Lecture #29

Lecture #29 - Lecture 29 Bacterial Toxins Bacterial Toxins...

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11/19/2007 1 Lecture 29 Bacterial Toxin Bacterial Toxins Horizontal Transfer of Pathogenesis genes Host Detection by Bacterial Pathogens BBOM 11e Sec. 4.9, 21.9 – 21.12, 8.10, 19.21, 10.10, 29.8, 28.5, 20.7 – 20.9, 20.12, 30.5 Antibiotics and Antibiotic Resistance Bacterial Toxins Endotoxins (Sections 4.9, 21.12) Lipopolysaccharides. Lipid A is the toxic component, while the polysaccharide increases water solubility. Cause a massive immune response, fever. Can be fatal in large amounts. Exotoxins (Sections 21.10, 21.11) Enzymes, exported from bacteria, enter host cells, and catalyze specific biochemical reactions. First described exotoxin: Diphtheria toxin. Cornyebacterium diphtheriae does not leave the site of infection yet causes systemic symptoms Emil Roux in 1880's leave the site of infection, yet causes systemic symptoms. Emil Roux, in 1880 s, postulated that the bacteria must release a toxin that spreads systemically. Roux grew a broth culture of the bacterium, removed the bacteria by filtration, and injected the cell free culture into mice, causing the disease symptoms. Birth of “Molecular Koch’s Postulates.”
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11/19/2007 2 Endotoxin, also known as Lipopolysaccharide (Fig. 4.34) Cytolytic toxins Bind to host cells and induce lysis. Often tested using animal red blood cells (because lysis is easy to detect on solid agar medium), and are therefore often called “hemolysins”, but natural substrate is generally other cell types. cytoplasmic contents released
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11/19/2007 3 The A domain of Diphtheria toxin covalently modifies EF 2, blocking protein synthesis. Exported from cytoplasm with cleavage of signal sequence. Two cysteine residues are covalently linked, forming a disulfide bond. Peptide backbone cleaved, so that two halves are joined only by the disulfide bond. Binds to host cell. “A” subunit is inserted through host membrane. Disulfide bond is cleaved, freeing A domain.
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11/19/2007 4 | | | | CO CO CO CO | | Extracellularly | | CH-CH2-SH + HS-CH2-CH ---------------> CH-CH2-S-S-CH2-CH | | <--------------- | | NH NH Intracellularly NH NH | | | | Cysteine Cysteine Disulfide bonds between two cysteine residues are formed outside the cell and are broken in the bacterial and host cytoplasms. Structure of NAD + . Toxin inhibits protein synthesis by inactivating Elongation Factor 2. Covalently modifies EF2. Uses NAD to donate ADP ribose to EF2, releasing nicotinamide. “ADP ribosylation” is a common reaction for toxins. Pseudomonas aeruginosa P. aeruginosa , unlike many pathogens, extremely versatile, colonizing many nonhuman niches. “Opportunistic” pathogen. Usually does not cause clinical problems, but can infect: burn patients immunocompromised individuals lung tissue of CF patients indwelling catheters. Causes “nosocomial” infections (infections obtained at a hospital). Exotoxin A Precursor Exotoxin A.
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Lecture #29 - Lecture 29 Bacterial Toxins Bacterial Toxins...

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