Cutaneous Mycetoma

Updated: Jun 09, 2020
  • Author: Oliverio Welsh, MD(DrSc); Chief Editor: Dirk M Elston, MD  more...
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Mycetoma is a chronic, granulomatous disease of the skin and subcutaneous tissue, which sometimes involves muscle, bone, and neighboring organs. [1] 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 appear in the general population. [2, 3, 4]

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. [5]

Also see the article Mycetoma.



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 that in some cases can reach more than 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 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). [6]

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. [7] Immunoglobulin M anti– N brasiliensis antibodies can protect mice from an experimental infection. [8] Activation of cellular immunity and production of cytokines are involved in resistance and elimination of the N brasiliensis bacterial cells.

Salinas-Carmona et al have unveiled aspects of the physiopathogenic mechanisms of experimental actinomycetoma in mice. [9]



Eumycetomas can be produced by a variety of fungi (see Table 1); however, actinomycetomas are mainly produced by bacteria of 4 genera: Nocardia, Actinomadura, Streptomyces, and Nocardiopsis (see Table 2), the last of which is rarely found.

Although traditionally it has been considered that mycetoma is produced by the pathogenic characteristics of the causative agents, it has been observed that genetic polymorphisms involved in neutrophil function are related to either the production of human mycetoma or its size, in the case of M mycetomatis infection. IL-8 (CXCL8), its receptor CXCR2, thrombospondin-4, nitric oxide synthase, and complement receptor 1 have significant differences in mycetoma patients compared with geographically and ethnically matched controls. These findings open the possibility that certain individuals are predisposed to this infection. [10]

Other agents have been identified as causing actinomycetoma (Nocardia harenae and Nocardia takedensis). The clinical pictures are similar, and identification has been achieved by genomic technique. [11, 12]

Table 1. Fungi Causing Mycetoma (Open Table in a new window)

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

Scedosporium apiospermum

(Pseudallescheria boydii)

Pyrenochaeta romeroi


Phlenodomus avramii

Table 2. Microorganisms Causing Actinomycetomas in Humans (Open Table in a new window)

Etiologic agent


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 [13]


Nocardia mexicana [14]


N harenae


N takedensis


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




United States

Mycetoma occasionally occurs in the United States, particularly in the South.


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 incidence 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%). [15] 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.


Mycetoma is more common in men than in women. The male-to-female ratio is 3:1.


Mycetoma predominates in individuals aged 20-40 years.



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).

Actinomycetomas generally respond well to trimethoprim-sulfamethoxazole/amikacin (see Medication) in 90% of cases. In those cases in which bacteria have become resistant to this treatment, antibiotic susceptibility testing should be performed to select the best antimicrobial agent or agents to be used.

Eumycetoma tends to be a more chronic disease, and success with medical therapy is observed in only about 40% of cases. If the response is partial or negative to medical treatment, surgery of the affected area should be performed, and antifungal drugs continued until complete remission of the disease.