La Crosse Encephalitis in West Virginia

Between July 6 and September 1, 1987, in central West Virginia, 19 cases of La Crosse encephalitis were serologically confirmed (Figure 1). After a cluster of meningo-encephalitis cases was reported from a referral pediatric service in Charleston, active hospital-based surveillance was undertaken in 15 counties in central and southern West Virginia, where La Crosse encephalitis had previously occurred. Cases were identified in five of these counties.

Eleven (58%) of the 19 patients were diagnosed as having viral encephalitis. Four (21%) had symptoms of meningitis alone, and four (21%) had meningo-encephalitis. The patients ranged in age from 1 to 14 years (mean = 7 years). Fifteen (79%) patients were male; the male-to-female ratio was 3.8:1. Eighteen (95%) children were hospitalized, and one child was treated as an outpatient. One patient, a 9-year-old boy with cerebral edema, died despite intensive supportive care.

All patients lived in rural areas of central West Virginia, a region with thick hardwood forests conducive to mosquito breeding. Attack rates varied by the patients' sex and place of residence (Table 1). Males were at much greater risk of becoming ill than females. The attack rate among children under 15 years of age in Nicholas County was over four times the rate in any other county. A case-control study is under way to test hypotheses regarding possible behavioral and environmental risk factors.

For six (32%) of the patients, diagnosis was based on compatible clinical findings and a single immunofluorescent antibody (IFA) titer greater than 128 during the convalescent stage of illness. For the other 13 (68%), a fourfold rise in antibody titer was demonstrated between the acute and convalescent stages of illness.

In the past, few cases of La Crosse encephalitis have been reported in West Virginia. Of 223 cases of encephalitis reported to the West Virginia Department of Health from 1980 through 1986, only eight (4%)--six in 1984 and two in 1985--were attributed to a California serogroup virus. Much of the increase in reported incidence in 1987 may be the result of intensive case-finding efforts. A change in the state laboratory's serologic procedure for La Crosse virus diagnosis may also have contributed to the increase in the number of identified cases. Previously, serologic diagnoses were made by measuring complement-fixing antibodies. The more sensitive IFA was adopted in 1987. Reported by: AA Kindle, JE McJunkin, MD, JR Meek, MD, Charleston Area Medical Center; MM Tomsho, MD, Summersville; DL Holbrook, DL Smith, MD, Nicholas County Health Dept; BA Crowder, DM Rosenberg, MD, Kanawha County Health Dept; JA Burke, DC Newell, DO, Fayette County Health Dept; SL Sebert, MD, Greenbrier County Health Dept; JH Wright, DO, Logan County Health Dept; JW Brough, DrPH, DM Cupit, MS, LE Haddy, MS, RC Baron, MD, Acting State Epidemiologist, West Virginia Dept of Health. Div of Field Svcs, Epidemiology Program Office; Div of Vector-Borne Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: La Crosse virus, a bunyavirus in the California serogroup, and its mosquito vector, Aedes triseriatus, are widely distributed in the central and eastern United States (1,2). Central nervous system (CNS) infections from La Crosse virus have been recognized chiefly in the upper Midwest. However, reports of sporadic cases from other states suggest that the disease may be endemic in a broader geographic distribution (3,4). The focus of cases in West Virginia in 1987 illustrates the high levels of endemic transmission that may remain undetected unless specific diagnoses are sought.

CNS infections from La Crosse virus occur nearly exclusively among children. Of the 929 cases reported to CDC from 1971-1983, 833 (89.7%) involved children under 15 years of age. Boys are affected more often than girls, presumably because they spend more time outdoors where they are exposed to the vector. Boys accounted for 66.3% of the 833 reported cases involving children. Although the proportion of reported cases involving males in West Virginia in 1987 was higher than the proportion reported elsewhere, it was not significantly greater than expected (pgreater than 0.17, binomial distribution). than girls, presumably because they spend more time outdoors where they are exposed to the vector. Boys accounted for 66.3% of the 833 reported cases involving children. Although the proportion of reported cases involving males in West Virginia in 1987 was higher than the proportion reported elsewhere, it was not significantly greater than expected (pgreater than 0.17, binomial distribution).

The incidence of La Crosse encephalitis in the five-county area of central West Virginia (20/100,000 children less than 15 years of age, 4.7/100,000 total population) was similar to rates reported from other locations where the disease is endemic. In 1978, active, hospital-based surveillance in 20 Wisconsin and Minnesota counties showed an incidence of 31.6/100,000 children under 15 years of age and 6.3/100,000 total population (5).

La Crosse encephalitis is infrequently recognized as a cause of childhood morbidity from CNS infection. Incidence rates for La Crosse encephalitis in endemic areas are similar to rates for Haemophilus influenzae meningitis, which range from 35 to 40/100,000 for children under 5 years of age and from 2.2 to 7.7/100,000 for the total population (6). The fatality rate for La Crosse encephalitis is less than 1%; however, during acute illness, convulsions occur in 50% of cases, and focal weakness, paralysis, or other localized signs occur in 25% (3). Residual convulsive disorders may persist in 10% of cases, and some recovered patients have impaired cognitive performance (3).

Public health measures to control La Crosse encephalitis have focused on eliminating breeding sites for Ae. triseriatus, but the importance of tree holes and breeding sites such as tires and other discarded containers in the spread of La Crosse encephalitis has not been well defined. The current case-control study addresses this issue; results of the study will help public health officials planning mosquito control programs to target breeding sites that pose the greatest risk.

References

1. Calisher CH. Taxonomy, classification, and geographic distribution of California serogroup bunyaviruses. Prog Clin Biol Res 1983;123:1-16.

2. Craig GB Jr. Biology of Aedes triseriatus: some factors affecting control. Prog Clin Biol Res 1983;123:329-41.

3. Tsai TF, Monath TP. Viral diseases in North America transmitted by arthropods or from vertebrate reservoirs. In: Feigin RD, Cherry JD, eds. Textbook of pediatric infectious diseases. Vol II. 2nd ed. Philadelphia: WB Saunders, 1987;1417-56.

4. Kappus KD, Monath TP, Kaminski RM, Calisher CH. Reported encephalitis associated with California serogroup virus infections in the United States, 1963-1981. Prog Clin Biol Res 1983;123:31-41.

5. Hurwitz ES, Schell W, Nelson D, Washburn J, LaVenture M. Surveillance for California encephalitis group virus illness in Wisconsin and Minnesota, 1978. Am J Trop Med Hyg 1983;32:595-601.

6. Fraser DW, Geil CC, Feldman RA. Bacterial meningitis in Bernalillo County, New Mexico: a comparison with three other American populations. Am J Epidemiol 1974;100:29-34.

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