Filovirus Outbreak Detection and Surveillance: Lessons From Bundibugyo
ABSTRACT The first outbreak of Ebola hemorrhagic fever (EHF) due to Bundibugyo ebolavirus occurred in Uganda from August to December 2007. During outbreak response and assessment, we identified 131 EHF cases (44 suspect, 31 probable, and 56 confirmed). Consistent with previous large filovirus outbreaks, a long temporal lag (approximately 3 months) occurred between initial EHF cases and the subsequent identification of Ebola virus and outbreak response, which allowed for prolonged person-to-person transmission of the virus. Although effective control measures for filovirus outbreaks, such as patient isolation and contact tracing, are well established, our observations from the Bundibugyo EHF outbreak demonstrate the need for improved filovirus surveillance, reporting, and diagnostics, in endemic locations in Africa.
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- "Several viruses within the Filoviridae family, including Ebola virus (EBOV), Sudan virus (SUDV), Taï Forest virus (TAFV), Bundibugyo virus (BDBV), Marburg virus (MARV) and Ravn virus (RAVV), cause severe viral hemorrhagic fevers (VHFs) with high casefatality (Hartman et al., 2010) in several equatorial African countries . A surveillance program to detect VHFs in Uganda was formally established in 2010 by the Centers for Disease Control and Prevention (CDC), Atlanta, USA, in collaboration with the Uganda Virus Research Institute (UVRI) and the Uganda Ministry of Health (UMoH) (MacNeil et al., 2011). Routine serologic and molecular diagnostic tests for various causative agents of VHF are performed on suspected case specimens submitted to the VHF reference laboratory located at UVRI, Entebbe. "
ABSTRACT: In 2012, an unprecedented number of four distinct, partially overlapping filovirus-associated viral hemorrhagic fever outbreaks were detected in equatorial Africa. Analysis of complete virus genome sequences confirmed the reemergence of Sudan virus and Marburg virus in Uganda, and the first emergence of Bundibugyo virus in the Democratic Republic of the Congo.Virology 05/2013; 442(2). DOI:10.1016/j.virol.2013.04.014 · 3.32 Impact Factor
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ABSTRACT: Twelve years after the Kikwit Ebola outbreak in 1995, Ebola virus reemerged in the Occidental Kasaï province of the Democratic Republic of Congo (DRC) between May and November 2007, affecting more than 260 humans and causing 186 deaths. During this latter outbreak we conducted several epidemiological investigations to identify the underlying ecological conditions and animal sources. Qualitative social and environmental data were collected through interviews with villagers and by direct observation. The local populations reported no unusual morbidity or mortality among wild or domestic animals, but they described a massive annual fruit bat migration toward the southeast, up the Lulua River. Migrating bats settled in the outbreak area for several weeks, between April and May, nestling in the numerous fruit trees in Ndongo and Koumelele islands as well as in palm trees of a largely abandoned plantation. They were massively hunted by villagers, for whom they represented a major source of protein. By tracing back the initial human-human transmission events, we were able to show that, in May, the putative first human victim bought freshly killed bats from hunters to eat. We were able to reconstruct the likely initial human-human transmission events that preceded the outbreak. This study provides the most likely sequence of events linking a human Ebola outbreak to exposure to fruit bats, a putative virus reservoir. These findings support the suspected role of bats in the natural cycle of Ebola virus and indicate that the massive seasonal fruit bat migrations should be taken into account in operational Ebola risk maps and seasonal alerts in the DRC.Vector borne and zoonotic diseases (Larchmont, N.Y.) 04/2009; 9(6):723-8. DOI:10.1089/vbz.2008.0167 · 2.30 Impact Factor
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ABSTRACT: Neisseria gonorrhoeae (GC), a major cause of pelvic inflammatory disease, can facilitate HIV transmission. In response to GC infection, genital epithelial cells can produce cytokines, chemokines and defensins to modulate HIV infection and infectivity. GC can also induce the production of cytokines and chemokines in monocytes and modulate T cell activation. In vivo, an increase in the number of endocervical CD4+ T cells has been found in GC-infected women. Additionally, GC appears to modulate HIV-specific immune responses in HIV-exposed sex workers. Interestingly, in vitro, GC exhibits HIV enhancing or inhibitory effects depending on the HIV target cells. This review summarizes molecular and immunological aspects of the modulation of HIV infection and transmission by GC. Future studies using a multi-cellular system or in animal models will offer insight into the mechanisms by which GC increases HIV transmission.Current HIV research 02/2012; 10(3):211-7. DOI:10.2174/157016212800618138 · 1.76 Impact Factor