SEP 08, 2019

Acute Flaccid Myelitis and Its Association With Enterovirus D68

WRITTEN BY: Dena Aruta

Acute flaccid myelitis (AFM), a polio-like infection, caught the attention of physicians in the U.S. during late summer and early fall in 2014. The outbreak was characterized by severe lower respiratory infections with paralysis and respiratory failure in a small subset of affected children. The CDC began tracking cases of AFM in August 2014, and there have been 587 confirmed cases to date. It is still unclear why only a small number of children get this disease, and a definitive etiology has not yet been determined. However, there is growing evidence that enterovirus D68 (EV-D68) is associated with AFM. The video below gives a brief overview of AFM:

 

group of researchers at the Children's Hospital of Philadelphia (CHOP) led by P. Uprety, MSPH, Ph.D.analyzed the prevalence of EV-D68 in children with AFM at CHOP between 2009-2018. Due to the paucity of longitudinal studies of the evolution of the virus, They also performed whole-genome sequencing (WGS) to track the occurrence of any mutations from year-to-year. 

During the 10-year surveillance of EV-D68 and AFM at CHOP, the researchers found that there was a peak in the circulation of the virus during even years except for a peak in 2009 and absence between 2010-2011. Half of the specimens tested were taken from samples stored in the laboratory. Also, AFM peaked during the same times in the study population with a correlation between the number of AFM cases and prevalence of EV-D68. 

In order to determine which clades of EV-D68 were present in the CHOP specimens, they performed WGS from 26 specimens of children without AFM and four diagnosed with AFM as well as completing polyprotein sequences from 28 of the 30 samples. Analyses revealed the presence of A and C clades in the 2009 specimens and one specimen containing the B1 clade. The B3 clade was introduced between 2014-2016, which probably emerged rather than evolved from an ancestor of B1. The implications of this finding suggest that in 2020 there may be another clade that emerges making future surveillance vital.  

One of the major controversies surrounding EV-D68 being the causative agent of AFM is the inability to isolate it from CSF specimens even though the disease affects the gray matter of the spinal cord. Other viruses may be involved including EV-A71 and coxsackievirus A16; all stool specimens tested from patients with AFM have been negative for poliovirus.