Comparative Prevalence of Superantigen Genes in Staphylococcus aureus Isolates Causing Sepsis With and Without Septic Shock

Ferry, Tristan; Thomas, Damien; Genestier, Anne-Laure; Bes, Michèle; Lina, Gérard; Vandenesch, François; Étienne, Jérôme

doi:10.1086/432798

Cited by 126 publications

(113 citation statements)

References 32 publications

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“…These results appeared similar somewhat to results reported by Ferry et al [42] who showed that 84% of the S. aureus clinical isolates harbored at least one toxin gene and results by Morandi et al [43] who reported that 79% of S. aureus from dairy products harbored at least one toxin gene. Further, Demir et al [44] reported that 65.8% of the clinical isolates exhibited at least one toxin gene.…”

Section: Discussionsupporting

confidence: 90%

Antibiograms, toxin profiling and molecular typing of Staphylococcus aureus isolates from two tertiary hospitals in Jordan

Jaradat

Hamdan

Hayajneh

et al. 2017

J Infect Dev Ctries

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Introduction: Methicillin-resistant Staphylococcus aureus (MRSA) is a major cause of hospital-associated infections. This study was undertaken to investigate toxin profiles as well as antibiotic resistance patterns of S. aureus isolates form two tertiary hospitals in Jordan. Methodology: A total of 250 S. aureus isolates from clinical samples of two tertiary hospitals were analyzed for the presence of the mecA, vanA, vanB, and 16 Staphylococcus toxin encoding genes using PCR. The isolates were further tested for antimicrobial sensitivities using the disc diffusion method. DNA from all the isolates were fingerprinted by coa gene Restriction Fragment Length Polymorphism (RFLP) to study relationships between isolates from the two hospitals. Results: 73.2% of the isolates contained the mecA gene and thus were designated MRSA. All MRSA isolates showed high levels of resistance to many of the antibiotics compared to those of MSSA. All MRSA isolates were susceptible to vancomycin and teicoplanin while all MSSA isolates were susceptible to nitrofurantoin, teicoplanin, vancomycin, cefoxitin, clindamycin, erythromycin and gentamycin. The isolates exhibited high prevalence of the toxin genes and none of the isolates contained less than 4 genes with one isolate contained 14 genes with no apparent differences in gene profiles among MRSA and MSSA. About 60% of the isolates contained 12 to 13 toxin genes and were isolated either from pus or blood. Conclusion: Antibiograms of the MRSA isolates were significantly different from MSSA antibiograms while there were no apparent differences in the toxin genes profiles. Further, coagulase gene RFLP of the isolates showed that the isolates are very heterogenic.

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Section: Discussionsupporting

confidence: 90%

Antibiograms, toxin profiling and molecular typing of Staphylococcus aureus isolates from two tertiary hospitals in Jordan

Jaradat

Hamdan

Hayajneh

et al. 2017

J Infect Dev Ctries

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“…Despite this, they are not a prominent cause of toxic shock syndrome (4,11,25) but their presence appears to be associated mainly with symptom-free carriage and inversely correlated with the severity of S. aureus infection (12,26). Astonishingly, neutralizing anti-egc serum Abs are very uncommon in healthy individuals (18).…”

Section: Discussionmentioning

confidence: 99%

“…However, they appear to cause toxic shock only very rarely (11). In fact, egc SAgs are significantly more frequent in commensal strains than in invasive isolates, and their presence is negatively correlated with severity of S. aureus sepsis (12,13). Because of this, it was suggested that SAgs might differ in their pro-inflammatory potential, and Dauwalder et al (14) reported that in PBMC from healthy donors the non-egc SAg SEA induces a stronger Th1-response than the egc SAg SEG.…”

mentioning

confidence: 99%

Immune Cell Activation by Enterotoxin Gene Cluster (egc)-Encoded and Non-egc Superantigens from Staphylococcus aureus

Grumann

Scharf

Holtfreter

et al. 2008

The Journal of Immunology

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The species Staphylococcus aureus harbors 19 superantigen gene loci, six of which are located in the enterotoxin gene cluster (egc). Although these egc superantigens are far more prevalent in clinical S. aureus isolates than non-egc superantigens, they are not a prominent cause of toxic shock. Moreover, neutralizing Abs against egc superantigens are very rare, even among carriers of egc-positive S. aureus strains. In search of an explanation, we have tested two non-exclusive hypotheses: 1) egc and non-egc superantigens have unique intrinsic properties and drive the immune system into different directions and 2) egc and non-egc superantigens are released by S. aureus under different conditions, which shape the immune response. A comparison of three egc (SEI, SElM, and SElO) and three non-egc superantigens (SEB, SElQ, and toxic shock syndrome toxin-1) revealed that both induced proliferation of human PBMC with comparable potency and elicited similar Th1/Th2-cytokine signatures. This was supported by gene expression analysis of PBMC stimulated with one representative superantigen from each group (SEI and SEB). They induced very similar transcriptional changes, especially of inflammation-associated gene networks, corresponding to a very strong Th1-and Th17-dominated immune response. In contrast, the regulation of superantigen release differed markedly between both superantigen groups. Egc-encoded proteins were secreted by S. aureus during exponential growth, while non-egc superantigens were released in the stationary phase. We conclude that the distinct biological behavior of egc and non-egc superantigens is not due to their intrinsic properties, which are very similar, but caused by their differential release by S. aureus. The Journal of Immunology, 2008, 181: 5054 -5061. Staphylococcus aureus is both a successful colonizer and an important pathogen in humans. These bacteria cause a wide spectrum of infectious diseases including several toxin-mediated diseases. Among the numerous toxins of S. aureus are the 19 known staphylococcal superantigens (SAgs) 3 : the toxic shock syndrome toxin (TSST-1), the staphylococcal enterotoxins (SEA-SEE, SEG-SEJ), and the staphylococcal enterotoxin-like toxins (SElK-SElR and SElU) (1-4). SAgs are the causative agents of toxic shock syndrome, and might also contribute to septic shock (3, 5). They directly cross-link conserved regions of the variable domains of the TCR ␤-chain (TCR V␤) with MHC class II molecules (outside the peptide-binding cleft) on APCs. This results in a strong stimulation of T cells that express the matching TCR V␤ element on their surface. Activated T cells respond with proliferation and massive cytokine release. In this way, SAgs activate up to 20% of all T cells. In contrast, conventional Ags only stimulate around 0.001% of T cells. They require uptake by APCs, processing into peptides, loading onto MHC-II molecules, and presentation on the cell surface, where their specific recognition is mediated by the hypervariable loops of TCR ␣-and ␤-chains.The recentl...

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“…CA-MRSA ST30 contains several genes that mediate adhesion (e.g., cna and bbp) and toxin genes (PVL and egc, which encode for at least 5 superantigens, including staphylococcal enterotoxin G, I, M, N, and O). The gene cluster egc is associated with septic shock (10). Further studies are needed to clarify the pathogenesis of community-acquired pneumonia caused by CA-MRSA.…”

Section: Lettersmentioning

confidence: 99%

Pediatric Pneumonia Death Caused by Community-acquired Methicillin-ResistantStaphylococcus aureus, Japan

Igarashi

Iijima

Fukushima

et al. 2008

Emerg. Infect. Dis.

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Comparative Prevalence of Superantigen Genes in Staphylococcus aureus Isolates Causing Sepsis With and Without Septic Shock

Abstract: Enterotoxin A (SEA) might play a key role in sea-positive S. aureus sepsis by triggering over-expression of inflammatory mediators associated with shock. Novel treatments targeting superantigens, especially the sea gene, might be beneficial in the treatment of S. aureus sepsis.

Cited by 126 publications

References 32 publications

Antibiograms, toxin profiling and molecular typing of Staphylococcus aureus isolates from two tertiary hospitals in Jordan

Antibiograms, toxin profiling and molecular typing of Staphylococcus aureus isolates from two tertiary hospitals in Jordan

Immune Cell Activation by Enterotoxin Gene Cluster (egc)-Encoded and Non-egc Superantigens from Staphylococcus aureus

Pediatric Pneumonia Death Caused by Community-acquired Methicillin-ResistantStaphylococcus aureus, Japan

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