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Toxic Shock Syndrome and Other Related Severe Infections
Published in Botros Rizk, A. Mostafa Borahay, Abdel Maguid Ramzy, Clinical Diagnosis and Management of Gynecologic Emergencies, 2020
Studies have demonstrated that although about 9% of the female population is vaginally colonized with S. aureus, only 1% of women carry the toxigenic strain [101]. In fact, the presence of the bacterium is transient, often depending on menstrual timing and changes in oxygenation, iron saturation, and pH [101]. This fluctuation in bacterial colonization is also thought to be due to the lack of binding sites for S. aureus; unlike the nasal passages, vaginal mucosa lacks the cytokeratin 10 that S. aureus clumping factor B can bind [101]. Original associations between TSS and tampon use were tied to the initiation of tampon use; typically, the symptom presents toward the middle or end of the menstrual cycle after a brief period of tampon use [89]. Although the subsequent mechanism of disease progression is poorly understood, it has been suggested that this bacterial colonization is exacerbated by the aerobic exposure promoted by tampon presence and the medium provided by persistence of endometrial blood in the vaginal canal [102].
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).
Staphylococcus aureus
Published in Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward, Case Studies in Infectious Disease, 2010
Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward
The patient has an infection caused by methicillin (oxacillin)-resistant Staphylococcus aureus (MRSA). Bacteria in the genus Staphylococcus are gram-positive cocci that grow in grape-like clusters and produce the enzyme catalase (see Section 4). The genus Staphylococcus comprises some 35 species, many of which are members of the endogenous microbiota of the skin and mucous membranes of the gastrointestinal and genitourinary tracts of humans. Interestingly, a number of these species have defined habitats on the human body. Three species account for most human disease, namely S. aureus, S. epidermidis, and S. saprophyticus. Of these, S. aureus is the most pathogenic. S. aureus has a typical gram-positive cell wall that features a thick peptidoglycan layer extensively cross-linked with pentaglycine bridges. The extensive cross-linking makes the cell very resistant to drying so that staphylococci can survive on fomites (inanimate objects) for long periods of time. The wall also contains covalently bound teichoic acid and lipoteichoic acid, which is anchored in the cytoplasmic membrane. There are a number of molecules that are exposed on the cell surface. These are either anchored in the cytoplasmic membrane and traverse the cell wall to the outside or they are anchored in the wall and extend from it (Figure 1). Among the important cell surface-exposed molecules of S. aureus are various microbial surface components that recognize adhesive matrix molecules (MSCRAMMs). These components recognize and bind various extracellular matrix proteins such as fibronectin, collagen, and fibrinogen (clumping factor), and the Fc region of mammalian IgG (protein A). In addition to wall-associated clumping factor that binds solid-phase fibrinogen, S. aureus secretes coagulase, which binds soluble fibrinogen. Coagulase binds prothrombin in a 1:1 molar ratio to form a complex termed staphylothrombin, which converts fibrinogen to fibrin. Because S. aureus is the only staphylococcal species that possesses coagulase and protein A their detection serves as a method to identify the bacterium (see Section 4). MSCRAMMs facilitate invasion of keratinocytes and endothelial cells by S. aureus. Once taken up by cells, the bacteria survive in vacuoles and free in the cytoplasm where some persist for several days. Bacterial invasion results in cytotoxicity and apoptotic cell death.
Inhibition of Streptococcus mutans adhesion and biofilm formation with small-molecule inhibitors of sortase A from Juniperus chinensis
Published in Journal of Oral Microbiology, 2022
Eunji Cho, Ji-Yeon Hwang, Jae Sung Park, Daehyun Oh, Dong-Chan Oh, Hyeung-Geun Park, Jongheon Shin, Ki-Bong Oh
Gram-positive pathogenic bacteria have many surface proteins related to bacterial adherence and host invasion, which play key roles in virulence. Sortase A (SrtA) is a transpeptidase that controls anchoring of surface proteins in the peptidoglycan cell walls of Gram-positive bacteria [1]. This protein recognizes the LPXTG motif in substrates, severs the amide bond between T and G residues, and forms a covalent bond between the substrate and cell wall [2]. Because numerous Gram-positive bacteria possess genes encoding SrtA and surface proteins with sorting signals recognized by SrtA, the SrtA-mediated anchoring system is considered a universal mechanism [3]. Knockout mutants of srtA fail to display surface proteins with the LPXTG motif which leads to diminished infectiousness without impacting bacterial viability [4–6]. For example, Staphylococcus aureus srtA mutants were not able to display Spa (protein A), FnbA (fibronectin-binding protein), ClfA (clumping factor) proteins, and showed impaired infections in mice [4]. Due to these properties, SrtA is closely associated with the virulence of Gram-positive pathogens and is considered a desirable anti-virulent drug target [7].
Statins potentiate the antibacterial effect of platelets on Staphylococcus aureus
Published in Platelets, 2021
Nadji Hannachi, Pierre-Edouard Fournier, Hélène Martel, Gilbert Habib, Laurence Camoin-Jau
We used a methicillin-sensitive strain of S. aureus (P6299). This strain was obtained from the CSUR (Collection des souches de l’unité des Rickettsies, IHU Mediterranée infection, Marseille, France) and isolated from positive blood cultures from patients with IE. Identification was confirmed using Maldi-Toff mass spectrometry and the Bio Typer database (Bruker, Dresden, Germany). In order to characterize this strain, the genes coding for proteins interacting with platelet GP IIbIIIa, namely the iron-regulated surface determinant system B (IsdB), the Clumping factor A (Clf A) and the Fibronectin binding protein A (FnBP A), were identified using metagenomic next-generation sequencing (mNGS) with protein homology of 100% in blastp (https://blast.ncbi.nlm.nih.gov/Blast.cgi) compared to the reference protein sequences available in GenBank (Supp material 1). The strain was cultured on 5% sheep blood-enriched Columbia agar (COS, BioMérieux, Marcy l’Etoile, France). After 18 hours of incubation at 37°C, colonies were removed and suspended in 0.9‰ NaCl medium to obtain 3 × 108 CFU/mL.
The distinct effects of aspirin on platelet aggregation induced by infectious bacteria
Published in Platelets, 2020
Nadji Hannachi, Jean-Pierre Baudoin, Arsha Prasanth, Gilbert Habib, Laurence Camoin-Jau
Several bacterial strains, such as staphylococci, streptococci, and enterococci play pivotal roles in the etiology of IE [5,6]. These roles are based on the presence of proteins and/or receptors on the surface of these bacteria that directly or indirectly interact with platelets. S. aureus is currently considered to be the main causative agent of IE [5]. S. aureus expresses surface proteins belonging to the microbial surface components that recognize the family of adhesive matrix molecules (MSCRAMM) such as clumping factor (ClfA and ClfB) and fibronectin-binding protein (Fnbp A and FnbpB). These molecules allow bacteria to adhere to tissues and induce platelet aggregation [3,7]. Furthermore, because of the presence of coagulases, S. aureus contributes to the development of fibrino-platelet vegetation during staphylococcal endocarditis [7,8].