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Few studies have analyzed the gut microbiota of child in unindustrialized countries, but none during the first month of life. Stool samples were collected from healthy newborns in hospitals of Gabon (n = 6) and Republic of the Congo (n = 9) at different time points during the first month of life: meconium, day 2 (D02), day 7 (D07) and day 28 (D28). In addition, one fecal sample was collected from each mother after delivery. Metagenomic sequencing was performed to determine the bacterial communities, and multiplex real-time PCR was used to detect the presence of seven enteric viruses (rotavirus a, adenovirus, norovirus I and II, sapovirus, astrovirus, enterovirus) in these samples. Bacterial diversity was high in the first days of life, and was dominated by the genus Prevotella. Then, it rapidly decreased and remained low up to D28 when the gut flora was composed almost exclusively of strictly anaerobic bacteria. Each infant’s fecal bacterial microbiota composition was significantly closer to that of their mother than to that of any other woman in the mothers’ group, suggesting an intrauterine, placental or amniotic fluid origin of such bacteria. Moreover, bacterial communities differed according to the delivery mode. Overall, the bacterial microbiota communities displayed a similar diversification and expansion in newborns within and between countries during the first four weeks of life. Moreover, six of the fifteen infants of this study harbored enteric viruses (rotavirus, enterovirus and adenovirus) in fecal samples, but never in the meconium. A maternal source for the viruses detected at D02 and D07 can be excluded because none of them was found also in the child’s mother. These findings improve our knowledge on the gut bacterial and viral communities of infants from two Sub-Saharan countries during their first month of life. [ABSTRACT FROM AUTHOR]

In 2006–2007 we observed an unusual mortality event among apes in northern Republic of Congo that, although not diagnostically confirmed, we believe to have been a disease outbreak. In 2007–2011 we conducted ape nest surveys in the region, recording 11,835 G. g. gorilla nests (2,262 groups) and 5,548 P. t. troglodytes nests (2,139 groups). We developed a statistical model to determine likely points of origin of the outbreak to help identify variables associated with disease emergence and spread. We modeled disease spread across the study area, using suitable habitat conditions for apes as proxy for local ape densities. Infectious status outputs from that spread model were then used alongside vegetation, temperature, precipitation and human impact factors as explanatory variables in a Generalized Linear Model framework to explain observed 2007–2011 ape nest trends in the region. The best models predicted emergence in the western region of Odzala-Kokoua National Park and north of the last confirmed Ebola virus disease epizootics. Roads were consistently associated with attenuation of modeled virus spread. As disease is amongst the leading threats to great apes, gaining a better understanding of disease transmission dynamics in these species is imperative. Identifying ecological drivers underpinning a disease emergence event and transmission dynamics in apes is critical to creating better predictive models to guide wildlife management, develop potential protective measures for wildlife and to reduce potential zoonotic transmission to humans. The results of our model represent an important step in understanding variables related to great ape disease ecology in Central Africa. [ABSTRACT FROM AUTHOR]

Enteroviruses, members of the Picornaviridae family, are ubiquitous viruses responsible for mild to severe infections in human populations around the world. In 2010 Pointe-Noire, Republic of Congo recorded an outbreak of acute flaccid paralysis (AFP) in the humans, caused by wild poliovirus type 1 (WPV1). One month later, in the Tchimpounga sanctuary near Pointe-Noire, a chimpanzee developed signs similar to AFP, with paralysis of the lower limbs. In the present work, we sought to identify the pathogen, including viral and bacterial agents, responsible for this illness. In order to identify the causative agent, we evaluated a fecal specimen by PCR and sequencing. A Human enterovirus C, specifically of the EV-C99 type was potentially responsible for the illness in this chimpanzee. To rule out other possible causative agents, we also investigated the bacteriome and the virome using next generation sequencing. The majority of bacterial reads obtained belonged to commensal bacteria (95%), and the mammalian virus reads matched mainly with viruses of the Picornaviridae family (99%), in which enteroviruses were the most abundant (99.6%). This study thus reports the first identification of a chimpanzee presenting AFP most likely caused by an enterovirus and demonstrates once again the cross-species transmission of a human pathogen to an ape. [ABSTRACT FROM AUTHOR]

In 2010, a large outbreak of poliomyelitis with unusual 47% lethality occurred in Pointe Noire, Republic of Congo. Vaccine-mediated immunity against the outbreak virus was never investigated. A wild poliovirus 1 (WPV1) isolated from a fatal case (termed PV1-RC2010) showed a previously unknown combination of amino acid exchanges in critical antigenic site 2 (AgS2, VP1 capsid protein positions 221SAAL→221PADL). These exchanges were also detected in an additional 11 WPV1 strains from fatal cases. PV1-RC2010 escaped neutralization by three different mAbs relevant for AgS2. Virus neutralization was tested in sera from fatal cases, who died before supplementary immunization (n = 24), Gabonese recipients of recent oral polio vaccination (n = 12), routinely vaccinated German medical students (n = 34), and German outpatients tested for anti-poliovirus immunity (n = 17) on Vero, human rhabdomyosarcoma, and human epidermoid carcinoma 2 cells. Fatal poliomyelitis cases gave laboratory evidence of previous trivalent vaccination. Neutralizing antibody titers against PV1-RC2010 were significantly lower than those against the vaccine strain Sabin-1, two genetically distinct WPV1s isolated in 1965 and 2010 and two genetically distinct vaccine-derived PV strains. Of German vaccinees tested according to World Health Organization protocols, 15-29% were unprotected according to their neutralization titers (<1:8 serum dilution), even though all were protected against Sabin-1. Phylogenetic analysis of the WPV1 outbreak strains suggested a recent introduction of virus progenitors from Asia with formation of separate Angolan and Congolese lineages. Only the latter carried both critical AgS2 mutations Antigenetically variant PVs may become relevant during the final phase of poliomyelitis eradication in populations with predominantly vaccine-derived immunity. Sustained vaccination coverage and clinical and environmental surveillance will be necessary. [ABSTRACT FROM AUTHOR]

Background: Crimean-Congo hemorrhagic fever (CCHF) is a severe tick-borne disease well recognized through Europe and Asia where diagnostic tests and medical surveillance are available. However, it is largely neglected in Africa, especially in the tropical rainforest of Central Africa where only sporadic human cases have been reported and date back to more than 30 years. We describe here an isolated human case that occurred in the Democratic Republic of the Congo in 2008 and performed phylogenetic analysis to investigate whether it resulted from a regional re-emergence or from the introduction of a novel virus in the area. Methods and Findings: Near complete segment S and partial segment M sequences were characterized. Bayesian phylogenetic analysis and datation were performed to investigate the relationship between this new strain and viral strains from Africa, Europe and Asia. The new strain is phylogenetically close to the previously described regional genotype (II) that appears to be specific to Central Africa. Phylogenetic discrepancy between segment S and M suggested genetic exchange among local sublineages, which was dated back to 130–590 years before present. Conclusions: The phylogenetic analyses presented here suggest ongoing CCHF virus circulation in Central Africa for a long time despite the absence of reported human cases. Many infections have most probably been overlooked, due to the weakness of healthcare structures and the absence of available diagnostic procedure. However, despite the lack of accurate ecological data, the sporadic reporting of human cases could also be partly associated with a specific sylvatic cycle in Central Africa where deforestation may raise the risks of re-emergence. For these reasons, together with the high risk of nosocomial transmission, public health authorities' attention should be drawn to this etiological agent. Author Summary: Crimean-Congo hemorrhagic fever virus (CCHFV) is transmitted to humans through tick-bite or contact with infected blood or tissues from livestock, the main vertebrate hosts in a peri-domestic natural cycle. With numerous outbreaks, a high case fatality rate (3%–30%) and a high risk for nosocomial transmission, CCHFV became a public health concern in Europe and Asia. However virus surveillance in Africa is difficult due to the limited sanitary facilities. Especially, CCHFV occurrence in Central Africa is very poorly described and seems highly in contrast with the temperate to dry environments to which the virus is usually associated with. We described a single human infection that occurred in Democratic Republic of the Congo after nearly 50 years of absence. The phylogenetic analysis suggests that CCHFV enzootic circulation in the area is still ongoing despite the absence of notification, and thus reinforces the need for the medical workers and authorities to be aware of the outbreak risk. The source of infection seemed associated with a forest environment while no link with the usual agro-pastoral risk factors could be identified. More accurate ecological data about CCHFV enzootic cycle are required to assess the risk of emergence in developing countries subjected to deforestation. [ABSTRACT FROM AUTHOR]

Background. Zaire ebolavirus was responsible for 2 outbreaks in Democratic Republic of the Congo (DRC), in 1976 and 1995. The virus reemerged in DRC 12 years later, causing 2 successive outbreaks in the Luebo region, Kasai Occidental province, in 2007 and 2008. Methods. Viruses of each outbreak were isolated and the full-length genomes were characterized. Phylogenetic analysis was then undertaken to characterize the relationships with previously described viruses. Results. The 2 Luebo viruses are nearly identical but are not related to lineage A viruses known in DRC or to descendants of the lineage B viruses encountered in the Gabon-Republic of the Congo area, with which they do, however, share a common ancestor. Conclusions. Our findings strongly suggest that the Luebo 2007 outbreak did not result from viral spread from previously identified foci but from an independent viral emergence. The previously identified epidemiological link with migratory bat species known to carry Zaire ebolavirus RNA support the hypothesis of viral spillover from this widely dispersed reservoir. The high level of similarity between the Luebo2007 and Luebo2008 viruses suggests that local wildlife populations (most likely bats) became infected and allowed local viral persistence and reemergence from year to year. [ABSTRACT FROM AUTHOR]

Abstract: Ebolavirus has caused highly lethal outbreaks of haemorrhagic fever in the Congo basin. The 2005 outbreak in the Republic of Congo occurred in the Etoumbi district of Cuvette Ouest Department between April and May. The two index cases were infected while poaching. The sanitary response consisted of active surveillance and contact tracing, public awareness campaigns and community mobilization, case management and safe burial practices, and laboratory confirmation. Twelve cases and ten deaths were reported (lethality 83%). A transmission tree was constructed from a sample collected by a medical team. This outbreak was remarkable by its short duration and limited size. Increased awareness among these previously affected populations and the rapid response of the healthcare system probably contributed to its extinction. [Copyright &y& Elsevier]

Background: Ebolavirus species Zaire (ZEBOV) causes highly lethal hemorrhagic fever, resulting in the death of 90% of patients within days. Most information on immune responses to ZEBOV comes from in vitro studies and animal models. The paucity of data on human immune responses to this virus is mainly due to the fact that most outbreaks occur in remote areas. Published studies in this setting, based on small numbers of samples and limited panels of immunological markers, have given somewhat different results. Methodology/Principal Findings: Here, we studied a unique collection of 56 blood samples from 42 nonsurvivors and 14 survivors, obtained during the five outbreaks that occurred between 1996 and 2003 in Gabon and Republic of Congo. Using Luminex technology, we assayed 50 cytokines in all 56 samples and performed phenotypic analyses by flow cytometry. We found that fatal outcome was associated with hypersecretion of numerous proinflammatory cytokines (IL-1β, IL-1RA, IL-6, IL-8, IL-15 and IL-16), chemokines and growth factors (MIP-1α, MIP-1β, MCP-1, M-CSF, MIF, IP-10, GRO-α and eotaxin). Interestingly, no increase of IFNα2 was detected in patients. Furthermore, nonsurvivors were also characterized by very low levels of circulating cytokines produced by T lymphocytes (IL-2, IL-3, IL-4, IL-5, IL-9, IL-13) and by a significant drop of CD3+CD4+ and CD3+CD8+ peripheral cells as well as a high increase in CD95 expression on T lymphocytes. Conclusions/Significance: This work, the largest study to be conducted to date in humans, showed that fatal outcome is associated with aberrant innate immune responses and with global suppression of adaptive immunity. The innate immune reaction was characterized by a "cytokine storm," with hypersecretion of numerous proinflammatory cytokines, chemokines and growth factors, and by the noteworthy absence of antiviral IFNα2. Immunosuppression was characterized by very low levels of circulating cytokines produced by T lymphocytes and by massive loss of peripheral CD4 and CD8 lymphocytes, probably through Fas/FasL-mediated apoptosis. Author Summary: Ebolavirus, especially the species Zaïre (ZEBOV), causes a fulminating hemorrhagic fever syndrome resulting in the death of most patients within a few days. In vitro studies and animal models have brought some insight as to the immune responses to ZEBOV infection. However, human immune responses have as yet been poorly investigated, mainly due to the fact that most outbreaks occur in remote areas of central Africa. Published studies, based on small numbers of biological samples have given conflicting results. We studied a unique collection of 50 blood samples obtained during five outbreaks that occurred between 1996 and 2003 in Gabon and Republic of Congo. We measured the plasma levels of 50 soluble factors known to be involved in immune responses to viral diseases. For the first time, using a cell staining technique, we analyzed circulating lymphocytes from ZEBOV-infected patients. We found that fatal outcome in humans is associated with aberrant innate immunity characterized by a "cytokine storm," with hypersecretion of numerous proinflammatory mediators and by the noteworthy absence of antiviral interferon. The adaptive response is globally suppressed, showing a massive loss of CD4 and CD8 lymphocytes and the immune mediators they produce. These findings may have important pathological and therapeutic implications. [ABSTRACT FROM AUTHOR]

Background. Patients who have refused to provide blood samples has meant that there have been significant delays in confirming outbreaks of Ebola virus hemorrhagic fever (EVHF). During the 2 EVHF outbreaks in the Republic of Congo in 2003, we assessed the use of oral fluid specimens versus serum samples for laboratory confirmation of cases of EVHF. Methods. Serum and oral fluid specimens were obtained from 24 patients with suspected Ebola and 10 healthy control subjects. Specimens were analyzed for immunoglobulin G antibodies by enzyme-linked immunosorbent assay (ELISA) and for Ebola virus by antigen detection ELISA and reverse-transcriptase polymerase chain reaction (RT-PCR). Oral fluid specimens were collected with a commercially available collection device. Results. We failed to detect antibodies against Ebola in the oral fluid specimens obtained from patients whose serum samples were seropositive. All patients with positive serum RT-PCR results also had positive results for their oral fluid specimens. Conclusions. This study demonstrates the usefulness of oral fluid samples for the investigation of Ebola outbreaks, but further development in antibodies and antigen detection in oral fluid specimens is needed before these samples are used for filovirus surveillance activities in Africa. [ABSTRACT FROM AUTHOR]

All human Ebola virus outbreaks during 2001-2003 in the forest zone between Gabon and Republic of Congo resulted from handling infected wild animal carcasses. After the first outbreak, we created an Animal Mortality Monitoring Network in collaboration with the Gabonese and Congolese Ministries of Forestry and Environment and wildlife organizations (Wildlife Conservation Society and Programme de Conservation et Utilisation Rationnelle des Ecosystemes Forestiers en Afrique Centrale) to predict and possibly prevent human Ebola outbreaks. Since August 2001, 98 wild animal carcasses have been recovered by the network, including 65 great apes. Analysis of 21 carcasses found that 10 gorillas, 3 chimpanzees, and 1 duiker tested positive for Ebola virus. Wild animal outbreaks began before each of the 5 human Ebola outbreaks. Twice we alerted the health authorities to an imminent risk for human outbreaks, weeks before they occurred. [ABSTRACT FROM AUTHOR]

Several human and animal Ebola outbreaks have occurred over the past 4 years in Gabon and the Republic of Congo. The human outbreaks consisted of multiple simultaneous epidemics caused by different viral strains, and each epidemic resulted from the handling of a distinct gorilla, chimpanzee, or duiker carcass. These animal populations declined markedly during human Ebola outbreaks, apparently as a result of Ebola infection. Recovered carcasses were infected by a variety of Ebola strains, suggesting that Ebola outbreaks in great apes result from multiple virus introductions from the natural host. Surveillance of animal mortality may help to predict and prevent human Ebola outbreaks. [ABSTRACT FROM AUTHOR]

The first recorded human outbreak of Ebola virus was in 1976, but the wild reservoir of this virus is still unknown. Here we test for Ebola in more than a thousand small vertebrates that were collected during Ebola outbreaks in humans and great apes between 2001 and 2003 in Gabon and the Republic of the Congo. We find evidence of asymptomatic infection by Ebola virus in three species of fruit bat, indicating that these animals may be acting as a reservoir for this deadly virus. [ABSTRACT FROM AUTHOR]

A survey was conducted in Befale and Boende in the Democratic Republic of the Congo. It revealed that the purchase of the game from hunters and the resale of these games in small pieces at the market are more practiced by women (100%). The experience of time spent in this activity varies from less than 10 years (33, 3 %) to 30 years and more (20%). Most (60%) have no preference for the choice of game meat to sell; they sell whatever they can find, as long as the operation brings them a profit. Many people buy meat from hunters (66, 7 %) but those who have not had time to reach the hunters, buy it from wholesalers (66, 7%). Some regular hunters or wholesalers take the game on credit and pay after the sale. Local markets are cited (80%) as the places where game meat is sold, especially when it is sold fresh. They alternate, one day to buy game from hunters in the surrounding villages, and another day to go and sell at the market. The profit from the sale of game meat and other products is allocated to medical care (90%), school fees (83, 3%), clothing (83, 3%), food for children (80%), etc. Among the other products sold, there are fish (63, 3%), goat or sheep (53, 3%), caterpillars (36, 7%), pork (33, 3%), etc. We suggest as an alternative to hunting, a program for the development of socio-economic activities for the local populations. [ABSTRACT FROM AUTHOR]

The article discusses a study on the outbreak of Ebola virus disease (EVD) in the Democratic Republic of Congo which started on July 26, 2014. Topics mentioned include simultaneous reports of EVD in equatorial and West Africa and whether the two outbreaks where linked, details of genome sequencing which confirmed the Ebola virus as the cause of the outbreak, and similar clinical and epidemiological characteristics of the EVD outbreak in Congo and previous outbreaks in equatorial Africa.

Since 1995, when the world was horrified by a deadly Ebola outbreak in Kikwit, Zaire, central Africa has suffered nearly a dozen outbreaks of the hemorrhagic fever, which can kill more than 80% of its victims. The human toll is tragic enough, but the disease is also threatening one of the world's largest populations of chimpanzees and gorillas. Researchers estimate that it has killed thousands of great apes in the past 5 years. One of the main puzzles is whether the recent outbreaks are all part of one larger epidemic that is spreading steadily through the forest from diseased animals to new victims, or whether each cluster stems from an independent introduction of the virus from its elusive host. Researcher Eric Leroy of the Institute of Research for Development in Franceville, Gabon, and his colleagues sequenced virus samples from human and animal victims of five outbreaks in Gabon and the Republic of Congo between 2001 and 2003.