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Bacteria Causing Gastrointestinal Infections
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
B. Vinoth, M. Krishna Raja, B. Agieshkumar
Alpha toxin is produced by type A strain and present frequently in humans. Zinc activates the toxin after which it interacts with the host cell receptors, and through a series of pathways, the permeability in blood vessels is increased and blood supply is reduced to tissues. Beta toxin is lethal and produced by type B and type C strains. Necrotizing enteritis (enteritis necroticans or pigbel), which is rare, is caused by toxins of type C strains and is often obtained by ingestion of undercooked pork. Epsilon toxin is most commonly isolated from animals. which are produced by type B and type D strains. Potassium ions and fluid leakage occurs due to perforation in tissues. Iota toxin, known as AB toxin, is produced by type E strain. B component interacts with the host cell surface receptor to facilitate the uptake of the toxin, while A component inhibits actin polymerization, thereby breaking down the cytoskeleton. Bacteremia and clostridial sepsis is uncommon, but both are fatal occurring with an infection of the uterus, colon, or biliary tract.
A Case of Hospital-Acquired Mrsa
Published in Meera Chand, John Holton, Case Studies in Infection Control, 2018
TSST-1 is a superantigen that stimulates a broad range of T-cells to release TNF and IL-1, leading to a generalized acute inflammatory reaction and shock. This leads to the toxic shock syndrome. S. aureus enterotoxins (SEA-SE/U2) are superantigens and have a similar mechanistic effect to TSST-1, but induce food poisoning with rapid onset of nausea, vomiting, and sometimes diarrhoea. Alpha toxin is a pore-forming toxin, which induces cell necrosis by allowing intracellular contents to leak out of the affected cells, causing local host cell death. PVL is associated with necrotizing pneumonia and severe invasive skin or bone infections. It induces cytolysis of cells, particularly neutrophils, thus abrogating the host innate immune response. Exfoliatin A and B produced by S. aureus affects cadherin intercellular adhesion proteins and their loss leads to separation of the upper skin layers, with desquamation of the epidermal layer. This illness is called scalded skin syndrome.
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
Almost all strains of S. aureus secrete a group of enzymes and cytotoxins that includes four hemolysins (alpha, beta, gamma, and delta), nucleases, proteases, lipases, hyaluronidase, and collagenase. Alpha-toxin is a pore-forming toxin that acts on many types of human cells. It is dermonecrotic and neurotoxic. Beta-toxin is a sphingomyelinase C whose role in pathogenesis remains unclear. Delta-toxin is able to damage the membrane of many human cells, possibly by inserting into the cytoplasmic membrane and disordering lipid chain dynamics, although there are suggestions that it may form pores. Two types of bicomponent toxin are made by S. aureus, gamma-toxin and Panton-Valentine leukocidin (PVL). While gamma-toxin is produced by almost all strains of S. aureus, PVL is produced by only a few percent of strains. The toxins affect neutrophils and macrophages. PVL has pore-forming activity and has been associated with necrotic lesions involving the skin and with severe necrotizing pneumonia in community-acquired S. aureus infections. Also, S. aureus produces a staphylokinase, which is a potent activator of plasminogen, the precursor of the fibrinolytic protease plasmin.
Staphylococcal alpha-toxin tilts the balance between malignant and non-malignant CD4+ T cells in cutaneous T-cell lymphoma
Published in OncoImmunology, 2019
Edda Blümel, Andreas Willerslev-Olsen, Maria Gluud, Lise M. Lindahl, Simon Fredholm, Claudia Nastasi, Thorbjørn Krejsgaard, Bas G. J. Surewaard, Sergei B. Koralov, Tengpeng Hu, Jenny L. Persson, Charlotte Menné Bonefeld, Carsten Geisler, Lars Iversen, Jürgen C. Becker, Mads Hald Andersen, Anders Woetmann, Terkild Brink Buus, Niels Ødum
Alpha-toxin is secreted as a monomer and elicits its toxicity by forming heptameric pores in the cell membrane. Its effect depends on the toxin concentration, duration of exposure and cell type.14 The surface receptor for alpha-toxin is the disintegrin and metalloproteinase domain-containing protein 10 (ADAM10).15 Accordingly, surface expression levels of ADAM10 largely determine the toxin susceptibility of a given cell.16 However, while ADAM10 levels are important, other mechanisms can further modulate the susceptibility to alpha-toxin. For instance, multiple lineages of cells are resistant to the alpha-toxin effects by blocking pore formation, shedding or internalizing affected parts of the membrane or by closing the pore itself.17–20