INTRODUCTION

Chromoblastomycosis is a slowly developing subcutaneous infection caused by dematiaceous fungi, usually acquired through traumatic inoculation of contaminated plant material. It is most common in rural areas of tropical or subtropical regions and primarily affects agricultural workers. Clinical presentations vary and may include verrucous, nodular, tumorous, cicatricial, or plaque-like forms. Psoriasiform presentations are uncommon and may mimic chronic inflammatory dermatoses, leading to diagnostic delays [1–7].

Fonsecaea monophora is a less frequent etiological agent with worldwide distribution and has been associated with both cutaneous and disseminated infections [1,2,8–10]. This report describes a case of psoriasiform chromoblastomycosis caused by F. monophora in an immunocompetent urban patient, highlighting the importance of clinical suspicion and mycological diagnosis.

CASE REPORT

A 63-year-old male civil engineer, residing in an urban area of Paraguay, with a history of ischemic heart disease, hypertension, and type 2 diabetes mellitus, reported trauma to the right forearm with a metal rod one month prior to symptom onset.

He presented to the dermatology consultation for a chronic skin lesion on the right forearm, present for approx. two months, with slow growth and no associated symptoms. He had self-medicated with topical corticosteroid–antifungal combinations without improvement.

A physical examination revealed an erythematous, scaly plaque measuring approx. 20 mm in diameter, with sharp, raised borders, a rough surface, diffuse scaling, and areas of hyperpigmentation on the extensor surface of the right forearm. No regional lymphadenopathy was palpable (Fig. 1).

Figure 1: Clinical picture: scaly, erythematous plaque on the right forearm with a central crust measuring 20 mm in length.

Histopathology revealed an epidermis showing marked pseudoepitheliomatous hyperplasia, hyperkeratosis, parakeratosis, and acanthosis. The dermis contained suppurative granulomas with multinucleated giant cells and abundant round brown cells with internal septa (fumagoid bodies) (Figs. 2 and 3).

	Figure 2: Histopathology: (a) (left) Epidermis with pseudoepithelial hyperplasia (H&E, 4x). (b) (right) Higher magnification of the chronic granulomatous inflammatory infiltrate of the dermis (H&E, 10x).
	Figure 3: Histopathology: (a) (left) Lower magnification of a tuberculoid-type granuloma with multinucleated foreign body-like giant cells without central necrosis (H&E, 20x). (b and c) (center and right) Fumagoid body in the center of the suppurating granuloma (H&E, 20–40x).

Microbiology:

Figure 4: Microbiology: direct examination with abundant fumagoid cells.

The diagnosis established was psoriasiform chromoblastomycosis due to Fonsecaea monophora, to be treated with itraconazole 200 mg/day combined with cryotherapy for six months, depending on clinical evolution.

Progressive reduction in the inflammation and lesion size was observed.

DISCUSSION

The psoriasiform presentation of chromoblastomycosis is rare and can be mistaken for psoriasis, eczema (particularly secondarily infected eczema), or squamous cell carcinoma. This clinical pattern may be related to epidermal hyperplasia induced by chronic inflammation [1–3,7].

Lesions most frequently occur on the lower limbs—particularly, the dorsum of the foot and leg. Upper limb involvement usually affects the dorsum of the hands and fingers. In our case, the lesion was located on the right forearm [1,5,6]. A characteristic feature is the presence of small, black dots on the lesion, which were absent in our patient [1,3,7].

Histopathology plays a fundamental role in differentiating infections from other dermatoses. In this case, the patient’s use of corticosteroid cream without improvement prompted a biopsy to exclude infectious versus neoplastic pathology [1,7].

Fonsecaea monophora accounts for a minority of chromoblastomycosis cases locally and worldwide, while F. pedrosoi remains the predominant species. However, F. monophora has been associated with a broader clinical spectrum, including disseminated infections. Definitive diagnosis requires mycological confirmation and, when possible, molecular identification [1-3,8.10].

In Paraguay, this represents the second published case of F. monophora infection, with the previous case not displaying a psoriasiform presentation [9].

A systematic review of PubMed, Scopus, and LILACS (2015–2025) identified six reported cases of psoriasiform presentation due to F. monophora. Most occurred in male patients, with a mean age of 55 years, and predominantly affected the upper extremities.

Treatment is long-term, typically combining systemic antifungals (itraconazole or terbinafine) with physical modalities such as cryotherapy, local heat, or surgery to improve cure rates and reduce recurrence [1–7,10]. In this case, the combination of itraconazole and cryotherapy achieved clinical remission, sustained during follow-up.

CONCLUSION

Psoriasiform chromoblastomycosis due to F. monophora is a rare entity that can mimic chronic inflammatory dermatoses. Mycological and molecular confirmation is essential for proper management. This case underscored the need to consider chromoblastomycosis in the differential diagnosis of psoriasiform plaques unresponsive to standard therapy, even in urban and immunocompetent patients. Combination therapy may yield a satisfactory outcome and should be considered in atypical clinical presentations.

REFERENCES

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