Abstract
Infection of the skin or throat by Streptococcus dysgalactiae subspecies equisimilis (SDSE) may result in a number of human diseases. To understand mechanisms that give rise to new genetic variants in this species, we used multi-locus sequence typing (MLST) to characterise relationships in the SDSE population from India, a country where streptococcal disease is endemic. The study revealed Indian SDSE isolates have sequence types (STs) predominantly different to those reported from other regions of the world. Emm-ST combinations in India are also largely unique. Split decomposition analysis, the presence of emm-types in unrelated clonal complexes, and analysis of phylogenetic trees based on concatenated sequences all reveal an extensive history of recombination within the population. The ratio of recombination to mutation (r/m) events (11∶1) and per site r/m ratio (41∶1) in this population is twice as high as reported for SDSE from non-endemic regions. Recombination involving the emm-gene is also more frequent than recombination involving housekeeping genes, consistent with diversification of M proteins offering selective advantages to the pathogen. Our data demonstrate that genetic recombination in endemic regions is more frequent than non-endemic regions, and gives rise to novel local SDSE variants, some of which may have increased fitness or pathogenic potential.
Highlights
Streptococcus dysgalactiae subspecies equisimilis (SDSE) is a bhaemolytic Gram-positive bacterium that typically colonises the oropharynx and skin of humans
Our findings suggest an evolutionary process in which novel genetic variants of SDSE, possibly with altered fitness or pathogenic potential, are more likely to arise in endemic regions than non-endemic regions
As recP22 is less than 90% identical to other so far known SDSE and S. pyogenes recP alleles, the allele was most likely acquired from S. agalactiae
Summary
Streptococcus dysgalactiae subspecies equisimilis (SDSE) is a bhaemolytic Gram-positive bacterium that typically colonises the oropharynx and skin of humans. Generally a less common cause of human infection, SDSE causes many of the same diseases as S. pyogenes, including pharyngitis, pyoderma, postglomerulonephritis, bacteraemia and other invasive diseases [2,3]. SDSE and S. pyogenes share in common many virulence factors that contribute to virulence, including the M-protein [7,8,9]. Nucleotide variation in emm, the gene encoding the M-protein, is used to type both SDSE and S. pyogenes at the subspecies level. More than 50 SDSE emm-genes are present in the Centre for Disease Control emm-gene database (http://www.cdc.gov/ncidod/biotech/strep/types_emm103-124.htm). Other typing methods such as vir-typing [10,11] and emm-pattern typing [12] target the locus encoding the emm-gene. Several studies have reported the emm-gene, and surrounding loci to be subject to lateral gene transfer (LGT) [13,14]
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