Staphylococcus aureus produces a wide variety of toxins including staphylococcal enterotoxins (SEs; SEA to SEE, SEG to SEI, SER to SET) with demonstrated emetic activity, and staphylococcal-like (SEl) proteins, which are not emetic in a primate model (SElL and SElQ) or have yet to be tested (SElJ, SElK, SElM to SElP, SElU, SElU2 and SElV). SEs and SEls have been traditionally subdivided into classical (SEA to SEE) and new (SEG to SElU2) types. All possess superantigenic activity and are encoded by accessory genetic elements, including plasmids, prophages, pathogenicity islands, vSa genomic islands, or by genes located next to the staphylococcal cassette chromosome (SCC) implicated in methicillin resistance. SEs are a major cause of food poisoning, which typically occurs after ingestion of different foods, particularly processed meat and dairy products, contaminated with S. aureus by improper handling and subsequent storage at elevated temperatures. Symptoms are of rapid onset and include nausea and violent vomiting, with or without diarrhea. The illness is usually self-limiting and only occasionally it is severe enough to warrant hospitalization. SEA is the most common cause of staphylococcal food poisoning worldwide, but the involvement of other classical SEs has been also demonstrated. Of the new SE/SEls, only SEH have clearly been associated with food poisoning. However, genes encoding novel SEs as well as SEls with untested emetic activity are widely represented in S. aureus, and their role in pathogenesis may be underestimated.

https://www.mdpi.com/2072-6651/2/7/1751/pdf

Food poisoning and Staphylococcus aureus enterotoxins.

https://waojournal.biomedcentral.com/track/pdf/10.1186/1939-4551-7-25.pdf

ICON: chronic rhinosinusitis

G. BLAIOTTA, D. ERCOLINI, C. PENNACCHIA, V. FUSCO, A. CASABURI, O. PEPE AND F. VILLANI. 2004. Aims: Evaluation of the occurrence of most known staphylococcal enterotoxin (SE) genes, egc (enterotoxin genecluster) and TSST1 (toxic shock syndrome toxin 1) gene in both coagulase-positive (CPS) and coagulase-negative(CNS) staphylococcal strains isolated from meat and dairy products.Methods and Results: Speciﬁcity and reliability of the PCR detection methods used were ascertained by usingnine reference strains of Staphylococcus (S. aureus) harbouring SE genes (seAtoseE; seG, seH, seI, seM, seJ, seN andseO) and egc (containing the following sequence of genes: seO, seM, seI, uent1, uent2, seN and seG). Of 109 wildStaphylococcus spp. strains analysed, only 11 S. aureus strains were SE and/or TSST1 PCR-positive. The last 11strains also appeared to harbour the egc. Restriction endonuclease analysis of part of the egc of both reference andwild strains showed that different variants of the egc exist. Moreover, nucleotide sequences of seG and seI indicatethat the egc of the strain AB-8802 is characterized by the presence of variants of these enterotoxins (seGv and seIv).Conclusions: The occurrence of SE genes in CNS and other non-S. aureus species isolated from Napoli-typesalami, raw water buffalo milk and natural whey cultures used for mozzarella cheese manufacturing is very rare.Signiﬁcance and Impact of the Study: During this study it was shown that at least ﬁve different egc may exist inS. aureus. A thorough study of egc polymorphism should provide further insight into the phylogenetics of the egc.Keywords: coagulase-negative staphylococci, enterotoxin gene cluster (egc), food, seGv (seG variant), seIv (seIvariant), staphylococcal enterotoxin (se) genes, Staphylococcus aureus.

https://sfamjournals.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2672.2004.02349.x

PCR detection of staphylococcal enterotoxin genes in Staphylococcus spp. strains isolated from meat and dairy products. Evidence for new variants of seG and seI in S. aureus AB-8802.

To test the hypothesis that the Staphylococcus aureus enterotoxin gene cluster (egc) can generate new enterotoxin genes by recombination, we analyzed the egc locus in a broad panel of 666 clinical isolates of S. aureus. egc was present in 63% of isolates, confirming its high prevalence. The archetypal organization of the egc locus, consisting of five enterotoxin genes plus two pseudogenes, was found in 409 of 421 egc-positive strains. The egc locus was incomplete in a few strains and occasionally harbored an insertion sequence and transposase genes. These strains may represent evolutionary intermediates of the egc locus. One strain with an atypical egc locus produced two new enterotoxins, designated SElV and SElU2, generated by (i) recombination between selm and sei, producing selv, and (ii) a limited deletion in the ϕent1-ϕent2 pseudogenes, producing selu2. Recombinant SElV and SElU2 had superantigen activity, as they specifically activated the T-cell families Vβ 6, Vβ 18, and Vβ 21 (SElV) and Vβ 13.2 and Vβ 14 (SElU2). Immunoscope analysis showed a Gaussian CDR3 size distribution of T-cell receptor Vβ chain junctional transcripts of expanded Vβ subsets in toxin-stimulated cultures, reflecting a high level of polyclonality. These data show that egc is indeed capable of generating new superantigen genes through recombination.

Staphylococcal Enterotoxin-Like Toxins U2 and V, Two New Staphylococcal Superantigens Arising from Recombination within the Enterotoxin Gene Cluster

Chronic rhinosinusitis (CRS) is presently classified into two subgroups: CRS without and CRS with nasal polyps. A variety of inflammatory mediators, including cytokines and chemokines, as well as adhesion molecules and matrix metalloproteinases, are upregulated in both subgroups of CRS; remodeling is also observed in both. However, there are also characteristic differences. Whereas CRS without nasal polyps has more neutrophilic infiltration, in CRS with nasal polyps (especially when associated with allergy/asthma) eosinophil infiltration is strikingly increased. Although several features of remodeling (eg, squamous metaplasia, basement membrane thickening, collagen deposition, hyperplasia of mucous glands, and goblet cells) are features seen in both subgroups of CRS, epithelial shedding as observed in asthma is not seen in either subgroup. Furthermore, pseudocyst formation seen in CRS with nasal polyps is not seen in CRS without nasal polyps.

Inflammatory mechanisms and remodeling in chronic rhinosinusitis and nasal polyps.

The present study was aimed at identifying a possible correlation between disease severity and colonization with superantigen-producing Staphylococcus aureus strains in patients with atopic eczema. To this end, Staphylococcus aureus strains from 91 patients with atopic eczema were screened for various staphylococcal superantigens such as SEA, SEB, SEC, SED, TSST1, the recently described enterotoxin gene cluster egc (which encodes the enterotoxins SEG, SEI, SEK, SEM, and SEO), and the see, seh, and sej loci. Swabs were taken from seven different sites in each patient. The rate of colonization with Staphylococcus aureus was 87.9%. Of those patients colonized, 35% were colonized with more than one different strain. Of the 120 genetically different strains investigated, the egc locus was found in 48.3% and the sej locus in 7.5%. The see and seh loci were not found in any strain. The presence of the classical superantigens SEA-SED or TSST1 was found in 38.3%. Overall, 71.3% of the Staphylococcus aureus-positive patients harbored at least one superantigen-producing strain on their skin. There was no difference in the prevalence of superantigens between atopic eczema patients and healthy volunteers. Moreover, there was no difference in the extent of disease expression between patients colonized by superantigen-positive Staphylococcus aureus strains and those with superantigen-negative strains as measured by the SCORAD system. However, patients colonized with Staphylococcus aureus had a significantly higher SCORAD score than those not colonized.

High prevalence of superantigens associated with the egc locus in Staphylococcus aureus isolates from patients with atopic eczema.

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High prevalence of superantigens associated with the egc locus in Staphylococcus aureus isolates from patients with atopic eczema.