| INCIDENCE AND SYMPTOMS
| TRANSMISSION CYCLE
| MOSQUITOES |
| SEASONALITY | SURVEILLANCE | TREATMENT AND PREVENTION | REFERENCES
St. Louis Encephalitis (SLE) is one of four main ¨encephalitides¨ that occur in the United States, the other three being eastern equine encephalitis (EEE), western equine encephalitis (WEE) and LaCrosse encephalitis (LAC). All are caused by arboviruses, a term that stands for arthropod borne viruses. These viruses are maintained in nature through biological transmission between vertebrate hosts and blood-feeding arthropods (mosquitoes, psychodid and ceratopogonid flies, and ticks).
More on Arboviruses.
SLE is the most important mosquito-transmitted disease in the United States (Goddard 1996). Although periodic epidemics have occurred only in the Midwest and Southeast, SLE virus is distributed throughout the lower continental United States. The viral organism causing the human disease, and the disease known as St. Louis Encephalitis are not synonymous; during an SLE epidemic, large numbers of people become infected, however, only a very small percentage of the SLE infections are clinically apparent and the majority are never diagnosed. Major SLE epidemics occurred in Florida in 1959, 1961, 1962, 1977, and 1990.
Confirmed SLE cases in Florida 1952-2003
Incidence and Symptoms: Incidence of the disease and manifestation of symptoms are highly correlated with age. During epidemics, people over 60 are 5 to 40 times more likely to be symptomatic than those under 10 years of age. Symptoms of encephalitis, the most grave consequence of infection with the SLE virus, also increase from approximately 50% in those 20 or younger, to close to 90% for those over 60. Mortality is less than 5% for those persons with the disease that are under 50 years of age, but from 7% to 25% in those over 50. When they do develop, symptoms usually start between 5 and 20 days after exposure.
Encephalitis is an inflamation of the brain that can drastically affect motor skills and cause permanent damage if not treated quickly. Symptoms range from mild headaches to coma and death. Other symptoms include fever, nausea, stiff neck and back, light sensitivity, confusion, drowsiness, irritability, and motor skill impairment. Invasion of the central nervous system the virus is thought to follow initial virus replication in peripheral sites and a period of viremia.
Clinically, it is essential to distinguish the arboviral encephalitides from two viral ones that are potentially deadly, but treatable. These are herpes simplex encephalitis, and the less common varicella-zoster encephalitis, which is deadly in patients with immunological deficiencies. In these cases, swift identification and immediate treatment can be lifesaving (Lazoff, 1998).
Transmission Cycle: The annual cycle of the SLE virus in Florida is still not completely understood. We know, however, that wild bird populations are central to the transmission cycle. When a bird becomes infected by the bite of a carrier mosquito, it produces more virus in its blood that can infect other susceptible mosquitoes that bite the bird. These mosquitoes can then further spread the virus. This process is called ¨amplification¨. An infected bird can produce an appreciable amount of virus in one or two days, but the virus disappears two to three days later, so a bird remains ¨infective¨ for only a few days. Birds do not show any symptoms of disease and become immune after exposure.
If amplification in the wild bird population is significant, then a large number of mosquitoes can become infected thus increasing the chances that a human or another vertebrate host may be bitten by an infected mosquito. Once a mosquito is infected, the virus replicates and invades other parts of the body including the salivary glands. When mosquitoes bite a host, they usually inject a small amount of saliva as an inti-coagulant before taking their blood meal and thus transfer the virus to the host.
As more and more birds recover from infection and become immune, however, the number of newly infected mosquitoes also diminish. Even though mosquitoes remain infected for life, they only live for a week or two, so as the infected mosquitoes die off, the epidemic subsides. Humans are dead-end hosts, but the role, if any, of other vertebrate animals in the maintenance and transmittal of SLE is not known yet.
Mosquitoes: Not all mosquitoes are capable of transmitting the virus. For example, of 76 species of mosquitoes that occur in Florida, only Culex nigripalpus has been definitely linked to SLE transmission. Several additional species, including the salt marsh mosquito Aedes taniorhynchus, have been found infected with SLE, but they have not yet been implicated in transmission. Elsewhere, other Culex species, particularly Culex pipiens in the midwest and Culex tarsalis in the west are the major vectors.
Seasonality: Although the SLE virus is probably present in Florida throughout the year, virus transmission is more prevalent during summer and fall. These time period corresponds with periods of high mosquito and bird activity in Florida, but direct correlations between these variables and SLE epidemics have not yet been established. Periods of heavy rainfall, preceded by approximately 2 weeks of drought appears to increase disease transmission in wild birds, possibly because of increased mosquito populations.
Surveillance: Mosquito Populations - Monitoring vector populations is done under the assumption that vector population densities correlate with the incidence of disease in humans. Although high densities of vectors do not invariably lead to human disease, human cases are not likely to occur if vector populations are kept below certain levels (Eldridge 1987). Vector surveillance is also conducted to evaluate the results of control efforts.
Virus Occurrence in Mosquitoes - Routine testing of mosquito samples for isolation of the virus can provide valuable epidemiological information. Although some studies have found a positive correlation between mosquito infestation rates and human cases (Kokernot et al. 1969), others found no correlation in studies encompassing several years (Bowen et al. 1980).
Sentinel Chickens - Many mosquito control programs use sentinel chicken flocks to monitor SLE virus activity. The chickens are placed inside cages and bled at frequent intervals. The blood is then analyzed to detect the presence of specific antibodies that are manufactured and circulated through the blood after infection with even small amounts of the SLE virus (seroconversion). Advantages of this method include the fact that it gives an estimate of the actual rates of transmission, rather than just rates of infection in nature; that depending upon the frequency of bleeding, it can also give an estimate of the timing of transmission (Eldridge 1987); and that long-term use can produce data that can yield information on seasonal patterns of virus transmission at specific locations. Disadvantages include the fact that the method is highly dependent upon the location of the sentinel chicken flock; the fact that there is a lag between infection and antibody formation; the possibility of non-specific antibody reactions; and the time, labor, and cost associated with development, maintenance, deployment and bleeding of sentinel chicken flocks.
Human Cases - Tracking of human cases is also a key element in any disease surveillance program. Very rarely does a historical record of human cases by itself help predict future disease epidemics. However, used with other data, long term human occurrence data can be useful in helping refine probability estimation of disease outbreaks. If nothing else, cases that occur early in the season can alert officials of possible need for emergency procedures. Additionally, lessons learned during the handling of human cases, whether epidemic or not, should better prepare officials for dealing with other cases and with full blown epidemics.
SLE Epidemic Zone in Florida.
Treatment and Prevention: There is no cure for the disease nor are there vaccines available. Medical treatment is only for the symptoms such as swelling of the brain and related effects like difficulties or stoppage of breathing, and for secondary complications such as bacterial infections.
Since there is no direct treatment, control of the disease relies upon preventing transmission to humans or breaking the virus cycle in nature. Transmission prevention involves significantly decreasing the probabilities of mosquito bites. Preventive measures includes avoiding outdoor activities after dark, when the Culex mosquitoes are most active, wearing protective clothing (long sleeves and pants, etc.), and using repellents that contain DEET as its active ingredients. Note that special care must be taken when applying concentrated repellents to children, and particularly, infants, because high concentrations of the active chemicals may be absorbed through the skin. DEET concentrations from 7 to 25% have been found to be effective in preventing mosquito bites, as long as the formulation persist on the individual.
Interrupting the virus cycle involves significantly reducing the mosquito populations. This is achieved through spraying of insecticides to directly kill adult and/or immature mosquitoes, or by elimination of mosquito breeding sites to prevent populations from ever reaching high levels.
Bowen, G. S. and D. B. Fancy. 1980. Surveillance. In: Monath T. P (ed), The Arboviruses: Epidemiology and Ecology. CRC Press, Boca Raton, FL.
Brinker K. R and T. P. Monath 1988. The Acute Disease, In: Monath, T. P. (ed.), The Arboviruses: Epidemiology and Ecology. CRC Press, Boca Raton, FL .
Chamberlain R. W. 1988. History of St. Louis Encephalitis. In: Monath TP (ed), The Arboviruses: Epidemiology and Ecology. CRC Press, Boca Raton, FL
Eldridge, B. F. 1987. Strategies for surveillance, prevention, and control of arbovirus diseases in western North America. Am. J. Tropical Medicine and Hygiene 37: 775-885.
Goddard J: 1996. Physician's Guide to Arthropods of Medical Importance., CRC Press, Boca Raton, FL.
Kokernot, R. H., J. Hayes, R. L. Will, C. H. Tempelis, D. M. H. Chan, and B Radivojevic. 1969. Arbovirus studies in the Ohio-Mississippi Basin, 1964-1967 II: St. Louis encephalitis virus. Am. J. Tropical Medicine and Hygiene 18: 750-761.
Lillie T. H, E. Schreck and A. J. Rahe. 1988. Effectiveness of personal protection against mosquitoes in Alaska. J. Med Entomol. 25:475-478.
Tsai T. F, and C. J. Mitchell 1988. St. Louis Encephalitis. In: Monath TP (ed), The Arboviruses: Epidemiology and Ecology. CRC Press, Boca Raton, FL.
Lazoff, M. 1998. Encephalitis. In: Emergency Medicine - An Online Reference.
Photos by Jim Newmann unless otherwise noted