Despite a greatly reduced incidence over the past 50 years, diphtheria remains endemic in many developing nations. Though immunization has had a dramatic effect on the incidence of diphtheria, a decline in incidence began well before the onset of widespread immunization. The major virulence of C. diphtheria is a result of its toxin production. Within a few days of respiratory infection, the toxin produces a local adherent pseudomembrane composed of dead host epithelial cells, leukocytes, fibrin, and red blood cells. This gray-green or black membrane can be local, or can extend widely to cover the entire pharyngeal or tracheobronchial mucosa. There is a marked underlying soft tissue edema and regional lymphadenitis producing the bull neck appearance. Palatal paralysis is an early local effect of the toxin. Myocarditis, renal tubular necrosis and demyelination, and axon degeneration within cranial or peripheral nerves are prominent features of the more severe infections with C. diphtheriae. Diphtheria can be prevented by active immunization with formalin-detoxified DT (toxoid). Diphtheria, at the end of the twentieth century, remains a serious disease, associated with a high case-fatality rate.

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