A new substrain of Enterovirus D68 is likely responsible for polio-like paralysis

Last summer (2014) there was a serious outbreak of the "summer cold" caused by a new strain of enterovirus named Enterovirus D68. What distinguished this outbreak was the severity of the symptoms which led to numerous hospitalizations and a large number of total cases (thousands or tens of thousands) [link]. As is typical of enterovirus infections, the vast majority of the patients were children (Figure 1).

Even more alarming was that approximately 115 children developed polio-like paralysis symptoms (NYTimes). Both enterovirus and poliovirus belong to the picornavirus family of viruses. In a previous post, I described how medical scientists suspected that Enterovirus D68 was the culprit, but did not know for sure because some of the kids did not have the enterovirus in their nasal mucus. One possibility was that the D68 diagnostic was not sensitive enough; the other possibility was that some other virus was the responsible agent.

A new paper from UCSF helps to resolve this question by providing strong evidence that D68 is indeed causing the paralysis in most if not all the kids.

The authors sequenced the DNA of the viruses found in the paralysis patients for more detailed identification. Among 25 patients with acute flaccid myelitis (i.e. polio-like partial paralysis), 12 possessed detectable Enterovirus D68 in their nasal secretions. More strikingly, sequencing revealed that all 12 were infected with the same special subtype of the D68 virus termed B1, and that this subtype contained mutations not found in other D68 viruses, but that instead resembled mutations in polio virus associated with paralysis. The fact that a significant fraction of the patients possessed one particular enterovirus subtype that contained mutations found in neuropathogenic poliovirus is compelling indirect evidence that Enterovirus D68 B1 is the causative agent of acute flaccid myelitis.

It is important to emphasize that most children who were infected by the D68-B1 substrain did not suffer the paralysis. Indeed, there were instances in which siblings were both infected by D68-B1 and while one suffered from acute flaccid myleitis, the other did not.

Finally, these numbers need to be put in perspective. By comparison in 1952 (Wikipedia), a few years before the polio vaccine was introduced, there were 57,628 cases of polio in the U.S., 3,145 patients died, and 21,269 were left with mild to disabling paralysis. Today thanks to the polio vaccine the number of polio cases has dropped to 0 in the U.S. and is closed to becoming eradicated worldwide. The 100 cases of partial paralysis caused by acute flaccid myelitis is small compared to the 25,000 serious polio cases in 1952.

With the end of last summer, the Enterovirus D68 outbreak has all but disappeared. The question is what will happen this summer (2015). Hopefully the D68-B1 virus will not return. Compared to the poliovirus infection rate the D68-B1 infection rate was much smaller boosting the chance that it could disappear altogether.

Figure 1. There is strong evidence that one subtype of Enterovirus D68 is responsible for the polio like paralysis (acute flaccid myelitis) that afflicted over 100 children last summer.