TAILIEUCHUNG - Chapter 131. Diphtheria and Other Infections Caused by Corynebacteria and Related Species (Part 2)

Pathogenesis and Immunology Diphtheria toxin, produced by toxigenic strains of C. diphtheriae, is the primary virulence factor in clinical disease. The toxin is synthesized in precursor form; is released as a 535-amino-acid, single-chain protein; and has an LD50 of ~100 ng/kg of body weight. The toxin is produced in the pseudomembranous lesion and is taken up into the bloodstream, through which it is distributed to all organ systems. Once bound to its cell surface receptor (a heparin-binding, epidermal growth factor–like precursor), the toxin is internalized by receptormediated endocytosis and enters the cytosol from an acidified early endosomal compartment. . | Chapter 131. Diphtheria and Other Infections Caused by Corynebacteria and Related Species Part 2 Pathogenesis and Immunology Diphtheria toxin produced by toxigenic strains of C. diphtheriae is the primary virulence factor in clinical disease. The toxin is synthesized in precursor form is released as a 535-amino-acid single-chain protein and has an LD50 of 100 ng kg of body weight. The toxin is produced in the pseudomembranous lesion and is taken up into the bloodstream through which it is distributed to all organ systems. Once bound to its cell surface receptor a heparin-binding epidermal growth factor-like precursor the toxin is internalized by receptor-mediated endocytosis and enters the cytosol from an acidified early endosomal compartment. In vitro the toxin may be separated into two chains after digestion with serine proteases the N-terminal A fragment and the C-terminal B fragment. Delivery of the A fragment into the eukaryotic cell cytosol results in irreversible inhibition of protein synthesis by NAD -dependent ADP ribosylation of elongation factor 2. The eventual result is the death of the cell. In 1926 Ramon at the Institut Pasteur found that formalinization of diphtheria toxin resulted in the production of diphtheria toxoid which was nontoxic but highly immunogenic. Subsequent studies showed that immunization with diphtheria toxoid elicited antibodies that neutralized the toxin and prevented most manifestations of diphtheria. In the 1930s mass immunization of children and susceptible adults commenced in the United States and Europe. Individuals with an antitoxin titer of unit mL are at low risk of diphtheria disease. In populations where a majority of individuals have protective antitoxin titers the carrier rate for toxigenic strains of C. diphtheriae decreases and the overall risk of diphtheria among susceptible individuals is reduced. Nevertheless individuals with nonprotective titers may contract diphtheria through either travel or exposure to .

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