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Is Ebola the “Bat-out-of Hell” and will we learn something from this experience?

Barry Michaels
September 16, 2014

Ebola outbreakMy esteemed blogging colleagues have written much on the subject of the most recent and deadly Ebola outbreak(s).  That's right; we now have the outbreak of two Ebola strains to be concerned about, one in Zaire and the other in the DR Congo.  Certainly unprecedented in modern times, if not for its scope, but for the shear terrifying manner in which the virus does its dirty deed.  Researchers say that the Zaire outbreak started when a fruit bat bit a 2-year old child and within a week both toddler and mother were dead.  Fruit bats live in colonies around the world of sometimes thousands or even millions strong.  This reminds me of the ‘super-herds’ represented by our large cities. In this case the butterfly effect so talked and written about has turned into a bat wing!

 

This disease leaves me almost speechless.  New projections are that it may infect another 20,000 people before the outbreak is under control; with current mortality rates of around 60%, the numbers are truly disturbing.  And now it seems we even have a second strain in what is now the fifth African country, the DR Congo.  With the West African strain named Zaire, are we about to see two deadly strains fight it out for dominance over the huge and under-developed continent?   For infection control practitioners, this is the stuff of our worst nightmares and we should be deeply indebted to Medecins Sans Frontieres (Doctors without Borders) for the work they do to both assist the sick, but also help prevent further transmission.

 

Clearly the developed world’s neglect of African public health infrastructure plays into the outbreak as it unfolds.  If we continue to ignore the plight of Africa’s health system it is at our own peril. And with all the brave and selfless healthcare experts sent out or volunteering to provide assistance to relieve the suffering and save as many lives as they can,  as they come back to our communities for treatment it might be good to review what we know in terms of hand hygiene and its ability to stop an outbreak as CDC assures us we can.  And is there anything to worry about with them coming home, or are there bigger issues looming just beyond  the horizon?

 

They say you can know a person by the company they keep, well so too for Ebola.  Significant is the fact that Ebola virus is in Baltimore Virus Group V (named after Nobel laureate David Baltimore).   Viruses in Group V are characterized by being enveloped, helical in capsid symmetry with single-stranded RNA genomes. The latter means they hit the ground running, something like the ‘bat-out-of-hell’ we are seeing unfold before our eyes. The deadly Ebola and Marburg viruses (Filovirus virus family) are well known members of this group, along with influenza where we have a good hand hygiene test history.  Also included in Group V are the viruses from other virus families, measles, mumps and rabies virus.  Some of these, while easy to kill, are known for their epidemic potential and of course, with rabies, we come back to the ‘bat’.  . 

 

Ebola virusThe recent Science article tells us that this virus has mutated 300 times since that first case and unfortunately, as we are finding out, Ebola is somewhat stable to freeze and thaw and poorly inactivated by UV, but then there is not much UV light back in those caves! However,on the bright sideEbola is  a virus surround by an ‘envelope’  andenveloped viruses are known to be very easily killed by alcohols, cationic surfactants and antimicrobials. Usually we spend our time talking about antiseptic or sanitizer effectiveness (or lack thereof) in virus groups that are much harder to kill, including viruses from groups IV, the naked non-enveloped viruses that include Adenoviruses, Caliciviruses, (think Norovirus) and Picornaviridae represented by Poliovirus.  These are by far the most difficult to kill with their tightly packed geometrical icosahedral protein coats. By comparison, Ebola should be a walk in the park (to kill) if it weren’t for the fact that profuse bleeding from every bodily orifice accompanies every symptomatic case, spreading virus far and wide. Perhaps this virus has the ability to get our attention to create a sustainable public health infrastructure for Africa, but only time will tell.

 

In respect to hand hygiene, with influenza viruses as an example, it is known that simple surfactant action is able to breakdown the virus envelope with effective hand washing.  With Ebola it is the envelope glycoprotein that binds with target cells and it is glycoprotein type that determines virus infectivity.  Fortunate for now, Ebola Zaire is not as hot as it can get, but then attenuation is the rule with extended human contact.  With some strains mortality rates are at 90%. In one of the few published reports on efficacy of sanitizing agents can be found a description of a “surfactant nanoemulsion” that is effective against Ebola in testing at 1% and 10% concentrations (see reference below) showing that chemistry and theory on effectiveness holds true.  This was made from simple surfactants and oils dispersed in a very fine emulsion making the mixture wet-out soils and eat holes in the virus envelope.  Common ingredients in antimicrobial soaps and hand sanitizers would be significantly active at disrupting virus envelopes as well. Heating serum at 60 degrees C for 1 hour renders viruses inactivated while dilution of blood in 3% acetic acid has also been found quite effective.

 

With any virus, it is not just the kill of the virus in vitro, but also the confounding effects of the soils in which it is found.  So while we know a lot about the virus’s relatives, we don’t know as much about where it comes from and the effects of those confounding soils. With Ebola, dried blood and other secretions will be of utmost importance. Therefore, it is really difficult to make any blanket statement about an antimicrobial agents effectiveness as these soils tend to totally protect viability of viruses until the soil can be broken down allowing the disinfectant or surfactant a chance to degrade the virus envelope.  In many cases the envelopes are destroyed by the simple act of drying out, but here the soil is the issue and the characteristics of blood so prized, its ability to clot, works against us. The search is now on for substances that can kill or effectively inhibit this virus at low cost and is readily available in the remote locations that are on fire with infections.

 

And is there more we should be worried about?  A 2000 study of the 1996 Gabon outbreak, caused by a closely related Zaire strain, tracked contacts and took blood samples and has uncovered a very high rate of asymptomatic Ebola cases.  These appear to commonly occur (~50%) among the surviving population of caregivers that manage not to become openly infected.  This means of course that the biggest risk is not from the healthcare worker who returns home extremely sick for needed treatment, but for all those that travel and are asymptomatic harboring the potential for risk of further spread. 

 

Is there is anything we should learn from this outbreak? When humankind walked out of Africa some 90 thousand years ago to establish the developed world, we unfortunately seldom looked back to our ancestral home.  Exploration of Africa in the 1800’s foretold infectious hazards, even the famous Dr. Livingston did not make it out alive.  Everything is indeed connected to everything else, and perhaps this is our Kilimanjaro moment.  We have the tools to conquer this but with climate change the snows are melting and bats are on the wing. There are a lot of lessons here, we are all in this together, and need to accelerate prevention efforts. With NIH and CDC taking an active role in vaccine development, perhaps these outbreaks can be rolled back sooner rather than later. Public health infrastructure is worth its weight in gold and if there is anything we can depend on it is change itself.

 

"Inactivation of Ebola virus with a surfactant nanoemulsion,"  Acta Trop. 2003 Aug; 87 (3): 315-2

 

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