Epidemiological and Molecular Characterization of an Invasive Group A Streptococcus
            <i>emm</i>
            32.2 Outbreak

Cornick, Jennifer; Kiran, Anmol; Vivancos, Roberto; Aartsen, Jon van; Clarke, Jenny; Bevan, Edward; Alsahag, Mansoor; Alaearts, Maaike; Bricio-Moreno, Laura; Jenkinson, Howard F.; Nobbs, Angela H.; Anson, James; Kadiolgu, Aras; French, Neil; Everett, Dean

doi:10.1128/jcm.00191-17

Cited by 12 publications

(15 citation statements)

References 38 publications

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“…Recent reports have described GAS outbreaks affecting homeless populations that were caused by strains of emm types 82, 83, 87, 101, and 114 in Canada [7], 44 in France [34], and 32 and 66 in Great Britain [35, 36]. One common theme between the current emm74 and prior emm59 epidemics, as well as in these other reports, is that the offending GAS strains belong to emm types of pattern D (skin tropism) or E (generalist, ie, both throat and skin tropism) [37, 38].…”

Section: Discussionmentioning

confidence: 99%

Canada-Wide Epidemic of emm74 Group A Streptococcus Invasive Disease

Teatero

McGeer

Tyrrell

et al. 2018

Open Forum Infectious Diseases

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BackgroundThe number of invasive group A Streptococcus (iGAS) infections due to hitherto extremely rare type emm74 strains has increased in several Canadian provinces since late 2015. We hypothesized that the cases recorded in the different provinces are linked and caused by strains of an emm74 clone that recently emerged and expanded explosively.MethodsWe analyzed both active and passive surveillance data for iGAS infections and used whole-genome sequencing to investigate the phylogenetic relationships of the emm74 strains responsible for these invasive infections country-wide.ResultsGenome analysis showed that highly clonal emm74 strains, genetically different from emm74 organisms previously circulating in Canada, were responsible for a country-wide epidemic of >160 invasive disease cases. The emerging clone belonged to multilocus sequence typing ST120. The analysis also revealed dissemination patterns of emm74 subclonal lineages across Canadian provinces. Clinical data analysis indicated that the emm74 epidemic disproportionally affected middle-aged or older male individuals. Homelessness, alcohol abuse, and intravenous drug usage were significantly associated with invasive emm74 infections.ConclusionsIn a period of 20 months, an emm74 GAS clone emerged and rapidly spread across several Canadian provinces located more than 4500 km apart, causing invasive infections primarily among disadvantaged persons.

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Section: Discussionmentioning

confidence: 99%

Canada-Wide Epidemic of emm74 Group A Streptococcus Invasive Disease

Teatero

McGeer

Tyrrell

et al. 2018

Open Forum Infectious Diseases

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“…Outbreaks of GAS disease have previously been linked to the acquisition of mobile genetic elements, such as an ongoing polyclonal emm12 and emm1 scarlet fever outbreak in Hong Kong and mainland China associated with horizontal acquisition of multidrug resistance and a superantigen-encoding prophage (6). Outbreaks of invasive GAS disease have also been associated with acquisition of, or mutations within, genotypic regulatory systems that result in increased phenotypic virulence (20,21). However, this clonal invasive GAS outbreak differs from previously reported outbreaks (6,20,21) because it was linked primarily to the acquisition of a transposable element with no obvious virulence determinant.…”

Section: Discussionmentioning

confidence: 99%

Biphasic Outbreak of Invasive Group A Streptococcus Disease in Eldercare Facility, New Zealand

Worthing¹,

Werno²,

Pink³

et al. 2020

Emerg. Infect. Dis.

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S treptococcus pyogenes, or group A Streptococcus (GAS), is a gram-positive, human-adapted opportunistic bacterial pathogen. GAS causes a wide variety of clinical manifestations, from relatively benign self-limiting infections of the nasopharynx or skin to life-threatening invasive infections such as bacteremia, pneumonia, and necrotizing fasciitis (1). The incidence of invasive GAS infections is highest among older adults (2,3), particularly those living in longterm care facilities (2,4). Outbreaks of GAS infections are often linked with distinct epidemiologic markers such as emm type (5,6). emm typing is a sequence-based method that analyzes heterogeneity in the 5′ end of the ubiquitous emm gene that encodes the Mprotein (7). Although emm typing provides useful information about the potential relatedness of outbreak isolates, whole-genome sequencing enables outbreak investigations to proceed with a far greater level of discrimination than single-gene typing of GAS isolates (8,9). For this study, we used multiple wholegenome-based approaches to examine the genetic relationships and molecular drivers of a biphasic GAS outbreak in an eldercare facility in which 14 persons became ill and 5 died. Methods Setting During winter 2014, an outbreak of invasive and noninvasive GAS disease occurred in an eldercare facility in South Island, New Zealand. The outbreak was recognized by a senior laboratory scientist who noted the sudden increase in positive blood cultures from the facility. The outbreak occurred in 2 phases. The first phase started in late May 2014 and ended when the last case-patient (a resident) was hospitalized in early June 2014. The initial 3 case-patients were admitted within 24 hours of each other, and GAS was isolated from blood or tissue cultures from all 3 case-patients. During the first phase, 6 casepatients with confirmed GAS infection were hospitalized; 5 died of presumed sepsis. Outbreak investigations and control measures were subsequently implemented and included screening staff members and residents by collecting throat swab samples and providing targeted chemoprophylaxis for residents and staff members who were in direct contact with case-patients. These interventions continued until early July 2014; however, in late July, the outbreak recurred

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“…We have previously shown that isolate 112327 is an outbreak strain with characteristics that suggest it is hypervirulent, e.g. it has 19 extra genes, five of which are associated with an increase in virulence 39 . We have shown in this current study that isolate 112327 is more virulent in an invasive bacteraemia model and produced significantly more SLO which is likely to be one of the causes of its increased capacity to cause host death.…”

Section: Discussionmentioning

confidence: 99%

“…As previously published in Cornick et al , between January 2010 to September 2012, the Respiratory and Vaccine Preventable Bacteria Reference Unit (RVPBRU) in the United Kingdom confirmed a total of 14 cases of emm type 32.2 invasive GAS in the Merseyside area. Over the same time period, 30 non- emm type 32.2 invasive GAS infections were collected alongside 20 non-invasive pharyngitis GAS isolates supplied by the Royal Liverpool University Hospitals Trust and Alder Hey Children’s Hospital 30 . The Merseyside outbreak emm type 32.2 isolates (n = 14) were selected for this study alongside a selection of non- emm type 32.2 isolates.…”

Section: Methodsmentioning

confidence: 99%

“…Despite all this however, substantial gaps still exist in our understanding of the contributory role of the variation and amount of SLO production to overall GAS pathogenesis. In order to address this, we developed a custom made ELISA to compare the production of SLO between a recently emerged hypervirulent outbreak strain (which resulted in an epidemic in Liverpool, UK, between 2010-2012) characterised as emm type 32.2 and invasive emm type 1.0. isolates 30 . Using in vivo GAS bacteraemia and novel septic arthritis models, we further investigated the role of SLO in establishing and maintaining different clinical pathotypes in vivo .…”

Section: Introductionmentioning

confidence: 99%

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Streptolysin production and activity is central toin vivopathotype and disease outcome in GAS infections

Clarke

Baltazar

Alsahag

et al. 2019

Preprint

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27Streptococcus pyogenes (GAS) is among the most diverse of all human pathogens, responsible 28 for a range of clinical manifestations, from mild superficial infections such as pharyngitis to 29 serious invasive infections such as necrotising fasciitis and sepsis. The drivers of these different 30 disease phenotypes are not known. The GAS cholesterol-dependent cytolysin, streptolysin O 31 (SLO), has well established cell and tissue destructive activity. We investigated the role of SLO 32 in determining disease outcome in vivo, by using two different clinical lineages; the recently 33 emerged hypervirulent outbreak emm type 32.2 strains, which result in sepsis, and the emm 34 type 1.0 strains which cause septic arthritis. Using clinically relevant in vivo mouse models of 35 sepsis and a novel septic arthritis model, we demonstrated that the amount and activity of SLO 36 is vital in determining the pathotype of infection. The emm32.2 strain produced large quantities 37 of highly haemolytic SLO that resulted in rapid development of sepsis. By contrast, the lower 38 levels and haemolytic activity of emm1.0 SLO led to translocation of bacteria to joints. 39 Importantly, sepsis associated strains that were attenuated by deletion or inhibition of SLO also 40 translocated to the joint, confirming the key role of SLO in determining infection niche. Our 41 findings demonstrate that SLO is key to in vivo pathotype and disease outcome. Careful 42 consideration should be given to novel therapy or vaccination strategies that target SLO. Whilst 43 neutralising SLO activity may reduce severe invasive disease, it has the potential to promote 44 chronic inflammatory conditions such as septic arthritis. 45 46 47 48 49 50 51 Group A Streptococcus (GAS), also called Streptococcus pyogenes, is a commensal of the 53 human upper respiratory tract and also an important human pathogen, accounting for over 750 54 million infections every year 1,2 . GAS is able to produce a variety of pyogenic infections that 55 range in severity and prevalence 3-5 . Diseases include pharyngitis, impetigo, cellulitis and more 56 life threating infections such as streptococcal toxic shock syndrome, necrotising fasciitis, and 57 sepsis 3,6 . The mechanisms that allow GAS to cause such diversity in disease types are 58 unknown, however a number of studies have shown that bacterial and host-specific components 59 may be involved 7 . 60 61 GAS strains are typed based on the sequence of the emm gene, which encodes the M-protein, 62 of which there are over 200 known emm types 8 . The epidemiology of GAS infections has been 63 changing globally over the last decade, with the emergence of new emm types and localised 64 outbreaks a main feature 9 . Within emm types of GAS, isolates may be causative of a range of 65 clinical outcomes, such that most lineages carry the potential for expression of a range of 66 phenotypes that may determine the course and nature of infection. Recent studies have shown 67 distinct correlations between the host niche of recovered GAS clin...

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Epidemiological and Molecular Characterization of an Invasive Group A Streptococcus emm 32.2 Outbreak

Cited by 12 publications

References 38 publications

Canada-Wide Epidemic of emm74 Group A Streptococcus Invasive Disease

Canada-Wide Epidemic of emm74 Group A Streptococcus Invasive Disease

Biphasic Outbreak of Invasive Group A Streptococcus Disease in Eldercare Facility, New Zealand

Streptolysin production and activity is central toin vivopathotype and disease outcome in GAS infections

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