On 23 March 2014, the World Health Organization (WHO) issued its first communique´ (WHO, 2014a) on a new outbreak of Ebola virus disease (EVD), which began in December 2013 in the Republic of Guinea, initially in the Prefecture (province) of Gue´cke´dou in Guinea’s eastern rainforest region, Guine´e Forestie`re (Forested Guinea), then spreading to the Prefecture of Macenta, 80 km to the east. Located on the Atlantic coast of West Africa, Guinea is the first country in this geographical region to report an EVD outbreak with more than one case (Fig. 1a). Cases have now also been reported at several other locations in Guinea, as well as in neighbouring Liberia (Fig. 1b). The appearance of cases in the Guinean capital, Conakry, represents the first large urban setting for EVD transmis-sion. Another case passed through the Liberian capital, Monrovia, but with no reports of any further transmission within the city. Suspected cases in the neighbouring republics of Mali and Sierra Leone have so far tested negative at the time of writing (Fig. 1b, 25 April 2014).
EVD is a severe haemorrhagic fever caused by negative-sense ssRNA viruses classified by the International Com-mittee on Taxonomy of Viruses as belonging to the genus Ebolavirus in the family Filoviridae (order Mononega-virales). Filovirus particles are 80 nm in diameter and form twisted filaments (hence the name) of up to 1.1 mm in length. One other genus in this family, Marburgvirus, contains viruses causing a similar disease to EVD. The third genus, Cuevavirus, is confined to bat hosts. The case fatality rate in EVD is so high, approaching 90 % in some outbreaks (Table 1), that members of the family Filoviridae have been classified as Category A potential bioterrorism agents by the Centers for Disease Control and Prevention (CDC, 2014). All bodily fluids are infectious, requiring the use of full-body protective clothing by medical and surveillance staff. Epidemiological control is also made especially difficult due to the highly variable incubation period of 1–25 days (Dowell et al., 1999), and the long Ebola virus-positive period of some recovered patients (Rodriguez et al., 1999; Rowe et al., 1999). These figures are necessarily approximate because of the low number of confirmed survivors in which testing has been carried out. Patients initially present with fever, headache, joint/muscle and abdominal pain accom-panied by diarrhoea and vomiting (Paessler & Walker, 2013). In its early stages, EVD is easily confused with other tropical fevers, such as malaria or dengue, until the appearance of the haemorrhagic terminal phase, presenting with the characteristic internal and subcutaneous bleeding, vomiting of blood and reddening of the eyes. If sufficient blood is lost, this leads to renal failure, breathing difficulties, low body temperature, shock and death (Paessler & Walker, 2013). ‘Cytokine storm’ with immune suppression of CD4 and CD8 lymphocytes is a candidate mechanism for production of the terminal haemorrhagic fever (Wauquier et al., 2010). Current treatment of EVD is purely symptomatic. However, the antiviral drug favipiravir has produced some promising results in laboratory-infected
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