Abstract
The development of inflammatory plaques on the lower extremities as a complication of dermatophytosis of the feet is well known. After McGlasson1 in 1926 called attention to the phenomenon, it was presumed that the lesions on the feet and legs were areas of erysipelas or cellulitis caused by lymphatic transmission of bacteria, usually hemolytic streptococci, which invaded through fissures and erosions of fungous origin situated between the toes and on the soles. According to this view, the fungi on the feet are passive actors in a dramatic episode, serving the casual role of throwing open the portals for bacterial penetration into deeper tissues and lymphatic channels, while they themselves remain bystanders, and often inconspicuous ones. The concept has much clinical evidence to support it, and at the present time it is widely held. Added support for this mechanism is provided by the efficacy of adequate treatment of the focus

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