Isolation of St. Louis encephalitis virus from a patient in Belém, Brazil

St. Louis encephalitis (SLE) virus was isolated from a 21-year-old female hospitalized on 4 October 1978 in Belém, Brazil. Symptomatology on admission included fever, chills, severe headache, abdominal pain, myalgia, arthralgia and jaundice. SLE virus was isolated from her blood drawn on the 8th day of illness and subsequent seroconversion was documented. Serological tests showed the isolate to be closely related to the Belém prototype of SLE virus but distinct from other flaviviruses tested. The patient was discharged without sequelae after 16 days of hospitalization. Epidemiological investigations where the patient worked and lived revealed no evidence of extensive transmission of SLE virus.     

Simulation studies of St. Louis encephalitis virus in south Florida

Two simulation models were used to investigate the epidemiology of St. Louis encephalitis virus (SLEv) in south Florida, one including sentinel hosts (chickens) and amplification hosts (wild birds), while the other one included age structure in the amplification host population. The overall population size of the vector, Culex nigripalpus, was a major factor in the likelihood of epizootics for both models, but the seasonal dynamics of the vector alone did not explain variation in transmission. Interactions between seasonal factors in the mosquito and reproduction in the wild amplification avian hosts appeared to be important in the likelihood of epizootics. Biased feeding between sentinel and amplification hosts affected the time course of virus prevalence and may have implications for the interpretation of sentinel data. The time of virus introduction strongly affected the timing of outbreaks but did not affect the likelihood of epizootics. In most cases, the outbreak occurred immediately after virus introduction; however, in some cases the outbreak was delayed until the mosquito population increased. This has implications for the timing of control strategies directed against mosquito populations.     

Transovarial transmission of St. Louis encephalitis virus by Culex pipiens complex mosquitoes

Experiments were conducted to determine whether transovarial transmission (TOT) of St. Louis encephalitis (SLE) virus occurs in Culex pipiens complex mosquitoes, the principal vectors of SLE virus in the central-eastern United States. In 1978, field-collected mosquitoes from Memphis, Tennessee, and McLeansboro, Illinois, were used; during 1979, colonized mosquitoes from Chicago, Illinois, and Memphis, Tennessee, were used. Mosquitoes were infected by feeding on viremic chicks inoculated with an SLE virus strain isolated from Cx. pipiens complex mosquitoes collected from Memphis, Tennessee, in 1976. During the 1979 experiments, progeny larval and adult mosquitoes were held at two temperatures, 18 and 25 degrees C. Progeny were tested for virus by plaque assay in duck embryo cell cultures and by inoculation of Aedes albopictus C6/36 cells and examination by immunofluorescence. In 1978, most of the progeny tested were from the first ovarian cycle, and a single occurrence of TOT was documented. In 1979, a single TOT occurred from 46,856 first ovarian cycle progeny, whereas 7 of 9,234 progeny of the second ovarian cycle were infected. The rate of TOT was higher for progeny of Memphis than Chicago mosquitoes, and for mosquitoes held at 18 degrees C than at 25 degrees C; however, these differences were not statistically significant. Four positive pools were females, and three were fed on chicks for transmission attempts. The positive Chicago mosquito pool failed to transmit, but both Memphis pools successfully transmitted virus. The overall rates of TOT of SLE virus in progeny of the first and second ovarian cycle were, respectively, 1/45, 151 and 1/1,460. The significance of these results as they relate to the natural history of SLE virus is discussed.     

St. Louis encephalitis: the Chicago experience.

The largest laboratory-documented outbreak of St. Louis encephalitis (SLE) in the United States occurred in the Chicago metropolitan area in the summer and early fall of 1975. Of 1,456 illnesses investigated, 326 cases of confirmed or probable SLE and 420 cases of suspected SLE were found in the six-county area. The outbreak peaked in early September, but cases continued to occur through October. Cases clustered geographically in the southwestern suburbs. There was a direct correlation between age and attack rate, severity of illness, and mortality rate--all of which increased with successive age groups. Thirty-six persons died. Males and females were equally affected. This epidemic marked the first time that St. Louis encephalitis has been documented in the Chicago area.     

Experimental transovarial transmission of St. Louis encephalitis virus by Culex and Aedes mosquitoes

Colonized and field-collected female Culex tarsalis, infected with St. Louis encephalitis, (SLE) virus by intrathoracic inoculation or by feeding on a viremic host, transmitted virus to their F1 adult and/or larval progeny when reared at 18(+/- 1) degree C but not when reared at 27(+/- 1) degrees C. The minimal infection rates (MIR) for different populations of Cx. tarsalis ranged from 1:32 to less than 1:250 (mean = 1:121) for larval progeny and from 1:32 to less than 1:1, 989 (mean = 1:1,571) for adult progeny. SLE virus also was transmitted transovarially by colonized and field-collected populations of Culex pipiens (mean MIRs = 1:340 and 1:1,815 for larval and adult progeny, respectively) and by a field population of Culex quinquefasciatus (MIR = 1:500 and less than 1:246 for larval and adult progeny, respectively), but not by colonized strains of Cx. quinquefasciatus and Culex peus. SLE virus was not recovered in tests on 5,522 Cx. tarsalis and 4,798 Cx. quinquefasciatus that were collected as larvae or pupae from field sites in Southern California and reared to adults at 18 degrees C in the laboratory. Transovarial transmission of SLE virus by Aedes epactius was confirmed and extended to a closely related species, Aedes atropalpus. Efforts to demonstrate transovarial transmission of SLE virus by Aedes melanimon, Aedes sierrensis, and Aedes triseriatus were unsuccessful. Aedes dorsalis, Cx. peus, and Toxorhynchites amboinensis were equally sensitive hosts for viral isolation when inoculated with suspensions of larvae transovarially infected with SLE virus.     

Serologic diagnosis of West Nile and St. Louis encephalitis virus infections in domestic chickens

Adult domestic chickens were infected with West Nile virus (WNV) or St. Louis encephalitis virus (SLEV) and challenged with homologous or heterologous virus at 21 or 56 days postinfection (dpi). Sera were collected at selected time points after infection and assayed by enzyme immunoassay (EIA), plaque reduction neutralization test (PRNT), and a Western blot (WB) alternative to PRNT. EIA results were sensitive and accurate (few false positives) but not specific, requiring a confirmatory test to determine virus infection history. PRNT results generally were specific until challenge, after which test results were frequently equivocal and inadequate to determine first or second infecting virus. WB results confirmed the serologic cross-reactivity between WNV and SLEV envelope protein. Non-structural protein 1 and pre-membrane protein reactivities were highly specific for WNV during SLEV infection, but less specific for SLEV during WNV infection. WB and PRNT specificities were similar for both viruses from 6 to 14 dpi, and sensitivities to WNV were virtually identical.     

The house sparrow (Passer domesticus) as a sentinel for St. Louis encephalitis virus

Birds are the primary hosts for St. Louis encephalitis (SLE) virus in most of North America. Because the increased prevalence of antibody in House Sparrows (Passer domesticus) has been related to human cases, this species has been frequently used as a sentinel of SLE virus activity in urban areas. This study investigated the susceptibility of House Sparrows to two strains of SLE virus, measured antibody profiles, and evaluated the use of House Sparrows in an urban surveillance system. House Sparrows were susceptible to both strains of SLE virus inoculated, although not equally, and produced viremias sufficient to infect vector mosquitoes. Both hemagglutination-inhibiting (HI) and neutralizing (N) antibody developed rapidly and to high titers within 2 weeks after inoculation. Detectable humoral antibody began to disappear by 3 months, but persisted for 2 years in 27% for HI and 36% for N antibody of the surviving birds. However, all of the surviving birds were resistant to reinfection with SLE virus at 2 years after inoculation. The titer of HI antibody appeared to be useful in determining recent exposure to SLE virus. The experimental data on HI antibody development and persistence was related to field serologic data from House Sparrows. The monthly prevalences of SLE antibody for independent samples of sera from House Sparrows collected in Memphis, Tennessee, in 1980 were similar. SLE amplification in the House Sparrow population was delayed until September. The Memphis arbovirus surveillance system detected the amplification quickly, and responded with increased adult mosquito control in the focal areas. Urban surveillance of SLE utilizing House Sparrows as sentinels is discussed.     

Comparison of biological properties of St. Louis encephalitis and Rio bravo viruses

St. Louis encephalitis (SLE) virus, an arbovirus, and Rio Bravo (RB) virus, a non-arthropod-borne virus, are flaviviruses which cross-react in neutralization tests. Several of their biological properties were compared. Viral growth curves revealed that greater than 99% of infectious SLE (Parton) virus remained cell-associated in Vero cells but was released slowly into the medium of infected BHK-21 cells. In contrast, RB (M-64) virus was released upon maturation into the fluids of Vero and BHK-21 cell cultures. Fortyfold more SLE virus than RB virus adsorbed to monolayer cultures of Aedes dorsalis cells. SLE but not RB virus replicated and reached high titers (10(8) pfu/ml) in Ae. dorsalis cell cultures maintained in media which were expected to enhance recovery of RB virus. Further, SLE but not RB virus replicated in cultured bat epithelial cells and primary duck embryo cells incubated at 42 degrees C. Clearly, the prototype strains of RB and SLE viruses are distinct viruses. Both the classification of RB virus in the genus flavivirus and the antigenic relationship between RB and SLE viruses require further clarification.