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Enterovirus D68 and acute flaccid myelitis-evaluating the evidence for causality

Kevin Messacar¹, Edwin J Asturias², Alison M Hixon³

¹Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO, USA; Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA; Children's Hospital Colorado, Aurora, CO, USA.

The Lancet. Infectious Diseases

|February 28, 2018

Abstract:

Increased circulation of enterovirus D68 in 2014 and 2016 temporally and geographically coincided with increases in cases of acute flaccid myelitis, an uncommon condition of paralysis due to lesions in the anterior horn of the spinal cord. The identification of enterovirus D68 in respiratory specimens from cases of acute flaccid myelitis worldwide further supports an association, yet the absence of direct virus isolation from affected tissues, infrequent detection in cerebrospinal fluid, and the absence, until recently, of an animal model has left the causal nature of the relationship unproven. In this Personal View we evaluate epidemiological and biological evidence linking enterovirus D68 and acute flaccid myelitis. We applied the Bradford Hill criteria to investigate the evidence for a causal relationship and highlight the importance of comprehensive surveillance and research to further characterise the role of enterovirus D68 in acute flaccid myelitis and pursue effective therapies and prevention strategies.

Insights

Enterovirus D68 (EV-D68) outbreaks coincided with acute flaccid myelitis (AFM) cases. Evaluating evidence suggests EV-D68 may cause AFM, necessitating further research and surveillance.

Area of Science:

Neurology
Virology
Epidemiology

Background:

Acute flaccid myelitis (AFM) is an uncommon paralytic condition.
Increased enterovirus D68 (EV-D68) circulation in 2014 and 2016 correlated with AFM outbreaks.
EV-D68 has been identified in respiratory samples from AFM patients globally.

Purpose of the Study:

To evaluate the epidemiological and biological evidence linking EV-D68 and AFM.
To assess the causal relationship using the Bradford Hill criteria.
To emphasize the need for enhanced surveillance and research.

Main Methods:

Review of epidemiological data on EV-D68 circulation and AFM incidence.
Evaluation of biological evidence supporting a link between EV-D68 and AFM.
Application of Bradford Hill criteria to assess causality.

Main Results:

Temporal and geographic association between EV-D68 circulation and AFM cases.
Identification of EV-D68 in respiratory specimens of AFM patients.
Challenges in proving causality include lack of direct isolation from affected tissues and infrequent CSF detection.

Conclusions:

Strong epidemiological and biological evidence suggests EV-D68 is linked to AFM.
Further comprehensive surveillance and research are crucial.
Understanding the role of EV-D68 is vital for developing therapies and prevention strategies.

Read full analysis

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