Chromoblastomycosis Clinical Presentation

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Apr 16, 2012
 

History

Patients usually do not report discomfort, and they tend to not seek medical care until secondary infection or elephantiasis ensues.

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Physical

The disease appears at the site of a previous often unnoticed or unremembered trauma to the skin. After several years, a small, raised, erythematous, asymptomatic papule develops. As the chromoblastomycosis lesion develops over years, it assumes a scaly and infiltrated aspect, generally leading to either of the 2 most common clinical variants: nodular or plaque. In both types, the surface is verrucous, and lesions spread laterally to contiguous healthy tissue. Note the images below.

Chromoblastomycosis, tumoral form. Chronic diseaseChromoblastomycosis, tumoral form. Chronic disease led to elephantiasis and involvement of the entire lower limb. Plaque lesion on the foot. The verrucous aspect ofPlaque lesion on the foot. The verrucous aspect of the lesion differentiates it from other infectious dermatoses that may present as a verrucous lesion, namely, cutaneous leishmaniasis, sporotrichosis, cutaneous tuberculosis, and cutaneous mycobacteriosis.

In general, the disease remains localized to the area of the initial infection or neighboring skin, but lymphatic and hematogenous dissemination may occur, producing metastatic lesions away from the primary site. The nodular type of lesion normally develops into verrucous, pedunculated, cauliflowerlike florets, while the plaque type spreads peripherally, with an active, raised border, leaving a central healed area with atrophic and yellowish scar tissue.

On the surface of both types of clinical variants, numerous black dots may be observed where the causative organisms are preferentially found. Hemopurulent material covering small ulcerations is commonly observed.

Cutaneous localized annular chromoblastomycosis has been described as well-circumscribed, slow-growing, annular, papulosquamous or papulosquamous-verrucous patches or plaques with no regression despite the use of topical antifungals.[32] These plaques may be atrophic.[33]

Secondary infection with bacteria is common, giving the lesion a characteristic ill odor. Secondary infection is believed to be important in the genesis of lymph stasis and consequently of elephantiasis. In old cases, lesions in different stages of development can be found. Extracutaneous spread may occur rarely, due to hematogenic and lymphatic dissemination. Contiguous spread to the underlying bone may produce an osteolytic lesion.[34]

The sites most commonly affected are the lower extremities, especially the feet. The hands, the arms, and the buttocks are also frequently involved, and sporadic reports mention lesions on the ears, the face, and the breasts.

Auricular chromoblastomycosis due to Fonsecaea pedrosoi, the most common agent found in Brazil, has been described.[35]

Morphological variants occur. Rarely, chromoblastomycosis may resemble sporotrichosis with verrucous nodules and a lymphatic distribution on the forearm expanding into verrucous plaques.[24] Chromoblastomycosis may also be evident as a large cauliflowerlike mass.[36]

Although it is most often evident ranging from a small ulcer, plaques, papulonodular lesions, or cauliflowerlike warty masses and cicatricial forms, it may rarely appear as a phagedenic ulcer on the face.[37]

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Causes

The isolation of the causative fungi from nature on several different occasions has added to the demonstration that fungi gain entry into the host's body through traumatic inoculation[1] ; this finding also confirmed that populations at risk are rural workers who walk barefoot in endemic regions where the causative agents are found.

A Brazilian study has suggested a link between the occurrence of lesions on the buttocks and the habit of sitting on babaçu (Orbignya phalerata) shells. The authors have failed to isolate the causative fungus from the shells.[38] In 2004, Salgado et al[39] were able to isolate the same F pedrosoi from a thorny bush (Mimosa pudica) and from a chromoblastomycosis patient. The lesion had developed after an accident at the site where those bushes grew.

On the other hand, in 1994, Zeppenfeldt et al[22] demonstrated that certain cactaceae from the Falcon state in Venezuela had fungi not only on their surfaces and thorns but also in the medulla. Not coincidentally, the fungus was identified as C carrionii, which is the most commonly found organism in chromoblastomycosis cases in that country. The histologic characteristics of the fungus in plant tissue resembled that found in humans. Experimental inoculation of C carrionii in goats, performed n Venezuela, demonstrated that although chromoblastomycosis affecting that genus of mammals has never been reported, C carrionii caused cellular reactions in goats identical to those seen in humans at the first stages of infection.[40]

In 1989, Tsuneto et al[41] demonstrated a higher frequency of HLA-A29 in patients with chromoblastomycosis; this finding suggests that genetics might have an influence in the acquisition of the disease.

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Contributor Information and Disclosures
Author

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

Eugeniusz Baran, MD, PhD  Professor, Department of Dermatology, Venereology and Allergology, Head, Clinic of Dermatology and Venereology, Wroclaw Medical University, Poland

Eugeniusz Baran, MD, PhD is a member of the following medical societies: European Confederation of Medical Mycology and International Society for Human and Animal Mycology

Disclosure: Nothing to disclose.

Specialty Editor Board

Alexa F Boer Kimball, MD, MPH  Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital

Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD  Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Celgene Honoraria Safety Monitoring Committee

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Luiz Guilherme M Castro, MD, to the development and writing of this article.

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Sclerotic cells on a potassium hydroxide preparation.
Micromorphology of Cladosporium carrionii (left) and Fonsecaea pedrosoi (right), the 2 most commonly isolated agents in chromoblastomycosis.
Chromoblastomycosis, tumoral form. Chronic disease led to elephantiasis and involvement of the entire lower limb.
Plaque lesion on the foot. The verrucous aspect of the lesion differentiates it from other infectious dermatoses that may present as a verrucous lesion, namely, cutaneous leishmaniasis, sporotrichosis, cutaneous tuberculosis, and cutaneous mycobacteriosis.
Culture of Fonsecaea pedrosoi on Sabouraud agar. The black velvety colony has the same macroscopic appearance as the colonies of other chromoblastomycosis-causing agents (eg, Cladosporium carrionii, Fonsecaea compacta, Phialophora verrucosa, Rhinocladiella aquaspersa, Exophiala species).
Hematoxylin and eosin–stained section shows typical sclerotic cells inside an abscess. Sclerotic cells present as round, thick-walled, cigar-colored structures.
 
 
 
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