By Dr. Simbo Davidson
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, 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).
[But] 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 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.