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
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.
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.
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 ...