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Detection of Streptococcus pyogenes M1 UK in Australia and characterization of the mutation driving enhanced expression of superantigen SpeA.

Authors :
Davies MR
Keller N
Brouwer S
Jespersen MG
Cork AJ
Hayes AJ
Pitt ME
De Oliveira DMP
Harbison-Price N
Bertolla OM
Mediati DG
Curren BF
Taiaroa G
Lacey JA
Smith HV
Fang NX
Coin LJM
Stevens K
Tong SYC
Sanderson-Smith M
Tree JJ
Irwin AD
Grimwood K
Howden BP
Jennison AV
Walker MJ
Source :
Nature communications [Nat Commun] 2023 Feb 24; Vol. 14 (1), pp. 1051. Date of Electronic Publication: 2023 Feb 24.
Publication Year :
2023

Abstract

A new variant of Streptococcus pyogenes serotype M1 (designated 'M1 <subscript>UK</subscript> ') has been reported in the United Kingdom, linked with seasonal scarlet fever surges, marked increase in invasive infections, and exhibiting enhanced expression of the superantigen SpeA. The progenitor S. pyogenes 'M1 <subscript>global</subscript> ' and M1 <subscript>UK</subscript> clones can be differentiated by 27 SNPs and 4 indels, yet the mechanism for speA upregulation is unknown. Here we investigate the previously unappreciated expansion of M1 <subscript>UK</subscript> in Australia, now isolated from the majority of serious infections caused by serotype M1 S. pyogenes. M1 <subscript>UK</subscript> sub-lineages circulating in Australia also contain a novel toxin repertoire associated with epidemic scarlet fever causing S. pyogenes in Asia. A single SNP in the 5' transcriptional leader sequence of the transfer-messenger RNA gene ssrA drives enhanced SpeA superantigen expression as a result of ssrA terminator read-through in the M1 <subscript>UK</subscript> lineage. This represents a previously unappreciated mechanism of toxin expression and urges enhanced international surveillance.<br /> (© 2023. The Author(s).)

Details

Language :
English
ISSN :
2041-1723
Volume :
14
Issue :
1
Database :
MEDLINE
Journal :
Nature communications
Publication Type :
Academic Journal
Accession number :
36828918
Full Text :
https://doi.org/10.1038/s41467-023-36717-4