scholarly journals Erratum for Cornick et al., “Epidemiological and Molecular Characterization of an Invasive Group A Streptococcus emm32.2 Outbreak”

2018 ◽  
Vol 56 (9) ◽  
Author(s):  
Jennifer E. Cornick ◽  
Anmol M. Kiran ◽  
Roberto Vivancos ◽  
Jon Van Aartsen ◽  
Jenny Clarke ◽  
...  
Keyword(s):  
Molecular Characterization ◽  
Group A Streptococcus ◽  
Invasive Group ◽  
Group A

scholarly journals Molecular Characterization of a Strain of Group A Streptococcus Isolated from a Patient with a Psoas Abscess

2003 ◽  
Vol 41 (10) ◽  
pp. 4888-4891 ◽  
Author(s):  
S. K. P. Lau ◽  
P. C. Y. Woo ◽  
T.-c. Yim ◽  
A. P. C. To ◽  
K.-y. Yuen
Keyword(s):  
Molecular Characterization ◽  
Group A Streptococcus ◽  
Psoas Abscess ◽  
Group A

scholarly journals Prevalence and Characterization of Invasive Isolates of Streptococcus pyogenes with Reduced Susceptibility to Fluoroquinolones

2005 ◽  
Vol 49 (5) ◽  
pp. 2130-2132 ◽  
Author(s):  
Jeff Powis ◽  
Allison McGeer ◽  
Carla Duncan ◽  
Ryan Goren ◽  
Joyce C. S. de Azavedo ◽  
...  
Keyword(s):  
Streptococcus Pyogenes ◽  
Susceptibility Testing ◽  
Group A Streptococcus ◽  
Invasive Group ◽  
Group A

ABSTRACT Fluoroquinolone susceptibility testing was performed on invasive group A streptococcus isolates from 1992-1993 and 2003 from Ontario, Canada. None were nonsusceptible to levofloxacin. Two of 153 (1.3%) from 1992-1993 and 7 of 160 (4.4%) from 2003 had a levofloxacin MIC of 2 μg/ml; all nine had parC mutations, and eight were serotype M6.

scholarly journals Epidemiological and Molecular Characterization of an Invasive Group A Streptococcusemm32.2 Outbreak

2017 ◽  
Vol 55 (6) ◽  
pp. 1837-1846 ◽  
Author(s):  
Jennifer E. Cornick ◽  
Anmol M. Kiran ◽  
Roberto Vivancos ◽  
Jon Van Aartsen ◽  
Jenny Clarke ◽  
...  
Keyword(s):  
Group A Streptococcus ◽  
Adult Population ◽  
Sequencing Analysis ◽  
Invasive Group ◽  
Disadvantaged Population ◽  
Specific Subset ◽  
Time Period ◽  
Case Comparison ◽  
Group A

ABSTRACTAnemm32.2 invasive group A streptococcus (iGAS) outbreak occurred in Liverpool from January 2010 to September 2012. This genotype had not previously been identified in Liverpool, but was responsible for 32% (14/44) of all iGAS cases reported during this time period. We performed a case-case comparison ofemm32.2 iGAS cases with non-emm32.2 control iGAS cases identified in the Liverpool population over the same time period to assess patient risk factors foremm32.2 iGAS infection. Theemm32.2 iGAS cases were confined to the adult population. We show that homelessness, intravenous drug use, and alcohol abuse predisposed patients toemm32.2 iGAS disease; however, no obvious epidemiological linkage between the patients withemm32.2 iGAS could be identified. Comparative whole-genome sequencing analysis ofemm32.2 iGAS and non-emm32.2 control isolates was also performed to identify pathogen factors which might have driven the outbreak. We identified 19 genes, five of which had previously been implicated in virulence, which were present in all of theemm32.2 iGAS isolates but not present in any of the non-emm32.2 control isolates. We report that a novelemm32.2 genotype emerged in Liverpool in 2010 and identified a specific subset of genes, which could have allowed this novelemm32.2 genotype to persist in a disadvantaged population in the region over a 3-year period.

scholarly journals Identification and Characterization of Bicistronic speB and prsA Gene Expression in the Group A Streptococcus

2006 ◽  
Vol 188 (21) ◽  
pp. 7626-7634 ◽  
Author(s):  
Yongsheng Ma ◽  
Amy E. Bryant ◽  
Dan B. Salmi ◽  
Susan M. Hayes-Schroer ◽  
Eric McIndoo ◽  
...  
Keyword(s):  
Group A Streptococcus ◽  
Genetic Regulation ◽  
Active Form ◽  
Prolyl Isomerase ◽  
Peptidyl Prolyl Isomerase ◽  
Invasive Group ◽  
Genes Encoding ◽  
Group A ◽  
Streptococcal Pyrogenic Exotoxin B

ABSTRACT Severe, invasive group A streptococcal infections have reemerged worldwide, and extracellular toxins, including streptococcal pyrogenic exotoxin B (SpeB), have been implicated in pathogenesis. The genetic regulation of SpeB is not fully understood, and the mechanisms involved in the processing of the protoxin to its enzymatically active form have not been definitively established. The present work demonstrated that the genes encoding SpeB (speB) and a peptidyl-prolyl isomerase (prsA) constitute an operon with transcription initiated from two promoters upstream of speB. Further, the speB-prsA operon was transcribed as a bicistronic mRNA. This finding is in contrast to the generally accepted notion that speB is transcribed only as a monocistronic gene. In addition, prsA has its own promoter, and transcription from this promoter starts in early log phase, prior to the transcription of speB. Genomic disruption of prsA decreased the production of enzymatically active SpeB but not the level of the pro-SpeB zymogen. Taken together, these results demonstrate that prsA is required for production of fully mature, enzymatically active SpeB.

Molecular characterization of four Group A Streptococcus causing invasive infection in a short time

2021 ◽  
Vol 39 (3) ◽  
pp. 158-159
Author(s):  
Alba Bellés Bellés ◽  
Pilar Villalón Panzano ◽  
Mar Miralbés Torner ◽  
Albert Bernet Sánchez
Keyword(s):  
Molecular Characterization ◽  
Group A Streptococcus ◽  
Invasive Infection ◽  
Group A ◽  
Short Time

Bilateral periorbital necrotising fasciitis associated with invasive group: a Streptococcus infection

2020 ◽  
Vol 13 (12) ◽  
pp. e236800
Author(s):  
Grace Anne McCabe ◽  
Thomas Hardy ◽  
Thomas Gordon Campbell
Keyword(s):  
Group A Streptococcus ◽  
Early Recognition ◽  
Skin Grafting ◽  
Final Diagnosis ◽  
Necrotising Fasciitis ◽  
Invasive Group ◽  
Group A ◽  
Tissue Microscopy ◽  
Periorbital Swelling ◽  
Multidisciplinary Teamwork

A previously independent 56-year-old immunocompetent woman presented with septic shock in the setting of periorbital swelling and diffuse infiltrates on chest imaging. Blood cultures were positive for growth of group A Streptococcus (GAS). Broad spectrum antimicrobials were initiated with the inclusion of the antitoxin agent clindamycin. Necrosis of periorbital tissue was noted and surgical consultation was obtained. Débridement of both eyelids with skin grafting was performed. GAS was isolated from wound cultures and also observed on periorbital tissue microscopy. The final diagnosis was bilateral periorbital necrotising fasciitis (PONF) associated with invasive GAS infection. The patient had a prolonged intensive care unit course with input from multiple specialist teams. This case demonstrates the importance of early recognition and treatment of PONF, the profound systemic morbidity caused by these infections, and illustrates successful multidisciplinary teamwork.

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