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Diphtheria, caused by Corynebacterium diphtheriae, occurs worldwide. Toxigenic strains produce a protein toxin that leads to the formation of pseudomembranes in the pharynx and respiratory tract, as well as systemic toxicity including myocarditis and polyneuropathy. It may present at any time of the year, although it is most common during winter. Because humans are the only significant reservoir, closeness and duration of contact with an ill person or a healthy carrier are important determinants of infection spread. As a result, attack rates in households and in crowded living conditions are high.


Human nasopharyngeal carriers of C diphtheriae are the principal source of new infections, but cutaneous lesions can transmit infection as well. In temperate climates, the skin lesions of diphtheria are superficial, indolent sores that resemble impetigo. Individuals with skin lesions generally do not develop toxic manifestations. Untreated, healthy nasopharyngeal carriers can be colonized for many weeks.

The incidence of diphtheria is inversely related to the percentage of immune individuals in an area and remains a common disease in countries without effective immunization programs. The incidence of diphtheria in the United States has declined dramatically since aggressive immunization efforts were begun in 1980; in fact, less than five patients with diphtheria are reported annually. Concurrently, diphtheria has shifted from a disease of children to a disease of adults with waning immunity.1 The potential for outbreaks continues, however, if segments of a community are not immunized.

C diphtheriae is comprised of irregularly staining gram-positive, nonspore-forming, unencapsulated slender rods. Branching and clubbed ends result in a cuneiform appearance. Metachromatic granules are common. There are three phenotypes of the organism: gravis, intermedius, and mitis, differentiated by colony morphology, growth characteristics, and biochemical reactions. All are capable of elaborating a cytotoxic exotoxin, which interferes with protein synthesis in host cells. The ability of a strain of C diphtheriae to produce toxin is conferred by a lysogenic bacteriophage that carries the gene for toxin production. The clinical signs and symptoms depend on the primary site of infection. Toxins produced by the three types are qualitatively similar, but the gravis and intermedius strains produce more toxin than does the mitis strain.

Clinical Manifestations

Diphtheria presents with respiratory infection that can cause respiratory obstruction, or with infected skin lesions that lack a characteristic appearance. With either presentation, toxin produced by the organism results in further symptoms.

Respiratory Diphtheria

This usually has an insidious onset with symptoms of a mild sore throat with slight redness and low-grade fever. Systemic signs of illness are absent in the early stages. Within 1 or 2 days, areas of yellow or “dirty” white exudate appear, most frequently on or adjacent to the tonsils; these areas subsequently coalesce to form a light reflective, sharply outlined pseudomembrane on the mucous membranes of the pharynx, tonsils, and uvula. Pseudomembranes ...

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