A case report of tinea pedis caused by Trichosporon faecale in Iran

Abstract

Trichosporon species are known as the causative agents of cutaneous infections and are involved in systemic, localized, as well as disseminated mycoses particularly in immunocompromised patients. Here we report a case of tinea pedis infection caused by Trichosporon faecale in a healthy 29-year-old woman in the north of Iran. Macroscopic and microscopic characteristics using direct examination as well as culture method revealed the causative agent as Trichosporon species.

Molecular analysis of the internal transcribed spacer region validated the initial result and indicated that this case of tinea pedis was caused by T. faecale. The patient was recovered after treatment with topical myconazole accompanied with oral fluconazole.

1. Introduction

Members of the genus Trichosporon have been identified from the mucosal surfaces of the human respiratory and gastrointestinal tracts as well as from stool, sputum and hair [1–3]. The species are the causative agents of cutaneous infections such as white piedra, an innocuous hair shaft infection encountered mostly in tropical and temperate countries [4]. Furthermore, they are also involved in systemic, localized, or disseminated mycoses [5–8]. In recent years, these fungi appear to have emerged as a life-threatening pathogen, especially in patients with underlying diseases, such as hematological malignancies, AIDS, burns, organ transplantation and solid tumors [9–12]. Owing to the usage of molecular techniques, the nomenclature within the genus; Trichosporon has been considerably revised [13]. Today, at least 13 Trichosporon species have been reported to be human pathogens including T. asahii, T. asteroides, T. coremiiforme, T. cutaneum, T. dermatis, T. domesticum, T. faecale, T. inkin, T. japonicum, T. jirovecii, T. loubieri, T. montevideense, and T. mucoides [13]. Among them, T. asahii is now regarded as the most common pathogenic agent of trichosporosis [1].

Few case reports have been published which identified T. faecale fungus as a causative agent of tinea pedis [14]. Here we report a case of tinea pedis due to T. faecale in an immune competent patient from Guilan province in the north of Iran.

2. Case

On February 2011, a 29-year old house-wife with a suspected tinea pedis and about six-month history of itching, scaling and erythematous patches on her right feet was referred to the laboratory of Medical Mycology in Tehran University of Medical Sciences (Day 0). The patient was in good health. However, her spreading lesions appeared pruritic and inflamed on the edges, especially those located on the right and left areas of her feet (Fig. 1). Treatment with unspecific topical agents was unsuccessful.

Fig. 1.

Lesions inflamed on the edges of feet.

Cutaneous samples were gathered by gently scraping of the active borders of the lesions. Direct microscopic examination of scale samples with 15% KOH showed septate hyaline hyphae and chains of arthroconidia which are usually produced by dermatophyte fungi in infected tissues (Fig. 2). Some portions of the scale specimens were inoculated on several locations in Sabouraud Dextrose Agar medium plates (Merck, Germany), containing chloramphenicol and cycloheximide. The plates were then kept at 28 °C. After 3 days, the macroscopic feature of the grown colony appeared white to creamy yeast-like colonies. The colonies were moist-shining similar to Candida colonies and showed radiating fissures extending from the center. Microscopic examination of the colonies revealed mycelium with septate hyphae, arthroconidia, and budding cells (Fig. 3a and b). Furthermore, sub culturing of obtained colonies on CHROM agar medium (Merck, Germany) yielded blue colonies (Fig. 3c).

Fig. 2.

15%KOH direct examination of samples showed septate hyaline hyphae and chains of arthroconidia (400×).

Fig. 3.

(a) Colony morphology of the causing agent of tinea pedis on SDA after incubating at 28 °C for 3 days. (b) Microscopic examination of the colony stained by LCB, the fungus possesses mycelium with septate hyphae, arthroconidia, and budding cells (Scale bar: 5 μm). (c) Colony morphology of the causing agent of tinea pedis on and CHROMagar after incubating at 28 °C for 3 days.

Based on the observed yeast-like colonies, abundant arthroconidia as well as rare budding cells, and according to previously described characteristics [15], a strain of Trichosporon species was likely to be the causative agent of this infection.

Fungal DNA was extracted from the colony by use of glass bead disruption [16]. Primers were designed based on the sequence of the rDNA regions. The sequences of primers are as follow: ITS1-F (5′-TCCGTAGGTGAACCTGCGG-3′) as forward and ITS4-R (5′-TCCTCCGCTTATTGATATGC-3′) as reverse. Polymerase chain reaction (PCR) was carried out in a thermal cycler (PeQLab, Germany) with the following temperature profile: 1 cycle of 5 min denaturation at 94 °C; 35 cycles of 45 s denaturation at 94 °C, primer annealing 45 s at 54 °C, primer extension 1.5 min at 72 °C; Final 10 min extension at 72 °C. A negative control was also run along with the experiment. PCR product was loaded onto 1% agarose gel and run in TBE buffer (90 mM Tris, 90 mM boric acid and 2 mM EDTA, [pH 8.3]) at 80 V for 1 h and detected by staining with ethidium bromide (0.5 μg/ml) and photographed. A single banding pattern with approximate size of 550 base pairs has been visualized and directly subjected for DNA sequencing. According to homology search in Gene Data Bank (NCBI, NIH, USA), the sequencing results demonstrated complete homology (100%) with the 28S rDNA regions of T. faecale.

Medication was immediately started according to the morphological results (Day 5). Fluconazole was prescribed in an oral dosage of 150 mg daily for four weeks. Along with oral treatment, topical myconazole nitrate was also applied twice a day. Complete remedy was obtained and no fungal elements were observed in the direct examination after six weeks.

3. Discussion

The frequency of infections caused by non-Candida yeast has increased recently due to increased population of immunocompromised patients and the use of anti-microbial prophylaxis [17]. Trichosporon species are widely distributed in rotting wood, sludge, soil, mushrooms, plants, leaf-cutting ants, birds and mammals. In humans, these species are occasionally isolated from skin, pharynges, urine as well as stool [18]. These fungi are also considered as emerging fungal pathogens responsible for causing localized or systemic mycoses.

Apart from white piedra, Trichosporon species are also responsible for causing superficial mycosis such as tinea pedis as well as onychomycosis [7,14]. In the present study, we reported a case of tinea pedis caused by one of the members of this genus. The reported patient was in good health and revealed no basic disorders or immunodeficiency. However, she has lived for several years in a humid area in the north of Iran. More investigations based on her living habits, revealed that she used to walk with bare feet in wet regions for a long time. Based on morphological characteristics, a strain of Trichosporon species was found as causative agent of this case. As phenotype-based methods are not sensitive enough for identification of Trichosporon species [13], a 550-bp PCR product of the rDNA region was sequenced. The latter analysis indicated the causative agent as T. faecale. This species has been previously reported as causative agent of summer-type hypersensitivity pneumonitis [19]. In addition, it has been isolated from the patients associated with asthma and liver diseases [20]. Besides, T. faecale was also isolated from forest area in Russia and from nails and skins of the patient in Argentina and Spain [21,22]. To the best of our knowledge, T. faecale has been rarely reported as causative agent of tinea pedis world wide.

The mentioned patient was medically followed and has been treated successfully.

Conflict of interest

There are none.