ena-STUDY-CGR-17-03-2017-13:58:15:156-371
Epidemiological and molecular characterization of an invasive Group A Streptococcus emm32.2 outbreak
An emm32.2 invasive Group A Streptococcus (iGAS) outbreak occurred in Liverpool from January 2010 to July 2012. This genotype had not previously been identified in Liverpool, but was responsible for 32% (14/44) of all iGAS cases reported during this time period. We performed case-case comparison of emm32.2 iGAS cases with non-emm32.2 control iGAS cases identified in the Liverpool population, over the same time period to assess patient risk factors for emm32.2 iGAS infection. The emm32.2 iGAS cases were confined to the adult population, we show that homelessness, intravenous drug use and alcohol abuse predisposed patients to emm32.2 iGAS disease, however no obvious epidemiological linkage between the patients with emm32.2 iGAS could be identified. Comparative whole genome sequencing analysis of emm32.2 iGAS to non-emm32.2 control isolates was also performed to identify pathogen factors, which might have driven the outbreak. We identified 19 genes, five of which had previously been implicated in virulence, which were present in all of the emm32.2 iGAS isolates but not present in any of the non-emm32.2 control isolates. We report that a novel emm32.2 genotype emerged in Liverpool in 2010 and identified a specific subset of genes, which could have allowed this novel emm32.2 genotype to persist in a disadvantaged population in the region over a three-year period.
An emm32.2 invasive Group A Streptococcus (iGAS) outbreak occurred in Liverpool from January 2010 to July 2012. This genotype had not previously been identified in Liverpool, but was responsible for 32% (14/44) of all iGAS cases reported during this time period. We performed case-case comparison of emm32.2 iGAS cases with non-emm32.2 control iGAS cases identified in the Liverpool population, over the same time period to assess patient risk factors for emm32.2 iGAS infection. The emm32.2 iGAS cases were confined to the adult population, we show that homelessness, intravenous drug use and alcohol abuse predisposed patients to emm32.2 iGAS disease, however no obvious epidemiological linkage between the patients with emm32.2 iGAS could be identified. Comparative whole genome sequencing analysis of emm32.2 iGAS to non-emm32.2 control isolates was also performed to identify pathogen factors, which might have driven the outbreak. We identified 19 genes, five of which had previously been implicated in virulence, which were present in all of the emm32.2 iGAS isolates but not present in any of the non-emm32.2 control isolates. We report that a novel emm32.2 genotype emerged in Liverpool in 2010 and identified a specific subset of genes, which could have allowed this novel emm32.2 genotype to persist in a disadvantaged population in the region over a three-year period.