Cutaneous Infection Caused by Plant Pathogen Colletotrichum gloeosporioides

Colletotrichum species are common pathogens for plant anthracnose but have recently emerged as a human opportunistic pathogen causing keratitis and subcutaneous fungal infection, which potentially can lead to life-threatening systemic dissemination.^1-4 Therefore, early recognition and intervention with debridement and systemic antifungal treatment are required to reduce the morbidity and mortality. Herein we described a case of cutaneous fungal infection by Colletotrichum gloeosporioides.

A woman in her 70s with a history of recurrent stasis dermatitis treated with long-term topical and systemic corticosteroids presented to the clinic with painful swelling over the right lower leg of 1 week’s duration. On physical examination, there were necrotic ulcers covered by hemorrhagic crusts and purulent debris on the right lower leg (Figure, A). She was afebrile. The blood tests revealed elevated C-reactive protein (18.1 mg/L) but no leukocytosis.

Histopathologically, the tissue fragments showed necrosis of the dermal and superficial subcutaneous tissue with a dense mixed inflammatory cell infiltrate and necrotic occlusion of blood vessels. Periodic acid–Schiff stain revealed abundant thin, septate hyphae on the base of the ulcer and in the lumen of necrotic blood vessels. Fontana-Masson stain revealed no pigmentation of the fungal elements (Figure, B). Fungal culture of the necrotic tissue from the ulcers grew colonies with white aerial mycelia, cylindrical conidia, and pigmented clavate appressoria (Figure, C).

Sequence analysis and a National Library of Medicine BLAST search revealed that the isolate had sequence similarities with reference sequences of ITS1 (100% similarity, 171 of 171 base pairs [bp]), ITS2 (99.4% similarity, 156 of 157 bp), and the D1-D2 domain (100% similarity, 553 of 553 bp) of C gloeosporioides in GenBank. The possible source of C gloeosporioides might be the plants, especially orchids,⁵ that she grew inside her bedroom and on the balcony. She also recalled that she had been traumatized by the plants on her right lower leg 3 months before presentation. The patient was treated with oral itraconazole, 100 mg twice daily, for 3 months, and the ulcers healed completely. A follow-up fungal culture showed no growth.

To our knowledge, there have been only 5 previously reported cases of cutaneous infection caused by Colletotrichum species (Table).^1,2,4 In 2 of these plus the present case (50%, 3 of 6), the patients recalled having experienced precedent trauma at botanical gardens or farms. All of them were immunocompromised due to malignant diseases or long-term use of systemic corticosteroids immunosuppressants. However, even with history of traumatic inoculation of the pathogen, subcutaneous fungal infection might not have manifested immediately, delayed “reactivation” possibly resulting from changes in the host’s immune status.²

Colletotrichum isolates, as determined by the minimal inhibitory concentrations, are susceptible to amphotericin B, itraconazole, and miconazole.^1,2,4 Infections caused by C gloeosporioides used to be classified as hyalohyphomycosis.¹ which is caused by nonpigmented fungi, as seen in our patient. However, the presence of dematiaceous hyphae was demonstrated by Gomori methenamine silver stain in a case of subcutaneous infection caused by C gloeosporioides.² This inconsistency could be explained by “C gloeosporioides species complex,” which contained at least 22 different species and was defined based on the basis of genetic proximity to a clade within the ColletotrichumITS gene tree.⁶

In summary, we present a case of cutaneous C gloeosporioides infection on the leg that was successfully treated with oral itraconazole. Physicians should be aware of Colletotrichum species as an emerging opportunistic life-threatening pathogen, especially in immunocompromised patients with history of trauma or wounds on the extremities and close contact with plants.

Corresponding Author: Chao-Chun Yang, MD, PhD, Department of Dermatology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 Sheng Li Rd, Tainan, Taiwan 704 (yangcc@mail.ncku.edu.tw).

Published Online: August 19, 2015. doi:10.1001/jamadermatol.2015.2102.

Conflict of Interest Disclosures: None reported.

Additional Contributions: We are indebted to Mark Ming-Long Hsu, MD, Department of Dermatology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan, for mycology consultation. Dr Hsu received no compensation for his contribution beyond that received in the normal course of his employment.