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Background Arbovirus surveillance and recurrence of outbreaks in Kenya continues to reveal the re-emergence of viruses of public health importance. This calls for sustained efforts in early detection and characterization of these agents to avert future potential outbreaks. Methods A larval survey was carried out in three different sites in Kwale County, Vanga, Jego and Lunga Lunga. All containers in every accessible household and compound were sampled for immature mosquitoes. In addition, adult mosquitoes were also sampled using CO2-baited CDC light traps and BG-Sentinel traps in the three sites and also in Tsuini. The mosquitoes were knocked down using trimethylamine and stored in a liquid nitrogen shipper for transportation to the laboratory where they were identified to species, pooled and homogenized ready for testing. Results A total of 366 houses and 1730 containers were inspected. The House Index (HI), Container Index (CI) and Breateau Index (BI) for Vanga Island were (3%: 0.66: 3.66) respectively. In Jego, a rural site, the HI, CI and BI were (2.4%: 0.48: 2.4) respectively. In Lunga Lunga, a site in an urban area, the HI, CI and BI were (22.03%: 3.97: 29.7) respectively. The indices suggest that this region is at risk of arbovirus transmission given they were above the WHO threshold (CI > 1, HI > 1% and BI > 5). The most productive containers were the concrete tanks (44.4%), plastic tank (22.2%), claypot (13.3%), plastic drums (8.9%), plastic basins (4%), jerricans (1.2%) and buckets (0.3%). Over 20,200 adult mosquitoes were collected using CDC light traps, and over 9,200 using BG- sentinel traps. These mosquitoes were screened for viruses by inoculating in Vero cells. Eleven Orthobunyavirus isolates were obtained from pools of Ae. pembaensis (4), Ae. tricholabis (1), Cx. quinquefasciatus (3), Culex spp. (1) and Cx. zombaensis (2). Five of the Orthobunyaviruses were sequenced and four of these were determined to be Bunyamwera viruses while one isolate was found to be Nyando virus. One isolate remained unidentified. Conclusions These results indicate circulation of Orthobunyaviruses known to cause diverse grades of febrile illness with rash in humans in this region and highlights the need for continued monitoring and surveillance to avert outbreaks.

Background Chikungunya virus is an alphavirus, primarily transmitted by Aedes aegypti and Ae. albopictus. In late 2017–2018, an outbreak of chikungunya occurred in Mombasa county, Kenya, and investigations were conducted to establish associated entomological risk factors. Methods Homes were stratified and water-filled containers inspected for immature Ae. aegypti, and larval indices were calculated. Adult mosquitoes were collected in the same homesteads using BG-Sentinel and CDC light traps and screened for chikungunya virus. Experiments were also conducted to determine the ability of Culex quinquefasciatus to transmit chikungunya virus. Results One hundred thirty-one houses and 1637 containers were inspected; 48 and 128 of them, respectively, were positive for immature Ae. aegypti, with the house index (36.60), container index (7.82) and Breteau index (97.71) recorded. Jerry cans (n = 1232; 72.26%) and clay pots (n = 2; 0.12%) were the most and least inspected containers, respectively, while drums, the second most commonly sampled (n = 249; 15.21%), were highly positive (65.63%) and productive (60%). Tires and jerry cans demonstrated the highest and lowest breeding preference ratios, 11.36 and 0.2, respectively. Over 6900 adult mosquitoes were collected and identified into 15 species comprising Cx. quinquefasciatus (n = 4492; 65.04%), Aedes vittatus (n = 1137; 16.46%) and Ae. aegypti (n = 911; 13.19%) and 2 species groups. Simpson’s dominance and Shannon-Wiener diversity indices of 0.4388 and 1.1942 were recorded, respectively. Chikungunya virus was isolated from pools of Ae. aegypti (1) and Cx. quinquefasciatus (4), two of which were males. Minimum infection rates of 3.0 and 0.8 were observed for female Ae. aegypti and Cx. quinquefasciatus, respectively. Between 25 and 31.3% of exposed mosquitoes became infected with CHIKV 7, 14 and 21 days post-exposure. For the experimentally infected Cx. quinquefasciatus mosquitoes, between 13 and 40% had the virus disseminated, with 100% transmission being observed among those with disseminated infection. Conclusions These results demonstrated high risk of chikungunya transmission for residents in the sampled areas of Mombasa. Transmission data confirmed the probable role played by Cx. quinquefasciatus in the outbreak while the role of Ae. vittatus in the transmission of chikungunya virus remains unknown. Graphical Abstract

Chikungunya virus (family Togavirdae and genus Alphavirus) is an emerging and reemerging virus of public health importance both regionally and globally. In Kenya, about 50–60% of the suspected meas...

On the last week of May of 2018, a community-based syndromic surveillance system detected mass abortions and deaths of young livestock in northeastern Kenya. Two weeks later, Rift Valley fever (RVF) was confirmed in humans presenting with febrile illness and hemorrhagic syndrome in the same region. A joint animal and human response team carried out an investigation to characterize the outbreak and identify drivers of disease transmission. Here, we describe the outbreak investigation and findings. A total of 106 human cases were identified in the months of May and June 2018: 92% (98) and 8% (8) of these cases occurring in the northern and western regions of Kenya, respectively. Seventy-six (72%) were probable cases, and 30 (28%) were laboratory confirmed by ELISA and/or PCR. Among the confirmed cases, the median age was 27.5 years (interquartile range = 20), and 60% (18) were males. Overall, the case fatality rate was 7% (n = 8). The majority of the confirmed cases, 19 (63%), reported contact with livestock during slaughter and consumption of meat from sick animals. All confirmed cases had fever, 40% (12) presented with hemorrhagic syndrome, and 23% (7) presented with jaundice. Forty-three livestock herds with at least one suspect and/or confirmed animal case were identified. Death of young animals was reported in 93% (40) and abortions in 84% (36) of livestock herds. The outbreak is indicative of the emergence potential of RVF in traditionally high- and low-risk areas and the risk posed by zoonosis to livestock keepers.

In May 2016, the Kenyan Ministry of Health (KMoH) reported an outbreak of chikungunya virus (CHIKV) in Mandera County on the border with Somalia. During this time in Somalia, outbreaks of CHIKV were occurring in the neighboring Bula Hawa region, originating from Mogadishu. In Mandera town, 1,792 cases were detected, and an estimated 50% of the health work force was affected by this virus. A cross-border joint response was coordinated between Kenya and Somalia to control the outbreak.1 This was the first reported outbreak of CHIKV in Kenya since 2004. The previous large CHIKV outbreak in Kenya occurred in Lamu Island in 2004, with an estimated 75% of the population infected.2 The disease also spread to the coastal city of Mombasa by the end of 2004, and further to the Comoros and La Reunion islands, causing large outbreaks in 2005–2006. On La Reunion island, unusual clinical complications were reported in association with CHIKV infection, and viral isolate sequences revealed the presence of an alanine-to-valine mutation in the E1 glycoprotein at position 226 (E1:A226V).3 This specific mutation was shown to confer significant increase in CHIKV infectivity for the Aedes albopictus vector, which was also the dominant mosquito species suspected to be responsible for the transmission of CHIKV on the island of La Reunion.4,5 Since then, the E1:A226V mutation has been observed in many of the genomes in the CHIKV lineage, spreading in the East, Central, and South African region (ECSA lineage), and has been shown to have emerged through convergent evolution in at least four different occasions.6 The remarkable emergence and spread of CHIKV adaptation to the Ae. albopictus vector prompted additional studies on the genetic plasticity of this virus, looking for additional biomarkers associated with virus transmission capacity, fitness, and pathogenicity.6–8 Mutations with the ability to enhance infection in this vector are of increased importance, as Ae. albopictus is rapidly expanding throughout the world.9 The Ae. albopictus mosquito is believed to have originated in Asia and is today most commonly found in east Asia. Aedes albopictus is also common in some parts of South and Southeast Asia, India, and Africa, and it has shown increased spread to regions with lower temperatures, such as southern Europe, southern Brazil, northern China, and the northern United States.9 In Europe, this vector has been associated with autochthonous transmission of CHIKV.10 Although some of the more recent CHIKV outbreaks have been transmitted by Ae. albopictus, most of the CHIKV transmissions in the world are associated with Aedes aegypti. Aedes aegypti is a container-breeding, domesticated mosquito mainly found in urban areas and feeding largely on humans during early and late daytime hours. Aedes aegypti originated from the ancestral zoophilic Ae. aegypti formosus native to Africa. Aedes aegypti now is most common in tropical and subtropical regions, such as Africa, India, Southeast Asia, and Australia.9 Recently, two mutations, E1:K211E and E2:V264A, have been reported in the CHIKV to be associated with increased fitness to Ae. aegypti vectors.11 These two mutations, in the background of the wild-type E1:226A, are believed to increase virus infectivity, dissemination, and transmission in Ae. aegypti, with no impact on virus fitness for the Ae. albopictus vector.6,11 E1:K211E was first observed in genomes sampled in 2006 from the Kerala and Puducherry regions, India, and simultaneous presence of both mutations was first observed in 2009–2010 in Tamil Nadu and Andhra Pradesh, India.12,13 In Kenya, the predominant CHIKV vector is Ae. aegypti, and vector competence studies using local vector populations have shown it is capable of transmitting the virus in this region.14 Given the recent large outbreak of CHIKV in the rural setting of Mandera County, Kenya, we analyzed CHIKV genomes sequenced from this outbreak for the presence of adaptive mutations associated with both Ae. albopictus and Ae. aegypti. Along with estimating origins and the time of emergence of a variant that carried two of these previously reported mutations, we also estimated time and origins of the Mandera CHIKV outbreak. Our results indicate the spread of a CHIKV that carries mutations previously associated with increased fitness for Ae. aegypti in Kenya. We also show that this variant is now connected with new large outbreaks in other regions of the world.

Dengue fever (DF) is an arboviral disease caused by dengue virus serotypes 1-4 (DENV 1-4). Globally, DF incidence and disease burden have increased in the recent past. Initially implicated in a 1982 outbreak, DENV-2 recently reemerged in Kenya causing outbreaks between 2011 and 2014 and more recently 2017–8. The origin and the evolutionary patterns that may explain the epidemiological expansion and increasing impact of DENV-2 in Kenya remain poorly understood. Using whole-genome sequencing, samples collected during the 2011–4 and 2017–8 dengue outbreaks were analyzed. Additional DENV-2 genomes were downloaded and pooled together with the fourteen genomes generated in this study. Bioinformatic methods were used to analyze phylogenetic relationships and evolutionary patterns of DENV-2 causing outbreaks in Kenya. The findings from this study have shown the first evidence of circulation of two different Cosmopolitan genotype lineages of DENV-2; Cosmopolitan-I (C-I) and Cosmopolitan-II (C-II), in Kenya. Our results put the origin location of C-I lineage in India in 2011, and C-II lineage in Burkina Faso between 1979 and 2013. C-I lineage was the most isolated during recent outbreaks, thus showing the contribution of this newly emerged strain to the increased DENV epidemics in the region. Our findings, backed by evidence of recent local epidemics that have been associated with C-I in Kenya and C-II in Burkina Faso, add to the growing evidence of expanding circulation and the impact of multiple strains of DENV in the region as well as globally. Thus, continued surveillance efforts on DENV activity and its evolutionary trends in the region, would contribute toward effective control and the current vaccine development efforts.

The 2016 Olympic Games happened at the time of heightened fears of Zika virus (ZIKV) that was causing microcephaly in newborns in Brazil. To avert or track introduction of ZIKV in Kenya, the Ministry of Health developed a public health response that involved screening of the Kenyan contingent before and after traveling to Brazil. Of the 92 team members that were screened, all but one tested negative for ZIKV IgM and IgG. The sero-positive individual had high IgM serum titers before and after travel to Brazil. When tested for potential antibody cross-reactivity to other flaviviruses that have been reported in Kenya, the sample showed high IgM cross-reactivity to West Nile, Tick-Borne Encephalitis and Yellow Fever Virus. Our data support the low risk predictions of acquiring ZIKV that were made before the Games and will help inform risk assessments for personnel traveling to endemic regions under similar circumstances in the future.

In 2016, a chikungunya virus (CHIKV) outbreak was reported in Mandera, Kenya. This was the first major CHIKV outbreak in the country since the global reemergence of this virus in Kenya in 2004. We collected samples and sequenced viral genomes from this outbreak. All Kenyan genomes contained two mutations, E1:K211E and E2:V264A, recently reported to have an association with increased infectivity, dissemination, and transmission in the

Between late 2017 and mid-2018, a chikungunya fever outbreak occurred in Mombasa, Kenya that followed an earlier outbreak in mid-2016 in Mandera County on the border with Somalia. Using targeted Next Generation Sequencing, we obtained genomes from clinical samples collected during the 2017/2018 Mombasa outbreak. We compared data from the 2016 Mandera outbreak with the 2017/2018 Mombasa outbreak, and found that both had the Aedes aegypti adapting mutations, E1:K211E and E2:V264A. Further to the above two mutations, 11 of 15 CHIKV genomes from the Mombasa outbreak showed a novel triple mutation signature of E1:V80A, E1:T82I and E1:V84D. These novel mutations are estimated to have arisen in Mombasa by mid-2017 (2017.58, 95% HPD: 2017.23, 2017.84). The MRCA for the Mombasa outbreak genomes is estimated to have been present in early 2017 (2017.22, 95% HPD: 2016.68, 2017.63). Interestingly some of the earliest genomes from the Mombasa outbreak lacked the E1:V80A, E1:T82I and E1:V84D substitutions. Previous laboratory experiments have indicated that a substitution at position E1:80 in the CHIKV genome may lead to increased CHIKV transmissibility by Ae. albopictus. Genbank investigation of all available CHIKV genomes revealed that E1:V80A was not present; therefore, our data constitutes the first report of the E1:V80A mutation occurring in nature. To date, chikungunya outbreaks in the Northern and Western Hemispheres have occurred in Ae. aegypti inhabited tropical regions. Notwithstanding, it has been suggested that an Ae. albopictus adaptable ECSA or IOL strain could easily be introduced in these regions leading to a new wave of outbreaks. Our data on the recent Mombasa CHIKV outbreak has shown that a potential Ae. albopictus adapting mutation may be evolving within the East African region. It is even more worrisome that there exists potential for emergence of a CHIKV strain more adapted to efficient transmission by both Ae. albopictus and Ae.aegypti simultaneously. In view of the present data and history of chikungunya outbreaks, pandemic potential for such a strain is now a likely possibility in the future. Thus, continued surveillance of chikungunya backed by molecular epidemiologic capacity should be sustained to understand the evolving public health threat and inform prevention and control measures including the ongoing vaccine development efforts.

BackgroundIn 2016, a chikungunya virus (CHIKV) outbreak was reported in Mandera, Kenya. This was the first major CHIKV outbreak in the country since the global re-emergence of this virus, which arose as an initial outbreak in Kenya in 2004. Therefore, we collected samples and sequenced viral genomes from the 2016 Mandera outbreak.Methodology/Principal FindingsAll Kenyan genomes contained two mutations, E1:K211E and E2:V264A, recently reported to have an association with increased infectivity, dissemination and transmission in the Aedes aegypti (Ae. aegypti) vector. Phylogeographic inference of temporal and spatial virus relationships using Bayesian approaches showed that this Ae. aegypti adapted strain emerged within the East, Central, and South African (ECSA) lineage of CHIKV between 2005 and 2008, most probably in India. It was also in India where the first large outbreak caused by this strain appeared, in New Delhi, 2010. More importantly, our results also showed that this strain is no longer contained to India, and that it has more recently caused several major outbreaks of CHIKV, including the 2016 outbreaks in India, Pakistan and Kenya, and the 2017 outbreak in Bangladesh. In addition to its capability to cause large outbreaks in different regions of the world, this CHIKV strain has the capacity to replace less adapted wild type strains in Ae. aegypti-rich regions. Indeed, all the latest full CHIKV genomes of the ECSA Indian Ocean Lineage (IOL), from the regions of high Ae. aegypti prevalence, carry these two mutations, including samples collected in Japan, Australia, and China.Conclusions/SignificanceOur results point to the importance of continued genomic-based surveillance of this strain’s global spread, and they prompt urgent vector competence studies in Asian and African countries, in order to assess the level of vector receptiveness, virus transmission, and the impact this might have on this strain’s ability to cause major outbreaks.Author summaryChikungunya virus (CHIKV) causes a debilitating infection with high fever, intense muscle and bone pain, rash, nausea, vomiting and headaches, and persistent and/or recurrent joint pains for months or years after contracting the virus. CHIKV is spread by two mosquito vectors, Aedes albopictus and Aedes aegypti, with increased presence around the globe. In this study, we report global spread of a CHIKV strain that carries two mutations that have been suggested to increase this virus’ ability to infect the Aedes aegypti mosquito, as well as to increase CHIKV’s ability to be transmitted by this vector. We show that this strain appeared sometime between 2005 and 2008, most probably in India, and has now spread to Africa, Asia, and Australia. We show that this strain is capable of driving large outbreaks of CHIKV in the human population, causing recent major outbreaks in Kenya, Pakistan, India and Bangladesh. Thus, our results stress the importance of monitoring this strain’s global spread, as well as the need of improved vector control strategies in the areas of Aedes aegypti prevalence.

Chikungunya is a reemerging vector borne pathogen associated with severe morbidity in affected populations. Lamu, along the Kenyan coast was affected by a major chikungunya outbreak in 2004. Twelve years later, we report on entomologic investigations and laboratory confirmed chikungunya cases in northeastern Kenya. Patient blood samples were received at the Kenya Medical Research Institute (KEMRI) viral hemorrhagic fever laboratory and the immunoglobulin M enzyme linked immunosorbent assay (IgM ELISA) was used to test for the presence of IgM antibodies against chikungunya and dengue. Reverse transcription polymerase chain reaction (RT-PCR) utilizing flavivirus, alphavirus and chikungunya specific primers were used to detect acute infections and representative PCR positive samples sequenced to confirm the circulating strain. Immature mosquitoes were collected from water-holding containers indoors and outdoors in the affected areas in northeastern Kenya. A total of 189 human samples were tested; 126 from Kenya and 63 from Somalia. 52.9% (100/189) tested positive for Chikungunya virus (CHIKV) by either IgM ELISA or RT-PCR. Sequence analysis of selected samples revealed that the virus was closely related to that from China (2010). 29% (55/189) of the samples, almost all from northeastern Kenya or with a history of travel to northern Kenya, tested positive for dengue IgM antibodies. Entomologic risk assessment revealed high house, container and Breteau indices of, 14.5, 41.9 and 17.1% respectively. Underground water storage tanks were the most abundant, 30.1%, of which 77.4% were infested with Aedes aegypti mosquitoes. These findings confirm the presence of active chikungunya infections in the northeastern parts of Kenya. The detection of dengue IgM antibodies concurrently with chikungunya virus circulation emphasizes on the need for improved surveillance systems and diagnostic algorithms with the capacity to capture multiple causes of arbovirus infections as these two viruses share common vectors and eco-systems. In addition sustained entomological surveillance and vector control programs targeting most productive containers are needed to monitor changes in vector densities, for early detection of the viruses and initiate vector control efforts to prevent possible outbreaks.

The first laboratory confirmed dengue outbreak in Kenya was reported in coastal towns of Malindi and Kilifi in 1982. Since then, no other outbreak had been confirmed in Kenya. Dengue outbreak was confirmed among African Mission soldiers in Somalia (AMISOM) between May to October 2011. From September 2011, an upsurge of febrile patients who were negative for malaria on microscopy were reported in several health facilities in Mandera town, an adjacent area to Somalia in northern Kenya. We investigated a suspected dengue outbreak in Mandera town from 26th September 2011 to 5th October 2011. A suspected case was defined as acute onset of fever with two or more of the following: headache, arthralgia, myalgia, rash and hemorrhages and negative malaria microscopy results in a person presenting to a health facility in Mandera town from 1st August to 2nd October 2011. We prospectively identified new cases meeting the suspect case definition from 2nd October to 5th October 2011 and we collected blood samples from consenting patients. Blood was collected into plastic vacutainers and stored in dry shipper at -80oc to laboratory for dengue virus testing using real time reverse transcriptase polymerase chain reaction (rRT-PCR). We administered a standardized form to obtain clinical information. We calculated descriptive statistics to describe the outbreak. A total of 1,332 patients had been line listed by the district surveillance team, of which 381 (29%) met our suspect case definition of dengue. Cases peaked between 10th September and 1st October 2011 and thereafter declined. We prospectively identified 33 cases meeting the suspect case definition, of whom 30 (91%) were positive for dengue virus serotype 3 by PCR. Among the 30 laboratory confirmed patients, 20 (67%) required hospitalization (Median hospitalization period, two days with a range: 1-4 days)). And of these, 26 (86%) patients reported aches and pain, 16 (53%) reported vomiting, and four (13%) gingival bleeding. Twenty-three (77%) received anti-malarial therapy. Among laboratory-confirmed dengue patients, seven (23%) had malaria co-infection. This was the second confirmed Dengue outbreak in Kenya, and highlighted the need for improved surveillance to better define disease burden and continuous education to medical personnel to improve detection and clinical management. We also recommended enhanced community education for disease prevention.

Background Dengue fever, a mosquito-borne disease, is associated with illness of varying severity in countries in the tropics and sub tropics. Dengue cases continue to be detected more frequently and its geographic range continues to expand. We report the largest documented laboratory confirmed circulation of dengue virus in parts of Kenya since 1982. Methods From September 2011 to December 2014, 868 samples from febrile patients were received from hospitals in Nairobi, northern and coastal Kenya. The immunoglobulin M enzyme linked immunosorbent assay (IgM ELISA) was used to test for the presence of IgM antibodies against dengue, yellow fever, West Nile and Zika. Reverse transcription polymerase chain reaction (RT-PCR) utilizing flavivirus family, yellow fever, West Nile, consensus and sero type dengue primers were used to detect acute arbovirus infections and determine the infecting serotypes. Representative samples of PCR positive samples for each of the three dengue serotypes detected were sequenced to confirm circulation of the various dengue serotypes. Results Forty percent (345/868) of the samples tested positive for dengue by either IgM ELISA (14.6 %) or by RT-PCR (25.1 %). Three dengue serotypes 1–3 (DENV1-3) were detected by serotype specific RT-PCR and sequencing with their numbers varying from year to year and by region. The overall predominant serotype detected from 2011–2014 was DENV1 accounting for 44 % (96/218) of all the serotypes detected, followed by DENV2 accounting for 38.5 % (84/218) and then DENV3 which accounted for 17.4 % (38/218). Yellow fever, West Nile and Zika was not detected in any of the samples tested. Conclusion From 2011–2014 serotypes 1, 2 and 3 were detected in the Northern and Coastal parts of Kenya. This confirmed the occurrence of cases and active circulation of dengue in parts of Kenya. These results have documented three circulating serotypes and highlight the need for the establishment of active dengue surveillance to continuously detect cases, circulating serotypes, and determine dengue fever disease burden in the country and region.

Background Minimal influenza surveillance has been carried out in sub-Saharan Africa to provide information on circulating influenza subtypes for the purpose of vaccine production and monitoring trends in virus spread and mutations. Objective The aim of this study was to investigate a surveillance program in Kenya to isolate and characterize influenza viruses. Results In the 2006–2007 influenza season, nine influenza A viruses were isolated. All were of H3N2 subtype with key amino acid (aa) changes indicating that they were more closely related to recent World Health Organization recommended vaccine strains than to older vaccine strains, and mirroring the evolution of circulating influenza A globally. Hemagglutination inhibition data showed that the 2006 Kenya isolates had titers identical to the 2005–2006 H3N2 vaccine strain but two- to threefold lower titers to the 2006–2007 vaccine strain, suggesting that the isolates were antigenic variants of the 2006–2007 vaccine strains. Analysis of aa substitutions of hemagglutinin-1 (HA1) protein of the 2006 Kenyan viruses revealed unique genetic variations with several aa substitutions located at immunodominant epitopes of the HA1 protein. These mutations included the V112I change at site E, the K 173 E substitution at site D and N 278 K change at site C, mutations that may result in conformational change on the HA molecule to expose novel epitopes thus abrogating binding of pre-existing antibodies at these sites. Conclusion Characterization of these important genetic variations in influenza A viruses isolated from Kenya highlights the importance of continuing surveillance and characterization of emerging influenza drift variants in sub-Saharan Africa.

An outbreak of Chikungunya virus (CHIKV) disease associated with high fever and severe protracted arthralgias was detected in Lamu, Kenya, peaking in July 2004. At least 1,300 cases were documented. We conducted a seroprevalence study to define the magnitude of transmission on Lamu Island. We conducted a systematic cross-sectional survey. We administered questionnaires and tested 288 sera from Lamu residents for IgM and IgG antibodies to CHIKV. Chikungunya virus infection (seropositivity) was defined as a person with IgG and/or IgM antibodies to CHIKV. IgM antibodies to CHIKV were detected in 18% (53/288) and IgG antibodies in 72% (206/288); IgM and/or IgG antibodies were present in 75% (215/288). The seroprevalence findings suggested that the outbreak was widespread, affecting 75% of the Lamu population; extrapolating the findings to the entire population, 13,500 (95% CI, 12,458-14328) were affected. Vector control strategies are needed to control the spread of this mosquito-borne infection.

Between the months of April and June 2004, an Ebola hemorrhagic fever (EHF) outbreak was reported in Yambio county, southern Sudan. Blood samples were collected from a total of 36 patients with suspected EHF and were tested by enzyme-linked immunosorbent assay (ELISA) for immunoglobulin G and M antibodies, antigen ELISA, and reverse-transcription polymerase chain reaction (PCR) of a segment of the Ebolavirus (EBOV) polymerase gene. A total of 13 patients were confirmed to be infected with EBOV. In addition, 4 fatal cases were classified as probable cases, because no samples were collected. Another 12 patients were confirmed to have acute measles infection during the same period that EBOV was circulating. Genetic analysis of PCR-positive samples indicated that the virus was similar to but distinct from Sudan EBOV Maleo 1979. In response, case management, social mobilization, and follow-up of contacts were set up as means of surveillance. The outbreak was declared to be over on 7 August 2004.

Numerous tickborne viruses, including Dhori virus and foot-and-mouth disease virus, were isolated., To identify tickborne viruses circulating in Kenya and the surrounding region, we conducted surveillance at abattoirs in Nairobi, Kenya. Species of ticks collected included Rhipicephalus pulchellus (56%), Amblyomma gemma (14%), R. appendiculatus (8%), A. variegatum (6%), and others. A total of 56 virus isolates were obtained, 26 from A. gemma, 17 from R. pulchellus, 6 from A. variegatum, and 7 from other species. Virus isolates included Dugbe virus (DUGV), an unknown virus related to DUGV, Thogoto, Bhanja, Kadam, Dhori, Barur, and foot-and-mouth disease (FMDV) viruses. This is the first report of Dhori virus isolation in East Africa and the first known isolation of FMDV associated with tick collection. Our results demonstrate the potential for tickborne dissemination of endemic and emergent viruses and the relevance of A. gemma in the maintenance of tickborne viruses in this region.

Highly pathogenic avian influenza virus A/H5N1 has been reported in 11 African countries. Migratory waterbirds have the potential of introducing A/H5N1 into east Africa through the Rift Valley of Kenya. We present the results of a wild bird surveillance system for A/H5N1 and other avian influenza viruses based on avian fecal sampling in Kenya. We collected 2630 fecal samples in 2008. Viral RNA was extracted from pools of 3-5 fecal samples and analyzed for presence of avian influenza virus RNA by real-time RT-PCR. Twelve (2.3%) of the 516 sample pools were positive for avian influenza virus RNA, 2 of which were subtyped as H4N6 viruses. This is the first report of avian influenza virus in wild birds in Kenya. This study demonstrates the success of this approach in detecting avian influenza virus in wild birds and represents an efficient surveillance system for avian influenza virus in regions with limited resources.

An outbreak of Chikungunya virus (CHIKV) disease associated with high fever and severe protracted arthralgias was detected in Lamu, Kenya, peaking in July 2004. At least 1,300 cases were documented. We conducted a seroprevalence study to define the magnitude of transmission on Lamu Island. We conducted a systematic cross-sectional survey. We administered questionnaires and tested 288 sera from Lamu residents for IgM and IgG antibodies to CHIKV. Chikungunya virus infection (seropositivity) was defined as a person with IgG and/or IgM antibodies to CHIKV. IgM antibodies to CHIKV were detected in 18% (53/288) and IgG antibodies in 72% (206/288); IgM and/or IgG antibodies were present in 75% (215/288). The seroprevalence findings suggested that the outbreak was widespread, affecting 75% of the Lamu population; extrapolating the findings to the entire population, 13,500 (95% CI, 12,458-14328) were affected. Vector control strategies are needed to control the spread of this mosquito-borne infection.

An outbreak of Chikungunya virus (CHIKV) illness associated with high fever combined with prolonged and severe arthralgias occurred on Grande Comore Island from January through May 2005; 5,202 cases were reported. A seroprevalence study was conducted to define the extent of transmission on the island. We conducted a cross-sectional survey using a multistage sampling technique. A total of 481 households were sampled. In each household, one resident was selected randomly for interview and blood collection. We administered questionnaires and tested 331 sera for CHIKV-specific IgM and IgG antibodies by capture enzyme-linked immunosorbent assay. Infection with CHIKV infection (seropositivity) was defined as presence of IgG and/or IgM antibodies to CHIKV. A total of 331 (69%) of 481 survey participants consented to blood collection. Antibodies to CHIKV were detected in 63% of sera; IgM antibodies were found in 60% of specimens and IgG antibodies were detected in 27% of specimens. Extrapolation of the findings to the entire Grande Comore population suggested that nearly 215,000 people were infected with CHIKV during the outbreak. A total of 79% of the seropositive persons were hospitalized or stayed at home in bed for a mean of 6 days (range = 1-30 days); 52% missed work or school for a mean of 7 days (range = 1-40 days). The findings suggest that CHIKV was broadly transmitted during the outbreak with a high attack rate. Although not fatal during this outbreak, CHIKV infection caused significant morbidity and decreased economic productivity.

Background Malaria is one of the most serious health problems in Kenya. In 2004, the Kenya Medical Research Institute and the US Army Medical Research Unit – Kenya surveyed adults in Samburu, Malindi, and Busia districts to determine socioeconomic risk factors for infection. Methods Sociodemographic, health, and antimalarial data were collected along with blood for malaria testing. A smear was considered negative only if no Plasmodium falciparum parasites were observed in 100 high-powered fields. Univariate analysis was performed with Pearson's Chi-square test and univariate logistic regression. A multivariate logistic regression model was then created which included only variables found to be at least marginally significant in univariate analysis. Results A total of 1,141 subjects were recruited: 238 from Samburu, 442 from Malindi, and 461 from Busia. Smear positivities for P. falciparum were 1.7% in Samburu, 7.2% in Malindi and 22.3% in Busia. Interdistrict differences were statistically significant (p < 0.001) in univariate analysis and in a multivariate logistic regression model which included district, literacy, occupation, and recent illness as independent variables. In the model, literacy and recent diarrhoeal illness were positively and at least marginally significantly associated with parasitaemia (p = 0.023 and p = 0.067, respectively). Neither age, sex, occupation, history of malaria in the previous three months, nor use of antimalarials in the previous four weeks were significantly associated with parasitaemia. Conclusion While district of residence was the variable most highly predictive for parasitaemia among Kenyan adults surveyed, both a recent history of diarrhoeal illness and literacy were at least marginally statistically significant predictors.

In May 2003, the World Health Organization received reports about a possible outbreak of a hemorrhagic disease of unknown cause in the Imatong Mountains of southern Sudan. Laboratory investigations were conducted on 28 serum samples collected from patients in the Imatong region. Serum samples from 13 patients were positive for immunoglobulin (Ig) M antibody to flavivirus, and serum samples from 5 patients were positive by reverse transcription–polymerase chain reaction with both the genus Flavivirus reactive primers and yellow fever virus–specific primers. Nucleotide sequencing of the amplicons obtained with the genus Flavivirus oligonucleotide primers confirmed yellow fever virus as the etiologic agent. Isolation attempts in newborn mice and Vero cells from the samples yielded virus isolates from five patients. Rapid and accurate laboratory diagnosis enabled an interagency emergency task force to initiate a targeted vaccination campaign to control the outbreak.

Cell fusing agent virus (CFAV) is an RNA insect virus that was isolated from a line of Aedes aegypti mosquito cells and has been assigned to the family Flaviviridae, genus Flavivirus. We report here the first isolation of a CFA-like virus from field-collected mosquitoes. Mosquito larvae and pupae were sampled from flooded dambos in Central Province, Kenya during the short rain season of 1999. Specimens were reared to adults, identified and pooled by species and were tested for the presence of virus. Two virus isolates were obtained from two pools of Aedes macintoshi mosquitoes. The virus isolates replicated only in invertebrate cells in culture and not in vertebrate cells or in mice. The virus isolates did not antigenically cross-react with known arboviruses but were identified to family by reverse-transcriptase polymerase chain reaction (RT-PCR) performed using primers specific to alphaviruses, bunyaviruses and flaviviruses; only the flavivirus-specific primers produced a DNA fragment of the expected size. Nucleic acid sequencing of this fragment showed the two isolates to be nearly identical. Comparison of sequences to the GenBank database using BLAST identified the virus as most closely related to CFAV. Results from cross-neutralization tests suggested that, although the BLAST search indicated homology to CFAV, the virus isolated represented a new insect flavivirus. Detailed characterization of this new virus, described in Crabtree et al. [7], further supports this finding. We propose this new flavivirus be designated Kamiti River virus (KRV). This is the first isolation of a CFA-like virus from field-collected mosquitoes and indicates the presence of this group of viruses in nature.

To the Editor: On October 21, 2000, a previously healthy 25-year-old male farmer was admitted to a mission hospital in western Kenya with an acute hemorrhagic illness. Four days before admission, the patient had rapid onset of fever, headache, nausea, vomiting, severe muscle pains, and diarrhea, which became bloody. On admission his temperature was 36.4°C, pulse was 60/minute, respiratory rate was 20/minute, and blood pressure was 90/40 mm Hg. In addition to the signs and symptoms listed above, the only other abnormal finding on admission was neck stiffness. The differential diagnoses included bacterial dysentery and meningitis. Results of a blood smear for malaria parasites and Widal test for typhoid were negative, and cerebrospinal fluid and urine examinations were normal. The patient was treated with doxycycline, cotrimoxazole, metronidazole, and intravenous fluids. On the day after admission, the patient’s vomitus became blood stained and blood was passed rectally. The patient was isolated and strict barrier nursing implemented on the suspicion of viral hemorrhagic fever (VHF). Progressive hypotension developed, resistant to resuscitation efforts with intravenous fluids and corticosteroids, and later massive bleeding from the nose, mouth, and upper and lower gastrointestinal tract occurred. The patient died on the second day of admission, 6 days after onset of illness. A serum sample was sent to the Arbovirus and Viral Hemorrhagic Fever Reference Laboratory in Nairobi for diagnostic screening. Serologic tests in Nairobi were negative for yellow fever, dengue, West Nile, Chikungunya, and Rift Valley fever (immunoglobulin [Ig] M–capture enzyme-linked immunosorbent assay) and reverse transcriptase-polymerase chain reaction (RT-PCR) tests for flaviviruses, alphaviruses, and Bunyamwera serogroup bunyaviruses were also negative. RT-PCR for Crimean-Congo hemorrhagic fever virus (C-CHFV) was positive. Tests for anti-C-CHFV–specific IgM antibody by indirect immunofluorescence were negative. Virus isolation attempts were then terminated because the cultivation of C-CHFV (the presumptive cause) requires biosafety level 4 facilities. The specimen was submitted to the Special Pathogens Unit in Johannesburg for confirmation of the result. The sample was positive by RT-PCR for C-CHFV and was IgM and IgG antibody negative. No isolation of the virus could be made from the serum sample, possibly because it was received by the Johannesburg laboratory 8 days after initial collection and following freeze-thaw conditions. The specimen was was insufficient to attempt C-CHVF antigen detection assays. Sequencing of the RT-PCR amplicon confirmed C-CHFV. C-CHFV is a tick-borne virus of the genus Nairovirus, family Bunyaviridae, and is widely distributed throughout eastern Europe and the Crimea, to the Middle East and western China, Pakistan, and Africa. Natural hosts for this virus are varied (including wild and domestic animals and birds) and may reflect the feeding preferences of the host tick (1). While C-CHFV infections are rare in humans, the virus is notorious for nosocomial outbreaks of VHF, typically following admission of an index case to a health-care facility where VHF was not suspected, with mortality rates up to 40%. Previous evidence for C-CHFV in Kenya is limited and based on serology (human and bovine) and two isolations of C-CHFV from non-human sources (1,2). This report represents the first documented case of acute human C-CHFV infection in Kenya. The hospital concerned belongs to a VHF surveillance network serving to increase awareness and preparedness within Kenyan health-care facilities. In this case suspicion of VHF was raised, and the patient was immediately isolated, noninvasive procedures were instigated, and barrier nursing was implemented to prevent nosocomial transmission. No family or hospital staff member who had close contact with the patient became ill. Although VHFs are rare, this report stresses the need for health facilities in Kenya and East/Central Africa to include VHFs in their differential diagnosis of unexplained fever with hemorrhagic tendencies, as well as the utility of the surveillance network. The causative agents of Ebola hemorrhagic fever, Marburg hemorrhagic fever, C-CHFV, Rift Valley fever, and yellow fever are all endemic in East and Central Africa, and sporadic cases, as well as outbreaks, are likely to continue to occur in this region (3–5).

A cornerstone of effective disease surveillance programs comprises the early identification of infectious threats and the subsequent rapid response to prevent further spread. Effectively identifying, tracking and responding to these threats is often difficult and requires international cooperation due to the rapidity with which diseases cross national borders and spread throughout the global community as a result of travel and migration by humans and animals. From Oct.1, 2008 to Sept. 30, 2009, the United States Department of Defense’s (DoD) Armed Forces Health Surveillance Center Global Emerging Infections Surveillance and Response System (AFHSC-GEIS) identified 76 outbreaks in 53 countries. Emerging infectious disease outbreaks were identified by the global network and included a wide spectrum of support activities in collaboration with host country partners, several of which were in direct support of the World Health Organization’s (WHO) International Health Regulations (IHR) (2005). The network also supported military forces around the world affected by the novel influenza A/H1N1 pandemic of 2009. With IHR (2005) as the guiding framework for action, the AFHSC-GEIS network of international partners and overseas research laboratories continues to develop into a far-reaching system for identifying, analyzing and responding to emerging disease threats.

Background Arthorpod-borne viruses (arboviruses) cause wide-spread morbidity in sub-Saharan Africa, but little research has documented the burden and distribution of these pathogens. Methods Using a population-based, cross-sectional study design, we administered a detailed questionnaire and used ELISA to test the blood of 1,141 healthy Kenyan adults from three districts for the presence of anti-viral Immunoglobulin G (IgG) antibodies to the following viruses: dengue (DENV), West Nile (WNV), yellow fever (YFV), Chikungunya (CHIKV), and Rift Valley fever (RVFV). Results Of these, 14.4% were positive for DENV, 9.5% were WNV positive, 9.2% were YFV positive, 34.0% were positive for CHIKV and 0.7% were RVFV positive. In total, 46.6% had antibodies to at least one of these arboviruses. Conclusions For all arboviruses, district of residence was strongly associated with seropositivity. Seroprevalence to YFV, DENV and WNV increased with age, while there was no correlation between age and seropositivity for CHIKV, suggesting that much of the seropositivity to CHIKV is due to sporadic epidemics. Paradoxically, literacy was associated with increased seropositivity of CHIKV and DENV.