California encephalitis virus has been recognized as a geographically extensive .annual, warm-season, epidemic, febrile central nervous system disease.Only since a sensitive CF antigen for the La Crosse strain was recently made available for routine serologic study of sera collected from patients who suffered febrile CNS signs that were demonstrated not to be due to WEE, EEE, and SLE or some enterovirus. From west of the Appalachians to the midwest, many general practitioners call the syndrome farm encephalitis.
Studies of 1964 and 1965 epidemics in Indiana and Ohio, supported by characterization of sporadic cases in Florida and North Carolina, establish that more than 90 per cent of the recognized cases were in persons under 16 years of age, the highest incidence being in those who were 5 to 7 years old.
Almost all cases can be associated with rural or sylvan exposure, primarily in recreational pursuits of picnicking, camping, fishing, or hunting in or adjacent to woods or the subtropical vegetation characteristic of Florida These habitats breed an abundance of a variety of an-minr mosquitoes, mostly Aedes species, from which nmnr low of California encephalitis virus have been isolated.
Mammalian species found tc contain. neutralizing antibody to these viruses also demonstrate the complicated zoonotic maintenance cycle that supports such a artet; of ecologic situations in which man can be infected Ties* include chipmunks, tree squirrels, and rabbits. A type of California encephalitis virus has been isolated from a snowshoe hare tn ’Montana. This evidence of mammalian rather than avian vertebrate hosts helps explain the widespread focal nature of California encephalitis virus activity as well as why there appear tc be so many antigenically distinct types.
At least six antigenically different types of virus of the California complex have beer, characterized in different regions of the United States. The La Crosse strain nich produces the most sensitive CF antigen for the cases diagnosed in the Ohio Valley, is the only strain of human inr.r. Related viruses of the California group have been isolated in tropical America, Europe, Africa, and Asia.
Whether all varieties the California complex in the United States or others of the group active in other con- raNv&t ‘Cue disease rembeci “here as California encephalitis is not yet known. It is therefore extremely important for the clinician who suspects this as the cause of a febrile CNS syndrome to collect appropriate sera— specimens for dispatch to a capable arbovirus laboratory for examination.An accurate mortality rate has not yet been established. It is not more than 5 per cent and is probably less, although sequelae of mental deterioration ar-d emotional instability may be more common.
Clinical Characteristics of California Encephalitis.
Limited circumstantial evidence suggests that the incubation period is between five and ten days. The time of the first symptoms is often difficult to establish because this is primarily a disease of young children and because California encephalitis usually has a more gradual and insidious onset than the other North American arboviral encephalitides. Mild fever and headache are often the only signs of illness for several days. The patient may then recover fully, the physician noting only a diagnosis of “summer fever.”
More severe cases are marked by gradual rise of the temperature over several days, the headache localizing and becoming severe in the frontal region. As primary complaints, the fever and headache are often attributed to some traumatic incident that the patient or parent remembers as having occurred within the previous few days. The fever and headache are frequently accompanied by vomiting.Mental confusion and lassitude may or may not precede sudden occurrence of convulsions. These have occurred spontaneously in a febrile child riding in a car, and have been so violent as to dislodge a reclining child from bed. Convulsive seizures may be the only overt sign of CNS involvement, but are often only a prelude to coma. Either may be the presenting condition for hospital admission.
In rural areas where the physician is called to see a feverish, confused, somnolent, convulsive, or comatose child, the condition is often diagnosed as “farm encephalitis.” It is well known by many general practitioners, who associate this children’s disease with summer or early autumn. In such environmental situations the most difficult differential diagnosis is from western equine and St. Louis encephalitis. Only appropriate laboratory examination can establish the diagnosis with certainty.
Meningeal signs occur but are uncommon. In contrast to the transient neurologic signs, such as changes in reflexes and shifting flaccid and spastic paralyses seen in the other encephalitides, these signs are not characteristic of California encephalitis. This may indicate localization of the neuropathologic process in the cortex more than involvement of the motor centers.Lumbar puncture following recognition of overt CNS signs yields clear cerebrospinal fluid under pressure, with a marked pleocytosis consisting of polymorphonuclear leukocytes and increase in lymphocytes as the disease progresses.
Fever continues to increase. This and dehydration are the two clinical conditions requiring close attention * and immediate treatment. Although death may occur suddenly, within a few hours, it may come only after several days’ progression of high fever, convulsions, coma, and respiratory difficulty that requires oxygen and a respirator. Upper respiratory signs are negligible.
Fever falls by lysis, and the convalescence is prolonged, weakness and lassitude continuing for some time. Although paralytic sequelae have not been observed, emotional lability at home and difficulty in learning at school have been noted in children following California encephalitis. Not enough cases have been studied to establish whether this is a permanent change.
During the summer or early autumn, severe frontal headache associated with gradually rising temperature over several days, leading to somnolence, irritability, disorientation, vomiting, convulsions, and coma, should stimulate consideration of California encephalitis. A history of exposure to mosquito bites in rural or wooded areas strengthens the suspicion.Mild leukocytosis, which may be lymphocytic, and significant polymorphonuclear or lymphocytic histiocytic pleocytosis in the cerebrospinal fluid, with or without abnormal increase in protein, further support the clinical diagnosis.
No virus has yet been isolated from the blood of an acutely ill patient. Virus has been recovered from brain tissue of a fatal case, but most patients survive. The laboratory diagnosis is therefore serologic. Because antibody levels tend to vary. widely in residents of areas where California encephalitis occurs most commonly, at least a fourfold rise in titer of CF or HI antibody is required to establish the diagnosis. A high titer of CF antibody in a single specimen of convalescent serum from a characteristic clinical case provides important circumstantial evidence of the possible cause.
California Encephalitis Treatment.
There being no specific antiviral therapy available, the treatment is symptomatic. The severe frontal headache may require powerful analgesics for relief. The fever will respond somewhat to antipyretics, but resolution of the fever is usually by lysis over a period of several days. The more severe cases of somnolence and coma require closest attention and constant nursing to ameliorate hyperthermia and to watch for respiratory difficulty that may require a respirator.Relatively slow convalescence is associated with malaise that may require environmental change as well as supportive treatment for recovery from depression. How much of this is due to CNS affliction is as yet unknown.
Although there has been no attempt to develop a vaccine, accumulating epidemiologic evidence increasingly focuses on a rural transmission of the virus by the Aedes mosquito. Protection against such sylvan mosquito attack is the most difficult mosquito control measure known. When children congregate in summer camps, extensive and frequent use of insecticides in the camp and at the periphery will destroy mosquitoes that otherwise might, bite during periods of rest or outdoor activities. Beyond the immediate environs of camping or picnic sites, personal protection from mosquito bite by use of protective clothing and application of repellents to exposed skin surfaces is recommended. The tree-hole breeding proclivity of sylvan Aedes complicates elimination of these mosquitoes immensely. In suburban areas, .where people are constantly or repeatedly enveloped by a sylvan environment, the expensive elimination of tree-hole breeding by drainage and filling holes in trees may prove to be the only practical Aedes control measure.