VEE, EEE and WEE virus in specimens was accomplished by microprecipitation within this time. In contrast to c...
Epidemic Venezuelan equine encephalitis in North America in 1971: vector studies. A major epidemic of Venezuelan equine encephalitis occurred in south Texas in the summer of 1971. More than 1500 equines died of VEE in Texas, and 110 human cases with no deaths were reported. Vector studies in south Texas and northern Tamaulipas revealed that the overall mosquito infection rates during the peak of the epidemic were about 1:100, one of the highest rates observed for a major epidemic. Mosquito infection rates of this magnitude could easily explain the intensity of VEE outbreaks in both equines and man. A total of 943 VEE virus isolations were made from mosquitoes. Eight of the ...
Possible evidence for interference with Venezuelan equine encephalitis virus vaccination of equines by pre-existing antibody to Eastern or Western Equine encephalitis virus, or both. During 1971, an epizootic of Venezuelan equine encephalitis (VEE) reached the United States. Laboratory tests were performed on a large number of sick, healthy, unvaccinated, and vaccinated horses. Neutralization (N) tests in cell cultures revealed that 153 of 193 (79.3%) equines outside the state of Texas and 175 of 204 (85.8%) within Texas (82.6% overall) had detectable N antibody to VEE virus a week or more after vaccination. Twenty-six of 40 (65%) non-Texas equines and 18 of 29 (62%) Texas equines which had no detectable antibody against VEE virus a week or more after vaccination had N ant...
An outbreak of Eastern equine encephalomyelitis in Upstate New York during 1971. During August 1971 three horses died and one human infant became ill during an outbreak of Eastern equine encephalomyelitis in Upstate New York. Fifteen of 93 wild avian sera collected in the area reacted in hemagglutination-inhibition (HI) tests with Eastern equine encephalomyelitis (EEE). EEE virus was isolated from four avian specimens (White-throated Sparrow, Towhee, Baltimore Oriole, Cedar Waxwing) and 5 of 159 arthropod pools (3 from Culiseta morsitans and 1 each from Culex territans and Culex restuans). Sera from 54 humans and 89 healthy equines were HI-negative for EEE. It is believed ...
