Chromomycosis B43.0

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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blastomycosis nigra; Chromoblastomycosis; Dematiacea mycosis; Dematiacea mycosis with round fungal cells in the tissue; Fonsecas disease; Moss foot; mossy foot; Pedrosos disease; verrucosa dermatitis

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Rudolph 1914; Lane 1915; Medlar 1915

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Chronic progressive mycosis endemic to Brazil, the southern USA and Russia, characterized by papular, nodular, verrucous and papillomatous-vegetative lesions of the skin.

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Roundish, yellow-brown fungal cells, which grow to 4-12 µm in size and reproduce by cleavage. Brown hyphae can occur in and on the epidermis. The currently recognized pathogens include 6 species with identical structures in the tissue as well as characteristic intrinsic colour. They are also called dematiacaea, dematiaceae or black fungus. These are the species listed below:

  • Phialophora verrucosa jeanselmii or gougerotii
  • Fonsecae pedrosoi
  • fonsecae compacta
  • Cladosporium (also Cladophialospora) carrionii
  • botromyces caespitosus
  • Rhinocladiella aquaspersa (so far only described in isolated cases).

Black fungus lives in the soil and in dead plant tissue. This fact explains the frequency of the disease in agricultural workers. Thus, the typical predilection sites are also the lower extremities.

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Described worldwide, mainly in tropical zones, e.g. in the south of the USA, South America, Russia and Japan; sporadically in Finland, Czech Republic, Slovakia, Germany. In Europe, infection may occur by crushing tropical boxwood.

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Penetration of the fungi sitting on wood and plants through small fissures or cracks in the skin. Rare inoculation after insect bites.

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Mainly rural population. Men are affected significantly more often than women. Preferably in the age group between 30-50 years. Less frequently in children and adolescents (Khan S et al. 2019).

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Mainly lower leg, foot and hand.

Clinical features
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Skin changes, especially on the lower extremities and exposed parts of the body. Rarely on the upper extremity of the face and trunk. Formation of slightly aching or even itching papules and pustules at the infection sites; later slowly swelling red lumps. These may ulcerate over time and become secondary bacterially superimposed. Sometimes there are only flat plaques with scarring. In other cases uncharacteristic psoriasiform or eczematous plaques are described. In the untreated state, large, partly map-like verrucous, sometimes cauliflower-like skin growths covered by crusts and dark scales are observed. Bizarrely configured flat ulcers may also occur.

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Tuberculoid granulation tissue, miliary abscesses, pseudoepitheliomatous epidermal hyperplasia. Fungi: Scleroting (fumagoid) bodies, Medlar bodies, copper-pennies, brownish, thick-walled cells, mycelium with lateral spore formation.

It is recommended to use the highly sensitive staining according to Gomori-Grocott or Fontana-Masson to detect the fungal elements.

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Cultural (Sabouraud glucose agar or cycloheximide-containing media) or histological pathogen detection from biopsy specimen. Culture: Dark, olive brown, velvety culture, pigmented septated hyphae.

General therapy
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The disease is often (especially when infected with Fonsecaea pedrosoi) resistant to therapy and protracted. Different forms of therapy are described. Circumscribed skin foci in early stages of the disease should be removed generously by surgery.

Alternatively cryosurgery. Icing times and frequencies depending on the location and depth of the skin changes.

Alternatively, local heat therapy (permanent for a few weeks at 44-46 °C) is also described as successful.

In case of development of elephantiasis chromomycetica, manual and intermittent lymphatic drainage measures(see below lymphedema).

External therapy
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In case of intolerance to systemic antimycotics, therapy with local Amphotericin B preparations or ketoconazole creams may be attempted.

Internal therapy
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  • Often the disease is too advanced for local therapy.
  • Therapy of choice is itraconazole (e.g. Sempera Kps.): 200-400 mg/day over 6-20 months (success rate approx. 65%).
  • Alternatively Terbinafine: 500 mg/day p.o. over 6-12 months.
  • For therapy-resistant courses: Posaconazole (Noxafil) 2 times/day 400 mg (10 ml) p.o. (daily dose 800 mg) or 4 times/day 200 mg (5 ml) p.o. The duration of therapy depends on the severity of the underlying disease, recovery from immunosuppression and clinical response.
  • Alternative: The former "classical therapy" consisted of Amphotericin B 0.1 mg/kg bw/day i.v. (slowly increasing to max. 1 mg/kg bw/day) in combination with 5-flucytosine (Ancotil) 150 mg/kg bw/day i.v. in 4 doses. The therapy is associated with considerable NW.

Operative therapie
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  • Because of the uncertain drug therapy, surgical treatment of circumscribed nodular foci is recommended. Cryosurgery or caustic measures have been recommended for extensive vegetative lesions.

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Chronic course, rarely also spontaneous standstill. S.a.u. Elephantiasis chromomycetica.

Case report(s)
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A 50-year-old farm worker from Nicaragua presented with a large, partly red, partly blackish discoloured, sharply defined, non-painful plaque on his right lower leg. The changes had existed for years and had not bothered him any further.

Findings: The skin lesions were extensive, keloidal solid, partly smooth, slightly scaly, reddish, partly circumscribed cauliflower-like verrucous, grey-blackish acuh crusty.

Histology: lymphocytic and epitheloid cell granulation tissue with miliary granulocytic abscesses, pseudoepitheliomatous epidermal hyperplasia. Detection of brownish, thick-walled spores, also mycelium with lateral spore formation.

Therapy: Itraconazole 200mg/day p.o. After 6 months slight flattening of the plaques. But still no final healing.

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  1. Artuz F (1997) Purple erythematous plaques on the face and left arm. Chromomycosis. Arch Dermatol 133: 1029, 1032
  2. Fernandez-Flores A et al (2014) Morphological findings of deep cutaneous fungal infections. At J Dermatopathol 36:531-553
  3. Khan S et al (2019) A Rare Case of Chromoblastomycosis in a 12-year-old boy. J Pak Med Assoc 69:1390-1393.
  4. Kimura M et al (2003) Multifocal subcutaneous phaeohyphomycosis caused by Phialophora verrucosa. Arch Catholic Lab Med 127: 91-93
  5. Lane CG (1915) A cutaneous disease caused by a new fungus, Phialophora verrucosa. J Cut Dis 33: 840-836
  6. Medlar EM (1915) A cutaneous infection caused by a new fungus, Phialophora verrucosa, with a study of the fungus J Med Res 32: 507-522
  7. Poirriez J et al (2000) A case of chromomycosis treated by a combination of cryotherapy, shaving, oral 5-fluorocytosine, and oral amphotericin B. Am J Trop Med Hyg 63: 61-63
  8. Queiroz cell fet al. (2015) chromoblastomycosis: a neglected tropical disease. Rev Inst Med Trop Sao Paulo 57 Suppl 19:46-50.
  9. Restrepo A (1994) Treatment of tropical mycosis. J Am Acad Dermatol 31: 91-102
  10. Rudolph M (1914) About the Brazilian "Figueira". Arch ship and tropics Hyg 18: 498-499
  11. Wortman PD (1995) Concurrent chromoblastomycosis caused by fonsecaea pedrosoi and actinomycetoma caused by nocardia brasiliensis. J Am Acad Dermatol 32: 390-392
  12. Yu R (1995) Successful treatment of chromoblastomycosis with itraconazole. Mycoses 38: 79-83


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Last updated on: 29.10.2020