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Cardiology
Published in Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan, Essential Notes for Medical and Surgical Finals, 2021
Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan
Precipitated by group A Streptococcal infection. Diagnosis: based on evidence of Strep. infection (positive throat swab, raised serum anti-streptolysin titre, etc) and on the Revised Jones Criteria which require 2 major, or 1 major + 2 minor criteria to be present for diagnosis.
Role of Bacteria in Blood Infections
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Kannan Balaji, Gnanasekaran JebaMercy, K. Balamurugan
In addition to its effect on erythrocytes, extracellular products released by such bacteria are toxic to a variety of cells and cell fractions, including polymorphonuclear leukocytes, platelets, tissue-culture cells, lysosomes, and isolated mammalian and amphibian hearts (Duncan & Schlegel, 1975; Bisno et al., 2003). Streptolysin S is a hemolysin produced by S. pyogenes in the presence of serum or several other substances such as serum albumin, alpha-lipoprotein, and ribonucleic acid. It exists in intracellular, cell-surface-bound, and extracellular forms, and it is one of the most potent cytotoxins known (Sierig et al., 2003; Datta et al., 2005; Sumitomo et al., 2011). Other extracellular antigenically distinct enzymes are DNases A, B, C, and D, which are involved in degradation of DNA, streptokinase, which causes dissolution of clots by catalyzing the conversion of plasminogen to plasmin, streptococcal pyrogenic exotoxin B (speB), a potent protease that cleaves the PMN binding site (Ji et al., 1996; Bisno et al., 2003), streptococcal inhibitor of complement, which inhibits lysis of the bacterium by binding to the insertion site of complement (Fernie-King et al., 2002).
Cytolytic Vaginosis, Aerobic Vaginitis, and Desquamative Inflammatory Vaginitis
Published in William J. Ledger, Steven S. Witkin, Vulvovaginal Infections, 2017
William J. Ledger, Steven S. Witkin
Both S. pyogenes and S. aureus have a multitude of mechanisms to prevent their detection and/or elimination by the host’s immune system. The major immune defense against S. pyogenes is recognition, phagocytosis and killing of the microorganism by polymorphonuclear leukocytes. One of the S. pyogenes proteins, known as M protein, has potent antiphagocytosis properties. It binds to factor H and C4b-binding protein, components of the complement system, and prevents complement deposition on the streptococcal surface and subsequent opsonization. Similarly, fibronectin binds to M protein, thereby masking the bacterial surface from recognition. Streptococcal-derived C5a peptidase, endoglycosidase, and Mac1-like protein also limit complement activation as well as antibody binding and leukocyte recruitment. Streptolysin O, a streptococcal virulence factor, also blocks phagocytic functions.18
Lactic acid bacteria: prominent player in the fight against human pathogens
Published in Expert Review of Anti-infective Therapy, 2022
Ujjayni B. Saha, Sunil D. Saroj
Streptococcus pneumoniae is one of the most prevalent causes of bacterial pneumonia, meningitis, bacteremia, and otitis media. Despite the availability of antibiotics, mortality and morbidity rates among high-risk groups remain high [111]. Lactic acid bacteria have been proven to promote protection in distant mucosae such as the respiratory mucosa by boosting the common mucosal immune system. In malnourished mice, including L. casei in the repletion diet has a positive impact because it speeds up the recovery of the innate immune response and improves certain immunological mechanisms against an S. pneumoniae respiratory infection [112] (Table 3). Lactobacillus strains L. rhamnosus Kx151A1 and L. reuteri PTA-5289 inhibited the hemolytic activity of Streptococcus pyogenes S165 in a study. The inhibition of hemolytic activity was due to a reduction in streptolysin S production (SLS) [113] (Table 3).
β-Hemolytic Streptococcus anginosus subsp. anginosus causes streptolysin S-dependent cytotoxicity to human cell culture lines in vitro
Published in Journal of Oral Microbiology, 2019
Atsushi Tabata, Takuya Yamada, Hiromi Ohtani, Kazuto Ohkura, Toshifumi Tomoyasu, Hideaki Nagamune
Our present investigation on the cytotoxicity of SLS produced from β-SAA was conducted in vitro. However, to reveal the mechanism of SLS-dependent cytotoxicity and virulence of β-SAA, further investigations in vivo would be required. In fact, it was reported that the contribution of SLS to the bacterial survival, neutrophil infiltration, and diffuse tissue necrosis is observed for the β-hemolytic group G streptococcus [32], and the contribution of SLS and streptolysin O to the early stages of infection and induction of necrotic lesions in mice is also observed for S. pyogenes [33]. In addition, it is also reported that the virulence factor of S. pyogenes is detected in some strains of S. anginosus [2]. Based on these accumulated recent findings on SLS and AGS, the underestimation in virulence of AGS, including SAA, as an opportunistic pathogen may increase the risk of misdiagnosis, prevention, and treatment of the infectious diseases caused by such a pathogenic sub-group of AGS producing the virulence factor(s) including the cytotoxic factor(s) such as SLS. In order to reveal and recognize the original pathogenicity of the β-hemolytic sub-group of AGS, further investigation is currently in progress.
Platelet interaction with bacterial toxins and secreted products
Published in Platelets, 2015
Streptococcus pyogenes produce a pore-forming toxin, Streptolysin O (SLO) that can mediate platelet activation and CD62P-dependent PNC formation [55]. Importantly, the authors demonstrated that SLO decreases local blood flow in an animal model and speculated that PNCs induced by SLO occlude the vasculature. The same authors have also demonstrated that phospholipase C (PLC) produced by Clostridium perfringens stimulates platelet aggregation and platelet–leukocyte complex formation [56]. Furthermore, local administration of PLC decreased blood flow in an animal model and platelet–platelet and platelet–leukocyte aggregates were evident in tissue sections of occluded vessels from the animals [57]. The ability of both SLO and PLC to induce platelet-dependent vessel occlusion may be highly relevant to the pathogenesis of necrotising local tissue infection caused by the toxin-producing organisms.