Dermatologic Manifestations of Mycetoma
- Author: Oliverio Welsh, MD DrSc; Chief Editor: Dirk M Elston, MD more...
Background
Mycetoma is a chronic, granulomatous disease of the skin and subcutaneous tissue, which sometimes involves muscle, bones, and neighboring organs. It is characterized by tumefaction, abscess formation, and fistulae. It typically affects the lower extremities, but it can occur in almost any region of the body. Mycetoma predominately occurs in farm workers, but it can also occur in the general population.[1]
Gill first described the disease in the Madura district of India in 1842, hence the term Madura foot. In 1860, Carter named the condition mycetoma, describing its fungal etiology. In 1913, Pinoy described the mycetoma produced by aerobic bacteria that belong to the actinomycete group and classified mycetomas as those produced by true fungi (eumycetoma) versus those due to aerobic bacteria (actinomycetoma). Both types have similar clinical findings.[2]
Also see the article Mycetoma.
Pathophysiology
Mycetoma is produced by the introduction of microorganisms (bacteria or fungi) via localized trauma of the skin with thorns, wood splinters, or implantation with solid objects. Clinically, the disease begins as small, firm nodules that can persist (mini-mycetomas) or evolve to form extensive suppurative lesions measuring up to 20 cm in diameter. Eumycetomas tend to be more localized than actinomycetomas.
In experimentally induced Nocardia brasiliensis actinomycetomas in mice, production of granules (or "grains") containing the bacterium can be observed 15 days after inoculation. The grains are surrounded by polymorphonuclear cells (PMNs), lymphocytes, plasma cells, and histiocytes. Murine infection can evolve into a chronic disease similar to the clinical manifestations observed in humans. Severe inflammation and deformity, abscesses, ulcers, and fistulae are present 28 days after infection.
The in situ production of cytokines in the microabscesses has been reported in the murine infection. Tumor necrosis factor-alpha is produced in the first days of infection, decreasing later to nondetectable quantities at day 90. Interleukin (IL) – 1-beta, interferon gamma, transforming growth factor-beta, IL-10, IL-4, and IL-6 are produced constantly during the 90 days, but IL-6 is the only one with a significant increase once the mycetoma is fully established (90 d).[3]
The host immune response in humans and mice involves the production of high levels of anti– N brasiliensis immunoglobulin G antibodies. Quantitation of these antibodies is useful for diagnosis.[4] Immunoglobulin M anti– N brasiliensis antibodies can protect mice from an experimental infection.[5] Activation of cellular immunity and production of cytokines are involved in resistance and elimination of the N brasiliensis bacterial cells.
Epidemiology
Frequency
United States
Mycetoma occasionally occurs in the United States, particularly in the South.
International
Mycetoma is endemic around the Tropic of Cancer (15° south and 30° north of the equator) in tropical, subtropical, and temperate regions. Sudan, Mexico, Venezuela, India, Pakistan, Senegal, and Somalia have the highest incidences of this disease worldwide. The United States, Asia, and other Latin American countries have reported cases less frequently.
The most common agents isolated in African countries are, among eumycetomas, Madurella mycetomatis, and in actinomycetomas, Streptomyces somaliensis and Actinomadura pelletieri. In Mexico, which shares common climatic conditions with the African countries, most cases are found in rural areas and 98% are caused by actinomycetes, mainly N brasiliensis (86%) and Actinomadura madurae (about 8%).[6] In India, 65% of cases are produced by actinomycetes and the rest by eumycetes, mostly M mycetomatis.
Worldwide, approximately 60% of mycetomas cases are of actinomycotic origin.
Mortality/Morbidity
Mycetoma is usually painless; individuals who are affected seek medical attention mainly because of tumefaction and draining sinuses. In cases affecting the thorax or the head, mycetoma can be potentially fatal because of the spread of microorganisms to adjacent organs. Rarely, the disease spreads by hematogenous dissemination (Nocardia asteroides and N brasiliensis).
Sex
Mycetoma is more common in men than in women. The male-to-female ratio is 3:1.
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| White grain | Black grain |
| Acremonium falciforme | Exophiala jeanselmei |
| Acremonium kiliense | Madurella grisea |
| Acremonium recifei | M mycetomatis |
| Cylindrocarpon destructans | M pseudomycetomatis |
| Fusarium moniliforme | Leptosphaeria tomkinsii |
| Fusarium solani | Leptosphaeria senegalensis |
| Neotestudina rosatii | Pyrenochaeta mackinnonii |
| Pseudallescheria boydii | Pyrenochaeta romeroi |
| ---------------- | Phlenodomus avramii |
| Etiologic agent | Grain |
| A madurae | White, large, 1-5 mm in diameter |
| A pelletieri | Red, hard, 1 mm in diameter |
| N brasiliensis | White to yellow, multilobed, soft, < 0.5 mm in diameter |
| N asteroides | Uncommon, white, soft, < 0.5 mm in diameter |
| Nocardia otitidiscaviarum | White to yellow, lobed, < 0.5 mm in diameter |
| Nocardia transvalensis | White to yellow, < 0.5 mm in diameter |
| Nocardia veterana[8] | -- |
| Nocardia mexicana[9] | -- |
| Nocardiopsis dassonvillei | White to yellow, < 0.5 mm in diameter |
| S somaliensis | Yellow, hard, 2 mm in diameter |
| Streptomyces sudanensis | Yellow, hard, 2 mm in diameter |

