Encephalitis Overview

A variety of causes exist for encephalitis, but for PCOs the most important are those related to mosquitoes. Here’s a review of mosquito-carried encephalitis viruses.

The recent outbreak of West Nile encephalitis in the New York area created quite a stir — both fear of the disease and fear of the pesticides being used to control the mosquito vectors. And it hasn’t stopped yet. West Nile encephalitis is spreading both in the North and South (as of this writing there were reports of the virus in 12 states and the District of Columbia). In light of the West Nile outbreak, an overview of all the common mosquito-carried encephalitis viruses occurring in the United States is in order for pest management professionals.

First, the reader must understand that there are many causes of encephalitis because encephalitis just means "inflammation of the brain." Symptoms of the disease include high fever, vomiting, drowsiness, seizures, twitching, convulsions and even coma and death. Encephalitis can be caused by a variety of bacterial or viral agents. You can develop it from a vaccination or from herpes or even an enterovirus (the "throw-up" viruses), among other things. So, if a person is diagnosed with encephalitis, it doesn’t mean that they have one of the mosquito-carried forms of the disease.

However, there are certain viruses — carried by mosquitoes — that cause encephalitis in people. These diseases are collectively called "encephalitides." They are essentially animal diseases, called "zoonoses," which only occasionally get transmitted to people. Most of them circulate among birds or small mammals by way of mosquito bites. Humans (or horses) get infected by accident — and thus are called "accidental hosts."

All encephalitides more or less cause similar symptoms in humans, although with great differences in severity. Some of them are extremely mild with a 1 percent or less mortality rate, while others may kill as many as half of the people infected. And, making matters worse, even for the survivors, there are sometimes long-lasting effects such as memory loss, personality changes, etc. The following is a breakdown of the common mosquito-carried encephalitis viruses in the United States and some characteristics of each.

EASTERN EQUINE ENCEPHALITIS. Eastern equine encephalitis (EEE) is generally the worst strain, being severe and frequently fatal (mortality rate 30 to 60 percent). It is especially bad in children. Fortunately, large and widespread outbreaks are not common; between 1961 and 1985 only 99 human cases were reported in the United States.

EEE occurs in late summer and early fall in the Central and Northcentral U.S., parts of Canada, southward along the coastal margins of the eastern U.S. and the Gulf of Mexico and sparsely throughout Central and South America. The life cycle of EEE is poorly understood. The virus circulates in wild bird populations by bird-feeding mosquitoes, but the exact mechanism of spread to humans is largely speculative. It is believed to be transmitted to humans by the mosquitoes Aedes sollicitans, Coquillettidia perturbans and possibly Ae. vexans and Anopheles crucians.

ST.LOUIS ENCEPHALITIS. St. Louis encephalitis (SLE) produces lower mortality rates than EEE (3 to 20 percent), but occurs occasionally in large epidemics over much of the U.S. In contrast to EEE, SLE is worse in older people. But, like EEE, most cases occur in late summer.

In 1933 there were 1,095 cases in the St. Louis area with more than 200 deaths. In 1975-76 there were more than 2,000 cases reported from 30 states, primarily in the Mississippi valley. SLE is transmitted by Culex tarsalis (western and southwestern U.S.), Cx. quinquefasciatus (central and southeastern U.S.) and Cx. nigripalpus (southeastern U.S.).

WESTERN EQUINE ENCEPHALITIS. Western equine encephalitis (WEE), occurring in the western and central U.S., parts of Canada and parts of South America, has occurred in several large outbreaks. There were large epidemics in the north central U.S. in 1941 and in the central valley of California in 1952. The 1941 outbreak involved 3,000 cases.

During 1964-1997, there were 639 human WEE cases reported to the CDC, for a national average of 19 cases per year. WEE is generally less severe than EEE and SLE, with a mortality rate of only 2 to 5 percent. Cases appear in early to midsummer and are primarily due to bites by infected Culex tarsalis mosquitoes.

LACROSSE ENCEPHALITIS. LaCrosse encephalitis (LAC) is a California group encephalitis that primarily affects children in the Midwestern states of Ohio, Indiana, Minnesota and Wisconsin. Cases have also occurred in the Southern states, but certainly not to the extent that they have in the Midwestern U.S. The mortality rate of LAC is less than 1 percent, but infection often leads to seizures.

In fact, that is one of the main symptoms — seizures in infants and children. The national average for LAC cases is 73 per year. Most cases occur in July, August and September. LAC is transmitted to humans by the tree hole mosquito, Aedes triseriatus. Interestingly, the virus may be transferred from adult female Ae. triseriatus to her offspring through the eggs. Some amplification of the virus takes place in nature through an Ae. triseriatus, wild vertebrate cycle.

MORE CALIFORNIA GROUP ENCEPHALITIS. Although LAC (above) encephalitis is probably the most notorious, several other California group encephalitis viruses exist. North American forms include California encephalitis (CE), Jamestown Canyon (JC), Jerry Slough (JS), Keystone (KEY), San Angelo (SA), Trivittatus (TVT) and others.

Viruses in the California serogroup are primarily pathogens of rodents and rabbits. They are transmitted to people by several species of mosquitoes, but especially the tree hole, floodwater and snow pool Aedes spp. California group encephalitis viruses generally produce only mild illness in humans (mortality rates 1 percent or so).

VENEZUELAN EQUINE ENCEPHALITIS. Venezuelan equine encephalitis (VEE) is relatively mild in humans and rarely affects the central nervous system. VEE is endemic in Mexico and Central and South America; epidemics occasionally reach the southern U.S. Cases generally appear during the rainy season. Although the mortality rate is generally less than 1 percent, significant morbidity is produced by this virus.

In an outbreak in Venezuela from 1962 to 1964, there were more than 23,000 reported human cases with 156 deaths. In 1971, an outbreak of VEE in Mexico extended into Texas resulting in 84 human cases. There has been a recent outbreak in Colombia and Venezuela during the summer of 1995 with at least 13,000 human cases.

WEST NILE ENCEPHALITIS. West Nile virus (WNV) was identified for the first time in the Western Hemisphere in New York in 1999 (see figure on page 82). By the end of the year, the virus had caused encephalitis in 62 people and numerous horses in and around New York City, resulting in 7 human and 10 equine deaths.

The virus continued to spread in 2000 and now evidence of WNV has been found in at least 12 states and the District of Columbia. WNV will likely eventually occur throughout the eastern United States. As far as severity of the disease, WNV is no more dangerous than SLE (one of our "native" encephalitis viruses). Like SLE, WNV is more serious in older patients.

A lot is yet unknown about the ecology of WNV in the United States, but we do know the virus causes a bird disease and is transmitted by mosquitoes (see figure above left).

WNV is believed to be transmitted to humans by Culex pipiens, Cx. restuans, Cx. salinarius and possibly Aedes japonicus.

CONCLUSION. The outbreak of WNV in New York and subsequent activities to slow its spread over the last year and a half have focused great attention on the mosquito-carried encephalitis viruses. And that’s good — at least from a pest control perspective. It has helped the public realize that there are some nasty diseases out there carried by insects. Also, it has pointed out the need for protection from insect pests.

People involved in pest control should hold their heads high during times like these, knowing that they serve a valid public health role — that of protectors of public health. Keep up the good work!

The author is a medical entomologist for the Mississippi Department of Health and clinical assistant professor of preventive medicine at the University of Mississippi Medical Center, Jackson, Miss. He can be reached at 601/576-7512 or jgoddard@pctonline.com.