Chromoblastomycosis is an infection caused by the traumatic implantation of species of dematiaceous fungi, primarily in the skin and subcutaneous tissues of the lower limbs. The disease generally starts as a cutaneous nodule or papule which gradually increases in the adjacent areas and develops a scaly, greyish surface. After the lesion may evolve into one of the following described clinical forms: the nodular, tumoral, verrucous, cicatricial and plaque types. Histologically, a granulomatous reaction associated with acanthosis and pseudoepitheliomatous hyperplasia in the stratum corneum and epidermis is observed. The fungal structure in infected scales or tissues appears as rounded, dark-brown yeast-like bodies (5–15μm in diameter) with thick, planate-dividing walls that are known as sclerotic cells (also referred as “copper pennies,” “fumagoid cells,” “Medlar bodies,” or “muriform cells”).1

Chromoblastomycosis is a frequent disease in countries with tropical and subtropical climates, particularly in Latin America, Africa and Asia. The most frequent causative agents are Fonsecaea pedrosoi, F. compacta, Phialophora verrucosa, Cladophialophora carrionii, and Rhinocladiella aquaspersa. These fungi inhabit the soil and vegetal matter; therefore, the disease is more frequent in rural populations.2

This work describes the case of a patient living in deficient hygienic and socioeconomic conditions who presented a chronic subcutaneous infection compatible with chromoblastomycosis. The identified etiological agent has not been previously associated with this pathology.

During a health campaign in rural areas organized by the Faculty of Chemical Sciences at the Autonomous University of Oaxaca the patient of this case was addressed. He was an indigent 79-year-old man, resident in Miahuatlan, Oaxaca (Mexico), and was a peasant with a history of chronic alcoholism and smoking. He began his current dermatological illness 27 years ago after the use of tight footwear that caused a laceration on his right heel. From that time, his lesion changed, with progressive thickening, pigmentation and peeling of the local skin. Several small nodules appeared and extended to the foot. The patient applied several empirical and aggressive treatments without improvement. He also sought medical assistance, but the treatment yielded unsatisfactory results. Five years ago, the presence of a progressive ulcerative lesion was detected.

On physical examination, pigmented verrucous plaques were observed, predominantly on the anterior side, heel and internal side of the right foot. Moderate oedema and thick, yellow and adherent squamae were noteworthy on the leg. The patient had an ulcer located on the internal side of the lower third of the leg (10cm×5cm), with a well-defined border and a haematopurulent and foetid exudate. Additionally, larvae (miasis) were observed in the ulcer. The patient did not report symptoms localized in the affected zone but manifested asthenia, adynamia and general discomfort. He presented pallor, hearing loss, uncontrolled salivation, involuntary movements of both hands, and urinary incontinence. Authorization to take an image of his lesion was obtained (Fig. 1a). Additionally, scales and blood samples were collected for mycological study and analysis, respectively.

Fig. 1.

(a) Pigmented verrucous lesions on the foot (arrows), an ulcerative lesion (*) on the lower part of the leg, and yellowish, thick, crusty lesions on the leg are observed. (b) Microscopic examination of scales, showing thick walled, round-to-ovoid brown cells with septa characteristic of fumagoid cells (40×). (c) Microscopic examination with lactophenol blue from primary culture: irregular and pigmented hyphae with internal guttules, chlamydoconidia-like cells and some septate globose structures similar to fumagoid cells (arrows) are observed (scale bar: 10μm).

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Morphological study

The fungus was grown on SDA, on potato dextrose agar (PDA) and on lactrimel agar (LA) for 6 days at 28°C. The microscopic morphology on SDA and PDA was similar to that observed for the primary isolate, but it revealed numerous chlamydoconidia on LA. After four weeks on PDA, many irregular and round pycnidia were observed. The fungus was later grown on malt extract agar (MEA) and on oat agar (OA) for 8 days at 28°C (Fig. 2a and b). The size of colony was 7.0 and 6.7cm of diameter, respectively. Microscopic morphology on two media was similar, but only description on OA is done. Abundant globose or piriformis, intercalary, terminal or in chains, of variable size (5–14μm diameter) chlamydospores, were observed (Fig. 2c). Numerous globose (200μm), piriformis (200μm×360μm) or irregular pycnidia, with one to three ostioles or pores (Fig. 2d) were observed. Polyhedral cells formed the pycnidial wall (Fig. 2e). Abundant ellipsoidal, hyaline conidia with one or two polar guttules emerging from picnidia were present (Fig. 2f). Conidial matrix whitish was evident. The morphological characteristics were integrated according to Boerema et al.3

Fig. 2.

Culture on OA (a) and MEA (b) after 8 days of growth, showing pigmented, woolly, green olivaceous colonies. (c) Abundant pigmented chlamydoconidia (10×); insert: magnification of a chlamydoconidium (scale bar: 10μm). (d) Globose picnidium (scale bar: 50μm), showing three ostiolae (arrows). (e) Polymorphic cells of the picnidium wall (scale bar: 10μm). (f) Abundant small and ellipsoidal conidia (40×); insert: magnification of conidia (scale bar: 5μm).

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Phoma (Saccardo 1880; Sacc emend. Boerema & G.J. Bollen) is an anamorphic, complex constituted by dematiaceous fungi. These organisms inhabit soil, organic debris, and water and include species that parasitize other fungi, insects and vertebrates. Approximately 10 species are reported as opportunistic or primary human pathogens.5

In 1970, Bakerspigel (cited in 6 and 7) reported the first case of human infection caused by Phoma (Phoma hibernica). Currently there are at least 30 reports of human infections caused by Phoma spp. as shown in Table 1.6–13

Different therapeutic resources have been used in clinical cases, most with satisfactory outcomes. In a recent in vitro antifungal susceptibility study, posaconazole and voriconazole showed the best activity against dematiaceous fungi including Phoma isolates. In that study amphotericin B and fluconazole were the least active drugs.14 These last findings are similar to those observed for P. insulana.

Five genera of dematiaceous fungi are the main causative agents of chromoblastomycosis in the world. In Mexico the frequency of the agents is: F. pedrosoi (95.8%), C. carrionii (1.1%), P. verrucosa (0.6%), R. aquaspersa (0.2%) and E. spinifera (0.2%).15 Here we inform an additional genus associated with this pathology.

In this work we report a case diagnosed as chromoblastomycosis based on the following data: (a) Disease began after skin trauma. (b) The clinical manifestations consisted of lesions with verrucous aspect and chronic evolution. (c) The microscopic examination of scales showed fumagoid cells, fungal structures associated only to chromoblastomycosis. (d) On culture developed several colonies of a dematiaceous fungus, kind of fungi described as etiological agents of phaeohyphomycosis or chromoblastomycosis. Due to patient’ reluctance, it was not possible to carry out the histopatological study which would reveal in addition fumagoid cells, a tissue response consisted of pseudoepitheliomatous hyperplasia, acanthosis and hyperkeratosis. Accordingly it was not possible prescribe him an appropriate treatment.

To the best of our knowledge, this is the first report of chromoblastomycosis caused by P. insulana.

The authors declare no conflict of interest.