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Role of Bacteria in Dermatological Infections
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Thirukannamangai Krishnan Swetha, Shunmugiah Karutha Pandian
The virulent enzymes sturdily aid survival of S. aureus by host tissue damage, whereas opsonization of S. aureus by surface expressed protein A and clumping factor helps in the evasion of host phagocytic attack. The production of hemolysins triggers the nuclear factor (NF-κB) inflammatory pathway through pore formation of targeted host cell membranes (Cogen et al., 2008). The exfoliative toxins ETA and ETB disrupt the cell-cell adhesion protein molecule desmoglein-1, which causes cutaneous blistering in SSSS (Hedrick, 2003). PVL in CA-MRSA complicates SSSIs by polymorphonuclear karyorrhexis, capillary dilation, and skin necrosis prompted by the production of severe inflammatory lesions (Dufour et al., 2002). The surface-expressed binding proteins elicit the severity of infections by promoting the invasive lifestyle of S. aureus through initial adhesion of S. aureus to host cell surface, followed by colonization and invasion (Shinji et al., 2011). Also, a novel class of virulent determinant (observed initially in CA-MRSA USA 300 clone and later in other S. aureus lineages) named arginine catabolic mobile element (ACMB) is involved in immune modulating functions such as conferring tolerance to polyamines (a nonspecific immune response), which in turn facilitate the successful survival of S. aureus by outnumbering the competitors, host colonization, and invasion (Shore et al., 2011).
Escalation of antimicrobial resistance among MRSA part 1: focus on global spread
Published in Expert Review of Anti-infective Therapy, 2023
Joseph P. Lynch, George G. Zhanel
Nearly all S. aureus strains express protein A on their surface. Protein A acts to prevent opsonization and phagocytosis [8]. S. aureus may produce numerous virulence factors that influence tissue invasion, cytotoxicity, membrane damage, and intracellular persistence [8–10]. S. aureus isolates exhibit considerable genetic diversity but specific genotypes have been associated with antimicrobial resistance (AMR) and toxin gene profiles [10,11]. More than 30 virulence factors have been reported including: Panton-Valentine leukocidin (PVL), arginine-catabolic mobile element (ACME), toxic-shock syndrome toxin-1 (tst-1), collagen adhesion and other adhesion factors (eno, fnbpA), staphylococcal enterotoxin A (sea), and myriad toxins [11,12]. Additionally, S. aureus produces biofilms that facilitate persistence and spread of the organism [11,12]. The genetic origin of S. aureus can be deduced using: pulse field gel electrophoresis (PFGE); multilocus sequence typing (MLST): Whole Genome Sequencing (WGS), S. aureus protein A (spa); accessory gene regulator (agr) allele; staphylococcus chromosomal cassette (SCC) mec typing (only for MRSA) [13–16].
Methicillin Resistant Staphylococcus aureus and public fomites: a review
Published in Pathogens and Global Health, 2020
Ziad W Jaradat, Qutaiba O Ababneh, Sherin T Sha’aban, Ayesha A Alkofahi, Duaa Assaleh, Anan Al Shara
In the United States, the USA 300 lineage is the most well-studied clonal group. It is associated with the production of high levels of cytotoxins such as α-toxin, arginine catabolic mobile element type 1 and a set of virulence genes including lukS-PV/lukF-PV, sek, and seq [16,21]. And thus, it is incriminated in most of the community-associated MRSA infections causing severe skin and soft-tissue infections [16]. USA300 has been classified as one of the highest pathogenic strains [22], as it became an increasingly common cause of health-care-associated MRSA infections as well [23]. Interestingly, a variant of the USA300 called USA300 LA is predominant in some countries in Latin America such as Columbia and Ecuador [24].
sesA, sesB, sesC, sesD, sesE, sesG, sesH, and embp genes are genetic markers that differentiate commensal isolates of Staphylococcus epidermidis from isolates that cause prosthetic joint infection
Published in Infectious Diseases, 2019
Silvestre Ortega-Peña, Carlos F. Vargas-Mendoza, Rafael Franco-Cendejas, Alejandra Aquino-Andrade, Guillermo J. Vazquez-Rosas, Gabriel Betanzos-Cabrera, Claudia Guerrero-Barajas, Janet Jan-Roblero, Sandra Rodríguez-Martínez, Mario E. Cancino-Diaz, Juan C. Cancino Diaz
Studies on the distribution and the presence of ses genes in S. epidermidis clinical isolates from pre-term infants and healthy skin isolates [18], from various sources of isolation [37] and from patients with orthopedic-device-related infections [33] show that the genes ses are highly distributed. Our results on the presence of ses genes in PJI and HS isolates showed that HS isolates have higher proportions of sesA, sesB, sesC, sesD, sesE, sesG, and sesH genes than PJI isolates (p < .05). This result suggests that ses genes can be considered as biomarkers for differentiating between commensal and PJI isolates. The high proportion of ses genes in HS isolates can be contrary to what was expected, because PJI isolates were high biofilm producers and Ses proteins are associated to the biofilm formation. We did not find a relationship between sesA, sesB, sesC, sesD, sesE, sesG, and sesH genes and the biofilm production; however, aap (sesF) gene was highly prevalent in the biofilm-producer PJI isolates suggesting that PJIs biofilm is of ica-independent type. Rohde et al. reported that PJI S. epidermidis isolates are high biofilm producers and they are aap gene positives [10]. On the other hand, it is commonly found that the differential biomarkers are more associated with clinical isolates than commensal isolates, there are scarce works that report the contrary, e.g. a high proportion in the commensal isolates of the arginine catabolic mobile element (ACME) [38] and the formate dehydrogenase gene [6] has been reported. The sesB gene is slightly more common among invasive isolates than contaminants [39]; however, the presence of the sesB gene was similar between hospital airborne S. epidermidis isolates (77.8%) and the patient isolates (88.5%) [40]. In this study, we found that the sesI gene is present only in biofilm-producer PJI isolates belonging to the B PFGE profile.