Climate and satellite indicators to forecast Rift Valley fever epidemics in Kenya.
(1/214)
All known Rift Valley fever virus outbreaks in East Africa from 1950 to May 1998, and probably earlier, followed periods of abnormally high rainfall. Analysis of this record and Pacific and Indian Ocean sea surface temperature anomalies, coupled with satellite normalized difference vegetation index data, shows that prediction of Rift Valley fever outbreaks may be made up to 5 months in advance of outbreaks in East Africa. Concurrent near-real-time monitoring with satellite normalized difference vegetation data may identify actual affected areas. (+info)
Rift valley fever surveillance in the lower Senegal river basin: update 10 years after the epidemic.
(2/214)
After the Rift valley fever (RVF) epidemic of 1987 in the Senegal River Basin, RVF surveillance based on serosurveys has been conducted for 10 years. Serum samples were obtained from 1336 persons and from sheep and goats in selected areas, and these were tested for IgG/IgM RVF antibodies by ELISA. After a period of regular decrease in RVF prevalence in domestic animals until 1993, an epizootic was observed in all herds in 1994-95 with increases in IgM levels and abortions. During the same period, no human cases or RVF IgM were detected. The RVF IgG prevalence significantly correlated with date of birth: children born after 1987 have a low prevalence (5%) in clear contrast to the older population (25.3%) in Podor district. A retrospective analysis of rainfall and RVF prevalence in small domestic animals over the last 10 years showed that the re-emergence correlated with heavy rainfall. A general analysis of the risk of re-emergence and the efficiency of this RVF surveillance system are presented. (+info)
Observations on the epidemiology of Rift Valley fever in Kenya.
(3/214)
The epizootic range of Rift Valley fever in Kenya is defined from the results of virus isolations during epizootics, and form an extensive serological survey of cattle which were exposed during an epizootic. A study of the sera from a wide range of wild bovidae sampled immediately after the epizootic, showed that they did not act as reservoir or amplifying hosts for RVF. Virus isolation attempts from a variety of rodents proved negative. Rift Valley fever did not persist between epizootics by producing symptomless abortions in cattle in areas within its epizootic range. A sentinel herd sampled annually after an epizootic in 1968 revealed not one single seroconversion from 1969 to 1974. Certain forest and forest edge situations were postulated as enzootic for Rift Valley fever, and a small percentage of seroconversions were detected in cattle in these areas, born four years after the last epizootic. This has been the only evidence for the persistence of the virus in Kenya since 1968, and may be a part of the interepizootic maintenance cycle for Rift Valley fever in Kenya, which otherwise remains unknown. (+info)
Resistance to Rift Valley fever virus in Rattus norvegicus: genetic variability within certain 'inbred' strains.
(4/214)
Rift Valley fever virus (RVFV) is the causative agent of Rift Valley fever, a widespread disease of domestic animals and humans in sub-Saharan Africa. Laboratory rats have frequently been used as an animal model for studying the pathogenesis of Rift Valley fever. It is shown here that Lewis rats (LEW/mol) are susceptible to infection with RVFV, whereas Wistar-Furth (WF/mol) rats are resistant to RVFV infection. LEW/mol rats developed acute hepatitis and died after infection with RVFV strain ZH548, whereas WF/mol rats survived the infection. Cross-breeding of resistant WF/mol rats with susceptible LEW/mol rats demonstrated that resistance is segregated as a single dominant gene. Primary hepatocytes but not glial cells from WF/mol rats showed the resistant phenotype in cell culture, indicating that resistance was cell type-specific. Moreover, when cultured hepatocytes were stimulated with interferon (IFN) type I there was no indication of a regulatory role of IFN in the RVFV-resistance gene expression in WF/mol rats. Interestingly, previous reports have shown that LEW rats from a different breeding stock (LEW/mai) are resistant to RVFV infections, whereas WF/mai rats are susceptible. Thus, inbred rat strains seem to differ in virus susceptibility depending on their breeding histories. A better genetic characterization of inbred rat strains and a revision in nomenclature is needed to improve animal experimentation in the future. (+info)
Outbreak of Rift Valley fever--Saudi Arabia, August-October, 2000.
(5/214)
On September 10, 2000, the Ministry of Health (MOH), Kingdom of Saudi Arabia, and subsequently the Ministry of Health of Yemen received reports of unexplained hemorrhagic fever in humans and associated animal deaths from the southwestern border of Saudi Arabia and Yemen. Signs and symptoms of ill persons included low grade fever, abdominal pain, vomiting, diarrhea, jaundice with liver and renal dysfunction often progressing to disseminated intravascular coagulation, hepatorenal syndrome, and death. On September 15, using ELISA (antigen detection and IgM), polymerase chain reaction, virus isolation, and immunohistochemistry, CDC confirmed the diagnosis of Rift Valley fever (RVF) in all four serum samples submitted from Saudi Arabia. This report summarizes the preliminary results of the collaborative epidemiologic investigation performed by the Saudi Arabian MOH, CDC, and the National Institute of Virology, South Africa, of the first confirmed occurrence of RVF outside Africa. (+info)
Update: outbreak of Rift Valley Fever--Saudi Arabia, August-November 2000.
(6/214)
On September 10, 2000, the Ministry of Health (MOH), Kingdom of Saudi Arabia and subsequently, the MOH of Yemen began receiving reports of unexplained hemorrhagic fever in humans and associated animal deaths and abortions from the far western Saudi-Yemeni border region. These cases subsequently were confirmed as Rift Valley fever (RVF), the first such cases on the Arabian peninsula. This report updates the findings of the ongoing investigation conducted by the Saudi Arabian MOH in collaboration with CDC and the National Institute of Virology, South Africa. (+info)
Outbreak of Rift Valley fever--Yemen, August-October 2000.
(7/214)
On September 17, 2000, the Ministry of Agriculture and Irrigation (MAI) and Ministry of Health (MOH) of Yemen received reports about the occurrence of disease compatible with Rift Valley fever (RVF) in El Zuhrah district of Hodeidah governorate. Reports of animal disease included abortions and deaths in young animals. Surveillance efforts by MOH and MAI documented widespread disease among humans and animals in the area of Wadi Mawr in El Zuhrah district, which is located on a coastal plain that extends from the southern tip of Yemen into the Jizan area of the Kingdom of Saudi Arabia (KSA). The Saudi Arabian Ministry of Health has described a simultaneous outbreak of RVF in the Jizan area in KSA (1,2). This report summarizes the investigation of the Yemen outbreak. (+info)
First isolation of the Rift Valley fever virus from Culex poicilipes (Diptera: Culicidae) in nature.
(8/214)
Following the reemergence of Rift Valley fever (RVF) virus in southeastern Mauritania in 1998, an entomological survey was undertaken in the boundary area in Senegal to assess the extent of the virus circulation. During this study, RVF virus (36 strains) was isolated for the first time from Culex poicilipes in nature. The possible role of Cx. poicilipes as an RVF vector is discussed regarding its biology and ecology. (+info)