Skin nontumor

Infectious disorders

Chromoblastomycosis


Author: Ha Kirsten Do

Last author update: 1 September 2010
Last staff update: 7 March 2024

Copyright: 2002-2024, PathologyOutlines.com, Inc.

PubMed Search: Fungi - Chromoblastomycosis

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Cite this page: Do HK. Chromoblastomycosis. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/skinnontumorfungiChromoblastomycosis.html. Accessed May 1st, 2024.
Definition / general
  • Chronic deep cutaneous fungal infection usually affecting the limbs at the inoculation site

  • Causative agents include several fungi found in soil, wood and decaying plant material:
    • Phialophora verrucosa
    • Fonsecaea pedrosi (most common pathogen, accounts for > 90% of the cases in South America)
    • Fonsecaea compacta
    • Cladosporium carrionii
    • Rhinocladiella aquaspersa (Ramichloridium cerophilum)
Epidemiology
  • First case of chromoblastomycosis was reported by Pedroso in Brazil in 1911
  • Incidence of chromoblastomycosis is greatest in tropical and subtropical regions, including Madagascar, Brazil, Gabon, Colombia, Venezuela, Cuba, the Dominican Republic and Mexico
  • Up to 70% of cases occur in males
  • Barefooted farmers account for almost 75% of patients with chromoblastomycosis
Clinical features
  • Common clinical presentation is verrucous lesion over extremities of adult men engaged in outdoor work (Indian J Pathol Microbiol 2010;53:666)
  • The disease is slowly progressive - the average time between the initial lesion and the clinical diagnosis is 15 years
  • Lesion starts as a small firm red / gray bump on the traumatized skin on the foot or hand
  • Grows slowly (2 mm/year) to form raised hyperkeratotic (crusted, warty-looking) plaque
  • The affected limp can be enlarged (elephantiasis)
  • Can develop satellites lesions (new lesions near primary lesion)
  • Rarely, squamous cell carcinoma develops within longstanding chromoblastomycosis (An Bras Dermatol 2010;85:267)

  • Diagnosis: culture at 25 - 30 degrees Celsius grows olive-green to black fungal colonies after 1 - 2 weeks
Treatment
  • Treatment is difficult and long
  • A Mexican study showed 30% cure rate, 60% improvement, and 10% failed therapy
  • Smaller lesions are best treated with surgical excision or cryotherapy (multiple treatments may span up to 10 years)
  • Extensive lesions can be treated with itraconazole (up to several years), or terbinafine (up to several months)
  • Often dramatic improvement at first, but difficult to cure
  • Some studies suggest a multidrug approach is more effective: itraconazole + flucytosine; flucytosine + amphotericin B
  • Recalcitrant lesions can be treated with a combination of itraconazole and cryotherapy or local hyperthermia or CO2 laser vaporization
Clinical images

Images hosted on other servers:

Hyperkeratotic plaque

Cultures are
typically olive
black with a
suede-like surface

Microscopic (histologic) description
  • Clinical suspicious is important to alert pathologists to check for sclerotic bodies, which may be rare
  • The classical histopathological hallmarks are pseudoepitheliomatous hyperplasia with intraepidermal abscess and pigmented fungal sclerotic bodies (Medlar bodies or copper bodies)
  • Fungi appear in clusters that reproduce by equatorial septation rather than budding
  • Fungal stains show fungi within macrophages and rarely in factor XIIIa positive dedrocytes or Langerhan cells
Microscopic (histologic) images

Images hosted on other servers:

Sclerotic bodies: H&E and KOH prep

H&E stain of
sclerotic bodies in
an intraepidermal
abscess

Skin biopsy specimen

Cladosporium carrionii (left) and Fonsecaea pedrosoi (right), the 2 most common pathogenic fungi causing chromoblastomycosis

Differential diagnosis
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