Mycetoma


Mycetoma

Description, Causes and Risk Factors:

A chronic infection involving the subcutaneous tissue, skin, and contiguous bone; characterized by the formation of localized lesions with tumefactions and multiple draining sinuses. The exudate contains granules that may be yellow, white, red, brown, or black, depending upon the causative agent. Mycetoma is caused by two principal groups of microorganisms: 1) actinomycetoma is caused by actinomycetes, including species of Streptomyces, Actinomadurae, and Nocardiae, 2) eumycetoma is caused by true fungi, including species of Madurellae, Exophialae, Pseudallescheria, Curvulariae, Neotestudina, Pyrenochaeta, Aspergillus, Leptosphaeria, Polycytella, Fusarium, Phialophorae, Corynespora, Cylindrocarpon, Pseudochaetosphaeronema, Bipolaris, and Acremonium.

Mycetoma is a chronic, suppurative infection of the subcutaneous tissue and contiguous bone. The clinical features are fairly uniform, regardless of the organism involved. The feet are the most common site for infection and account for at least two-thirds of cases. Other sites include the lower legs, hands, head, neck, chest, shoulder and arms. Most cases start out as a small hard painless nodule which over time begins to soften on the surface and ulcerate to discharge a viscous, purulent fluid containing grains. The infection slowly spreads to adjacent tissue, including bone, often causing considerable deformity. Sinuses continue to discharge serosanguineous fluid containing the granules which vary in size, color and degree of hardness, depending on the etiologic species. These grains are the hallmark of mycetoma.

The agents of mycetoma are fungi and aerobic filamentous bacteria that have been found on plants and in the soil. The predominance of bacterial versus fungal causes of mycetoma varies among geographic location. The disease is caused by a variety of fungal organisms. These can be divided into those that form dark grains and those that form pale or white grains. Color distinctions are made by observing unstained specimens. Among the fungi causing dark-grained mycetoma, the most common are Madurella mycetomi, Madurella grisea. Other agents include Corynespora cassiicola, Curvularia geniculata, Curvularia lunata, Exophiala jeanselmei, Exophiala oligosperma, Leptosphaeria tompkinsii, Phialophora verrucosa, Plenodomas avramii, Pseudochaetosphaeronema larense, Rhinocladiella atrovirens, Pyrenochaeta mackinnonii, and Pyrenochaeta romeroi. Pseudallescheria boydii is the most common cause of pale-colored grains. Other fungi in that category include Acremonium (Fusarium) falciforme, Acremonium kiliense, Acremonium recifei, Aspergillus flavus, Aspergillus hollandicus, Aspergillus (Emericella) nidulans, Cylindrocarpon cyanescens, Cylindrocarpon destructans, Fusarium solani, Fusarium moniliforme (verticillioides), Neotestudina rosatii, Phaeoacremonium species, and Polycytella hominis. Actinomycetoma is caused by members of the order Actinomycetales, most commonly Nocardia brasiliensis, Actinomadura madurae, Streptomyces somaliensis, and Actinomadura pelliertieri. Cases have been reported that were caused by Actinomadura latina, Nocardia asteroides, Nocardia caviae, Nocardia farcinica, Nocardia otitidiscaviarum, Nocardia mexicana, Nocardia transvalensis, Nocardia veterana, Nocardiopsis dassonvillei, and Streptomyces sudanensis. Actinomycetoma grains are typically white or pale yellow, except those caused by Actinomadura pelliertieri, which are red to pink.

Mycetoma is most commonly found in tropical and subtropical climates, with the highest incidence being reported from endemic areas in the India subcontinent, Sri Lanka, the Middle East, Africa, and Central and South America.

Disease is more common in agricultural workers and outdoor laborers, but is not exclusively seen in rural areas. Disease occurs sporadically throughout most areas of the world, and some postulate that the increased numbers in tropical regions may also be in part the result of decreased use of protective clothing, chiefly shoes, in the warmer, poorer endemic regions.

Symptoms:

Disease begins in most cases as a single, small, painless subcutaneous nodule. This nodule slowly increases in size, becomes fixed to the underlying tissue, and ultimately develops sinus tracts beneath the lesion. These tracts open to the surface and drain purulent material with grains. Grains are several millimeters in diameter and may be seen by close inspection of a gauze bandage covering the sinus tract. Progression to draining sinus tracts can take weeks, months, and even years, occurring more rapidly in actinomycetoma.

Disease can affect the skin, subcutaneous tissue, and eventually contiguous bone, spreading along fascial planes. Overlying skin appears smooth and shiny, and is commonly fixed to the underlying tissue. Skin may be hypo- or hyperpigmented, with signs of both old healed and active sinuses, displaying the cycle of spontaneous healing of older sinuses tracts and simultaneous spread of infection to new areas typical of this disease. Swelling is often firm and nontender, and the overlying skin is not erythematous. Muscle, tendons, and nerves are generally spared direct infection, but extensive local damage may lead to muscle wasting, bone destruction, and limb deformities. Lymphatic spread is rare, although it may follow surgical manipulation.

Diagnosis:

Differential diagnosis includes botryomycosis, chronic bacterial osteomyelitis, tuberculous osteomyelitis, chromoblastomycosis, phaeohyphomycosis, and soft tissue or bone tumor.

    Clinical Material: Tissue biopsy or excised sinus, serosanguineous fluid containing the granules which vary in size, color and degree of hardness, depending on the etiologic species.

  • Direct Microscopy: Serosanguineousfluid containing the granules should be examined using either 10% KOH and Parker ink or calcofluor white mounts, and tissue sections should be stained using H&E (hematoxylin and eosin), PAS digest, and Grocott's methenamine silver (GMS).

  • Interpretation: The presence of white to yellow or black pigmented grains, from a patient with supporting clinical symptoms should be considered significant. Biopsy and evidence of tissue invasion is of particular importance. Remember direct microscopy or histopathology does not offer a specific identification of the causative agent.

  • Culture: Clinical specimens should be inoculated onto primary isolation media, like Sabouraud's dextrose agar.

  • Serology: There are currently no commercially available serological procedures for the diagnosis of mycetoma.

  • Identification: Characteristic clinical, microscopic and culture features.

Treatment:

Treatment of this disease has proven to be difficult, and typically includes antimicrobial agents and surgery. Short of amputation, surgery alone is rarely successful in the treatment of mycetoma, but removal of smaller lesions or debulking of larger ones does play an important role, especially in the management of fungal disease. Because chemotherapy varies for actinomycetoma and eumycetoma, at a minimum the clinician must differentiate whether a mycetoma is caused by actinomycetes or fungi. Ideally, recovery of the causative organism can allow identification of species, and perhaps even susceptibility testing, to guide therapy. Treatment regimens are currently based on expert opinion because no randomized controlled trials have been performed. Duration of therapy is also not defined, and most patients receive 3 to 24 months of therapy to obtain an adequate response.

The most commonly described regimens include streptomycin plus either sulfamethoxazole and trimethoprim (SMZ-TMP) or dapsone.

Antifungal therapy of eumycetoma most commonly includes the use of azole antifungals, because amphotericin B has not been effective in producing long-term cures. Itraconazole (400 mg/day) or ketoconazole (200 to 400 mg/day) are considered first-line azole agents in the treatment of this disease.

No preventive vaccine is available against any of the causative agents of mycetoma. Disease prevention is best accomplished by reduction of the incidence of the traumatic inoculation of the causative organisms. Wearing of shoes and clothing to protect against splinters and thorn pricks should be stressed. Debilitating disease can be prevented by early identification and treatment of lesions, usually with minor surgery and chemotherapy.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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