Chromoblastomycosis Workup

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

Laboratory Studies

Among the possible laboratory tests to be obtained, direct examination of 10% potassium hydroxide cleared lesion scrapings is by far the most useful. Typical, thick-walled, cigar-colored, sclerotic cells, also known as Medlar bodies, are readily seen. Although these cells are pathognomonic of chromoblastomycosis, they do not give specific information on the agent. Eventually, dematiaceous hyphae can also be observed. Identifying the agent is easier when the specimens collected include the black dots present in the lesions. In 2005, Miranda et al[43] suggested the use of vinyl adhesive tape for collecting and identifying some types of deep-seated mycoses in which the infectious agents can be observed in the horny layer of the epidermis in transepidermal elimination events. Note the image below.

Sclerotic cells on a potassium hydroxide preparatiSclerotic cells on a potassium hydroxide preparation.

In culture, each causative agent produces a similar pattern, that of a slow-growing, dark, velvety colony with a black obverse. Identification of individual species is handled in the usual manner by observing various characteristics, including conidia production. Note the image below.

Micromorphology of Cladosporium carrionii (left) aMicromorphology of Cladosporium carrionii (left) and Fonsecaea pedrosoi (right), the 2 most commonly isolated agents in chromoblastomycosis.

Serologic tests are exclusively used for research matters, and they are not routinely used or available. A recently isolated, highly specific and sensitive immunoblotting method depicted a 54-kd antigen from F pedrosoi[44] that may prove to be helpful in the study of the disease. Note the image below.

Culture of Fonsecaea pedrosoi on Sabouraud agar. TCulture 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).

An enzyme-linked immunosorbent assay (ELISA) using a somatic antigen of C carrionii was tested to serologically follow cases of chromoblastomycosis due to C carrionii before, during, and after therapy. ELISA proved to be a valuable tool for the diagnosis and follow-up of patients with chromomycosis (due to C carrionii). According to the authors[45] in 2005, the use of an ELISA might be useful to establish remission criteria in chromoblastomycosis caused by C carrionii.

Duplex polymerase chain reaction is a rapid and specific assay for identification of Fonsecaea isolates, mainly for the strains that are difficult to identify using morphologic methods.[46]

A rapid and sensitive assay for identification of pathogenic species of Fonsecaea without sequencing can be obtained using rolling circle amplification (RCA). This simple, sensitive, and low-cost method may prove practical.[47]

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Imaging Studies

Bone involvement is not a typical finding in chromoblastomycosis. Long-lasting lesions may lead indirectly to bone changes, making it necessary to evaluate possible bone compromise with regular radiography, especially when lesions are old, located at sites with scarce subcutaneous tissue, or associated with lymphedema.

Lymphoscintigraphy has been used to evaluate lymphedema, but it is not routinely used.[48]

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Histologic Findings

In cutaneous lesions, the cigar-colored fungi are easily seen in hematoxylin and eosin–stained sections. No special stains are needed. The typical finding is a pseudoepitheliomatous hyperplasia of the epidermis with a diffuse, lymphomononuclear inflammatory infiltrate in the dermis. The tissue response to the fungus is typically mixed.

True and pure abscesses or microabscesses, granulomas, granulomatous reactions, and abscesses surrounded by a granulomatous reaction with giant cells may be seen in the same section.[49] Inside the giant cells, brown-colored, thick-walled fungal cells may be seen. These muriform fungal cells may be single, 2-celled, or multiple-celled; this feature is a result of multiplication by septation rather than budding. Note the image below.

Hematoxylin and eosin–stained section shows typicaHematoxylin and eosin–stained section shows typical sclerotic cells inside an abscess. Sclerotic cells present as round, thick-walled, cigar-colored structures.

Transepidermal elimination of the fungal cells is the histologic counterpart of the black dots clinically evident in chromoblastomycosis lesions. An unusual dermal response has been described by Jawitz et al[50] in 2007, consisting of dermal effacement by a spindle cell proliferation arranged in sweeping fascicles.

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Staging

Staging of the disease is especially useful for academic matters. Because treatment is still difficult, several papers in the literature describe the results obtained with different therapeutic methods. Unfortunately, most papers are single case reports, and follow-up tends to be short. The lack of uniformity in staging contributes to the low reproducibility of the proposed regimens.

In 1999, Castro devised an elegant, clinically based, physician friendly index to stage chromoblastomycosis. The severity index is based on the extension of the diseased area, the number of lesions, the presence of complications (eg, lymphedema, ulceration, secondary infection), and the unresponsiveness to previous treatments. According to this scoring system, patients are classified as having mild (up to 3 points), moderate (4-6 points), or severe (7-10 points) disease.

A scoring system for staging chromoblastomycosis is as follows:

  • Area of lesions: Small lesions up to 25 cm2 are 1 point. Medium lesions larger than 25 cm2 and smaller than 100 cm2 are 2 points. Lesions larger than 100 cm2 are 3 points.
  • Number of lesions: A single lesion is 1 point. One to 5 lesions is 2 points. More than 5 lesions or metastatic lesions is 3 points.
  • Complications (1 point for each complication present): Lymphedema is 1 point. Ulceration is 1 point. Secondary infection is 1 point.
  • Resistance to previous treatment or previous unsuccessful treatment is 1 point.
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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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