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.
References
California State Department of Health Services. St. Louis
encephalitis in southern California. California Morbidity,
October 26, 1984.
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.
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.
Monath TP. Epidemiology. In: Monath TP, ed. St. Louis
encephalitis. Washington, D.C.: American Public Health
Association, 1980:239-312.
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.
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.
Luby JP. St. Louis encephalitis. Epidemiol Rev 1979;1:55-73.
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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