The virulence factors of group A streptococcus strains isolated from invasive and non-invasive infections in Polish and German centres, 2009–2011

2017 ◽  
Vol 36 (9) ◽  
pp. 1643-1649 ◽  
Author(s):  
M. Strus ◽  
P. B. Heczko ◽  
E. Golińska ◽  
A. Tomusiak ◽  
A. Chmielarczyk ◽  
...  
2006 ◽  
Vol 55 (8) ◽  
pp. 1115-1123 ◽  
Author(s):  
Alba Rivera ◽  
Montserrat Rebollo ◽  
Elisenda Miró ◽  
Míriam Mateo ◽  
Ferran Navarro ◽  
...  

Group A streptococcus (GAS) has been described as an emerging cause of severe invasive infections. A retrospective hospital-based study was conducted, including GAS isolates causing invasive or non-invasive infections from January 1999 to June 2003 in Barcelona. Demographic and clinical information on the invasive cases was obtained from medical files. GAS isolates collected from 27 patients with invasive infections and 99 patients with non-invasive infections were characterized by emm type and subtype, superantigen (SAg) gene profile (speA–C, speF–J, speL, speM, ssa and smeZ), allelic variants of speA and smeZ genes, antibiotic susceptibility and genetic resistance determinants. The most prevalent emm type was emm1 (17.5 %), followed by emm3 (8.7 %), emm4 (8.7 %), emm12 (7.1 %) and emm28 (7.1 %). The smeZ allele and SAg gene profiles were closely associated with the emm type. The speA2, speA3 and speA4 alleles were found in emm1, emm3 and emm6 isolates, respectively. Overall, 27.8, 25.4 and 11.9 % of isolates were resistant to erythromycin, tetracycline or both agents, respectively. Reduced susceptibility to ciprofloxacin and levofloxacin (MIC 2–4 μg ml−1) was found in 3.2 % of isolates. mef(A)-positive emm types 4, 12 and 75, and erm(B)-positive emm types 11 and 25 were responsible for up to 80 % of the erythromycin-resistant isolates. No significant differences in emm-type distribution, SAg gene profile or resistance rates were found between invasive and non-invasive isolates. The SAg and antibiotic resistance genes appeared to be associated with the emm type and were independent of the disease type.


Author(s):  
Shyra Wilde ◽  
Anders F. Johnson ◽  
Christopher N. LaRock

Group A Streptococcus is an obligate human pathogen that is a major cause of infectious morbidity and mortality. It has a natural tropism for the oropharynx and skin, where it causes infections with excessive inflammation due to its expression of proinflammatory toxins and other virulence factors. Inflammation directly contributes to the severity of invasive infections, toxic shock syndrome, and the induction of severe post-infection autoimmune disease caused by autoreactive antibodies. This review discusses what is known about how the virulence factors of Group A Streptococcus induce inflammation and how this inflammation can promote disease. Understanding of streptococcal pathogenesis and the role of hyper-immune activation during infection may provide new therapeutic targets to treat the often-fatal outcome of severe disease.


Author(s):  
Tarah Lynch ◽  
Tannistha Nandi ◽  
Teenus Jayaprakash ◽  
Dan Gregson ◽  
Deirdre L Church

Background: In 2004–2005, an outbreak of impetigo occurred at a correctional facility during a sentinel outbreak of methicillin-resistant Staphylococcus aureus (MRSA) in Alberta, Canada. Next-generation sequencing (NGS) was used to characterize the group A Streptococcus (GAS) isolates and evaluate whether genomic biomarkers could distinguish between those recovered alone and those co-isolated with S. aureus. Methods: Superficial wound swabs collected from all adults with impetigo during this outbreak were cultured using standard methods. NGS was used to characterize and compare all of the GAS and S. aureus genomes. Results: Fifty-three adults were culture positive for GAS, with a subset of specimens also positive for MRSA ( n = 5) or methicillin-sensitive S. aureus ( n = 3). Seventeen additional MRSA isolates from this facility from the same time frame (no GAS co-isolates) were also included. All 78 bacterial genomes were analyzed for the presence of known virulence factors, plasmids, and antimicrobial resistance (AMR) genes. Among the GAS isolates were 12 emm­ types, the most common being 41.2 ( n = 27; 51%). GAS genomes were phylogenetically compared with local and public datasets of invasive and non-invasive isolates. GAS genomes had diverse profiles for virulence factors, plasmids, and AMR genes. Pangenome analysis did not identify horizontally transferred genes in the co-infection versus single infections. Conclusions: GAS recovered from invasive and non-invasive sources were not genetically distinguishable. Virulence factors, plasmids, and AMR profiles grouped by emm­­ type, and no genetic changes were identified that predict co-infection or horizontal gene transfer between GAS and S. aureus.


2018 ◽  
Vol 86 (11) ◽  
Author(s):  
Paul E. Bernard ◽  
Priyanka Kachroo ◽  
Luchang Zhu ◽  
Stephen B. Beres ◽  
Jesus M. Eraso ◽  
...  

ABSTRACTSerotype M28 group A streptococcus (GAS) is a common cause of infections such as pharyngitis (“strep throat”) and necrotizing fasciitis (“flesh-eating” disease). Relatively little is known about the molecular mechanisms underpinning M28 GAS pathogenesis. Whole-genome sequencing studies of M28 GAS strains recovered from patients with invasive infections found an unexpectedly high number of missense (amino acid-changing) and nonsense (protein-truncating) polymorphisms inrocA(regulatorofCov), leading us to hypothesize that altered RocA activity contributes to M28 GAS molecular pathogenesis. To test this hypothesis, an isogenicrocAdeletion mutant strain was created. Transcriptome sequencing (RNA-seq) analysis revealed that RocA inactivation significantly alters the level of transcripts for 427 and 323 genes at mid-exponential and early stationary growth phases, respectively, including genes for 41 transcription regulators and 21 virulence factors. In contrast, RocA transcriptomes from other GAS M protein serotypes are much smaller and include fewer transcription regulators. TherocAmutant strain had significantly increased secreted activity of multiple virulence factors and grew to significantly higher colony counts under acid stressin vitro. RocA inactivation also significantly increased GAS virulence in a mouse model of necrotizing myositis. Our results demonstrate that RocA is an important regulator of transcription regulators and virulence factors in M28 GAS and raise the possibility that naturally occurring polymorphisms inrocAin some fashion contribute to human invasive infections caused by M28 GAS strains.


2021 ◽  
Vol 14 (4) ◽  
pp. e241339
Author(s):  
Kaori Amari ◽  
Masaki Tago ◽  
Naoko E Katsuki ◽  
Shu-ichi Yamashita

We herein report three cases of group A Streptococcus (GAS) infection in a family. Patient 1, a 50-year-old woman, was transferred to our hospital in shock with acute respiratory distress syndrome, swelling in the right neck and erythemata on both lower extremities. She required intubation because of laryngeal oedema. At the same time, patient 2, a 48-year-old man, was admitted because of septic shock, pneumonia and a pulmonary abscess. Five days later, patient 3, a 91-year-old woman, visited our clinic with bloody stool. All three patients were cured by antibiotics, and GAS was detected by specimen cultures. During these patients’ clinical course, an 84-year-old woman was found dead at home after having been diagnosed with type A influenza. All four patients lived in the same apartment. The GAS genotypes detected in the first three patients were identical. When treating patients with GAS, appropriate management of close contacts is mandatory.


2011 ◽  
Vol 60 (3) ◽  
pp. 187-201 ◽  
Author(s):  
ANNA L. BOREK ◽  
JOANNA WILEMSKA ◽  
RADOSŁAW IZDEBSKI ◽  
WALERIA HRYNIEWICZ ◽  
IZABELA SITKIEWICZ

Streptococcus pyogenes (group A Streptococcus, GAS) is a human pathogen that causes diseases of various intensity, from mild strep throat to life threatening invasive infections and postinfectional sequelae. S. pyogenes encodes multiple, often phage encoded, virulence factors and their presence is related to severity of the disease. Acquisition of mobile genetic elements, carrying virulence factors, as phages or ICEs (integrative and cojugative elements) has been shown previously to promote selection of virulent clones. We designed the system of eight low volume multi- and one singleplex PCR reactions to detect genes encoding twenty virulence factors (spd3, sdc, sdaB, sdaD, speB, spyCEP, scpA, mac, sic, speL, K, M, C, I, A, H, G, J, smeZ and ssa) and twenty one phage and ICE integration sites described so far for S. pyogenes. Classification of strains based on the phage and virulence factors absence or presence, correlates with PFGE MLST and emm typing results. We developed a novel, fast and cost effective system that can be used to detect GAS virulence factors. Moreover, this system may become an alternative and effective system to differentiate between GAS strains.


2003 ◽  
Vol 51 (1) ◽  
pp. 123-134 ◽  
Author(s):  
Ramy K. Aziz ◽  
Michael J. Pabst ◽  
Arthur Jeng ◽  
Rita Kansal ◽  
Donald. E. Low ◽  
...  

2013 ◽  
Vol 81 (11) ◽  
pp. 4121-4127 ◽  
Author(s):  
Ayelet Michael-Gayego ◽  
Mary Dan-Goor ◽  
Joseph Jaffe ◽  
Carlos Hidalgo-Grass ◽  
Allon E. Moses

ABSTRACTGroup G beta-hemolytic streptococcus (GGS) strains cause severe invasive infections, mostly in patients with comorbidities. GGS is known to possess virulence factors similar to those of its more virulent counterpart group A streptococcus (GAS). A streptococcal invasion locus,sil, was identified in GAS.silencodes a competence-stimulating peptide named SilCR that activates bacterial quorum sensing and has the ability to attenuate virulence in GAS infections. We found thatsilis present in most GGS strains (82%) but in only 25% of GAS strains, with a similar gene arrangement. GGS strains that containedsilexpressed the SilCR peptide and secreted it into the growth medium. In a modified murine model of GGS soft tissue infection, GGS grown in the presence of SilCR caused a milder disease than GGS grown in the absence of SilCR. To further study the role of the peptide in bacterial virulence attenuation, we vaccinated mice with SilCR to produce specific anti-SilCR antibodies. Vaccinated mice developed a significantly more severe illness than nonvaccinated mice. Our results indicate that thesillocus is much more prevalent among the less virulent GGS strains than among GAS strains. GGS strains express and secrete SilCR, which has a role in attenuation of virulence in a murine model. We show that the SilCR peptide can protect mice from infection caused by GGS. Furthermore, vaccinated mice that produce specific anti-SilCR antibodies develop a significantly more severe infection. To our knowledge, this is a novel report demonstrating that specific antibodies against a bacterial component cause more severe infection by those bacteria.


Sign in / Sign up

Export Citation Format

Share Document