Epidemiology

The ultimate sources of diphtheritic contagion are humans. In addition to respiratory transmission of the bacillus through cutaneous diphtheritic lesions, the disease can be spread by touch and by fomites - such as schoolchildren’s pencils.

The experience with diphtheria in England and Wales, from 1915 to 1942, is probably typical of industrialized countries in the twentieth century. Early in this period, over 50,000 cases were reported each year, and it was the leading cause of death for children aged 4 to 10 years. Over this time period, however, case fatality rates declined by 40 percent as a result of more rapid diagnosis and therapeutic interventions in the form of antitoxin and trache­ostomy (surgically providing a way to breathe when the upper pharynx is occluded).

After World War II, mass immunization efforts effected a rapid decline in the overall number of cases, and the age of incidence rose. In virulent cases of diphtheria, mortality remains today around 5 per­cent, a fact that leads A. B. Christie (1974) to assert that we do not possess convincing proof that anti­toxin alone reverses the clinical course of diphthe­ria. The organism itself is sensitive to penicillin.

Unlike measles, the common early springtime vi­ral disease of childhood, diphtheria in temperate climates usually peaks in incidence in autumn and early winter. Most cases during the last 200 years have occurred among individuals under 15 years of age. Crowded conditions to which the poor are sub­jected facilitate passage of the organism, and so ac­counts of diphtheria before the germ theory of dis­ease was widely accepted often described it as a filth disease naturally favoring the poor (Ziporyn 1988). In tropical regions cutaneous diphtheria is much more common, resulting in “punched,” weeping ul­cers sometimes called “desert sores.” Contact with these lesions, usually on the extremities, is probably an important means of spreading the disease in such regions.