Dr. Simbo Davidson believes sufferers of Ebola can be treated with a drug available in the market and which was once used to contain a deadly virus in South Africa

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On 22 July 2014, the first case of the dreaded Ebola virus arrived in Nigeria via an Asky aircraft. However, no one knew it at the time. How did this happen? How had this patient been screened at his port of departure, that is Liberia airport? We can also ask ourselves yet another question. Why is it taking so long to curtail the epidemic? For instance, the World Health Organisation (WHO) recently announced that as at 23 July 2014, the Ebola epidemic had claimed 672 lives. Furthermore, there are currently 1201 suspected and confirmed cases across West Africa. In terms of intervention, the current strategy appears to be related to the use of universal precautions: case isolation, hand-washing, and health worker protection and palliative treatments (such as pain management, and rehydrating fluids).

In theory, this strategy may be quite effective. This is because epidemic control strategies usually aim to reduce person-to-person transmission through avoidance related methods (WHO, 2014). In this case, persons at risk will need to avoid contact with the body fluids of infected person, including sweat, semen, vomit, faeces, urine, blood and saliva (Infection Control for Viral Hemorrhagic Fevers, WHO 2014).

In practice, avoidance techniques may not work, as in reality, these are the most basic of preventive measures. Firstly, a high level of hygiene is required and this may be relatively impossible in the urban slums and rural areas of many African countries. Secondly, isolation centres will need to be stationed in every single district or local government area. In many developing African countries, such centres may not be adequately manned, suitably stationed, or reasonably equipped. So, invariably, many infected persons are nursed at home or buried at home. Hence, the cycle of transmission continues. What then can be done?

From a Public Health perspective, there are several ways that epidemics may be subdued: 1). Interrupt the cycle of transmission e.g prevent cross-contamination 2). Protect the susceptible host e.g through vaccination or 3). Eliminate the reservoir of infection e.g. kill all animals that harbour the Ebola virus.

Starting from the third option, we immediately encounter the difficulty of which animals to slaughter. Unlike Avian flu, it isn’t clear which animal is involved here? Bats? Rodents? Monkeys? In addition, the Ebola virus has no vaccine to date; so that leaves only one other option: interrupt the cycle of transmission. The question then is ‘Has this been effectively done? How have other nations contained similar epidemics?

On 21 September 2008, a woman was admitted at a South African hospital for fever, vomiting and diarrhea, “followed by a rash,” and signs of organ failure (Keeton, 2008). The woman died the next day. Three more cases were reported, in quick succession, to the National Institute for Communicable Disease in South Africa. They all died within a few days of admission. Three of the patients were medical staff. Researcher Keeton (2008) noted that all cases presented with “ flu-like illness (in a similar way to Ebola) and had fever, headache and muscle pain. When the fifth patient surfaced, the institute had diagnosed an outbreak of an old world arena virus infection. While this specific virus did not cause internal bleeding, it belonged to the same class of viruses that did, e.g West African LASSA fever causes fever and bleeding (Keeton ,2008). According to Keeton (2008), the fifth patient (a nurse) was “treated with Ribavirin, which has been effective in patients with LASSA fever, and she has since made a good recovery” (Keeton, 2008).

Ribavirin then was the deciding factor in this case. All other palliative methods failed, intravenous fluids, etc. Why then should we expect such interventions to work now in 2014? Surely an antiviral, which worked in a similar situation six years ago, should also be a consideration in this case? The virus isolated in South Africa had never been subjected to Ribavirin in a research setting (Keeton 2008). In effect, there was no guarantee that it would work. But this was nevertheless the most logical approach to the impending threat.

Ribavirin is a broad-spectrum antiviral agent. It is effective against a wide range of RNA viruses including viral hemorrhagic viruses such as LASSA fever (Crotty, Cameron, & Andino, 2001). According to the trio, Ribavirin was discovered in 1972. It can therefore not be classified as an experimental drug. Ribavirin also acts independently of the viral RNA sequence. Therefore flaviruses (of which Yellow fever is a member) and arena viruses (of which Lassa fever is a member) differ somewhat in structure but are still responsive to the antiviral. The critical success factor, however, may be timely intervention. Ribavirin is contraindicated after organ (e.g. kidney or liver failure) sets in. It may therefore be imperative that treatment be commenced during the early phase of the illness. While the antiviral may not be available as an OTC, (non prescription drug) large orders (in tablet or injectable form) may be made directly from the manufacturers. Fortunately, no fewer than six global pharmaceutical giants, including Sandoz and Roche, are currently manufacturing the antiviral.

In terms of potential impact, the Ebola virus is an RNA virus, and a member of the viral hemorrhagic fevers, such as LASSA fever, Rift valley fever, Marburg virus, Crimean Congo hemorrhagic virus and Yellow fever (Crotty et al.,2001; Keeton, 2008). Most of the VHF viruses present with similar symptoms such as flu-like illness, vomiting, diarrhea, high fever, skin rashes and bleeding (Keeton, 2008). Most are invariably fatal without therapeutic intervention, or vaccination (if available). These statistics clearly indicate that the VHF viruses have similar molecular mechanisms.

Therefore, in view of the current status of the epidemic, the next logical approach should be related to therapeutic intervention. There is certainly no hard evidence that such an approach would be fruitless, while there is certainly compelling evidence that the outcome may be positive.

References

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Crotty, S., Cameron, C., & Andino R.(2001).Ribavirin’s antiviral mechanism of action: Lethal mutagenesis? Journal of Molecular Medicine,(2002) 80 :86-95

Infection Control for Viral Hemorrhagic Fevers in the African Setting.

(World Health Organisation and CDC. 2014)

Keeton, C.(2008).South African Doctors move quickly to contain a new virus. World Health Organization. Bulletin of The World Health Organisation 86.12(Dec 2008) :912-3

Simbo Davidson (MBBS, MPH, PCQI) is a Public Health specialist working in a private hospital in Lagos, Nigeria.

She wrote this article exclusively for PREMIUM TIMES.

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