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Wound care
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
Type II. Monomicrobial. Although more recently methicillin-resistant Staphylococcus aureus (MRSA) has been implicated, the causative agent is usually group A β-haemolytic streptococci (e.g. Streptococcus pyogenes) carried in the nose/throat of 15% of the population. This is the classic ‘flesh-eating bacteria’; it can also contribute to type I infections. Type II NF can affect all age groups and the healthy (up to a half); there is an association with varicella zoster and NSAIDs. The (lower) extremity is affected most often. There are a number of virulence factors: Exotoxin, e.g. streptococcal pyrogenic exotoxin A (SpeA); this superantigen (antigens that cause non-specific activation of T-cells resulting in polyclonal T-cell activation and massive cytokine release) causes systemic upset.Streptokinase that activates plasminogen and fibrinolysis.Hyaluronidase.Haemolysins.M proteins that inhibit opsonisation by an alternative complement pathway.
Streptococcus and Streptococcal Toxins
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Udayakumar Prithika, Krishnaswamy Balamurugan
Determination of the pathogenicity of a microorganism depends on the factors that help its invasion and establishment inside the host. A microorganism is considered pathogenic only if it causes disease in the healthy host [5]. S. pyogenes can spread expeditiously to various organs and has been conjectured to have escaped from the human immune system, enabling the organisms to initiate acute and chronic infections [46]. S. pyogenes invade the host system through numerous virulence factors: M protein and lipoteichoic acid (attachment); a hyaluronic acid capsule (inhibits phagocytosis); other extracellular products, such as pyrogenic (erythrogenic) toxin; streptokinase, streptodornase (DNase B), and streptolysins [17] (Figure 21.3). GAS responds rapidly and in a regulated manner to the distinct environments encountered in the host during the establishment and propagation of disease [47,48]. One of the most common S. pyogenes strains is the M1T1 strain, which is equipped with flagella referred to as antigen T that helps in increased invasiveness. Despite the presence of flagella, S. pyogenes has several toxins, among which, streptococcal pyrogenic exotoxin B (SpeB) is found to have cysteine protease activity [8]. The decrease in the virulence of the pathogen can also be attributed to the inhibition or lesser activity of SpeB. GAS also plays a crucial role in adaptation of microbes to various environmental conditions through a two-component system (TCS) [49]. Another major virulence factor extensively studied was the M protein serotype. The individuals’ immune system soon after acute GAS infection develops a very strong, long-lasting immunity to the serotype [50]. The M protein essentially offers protection through diversity, providing immunologically distinct surface coats to different serotypes. Novel serotypes thereby avoid antibodies raised by hosts in response to previous infections [51,52].
Linezolid
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
A number of studies have demonstrated that linezolid reduces bacterial exotoxin secretion (Diep et al., 2012). Subinhibitory concentrations of linezolid reduce virulence factor production by S. aureus, including staphylococcal enterotoxins A and B, alpha- and beta-hemolysins, protein A, and coagulase (Gemmell and Ford, 2002; Bernardo et al., 2004; Otto et al., 2013; Yamaki et al., 2013; Cardot Martin et al., 2015), in some cases in spite of an increase in gene expression; the mechanism is presumably blockade of RNA transcription (Pichereau et al., 2012). In addition, linezolid has been shown to reduce production of the toxin Panton-Valentine leukocidin (PVL) (Dumitrescu et al., 2007; Stevens et al., 2007; Pichereau et al., 2012; Otto et al., 2013; Cardot Martin et al., 2015), although in the case of the USA300 strain of MRSA, data are conflicting: one in vitro study showed no suppression (Cardot Martin et al., 2015) whereas an in vivo rabbit pneumonia study demonstrated decreased PVL production and improved mortality outcomes (Diep et al., 2013). Conversely, subinhibitory concentrations of linezolid increased S. aureus expression of fibronectin-binding protein, leading to a hyperadhesive phenotype in vitro, but this translated into neither increased cell adhesion nor invasion in vivo (Rasigade et al. 2011). Linezolid also increased production of phenol-soluble modulins in some strains of MRSA, although to a lesser extent than clindamycin, whereas production was inhibited in others (Yamaki et al., 2013). This highlights a finding shared by many studies: that the effect of linezolid (and other antimicrobials) on toxin production can be heterogeneous and strain specific, which should be borne in mind when considering the generalizability of results to other strains and clinical situations. Linezolid alone, or in combination with penicillin, led to reduced streptococcal pyrogenic exotoxin A (SPE A) from group A streptococci in an in vitro model (Coyle, 2003), and linezolid alone at subinhibitory concentrations reduced streptolysin O and DNAase production from S. pyogenes (Gemmell and Ford, 2002). Linezolid has also been shown to fully suppress in vitro toxin production by the toxigenic Sterne strain of B. anthracis. This is in spite of most bacteria remaining in the toxin-producing vegetative stage, because linezolid also prevented spore formation (Louie et al., 2012a, 2012b). A gene microarray study of the response of M. tuberculosis to linezolid exposure found up- or down-regulation of a range of genes involved in different pathways; the implications of these alterations remain to be clarified (Liang et al., 2012).
Acute post-streptococcal glomerulonephritis: analysis of the pathogenesis
Published in International Reviews of Immunology, 2021
Jesús Mosquera, Adriana Pedreañez
Many attempts have been made to identify a streptococcal factor(s) capable of triggering APSGN. Since glomerular C3 deposition is generally demonstrated before IgG or immune complexes, it is likely that the inflammatory processes are initiated by early renal deposition of streptococcal compounds, instead of deposition of immune complexes. APSGN is a consequence of streptococcal infection and assumed to be caused by an antigen(s) present in group A streptococci, related to M types 1, 2, 4, 12, 18, 25, 49, 55, 57, and 60 [1, 5]. However, group C streptococci, have caused epidemics of APSGN, specifically S. zooepidemicus and, therefore, nephritogenic antigens are present and possibly shared by streptococci from several groups [2]. Previous studies have tried to define the specific causative antigen of the APSGN. In this regard, several proteins from the streptococcus have been studied. Streptococcal proteins such as streptokinase [66,67], streptococcal pyrogenic exotoxin B (ETB/ETBP) [12, 68,69] and nephritis-associated plasmin receptor (NAPlr) [13, 43] have been reported as potent nephritogenic antigens in APSGN. However, several other streptococcal proteins could be involved in the pathogenesis of the disease (Figure 3).
Necrotizing myositis case report and brief literature study
Published in Acta Clinica Belgica, 2020
Arthur Basso, Filip Moerman, Christophe Ronsmans, Martine Demarche
Group A Streptococci (GAS) are a virulent strain because of their capacity to produce several exotoxins of which some have ‘super antigen properties’. The streptococcal pyrogenic exotoxin A (SPEA) is responsible for a major immune response with potentially devastating consequences. The reaction causes ischemia and necrosis of infected tissue and its surrounding area through the development of microthrombi. Moreover, infection spreads more easily on necrotic tissue. M protein is a virulence factor produced by streptococci. It contributes to the invasiveness of the germ by preventing phagocytosis by polymorphonuclear leukocytes. Based on these factors of virulence, D.L. Steven proposed an explanation for the development of the streptococcal toxic shock syndrome, and necrotizing fasciitis and myositis without direct entry point [3] (Figure 1). Thus, the GAS, producing exotoxins and carrying M proteins, locally accountable for a pharyngitis, would sometimes undergo a translocation leading to bacteraemia. This phenomenon is rare and arises only in 0.3% of the pharyngitis cases caused by GAS. The strained muscle, due to the discontinuity of its fibres and the bruise, is a fertile ground enhancing bacterial growth and hence the potential development of myositis. The phenomenon is favoured by the intake of nonsteroidal anti-inflammatory drugs. It was demonstrated in vitro that GAS can develop in areas of induced muscular injuries and that this phenomenon is 10 times more frequent when taking nonsteroidal anti-inflammatory drugs [4].
Coexistence of acute poststreptococcal glomerulonephritis and acute rheumatic fever in a Japanese girl with primary Sjögren’s syndrome
Published in Modern Rheumatology Case Reports, 2020
Ichiro Kobayashi, Shunichiro Takezaki, Yusuke Tozawa, Masahiro Ueki, Asako Hayashi, Takeshi Yamazaki, Yasuyuki Sato, Takayuki Okamoto, Masafumi Yamada, Tadashi Ariga
Despite the association of several M types with APSGN, pathological roles of the M antigens in APSGN are not clear. Recent reports have suggested in-situ immune complex formation with streptococcal nephritogenic antigens such as nephritis-associated plasmin receptor and streptococcal pyrogenic exotoxin B within the glomeruli, which activate alternate complement pathway [35]. These suggest a central role of antibody-mediated mechanisms in the development of APSGN. On the other hand, studies of patients with ARF and model mice have suggested pathological roles of both antibody- and cell-mediated immunity to self-components cross-reactive with certain M proteins such as cardiac myosin in the development of myocarditis and valvular disease [36–38]. SS is characterised by the production of autoantibodies and polyclonal hypergammaglobulinemia as well as T cell activation [39]. Some patients with SS produce anti-myosin autoantibodies cross-reactive with streptococcal M protein, although the pathological role of the antibody in the development of carditis is still unclear [40,41]. Thus, APSGN and ARF may have coexisted under an autoimmune-prone status of underlying SS following GAS infection in our patient.