THE QUESTION OF IMMUNITY IN RINGWORM INFECTIONS *

There is some indication that an immune response against dermatophytes is developed in experimental animals in view of the early work of Delamater’ and Delamater and Benham2 with Trichophylon menfagrophytes and of the more recent work of Reiss and Leonard3 with Microsporum canis and of Keeney and Huppert4 with T . menfagrophyfes. Also, Huppert and Keeney5 felt that they had demonstrated an acquired resistance against dermatophyte infections in human volunteers previously immunized with antigens of T. menlagrophytes. For the most part, however, the immunity developed has been partial in that the course of the disease following immunization was only shorter and milder than that normally observed. The role of such an altered response under natural conditions is nebulous, in part because of so-called “natural resistance” to dermatophyte infections that has been described by many, particularly well by Barlow.G I t is generally assumed that most persons are exposed to dermatophyte infections, yet relatively few develop clinical disease. This is well exemplified by the study of Kligman? who found that only 5 per cent of a group of institutionalized children had acquired a natural infection during an epidemic of tinea capitis caused by Microsforon audouini, despite the intimate and prolonged contact this situation provided. The factors that limit the spread of such epidemics would seem to be more complex than merely the natural resistance of certain individuals and might well be strongly influenced by other factors such as infectivity and virulence of the strain, size of the inoculum received by the individual, and the effect of local trauma, as well as the possibility of altered response following infection. For example, it is our impression, based more on speculation than data, that M . audouini, although perhaps more virulent than other of the causative agents of tinea capitis, may not be a5 infectious. I t was our desire to determine the presence, or absence, of immunity under natural conditions following recovery from naturally acquired tinea capitis. The observation that children usually do not have second bouts with this disease would seem a t first glance sufficient evidence for a concept of acquired immunity. However, since the opportunity for first infections often is not great, the failure to acquire a second infection might well be attributable to lack of opportunity rather than immunity. Of 718 children treated for tinea capitis in the Tulane University clinic during a threeyear period, not one returned with a second infection, despite entirely free medical care, including medication. At the time griseofulvin first became available, a deliberate effort was made to set up studies to explore the possibility of immunity following infection. I t seemed to us that treating one sibling and then leaving that child exposed to one or more untreated children would provide a long-awaited opportunity. * The work described in this paper was supported in part by Grant F, 1224 from the National Institute of Allergy and Infectious Diseases, Public Health Service, Bethesda, Md.