A new Streptococcus pyogenes genotype (designated M1UK) emerged in 2014 in England causing an increase in scarlet fever “unprecedented in modern times.” Researchers discovered that this new genotype became dominant during this increased period of scarlet fever. This new genotype was characterized by an increased production of streptococcal pyrogenic exotoxin A (SpeA, also known as scarlet fever or erythrogenic toxin A) compared to previous isolates, according to a report in The Lancet Infectious Diseases.
The researchers analyzed changes in S. pyogenes emm1 genotypes sampled from scarlet fever and invasive disease cases in 2014-2016. The emm1 gene encodes the cell surface M virulence protein and is used for serotyping S. pyogenes isolates. Using regional (northwest London) and national (England and Wales) data, they compared genomes of 135 noninvasive and 552 invasive emm1 isolates from 2009-2016 with 2,800 global emm1 sequences.
During the increase in scarlet fever and invasive disease, emm1 S. pyogenes upper respiratory tract isolates increased significantly in northwest London during the March to May periods over 3 years from 5% of isolates in 2014 to 19% isolates in 2015 to 33% isolates in 2016. Similarly, invasive emm1 isolates collected nationally in the same period increased from 31% of isolates in 2015 to 42% in 2016 (P less than .0001). Sequences of emm1 isolates from 2009-2016 showed emergence of a new emm1 lineage (designated M1UK), which could be genotypically distinguished from pandemic emm1 isolates (M1global) by 27 single-nucleotide polymorphisms. In addition, the median SpeA protein concentration was 9 times greater among M1UK isolates than among M1global isolates. By 2016, M1UK expanded nationally to comprise 84% of all emm1 genomes tested. Dataset analysis also identified single M1UK isolates present in Denmark and the United States.
“The expansion of such a lineage within the community reservoir of S. pyogenes might be sufficient to explain England’s recent increase in invasive infection. Further research to assess the likely effects of M1UK on infection transmissibility, treatment response, disease burden, and severity is required, coupled with consideration of public health interventions to limit transmission where appropriate,” Dr. Lynskey and colleagues concluded.
The authors reported that they had no disclosures.
SOURCE: Linskey NN et al. Lancet Infect Dis. 2019. doi: 10.1016/S1473-3099(19)30446-3.