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Emerging Infectious Diseases | 2004

Yellow Fever Outbreak, Southern Sudan, 2003

Clayton O. Onyango; Antoinette A. Grobbelaar; Georgina V.F. Gibson; Rosemary Sang; Abdourahmane Sow; Robert Swanepoel; Felicity J. Burt

In May 2003, an outbreak of fatal hemorrhagic fever, caused by yellow fever virus, occurred in southern Sudan. Phylogenetic analysis showed that the virus belonged to the East African genotype, which supports the contention that yellow fever is endemic in East Africa with the potential to cause large outbreaks in humans.


Emerging Infectious Diseases | 2004

Yellow Fever Outbreak, Imatong, Southern Sudan

Clayton O. Onyango; Victor Ofula; Rosemary Sang; Samson L. Konongoi; Abdourahmane Sow; Kevin M. De Cock; Peter M. Tukei; Fredrick A. Okoth; Robert Swanepoel; Felicity J. Burt; Norman C. Waters; Rodney L. Coldren

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 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.


Emerging Infectious Diseases | 2014

Rift Valley Fever Outbreak, Southern Mauritania, 2012

Abdourahmane Sow; Ousmane Faye; Yamar Ba; Hampathé Ba; Diawo Diallo; Oumar Faye; Cheikh Loucoubar; Mohamed Boushab; Yahya Barry; Mawlouth Diallo; Amadou A. Sall

Rift Valley Fever Outbreak, Mauritania, 2012


Journal of Clinical Microbiology | 2015

Detection of chikungunya virus antigen by a novel rapid immunochromatographic test.

Tamaki Okabayashi; Tadahiro Sasaki; Promsin Masrinoul; Nantarat Chantawat; Sutee Yoksan; Narong Nitatpattana; Sarunyou Chusri; Ronald Enrique Morales Vargas; Marc Grandadam; Paul T. Brey; Soegeng Soegijanto; Kris Cahyo Mulyantno; Siti Churrotin; Tomohiro Kotaki; Oumar Faye; Ousmane Faye; Abdourahmane Sow; Amadou A. Sall; Orapim Puiprom; Panjaporn Chaichana; Takeshi Kurosu; Seiji Kato; Mieko Kosaka; Pongrama Ramasoota; Kazuyoshi Ikuta

ABSTRACT Chikungunya fever is a mosquito-borne disease of key public health importance in tropical and subtropical countries. Although severe joint pain is the most distinguishing feature of chikungunya fever, diagnosis remains difficult because the symptoms of chikungunya fever are shared by many pathogens, including dengue fever. The present study aimed to develop a new immunochromatographic diagnosis test for the detection of chikungunya virus antigen in serum. Mice were immunized with isolates from patients with Thai chikungunya fever, East/Central/South African genotype, to produce mouse monoclonal antibodies against chikungunya virus. Using these monoclonal antibodies, a new diagnostic test was developed and evaluated for the detection of chikungunya virus. The newly developed diagnostic test reacted with not only the East/Central/South African genotype but also with the Asian and West African genotypes of chikungunya virus. Testing of sera from patients suspected to have chikungunya fever in Thailand (n = 50), Laos (n = 54), Indonesia (n = 2), and Senegal (n = 6) revealed sensitivity, specificity, and real-time PCR (RT-PCR) agreement values of 89.4%, 94.4%, and 91.1%, respectively. In our study using serial samples, a new diagnostic test showed high agreement with the RT-PCR within the first 5 days after onset. A rapid diagnostic test was developed using mouse monoclonal antibodies that react with chikungunya virus envelope proteins. The diagnostic accuracy of our test is clinically acceptable for chikungunya fever in the acute phase.


One Health | 2017

Emergence of Wesselsbron virus among black rat and humans in Eastern Senegal in 2013

Moussa M. Diagne; Martin Faye; Oumar Faye; Abdourahmane Sow; Fanny Balique; Mbacké Sembène; Laurent Granjon; Pascal Handschumacher; Ousmane Faye; Mawlouth Diallo; Amadou A. Sall

Wesselsbron disease is a neglected mosquito transmitted Flavivirus infection that causes abortions and has teratogenic effects on sheep and cattle in Africa. Human can also be infected. The detection of human or animal cases is complicated by the non-specific symptoms close to Rift Valley Fever (RVF) in domestic livestock species or Dengue like syndrome in humans. Then, these detections are usually made during RVF investigations in sheep. These domestic animals should take a role in the life cycle of the virus but some evidences of Wesselsbron virus (WSLV) presence in wild animals suggest that the latter may be involved in the virus maintenance in nature. However, the reservoir status of wild vertebrate in general and rodents particularly for WSLV is only based on an isolation from a Cape short-eared gerbil in southern Africa. Most of WSLV isolations are from southern parts of Africa even if it has been found in western and central Africa or Madagascar. In Senegal, there are serological evidences of WSLV circulation in human since the 1970s and some isolations, the last one of which dates back in 1992. Despite the detection of the virus on mosquitoes until the 2000s in different parts of the country, no new human case has been noted. In this paper, we report the WSLV re-emergence in eastern Senegal in 2013 with 2 human cases and its first isolation from a black rat Rattus rattus. Sequencing analyses show the circulation of the same strain between these humans and the commensal rodent. The putative impact on WSLV transmission to human populations could be more important if the reservoir status of the black rat is confirmed. Focused survey in human populations, specific entomological and mammalogical investigations would permit a better understanding of the life cycle of the virus and its impact on public health.


Emerging Infectious Diseases | 2014

Rift Valley fever in Kedougou, southeastern Senegal, 2012.

Abdourahmane Sow; Oumar Faye; Ousmane Faye; Diawo Diallo; Bakary Djilocalisse Sadio; Scott C. Weaver; Mawlouth Diallo; Amadou A. Sall

To the Editor: Rift Valley fever (RVF) is an acute, febrile, viral disease caused by Rift Valley fever virus (RVFV), a phlebovirus of the family Bunyaviridae that is endemic to sub-Saharan Africa. RVF mortality and abortion rates among young domesticated ruminants and pregnant females are high. In humans, clinical manifestations range from mild to severe syndromes, which can include neurologic, hemorrhagic, and hepatic features and retinitis, and which sometimes result in death (1). Diagnosis of RVF is challenging for clinicians because clinical manifestations are not specific (2). Heavy rainfall and flooding create conditions for emergence of RVF vectors (Aedes and Culex spp. mosquitoes), and dispersion of this disease into new areas is linked to migration of infected livestock, wildlife, or mosquitoes. Since 1987, when the Diama dam was built, RVF outbreaks in Mauritania have been reported regularly (3). In Kedougou, southeastern Senegal, RVFV was isolated 4 times from Ae. dalzieli mosquitoes and once from a person with a mild case of RVF (4). We report results of a field investigation and laboratory findings for a human case of RVF detected by surveillance of acute febrile illnesses in Kedougou. On October 16, 2012, a 27-year-old man (school teacher) who lived and worked in Baya village in the Kedougou region of Senegal (12°27′50″N, 12°28′6″W) visited the Kedougou military health post because of high fever, chills, headache, back pain, myalgia, and arthralgia that started on October 14. He reported regular contact with domesticated animals (cows, sheep, and goats) during farming. A thick blood smear for the patient showed a positive result for malaria, and specific treatment was given. As part of surveillance for acute febrile illnesses, blood samples from the patient were tested for IgM against RVF, chikungunya, dengue, West Nile, yellow fever, Zika, and Crimean-Congo hemorrhagic fever viruses; and for viral RNA and virus (5,6). All test results for IgM against the 7 viruses were negative RVFV was isolated from newborn mice that were intracerebrally inoculated with a blood sample from the patient. Viral RNA was detected by reverse transcription PCR in serum from the patient. Phylogenetic analysis of the partial nonstructural protein gene on the small RNA segment showed that the RVFV isolate was closely related to a strain that had circulated in Mauritania in 2012 (Figure). Figure Phylogenetic tree of a 581-bp sequence of the nonstructural protein gene on the small RNA segment of Rift Valley fever viruses. Boldface indicates strain isolated in this study. Bootstrap values are indicated along branches. Scale bar indicates nucleotide ... An epidemiologic field investigation was conducted to assess the extent of RVFV circulation. During this investigation, the case-patient provided an additional blood sample. In addition, 115 contacts of the case-patient, including primary school students, friends, family members and neighbors (median age 12 years, range 6–75 years; female:male sex ratio 1.6) were also sampled and questioned to identify asymptomatic and benign cases. A total of 218 samples from patients attending the nearest health posts in Ibel and Thiokoye villages during October 2012 were also tested during surveillance of acute febrile illnesses. All 334 samples were negative for RVFV RNA and IgM and IgG against RVFV except for samples from 3 patients, including the case-patient, which were positive for RVFV-specific IgG and malaria parasites. The 2 other patients were a 32-year-old tradesman and a 20-year-old housewife sampled during surveillance of acute febrile illnesses in Kedougou and Bandafassi, which is 30 km from Baya (Technical Appendix Figure). No RVFV RNA was detected from 519 mosquito pools sampled in the Kedougou region during October 2012, although these pools included 7 species previously found associated with RVFV and which represented 26.6 % of the pools. The patient reported no travel outside Kedougou in the 2-year period before his illness. Because no evidence of recent RVFV circulation among humans and mosquitoes was found, we believe that the patient was infected by contact with an animal imported from Mauritania. This hypothesis is based on reports by farmers from neighboring villages (Baya, Ibel, Thiokoye, and Dondol) of the presence of ruminants imported from Mauritania in the market in Thiokoye village and of deaths and abortions among sheep and goats in their villages during October–November 2012. However, no animals were sampled during the investigation. There is an abundance of competent vectors for RVFV in Kedougou (4). In addition, there are massive human migrations resulting from gold mining and regular importation of animals from RVF-endemic regions of western Africa. Thus, an integrated human and animal surveillance system should be implemented or reinforced to avoid large-scale RVF outbreaks in Kedougou. Technical Appendix: Figure. Geographic distribution of Rift Valley fever cases, southeastern Senegal, 2012. Click here to view.(64K, pdf)


Nature Communications | 2018

Role of monkeys in the sylvatic cycle of chikungunya virus in Senegal

Benjamin M. Althouse; Mathilde Guerbois; Derek A. T. Cummings; Ousmane M. Diop; Ousmane Faye; Abdourahmane Faye; Diawo Diallo; Bakary Djilocalisse Sadio; Abdourahmane Sow; Oumar Faye; Amadou A. Sall; Mawlouth Diallo; Brenda R. Benefit; Evan Simons; Douglas M. Watts; Scott C. Weaver; Kathryn A. Hanley

Arboviruses spillover into humans either as a one-step jump from a reservoir host species into humans or as a two-step jump from the reservoir to an amplification host species and thence to humans. Little is known about arbovirus transmission dynamics in reservoir and amplification hosts. Here we elucidate the role of monkeys in the sylvatic, enzootic cycle of chikungunya virus (CHIKV) in the region around Kédougou, Senegal. Over 3 years, 737 monkeys were captured, aged using anthropometry and dentition, and tested for exposure to CHIKV by detection of neutralizing antibodies. Infant monkeys were positive for CHIKV even when the virus was not detected in a concurrent survey of mosquitoes and when population immunity was too high for monkeys alone to support continuous transmission. We conclude that monkeys in this region serve as amplification hosts of CHIKV. Additional efforts are needed to identify other hosts capable of supporting continuous circulation.The authors examine the role of monkey populations in the sylvatic cycle of chikungunya virus in the Kédougou region, Senegal. The authors show that monkeys are amplification hosts, as opposed to reservoir hosts for infection. These findings expand our knowledge of the transmission dynamics of chikungunya virus in this region of Senegal.


bioRxiv | 2016

Monkey in the middle: monkeys serve as amplification hosts but not reservoir hosts of sylvatic chikungunya virus

Benjamin M. Althouse; Matilde Guerbois; Derek A. T. Cummings; Ousmane M. Diop; Ousmane Faye; Abdourahmane Faye; Diawo Diallo; Bakary Djilocalisse Sadio; Abdourahmane Sow; Oumar Faye; Amadou A. Sall; Mawlouth Diallo; Brenda R. Benefit; Evan Simmons; Douglas M. Watts; Scott C. Weaver; Kathryn A. Hanley

Background Novel pathogens can emerge into humans via one-step transmission from a reservoir host, an animal species in which the pathogen is maintained, or a two-step process in which the pathogen is transmitted from the reservoir host into a different amplification host species and thence to humans. Here we use serosurveillance and mathematical modeling to discover whether monkeys serve as reservoir or amplification hosts for mosquito-borne chikungunya virus (CHIKV). CHIKV invaded the Americas in 2013, and our study provides key data for predicting whether and where CHIKV will establish enzootic transmission among animal hosts in the New World. Results Over three years we captured 219 African green monkeys, 78 patas monkeys, and 440 Guinea baboons, the three monkey species near Kédougou, Senegal. Monkey age was determined by anthropometry and dentition, and exposure of each animal to CHIKV was determined via detection of neutralizing antibodies. Age and exposure were used to estimate age-specific CHIKV seroprevalence, force of infection (FoI), and basic reproductive number (R0) in each species. CHIKV FoI were extremely high, ranging from 0.13 (95% CI, 0.07–0.22) in patas in 2012 to 1.12 (95% CI, 0.81–2.28) in African greens in 2011. R0 ranged from 1.5 (95% CI, 1.3–1.9) in patas in 2012, to 6.6 (95% CI, 5.1–10.4) in baboons in 2011. Conclusions These findings demonstrate that monkeys in this region are constantly exposed to CHIKV transmission, even when population seropositivity, and therefore immunity, was too high for monkeys themselves to support continuous CHIKV transmission. We therefore conclude that monkeys in this system serve as amplification rather than reservoir hosts of CHIKV. Considering the potential for CHIKV to spill back in to monkeys in the Americas and elsewhere, improved understanding of its sylvatic cycle is essential to understanding and perhaps controlling the spread of this virus.Athropod-borne viruses (arboviruses) pose the greatest risk of spillover into humans of any class of pathogens. Such spillover may occur as a one-step jump from a reservoir host species into humans or as a two-step jump from the reservoir to a different amplification host species and thence to humans. Despite the widespread havoc wreaked by emerging arboviruses, little is known about their transmission dynamics in reservoir and amplification hosts. Here we used serosurveillance and mathematical modeling to elucidate the role of monkeys in the sylvatic, enzootic cycle of chikungunya virus (CHIKV). Over three years, 219 African green monkeys, 78 patas monkeys, and 440 Guinea baboons were captured in the region surrounding Kedougou, Senegal. The age of each animal was determined by anthropometry and dentition, and exposure to CHIKV was determined by detection of neutralizing antibodies. We estimate age-specific CHIKV seroprevalence, force of infection (FoI), and basic reproductive number (R0) in each species. Among the different species, CHIKV FoI ranged from 0.13 to 1.12 (95% CI, 0.81-2.28) and R0 ranged from 1.5 (95% CI, 1.3-1.9) to 6.6 (95% CI, 5.1-10.4). CHIKV infection of infant monkeys was detected even when the virus was not detected in a concurrent survey of primatophilic mosquitoes and when population seropositivity, and therefore immunity, was too high for monkeys themselves to support continuous CHIKV transmission. We therefore conclude that monkeys in this region serve primarily as amplification rather than reservoir hosts of CHIKV. Additional efforts are needed to identify other vertebrate hosts capable of supporting continuous circulation.


Open Forum Infectious Diseases | 2018

Chikungunya Outbreak in Kedougou, Southeastern Senegal in 2009–2010

Abdourahmane Sow; Oumar Faye; Mawlouth Diallo; Rubing Chen; Ousmane Faye; Cheikh T. Diagne; Mathilde Guerbois; Manfred Weidmann; Youssoupha Ndiaye; Cheikh Sadibou Senghor; Abdourahmane Faye; Ousmane M. Diop; Bakary Djilocalisse Sadio; Oumar Ndiaye; Douglas M. Watts

Abstract Background In Senegal, Chikungunya virus (CHIKV), which is an emerging mosquito-borne alphavirus, circulates in a sylvatic and urban/domestic cycle and has caused sporadic human cases and epidemics since 1960s. However, the real impact of the CHIKV sylvatic cycle in humans and mechanisms underlying its emergence still remains unknown. Methodology One thousand four hundred nine suspect cases of CHIKV infection, recruited from 5 health facilities located in Kedougou region, south-eastern Senegal, between May 2009 to March 2010, together with 866 serum samples collected from schoolchildren from 4 elementary schools in May and November 2009 from Kedougou were screened for anti-CHIKV immunoglobulin (Ig)M antibodies and, when appropriate, for viral nucleic acid by real-time polymerase chain reaction (rPCR) and virus isolation. In addition, mosquitoes collected in the same area from May 2009 to January 2010 were tested for CHIKV by rPCR and by virus isolation, and 116 monkeys sera collected from March 2010 to May 2010 were tested for anti-CHIKV IgM and neutralizing antibodies. Results The main clinical manifestations of the CHIKV suspect cases were headache, myalgia, and arthralgia. Evidence for CHIKV infection was observed in 1.4% (20 of 1409) of patients among suspect cases. No significant difference was observed among age or sex groups. In addition, 25 (2.9%) students had evidence of CHIKV infection in November 2009. Chikungunya virus was detected in 42 pools of mosquitoes, mainly from Aedes furcifer, and 83% of monkeys sampled were seropositive. Conclusions Our findings further documented that CHIKV is maintained in a sylvatic transmission cycle among monkeys and Aedes mosquitoes in Kedougou, and humans become infected by exposure to the virus in the forest.


Open Forum Infectious Diseases | 2017

Detection of the Northeastern African Rift Valley Fever Virus Lineage During the 2015 Outbreak in Mauritania.

Ndeye Sakha Bob; Hampâté Bâ; Gamou Fall; Elkhalil Ishagh; Mamadou Y. Diallo; Abdourahmane Sow; Pape Mbacké Sembène; Ousmane Faye; Brahim El Kouri; Mohamed Lemine Sidi; Amadou A. Sall

Abstract Background Rift Valley fever (RVF) is an acute viral anthropozoonosis that causes epizootics and epidemics among livestock population and humans. Multiple emergences and reemergences of the virus have occurred in Mauritania over the last decade. This article describes the outbreak that occurred in 2015 in Mauritania and reports the results of serological and molecular investigations of blood samples collected from suspected RVF patients. Methods An RVF outbreak was reported from 14 September to 26 November 2015 in Mauritania. Overall, 184 suspected cases from different localities were identified by 26 health facilities. Blood samples were collected and tested by enzyme-linked immunosorbent assay (ELISA) and real-time reverse-transcription polymerase chain reaction (RT-PCR) at the Institut Pasteur de Dakar (IPD). Sequencing of partial genomes and phylogenetic analyses were performed on RT-PCR–positive samples. As part of routine surveillance at IPD, samples were also screened for dengue, yellow fever, West Nile, Crimean Congo hemorrhagic fever, Zika, and Chikungunya viruses by ELISA and RT-PCR. Results Of the 184 suspected cases, there were 57 confirmed cases and 12 deaths. Phylogenetic analysis of the sequences indicated an emergence of a virus that originated from Northeastern Africa. Our results show co-circulation of other arboviruses in Mauritania—dengue, Crimean Congo hemorrhagic fever, and West Nile viruses. Conclusion The Northeastern Africa lineage of RVF was responsible for the outbreak in Mauritania in 2015. Co-circulation of multiples arboviruses was detected. This calls for systematic differential diagnosis and highlights the need to strengthen arbovirus surveillance in Africa.

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