Western Equine Encephalomyelitis;Diagnosis,Treatment,Epidemiology

Western equine encephalomyelitis (WEE) virus was first isolated by Meyer in 1930 from the brain of a paralyzed horse in the San Joaquin Valley of California. Howitt was the first to recover it from human tissue and blood in 1938, at which time it became evident from serologic studies of suspected cases that human encephalitis was caused by WEE virus. In the summer of 1941, WEE virus was Erst isolated from mosquitoes (Culex tarsal:s in the Yakima Valley of Wash­ington.

It Is  mis species  of mosquito that most isolates of WEE have been recovered, estab­lishing it as the vector to man from avian hosts in a wild cycle on which they also preferentially feed. Following serologic ti-.-lier.ee of infection of wild birds, the virus has been repeatedly and con­sistently isolated from blood of birds in the recog­nized epizootic, epidemic, and endemic areas. In addition, WEE virus has been isolated from birds or mosquitoes or from both, in as widely separated localities as Massachusetts. New Jersey, Alabama, Georgia, and Florida where it has only rarely been associated with human and equine disease.

Evidence of virus isolation or serology has indi­cated that WEE viral infection also occurs widely throughout the western hemisphere, in Canada, Mexico, Guiana, and Argentina.

Epidemiology.

In the United States and Canada, WEE virus infection of man occurs in the Mississippi drainage basin, the Great Plains, and in the valleys and basins between the western mountain ranges where a rich fauna supports the Culex tarsaLis-wild bird cycle.Numerous serologic surveys show a high rate of inapparent or at least subclinical infection of indigenous residents of these areas. Epizootics in horses are often the firs: indication of WEE virus in an area.

Where facilities are available, virologic exam­ination of mosquitoes and nestling and mobile wild birds and serologic study of sentinel chicken flocks turn up simitar evidence of viral activity, which has appeared as earl;- as late May in Illinois. Transmission continues until the firs: hard freeze in October or November; where freezing may not occur, as in Cali­fornia, virus may be recoverable from mosquitoes on into the winter.Highest attack rates have been observed in young adult males, probably occupationally exposed, and in infants under one year of age. Mortality rates in cases of overt CNS disease range up to 10 per cent.

Clinical Characteristics.

Mild, nondescript fe­brile illness may be virologically diagnosed, par­ticularly as a component of an extensive epi­demic, but the encephalitic cases are of prime concern here. Following an incubation period of five to ten days, which may rarely be shorter and is sometimes twice as long, there is a two- to four- day prodrome of fever, headache, and malaise that usually precedes onset of CNS signs in children.

The onset in adults, especially the elderly, is more commonly marked by a suddenness of fever and headache, accompanied by stiff neck and drowsi­ness. It is not possible on clinical grounds to diag­nose the cause specifically as WEE virus because it occurs as a syndrome common to St. Louis en­cephalitis (SLE) in the same geographic areas. The same prodrome and nonparalytic CNS signs can also result from a variety of enteroviral infections that may be circulating in the same population at the same time. Affliction of infants, however, is a key feature, few cases of SLE ever having been observed in the very young.

Somnolence, disorientation, and coma are the most universal signs. Although convulsions are common in children, they almost never occur in adults. Neurologic manifestations, such as flaccid and spastic paralyses and abnormal reflexes, are seen more often in children; they are uncommon in adults. The temperature exceeds 102° F., often reaching 104° F. A fever that exceeds that level is ominous. Every effort should be made to de­crease such hyperthermia by application of ex­ternal measures.

The febrile phase lasts more than a week, but seldom for two, A dramatic im­provement, usually about the ninth or tenth day of illness, frequently occurs, especially in older patients, who proceed to recover completely; per­manent sequelae, such as personality change, are very unusual in adults. On the other hand, more than half of the children under a year old can be expected to suffer some permanent neurologic damage resulting in mental retardation, emo­tional changes, and spastic paralysis in one or more extremities.

Leukopenia may be observed in the very early stages of illness, although a mild • polymorpho­nuclear leukocytosis up to 15,000 cells per cubic millimeter is usual. Cerebrospinal fluid is color­less, sometimes under pressure, almost always presenting a mild but significant pleocytosis, accompanied by increased protein.

Diagnosis of Western equine encephalomyelitis

A summer syndrome of prodromal fever, headache, anorexia, vomiting, stiff neck, drowsiness in young children or sudden, se­vere onset of the same signs in adults should focus suspicion on an arboviral encephalitis. The appro­priateness of the region and history of exposure further suggest the possibility of western equine encephalitis, which only laboratory examination of proper serum specimens can establish with certainty.

Although WEE virus has been isolated on occa­sion from cerebrospinal fluid, isolation of the virus from other than the brain tissue collected at autopsy following death during the first week of illness has seldom succeeded. The laboratory diag­nosis in living patients is therefore dependent upon demonstration of a fourfold or greater rise of complement-fixation (CF) and/or hemagglutination-inhibition (HI) antibody in sequentially collected sera, the earliest being obtained as soon as an arbovirus is suspected, because antibody may appear early in the course of illness. Because of widespread high incidence of inapparent infec­tion in the rural areas west of the Mississippi, where WEE has widespread occurrence annually, demonstration of WEE antibody in a single serum specimen has little diagnostic significance.

Treatment

Maintenance of hydration and electrolyte balance, control of high fever, and fre­quent confirmation , that the airway is patent are the only measures that can be prescribed for good medical care. The objective is physiologic support as the’viral disease runs its course, with as little discomfort to the patient as possible.

Although dramatic improvement and spectac­ular recoveries occur, prolonged convalescence is often required to overcome weakness and fatigue. The common occurrence of irreversible sequelae in young children may require institutional psy­chiatric and occupational therapy. 

Prophylaxis.

The primary objective of preven­tion or control in an epidemic or epizootic situation is to prevent infected mosquitoes from biting and infecting babies. Infants should be kept inside screened houses whenever possible. When they are outside, or otherwise not protected by screened premises, buggies, cribs, or bassinets should be covered by suspended mosquito nets. Enough cases of infection of pregnant women have occurred with transmission of WEE virus in utero that special precautions against exposure of pregnant women to bites of Culex tarsalis mosquitoes should be emphasized. Frequent application of residual and knockdown adjunct agents within and around residences is also recommended.

More mobile adults can best be protected by appropriate clothing, mosquito repellents such as Rutgers’ 612 (2-ethyl-l,3-hexanediol), and a com­munity-wide mosquito control program that di­minishes mosquito breeding. The effectiveness of these mosquito control measures has been demon­strated by Reeves and Hess in California, Colorado, and Texas.

Epizootic equine encephalitis has been the pre­cursor of many human epidemics in the West. Effective formalin-killed chick embryo virus vac­cine has been produced for protection of horses. A dilution of this same product has been used to immunize laboratory and field workers subjected to a high risk of WEE viral infection, but it is no longer available.

Recently a non-neurotropic hamster-kidney tissue culture strain of WEE virus, derived from a wild bird infection, has been used successfully as an immunizing agent for equines by Johnson. Perhaps this is the precursor of a vaccine for more widespread human use, although it has not yet reached human volunteers.

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