Clinical and population genomic epidemiology of invasive group A streptococcus in Scotland, 2014-2024
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Objectives
Following the COVID-19 pandemic, multiple countries reported a surge in invasive group A streptococcus (iGAS) infections. Posited explanations include reduced population immunity, increased respiratory virus co-infection, and emergence of hypervirulent GAS clones. To assess the relative contribution of these factors, we analyzed the epidemiology and genomics of 3,408 iGAS infections in Scotland.
Methods
National surveillance data from 2014–2024 were analyzed to characterize iGAS incidence. Hybrid whole genome sequencing was used to comprehensively genetically characterize 404 emm 1 isolates collected from invasive and tonsillitis infections.
Results
iGAS incidence markedly increased in late 2022 and early 2023, disproportionately affecting children and older adults. This surge was not associated with a proportional increase in bacteremia but did coincide with increased influenza and respiratory syncytial virus infections. Genomic analyses found that emm 1 post-pandemic isolates were not genetically distinct from pre-pandemic isolates in genome-wide polymorphisms, accessory genes including virulence and antimicrobial resistance determinants, mobile genetic elements, or chromosomal structural variants.
Conclusions
The post-pandemic iGAS surge in Scotland was not associated with emergence of a novel hypervirulent emm 1 clone. Instead, the epidemiologic and population genomic findings are consistent with increased host susceptibility following reduced pathogen exposure during the pandemic and increased respiratory virus co-infection as predominant contributing factors.
Highlights
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Post-COVID-19 iGAS surged disproportionately affecting children and the elderly
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The iGAS surge was associated with an overall decreased odd of bacteremia
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Peaks in influenza and RSV activity coincided with the post-pandemic iGAS surge
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Emm1 was the most prevalent emm type, accounting for 56% of the iGAS surge isolates
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Emergence of a more virulent emm 1 clone was not supported by genomic analyses