A molecular epidemiology of invasive Group A Streptococcus (iGAS) infection detected within the Hunter New England Local Health District (HNELHD) of New South Wales (NSW), Australia from 2007 to 2017 — ASN Events

A molecular epidemiology of invasive Group A Streptococcus (iGAS) infection detected within the Hunter New England Local Health District (HNELHD) of New South Wales (NSW), Australia from 2007 to 2017 (#134)

Pappu K Mandal 1 , Trent A J Butler 2 , Emily Green 1 , Kirsten M Williamson 3 , Sebastiaan Van Hal 4 , Hemalatha Varadhan 1
  1. Microbiology, NSW Health Pathology, John Hunter Hospital, New Lambton Heights, New South Wales, Australia
  2. Molecular Medicine, NSW Health Pathology, John Hunter Hospital, New Lambton Heights, New South Wales, Australia
  3. Hunter New England Population Health, Hunter New England Local Health District, Newcastle, New South Wales, Australia
  4. Infectious Diseases and Microbiology, NSW Health Pathology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia

Invasive Group A Streptococcal infection (iGAS) is an uncommon but serious infection with reported case fatality rates of up to 15%. The incidence of GAS bacteraemia in the HNELHD has gradually increased over the last two decades; however, there remains a scarcity of reports on the molecular epidemiology of iGAS strains found within the region. To better understand iGAS infections occurring within the HNELHD region, we performed whole genome sequencing of 181 iGAS isolates collected from 2007 to 2017. 54 different emm types associated with iGAS infections were detected during the period. Type emm1 was dominant, followed by emm28, emm89, emm3.1, emm12, and emm4, whilst the other emm-types were sporadically detected. The M1UK variant of emm1 was detected from 2013, and 60% in 2017 was M1UK. Virulence genes fbb54, lmb, scpA/scpB, ides/mac, mf/spd, ska, and slo were detected across all strains in our collection. All strains but emm4, emm22, and emm89 consistedĀ hasA and hasB. All except one strain possessed speB, while all but emm4 strains contained speG. Different emm types differed in the pattern and quantity of additional exotoxin-coding genes. Notably, emm1 consisted of a distinct fct-type pili (fctA, fctB, lepA, and srtC1), and a gene encoding complement inhibitor (sic), which were absent in other emm-types. 5.5% of our isolates harboured tetM, and 2.2% had either ermA or ermB. Overall, our findings contribute rich information on molecular epidemiology of iGAS and serve as a useful guide for future iGAS surveillance to investigate outbreaks or strain emergence inĀ  HNELHD region.

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