Complete sequencing of p54-gene from 67 European, American, and West and East African Swine Fever virus (ASFV) isolates revealed that West African and European ASFV isolates classified within the predominant Genotype I according to partial sequencing of p72 were discriminated into four major sub-types on the basis of their p54 sequences. This highlighted the value of p54 gene sequencing as an additional, intermediate-resolution, molecular epidemiological tool for typing of ASFV viruses. We further evaluated p54-based genotyping, in combination with partial sequences of two other genes, for determining the genetic relationships and origin of viruses responsible for disease outbreaks in Kenya. Animals from Western and central Kenya were confirmed as being infected with ASFV using a p72 gene-based PCR assay, following outbreaks of severe hemorrhagic disease in domestic pigs in 2006 and 2007. Eleven hemadsorbing viruses were isolated in macrophage culture and genotyped using a combination of full-length p54-gene sequencing, partial p72-gene sequencing, and analysis of tetrameric amino acid repeat regions within the variable region of the B602L gene (CVR). The data revealed that these isolates were identical in their p72 and p54 sequence to viruses responsible for ASF outbreaks in Uganda in 2003. There was a minor difference in the number of tetrameric repeats within the B602L sequence of the Kenyan isolates that caused the second Kenyan outbreak in 2007. A practical implication of the genetic similarity of the Kenyan and Ugandan viral isolates is that ASF control requires a regional approach.

We analyzed the extent of livestock involvement in the latest Rift Valley fever (RVF) outbreak in Kenya that started in December 2006 and continued until June 2007. When compared with previous RVF outbreaks in the country, the 2006-07 outbreak was the most extensive in cattle, sheep, goats, and camels affecting thousands of animals in 29 of 69 administrative districts across six of the eight provinces. This contrasted with the distribution of approximately 700 human RVF cases in the country, where over 85% of these cases were located in four districts; Garissa and Ijara districts in Northeastern Province, Baringo district in Rift Valley Province, and Kilifi district in Coast Province. Analysis of livestock and human data suggests that livestock infections occur before virus detection in humans, as supported by clustering of human RVF cases around livestock cases in Baringo district. The highest livestock morbidity and mortality rates were recorded in Garissa and Baringo districts, the same districts that recorded a high number of human cases. The districts that reported RVF in livestock for the first time in 2006/07 included Kitui, Tharaka, Meru South, Meru central, Mwingi, Embu, and Mbeere in Eastern Province, Malindi and Taita taveta in Coast Province, Kirinyaga and Murang'a in Central Province, and Baringo and Samburu in Rift Valley Province, indicating that the disease was occurring in new regions in the country.

Rift Valley fever virus (RVFV) is an arbovirus associated with periodic outbreaks, mostly on the African continent, of febrile disease accompanied by abortion in livestock, and a severe, fatal haemorrhagic syndrome in humans. However, the maintenance of the virus during the inter-epidemic period (IEP) when there is low or no disease activity detected in livestock or humans has not been determined. This study report prevalence of RVFV-neutralizing antibodies in sera (n=896) collected from 16 Kenyan wildlife species including at least 35% that were born during the 1999-2006 IEP. Specimens from seven species had detectable neutralizing antibodies against RVFV, including African buffalo, black rhino, lesser kudu, impala, African elephant, kongoni, and waterbuck. High RVFV antibody prevalence (>15%) was observed in black rhinos and ruminants (kudu, impala, buffalo, and waterbuck) with the highest titres (up to 1:1280) observed mostly in buffalo, including animals born during the IEP. All lions, giraffes, plains zebras, and warthogs tested were either negative or less than two animals in each species had low (or= 1:80. These data provide evidence that wild ruminants are infected by RVFV but further studies are required to determine whether these animals play a role in the virus maintenance between outbreaks and virus amplification prior to a noticeable outbreak.

No abstract

Since Kenya first reported Rift Valley fever (RVF)-like disease in livestock in 1912, the country has reported the most frequent epizootics of RVF disease. To determine the pattern of disease spread across the country after its introduction in 1912, and to identify regions vulnerable to the periodic epizootics, annual livestock disease records at the Department of Veterinary Services from 1910 to 2007 were analysed in order to document the number and location of RVF-infected livestock herds. A total of 38/69 (55%) administrative districts in the country had reported RVF epizootics by the end of 2007. During the 1912-1950 period, the disease was confined to a district in Rift Valley province that is prone to flooding and where livestock were raised in proximity with wildlife. Between 1951 and 2007, 11 national RVF epizootics were recorded with an average inter-epizootic period of 3·6 years (range 1-7 years); in addition, all epizootics occurred in years when the average annual rainfall increased by more than 50% in the affected districts. Whereas the first two national epizootics in 1951 and 1955 were confined to eight districts in the Rift Valley province, there was a sustained epizootic between 1961 and 1964 that spread the virus to over 30% of the districts across six out of eight provinces. The Western and Nyanza provinces, located on the southwestern region of the country, had never reported RVF infections by 2007. The probability of a district being involved in a national epizootic was fivefold higher (62%) in districts that had previously reported disease compared to districts that had no prior disease activity (11%). These findings suggests that once introduced into certain permissive ecologies, the RVF virus becomes enzootic, making the region vulnerable to periodic epizootics that were probably precipitated by amplification of resident virus associated with heavy rainfall and flooding.