Viral Encephalomyelitis of Equines and Domestic Ruminants in the Near East: Part I

Abstract

Near eastern equine encephalomyelitis is a non-purulent lymphocytic meningo-encephalomyelitis characterized by a varying, but commonly quite modest, degree of perivascular infiltration with round cells, diffuse lymphocytic infiltration, marked microgliosis, satellitosis of neurons, which show chromatolysis and neuronophagia, formation of glial nodules and occasional rarefaction of tissue. Polymorphonuclear leucocytes do not participate in the infiltrative process at any stage of the disease. Sites of election for histopathological changes arc cerebral cortex, hippocampal and periventricular areas, basal nuclei, pons and medulla. An account is given of 5 outbreaks of the equine disease that were observed in Egypt and Syria between 1949 and 1957. In 3 of the outbreaks it was possible to isolate strains of virus by intracerebral inoculation of rabbits with suspensions of equine brain tissue or blood serum; in one other outbreak, vims was isolated from ticks taken on sick and recovered animals. Strains of virus isolated from horses and donkeys were regularly pathogenic by the intracerebral route for rabbits, sheep and day-old chicks, but much less pathogenic for mice and guinea-pigs. Some strains were pathogenic for rabbits by intramuscular or subcutaneous inoculation. Kittens were infected per os. Histopathologically, there is no significant difference between the lesions produced in sheep and rabbits and the lesions observed in naturally infected horses. The few attempts that were made to reproduce the disease in horses with rabbit-passaged virus were unsuccessful, but in one case prolonged viraemia followed inoculation. Five outbreaks of encephalitis in ruminants are described, 4 in sheep and one in cattle, from each of which virus isolates indistinguishable from the equine strains were recovered. The disease occurs seasonally, and outbreaks are self-limited. Outbreaks in horses tend to occur in early spring and, to a lesser degree, in the autumn. The season at which outbreaks occur in sheep is affected by migrations between desert and farming areas. Apparently identical virus isolates have been obtained from ticks, principally Hyalomma anatolicum anatolicum, collected from horses, cattle and sheep at the site of outbreaks. The virus is transmitted transovarially to the larvae of this tick. Further virus isolations have been made from the brains of a variety of wild birds shot in a heavily infected area near Lake Ateibe, Syria. The virus is small, since in saline or broth suspension it can traverse gradocol membranes of 34mµ average pore diameter (A.P.D.). A few attempts to immunize rabbits with inactivated adjuvant vaccines jailed. Demonstration of antibodies in the sera of recovered or hyperimmunized animals was not achieved. There may be a long period of viraemia in sheep and horses inoculated with virus. The disease and the virus isolates have much in common with Borna disease and the Borna virus. Comparison of the 2 viruses by cross-immunity tests in rabbits is feasible.