St. Louis Encephalitis Virus Disease in the United States, 2003-2017.

St. Louis encephalitis virus (SLEV), an arthropod-borne flavivirus, can cause disease presentations ranging from mild febrile illness through severe encephalitis. We reviewed U.S. national SLEV surveillance data for 2003 through 2017, including human disease cases and nonhuman infections. Over the 15-year period, 198 counties from 33 states and the District of Columbia reported SLEV activity; 94 (47%) of those counties reported SLEV activity only in nonhuman species. A total of 193 human cases of SLEV disease were reported, including 148 cases of neuroinvasive disease. A median of 10 cases were reported per year. The national average annual incidence of reported neuroinvasive disease cases was 0.03 per million. States with the highest average annual incidence of reported neuroinvasive disease cases were Arkansas, Arizona, and Mississippi. No large outbreaks occurred during the reporting period. The most commonly reported clinical syndromes were encephalitis (N = 116, 60%), febrile illness (N = 35, 18%), and meningitis (N = 25, 13%). Median age of cases was 57 years (range 2-89 years). The case fatality rate was 6% (11/193) and all deaths were among patients aged > 45 years with neuroinvasive disease. Nonhuman surveillance data indicated wider SLEV activity in California, Nevada, and Florida than the human data alone suggested. Prevention depends on community efforts to reduce mosquito populations and personal protective measures to decrease exposure to mosquitoes.

Tissue tropism of Saint Louis encephalitis virus: Histopathology triggered by epidemic and non-epidemic strains isolated in Argentina.

Saint Louis encephalitis virus (SLEV) reemerged in South America, and caused encephalitis outbreaks at the beginning of the 21st century. To enhance our knowledge about SLEV virulence, we performed comparative pathogenesis studies in Swiss albino mice inoculated with two different variants, the epidemic strain CbaAr-4005 and the non-epidemic strain CorAn-9275. Only the infection of mice with SLEV strain CbaAr-4005 resulted in high viremia, invasion of peripheral tissues including the lungs, kidney, and spleen, and viral neuroinvasion. This was associated with inflammatory pathology in the lungs, spleen, and brain as well as morbidity and mortality. In contrast, neither signs of desease nor viral replication were observed in mice infected with strain CorAn-9275. Interestingly, important loss of B cells and development of altered germinal centers (GC) were detected in the spleen of mice infected with strain CbaAr-4005, whereas mice infected with SLEV CorAn-9275 developed prominent GC with conserved follicular architecture, and neutralizing antibodies.

Human outbreak of St. Louis encephalitis detected in Argentina, 2005.

BACKGROUND: An outbreak of flavivirus encephalitis occurred in 2005 in Córdoba province, Argentina. OBJECTIVES: To characterize the epidemiologic and clinical features of that outbreak and provide the serologic results that identified St. Louis encephalitis virus (SLEV) as the etiologic agent. STUDY DESIGN: From January to May 2005, patients with symptoms of encephalitis, meningitis, or fever with severe headache were evaluated and an etiologic diagnosis achieved by detection of flavivirus-specific antibody sera and cerebrospinal fluid. RESULTS: The epidemic curve of 47 cases showed an explosive outbreak starting in January 2005 with one peak in mid-February and a second peak in mid-March; the epidemic ended in May. Cases occurred predominantly among persons 60 years and older. Nine deaths were reported. SLEV antibodies, when detected in 47 patients studied, had a pattern characteristic of a primary SLEV infection. CONCLUSIONS: Even though isolated cases of St. Louis encephalitis have been reported in Argentina, this is the first description of a large SLEV encephalitis outbreak in Argentina.

Simulation studies of St. Louis encephalitis and West Nile viruses: the impact of bird mortality.

West Nile virus (WNv) has spread through much of the eastern United States following its introduction in 1999, and arrived in Florida in 2001. Prior to its arrival, we anticipated that its transmission cycle was likely to be similar to that of St. Louis encephalitis virus (SLEv). However, high levels of avian mortality have been reported for WNv in the northeastern United States, and it was unknown how this would impact the transmission dynamics of WNv. Simulation models were used to compare the two viruses by considering the impact of bird mortality on the transmission dynamics of arboviruses in south Florida. Transmission models without disease-induced mortality (SLEv) were compared with models including disease-induced mortality (WNv). Disease-induced mortality depressed transmission, eliminating epizootics in two of 14 simulations that were epizootic without the additional mortality. In both models, the most important factor in the likelihood of epizootics was mosquito population size; the mosquito mortality rate was also important. The additional avian mortality altered the factors most important in the size and timing of epizootics, although it did not always directly affect the outcome of the simulations. In some cases, low-level transmission occurred prior to the epizootic peak. When disease-induced avian mortality was included in the simulations, appreciable numbers of dead birds occurred prior to high levels of infection in mosquitoes. This has implications for the use of dead birds as a surveillance tool monitoring the spread and transmission of WNv.

St. Louis encephalitis: clinical and epidemiologic aspects, Mississippi, 1974.

During July, August, and September 1974, 23 confirmed or presumptive cases of St. Louis encephalitis occurred in Mississippi. Attack rates were highest in the northwest corner of the state and among persons over 70 years of age. Rural and urban residents had similar attack rates. Nine persons have not resumed their pre-illness level of activity because of residual neurologic impairment six months after their illness. Additional cases of St. Louis encephalitis are expected in the next few years.

The epidemiology of St. Louis encephalitis in Dallas, Texas, 1966.

An epidemic of St. Louis encephalitis (SLE) occurred in Dallas, Texas, in the summer of 1966. A total of 545 suspected cases within Dallas city and county were reported, of which 145 were laboratory-confirmed as SLE virus infection. The greatest concentration of cases occurred in lower socioeconomic areas of the central part of the city in black populations. The attack rate and mortality rate increased markedly with age. The overall attack rate was 15.2 per 100,000, with a case fatality rate of 9.7%. During the course of the epidemic, most of the county was sprayed aerially with an ultra-low volume (ULV), high-concentration malathion mist. The effects of this treatment cannot be adequately assessed from the human epidemiologic aspect alone, but the spraying clearly reduced the number and infection rate of the vector mosquitoes.

The epidemiology of St. Louis encephalitis in Corpus Christi, Texas, 1966.

In the summer of 1966, an epidemic of St. Louis encephalitis occurred in Corpus Christi, Texas, coincident with one occurring in Dallas about 563 km to the north. Among the 76 cases confirmed in Corpus Christi, there were two deaths; the attack rate was 41.0 per 100,000. In contrast with a concurrent outbreak in Dallas and the 1964 outbreak in Houston, attack rates were much higher in populations of the upper socioeconomic districts. This distribution may have resulted from the combined effects of an unusual concentration of vector mosquito breeding sites in storm sewers in the upper socioeconomic districts and a higher degree of residual immunity in the residents of the lower socioeconomic areas.

Influence of sex and age on natural resistance to St. Louis encephalitis virus infection in mice.

A difference was observed in susceptibility of adult male and female mice to St. Louis encephalitis (SLE) virus as measured by the death rate after intravenous challenge. Female mice that had susceptibility similar to that of males at 2 months of age had increased resistance to SLE virus at 3 and 4 months of age. The increased resistance occurred after sexual maturity, indicating that the resistance factor possibly was related to an aging process in the female. The susceptibility of male mice remained unchanged over the 2- to 4-month period. Neither pregnancy nor castration had any effect on resistance of adult mice to St. Louis encephalitis virus.