Clonal basis for resurgence of serious Streptococcus pyogenes disease in the 1980s

P. P. Cleary; P. M. Schlievert; J. P. Handley; M. H. Kim; A. R. Hauser; E. L. Kaplan; A. Wlazlo

doi:10.1016/0140-6736(92)90339-5

Clonal basis for resurgence of serious Streptococcus pyogenes disease in the 1980s

P. P. Cleary^*, P. M. Schlievert, J. P. Handley, M. H. Kim, A. R. Hauser, E. L. Kaplan, A. Wlazlo

^*Corresponding author for this work

Microbiology-Immunology

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Abstract

During the 1980s there was a resurgence of serious Streptococcus pyogenes infections with complications, including rheumatic fever, sepsis, severe soft-tissue invasion, and toxic-shock-like syndrome (TSLS). We have investigated the suggested association between expression of a scarlet fever toxin, SPE A, and systemic toxicity, and the possibility that a new highly virulent clone of S pyogenes has emerged and spread world wide. We studied serotype M1 strains, the serotype most commonly associated with serious complications. 19 isolates from patients with sepsis, with or without TSLS, and 48 from patients with uncomplicated pharyngitis or superficial skin infection were subjected to restriction-enzyme digestion and electrophoresis; 56 isolates (19 serious, 37 uncomplicated disease) were then examined by hybridisation to an speA gene probe. 17 (90%) of the 19 serious-disease isolates had a characteristic ("invasive", I) restriction-fragment profile and were positive for the speA gene. Significantly lower proportions of the isolates from patients with uncomplicated disease had the I profile (21/48 [44%]; p=0·0035) and speA (20/37 [54%]; p<0·001). These findings suggest that the strains from patients with serious disease are a unique clone, which became the predominant cause of severe streptococcal infections in the United States and elsewhere in the late 1980s.

Original language	English (US)
Pages (from-to)	518-521
Number of pages	4
Journal	The Lancet
Volume	339
Issue number	8792
DOIs	https://doi.org/10.1016/0140-6736(92)90339-5
State	Published - Feb 29 1992

Funding

toxin gene. Although our results show a link between these genotypic changes and the epidemiological spread, we cannot conclude that those changes enhanced the dissemination of the highly virulent clone through human populations. SPE A in vitro so invasiveInvasive strains that have the speA gene do not uniformly express (unpublished), potential may not be related to possession of the gene. Our findings are consistent with the possibility that invasive genes are horizontally transmissible between members of the species. The speA gene is carried by a temperate bacteriophage,15 and bacteriophages are the most likely vehicle of transmission. Infection and lysogenisation of other serotypes could account for their association with invasive disease in this outbreak. We thank Mr Dwight Johnson for serotyping S pyogenes strains and Mrs Helen Pederson for preparing the paper. This study was supported by grants from the National Institutes of Health, AI16722(PC), HL36611(PS), and the Emma B. Howe Foundation (E. L. K.). REFERENCES

ASJC Scopus subject areas

General Medicine

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title = "Clonal basis for resurgence of serious Streptococcus pyogenes disease in the 1980s",

abstract = "During the 1980s there was a resurgence of serious Streptococcus pyogenes infections with complications, including rheumatic fever, sepsis, severe soft-tissue invasion, and toxic-shock-like syndrome (TSLS). We have investigated the suggested association between expression of a scarlet fever toxin, SPE A, and systemic toxicity, and the possibility that a new highly virulent clone of S pyogenes has emerged and spread world wide. We studied serotype M1 strains, the serotype most commonly associated with serious complications. 19 isolates from patients with sepsis, with or without TSLS, and 48 from patients with uncomplicated pharyngitis or superficial skin infection were subjected to restriction-enzyme digestion and electrophoresis; 56 isolates (19 serious, 37 uncomplicated disease) were then examined by hybridisation to an speA gene probe. 17 (90%) of the 19 serious-disease isolates had a characteristic ({"}invasive{"}, I) restriction-fragment profile and were positive for the speA gene. Significantly lower proportions of the isolates from patients with uncomplicated disease had the I profile (21/48 [44%]; p=0·0035) and speA (20/37 [54%]; p<0·001). These findings suggest that the strains from patients with serious disease are a unique clone, which became the predominant cause of severe streptococcal infections in the United States and elsewhere in the late 1980s.",

author = "Cleary, {P. P.} and Schlievert, {P. M.} and Handley, {J. P.} and Kim, {M. H.} and Hauser, {A. R.} and Kaplan, {E. L.} and A. Wlazlo",

note = "Funding Information: toxin gene. Although our results show a link between these genotypic changes and the epidemiological spread, we cannot conclude that those changes enhanced the dissemination of the highly virulent clone through human populations. SPE A in vitro so invasiveInvasive strains that have the speA gene do not uniformly express (unpublished), potential may not be related to possession of the gene. Our findings are consistent with the possibility that invasive genes are horizontally transmissible between members of the species. The speA gene is carried by a temperate bacteriophage,15 and bacteriophages are the most likely vehicle of transmission. Infection and lysogenisation of other serotypes could account for their association with invasive disease in this outbreak. We thank Mr Dwight Johnson for serotyping S pyogenes strains and Mrs Helen Pederson for preparing the paper. This study was supported by grants from the National Institutes of Health, AI16722(PC), HL36611(PS), and the Emma B. Howe Foundation (E. L. K.). REFERENCES Copyright: Copyright 2014 Elsevier B.V., All rights reserved.",

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N1 - Funding Information: toxin gene. Although our results show a link between these genotypic changes and the epidemiological spread, we cannot conclude that those changes enhanced the dissemination of the highly virulent clone through human populations. SPE A in vitro so invasiveInvasive strains that have the speA gene do not uniformly express (unpublished), potential may not be related to possession of the gene. Our findings are consistent with the possibility that invasive genes are horizontally transmissible between members of the species. The speA gene is carried by a temperate bacteriophage,15 and bacteriophages are the most likely vehicle of transmission. Infection and lysogenisation of other serotypes could account for their association with invasive disease in this outbreak. We thank Mr Dwight Johnson for serotyping S pyogenes strains and Mrs Helen Pederson for preparing the paper. This study was supported by grants from the National Institutes of Health, AI16722(PC), HL36611(PS), and the Emma B. Howe Foundation (E. L. K.). REFERENCES Copyright: Copyright 2014 Elsevier B.V., All rights reserved.

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N2 - During the 1980s there was a resurgence of serious Streptococcus pyogenes infections with complications, including rheumatic fever, sepsis, severe soft-tissue invasion, and toxic-shock-like syndrome (TSLS). We have investigated the suggested association between expression of a scarlet fever toxin, SPE A, and systemic toxicity, and the possibility that a new highly virulent clone of S pyogenes has emerged and spread world wide. We studied serotype M1 strains, the serotype most commonly associated with serious complications. 19 isolates from patients with sepsis, with or without TSLS, and 48 from patients with uncomplicated pharyngitis or superficial skin infection were subjected to restriction-enzyme digestion and electrophoresis; 56 isolates (19 serious, 37 uncomplicated disease) were then examined by hybridisation to an speA gene probe. 17 (90%) of the 19 serious-disease isolates had a characteristic ("invasive", I) restriction-fragment profile and were positive for the speA gene. Significantly lower proportions of the isolates from patients with uncomplicated disease had the I profile (21/48 [44%]; p=0·0035) and speA (20/37 [54%]; p<0·001). These findings suggest that the strains from patients with serious disease are a unique clone, which became the predominant cause of severe streptococcal infections in the United States and elsewhere in the late 1980s.

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Clonal basis for resurgence of serious Streptococcus pyogenes disease in the 1980s

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