Indian Journal of Transplantation

: 2019  |  Volume : 13  |  Issue : 3  |  Page : 219--220

Primary cutaneous aspergillosis in a renal allograft recipient

Luvdeep Dogra, Manisha Sahay, Kiranmai Ismal, PS Vali, Anuradha K 
 Department of Nephrology, Osmania General Hospital, Hyderabad, Telangana, India

Correspondence Address:
Dr. Manisha Sahay
Department of Nephrology, OGH, Hyderabad, Telangana


Cutaneous fungal infection due to aspergillus is relatively less known. Mostly it occurs due to Aspergillus flavus. This entity should be included in differential diagnosis of cutaneous fungal infections

How to cite this article:
Dogra L, Sahay M, Ismal K, Vali P S, Anuradha. Primary cutaneous aspergillosis in a renal allograft recipient.Indian J Transplant 2019;13:219-220

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Dogra L, Sahay M, Ismal K, Vali P S, Anuradha. Primary cutaneous aspergillosis in a renal allograft recipient. Indian J Transplant [serial online] 2019 [cited 2020 Mar 28 ];13:219-220
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Aspergillosis is a common fungal infection in immunocompromised patients.[1] It is caused by infection with ubiquitous soil-and water-dwelling saprophytes of the Aspergillus genus. Disseminated human disease is usually caused by Aspergillus fumigatus and rarely by other species. Primary cutaneous disease is rare and is most commonly caused by A. fumigatus and Aspergillus flavus.[2],[3] We report a case of primary cutaneous aspergillosis caused by A. flavus in a renal allograft recipient.

 Case Report

A 35-year-old male patient, a case of end-stage renal disease on maintenance hemodialysis, underwent a deceased donor renal allograft transplant. Native kidney disease was presumed chronic interstitial nephritis. The donor was 26 years old and had no known comorbidities except hypertension. The cause of donor death was road traffic accident. Antithymocyte globulin induction at 4 mg/kg was started followed by triple immunosuppression with tacrolimus, mycophenolate mofetil, and prednisolone. The postoperative period was uneventful, and he was discharged with a serum creatinine of 1.1 mg/dl. There was no history of new-onset diabetes post transplant or any prior opportunistic infections. He had a stable posttransplant course until 6 months after transplant when he presented with complaints of gradually progressive painless swelling over the medial border of the sole of the left foot and over the right calf noticed for the last 15 days. The lesions had increased from the size of a small nodule to the size of almost a lemon over this period. There was no history of fever, weight loss, or trauma prior to the onset. Local examination revealed two verrucous hyperpigmented plaques with erythematous base. One lesion was on the medial side of the sole of the left foot measuring around 3 cm × 3 cm [Figure 1] and the other over the right calf of around 3 cm × 2 cm in size. The lesions were associated with superficial crusting, and there was no discharge or bleeding from the site. There was no lymphadenopathy. The patient was admitted and baseline investigations were done, which were essentially normal including total and differential leukocyte counts. Blood culture (aerobic and fungal) and sputum culture were sterile. Chest X-ray was normal. Skin consultation was sought, and tissue sample was taken by punch biopsy. Gram staining and acid-fast bacillus staining done were negative. Tissue sample for histopathology revealed ulceration with acute and chronic dermal inflammation and microabscess formation, with branching septate hyphae, suggestive of Aspergillus infection. However, the tissue culture specimen clinched the diagnosis in our case and grew A. flavus. Surgical debridement was deferred, and the patient was started on oral voriconazole at a dose of 400 mg/day in two divided doses. He responded to the above management well. The lesions reduced in size significantly by the first 2 weeks of treatment [Figure 2]. Oral voriconazole was given for a total duration of 6 weeks while monitoring for tacrolimus levels, in view of financial constraints. There was a complete resolution of the lesions. However, longer durations of therapy are usually advocated for aspergillosis.{Figure 1}{Figure 2}


Aspergillosis is the second most common fungal infection in immunocompromised patients next only to Candida. Primarily, respiratory system infection occurs via inhalation of fungal spores, which then leads to disseminated hematogenous spread. Aspergillosis has been reported from approximately 0.7% to up to 4% of the renal transplant recipients. Primary cutaneous involvement represents only 15%–20% of the total disease burden. A. fumigatus is the most common species associated with disseminated disease with cutaneous involvement, whereas A. flavus most often causes the less frequent primary skin infections.[2],[3] Cutaneous manifestations of aspergillosis usually follow traumatic implantation of the fungus, commonly involving the peripheries, and include single or multiple erythematous-to-violaceous plaques or papules, often characterized by a central necrotic ulcer or eschar. Key risk factors for cutaneous aspergillosis include neutropenia from hematologic malignancy or chemotherapy, immunosuppressive therapy, AIDS, diabetes, tissue damage, allogenic hematopoietic stem cell transplant, and cytomegalovirus infection.[2],[3]

The diagnosis is usually suggested by tissue biopsy and culture of tissue specimen. Our patient was a deceased donor renal allograft recipient and was on triple immunosuppression. A possibility of local implantation of the foot was considered as the possible etiology as our patient was a farmer by occupation and a history of irregular use of footwear was forthcoming. Treatment of cutaneous aspergillosis includes a combination of surgical debridement and multidrug antifungal chemotherapy.[4] In view of local tissue involvement and immunocompromised state, debridement was deferred. Usual antifungals include oral voriconazole and itraconazole for a duration of 6–8 weeks or until resolution; however, longer courses are usually advocated.[4],[5],[6] Intravenous amphotericin is used in patients who develop worsening of symptoms or poor response to therapy.[7]

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.


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