|Year : 2019 | Volume
| Issue : 1 | Page : 62-64
Chromoblastomycosis in a renal allograft recipient on calcineurin inhibitor-free immunosuppression
PK Bipi1, VN Unni1, Nanda Kachare2, K Vinod Kumar1
1 Department of Nephrology, Aster Medcity, Kochi, Kerala, India
2 Department of Pathology, Aster Medcity, Kochi, Kerala, India
|Date of Web Publication||29-Mar-2019|
Dr. P K Bipi
Flat 2A, Cheloor Pushpak Apartments, Ravipuram, Kochi - 682 015, Kerala
Source of Support: None, Conflict of Interest: None
Superficial cutaneous fungal infections are common in our country in the kidney transplant recipients. However, deep fungal infections involving the skin and subcutaneous tissue are relatively rare. Here, we report a case of chromoblastomycosis in a renal allograft recipient on a calcineurin inhibitor-free immunosuppression. The case highlights the importance of skin biopsy in differentiating various skin lesions in transplant patients and the role of the early institution of appropriate treatment in successfully treating these infections.
Keywords: Chromoblastomycosis, fungal infections, renal transplant
|How to cite this article:|
Bipi P K, Unni V N, Kachare N, Kumar K V. Chromoblastomycosis in a renal allograft recipient on calcineurin inhibitor-free immunosuppression. Indian J Transplant 2019;13:62-4
|How to cite this URL:|
Bipi P K, Unni V N, Kachare N, Kumar K V. Chromoblastomycosis in a renal allograft recipient on calcineurin inhibitor-free immunosuppression. Indian J Transplant [serial online] 2019 [cited 2019 Jun 26];13:62-4. Available from: http://www.ijtonline.in/text.asp?2019/13/1/62/255182
| Introduction|| |
Infections are the bane of tranplant programmes worldwide, more so in developing countries. The risk of infections depend on the dose and duration of immunosupression. We however describe a case of Chromoblastomycosis diagnosed following skin biopsy by the presence of the characteristic sclerotic bodies; while being on a Calcineurin inhibitor free immunosupression. He was successfully treated with oral antifungal agent for a period of six months with no recurrence of lesions even after stopping treatment.
| Case Report|| |
A 58-year-old male patient, an agriculturist by profession, underwent live donor (spouse) renal transplantation 3 years back. The postoperative period was uneventful; he was started on triple immunosuppression (cyclosporine, mycophenolate mofetil, and prednisolone). About 6 months later, he developed new-onset diabetes after transplantation for which he was started on insulin, with which his blood sugars were well controlled. One year after transplantation, he underwent a graft kidney biopsy for graft dysfunction (serum creatinine 2.1 mg/dL) which revealed 30%–40% of interstitial fibrosis and tubular atrophy with no evidence of rejection. Cyclosporine was gradually withdrawn over 12 weeks, and he was continued on mycophenolate mofetil 750 mg twice daily and wysolone 7.5 mg once daily. The graft functions remained stable after withdrawing cyclosporin.
Three years after transplantation, he presented with multiple hyperpigmented warty nodular lesions of size 0.5–1.5 cm in diameter over the back, upper arms, and posterior aspect of lower limbs [Figure 1]. There was no known history of preceding trauma. Excision biopsy of the lesion was done. Histopathology showed epidermis with marked pseudoepitheliomatous hyperplasia, hyperkeratosis, and parakeratosis. The dermis showed multiple epithelioid granulomas with epitheliod cells, lymphocytes, plasma cells, and Langhan's and foreign-body type giant cells with central suppuration and multiple foci of intraepidermal and dermal microabcesses. In the granulomas, there were numerous 5–12 μ-sized pigmented brown-colored fungal forms with thick double walls, morphologically consistent with “sclerotic bodies≵ characteristic of chromoblastomycosis [Figure 2].
|Figure 1: Photograph showing multiple hyperpigmented warty nodular lesions of size 0.5 - 1.5 cm in diameter over the back|
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|Figure 2: Skin biopsy showing (a) pseudoepitheliomatous hyperplasia (H and E, ×10). (b) Intraepidermal and dermal infiltration of multiple round pigemented brown sclerotic bodies (black arrow) consistent with chromoblastomycosis (H and E, ×40)|
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Based on the presence of the characteristic sclerotic bodies, the patient was diagnosed to have chromoblastomycosis and was started on oral itraconazole for 6 months. The skin lesions responded well to treatment and the lesions gradually healed. His renal functions remained stable during treatment. There was no relapse of lesions for 1 year after stopping itraconazole.
| Discussion|| |
Chromoblastomycosis is a chronic fungal infection of the skin and subcutaneous tissue, usually following a traumatic injury. It was first described by Max Rudolph in 1914. The disease is most commonly found in the tropical and subtropical regions of Africa and Latin America. It has also been reported from Asia. Till date, there are about 34 case reports from India. There are a couple of reported cases of chromoblastomycosis in renal allograft recipients from India; however, they were on triple immunosuppression comprising tacrolimus, mycophenolate mofetil, and steroids at the time of diagnosis.
The fungi responsible are dematiaceous fungi, forming black colonies due to the presence of melanin in their cell walls. The most commonly reported species are Fonsecaea pedrossi, Phialophora verrucosa, Cladophialophora carroni, and Rhinocladiella aquaspersa. These are found as part of the normal flora of the environment.
The disease is more prevalent in middle-aged males predominantly involved in agricultural activities. Predisposing factors for the disease include tropical climate, male sex, and engagement in agricultural activities which increases the possibility of injury to the skin. The individuals with human leukocyte antigen-A 29 antigen are also found to be more susceptible to chromoblastomycosis. The source of infection is through transcutaneous puncture wounds. The primary lesion is an erythematous papule which gradually enlarges to various sizes. Satellite lesions can occur either from autoinoculation or via lymphatic spread. The lesions can present in various forms nodular, tumoral, verrucous, plaque, and cicatricial forms. In the tissue, the fungi produce characteristic sclerotic cells or muriform cells. Complications that can develop include secondary bacterial infection, lymphedema, and rarely squamous cell carcinoma. Rarely, the disease can involve lymph nodes, pleural cavity, oropharynx, trachea, and ileocecal regions.
Diagnosis is made by histopathology and/or culture. The chromoblastomycosis needs to be differentiated from other fungal infections, tuberculosis of the skin, tertiary syphilis as well as noninfectious causes such as skin malignancies, psoriasis, and sarcoidosis. The diagnosis is confirmed by the presence of sclerotic bodies (Medlar bodies) in the potassium hydroxide treated skin scrapings or histopathology specimens. Medlar bodies also known as sclerotic cells, are globe-shaped, cigar-colored, thick-walled structures that are 4–12 μm in diameter. Microbiological culture using sabarouds agar can be helpful in microbiological diagnosis, but the fungi implicated are slow growing and can form green-to-black colonies after weeks to months.
Antifungal therapy with itraconazole forms the mainstay of therapy. Mild-to-moderate forms heal after 6–12 months of treatment. However, relapses can be frequent after completion of treatment. Other drugs used are terbinafine, posaconazole, and 5-fluorocytosine. Various physical methods which were tried include surgical excision, cryosurgery, thermotherapy, and laser vaporization even though none have been recommended.
Our patient was on a calcineurin inhibitor-free immunosuppressive regimen for >2 years at the time of diagnosis of chromoblastomycosis. This case highlights the high risk of infections among renal allograft recipients in our country even if the immunosuppression is less than the usual triple-drug regimen. The case also stresses the importance of considering an early skin biopsy in transplant recipients with skin lesions so that an accurate diagnosis can be made.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Castro RM, Castro LG. On the priority of description of chromomycosis. Mycoses 1987;30:397-403.
Ameen M. Chromoblastomycosis: Clinical presentation and management. Clin Exp Dermatol 2009;34:849-54.
Rubin HA, Bruce S, Rosen T, McBride ME. Evidence for percutaneous inoculation as the mode of transmission for chromoblastomycosis. J Am Acad Dermatol 1991;25:951-4.
Sharma NL, Sharma RC, Grover PS, Gupta ML, Sharma AK, Mahajan VK, et al.
Chromoblastomycosis in India. Int J Dermatol 1999;38:846-51.
Krzyściak PM, Pindycka-Piaszczyńska M, Piaszczyński M. Chromoblastomycosis. Adv Dermatol Allergol 2014;31:310.
[Figure 1], [Figure 2]