EXTRAORDINARY CASE REPORT
Chromoblastomycosis in a Diabetic Patient Without a History of Trauma Mina Zarei, MD, Samantha Schneider, BS, Alexandra Villasante, BS, Gabriel Villada, MD, Tejas Patel, MD, Shasa Hu, MD, and Paolo Romanelli, MD
Abstract: Chromoblastomycosis (CBM) is a slowly progressive cutaneous and subcutaneous mycosis mostly seen in tropical and subtropical areas and Fonsecaea pedrosoi is the most common cause. The authors describe the case of a diabetic Haitian woman, presenting with a chronic verrucous plaque without any history of trauma. Her histopathologic results showed epidermal hyperplasia and sclerotic bodies, which are diagnostic for CBM. Her therapy began with itraconazole 200 mg tablets twice a day. The unique feature of this patient is the coincidence of diabetes and CBM. However, to the best of our knowledge, this is the first documented case of human CBM in Miami, FL, which develops the awareness regarding this diagnosis among doctors in this area. There should be a close communication between dermatologists and pathologists to make an early diagnosis of CBM and also adequate therapy, which both are fundamental to improve patient’s quality of life. Key Words: chromoblastomycosis, diabetes, Medlar bodies, trauma, itraconazole (Am J Dermatopathol 2015;37:e112–e115)
CASE REPORT A 78-year-old Haitian woman was referred to our dermatology clinic at the University of Miami from her nursing home residence by her endocrinologist. This physician had been managing her type 2 diabetes, which was well controlled with metformin 850 mg twice a day. Before 10 years, this patient immigrated to the United States and has been living in the Miami area ever since. On her presentation, the patient reported a growing lesion on her right lower leg, which had appeared approximately before 9 months as a small pruritic/painful papule on the anterolateral aspect of the right lower leg. It has been slowly increasing in size. The patient assumed that the lesion was due to diabetes and therefore did not seek any treatment for it. She denied any history of trauma or injury to the site of the lesion, and there was no occupational activity that could explain any fungal inoculation. She had neither personal or family history of skin cancer nor any similar lesions in the past and also no known allergies nor history of tuberculosis. She was not smoking or using any alcohol or illicit drugs. The lesion was a 10 · 7-cm large verrucous skin-colored plaque with varying firm nodularity throughout (Fig. 1). The patient did not have any regional lymphadenopathy. Incisional biopsy (1.5 · 1 cm)
INTRODUCTION Chromoblastomycosis (CBM) is a slowly progressive cutaneous and subcutaneous mycosis. The most common species is Fonsecaea pedrosoi, followed by Phialophora verrucosa and Cladophialophora carrionii, which are found in dirt and vegetation near tropical forests.1,2 Typically, there is a history of mechanical trauma or injury to the site of infection. CBM has a male predominance and is rarely seen before adolescence. CBM can develop on any part of the body but most commonly affects the lower extremities. The infection usually begins as small erythematous papules that can develop to large verrucous lesions.2,3 Here, we describe the case of a diabetic Haitian woman presenting with a chronic verrucous plaque on her right leg without any history of trauma, which was diagnosed as CBM. This report discusses the clinical presentation, diagnosis, and treatment of this condition. From the Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL. The authors declare no conflicts of interest. Reprints: Paolo Romanelli, MD, Associate Professor, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, 1600 NW 10th Avenue, Room 2023-C, Miami, FL 33136 (e-mail: [email protected]). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
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FIGURE 1. Large verrucous skin-colored plaque on the anterolateral aspect of the right lower leg. Am J Dermatopathol Volume 37, Number 9, September 2015
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol Volume 37, Number 9, September 2015 was taken with the clinical suspicion of dermatofibrosarcoma protuberans versus deep fungal infection. The specimen was sent for histopathology and tissue culture evaluations. The patient was instructed to keep the area clean and continue to apply Bactroban to the site twice a day. Aerobic and anaerobic bacterial cultures of the biopsy tissue revealed no growth. Ziehl–Neelsen staining was negative for acidfast bacilli, and no mycobacterium species were isolated after 4 weeks of incubation. The patient had a point-of-care glucose of 147 mg/dL (74–106 mg/dL normal) and HbA1C of 5.7%. The fungal culture showed mold on second week, and the final report was Scytalidium species. However, the hematoxylin and eosin (H&E)–stained section of the biopsy material revealed epidermal hyperplasia with a granulomatous dermal infiltrate. Admixed within the granulomatous inflammation were numerous neutrophils and scattered Medlar (sclerotic) bodies, which are characteristic for CBM (Figs. 2–4). Periodic acid–Schiff, Gomori methenamine silver, and the Fontana–Masson special stains displayed the fungal organisms (Fig. 5). Since Scytalidium species are very likely to be cultured as contaminants and Medlar bodies are pathognomonic for CBM, the patient was diagnosed with CBM. Therefore, itraconazole (ITZ) 200 mg tablets twice a day were prescribed and the patient was asked to return to clinic in 2 months. After a 2-month followup, the lesion had a good response to the antifungal treatment and was slowly regressing.
DISCUSSION CBM is a slowly progressive cutaneous and subcutaneous mycosis caused by dematiaceous (darkly pigmented) fungi, which include the genera Fonsecaea, Phialophora, and Cladophialophora.2,3 Slow progression of this disease brings up the possibility that our patient has been infected many years ago when she was living in Hawaii and may be quiescent without signs and symptoms that induce the patient to search for medical assistance. Extra dermal and systemic types of CBM are very rare and are suggestive of immunosuppression
FIGURE 2. Granulomas with multinucleated giant cells in the reticular dermis (H&E, scanning magnification). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Chromoblastomycosis in a Diabetic Patient
FIGURE 3. Dermal granulomas with pigmented spores, anetoderma in the superficial dermis, and epidermal acanthosis (H&E, ·40).
in the patient. CBM involvement has been reported in the cerebrum, cornea, liver, lymph nodes, and lungs.4 The infection initially presents as small papules and pustules on the lower extremities, which gradually transform into papillous hyperkeratotic lesions. Damage to the lymphatic system might be seen in some cases.2,3 In an epidemiological study by Pires et al5 on 65 CBM patients from the Eastern Amazon, the majority of the patients were male agricultural workers of 45–55 years of age. Additionally, most of the lesions were of the verrucous type and located principally on the lower limbs. Higher rates of the infection in lower extremities might be because of increased susceptibility to trauma in these areas. The location of the CBM lesion on our patient’s lower leg is consistent with the results of the study above; however, she denied any trauma to the site of infection. There are a few reports regarding the development of squamous cell carcinoma (SCC) in long-standing CBM cases.6 In most of the reported cases, the risk of malignancy increased after 20–30 years of CBM infection particularly in male patients older than 60 years. Because our patient reported the presence of the lesion for only 9 months, SCC transformation is not a large concern for our patient; however, we will consider close follow-up. Diagnosis of CBM might be challenging outside the endemic regions. The disease might be misdiagnosed as other infectious etiologies such as granulomatous candidiasis, trichophytosis, skin tuberculosis, leprosy, tertiary syphilis, mycobacteriosis, leishmaniasis, and noninfectious diseases including SCC, sporotrichosis, blastomycosis, and systemic lupus erythematosus.3,7 For CBM, the diagnosis is made on the basis of direct examination, histopathological features, and fungal culture. The existence of Medlar bodies, also named as sclerotic cells, muriform cells, or copper pennies, is a pathognomonic feature of CBM.8 In the reported patient, the initial differential diagnoses were dermatofibrosarcoma protuberans versus atypical infections such as lobomycosis or nocardia. Since the patient had type 2 diabetes, phaeohyphomycosis www.amjdermatopathology.com |
e113
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Zarei et al
Am J Dermatopathol Volume 37, Number 9, September 2015
FIGURE 4. Intracellular and extracellular pigmented spores (Medlar bodies) within granulomas, with focal microabscesses [H&E, ·200 (A), ·400 (B)].
can be another differential diagnosis. Phaeohyphomycosis is a heterogeneous group of mycotic infections caused by dematiaceous fungi and is commonly associated with immunocompromised patients.9 However, the histopathological results revealed CBM as the final diagnosis. Figure 4 shows the histopathological section of our patient’s biopsy revealing brown spores of CBM, known as sclerotic bodies. Other histopathological features of cutaneous CBM include epithelial hyperplasia, dermal abscess formation, and chronic granulomatous inflammation with multinucleated giant cells.10 H&E staining of our patient’s biopsy showed epidermal hyperplasia with a granulomatous dermal infiltrate and granulomatous
inflammation with numerous neutrophils and scattered Medlar (sclerotic) bodies (Figs. 2–4). CBM is difficult to treat and relapses may occur; therefore, it is very important to choose the best treatment for the patient based on the severity of the disease and its clinical and histopathological features. The methods of treatment include physical intervention, chemotherapy, and a combination of both. The physical methods include surgical excision of initial lesions, thermotherapy, photodynamic therapy, and cryosurgery. These methods may decrease the duration of treatment particularly when combined with systemic antifungal.2,11
FIGURE 5. Spores stain positive for Gomori methenamine silver (A), periodic acid–Schiff (B) and Fontana– Masson (C) (special stain, ·400).
e114
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Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol Volume 37, Number 9, September 2015
Chemotherapy options for CBM include various drugs such as ITZ, terbinafine (TBF), posaconazole, voriconazole, amphotericin B, 5-flucytosine, and ketoconazole.12 Systemic antifungal therapy is validated for all patients whose initial lesions were not diagnosed at early stages nor surgically removed such as in our patient. The different treatment modalities available have not been compared in clinical settings and are mostly based on the successful therapies in reported cases. Noncomparative trials showed that ITZ, TBF, or their combinations remain the drug(s) of choice with the average duration of therapy ranging from 6 to 12 months.8,11,13–15 Cure rates with ITZ or TBF vary from 15% to 80%, according to the published data.10,14 The results of such studies depend primarily on the etiologic agent and the severity of the infection.11 Queiroz-Telles et al16 evaluated the efficacy and tolerability of ITZ (200–400 mg/d) in 19 Brazilian patients with CBM because of F. pedrosoi demonstrating its effectiveness. Based on the available evidence and also the severity of the infection in our patient, 200 mg of ITZ was prescribed twice daily to treat CBM with a 2 month follow-up. In conclusion, clinicians and dermatologists must consider CBM as one of the differential diagnoses of chronic skin conditions, especially in tropical and subtropical regions such as Miami. To the best of our knowledge, this is the first documented case of human CBM in Miami, FL. The coincidence of diabetes and CBM is another unique feature of our case report. Although diabetic patients have an increased risk of mycotic infections such as mucormycosis, current evidence shows only 2 documented cases of CBM in these patients.17,18 The fact that CBM was diagnosed by a dermatopathologist in our reported patient demonstrates the importance of close communication between dermatologists and pathologists to make an early diagnosis and to provide the patient with early appropriate therapy, both of which are fundamental to improving patients’ quality of life.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Chromoblastomycosis in a Diabetic Patient
REFERENCES 1. Correia RT, Valente NY, Criado PR, et al. Chromoblastomycosis: study of 27 cases and review of medical literature. An Bras Dermatol. 2010;85:448–454. 2. Ameen M. Chromoblastomycosis: clinical presentation and management. Clin Exp Dermatol. 2009;34:849–854. 3. López Martínez R, Méndez Tovar LJ. Chromoblastomycosis. Clin Dermatol. 2007;25:188–194. 4. Camara-Lemarroy CR, Soto-Garcia AJ, Preciado-Yepez CI, et al. Case of chromoblastomycosis with pulmonary involvement. J Dermatol. 2013; 40:746–748. 5. Pires CA, Xavier MB, Quaresma JA, et al. Clinical, epidemiological and mycological report on 65 patients from the Eastern Amazon region with chromoblastomycosis. An Bras Dermatol. 2012;87:555–560. 6. Jamil A, Lee YY, Thevarajah S. Invasive squamous cell carcinoma arising from chromoblastomycosis. Med Mycol. 2012;50:99–102. 7. Queiroz-Telles F, Esterre P, Perez-Blanco M, et al. Chromoblastomycosis: an overview of clinical manifestations, diagnosis and treatment. Med Mycol. 2009;47:3–15. 8. Torres-Guerrero E, Isa–Isa R, Isa M, et al. Chromoblastomycosis. Clin Dermatol. 2012;30:403–408. 9. Yoon YA, Park KS, Lee JH, et al. Subcutaneous phaeohyphomycosis caused by Exophiala salmonis. Ann Lab Med. 2012;32:438–441. 10. Bandyopadhyay A, Majumdar K, Gangopadhyay M, et al. Cutaneous chromoblastomycosis mimicking tuberculosis verrucosa cutis: look for copper pennies! Turk Patoloji Derg. 2013. doi: 10.5146/tjpath.2013. 01197. Epub ahead of print. 11. Queiroz-Telles F, Santos DW. Challenges in the therapy of chromoblastomycosis. Mycopathologia. 2013;175:477–488. 12. Daboit TC, Magagnin CM, Heidrich D, et al. A case of relapsed chromoblastomycosis due to Fonsecaea monophora: antifungal susceptibility and phylogenetic analysis. Mycopathologia. 2013;176:139–144. 13. Ameen M. Managing chromoblastomycosis. Trop Doct. 2010;40:65–67. 14. Minotto D, Varejao Bernarti CD, Mallmann LF, et al. Chromoblastomycosis: a review of 100 cases in the state of Rio Grande do Sul, Brazil. J Am Acad Dermatol. 2001;44:585–592. 15. Bonifaz A, Paredes-Solis V, Saul A. Treating chromoblastomycosis with systemic antifungals. Expert Opin Pharmacother. 2004;5:247–254. 16. Queiroz-Telles F, Purim KS, Fillus JN, et al. Itraconazole in the treatment of chromoblastomycosis due to Fonsecaea pedrosoi. Int J Dermatol. 1992;31:805–812. 17. Pilar Santana L, Rojas-Hidalgo E. A case of chromoblastomycosis in a diabetic [in Spanish]. Rev Clin Esp. 1978;148:625–626. 18. Radouane N, Hali F, Khadir K, et al. Generalized chromomycosis caused by Phialophora verrucosa [in French]. Ann Dermatol Venereol. 2013; 140:197–201.
www.amjdermatopathology.com |
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Chromoblastomycosis in a Diabetic Patient Without a History of Trauma Mina Zarei, MD, Samantha Schneider, BS, Alexandra Villasante, BS, Gabriel Villada, MD, Tejas Patel, MD, Shasa Hu, MD, and Paolo Romanelli, MD
Abstract: Chromoblastomycosis (CBM) is a slowly progressive cutaneous and subcutaneous mycosis mostly seen in tropical and subtropical areas and Fonsecaea pedrosoi is the most common cause. The authors describe the case of a diabetic Haitian woman, presenting with a chronic verrucous plaque without any history of trauma. Her histopathologic results showed epidermal hyperplasia and sclerotic bodies, which are diagnostic for CBM. Her therapy began with itraconazole 200 mg tablets twice a day. The unique feature of this patient is the coincidence of diabetes and CBM. However, to the best of our knowledge, this is the first documented case of human CBM in Miami, FL, which develops the awareness regarding this diagnosis among doctors in this area. There should be a close communication between dermatologists and pathologists to make an early diagnosis of CBM and also adequate therapy, which both are fundamental to improve patient’s quality of life. Key Words: chromoblastomycosis, diabetes, Medlar bodies, trauma, itraconazole (Am J Dermatopathol 2015;37:e112–e115)
CASE REPORT A 78-year-old Haitian woman was referred to our dermatology clinic at the University of Miami from her nursing home residence by her endocrinologist. This physician had been managing her type 2 diabetes, which was well controlled with metformin 850 mg twice a day. Before 10 years, this patient immigrated to the United States and has been living in the Miami area ever since. On her presentation, the patient reported a growing lesion on her right lower leg, which had appeared approximately before 9 months as a small pruritic/painful papule on the anterolateral aspect of the right lower leg. It has been slowly increasing in size. The patient assumed that the lesion was due to diabetes and therefore did not seek any treatment for it. She denied any history of trauma or injury to the site of the lesion, and there was no occupational activity that could explain any fungal inoculation. She had neither personal or family history of skin cancer nor any similar lesions in the past and also no known allergies nor history of tuberculosis. She was not smoking or using any alcohol or illicit drugs. The lesion was a 10 · 7-cm large verrucous skin-colored plaque with varying firm nodularity throughout (Fig. 1). The patient did not have any regional lymphadenopathy. Incisional biopsy (1.5 · 1 cm)
INTRODUCTION Chromoblastomycosis (CBM) is a slowly progressive cutaneous and subcutaneous mycosis. The most common species is Fonsecaea pedrosoi, followed by Phialophora verrucosa and Cladophialophora carrionii, which are found in dirt and vegetation near tropical forests.1,2 Typically, there is a history of mechanical trauma or injury to the site of infection. CBM has a male predominance and is rarely seen before adolescence. CBM can develop on any part of the body but most commonly affects the lower extremities. The infection usually begins as small erythematous papules that can develop to large verrucous lesions.2,3 Here, we describe the case of a diabetic Haitian woman presenting with a chronic verrucous plaque on her right leg without any history of trauma, which was diagnosed as CBM. This report discusses the clinical presentation, diagnosis, and treatment of this condition. From the Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL. The authors declare no conflicts of interest. Reprints: Paolo Romanelli, MD, Associate Professor, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, 1600 NW 10th Avenue, Room 2023-C, Miami, FL 33136 (e-mail: [email protected]). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
e112
| www.amjdermatopathology.com
FIGURE 1. Large verrucous skin-colored plaque on the anterolateral aspect of the right lower leg. Am J Dermatopathol Volume 37, Number 9, September 2015
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol Volume 37, Number 9, September 2015 was taken with the clinical suspicion of dermatofibrosarcoma protuberans versus deep fungal infection. The specimen was sent for histopathology and tissue culture evaluations. The patient was instructed to keep the area clean and continue to apply Bactroban to the site twice a day. Aerobic and anaerobic bacterial cultures of the biopsy tissue revealed no growth. Ziehl–Neelsen staining was negative for acidfast bacilli, and no mycobacterium species were isolated after 4 weeks of incubation. The patient had a point-of-care glucose of 147 mg/dL (74–106 mg/dL normal) and HbA1C of 5.7%. The fungal culture showed mold on second week, and the final report was Scytalidium species. However, the hematoxylin and eosin (H&E)–stained section of the biopsy material revealed epidermal hyperplasia with a granulomatous dermal infiltrate. Admixed within the granulomatous inflammation were numerous neutrophils and scattered Medlar (sclerotic) bodies, which are characteristic for CBM (Figs. 2–4). Periodic acid–Schiff, Gomori methenamine silver, and the Fontana–Masson special stains displayed the fungal organisms (Fig. 5). Since Scytalidium species are very likely to be cultured as contaminants and Medlar bodies are pathognomonic for CBM, the patient was diagnosed with CBM. Therefore, itraconazole (ITZ) 200 mg tablets twice a day were prescribed and the patient was asked to return to clinic in 2 months. After a 2-month followup, the lesion had a good response to the antifungal treatment and was slowly regressing.
DISCUSSION CBM is a slowly progressive cutaneous and subcutaneous mycosis caused by dematiaceous (darkly pigmented) fungi, which include the genera Fonsecaea, Phialophora, and Cladophialophora.2,3 Slow progression of this disease brings up the possibility that our patient has been infected many years ago when she was living in Hawaii and may be quiescent without signs and symptoms that induce the patient to search for medical assistance. Extra dermal and systemic types of CBM are very rare and are suggestive of immunosuppression
FIGURE 2. Granulomas with multinucleated giant cells in the reticular dermis (H&E, scanning magnification). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Chromoblastomycosis in a Diabetic Patient
FIGURE 3. Dermal granulomas with pigmented spores, anetoderma in the superficial dermis, and epidermal acanthosis (H&E, ·40).
in the patient. CBM involvement has been reported in the cerebrum, cornea, liver, lymph nodes, and lungs.4 The infection initially presents as small papules and pustules on the lower extremities, which gradually transform into papillous hyperkeratotic lesions. Damage to the lymphatic system might be seen in some cases.2,3 In an epidemiological study by Pires et al5 on 65 CBM patients from the Eastern Amazon, the majority of the patients were male agricultural workers of 45–55 years of age. Additionally, most of the lesions were of the verrucous type and located principally on the lower limbs. Higher rates of the infection in lower extremities might be because of increased susceptibility to trauma in these areas. The location of the CBM lesion on our patient’s lower leg is consistent with the results of the study above; however, she denied any trauma to the site of infection. There are a few reports regarding the development of squamous cell carcinoma (SCC) in long-standing CBM cases.6 In most of the reported cases, the risk of malignancy increased after 20–30 years of CBM infection particularly in male patients older than 60 years. Because our patient reported the presence of the lesion for only 9 months, SCC transformation is not a large concern for our patient; however, we will consider close follow-up. Diagnosis of CBM might be challenging outside the endemic regions. The disease might be misdiagnosed as other infectious etiologies such as granulomatous candidiasis, trichophytosis, skin tuberculosis, leprosy, tertiary syphilis, mycobacteriosis, leishmaniasis, and noninfectious diseases including SCC, sporotrichosis, blastomycosis, and systemic lupus erythematosus.3,7 For CBM, the diagnosis is made on the basis of direct examination, histopathological features, and fungal culture. The existence of Medlar bodies, also named as sclerotic cells, muriform cells, or copper pennies, is a pathognomonic feature of CBM.8 In the reported patient, the initial differential diagnoses were dermatofibrosarcoma protuberans versus atypical infections such as lobomycosis or nocardia. Since the patient had type 2 diabetes, phaeohyphomycosis www.amjdermatopathology.com |
e113
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Zarei et al
Am J Dermatopathol Volume 37, Number 9, September 2015
FIGURE 4. Intracellular and extracellular pigmented spores (Medlar bodies) within granulomas, with focal microabscesses [H&E, ·200 (A), ·400 (B)].
can be another differential diagnosis. Phaeohyphomycosis is a heterogeneous group of mycotic infections caused by dematiaceous fungi and is commonly associated with immunocompromised patients.9 However, the histopathological results revealed CBM as the final diagnosis. Figure 4 shows the histopathological section of our patient’s biopsy revealing brown spores of CBM, known as sclerotic bodies. Other histopathological features of cutaneous CBM include epithelial hyperplasia, dermal abscess formation, and chronic granulomatous inflammation with multinucleated giant cells.10 H&E staining of our patient’s biopsy showed epidermal hyperplasia with a granulomatous dermal infiltrate and granulomatous
inflammation with numerous neutrophils and scattered Medlar (sclerotic) bodies (Figs. 2–4). CBM is difficult to treat and relapses may occur; therefore, it is very important to choose the best treatment for the patient based on the severity of the disease and its clinical and histopathological features. The methods of treatment include physical intervention, chemotherapy, and a combination of both. The physical methods include surgical excision of initial lesions, thermotherapy, photodynamic therapy, and cryosurgery. These methods may decrease the duration of treatment particularly when combined with systemic antifungal.2,11
FIGURE 5. Spores stain positive for Gomori methenamine silver (A), periodic acid–Schiff (B) and Fontana– Masson (C) (special stain, ·400).
e114
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Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol Volume 37, Number 9, September 2015
Chemotherapy options for CBM include various drugs such as ITZ, terbinafine (TBF), posaconazole, voriconazole, amphotericin B, 5-flucytosine, and ketoconazole.12 Systemic antifungal therapy is validated for all patients whose initial lesions were not diagnosed at early stages nor surgically removed such as in our patient. The different treatment modalities available have not been compared in clinical settings and are mostly based on the successful therapies in reported cases. Noncomparative trials showed that ITZ, TBF, or their combinations remain the drug(s) of choice with the average duration of therapy ranging from 6 to 12 months.8,11,13–15 Cure rates with ITZ or TBF vary from 15% to 80%, according to the published data.10,14 The results of such studies depend primarily on the etiologic agent and the severity of the infection.11 Queiroz-Telles et al16 evaluated the efficacy and tolerability of ITZ (200–400 mg/d) in 19 Brazilian patients with CBM because of F. pedrosoi demonstrating its effectiveness. Based on the available evidence and also the severity of the infection in our patient, 200 mg of ITZ was prescribed twice daily to treat CBM with a 2 month follow-up. In conclusion, clinicians and dermatologists must consider CBM as one of the differential diagnoses of chronic skin conditions, especially in tropical and subtropical regions such as Miami. To the best of our knowledge, this is the first documented case of human CBM in Miami, FL. The coincidence of diabetes and CBM is another unique feature of our case report. Although diabetic patients have an increased risk of mycotic infections such as mucormycosis, current evidence shows only 2 documented cases of CBM in these patients.17,18 The fact that CBM was diagnosed by a dermatopathologist in our reported patient demonstrates the importance of close communication between dermatologists and pathologists to make an early diagnosis and to provide the patient with early appropriate therapy, both of which are fundamental to improving patients’ quality of life.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Chromoblastomycosis in a Diabetic Patient
REFERENCES 1. Correia RT, Valente NY, Criado PR, et al. Chromoblastomycosis: study of 27 cases and review of medical literature. An Bras Dermatol. 2010;85:448–454. 2. Ameen M. Chromoblastomycosis: clinical presentation and management. Clin Exp Dermatol. 2009;34:849–854. 3. López Martínez R, Méndez Tovar LJ. Chromoblastomycosis. Clin Dermatol. 2007;25:188–194. 4. Camara-Lemarroy CR, Soto-Garcia AJ, Preciado-Yepez CI, et al. Case of chromoblastomycosis with pulmonary involvement. J Dermatol. 2013; 40:746–748. 5. Pires CA, Xavier MB, Quaresma JA, et al. Clinical, epidemiological and mycological report on 65 patients from the Eastern Amazon region with chromoblastomycosis. An Bras Dermatol. 2012;87:555–560. 6. Jamil A, Lee YY, Thevarajah S. Invasive squamous cell carcinoma arising from chromoblastomycosis. Med Mycol. 2012;50:99–102. 7. Queiroz-Telles F, Esterre P, Perez-Blanco M, et al. Chromoblastomycosis: an overview of clinical manifestations, diagnosis and treatment. Med Mycol. 2009;47:3–15. 8. Torres-Guerrero E, Isa–Isa R, Isa M, et al. Chromoblastomycosis. Clin Dermatol. 2012;30:403–408. 9. Yoon YA, Park KS, Lee JH, et al. Subcutaneous phaeohyphomycosis caused by Exophiala salmonis. Ann Lab Med. 2012;32:438–441. 10. Bandyopadhyay A, Majumdar K, Gangopadhyay M, et al. Cutaneous chromoblastomycosis mimicking tuberculosis verrucosa cutis: look for copper pennies! Turk Patoloji Derg. 2013. doi: 10.5146/tjpath.2013. 01197. Epub ahead of print. 11. Queiroz-Telles F, Santos DW. Challenges in the therapy of chromoblastomycosis. Mycopathologia. 2013;175:477–488. 12. Daboit TC, Magagnin CM, Heidrich D, et al. A case of relapsed chromoblastomycosis due to Fonsecaea monophora: antifungal susceptibility and phylogenetic analysis. Mycopathologia. 2013;176:139–144. 13. Ameen M. Managing chromoblastomycosis. Trop Doct. 2010;40:65–67. 14. Minotto D, Varejao Bernarti CD, Mallmann LF, et al. Chromoblastomycosis: a review of 100 cases in the state of Rio Grande do Sul, Brazil. J Am Acad Dermatol. 2001;44:585–592. 15. Bonifaz A, Paredes-Solis V, Saul A. Treating chromoblastomycosis with systemic antifungals. Expert Opin Pharmacother. 2004;5:247–254. 16. Queiroz-Telles F, Purim KS, Fillus JN, et al. Itraconazole in the treatment of chromoblastomycosis due to Fonsecaea pedrosoi. Int J Dermatol. 1992;31:805–812. 17. Pilar Santana L, Rojas-Hidalgo E. A case of chromoblastomycosis in a diabetic [in Spanish]. Rev Clin Esp. 1978;148:625–626. 18. Radouane N, Hali F, Khadir K, et al. Generalized chromomycosis caused by Phialophora verrucosa [in French]. Ann Dermatol Venereol. 2013; 140:197–201.
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