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Published on: March 28, 2013
Epidemiology of invasive group A streptococcal infections in Norway 2010-2014: A retrospective cohort study
U Naseer1,2, M Steinbakk3, H Blystad3
1Domain for Environmental Health and Infectious Disease Control, Norwegian Institute of Public Health, P. O. Box 4404, Nydalen, 0403, Oslo, Norway. mohammed.umaer.naseer@fhi.no.
Abstract:
Streptococcus pyogenes or group A streptococcus (GAS) causes mild to severe infections in humans. GAS genotype emm1 is the leading cause of invasive disease worldwide. In the Nordic countries emm28 has been the dominant type since the 1980s. Recently, a resurgence of genotype emm1 was reported from Sweden. Here we present the epidemiology of invasive GAS (iGAS) infections and their association with emm-types in Norway from 2010-2014. We retrospectively collected surveillance data on antimicrobial susceptibility, multilocus sequence type and emm-type, and linked them with demographic and clinical manifestation data to calculate age and sex distributions, major emm- and sequence types and prevalence ratios (PR) on associations between emm-types and clinical manifestations. We analysed 756 iGAS cases and corresponding isolates, with overall incidence of 3.0 per 100000, median age of 59 years (range, 0-102), and male 56 %. Most frequent clinical manifestation was sepsis (49 %) followed by necrotizing fasciitis (9 %). Fifty-two different emm-types and 67 sequence types were identified, distributed into five evolutionary clusters. The most prevalent genotype was emm1 (ST28) in all years (range, 20-33 %) followed by 15 % emm28 in 2014. All isolates were susceptible to penicillin, 15 % resistant to tetracycline and <4 % resistant to erythromycin. A PR of 4.5 (95 % CI, 2.3-8.9) was calculated for emm2 and necrotizing fasciitis. All emm22 isolates were resistant to tetracycline PR 7.5 (95 % CI, 5.8-9.9). This study documented the dominance of emm1, emergence of emm89 and probable import of tetracycline resistant emm112.2 into Norway (2010-2014). Genotype fluctuations between years suggested a mutual exclusive dominance of evolutionary clades.
Insights
Invasive group A Streptococcus (GAS) infections in Norway were dominated by emm1 genotype between 2010-2014. The study also noted the emergence of emm89 and imported tetracycline-resistant emm112.2 strains.
Area of Science:
- Microbiology
- Epidemiology
- Infectious Diseases
Background:
- Streptococcus pyogenes, or group A Streptococcus (GAS), causes a spectrum of human infections.
- The emm1 genotype is a leading cause of invasive GAS (iGAS) disease globally, while emm28 has predominated in Nordic countries.
- A recent resurgence of emm1 in Sweden prompted this investigation into Norwegian iGAS epidemiology.
Purpose of the Study:
- To investigate the epidemiology of iGAS infections in Norway from 2010-2014.
- To analyze the association between emm-types and clinical manifestations of iGAS disease.
- To track antimicrobial susceptibility patterns and genotypic diversity of circulating iGAS strains.
Main Methods:
- Retrospective analysis of surveillance data for iGAS cases and isolates.
- Collection of data on antimicrobial susceptibility, multilocus sequence typing, and emm-typing.
- Linking epidemiological data with demographic and clinical manifestation information.
Main Results:
- A total of 756 iGAS cases were analyzed, with an overall incidence of 3.0 per 100,000 population.
- The emm1 genotype (ST28) was the most prevalent throughout the study period (20-33%), followed by emm28 (15% in 2014).
- Sepsis was the most common manifestation (49%), and a significant association was found between emm2 and necrotizing fasciitis (PR 4.5). Tetracycline resistance was noted in emm22 isolates (PR 7.5).
Conclusions:
- The study confirms the dominance of the emm1 genotype in Norwegian iGAS infections during 2010-2014.
- Emergence of emm89 and the probable introduction of tetracycline-resistant emm112.2 were observed.
- Fluctuations in genotype prevalence suggest potential competitive exclusion between different evolutionary clades of GAS.
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