May 2004 St. Louis Encephalitis - Another Mosquito Borne Disease St. Louis encephalitis (SLE) is caused by a virus that normally infects a variety of birds and mammals, without any apparent disease. Infection in these vertebrate hosts results in a multiplication of virus, creating a viremia, sufficient virus particles per unit of blood, which makes them infective. This viremia lasts a few days, during this time the virus can be picked up by a blood feeding mosquito. The virus infects and multiplies within the mosquito, making the mosquito infective to other animals that it subsequently feeds on. Transmission of SLE is done primarily by mosquitoes of the genus Culex. In Florida, the main vector is Culex nigripalpus, a species found throughout the state.
Humans are incidental, dead-end hosts to SLE, never developing a high enough viremia in our blood to become infective. The clinical symptoms of SLE infections in humans can be: no symptoms at all, a mild flu-like illness, or aseptic meningitis and encephalitis which can progress to coma and death. Inapparent illness is common in young people, whereas encephalitis and its complications is most common in the elderly. The overall mortality of symptomatic cases is between 3% to 30%, depending upon the age makeup of the population and the virulence of the virus. SLE epidemics in the human population usually occurs from August through December of any given year.
The first outbreak of SLE in humans occurred in, where else, St. Louis, Missouri, in 1933. Since then many SLE epidemics have occurred in the U.S. From 1964 to 1998, 4,478 human cases have been reported, an average of 128 cases annually. In Florida, SLE outbreaks have occurred in 1959, 1961, 1962, 1977, and 1990.
The transmission cycle leading to SLE epidemics is very complicated and poorly understood. Outbreaks in humans is thought to coincide with the infection of various, specific species of wild birds, initiated by the bite of an infected mosquito. Once infected, the virus will multiply in the bird and, within 2 days, produce large enough quantities of virus in its blood to become infective to other mosquitoes that feed from such a bird. Infected birds produce antibodies to the SLE virus and, within 3 days, the virus disappears and the bird is no longer a source of infection. The 1 - 3 days that it takes for a bird to develop antibodies is the only “window of opportunity” a mosquito has to pick up the virus and become infective. Once infected and antibodies are produced, the bird is forever immune to re-infection by SLE. The SLE virus does not cause mortality in birds, and birds cannot infect one another, the virus can only be transmitted by mosquitoes. As ever greater numbers of susceptible birds are infected and become immune, the infection rate in mosquitoes dwindles. Since mosquitoes are short-lived, mosquitoes with “old” SLE infections rapidly disappear and the epidemic quickly ends. So, how is the SLE virus maintained if the birds become immune and the mosquitoes die off? It is thought that the virus is maintained or reservoired in several ways. In incidental hosts, such as rodents, that maintain an active viremia and are unaffected by the infection, by infected, migrating birds that come into an area, or the virus can overwinter in an infected mosquito, as an adult or larva. The virus can get into the immature mosquitoes by what is termed transovarian transmission. Transovarian transmission is when the virus in an infected female mosquito infects the eggs she produces. When the eggs hatch, the larva are infected and, when they emerge as adults, are already infective.
Conditions needed for an SLE epidemic in the bird population and a consequent spillover into the human population is an abnormally high mosquito population capable of vectoring SLE (Culex nigripalpus), a large population of susceptible birds (hatchlings), and the presence of the virus - all of which needs to occur at the same time. An excessively wet spring can provide for 2 of the 3 variables. Abnormally high rainfall provides for more mosquito habitat/production and more food for nesting birds. An abundance of food for birds allows them to produce more eggs thus more hatchlings or susceptible birds. The only ingredient missing is the SLE virus and that is usually available, as previously mentioned, in the natural environment. Again, all of these variables need to coincide precisely for an epidemic in birds to occur. All of the steps in the SLE virus transmission cycle are still not known and research on the SLE transmission cycle is on-going.
Fortunately, SLE in the northern half of Florida is quite rare. Most SLE outbreaks have occurred from the central part of the state, the Tampa-Vero Beach areas, southward. Coincidently, this is the point where freezing weather normally reaches in our state. This “freeze line” may have something to do with outbreaks of SLE, along with the other factors previously mentioned. It is theorized that a hard freeze that extends into the sub-tropical area of Florida kills off the cold sensitive ground covering vegetation. This die-off of ground cover increases the habitat/food supply for ground foraging birds, such as mourning doves. This increased food supply results in the production and ability to support more hatchlings - susceptible birds. This theory is recent and we are still awaiting a winter with a hard freeze in the sub-tropical region of the state and the subsequent coincidence of the other factors needed for an SLE transmission cycle to occur. If a hard freeze is shown to be an essential prerequisite for an SLE outbreak, it would become an early warning system, alerting mosquito control programs to better prepare for the possibility of an SLE outbreak in Florida. |