Testing of 14 patients with acute flaccid myelitis, or AFM, showed they had antibodies against enteroviruses, especially EV-D68, in their cerebrospinal fluid at a significantly higher rate than controls, supporting “the plausibility of a link” between enterovirus infection and AFM, researchers reported in mBio.
“Physicians and scientists have long suspected that enteroviruses — a family of viruses responsible for polio, another paralyzing disease — are behind AFM, but there has been little evidence to support this idea," Nischay Mishra, PhD, assistant professor of epidemiology at the Columbia University Mailman School of Public Health’s Center for Infection and Immunity, said in a news release. "Further work is needed with larger, prospective studies. Nonetheless, these results take us one step closer to understanding the cause of AFM, and one step closer to developing diagnostic tools and treatments.”
According to Mishra and colleagues, AFM has caused more than 560 cases of motor paralysis in the United States in the last 5 years.
To explore the possible relationship between AFM and enteroviruses, the researchers used a viral-capture high-throughput sequencing system to analyze CSF collected from 14 people with AFM and five people with other central nervous system diseases. They then tested CSF and serum samples from patients and controls for antibodies to enteroviruses using peptide microarrays.
They identified enterovirus RNA in CSF from only one adult with AFM and one non-AFM case. However, most patients with AFM (n = 11; 79%) had antibodies to enterovirus peptides in their spinal fluid, according to Mishra and colleagues. This prevalence was significantly higher than the prevalence identified among non-AFM patients (n = 1 of 5; 20%), adults with other non-AFM central nervous system diseases (n = 2 of 11; 18%) and children with Kawasaki disease (n = 0 of 10), they reported.
According to the study, peptides to EV-D68 — an enterovirus that has been suspected to cause AFM among children — were commonly identified among patients with AFM (CSF: n = 6 of 14 [43%]; serum samples: n = 8 of 11 [73%]). Furthermore, the researchers identified no immunoreactivity against EV-D68 in three control groups through their CSF (group 1: n = 0 of 5; P = .008; group 2: n = 0 of 10; P = .0003; group 3: n = 0 of 11; P = .035) or serum (n = 0 of 2; P = .139; group 2: n = 0 of 8; P = .002; group 3: n = 0 of 5; P = .009).
“Pathogen discovery has historically focused on direct detection of infectious agents. The introduction of new methods that allow us to also test for footprints of exposure will lead to new insights into infectious diseases,” W. Ian Lipkin, MD, director of Center for Infection and Immunity, said in the release. – by Katherine Bortz
Disclosures: The authors report no relevant financial disclosures.