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The Connundrum of EV68 Infection Control

Jason Tetro
October 21, 2014

child-sick.jpgThis summer, a virus has spread across the United States and Canada leaving hundreds of children infected many of whom required hospitalization.  The cause is enterovirus D species, serotype 68 (EVD68 or EV68).  This virus is well known to microbiologists but has rarely grabbed media headlines.  Yet for some reason, whether due to evolution or some other unresolved risk factor, the pathogen has sparked concern for parents and public health officials alike.

 

 

Biologically, EV68 is classified as a member of the enterovirus genus within the Picornaviridae family.  This group of non-enveloped viruses includes a number of much better known species including the common cold-causing rhinoviruses; the agent of hand, foot, and mouth disease, the coxsackievirus; a form of viral meningitis, enterovirus A species, serotype 71 (EV71); and most infamously, the polioviruses.  All are ubiquitous in nature and have caused outbreaks in various areas of the world, primarily in clusters. 

 

EV68 was first recognized in 1962 when 4 children became ill from a respiratory virus.  Since then, the virus has gained significant study for its ability to infect and also spread.  Due to its genetic similarity to both the rhinoviruses and the polioviruses, the virus has been suspected of not only causing cold-like symptoms, but worsening conditions including wheezing, respiratory distress, and quite possibly acute flaccid paralysis. 

 

While the clinical nature of EV68 infection has been and continues to be explored, the environmental survival of the virus has been less robust.  It wasn’t until 2001 that environmental spread was even considered as a concern.  By 2011, this had magnified due in part to an increase in cases in the Philippines, Japan, Europe and the United States.  By 2012, the virus was found in the waters of Hawaii.  This confirmed the virus could easily survive in the environment and could pose a risk for environmental spread.

 

With environmental persistence shown, the potential for spread indoors became apparent.  In the context of fomites, standard disinfection tests have been established for the picornaviruses and a plethora of products are now available to reduce the levels of these pathogens.  For skin, however, there are still gaps in our knowledge base.  This has meant public health officials need to look back in time to identify the means necessary to inactivate and/or kill other picornaviruses on hands. 

 

The initial work stemmed back decades and was based on the model of poliovirus.  In 1985, researchers learned the virus tended to bind tightly to the outer dermal layer albeit reversibly.  In their handwashing experiments, 5 minutes of washing with soap and water was ineffective at achieving today’s requirement of 4 log10 reduction.  When other products were used in place of soap – including sand – the reduction was more efficient but still ultimately ineffective.  This led to the suggestion of using chemical additives to inactivate the virus.

 

In 1993, several hand disinfectants were tested against poliovirus.  In this case, a wide scope of products was included with active ingredients such as ethanol, chlorhexidine gluconate, quaternary ammonium chlorides, hexaclorophene and tap water as a control.  Unlike the 1985 study, handwashing was conducted in a more realistic manner with a lathering time of only ten seconds.  Not surprisingly, none of the products could reach more than a 2 log10 reduction suggesting a need to think about viral load rather than efficacy of kill. 

 

When hand sanitizers came around, they were thought to be superior to handwashing.  Yet, the same picornavirus problems appeared to be apparent. In 2005 researchers attempted to determine the ability of 62% alcohol as well as a number of other organic acids on the survival of rhinovirus.  Much like the poliovirus counterpart, the reductions were minimal at best and did little to prevent infection spread.  A silver lining did appear in 2010 in a study that attempted to mimic minimal contamination.  When only 125 viruses were used and the amount of sanitizer was doubled such that contact time was increased, efficacy was finally seen.  But to get to that low load, prior handwashing would have had to occur.      

 

By looking at the nature of the virus, its transmission, which is primarily through respiratory droplets, and its excellent persistence in the environment and on human skin, the need for proper hand hygiene is apparent.  To accomplish this, one needs to ensure handwashing and hand sanitizer use is performed after each consultation with an infected patient.  This may be supplemented with hand sanitizer during consultation as per the 5 moments of hand hygiene, but cannot be considered to be fully protective.  In addition, any contact with individuals other than the patient should be done after handwashing and the use of hand sanitzer in combination is performed to reduce the potential for spread.       

 

The wave of EVD68 has been a rather bad one, taking both the public and health officials off guard.  At the individual level, an increased adherence to hand hygiene is needed to prevent transmission.  Granted, the path forward may seem difficult in operations but it is nonetheless feasible and necessary. Considering the health and lives of children are at stake, it’s undoubtedly worth the effort. 

 

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