Key result
Acute flaccid myelitis shares important similarities with poliomyelitis, and the inability to detect enteroviruses in cerebrospinal fluid does not eliminate them as etiologic agents.
Why the study?
With the eradication of poliomyelitis in the United States, the emergence of acute flaccid myelitis outbreaks raised questions regarding their causation.
The inability to detect enteroviruses in the cerebrospinal fluid of patients with acute flaccid myelitis does not rule them out as etiologic agents, drawing parallels to historical findings in poliomyelitis.
With the eradication of poliomyelitis in the United States, the appearance of acute flaccid myelitis outbreaks has raised questions regarding their causation. Review of the epidemiology, clinical aspects, and laboratory findings of bygone cases of poliomyelitis have revealed shows important similarities with those of newer cases of acute flaccid myelitis. Many occurrences are preceded by an apparent viral illness, and a number of viruses, particularly enteroviruses A71 and D68, can be isolated from respiratory or stool specimens. Our inability to detect these viruses in cerebrospinal fluid samples from these patients does not eliminate them as etiologic agents, because poliovirus is often not detected in cerebrospinal fluid samples of patients with paralysis caused by poliomyelitis.
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Janet R. Gilsdorf (2019) conducted a review in Acute Flaccid Myelitis. Enteroviruses A71 and D68 was evaluated. Acute flaccid myelitis shares important similarities with poliomyelitis, and the inability to detect enteroviruses in cerebrospinal fluid does not eliminate them as etiologic agents.
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