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Streptococcus Toxins

CM101 Analog of group B streptococcus toxin, binds to tumor endothelium, induces inflammation... [Pg.85]

Vaccines can be roughly categorized into killed vaccines and Hve vaccines. A killed vaccine can be (/) an inactivated, whole microorganism such as pertussis, (2) an inactivated toxin, called toxoid, such as diphtheria toxoid, or (J) one or more components of the microorganism commonly referred to as subunit vaccines. The examples are capsular polysaccharide of Streptococcus pneumoniae and the surface antigen protein for Hepatitis B vims vaccine. [Pg.356]

Streptococcus pyogenes can be an extremely dangerous pathogen it produces a series of toxins, including an erythrogenic toxin which induces a characteristic red rash, and a family of toxins which destroy the formed elements of blood. [Pg.26]

Toxic shock syndrome is a very damaging, often fatal condition caused by toxins from Staphylococcus aureus or Streptococcus pyogenes. First reported in children in 1978, it is manifested by high fever, erythroderma (a skin rash condition), and severe diarrhea.6 Patients may exhibit confusion, hypotension, and tachycardia, and they may go into shock with failure of several organs. Survivors often suffer from skin desquamation (flaky skin). [Pg.399]

Antigen delivery through liposomes, hollow membrane-bound spheres, can be achieved by entrapping the molecule in the lipid membrane or inside the hollow cavity. Modified liposomes have been able to induce mucosal IgA responses compared to free antigen (Ann Clark et al. 2001 Aziz et al. 2007). Liposomes containing pertussis toxin (Guzman et al. 1993), Streptococcus mutans (Childers et al. 2002), or bovine serum albumin (Therien et al. 1990) as vaccine antigens have been tested in experimental models and induced effective antibody- and cell-mediated immune responses. [Pg.204]

Streptococcus pyogenes and Staphylococcus aureus secrete a number of enterotoxins and pyrogenic exotoxins, respectively. These toxins are known as superantigens, since they simultaneously form complexes with the major histocompatibility class II (MHC-II) molecules and T-cell receptors (TCRs) enabling them to activate a number of T-cell lymphocytes. Thus, superantigens stimulate up to... [Pg.5162]

Pinkney M, Kapur V, Smith J et al. (1995) Different forms of streptolysin O produced by Streptococcus pyogenes and by Escherichia coli expressing recombinant toxin cleavage by streptococcal cystein protease. In Infect Immun 63 2776-2779. [Pg.256]

Weeks OR, Ferretti JJ Nucleotide sequence of the type A streptococcal exotoxin (erythrogenic toxin) gene from Streptococcus pyogenes bacteriophage T12. Infect Immun 1986 52 144-150. [Pg.19]

Kamezawa Y, Nakahara T, Nakano S, Abe Y, Nozaki-Renard J, Isono T Streptococcal mitogenic exotoxin Z, a novel acidic superantigenic toxin produced by a T1 strain of Streptococcus pyogenes. Infect Immun 1997 65 3828-3833. [Pg.19]

YuCE, Ferretti JJ Molecular epidemiologic analysis of the type A streptococcal exotoxin (erythrogenic toxin) gene (speA) in clinical Streptococcus pyogenes strains. Infect Immun 1989 57 3715-3719. Hauser A, Stevens D, Kaplan E, Schlievert P Molecular analysis of pyrogenic exotoxins from Streptococcus pyogenes isolates associated with toxic shock-like syndrome. J Clin Microbiol 1991 29 1562-1567. [Pg.21]

Reichardt W, Muller-Alouf H, Alouf J, Kohler W Erythrogenic toxins A, B, and C occurrence of the genes and exotoxin formation from clinical Streptococcus pyogenes strains associated with streptococcal toxic shock-like syndrome. FEMS Microbiol Lett 1992 79 313-322. [Pg.22]

Smoot LM, McCormick JK, Smoot JC, Hoe NP, Strickland I, Cole RL, Barbian KD, Earhart CA, Ohlendorf DH, Veasy LG, Hill HR, Leung DYM, Schlievert PM, Musser JM Characterization of two novel pyrogenic toxin superantigens made by an acute rheumatic fever clone of Streptococcus pyogenes associated with multiple disease outbreaks. Infect Immun 2002 70 7095-7104. [Pg.22]

In 1893, William Coley, a surgeon at Memorial Hospital in New York City, deliberately injected a mixture of heat-treated bacterial cells into the tumours of his cancer patients. In all, he treated over 900 patients, and there were several dramatic remissions. He was inspired to do this by the observation that cancer patients sometimes experienced remarkable improvement in their condition following a serious bacterial infection. It was as if their already severely damaged bodies were somehow activated by the bacterial onslaught to mount a sustained attack on both the bacterial and cancer cells. Coley s toxins - usually a mixture of killed bacteria of the species Streptococcus... [Pg.211]

KATZ, J HARMON, C.C., BUCKNER, G.P., RICHARDSON, G.J., RUSSELL, M.W. MICHALEK, S.M. (1993) Protective salivary immunoglobulin A responses against Streptococcus mutans infection after intranasal immunization with S. mutans antigen I/II coupled to the B subunit of cholera toxin. Infection and Immunity, 61, 1964—1971. [Pg.147]

Toxins that act directly on cell membranes, called cytolytic toxins, disturb and ultimately kill the target cells. Produced by many organisms (e.g., bacteria, fungi, plants, fish, and snakes), cytolytic toxins may cause damage in several ways. For example, streptolysin O (67,000 D), produced by the bacterium Streptococcus pyogenes, causes pores to form in the target cell membranes. Affected cells are rapidly lysed because the cell membrane is much more permeable to ions such as Na+. Streptolysin O is believed to cause some of the damage in rheumatic fever. [Pg.149]

The role of glycolipids is still unclear. Certain glycolipid molecules may bind bacterial toxins, as well as bacterial cells, to animal cell membranes. For example, the toxins that cause cholera, tetanus, and botulism bind to glycolipid cell membrane receptors. Bacteria that have been shown to bind to glycolipid receptors include E. coli, Streptococcus pneumoniae, and Neisseria gonorrhoeae, the causative agents of urinary tract infections, pneumonia, and gonorrhea, respectively. [Pg.346]

Bacteria can permanently acquire the capacity to produce a toxin when the viral toxin gene becomes incorporated into the bacterial chromosome or a self-replicating plasmid. Comparison of modem group A streptococcus with the organism that caused a similar disease in the 1920s requires the production via PCR of a series of DNA probes from the modem organism. These probes are then used in an in situ hybridization... [Pg.733]

Coley s Toxins are the by-products from two common bacteria. Streptococcus pyrogenes and Serratia marcescens. The toxins can cause a fever anywhere from slightly above normal to 105°F, and a pulse rate of 100 or more, and accompanying chills. In other words, flu-like symptoms. To quote directly from Moss s book ... [Pg.78]


See other pages where Streptococcus Toxins is mentioned: [Pg.248]    [Pg.283]    [Pg.1021]    [Pg.123]    [Pg.122]    [Pg.150]    [Pg.205]    [Pg.206]    [Pg.1857]    [Pg.369]    [Pg.153]    [Pg.315]    [Pg.248]    [Pg.5162]    [Pg.242]    [Pg.23]    [Pg.406]    [Pg.936]    [Pg.1970]    [Pg.277]    [Pg.1]    [Pg.8]    [Pg.20]    [Pg.162]    [Pg.215]    [Pg.651]    [Pg.115]    [Pg.1421]   


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