Distribution Incidence and Immunity

Corynebacteria are distributed throughout the world, but C. diphtheriae occurs naturally only in humans. Farm animals can be infected through human cases, and many laboratory animals are susceptible to deliberate infection. Indeed, diphtheria's wide host range accounts for part of the success in studying this organism during the early bacteriologic revolution.

In historical accounts, it is often described as a malignant sore throat, and one of the most puzzling features is the sudden appearance of an epidemic. In the "throat distemper" epidemic of colonial New England, Boston was spared the high childhood mortality and morbidity experience elsewhere in Massachusetts and New Hampshire, illustrating the patchy geographic distribution of severe cases that one could observe even during an epidemic. Peter English (1985) describes how a phage virus is associated with the virulence of the diphtheria bacilli in that the "tox" gene can either elaborate toxin (tox+) or not (tox"). But in both cases the presence of this gene incorporated into the bacterial DNA stimulates immunity to virulent diphtheria. Because a low-iron environment or medium tends to stimulate or facilitate the production of toxin, English further speculates that the nutritional poverty of many premod-ern populations helped to discourage the frequent recurrence of epidemic diphtheria. Many other researchers, including Ernest Caulfield (1939), point to a mixture of organisms during epidemics of sore throat, diphtheritic and pseudodiphtheritic. In the Boston epidemic of sore throat in 1735, for example, a rash accompanied clinical cases, suggesting coin-fection with streptococcal organisms. Suprainfection with streptococcus is common even for true diphtheria, but it is not known what influence, if any, the presence of a copathogen has in the elaboration of toxin.

The phage carrying the tox+ genome does enhance iron binding, permitting the microorganism to acquire this essential metabolite for its reproduction. Normally the human immune system is able to withhold iron and "starve" a pathogen (Weinberg 1978). Thus the production of toxin and the emergence of virulent strains should not depend upon an individual host's nutritional status. Epidemiolog-ically the appearance of virulent diphtheria epidem ics should reflect increased opportunities for transmitting the bacillus to susceptible hosts, as through crowding or urbanization. Historically diphtheria epidemics were recorded only after medical theories supported recognition of the clinical specificity of this disease.

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