PHa JOURNAL OF INVESTIGATIVE DERMATOLOGY

Several years ago (1, 2) we conducted studies attempting to deliberately produce tinea pedis by immersing the healthy (fungus-free) feet of volunteer subjects in suspensions of living dermatophytes for 30 minutes. The source of these fungi was either fragmented cultures of dermatophytes or the foot bath water of persons with myeologically proven, clinically active tinea pedis. Among 68 subjects thus exposed, not a single case of acute tinea pedis was observed during the 6 weeks of observation following the exposure, although a transient, asymptomatic infection was apparently induced in about one half of these subjects. The studies referred to above appeared to simulate naturally occurring conditions more closely than did the technies used by earlier investigators (3, 4, 5) who induced experimental superficial fungous infections of the feet by maeeration and occlusion of the interdigital spaces. We concluded from the results of our studies that mere exposure of healthy feet to fungi was not sufficient to induce clinical disease. The demonstration of pathogenic fungi on clinically healthy skin (6) strongly suggested that these organisms maintain themselves without producing disease, perhaps for considerable periods of time. Clinical disease might well result under altered conditions of host-parasite relationship. Strauss and Kligman (7) demonstrated that in many persons with a fungous infection of the foot, a normal interdigital space would become infected as evidenced by a KOH positive examination if the webs or the entire foot were occluded. In persons with normal feet, however, experimental infections were most difficult to induce. Prolonged wetness of the inoculated site was essential to an experimental in-