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St. Louis Encephalitis -- California

In early October 1984, a private physician notified the Long Beach City Health Department that a local private medical laboratory had confirmed the diagnosis of St. Louis encephalitis (SLE) in a city resident with encephalitis. Subsequently, the health department learned that the laboratory also had serologic evidence of recent SLE infection in several other patients with central nervous system infections. As of October 22, SLE had been confirmed in 11 persons--seven from Los Angeles County, three from Orange County, and one from Riverside County. Dates of onset ranged from August 2 to October 5 (Figure 1). There were no deaths. All but two of the patients were 50 years of age or over. Investigations suggest that all patients were infected locally, because none had recently traveled far from home. At least five additional suspected cases are under investigation.

Routine surveillance of arboviral activity in 1984 had been unremarkable until seroconversions to SLE virus were noted in sentinel chickens from Harbor City (Los Angeles County) and Irvine (Orange County) bled on August 30. SLE virus was isolated from pools of Culex tarsalis mosquitoes collected from the Harbor City site on September 13 and September 18. More seroconversions were found in bleedings of the Harbor City flock on September 21 and the Irvine flock on October 11. These seroconversions probably reflected viral transmission in the previous 2 weeks. With the onset of cooler weather, by mid-October, mosquito populations had decreased below levels normally associated with risk of transmission to humans (1). Reported by Local mosquito control agencies, Microbiology Reference Laboratory, Long Beach, Long Beach City Health Dept, Arbovirus Research Unit, School of Public Health, University of California, Berkeley, Epidemiology, Laboratory, and Vector Control Svcs, County of Los Angeles Dept of Health Svcs, Orange County Health Care Agency, County of Riverside, California State Dept of Health Svcs; Div of Vector-borne Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: From 1945 to 1959, major combined outbreaks of western equine encephalitis (WEE) and SLE occurred in California, principally in the Sacramento and San Joaquin Valleys, although 10% of cases were reported from Imperial and Riverside Counties (2). In 1952, when the largest arbovirus encephalitis outbreak in the state's history occurred, no human cases occurred in Los Angeles or Orange Counties (2). The epidemiology of WEE and SLE in the central valley was characterized by endemic transmission, resulting in increased immunity in the population with increasing length of residence (3). Consequently, most clinical infections occurred among children and young adults (3). In contrast to this pattern, in east-central and Atlantic states, where SLE transmission occurs intermittently and the population is largely susceptible, major, often urban-centered outbreaks occur, affecting principally the elderly, who are biologically more susceptible (4).

Most of the persons in the current outbreak were over 50 years of age, indicating that larger numbers of milder clinical cases in younger age groups may not have been recognized. The crude attack rate to date for Long Beach, where cases clustered, was 3/100,000 population among persons 60 years of age or older. Although this is a relatively low attack rate, compared with previously described urban SLE outbreaks (3), case finding in Los Angeles has been passive thus far. The age distribution in this outbreak suggests that endemic SLE-virus transmission has not previously occurred in the area and that the underlying level of immunity in the population may be low.

In urban SLE outbreaks in the east, Cx. p. pipiens and Cx. p. quinquefasciatus are the principal vectors. Cx. tarsalis is the vector of SLE and WEE in the rural west; however, investigations have indicated a potential role for Cx. p. quinquefasciatus in SLE transmission in Imperial County, California (5), and, in 1966, in Tucson, Arizona (6). In Dallas, Texas, an outbreak in 1966 was attributed to introduction of SLE virus from the rural Cx. tarsalis cycle to urban Cx. p. quinquefasciatus (7,8). The identity of the vector species in this outbreak was not determined. Comprehension of the vector ecology and epidemiology of SLE in Los Angeles will be essential to guide surveillance and control programs to prevent future outbreaks in this populous area, where a substantial proportion of the population appears to be susceptible.


  1. California State Department of Health Services. St. Louis encephalitis in southern California. California Morbidity, October 26, 1984.

  2. Longshore WA Jr, Stevens IM, Hollister AC Jr, Gittelsohn A, Lennette EH. Epidemiologic observations on acute infectious encephalitis in California, with special reference to the 1952 outbreak. Am J Hyg 1956;63:69-86.

  3. Reeves WC, Hammon WM. Epidemiology of the arthropod-borne viral encephalitides in Kern County, California, 1943-1952. In: Smith CE, Griffiths W, Reeves WC, eds. University of California Publications in Public Health, Vol. 4. Berkeley, California: University of California Press, 1962.

  4. Monath TP. Epidemiology. In: Monath TP, ed. St. Louis encephalitis. Washington, D.C.: American Public Health Association, 1980:239-312.

  5. Magy HI, Work TH, Thomas CV. A reassessment of Culex pipiens as a potential St. Louis encephalitis vector in Imperial County. Proc Pap Annu Conf Calif Mosq Control Assoc 1976;44:41-5.

  6. Smith HH, Janssen RJ, Mail GA, Wood SA. Arbovirus activity in southern Arizona. Isolations of virus and observations of sentinel chickens. Am J Trop Med Hyg 1969;18:448-54.

  7. Luby JP. St. Louis encephalitis. Epidemiol Rev 1979;1:55-73.

  8. Monath TP, Cropp CB, Bowen GS, Kemp GE, Mitchell CJ, Gardner JJ. Variation in virulence for mice and rhesus monkeys among St. Louis encephalitis virus strains of different origin. Am J Trop Med Hyg 1980;29:948-62.

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