Background: A group A Streptococcus (GAS) lineage of genotype emm3, sequence type 15 (ST15) was associated with a 6 month upsurge in invasive GAS disease in the UK. The epidemic lineage (Lineage C) had lost 2 typical emm3 prophages, Φ315.1 and Φ315.2 associated with the superantigen ssa, but gained a different prophage (ΦUK-M3.1) associated with a different superantigen, speC and a DNAse spd1. Methods and Results: The presence of speC and spd1 in Lineage C ST15 strains enhanced both in vitro mitogenic and DNase activities over non-Lineage C ST15 strains. Invasive disease models in Galleria mellonella and SPEC-sensitive transgenic mice, revealed no difference in overall invasiveness of Lineage C ST15 strains compared with non-Lineage C ST15 strains, consistent with clinical and epidemiological analysis. Lineage C strains did however markedly prolong murine nasal infection with enhanced nasal and airborne shedding compared with non-Lineage C strains. Deletion of speC or spd1 in 2 Lineage C strains identified a possible role for spd1 in airborne shedding from the murine nasopharynx. Conclusions: Nasopharyngeal infection and shedding of Lineage C strains was enhanced compared with non-Lineage C strains and this was, in part, mediated by the gain of the DNase spd1 through prophage acquisition.
Bibliographical notePublisher Copyright:
© 2017 The Author(s). Published with license by Taylor & Francis © 2017, © Baharak Afshar, Claire E. Turner, Theresa L. Lamgni, Ken C. Smith, Ali Al-Shahib, Anthony Underwood, Matthew T. G. Holden, Androulla Efstratiou, and Shiranee Sriskandan.
- Streptococcus pyogenes
- epidemic upsurge
- genotype emm3
- group A Streptococcus
- invasive group A streptococcal disease
- nasopharyngeal infection
- serotype M3