Developments in the management of mycetomas M. Ameen and R. Arenas* Department of Dermatology, St. John’s Institute of Dermatology, London, UK; and *Department of Mycology, Dr Manuel Gea Gonzalez General Hospital, Mexico City, Mexico doi:10.1111/j.1365-2230.2008.03028.x Summary Mycetomas are chronic, granulomatous, subcutaneous infections caused by either eumycetes fungi or actinomycetes bacteria, giving rise to eumycetomas and actinomycetomas, respectively. The disease is endemic in many tropical countries, and is characterized by slow progression with risks of bone and visceral involvement. Treatment consists of long courses of antifungals and antibacterials, often combined with surgery. Drug resistance, poor response to treatment, and high rates of relapse have prompted trials of novel antibiotics and antifungals. This article discusses the potential of new treatment regimens and recent developments and improvements in diagnostics and prognostics, which will improve disease management. Introduction Mycetomas are an important group of subcutaneous infections that have been notoriously difficult to treat. For many decades, there was little progress in their management or treatment, and little recognition of their propensity to cause profound disability. Mycetoma is a disease of poverty, most commonly affecting agricul- tural workers and people who are habitually barefoot. It is most common in young men, and therefore has a socioeconomic effect on dependent family members. The introduction of new broad-spectrum antimicrobials and antifungals offers the hope of improved drug efficacy. Advances in the molecular identification of the causa- tive species, and the development of genetic and molecular markers for disease susceptibility and prog- nosis will facilitate disease management. 1–5 Aetiology and clinical presentation Mycetomas are caused by micro-organisms. Actino- mycetes are Gram-positive filamentous bacteria, whereas eumycetes are eukaryotic fungi, and they cause actino- mycetomas and eumycetomas, respectively. Both types of organism are important soil saprophytes, and there- fore infection is normally acquired by traumatic inoc- ulation of the skin by contaminated material, such as thorns. Clinically, mycetomas are characterized by tumefaction, draining sinuses and discharging grains. The grains are aggregates of fungal hyphae or bacterial filaments, and their size, colour and consistency provide the initial clue to the causative species (Table 1). The legs and feet are the most commonly affected site (Fig. 1), and in Mexico, the back is the second most common location for mycetomas. Early lesions begin as subcutaneous nodules that suppurate and drain through sinus tracts (Fig. 2). Without effective treat- ment, infection can spread to deeper structures such as soft tissue and bone, causing osteomyelitis (Fig. 3). Actinomycetomas characteristically progress more rap- idly than eumycetomas, and their lesions are more inflammatory and destructive. They can affect viscerae such as the lungs and peritoneum through contiguous spread, as in the case of severe infection of the trunk (Fig. 4). Infection of the vertebrae bodies can lead to spinal-cord compression, giving rise to neurological complications including paraplegia. 6,7 Mycetomas are endemic in Latin America, the Indian subcontinent and Africa, and a ‘mycetoma belt’ describ- ing the region of greatest endemnicity extends between the latitudes of 15°S and 30°N around the Tropic of Cancer. Worldwide, approximately 60% of all mycetomas are caused by actinomycetes, the commonest agent being Nocardia brasiliensis. The geographical distribution of Correspondence: M. Ameen, St. John’s Institute of Dermatology, St. Thomas’ Hospital, Westminster Bridge Road, London SE1 7EH. E-mail: mahreenameen@hotmail.com Conflict of interest: none declared. Accepted for publication 15 June 2008 Clinical dermatology • Review article Clinical and Experimental Dermatology Ó 2008 The Author(s) Journal compilation Ó 2008 British Association of Dermatologists • Clinical and Experimental Dermatology, 34, 1–7 1