Mycetoma

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Background

Mycetoma is a chronic subcutaneous infection caused by actinomycetes or fungi. This infection results in a granulomatous inflammatory response in the deep dermis and subcutaneous tissue, which can extend to the underlying bone. Mycetoma is characterized by the formation of grains containing aggregates of the causative organisms that may be discharged onto the skin surface through multiple sinuses.[1] Mycetoma was first described in the mid 1800s and initially named Madura foot, after the region of Madura in India where the disease was first identified.

Mycetoma caused by microaerophilic actinomycetes is termed actinomycetoma, and mycetoma caused by true fungi is called eumycetoma.[2]

These conditions are to be differentiated from actinomycosis, which is an endogenous suppurative infection caused by Actinomyces israelii or other species of Actinomyces or related bacteria, affecting the cervical-facial, thoracic, and pelvic sites (the latter is usually associated with the use of intrauterine devices). The branching bacteria that cause actinomycosis are non–acid-fast anaerobic or microaerophilic bacteria. These bacteria are smaller than 1 µm in diameter, smaller than eumycotic agents. On the other hand, the agents that cause actinomycetoma are always aerobic and are sometimes weakly acid-fast.

The term mycetoma can also be found incorrectly referring to a fungus ball in a preexisting cavity in the lung or within a paranasal sinus, most often caused by Aspergillus species.[3]

More than 20 species of fungi and bacteria can cause mycetoma. The ratio of mycetoma cases caused by bacteria (actinomycetoma) to those caused by true fungi (eumycetoma) is 197:67.

Pathophysiology

The body parts affected most commonly in persons with mycetoma include the foot or lower leg, with infection of the dorsal aspect of the forefoot being typical. The hand is the next most common location; however, mycetoma lesions can occur anywhere on the body. Lesions on the chest and back are frequently caused by Nocardia species, whereas lesions on the head and neck are usually caused by Streptomyces somaliensis.

The causative organism enters through sites of local trauma (eg, cut on the hand, foot splinter, local trauma related to carrying soil-contaminated material). A neutrophilic response initially occurs, which may be followed by a granulomatous reaction. Spread occurs through skin facial planes and can involve the bone. Hematogenous or lymphatic spread is uncommon.

Epidemiology

Frequency

United States

Mycetoma is rare in the United States. Some cases are due to increasing international travel. Rarely, mycetoma is acquired on US soil.[4] Pseudallescheria boydii (Scedosporium apiospermum) is the most common cause of this condition.

International

Mycetoma is endemic in Africa, from Sudan and Somalia through Mauritania and Senegal. Other endemic countries include Mexico and India. Mycetoma can also be found in natives of areas of Central and South America and the Middle or Far East between latitudes 15°S and 30°N.

Eumycetoma is more common in areas where the average rainfall is scarce (ie, < 350 mm), whereas actinomycetoma tends to appear in areas with abundant rainfall (ie, >600 mm)[5] and has been described in Southeast Asia.[6]

In Sudanese hospitals, at least 300-400 patients are diagnosed with mycetoma every year.

Mortality/Morbidity

Mycetoma causes disfigurement but is rarely fatal in the absence of skull involvement. The lesions are painless and slowly progressive; however, secondary bacterial infection or bone expansion may cause pain. In advanced cases, deformities or ankylosis and their corresponding disabilities can appear. Patients who are immunocompromised or who have undergone transplantation can develop invasive infection.


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Mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years.


View Image

Frontal view of mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years.

Race

Mycetoma has no apparent racial predilection.

Sex

Mycetoma has a male-to-female ratio of 183:81.

Age

Mycetoma is most common in persons aged 20-50 years.

History

Physical

Causes

Laboratory Studies

Imaging Studies

Procedures

Perform a deep wedge biopsy or puncture and fine-needle aspiration to obtain a grain sample. The aspirated material is processed to form cell blocks and further studied as for routine tissue histopathological examination.[13] Fine-needle aspiration cytology allows differentiating actinomycetoma from eumycetoma.[14]

Histologic Findings

Grains are surrounded closely and sometimes infiltrated by neutrophils. The causal agent can be stained better in biopsy samples with Gram stain (actinomycetoma) or Gomori methenamine silver or periodic acid-Schiff stains (eumycetoma).

For mycetomas in which causative infectious agents cannot be isolated, histology may prove beneficial by avoiding inadvertent use of combined antifungal and antimicrobial agents so that a correct therapeutic modality can be decided.[15]

Staging

Radiographic staging of bone involvement can be found in Imaging Studies.

Medical Care

In the treatment of mycetoma, antibiotic or antifungal therapy should be attempted first and may need to be combined with surgery,[1] especially for eumycetoma lesions in the extremities.[16]

External beam radiotherapy in doses ranging from 3.5-14 Gy has been considered successful treatment in a few selected cases.[17]

Surgical Care

Surgery is recommended for localized mycetoma lesions that can be excised completely without residual disability. Surgical reduction of large lesions can improve the patient's response to medical treatment.[18] However, partial surgical resection without subsequent use of appropriate antimicrobial or antifungal agents is prone to failure.

Consultations

Consultation with specialists in infectious disease or tropical medicine is advised in areas of the world where mycetoma is unfamiliar.

Medication Summary

Actinomycetoma is a bacterial infection that can respond to antibiotics[19] if treatment is administered early in the course of the disease.[20] A combination of 2 drugs in 5-week cycles is used. If needed, the cycles can be repeated once or twice. The following agents have been used in combination: trimethoprim-sulfamethoxazole (TMP-SMZ), dapsone (diaminodiphenylsulfone), and streptomycin sulfate. Amikacin can be substituted for streptomycin but is usually kept as a second-line drug because of its cost.

The combination of amikacin with cotrimoxazole is known as the Welsh regimen. Adding rifampin to the Welsh regimen allows for remissions without recurrence.[21]

In one case report, a patient required salvage therapy with amikacin and imipenem for 6 months.[22] An effective and convenient regimen combining a short course of intravenous gentamicin with a 6-month oral course of cotrimoxazole and doxycycline has been described.[23, 24]

Although eumycetoma may respond partially to antifungal agents, surgical removal is usually done first.[25] Madurella mycetomatis mycetoma may respond to ketoconazole but is best treated with itraconazole.[26] P boydii (S apiospermum) mycetoma should be treated primarily with voriconazole, although it may also respond to itraconazole. Other agents that cause eumycetoma may respond intermittently to itraconazole or amphotericin B. The minimum treatment duration is 10 months.

Voriconazole is the drug of choice for invasive infections caused by agents of eumycetoma in immunocompromised patients.

Posaconazole is highly active in vitro against Madurella mycetomatis, but terbinafine is only moderately active. Since posaconazole has an excellent safety profile, it might provide an important alternative in mycetoma therapy.[27]

Madurella mycetomatis is not susceptible to the echinocandins.[28]

Doxycycline (Bio-Tab, Doryx, Doxy, Periostat, Vibramycin, Vibra-Tabs)

Clinical Context:  Drug of choice. Broad-spectrum, synthetically derived bacteriostatic antibiotic in the tetracycline class. Almost completely absorbed, concentrates in bile, and is excreted in urine and feces as a biologically active metabolite in high concentrations. Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. May block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Trimethoprim-sulfamethoxazole (Bactrim DS, Septra)

Clinical Context:  DOC; inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Should be used continuously in combination with another antimicrobial for 5 wk. Cycle may be repeated prn.

Amikacin (Amikin)

Clinical Context:  Irreversibly binds to 30S subunit of bacterial ribosomes, blocks recognition step in protein synthesis, and causes growth inhibition.

Should be given continuously for 3 wk. Although somewhat expensive, it usually is active against the bacteria causing actinomycetoma. Use the patient's IBW for dosage calculation.

Dapsone (Avlosulfon)

Clinical Context:  Bactericidal and bacteriostatic against mycobacteria. Mechanism of action is similar to sulfonamides where competitive antagonists of PABA prevent formation of folic acid, inhibiting bacterial growth. Lowest-cost regimen. Change to TMP-SMZ if no response occurs after 1 mo.

Rifampin (Rimactane, Rifadin)

Clinical Context:  For use in combination with at least 1 other agent. Inhibits DNA-dependent bacterial but not mammalian RNA polymerase. Cross-resistance may occur.

Imipenem and cilastatin (Primaxin)

Clinical Context:  For treatment of multiple-organism infections in which other agents do not have wide spectrum coverage or are contraindicated due to potential for toxicity.

Gentamicin (Garamycin)

Clinical Context:  Aminoglycoside antibiotic for gram-negative coverage bacteria, including Pseudomonas species. Synergistic with beta-lactamase against enterococci. Interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits. Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of distribution, as well as body space into which agent needs to distribute. Gentamicin may be given IV/IM. Each regimen must be followed by at least trough level drawn on third or fourth dose, 0.5 h before dosing; may draw peak level 0.5 h after 30-min infusion.

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of a clinical setting suggestive of actinomycetoma.

Ketoconazole (Nizoral)

Clinical Context:  Fungistatic activity. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.

Itraconazole (Sporanox)

Clinical Context:  Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Amphotericin B (Fungizone)

Clinical Context:  Polyene antibiotic produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death.

Conventional formulation (complexed with deoxycholate) has a poor tolerability profile. Liposomal amphotericin B incorporates the drug into small unilamellar liposomes; this formulation retains the antifungal activity with less hypokalemia, anemia and infusion reactions, and far less nephrotoxicity than the conventional formulation.

Although the acquisition cost of liposomal amphotericin B is considerably higher than that of the conventional formulation, when adverse effects are considered, the calculated total costs of treatment for fungal infections are not clearly different.

Voriconazole (VFEND)

Clinical Context:  Used for primary treatment of invasive aspergillosis and salvage treatment of Fusarium species or S apiospermum infections. A triazole antifungal agent that inhibits fungal cytochrome P450-mediated 14 alpha-lanosterol demethylation, which is essential in fungal ergosterol biosynthesis.

Class Summary

In combination with surgical therapy, antifungal agents may help to attain partial response in cases of eumycetoma.

Further Outpatient Care

Patients with mycetoma should receive maintained medical treatment and follow-up care for at least 10 months.

Deterrence/Prevention

Educate patients to avoid activities that expose them to agents of mycetoma. Instruct patients to avoid carrying sticks and thorny branches that have had contact with soil, especially if contaminated with cattle dung.[8]

The glycolytic enzyme fructose-bisphosphate aldolase (FBA) is expressed on the hyphae present in the mycetoma grain. FBA antibody levels were found to be significantly higher in eumycetoma patient sera when compared with healthy Sudanese controls. Therefore, FBA might be useful as candidate antigen for a future vaccine against mycetoma.[29]

Complications

Complications of mycetoma result mainly from toxicity due to prolonged administration of antimicrobial or antifungal drugs.

Amputation may result from neglected chronic infections.

Secondary bacterial infections can progress to full-blown bacteremia or septicemia, resulting in death.[1]

Prognosis

Mycetoma carries a good prognosis if the disease is promptly diagnosed and treated. Although mycetoma carries a low risk of mortality, amputations or ankylosis can lessen the quality of life.[30]

In late stages of mycetoma, the treatment response is limited.

Author

Basilio J Anía, MD, Associate Professor of Infectious Diseases, Universidad de Las Palmas de Gran Canaria; Consultant in Internal Medicine, Hospital Universitario Dr. Negrín, Spain

Disclosure: Nothing to disclose.

Coauthor(s)

Margarita Asenjo, MD, Associate Professor, Department of Radiology, Medical School of the University of Las Palmas De Gran Canaria, Spain

Disclosure: Nothing to disclose.

Raphael J Kiel, MD, Associate Professor of Medicine, Wayne State University School of Medicine; Associate Professor of Medicine, Oakland University William Beaumont School of Medicine; Consulting Staff, Infectious Diseases Division, William Beaumont Hospital; Consulting Staff, Infectious Diseases Division Providence Hospital

Disclosure: Nothing to disclose.

Specialty Editors

Larry I Lutwick, MD, Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Disclosure: Nothing to disclose.

References

  1. Venkatswami S, Sankarasubramanian A, Subramanyam S. The madura foot: looking deep. Int J Low Extrem Wounds. Mar 2012;11(1):31-42. [View Abstract]
  2. van Belkum A, Fahal A, van de Sande WW. Mycetoma caused by Madurella mycetomatis: a completely neglected medico-social dilemma. Adv Exp Med Biol. 2013;764:179-89. [View Abstract]
  3. Hospenthal DR. Agents of Mycetoma. In: Mandell GL, Bennett JE, Dolin R. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 2. 7th. Philadelphia, PA (U.S.A.): Churchill Livingstone Elsevier; 2010:3281-3285.
  4. Rouphael NG, Talati NJ, Franco-Paredes C. A painful thorn in the foot: a case of eumycetoma. Am J Med Sci. Aug 2007;334(2):142-4. [View Abstract]
  5. Bakshi R, Mathur DR. Incidence and changing pattern of mycetoma in western Rajasthan. Indian J Pathol Microbiol. Jan-Mar 2008;51(1):154-5. [View Abstract]
  6. Rattanavong S, Vongthongchit S, Bounphamala K, Vongphakdy P, Gubler J, Mayxay M, et al. Actinomycetoma in SE Asia: the first case from Laos and a review of the literature. BMC Infect Dis. Dec 12 2012;12:349. [View Abstract]
  7. Ahmed AO, van Leeuwen W, Fahal A, et al. Mycetoma caused by Madurella mycetomatis: a neglected infectious burden. Lancet Infect Dis. Sep 2004;4(9):566-74. [View Abstract]
  8. de Hoog GS, Ahmed SA, Najafzadeh MJ, Sutton DA, Keisari MS, Fahal AH, et al. Phylogenetic findings suggest possible new habitat and routes of infection of human eumyctoma. PLoS Negl Trop Dis. May 2013;7(5):e2229. [View Abstract]
  9. Abd El-Bagi ME, Fahal AH. Mycetoma revisited. Incidence of various radiographic signs. Saudi Med J. Apr 2009;30(4):529-33. [View Abstract]
  10. El Shamy ME, Fahal AH, Shakir MY, Homeida MM. New MRI grading system for the diagnosis and management of mycetoma. Trans R Soc Trop Med Hyg. Dec 2012;106(12):738-42. [View Abstract]
  11. Kumar J, Kumar A, Sethy P, et al. The dot-in-circle sign of mycetoma on MRI. Diagn Interv Radiol. Dec 2007;13(4):193-5. [View Abstract]
  12. Jain V, Makwana GE, Bahri N, Mathur MK. The "dot in circle" sign on MRI in maduramycosis: a characteristic finding. J Clin Imaging Sci. 2012;2:66. [View Abstract]
  13. Yousif BM, Fahal AH, Shakir MY. A new technique for the diagnosis of mycetoma using fixed blocks of aspirated material. Trans R Soc Trop Med Hyg. Jan 2010;104(1):6-9. [View Abstract]
  14. Hemalata M, Prasad S, Venkatesh K, Niveditha SR, Kumar SA. Cytological diagnosis of actinomycosis and eumycetoma: a report of two cases. Diagn Cytopathol. Dec 2010;38(12):918-20. [View Abstract]
  15. Chufal SS, Thapliyal NC, Gupta MK. An approach to histology-based diagnosis and treatment of Madura foot. J Infect Dev Ctries. Sep 17 2012;6(9):684-8. [View Abstract]
  16. Ahmed AA, van de Sande WW, Fahal A, et al. Management of mycetoma: major challenge in tropical mycoses with limited international recognition. Curr Opin Infect Dis. Apr 2007;20(2):146-51. [View Abstract]
  17. Falkson C, Sur R, Pacella J. External beam radiotherapy: a treatment option for massive haemoptysis caused by mycetoma. Clin Oncol (R Coll Radiol). Jun 2002;14(3):233-5. [View Abstract]
  18. Maina AM, Macharia JT. Alleviating a Nomad's Anguish: Successful Treatment of a Case of Leg Mycetoma-A Case Report. Case Rep Orthop. 2012;2012:753174. [View Abstract]
  19. Welsh O, Vera-Cabrera L, Welsh E, Salinas MC. Actinomycetoma and advances in its treatment. Clin Dermatol. Jul 2012;30(4):372-81. [View Abstract]
  20. Agarwal US, Besarwal RK, Gupta R, Agarwal P. Treatment of actinomycetoma foot - our experience with ten patients. J Eur Acad Dermatol Venereol. Nov 26 2012;[View Abstract]
  21. Damle DK, Mahajan PM, Pradhan SN, Belgaumkar VA, Gosavi AP, Tolat SN, et al. Modified Welsh regimen: a promising therapy for actinomycetoma. J Drugs Dermatol. Sep 2008;7(9):853-6. [View Abstract]
  22. Baril L, Boiron P, Manceron V, et al. Refractory craniofacial actinomycetoma due to Streptomyces somaliensis that required salvage therapy with amikacin and imipenem. Clin Infect Dis. Aug 1999;29(2):460-1. [View Abstract]
  23. Ramam M, Bhat R, Garg T, et al. A modified two-step treatment for actinomycetoma. Indian J Dermatol Venereol Leprol. Jul-Aug 2007;73(4):235-9. [View Abstract]
  24. Palit A, Ragunatha S, Inamadar AC. Actinomycetoma: dramatic response to modified two-step regimen. Int J Dermatol. Apr 2011;50(4):446-9. [View Abstract]
  25. Estrada R, Chávez-López G, Estrada-Chávez G, López-Martínez R, Welsh O. Eumycetoma. Clin Dermatol. Jul 2012;30(4):389-96. [View Abstract]
  26. Fahal AH, Rahman IA, El-Hassan AM, Rahman ME, Zijlstra EE. The safety and efficacy of itraconazole for the treatment of patients with eumycetoma due to Madurella mycetomatis. Trans R Soc Trop Med Hyg. Mar 2011;105(3):127-32. [View Abstract]
  27. van Belkum A, Fahal AH, van de Sande WW. In vitro susceptibility of Madurella mycetomatis to posaconazole and terbinafine. Antimicrob Agents Chemother. Apr 2011;55(4):1771-3. [View Abstract]
  28. van de Sande WW, Fahal AH, Bakker-Woudenberg IA, van Belkum A. Madurella mycetomatis is not susceptible to the echinocandin class of antifungal agents. Antimicrob Agents Chemother. Jun 2010;54(6):2738-40. [View Abstract]
  29. de Klerk N, de Vogel C, Fahal A, van Belkum A, van de Sande WW. Fructose-bisphosphate aldolase and pyruvate kinase, two novel immunogens in Madurella mycetomatis. Med Mycol. Jul 5 2011;[View Abstract]
  30. Zein HA, Fahal AH, Mahgoub el S, El Hassan TA, Abdel-Rahman ME. Predictors of cure, amputation and follow-up dropout among patients with mycetoma seen at the Mycetoma Research Centre, University of Khartoum, Sudan. Trans R Soc Trop Med Hyg. Nov 2012;106(11):639-44. [View Abstract]
  31. Abd El Bagi ME. New radiographic classification of bone involvement in pedal mycetoma. AJR Am J Roentgenol. Mar 2003;180(3):665-8. [View Abstract]
  32. Akhtar MA, Latief PA. Actinomycetoma pedis. Postgrad Med J. Nov 1999;75(889):671. [View Abstract]
  33. Bapat KC, Pandit AA. Actinomycotic mycetoma. Report of a case with diagnosis by fine needle aspiration. Acta Cytol. Nov-Dec 1991;35(6):770-2. [View Abstract]
  34. Boiron P, Locci R, Goodfellow M, et al. Nocardia, nocardiosis and mycetoma. Med Mycol. 1998;36 Suppl 1:26-37. [View Abstract]
  35. Bouza E, Munoz P. Invasive infections caused by Blastoschizomyces capitatus and Scedosporium spp. Clin Microbiol Infect. Mar 2004;10 Suppl 1:76-85. [View Abstract]
  36. Campagnaro EL, Woodside KJ, Early MG, et al. Disseminated Pseudallescheria boydii (Scedosporium apiospermum) infection in a renal transplant patient. Transpl Infect Dis. Dec 2002;4(4):207-11. [View Abstract]
  37. Chaveiro MA, Vieira R, Cardoso J, et al. Cutaneous infection due to Scedosporium apiospermum in an immunosuppressed patient. J Eur Acad Dermatol Venereol. Jan 2003;17(1):47-9. [View Abstract]
  38. Chávez G, Estrada R, Bonifaz A. Perianal actinomycetoma experience of 20 cases. Int J Dermatol. Aug 2002;41(8):491-3. [View Abstract]
  39. Coukell AJ, Brogden RN. Liposomal amphotericin B. Therapeutic use in the management of fungal infections and visceral leishmaniasis. Drugs. Apr 1998;55(4):585-612. [View Abstract]
  40. Develoux M, Dieng MT, Kane A, et al. [Management of mycetoma in West-Africa]. Bull Soc Pathol Exot. Jan 2003;96(5):376-82. [View Abstract]
  41. Dieng MT, Sy MH, Diop BM, et al. [Mycetoma: 130 cases]. Ann Dermatol Venereol. Jan 2003;130(1 Pt 1):16-9. [View Abstract]
  42. EL Hag IA, Fahal AH, Gasim ET. Fine needle aspiration cytology of mycetoma. Acta Cytol. May-Jun 1996;40(3):461-4. [View Abstract]
  43. Fahal AH. Mycetoma: a thorn in the flesh. Trans R Soc Trop Med Hyg. Jan 2004;98(1):3-11. [View Abstract]
  44. Fahal AH, Hassan MA. Mycetoma. Br J Surg. Nov 1992;79(11):1138-41. [View Abstract]
  45. Fahal AH, Sheik HE, Homeida MM, et al. Ultrasonographic imaging of mycetoma. Br J Surg. Aug 1997;84(8):1120-2. [View Abstract]
  46. Fletcher CL, Moore MK, Hay RJ. Eumycetoma due to Madurella mycetomatis acquired in Jamaica. Br J Dermatol. Dec 2001;145(6):1018-21. [View Abstract]
  47. Greenberg AK, Knapp J, Rom WN, et al. Clinical presentation of pulmonary mycetoma in HIV-infected patients. Chest. Sep 2002;122(3):886-92. [View Abstract]
  48. Hay RJ. Fungal infections. In: Cook GC, ed. Manson's Tropical Diseases. 20th ed. London, UK: WB Saunders; 1996:1047-74.
  49. Hay RJ, Moore M. Mycology. In: Champion RH, Wilkinson DS, Ebling FJG, Breathnach SM, eds. Rook/Wilkinson/Ebling Textbook of Dermatology. Vol 2. 6th ed. Oxford, UK: Blackwell Science; 1998:1277-376.
  50. Khatri ML, Al-Halali HM, Fouad Khalid M, et al. Mycetoma in Yemen: clinicoepidemiologic and histopathologic study. Int J Dermatol. Sep 2002;41(9):586-93. [View Abstract]
  51. Lichon V, Khachemoune A. Mycetoma : a review. Am J Clin Dermatol. 2006;7(5):315-21. [View Abstract]
  52. Mahgoub ES. Medical management of mycetoma. Bull World Health Organ. 1976;54(3):303-10. [View Abstract]
  53. Maiti PK, Ray A, Bandyopadhyay S. Epidemiological aspects of mycetoma from a retrospective study of 264 cases in West Bengal. Trop Med Int Health. Sep 2002;7(9):788-92. [View Abstract]
  54. Mellinghoff IK, Winston DJ, Mukwaya G, et al. Treatment of Scedosporium apiospermum brain abscesses with posaconazole. Clin Infect Dis. Jun 15 2002;34(12):1648-50. [View Abstract]
  55. Mendez-Tovar LJ, Mondragon-Gonzalez R, Manzano-Gayosso P, et al. [Immunoglobulins in patients with Nocardia brasiliensis actinomycetoma]. Rev Argent Microbiol. Oct-Dec 2004;36(4):174-8. [View Abstract]
  56. O'Bryan TA. Pseudallescheriasis in the 21st century. Expert Rev Anti Infect Ther. Oct 2005;3(5):765-73. [View Abstract]
  57. Poncio Mendes R, Negroni R, Bonifaz A, et al. New aspects of some endemic mycoses. Med Mycol. 2000;38 Suppl 1:237-41. [View Abstract]
  58. Queiroz-Telles F, McGinnis MR, Salkin I, et al. Subcutaneous mycoses. Infect Dis Clin North Am. Mar 2003;17(1):59-85, viii. [View Abstract]
  59. Ramam M, Garg T, D'Souza P, et al. A two-step schedule for the treatment of actinomycotic mycetomas. Acta Derm Venereol. Sep-Oct 2000;80(5):378-80. [View Abstract]
  60. Saag MS. Mycetoma. In: Goldman L, Bennett JC, eds. Cecil Textbook of Medicine. ed. Philadelphia, Pa: WB Saunders; 2000:1885-7.
  61. Saarinen KA, Lestringant GG, Czechowski J, et al. Cutaneous nocardiosis of the chest wall and pleura--10-year consequences of a hand actinomycetoma. Dermatology. 2001;202(2):131-3. [View Abstract]
  62. Sharma N, Mendiratta V, Sharma RC, et al. Pulse therapy with amikacin and dapsone for the treatment of actinomycotic foot: a case report. J Dermatol. Oct 2003;30(10):742-7. [View Abstract]

Mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years.

Frontal view of mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years.

MRI coronal section of mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years. On this T1-potentiated image, a large heterogenous mass surrounds the cranium. Bone invasion can be observed only in the area of the zygomatic fossa.

MRI with coronal view of mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years. The mycetoma mass invades the left parapharyngeal space and almost reaches the lumen of the pharynx.

Mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years.

Frontal view of mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years.

MRI coronal section of mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years. On this T1-potentiated image, a large heterogenous mass surrounds the cranium. Bone invasion can be observed only in the area of the zygomatic fossa.

MRI with coronal view of mycetoma in a 47-year-old shepherd from Mauritania who had a painless progressive swelling of the face for more than 20 years. The mycetoma mass invades the left parapharyngeal space and almost reaches the lumen of the pharynx.