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Group A  Streptococcus  (GAS) genotype  emm 89 is increasingly recognized as a leading cause of disease worldwide, yet factors that underlie the success of this  emm  type are unknown. Surveillance identified a sustained nationwide increase in  emm 89 invasive GAS disease in the United Kingdom, prompting longitudinal investigation of this genotype. Whole-genome sequencing revealed a recent dramatic shift in the  emm 89 population with the emergence of a new clade that increased to dominance over previous  emm 89 variants. Temporal analysis indicated that the clade arose in the early 1990s but abruptly increased in prevalence in 2008, coinciding with an increased incidence of  emm 89 infections. Although standard variable typing regions ( emm  subtype,  tee  type,  sof  type, and multilocus sequence typing [MLST]) remained unchanged, uniquely the emergent clade had undergone six distinct regions of homologous recombination across the genome compared to the rest of the sequenced  emm 89 population. Two of these regions affected known virulence factors, the hyaluronic acid capsule and the toxins NADase and streptolysin O. Unexpectedly, and in contrast to the rest of the sequenced  emm 89 population, the emergent clade-associated strains were genetically acapsular, rendering them unable to produce the hyaluronic acid capsule. The emergent clade-associated strains had also acquired an NADase/streptolysin O locus nearly identical to that found in  emm 12 and modern  emm 1 strains but different from the rest of the sequenced  emm 89 population. The emergent clade-associated strains had enhanced expression of NADase and streptolysin O. The genome remodeling in the new clade variant and the resultant altered phenotype appear to have conferred a selective advantage over other  emm 89 variants and may explain the changes observed in  emm 89 GAS epidemiology.

Emergence of a New Highly Successful Acapsular Group A Streptococcus Clade of Genotype emm 89 in the United Kingdom