BackgroundEnterovirus D68 (EV-D68) has historically been a sporadic disease, causing occasional small outbreaks of generally mild infection. In recent years, there has been evidence of an increase in EV-D68 infections globally. Large outbreaks of EV-D68, with thousands of cases, occurred in the United States, Canada and Europe in 2014. The outbreaks were associated temporally and geographically with an increase in clusters of acute flaccid myelitis (AFM). Aims: We aimed to evaluate a causal association between EV-D68 and AFM. Methods: Using data from the published and grey literature, we applied the Bradford Hill criteria, a set of nine principles applied to examine causality, to evaluate the relationship between EV-D68 and AFM. Based on available evidence, we defined the Bradford Hill Criteria as being not met, or met minimally, partially or fully. Results: Available evidence applied to EV-D68 and AFM showed that six of the Bradford Hill criteria were fully met and two were partially met. The criterion of biological gradient was minimally met. The incidence of EV-D68 infections is increasing world-wide. Phylogenetic epidemiology showed diversification from the original Fermon and Rhyne strains since the year 2000, with evolution of a genetically distinct outbreak strain, clade B1. Clade B1, but not older strains, is associated with AFM and is neuropathic in animal models. Conclusion: While more research is needed on dose–response relationship, application of the Bradford Hill criteria supported a causal relationship between EV-D68 and AFM.
Superspreading events have characterised previous epidemics of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) infections. Using contact tracing data, we identified and characterized SARS-CoV-2 clusters in Hong Kong. Given a superspreading threshold of 6-8 secondary cases, we identified 5-7 probable superspreading events and evidence of substantial overdispersion in transmissibility, and estimated that 20% of cases were responsible for 80% of local transmission. Among terminal cluster cases, 27% (45/167) ended in quarantine. Social exposures produced a greater number of secondary cases compared to family or work exposures (p<0.001) while delays between symptom onset and isolation did not reliably predict the number of individual secondary cases or resulting cluster sizes. Public health authorities should focus on rapid tracing and quarantine of contacts, along with physical distancing to prevent superspreading events in high-risk social environments.
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