Chromoblastomycosis Clinical Presentation: History, Physical Examination, Complications

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Presentation

History

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

Physical Examination

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 two 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 disease led to elephantiasis and involvement of the entire lower limb.

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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.

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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.^[40]These plaques may be atrophic.^[41]

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.^[42]

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, face, breasts, and axillae.^[43]

Auricular chromoblastomycosis due to Fonsecaea pedrosoi, the most common agent found in Brazil, has been described.^[44]

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.^[45]

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.^[46]The dermatoscopic features can be variable, with red dots, white vague areas, black globules, and sandlike patterns sometimes evident.^[34]

Complications

The most common complications of chromoblastomycosis are ulceration, secondary bacterial infection, lymphedema that leads to elephantiasis, and myiasis.^[47]Leech bites may predispose to bacterial infection. Rare cases of malignant transformation (squamous cell carcinoma) of chromoblastomycosis have been documented.^[48] Cutaneous chromoblastomycosis with dissemination to brain has been described.^[49]

Differential Diagnoses

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Media Gallery

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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Author

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

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

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for MOHS Surgery, 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, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: Lilly; Amgen <br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Allergen; Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Acknowledgements

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.

Luiz Guilherme M Castro, MD Supervising Physician, Master and Doctor in Dermatology, Division of Dermatology, Hospital Das Clinicas, University of São Paulo, Brazil

Luiz Guilherme M Castro is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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