Abstract

Mycetoma pedis, or Madura foot, was first described as a clinical entity by Gill in 1842, from the Madura dispensary in India. In 1858, Rustomji first recognized the fact that in some cases black granules and in others yellow granules were present in the tissues. Carter, in 1880, used the color of the granules as a basis of classification. He believed, however, that all cases were due to the same fungus, and from this he called the disease mycetoma. In 1894 Boyce and Surveyor discovered that the condition was produced by more than one group of organisms. Further studies isolated Actinomyces from some cases and true fungi from others. Pinoy, in 1913, suggested that the name mycetoma be reserved for the latter group of cases, and that those due to Actinomyces be called actinomycosis. In 1916, however, Chalmers and Archibald redefined the term mycetoma to include all infections caused by mycotic organisms in which granules, comprised of the organisms, are present in the tissues. Madura foot is not an uncommon occurrence in the tropical regions of the world—India, Africa, Central America, South America, and the Netherland East Indies. In temperate climates it is more unusual, although a considerable number of cases have been reported in the United States, chiefly in the South, and a few in Canada. The usual mode of infection is thought to be from the soil, through an abrasion in a foot unprotected by a shoe. Consequently, laborers and particularly farmers of the poorer class, who go barefoot, are most commonly affected. A history of trauma and contact with the soil is not always obtainable, however, and it may be impossible to trace the source of infection. The causative agent of mycetoma may be anyone of a variety of species of Actinomyces or true fungi. The pathologic changes and the clinical course, however, are the same regardless of the etiologic agent. Laboratory studies are necessary in order to differentiate one infection from another. The clinical course is slow and progressive, cases having been reported with a duration of twenty years. Early symptoms may consist of pain and tenderness. Then a hard, deep-seated, fixed nodule develops. Swelling gradually extends peripherally about the nodule and other nodules appear. These soften and after a few days rupture spontaneously, discharging fluid containing the characteristic granules. Drainage continues for a few days and then gradually diminishes, the fistula crusting and healing over. As the disease progresses, all stages may be present—draining sinuses, encrusted lesions, and small scars from old lesions. The individual sinuses lead to deep-seated abscesses. The swelling gradually involves the entire foot, leading to a massive globose deformity. The subjective symptoms are usually slight. There may be some pain just before rupture of a nodule, and patients sometimes complain of a deep aching or sensation of fullness.

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