Acute Flaccid Myelitis Cases Stable Despite Enterovirus Rise

Acute flaccid myelitis, a severe neurological disorder characterised by rapid onset of limb weakness, has historically presented in clusters, often coinciding with peaks in enterovirus circulation. The condition primarily affects the grey matter of the spinal cord, leading to flaccid paralysis that can range from mild to life-threatening, particularly if respiratory muscles are involved. The clinical presentation often follows a febrile illness, typically respiratory or gastrointestinal, suggesting a post-infectious or direct viral aetiology.¹

The European Centre for Disease Prevention and Control (ECDC) has maintained surveillance for AFM cases, especially since the notable increase in cases observed in North America in 2014. This surveillance aims to monitor trends and identify potential triggers, with a particular focus on enteroviruses, specifically EV-D68 and EV-A71. These viruses are known neurotropic pathogens, capable of causing a spectrum of neurological diseases, from aseptic meningitis to encephalitis and paralysis.¹

Monitoring the viral landscape

Recent epidemiological data from across Europe indicate a discernible increase in the overall incidence of enterovirus infections. This rise encompasses a variety of serotypes, including EV-D68, which has been implicated in previous AFM outbreaks. Public health agencies track these trends through sentinel surveillance networks and laboratory reporting systems, which collect data on respiratory and neurological samples. The increased detection of enteroviruses reflects improved diagnostic capabilities and heightened awareness among clinicians, but also genuine shifts in viral circulation patterns.²

But, despite this documented increase in enterovirus activity, the incidence of acute flaccid myelitis has not followed suit. Surveillance reports show no statistically significant increase in AFM cases across European countries during periods of heightened enterovirus detection. This observation challenges the previously assumed direct, dose-response relationship between general enterovirus circulation and AFM incidence. The number of confirmed AFM cases has remained relatively stable, hovering around baseline levels, even as laboratory confirmations of enterovirus infections have climbed.²

This decoupling suggests that while enteroviruses are undoubtedly aetiological agents for AFM, the mere presence or increased circulation of these viruses does not automatically translate into a surge in AFM. Other factors, such as specific viral clades, host susceptibility, or environmental co-factors, likely play a critical role in determining whether an enterovirus infection progresses to AFM. The pathogenesis of AFM is complex, involving direct viral invasion of motor neurons, immune-mediated damage, or a combination of both. Not all individuals infected with neurotropic enteroviruses develop neurological complications; indeed, the vast majority experience mild, self-limiting illness.³

The surveillance methodology for AFM typically involves active case finding through paediatric neurology departments and infectious disease units, coupled with retrospective chart reviews. Case definitions are standardised, requiring acute onset of flaccid limb weakness and characteristic MRI findings of spinal cord grey matter lesions spanning one or more vertebral segments. Laboratory confirmation of enterovirus in cerebrospinal fluid (CSF) is highly indicative but not always achieved, as viral shedding can be transient. Respiratory and stool samples are also routinely collected, though their correlation with neurological disease is less direct.¹

The open-label nature of enterovirus surveillance is the obvious caveat. Detection rates are influenced by testing practices, which can vary between regions and over time. An increase in testing for enteroviruses, driven by clinical suspicion or public health alerts, could artificially inflate reported infection rates without a true increase in viral prevalence. Still, the consistent reporting of stable AFM numbers across multiple surveillance systems, even with increased enterovirus detection, lends weight to the observation. The trial was not powered to detect subtle changes in very rare subgroups, and that gap matters for understanding the full spectrum of viral neuroinvasion.²

The data also do not differentiate between specific enterovirus serotypes in all reported cases. While EV-D68 is a primary suspect, other enteroviruses, such as EV-A71, have also been linked to AFM. A more granular analysis of serotype-specific circulation alongside AFM incidence could provide further clarity. Without this detailed breakdown, it remains difficult to definitively rule out a shift in dominant circulating strains that might be less neurovirulent, or a change in population immunity.³

The current understanding of AFM pathogenesis is still evolving. While direct viral damage to motor neurons is a leading hypothesis, immune-mediated mechanisms, where the body's own immune response to the virus inadvertently attacks the spinal cord, are also considered. This complex interplay means that a simple increase in viral exposure may not be sufficient to trigger the disease in all susceptible individuals. The absence of a corresponding rise in AFM cases, despite increased enterovirus activity, underscores the need for continued research into host genetic factors and specific viral determinants that predispose individuals to this severe outcome.³