Western Equine Encephalomyelitis
Western equine encephalomyelitis (WEE) is a mosquito-borne zoonotic infection, primarily involving wild birds and Culex tarsalis, that can produce acute central nervous system (CNS) disease in infected horses and humans. WEE is transmitted, primarily by Cx. tarsalis to a variety of avian and mammalian hosts. People and horses are dead-end hosts for the virus, in that the concentration of virus particles circulating in the blood stream of humans and horses is too low to infect a blood feeding mosquito.
Symptoms of infection appear 7 to 21 days after a bite from an infected mosquito. The disease is most severe in infants and small children and can result in permanent brain damage or death. Symptoms range from mild to severe and may include only fever and headache to encephalitis with delirium, disorientation or coma.
Passerine birds, primarily house sparrows and house finches, are highly preferred hosts of Cx. tarsalis and are an important source of vector infections. Infections in house sparrows, particularly nestlings, amplify WEE virus that is present. Attempts to use these birds in testing programs as an "early warning system" for avian-Cx. tarsalis transmitted WEE virus have proven unsuccessful. The use of sentinel chicken flocks continues to be the most effective means of monitoring the presence and amplification of this disease in any given area.
Seroconversions to St. Louis Encephalitis (SLE) and Western Equine Encephalomyelitis (WEE) viruses from pooled mosquitoes (Culex tarsalis) in California, 1990-1999
Weather is an important influence of WEE virus transmission and vector abundance. In North America, WEE epidemics are often associated with cool temperatures in the early spring, when Cx. tarsalis populations are generally more susceptible to infection. Once the Cx. tarsalis population increases and they begin transmitting WEE virus to wild birds, the rate of virus amplification increases correlated with ambient temperatures.
During the summer of 1930, the San Joaquin Valley of California had clinical cases of encephalitis in horses. The initial epizootic of WEE in the San Joaquin Valley in 1930 affected approximately 6,000 horses with a case fatality rate of 50%. Several outbreaks occurred in several western states from 1931 to 1934. In 1938, more than 300,000 horses and mules were stricken in the U.S. In 1941, there were 1,094 human cases reported in Canada and 2,242 human cases in the U.S. An outbreak in California's Central Valley in 1952 resulted in 813 cases of encephalitis in humans with an attack rate in Kern County of 50/100,000 humans and 1120/100,000 horses. Outbreaks of WEE in the 1930's and 1940's caused serious losses in horses and mules used as draught animals, adversely affecting agricultural production.
Organized mosquito abatement has reduced the incidence of WEE in California over the past two decades. Despite low numbers of human cases in recent years, mosquito-borne encephalitis remains an alarming disease to both the public and medical community. Diseases which appear suddenly as epidemics, cause severe illness in children, and are transmitted by mosquitoes, producing a high level of public concern. In 1969, the threat of an impending encephalitis outbreak in California resulted in the appropriation of $1.25 million of emergency funding in addition to the $10 million already budgeted for vector control.
Because both the vector, Cx. tarsalis, and WEE virus are still present over a widespread geographic range, public health agencies maintain preventative programs including reporting systems, surveillance programs, and vector control. Vector control is presently the only practical approach to the control of WEE. Organized mosquito abatement practices have led to the gradual reduction of human cases in California over the past two decades.
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