Emerging diseases, notably zoonoses caused by negative-stranded RNA viruses continue to be a formidable problem for public health and veterinary communities globally. Arenaviruses, principally rodent-borne viruses, are capable of causing severe syndrome of viral haemorrhagic fevers (VHFs) in humans. The family Arenaviridae includes 23 recognised species, of which 6 can cause outbreaks of VHFs with high case fatality rates. Until recently, Lassa virus was the only known arenavirus to cause VHFs in humans in West Africa (Buchmeier et al. 2007; Charrel et al. 2008). However, the importation of a previously unrecognised arenavirus to South Africa after air medical transfer of a critically ill patient from Lusaka, Zambia in September 2008 resulted in a dramatic VHF nosocomial outbreak in Johannesburg with a case fatality rate of 80 %. International collaboration during this outbreak allowed for rapid identification of the novel virus, thus reassuring that health and scientific communities are committed and have powerful tools to rapidly detect and respond to the challenges of emerging unknown pathogens. The history of the outbreak, however, is a serious warning that highly pathogenic arenaviruses could be more widely prevalent in Africa (Paweska et al. 2009). It also evidences that international movement of patients contributes to unintentional spread of dangerous pathogens with dramatic public health consequences. Genome molecular study, including the application of unbiased high-throughput sequencing, allowed for rapid characterisation of a new member of the family Arenaviridae (Briese et al. 2009) provisionally named Lujo virus (LUJV), but our knowledge on its ecology, epidemiology, including host range, natural transmission cycle and distribution is in paucity. In the light of an unusual highly mortality rate in patients infected with LUJV, studies on tissue tropism, dynamics of viral replication and dissemination, mechanisms of pathogenesis in rodent host species and other potential vertebrate hosts, including primates, are needed.

The natural reservoir host of LUJV remains unknown likewise the source and route of infection of the first (index) case. She kept domestic pets and horses on her agricultural holding near Lusaka and there was evidence of rodent activity in the stables. Rodents could contaminate objects left unattended on the ground by excretion of virus in urine, including broken glass which apparently resulted in a deep cut to her foot about 10 days before medical evacuation to South Africa (Paweska et al. 2009). These circumstances might be of potential epidemiological relevance as she developed first symptoms within the incubation period of arenavirus infection after the cut. The natural reservoirs of arenavirus in Africa are rodents of the family Muridae, especially Mastomys natalensis. To-date only non-pathogenic arenaviruses have been found in areas surrounding Zambia. A study on the prevalence of arenaviruses among M. natalensis rodents in Zambia was conducted less than 1 year after the LUJV outbreak, from May to August 2009, including areas surrounding the cities of Lusaka, Namwala and Mfuwe, but not specifically on the farm of the index case. Nevertheless, of the total of 263 rodents captured, 5 were positive for an arenavirus infection in kidneys, of which 17 % of the 23 rodents captured near Lusaka and 4 % of the 24 captured in Namwala were positive, but none of the 143 rodents captured in Mfuwe were positive for arenavirus. Phylogenetic analysis of the four Zambian arenavirus isolates showed distinct sequences between Old World and New World arenaviruses. The novel Lusaka and Namwala strains, collectively designated Luna virus (LUNV), are genetically different from the LUJV, but closely related to nonpathogenic arenaviruses that have been found from central to eastern Africa (Ishii et al. 2011).

Rift Valley fever (RVF) was first reported in South Africa when a large outbreak occurred during 1950 and 1951. Subsequently, outbreaks with confirmed human cases occurred in South Africa in 1953, between 1974 and 1976, and in 1999. Limited and isolated outbreaks occurred in South Africa in 2008 and 2009 (Swanepoel and Paweska 2011; Bret et al. 2011), followed by a large, widespread outbreak during 2010 and 2011. Between 2008 and 2011, more than 2000 specimens from suspected human RVF cases were submitted to the Special Pathogens Unit of the National Institute for Communicable Diseases of the National Health Laboratory Service for laboratory confirmation. In 2008 and 2009, a total of 24 non-fatal human RVF cases were laboratory confirmed. In 2010, a total of 241 human cases were confirmed of which 25 were fatal. No human fatalities were recorded among 37 confirmed cases during 2011. The outbreaks were geographically linked with outbreaks in domestic ruminants and occurred mostly on the inland plateau of the country, notably in the Free State, Northern Cape, North-West, Eastern Cape and Western Cape provinces. The RVF outbreaks in humans peaked in March 2010 when more than 100 cases were laboratory confirmed. No new cases have been recorded in 2012 to date. In total, 302 human cases were confirmed from 2008 to 2011. In the same period, a total of 13,902 animal cases were confirmed of which 8,581 were fatal. Animal cases involved primarily domestic ruminants, but wild animals, including buffalo, sable, nyala, alpaca, llama and Asian buffalo were also affected. Overlap of geographic distribution of animal and human cases indicates that most humans were infected through direct contact with infected animals. Indeed, 254 (89 %) of the confirmed cases reported a history of contact with animal tissues or bodily fluids. All fatal cases occurred in 2010 (case fatality ratio 10 %). The overall case fatality ratio from 2008 to 2011 was 8 % (Jansen van Vuren et al. 2012). The 2008 and 2009 outbreaks were caused by the virus genetic variants representing lineage C comprising virus isolates from Zimbabwe (1978–1979), Madagascar (1991), Kenya (1997–1998, 2006–2007), South Africa (1999) and Madagascar (2003). The 2010 and 2011 outbreaks were caused by virus genetic variants related to a Namibian isolate from of lineage H first identified in 2004. One isolate from the 2010 outbreaks was genetically distinct, and was closely related to the Smithburn neurotropic vaccine strain. The virus was isolated from a veterinarian who experienced a needle stick injury while vaccinating livestock that likely was already infected by wild-type circulating virus. This isolate is therefore likely a reassortant of the wild-type and the vaccine RVFV strains (Grobbelaar et al. 2011).

The sporadic outbreaks of filovirus infections in humans are believed to result from contact with an infected animal and subsequent transmission between persons by direct contact with infected blood or body fluids. Infected individuals succumbing to filovirus infection exhibit virus-mediated impairment of early innate immune responses allowing for rapid progression of filovirus infection. The unavailability of antiviral therapy or approved vaccines, and the elusive nature of the spillover of filoviruses from a reservoir source to humans hamper countermeasures to effectively prevent the severe course of filovirus disease and transmission. Viruses belonging to the filovirus group were first discovered in 1967 for Marburg virus (Saijo et al. 2006) and in 1976 for Ebola virus (WHO 1978a, b). For a long time, the epidemiological circumstances surrounding filovirus outbreaks suggested that bats may have served as the primary source of infection in humans and non-human primates. Despite intensive efforts to trap thousands of vertebrate and invertebrate hosts in filovirus outbreak areas, isolation of live Ebola virus was unsuccessful, and the ecology and epidemiology of filoviruses are still not well understood. This is mostly because filovirus outbreaks occur irregularly, in poor resource, and remote areas of Africa, consequently investigations of filovirus outbreaks are hugely delayed and dependent on international support. In addition, handling of filoviruses requires the use of biosafety level four (BSL 4) facilities which are unavailable in these countries. Therefore, investigation of filovirus outbreaks, biology, ecology and epidemiology of filoviruses require a collaborative approach involving local researchers and overseas partners in order to secure required funding, training, diagnostic materials and laboratory support.

The SACIDS study of the ecology of filoviruses is undertaken in the Congo basin and particularly in the Democratic Republic of Congo (DRC) where several filovirus outbreaks occurred in the past. The programme is based on a collaborative approach involving several Congolese institutions (e.g. National Institute of Biomedical Research, Veterinary Laboratory of Kinshasa, University of Kinshasa), the National Institute of Communicable Diseases (NICD) a branch of the National Health Laboratory Services of South Africa plus the World Health Organisation (WHO). In this collaborative approach, the Congolese institutions provide administrative and human resources for sample collection in the field, the SACIDS, the NICD/NHLS and the WHO provide maximum security laboratory facility, training, financial and logistic support. Specific objectives of these studies are to collect samples from putative filovirus reservoirs in the DRC, notably from targeted bat species, and conduct their laboratory analysis in the BSL4 facility at NICD/NHLS (Fig. 2). These studies are based on the hypothesis of bats being reservoirs of Ebola virus and thus aim at isolating Ebola virus from bat organs.