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We studied the capacity of 44 strains of St. Louis encephalitis (SLE) virus to induce viremia in an epidemiologically important wild avian host, the House Sparrow (Passer domesticus). Selected virus strains were also inoculated at varying doses into 3-week-old chicks. Viremic responses were analyzed in terms of the proportion of inoculated nestling and adult birds which became viremic, the mean duration and the mean peak titer of viremia. Infectivity of avian sera was determined by plaque assay in primary duck embryo cell cultures. The susceptibility of the House Sparrow to viremic infection with different SLE virus strains varied markedly. Nestling sparrows 6-10 days of age were generally more susceptible than adult birds. All virus strains isolated during Culex pipiens-borne epidemics in the eastern United States were highly viremogenic [viremia in 80% of birds with a mean duration of greater than or equal to 1.6 days in adults or greater than or equal to 2.7 days in nestlings and a mean peak titer of greater than or equal to 10(3.0) plaque-forming units (PFU)/ml in adults and 10(4.0) PFU/ml in nestlings]. All virus strains isolated from Culex tarsalis in the western United States, strains isolated from rodents in South America. and six of 16 strains isolated from various sources elsewhere in tropical America were partially or fully attenuated. A high degree of concordance was demonstrated between experimental viremia in sparrows, viremia in 3-week-old chicks, and neurovirulence for weanling mice. The epidemilogic significance of these findings is discussed.

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A second virus with distinct biological, serological, and physiochemical properties was detected as a minority viral subpopulation in specimens of Cliff Swallow nest bugs (Oeciacus vicarius) and nestling bird sera containing Fort Morgan (FM) virus. The second virus, detected by a breakthrough neutralization test employing FM antiserum, was present in 5 of 11 FM virus-positive pools of nest bugs and in 4 of 38 birds from Colorado and South Dakota. The concentration of the second virus was 10-fold to 1,000-fold lower than that of FM virus. The second virus, which was provisionally named "Bijou Bridge" (BB) virus was shown by conventional serological tests to be a member of the Venezuelan equine encephalomyelitis (VEE) complex, and by tests employing antisera to the E2 viral glycoprotein to be identical with Tonate virus, previously isolated from birds and mosquitoes only in French Guiana. Experimental infection of House Sparrows and Cliff Swallows showed that they develop brief BB viremias and antibodies. Oe. vicarius bugs were resistant to oral infection with BB virus. The epidemiological significance of recovery of Tonate virus in North American is discussed.

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Previous studies have demonstrated a diabetogenic effect of Venezuelan equine encephalitis (VEE) virus in hamsters. A preliminary study was conducted in which five 2- to 3-year-old rhesus monkeys were infected with the virulent Trinidad donkey strain of VEE virus and their carbohydrate metabolism was studied over 10 months. All animals developed mild clinical illness (rhinorrhea, cough, fever), were viremic, and developed antibodies. As compared with the results of preinoculation intravenous glucose tolerance tests (IVGTT), the monkeys had abnormally high glucose values by 2 months postinoculation (PI), progressively diminished insulin responses between 8 days and 5 months PI, and significantly lower glucagon curves 2, 5, and 10 months PI. Pancreatic histology and insulin content were normal. A second, controlled study was conducted of glucose and insulin metabolism in somewhat older (3- to 8-year-old) rhesus monkey after they were infected with both the Trinidad donkey strain of VEE virus and the attenuated VEE vaccine (TC-83). Groups of six monkeys received the virulent virus and the TC-83 vaccine, and five animals were sham-inoculated with saline. Monkeys inoculated with virulent virus became viremic, and 50% became febrile without overt signs of illness, whereas those given TC-83 virus remained afebrile and did not become viremic, but five of six developed antibodies. Intravenous glucose tolerance tests were performed and serum immunoreactive insulin responses to glucose administration measured before infection and 2 and 5 months later. No significant and consistent alterations of glucose or insulin responses were detected in the infected or control groups. Although several animals had preinoculation anti-islet cell antibodies, none developed new antibodies during the study.

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Epidemics of dengue fever occurring in Puerto Rico in 1963 to 1964 and 1969 were caused by dengue-3 and dengue-2 (DN-2) viruses, respectively, but endemic dengue transmission has never been documented on the Island. Since the 1969 epidemic, a surveillance system has detected DN-2 activity on the Island during each of the years 1970 through 1973, which suggests endemic persistence of the virus. This report describes the investigation of localized outbreaks of DN-2 in Guanica-Ensenada (1972) and Villalba (1973), and presents epidemiological, serological, and virological data from the outbreaks. Analysis of geographic distribution of dengue activity in Puerto Rico in recent years indicates that the DN-2 transmission in 1970 to 1973 may represent a long tail-off of the 1969 epidemic rather than the emergence of a truly endemic situation.

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