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Med Microbiol Immunol. 2018 Jun 23. doi: 10.1007/s00430-018-0546-1. [Epub ahead of print]

A clone of the emergent Streptococcus pyogenes emm89 clade responsible for a large outbreak in a post-surgery oncology unit in France.

Author information

1
INSERM, U1016, Institut Cochin, 75014, Paris, France.
2
Université Sorbonne Paris Descartes, 75014, Paris, France.
3
CNRS (UMR 8104), 75014, Paris, France.
4
Assistance Publique Hôpitaux de Paris, Service de Bactériologie, Centre National de Référence des Streptocoques, Groupe Hospitalier Paris Centre Cochin-Hôtel Dieu-Broca, 75014, Paris, France.
5
Centre de Prévention des infections associées aux soins, Assistance Publique Hôpitaux de Paris, 75014, Paris, France.
6
Unité Ecologie et Evolution de la Résistance aux Antibiotiques, Institut Pasteur, 75724, Paris, France.
7
CNRS UMR3525, Paris, 75724, France.
8
Institut Pasteur, Pôle Biomics, 75724, Paris, France.
9
GGIV Unit, Institut Pasteur, 75724, Paris, France.
10
Centre Médical de Forcilles, 77150, Lesigny, France.
11
Faculté de Médecine, APHP, Pitie-Salpétrière, Sorbonne Université, 75013, Paris, France.
12
INSERM, U1016, Institut Cochin, 75014, Paris, France. claire.poyart@aphp.fr.
13
Université Sorbonne Paris Descartes, 75014, Paris, France. claire.poyart@aphp.fr.
14
CNRS (UMR 8104), 75014, Paris, France. claire.poyart@aphp.fr.
15
Assistance Publique Hôpitaux de Paris, Service de Bactériologie, Centre National de Référence des Streptocoques, Groupe Hospitalier Paris Centre Cochin-Hôtel Dieu-Broca, 75014, Paris, France. claire.poyart@aphp.fr.

Abstract

An outbreak of nosocomial infections due to Streptococcus pyogenes (Group A Streptococcus; GAS) occurred in a post-surgery oncology unit and concerned more than 60 patients and lasted 20 months despite enhanced infection control and prophylaxis measures. All GAS strains were characterized (emm genotype, toxin gene profile and pulse-field gel electrophoresis subtype). Selected strains were sequenced and phylogenetic relationship established. Capacity to form biofilm and interaction with human pulmonary epithelial cells and macrophages were determined. Twenty-six GAS strains responsible for invasive infections (II) and 57 for non-II or colonization were isolated from patients (n = 66) or healthcare workers (n = 13). Seventy strains shared the same molecular markers and 69 the same PFGE pattern; 56 were sequenced. They all belonged to the emerging emm89 clade 3; all but 1 were clonal. Whole genome sequencing identified 43 genetic profiles with sporadic mutations in regulatory genes and acquired mutations in 2 structural genes. Except for two regulatory gene mutants, all strains tested had the same biofilm formation capacity and displayed similar adherence and invasion of pulmonary epithelial cells and phagocytosis and survival in human macrophages. This large outbreak of GAS infection in a post-surgery oncology unit, a setting that contains highly susceptible patients, arose from a strain of the emergent emm89 clade. No relationship between punctual or acquired mutations, invasive status, and strain phenotypic characteristics was found. Noteworthy, the phenotypic characteristics of this clone account for its emergence and its remarkable capacity to elicit outbreaks.

KEYWORDS:

Bacterium–cell interaction; Biofilm; Emerging clade; Group A Streptococcus; Outbreak; Phylogeny; emm89

PMID:
29936564
DOI:
10.1007/s00430-018-0546-1
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