Genomic Characterization of Group A Streptococci Causing Pharyngitis and Invasive Disease in Colorado, USA, June 2016- April 2017.
Group A streptococcus
antimicrobial resistance
genomic cluster
invasive disease
pharyngitis
Journal
The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675
Informations de publication
Date de publication:
16 05 2022
16 05 2022
Historique:
received:
10
08
2021
accepted:
08
11
2021
pubmed:
18
11
2021
medline:
20
5
2022
entrez:
17
11
2021
Statut:
ppublish
Résumé
The genomic features and transmission link of circulating Group A Streptococcus (GAS) strains causing different disease types, such as pharyngitis and invasive disease, are not well understood. We used whole-genome sequencing to characterize GAS isolates recovered from persons with pharyngitis and invasive disease in the Denver metropolitan area from June 2016 to April 2017. The GAS isolates were cultured from 236 invasive and 417 pharyngitis infections. Whole-genome sequencing identified 34 emm types. Compared with pharyngitis isolates, invasive isolates were more likely to carry the erm family genes (23% vs 7.4%, P<.001), which confer resistance to erythromycin and clindamycin (including inducible resistance), and covS gene inactivation (7% vs 0.5%, P<.001). Whole-genome sequencing identified 97 genomic clusters (433 isolates; 2-65 isolates per cluster) that consisted of genomically closely related isolates (median single-nucleotide polymorphism=3 [interquartile range, 1-4] within cluster). Thirty genomic clusters (200 isolates; 31% of all isolates) contained both pharyngitis and invasive isolates and were found in 11 emm types. In the Denver metropolitan population, mixed disease types were commonly seen in clusters of closely related isolates, indicative of overlapping transmission networks. Antibiotic-resistance and covS inactivation was disproportionally associated with invasive disease.
Sections du résumé
BACKGROUND
The genomic features and transmission link of circulating Group A Streptococcus (GAS) strains causing different disease types, such as pharyngitis and invasive disease, are not well understood.
METHODS
We used whole-genome sequencing to characterize GAS isolates recovered from persons with pharyngitis and invasive disease in the Denver metropolitan area from June 2016 to April 2017.
RESULTS
The GAS isolates were cultured from 236 invasive and 417 pharyngitis infections. Whole-genome sequencing identified 34 emm types. Compared with pharyngitis isolates, invasive isolates were more likely to carry the erm family genes (23% vs 7.4%, P<.001), which confer resistance to erythromycin and clindamycin (including inducible resistance), and covS gene inactivation (7% vs 0.5%, P<.001). Whole-genome sequencing identified 97 genomic clusters (433 isolates; 2-65 isolates per cluster) that consisted of genomically closely related isolates (median single-nucleotide polymorphism=3 [interquartile range, 1-4] within cluster). Thirty genomic clusters (200 isolates; 31% of all isolates) contained both pharyngitis and invasive isolates and were found in 11 emm types.
CONCLUSIONS
In the Denver metropolitan population, mixed disease types were commonly seen in clusters of closely related isolates, indicative of overlapping transmission networks. Antibiotic-resistance and covS inactivation was disproportionally associated with invasive disease.
Identifiants
pubmed: 34788828
pii: 6426048
doi: 10.1093/infdis/jiab565
pmc: PMC9125432
mid: NIHMS1798262
doi:
Substances chimiques
Anti-Bacterial Agents
0
Types de publication
Journal Article
Research Support, U.S. Gov't, P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
1841-1851Subventions
Organisme : Intramural CDC HHS
ID : CC999999
Pays : United States
Informations de copyright
Published by Oxford University Press for the Infectious Diseases Society of America 2021.
Références
Mol Microbiol. 1998 Oct;30(1):209-19
pubmed: 9786197
Nat Genet. 2015 Jan;47(1):84-7
pubmed: 25401300
Clin Microbiol Infect. 2019 Jan;25(1):96-101
pubmed: 29698817
Am J Pathol. 2012 Apr;180(4):1522-34
pubmed: 22330677
Future Microbiol. 2010 Apr;5(4):623-38
pubmed: 20353302
N Engl J Med. 2009 Dec 24;361(26):2584-5
pubmed: 20032333
Clin Microbiol Infect. 2019 Feb;25(2):248.e1-248.e7
pubmed: 29783026
Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):4371-6
pubmed: 20142485
Vaccine. 2020 Feb 5;38(6):1384-1392
pubmed: 31843270
Clin Infect Dis. 2021 Mar 15;72(6):1004-1013
pubmed: 32060499
PLoS Pathog. 2011 Oct;7(10):e1002361
pubmed: 22046138
PLoS Pathog. 2006 Jan;2(1):e5
pubmed: 16446783
Bioinformatics. 2015 Nov 15;31(22):3691-3
pubmed: 26198102
Bioinformatics. 2018 Dec 15;34(24):4310-4312
pubmed: 30535304
Clin Infect Dis. 2019 Aug 16;69(5):877-883
pubmed: 30624673
Genome Biol. 2004;5(2):R12
pubmed: 14759262
Infect Genet Evol. 2020 Dec;86:104609
pubmed: 33147506
Proc Natl Acad Sci U S A. 2011 Mar 22;108(12):5039-44
pubmed: 21383167
Vaccine. 2019 Jun 6;37(26):3485-3494
pubmed: 31101422
Nat Genet. 2019 Jun;51(6):1035-1043
pubmed: 31133745
Lancet Infect Dis. 2019 Nov;19(11):1209-1218
pubmed: 31519541
mBio. 2015 Oct 06;6(5):e01378-15
pubmed: 26443457
Eur J Clin Microbiol Infect Dis. 2014 May;33(5):735-43
pubmed: 24158687
Clin Infect Dis. 2021 Dec 6;73(11):e3718-e3726
pubmed: 32803254
Clin Exp Vaccine Res. 2017 Jan;6(1):45-49
pubmed: 28168173
mBio. 2015 Jul 14;6(4):e00622
pubmed: 26173696
Clin Microbiol Rev. 2014 Apr;27(2):264-301
pubmed: 24696436
Antimicrob Agents Chemother. 2007 Apr;51(4):1209-16
pubmed: 17261630
J Bacteriol. 2004 Jul;186(13):4285-94
pubmed: 15205431
Front Microbiol. 2020 Jul 24;11:1547
pubmed: 32849323
Clin Infect Dis. 2016 Aug 15;63(4):478-86
pubmed: 27105747
PLoS Pathog. 2010 Apr 01;6(4):e1000832
pubmed: 20368967
Microb Genom. 2019 Nov;5(11):
pubmed: 31755853
Sci Rep. 2015 Jul 15;5:12057
pubmed: 26174161
mBio. 2017 Sep 19;8(5):
pubmed: 28928212
Clin Infect Dis. 2020 Jun 24;71(1):201-204
pubmed: 31630171
Sci Rep. 2017 Aug 17;7(1):8554
pubmed: 28819111