More Evidence Supports an Enterovirus-AFM Link
Enterovirus-specific antibodies were detected in the cerebrospinal fluid of 79% (11 of 14) of the AFM cases included in a new study.
New research presents additional evidence bolstering the argument that enterovirus infection may be the cause of acute flaccid myelitis (AFM), the “polio-like” disease that primarily affects children.
A team of investigators from the Center for Infection and Immunity (CII) at Columbia University Mailman School of Public Health, the US Centers for Disease Control and Prevention (CDC), and the University of California, San Diego analyzed the cerebrospinal fluid of AFM patients in search of enterovirus antibodies.
According to the CDC, there have been more than 570 cases of AFM in the United States since 2014, with patients reporting extreme weakness in 1 or more limbs, even partial paralyzation, usually within a month of a respiratory or gastrointestinal illness. Investigators hypothesize that a pathogen may be responsible for AFM, and a bulk of the research to date has been focused on identifying one.
The new study, funded by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, and published in mBio, included 14 patients with confirmed AFM (all but 1 were pediatric patients with a median age of 3 years [range, 1 to 7 years]; 69% male) and a control group made up of patients with either a non-AFM central nervous system or inflammatory disease.
Investigators used 2 methods to test study participants for enterovirus antibodies; first, they ran cerebrospinal fluid samples from the 14 patients in the AFM arm and 5 patients in the non-AFM control group through a specialized high throughput sequencing technology developed by CII called VirCapSeq-VERT. Second, they processed the same 14 AFM cerebrospinal fluid samples and blood serum, along with cerebrospinal fluid samples from 11 non-AFM adults with a central nervous system condition and 10 non-AFM children with Kawasaki disease, using high density peptide microarrays that span all the capsid proteins of all species of human EV (species EV-A, EV-B, EV-C, and EV-D).
Nischay Mishra, PhD, associate research scientist at Columbia University’s Mailman School of Public Health and lead author on the study, explained his team’s key findings.
“Our study strongly supports the plausibility of a link between EV-D 68 infection and AFM,” he told Contagion®. “Antibodies to enteroviruses were present 11 of 14 AFM patients (79%), significantly higher than controls. Eight of 11 AFM patients (73%) were immunoreactive to an EV-D68-specific peptide, whereas the 3 control groups were not immunoreactive.”
According to Mishra, the biggest takeaway for clinicians is, moving forward, to keep updating themselves on AFM and report to agencies if they come across any cases.
“Collect and store samples with CDC recommendations,” he advised, “[and] provide more and more information to families and parents about the ill one so they do not panic. Pediatricians should contact infectious diseases specialists in case they have more questions.”