Dermatophytoses are common superficial fungal infections, most frequently caused by Trichophyton species. Among them, Trichophyton tonsurans is increasingly recognized as an important cause of tinea capitis and other dermatophytic infections. We conducted a retrospective review spanning three- years and six months (January 2022 - June 2025) in the Parasitology-Mycology Laboratory of La Rabta University Hospital (Tunis, Tunisia). The study included patients with dermatophytosis confirmed to be caused by Trichophyton tonsurans. Clinical samples (skin, scalp, nails) were examined by direct microscopy, following potassium hydroxide clarification and cultured on Sabouraud agar with chloramphenicol and with or without actidione at 27 °C. Identification was based on colony morphology, microscopic examinations and confirmed by ITS2 sequencing. Eight cases of T. tonsurans infection were diagnosed during the study period. Patients ranged in age from 8 to 59 years. Seven presented with scaly alopecic patches on the scalp and one with generalized erythematous-squamous lesions associated with onychomycosis. Four patients (three children and one adult) reported similar infections among close contacts, suggesting possible intra-familial or community transmission. Direct microscopy was positive in six cases, revealing endothrix parasitism or septate hyphae. Cultures yielded powdery white to beige colonies with a yellowbrown reverse within 8-14 days. Molecular analysis confirmed the isolates as T. tonsurans. This case series documents the occurrence of T. tonsurans infections identified over a recent three-year period in Tunisia. Accurate laboratory diagnosis and molecular confirmation remain essential for clinical management and for monitoring evolving dermatophyte epidemiology in the region.

Pityriasis versicolor is a superficial fungal infection of the skin caused by fungi of the genus Malassezia. Typically, patients present with well-defined, hypopigmented, scaly macules, or patches over seborrheic areas. However, rare presentations include papular, confetti-like spots, and folliculocentric, atrophic, and inverse forms. Diagnosis may be established clinically with the help of noninvasive diagnostic tools such as dermoscopy, Wood's lamp, and direct microscopic examinations. However, skin biopsies are imperative in equivocal cases. To date, 34 cases have been reported. This study presents a rare presentation of atrophying skin lesions in a patient with pityriasis versicolor.

Inverse pityriasis versicolor (PV) involving the groin and scrotum is an uncommon presentation of PV. Despite its uncommon location, PV should be suspected in patients with scaly and persistent hypo or hyperpigmented lesions, especially in regions with hot and humid environment. Early recognition allows effective antifungal therapy, preventing chronicity and recurrence.

Vasculitis comprises a spectrum of disorders defined inflammation of the blood vessel walls and is categorized based on vessel size into small-, medium-, and large-vessel vasculitis. The histological characteristics of leukocytoclastic vasculitis include neutrophil infiltration around small cutaneous blood arteries and fibrinoid necrotizing inflammation. Annular morphology is a unique and rare type of leukocytoclastic vasculitis. We report a case of annular leukocytoclastic vasculitis in a 39-year-old Saudi man who presented with scaly annular erythema and targetoid lesion configurations with prominent, raised borders. He was managed with oral prednisolone 40 mg daily as a tapered dosage regimen, in combination with topical mometasone furoate 0.1% cream applied twice daily, resulting in complete resolution of lesions. To the best of our knowledge, this is the first reported case of annular morphology of leukocytoclastic vasculitis with microvascular occlusions in the Middle East.

Seborrheic dermatitis (SD) is a common, chronic inflammatory skin disorder that can be challenging to manage when refractory to conventional topical therapies. This case report describes the use of a 532-nm Potassium Titanyl Phosphate (KTP) Q-switched laser in a patient with refractory SD. A 25-year-old male patient presented with persistent erythematous, scaly, and pruritic facial lesions. Clinical evaluation included histopathological confirmation and Seborrheic Dermatitis Area and Severity Index (SEDASI) scoring, with an initial score of 46 points. The patient underwent four sessions of 532-nm KTP Q-switched laser treatment (8 J/cm[2], 10-ns pulse duration, 3-mm spot size, 5 Hz frequency, three non-overlapping passes per session), in combination with standard topical therapy (ketoconazole 2% shampoo and ceramide-based sunscreen). Following the fourth session, the SEDASI score decreased from 46 to 23 points, corresponding to a reduction from "very severe" to "moderate" disease severity. This was accompanied by clinical improvement in erythema, scaling, and pruritus. A three-month follow-up demonstrated sustained improvement without recurrence. No adverse effects were observed apart from transient erythema. Immediate whitening noted during treatment was consistent with a possible photomechanical effect. In this single case, 532-nm KTP Q-switched laser therapy was well tolerated and associated with clinical improvement. Given the inherent limitations of a case report, these findings should be interpreted with caution. Further controlled studies are required to better define the safety, efficacy, and potential role of this modality in refractory SD.

Cutaneous squamous cell carcinoma (cSCC) is the second most prevalent skin cancer diagnosed worldwide after basal cell carcinoma. CSCC represents a growing global public health challenge due to its higher potential of local invasion, recurrence, and metastasis. Incidence rates of cSCC are projected to increase due to rising exposures to risks factors. Ultraviolet light exposure is the primary cause, and lighter skin pigmentation, immunosuppressive conditions and skin phototype are the primary risk factors. CSCC typically presents as a red, scaly, flat lesion (in situ tumors) or a red, firm, raised lesion with scale or erosion (invasive tumors). Surgical excision remains the standard-of-care for localized cSCC and is often curative. Although, most patients achieve favorable outcomes, a subset of cSCC exhibits a highly aggressive and metastatic phenotype (postoperative recurrence rates are approximately 5%). Addressing the clinical challenge posed by these high-risk cases requires a more comprehensive understanding of the underlying molecular drivers. This review examines the interaction between transglutaminase 2 (TG2) and the G-protein-coupled receptor 56 (GPR56) as a pivotal driver of the aggressive cSCC phenotype. This molecular axis is particularly significant for its role in the maintenance of epidermal cancer stem (ECS) cells, which contribute to tumor progression and therapy resistance. While the definitive link between the TG2-GPR56 complex and systemic metastasis in cSCC is currently being elucidated, significant evidence from analogous malignancies and in vitro keratinocyte models provides a clear mechanistic roadmap for its involvement in tumor invasion.

Dermal leishmaniasis, particularly postkala-azar dermal leishmaniasis (PKDL), is an uncommon entity that may closely mimic lepromatous leprosy in endemic regions. Both conditions present with chronic, symmetric nodular or plaque-like lesions, leading to frequent diagnostic confusion, especially when peripheral nerve thickening is absent. We report a 71-year-old male with a 15-year history of diffuse erythematous nodules and scaly plaques over the palms and dorsum of the feet, repeatedly managed as lepromatous leprosy without clinical improvement. The absence of peripheral nerve thickening and a negative slit-skin smear prompted further evaluation. Skin biopsy demonstrated macrophages packed with Leishmania donovani (LD) bodies, and polymerase chain reaction (PCR) targeting the ITS-1 gene confirmed LD. The patient was initiated on miltefosine 50 mg twice daily for 12 weeks (standard regimen). At 4-week follow-up, lesions showed approximately 30% flattening, and at 12 weeks, more than 60% regression was noted, without adverse effects. This rare case of a 71-year-old male with >15 years of misdiagnosis highlights that chronic diffuse nodular dermatosis without nerve involvement should prompt consideration of PKDL even in the absence of documented prior visceral leishmaniasis. Accurate diagnosis using histopathology and PCR prevents prolonged inappropriate therapy and reduces the risk of community transmission.

Chromoblastomycosis is a chronic mycosis of the skin and subcutaneous tissue typically caused by traumatic inoculation of dematiaceous fungi of the Herpotrichiellaceae. A 59-year-old male presented with a 12-month history of an asymmetrical, scaly plaque on the left forearm that has been slowly increasing in size. Past medical history included atrial fibrillation on apixaban, hypertension and a cardiac stent. A 4 mm punch biopsy of the left forearm revealed superficial dermal fibrosis with mild pseudoepitheliomatous hyperplasia and granulomatous inflammation with scattered multinucleate histiocytes. There were giant cells with dark brown, somewhat round, yeast-like structures, some with internal septation exhibiting moderate staining for PAS, compatible with Medlar bodies suggestive of chromoblastomycosis. The patient was on rosuvastatin, rendering itraconazole not a possible treatment option, and instead the patient underwent curettage and cautery with two bouts of cryotherapy freeze and thaw cycles. A twelve-month follow-up noted a crusted area on the distal aspect of the scar. A shave biopsy of this area revealed pigmented organisms suggesting a recurrence of chromoblastomycosis. A further excisional biopsy was performed, with no evidence of chromoblastomycosis. This case highlights multiple surgical options for the management of chromoblastomycosis in patients where medical management is contraindicated. It highlights the therapeutic challenge of this disease due to frequent recurrence of lesions and that repeat biopsy may be efficacious in monitoring for recurrence.

The aim of this study is to illustrate the coexistence of these autoimmune conditions in the same patient, through the presentation of two case reports. Clinical Case 1: Male patient, fair-skinned, 43 years old, presenting with ulcerated and disseminated oral lesions for approximately six months, along with scaly lesions on the neck and elbows, previously diagnosed as psoriasis. An oral biopsy confirmed a diagnosis consistent with pemphigus vulgaris. Clinical Case 2: A 51-year-old fair-skinned male reported pain in the inner region of the mouth and throat for the past four months, associated with widespread ulcerative lesions. In addition, he presented scaly areas on the scalp. The findings confirmed a concomitant diagnosis of pemphigus vulgaris and psoriasis. In all cases, systemic corticosteroid therapy was prescribed, and the patients remain under joint follow-up care in the of Stomatology and Dermatology. Therefore, a thorough investigation through clinical, laboratory, and histopathological examinations is indispensable for the proper management of these conditions, ensuring effective treatment.

Psoriasiform eruption is an uncommon cutaneous immune-related adverse event (irAE) associated with anti-PD-1 therapy, and its rapid recurrence upon switching to a different anti-PD-1 agent is a scarcely documented phenomenon. We report the case of a 59-year-old man with stage IIB lung adenocarcinoma who developed a pruritic, scaly eruption after his fourth cycle of pembrolizumab. Histopathological examination confirmed a diagnosis of grade 2 psoriasiform dermatitis according to the Common Terminology Criteria for Adverse Events (CTCAE) version 5.0. The initial episode was resolved with systemic corticosteroids. However, upon switching anti-PD-1 therapy to tislelizumab, a similar but more widespread eruption recurred rapidly within a week. The recurrence was successfully managed with topical corticosteroid and antihistamines, and the anti-PD-1 therapy was subsequently discontinued. During the 3-year follow-up after discontinuation, the patient's skin lesions resolved completely with no recurrence, and no tumor progression was observed. The reduced latency of psoriasiform dermatitis recurrence upon anti-PD-1 inhibitor rechallenge suggests a memory T cell-driven immune response. It also highlights that such irAEs were observed with the two PD-1 inhibitors pembrolizumab and tislelizumab used in this case and can be effectively managed. In this case, tumor progression was not observed after treatment cessation, although causality cannot be inferred.

Dermatosis neglecta (DN) is a rare psychocutaneous disorder. To the best of our knowledge, this is the first reported case of DN localized to the periumbilical region. We present a case of 19-year-old male patient who developed extensive, persistent, scaly plaques on his abdomen over two years, which were resistant to routine washing with soap and water. Dermoscopy revealed no hemorrhage or other significant abnormalities. Wood's lamp examination demonstrated white fluorescence, and direct mycological tests were negative. The diagnosis was confirmed by the complete resolution of the lesions after wiping with 70% isopropyl alcohol, which revealed normal underlying skin. Based on the clinical presentation and diagnostic evaluation, a diagnosis of DN was established.

Sexually transmitted dermatophytosis caused by Trichophyton mentagrophytes genotype VII (TMVII) has recently emerged as a novel clinical entity, particularly within sexual networks. This pathogen is characterized by inflammatory genital lesions, diagnostic challenges, and increasing antifungal resistance. We report a case of genital dermatophytosis caused by terbinafine-resistant TMVII in a heterosexual woman following sexual exposure abroad. A 35-year-old otherwise healthy woman presented with a 3-week history of rapidly progressive, intensely pruritic genital lesions unresponsive to topical antifungal therapy. Clinical examination revealed well-demarcated annular erythematous plaques with central clearing and an active scaly border confined to the pubic and inguinal regions. Direct microscopic examination demonstrated fungal hyphae, and fungal culture identified Trichophyton mentagrophytes. Molecular analysis by PCR sequencing confirmed genotype VII. The patient denied animal contact or fomite exposure but reported unprotected sexual intercourse during recent travel to Turkey. Screening for sexually transmitted infections, including HIV, hepatitis B, and syphilis, was negative. Oral terbinafine therapy (250 mg/day for 4 weeks) was ineffective. Antifungal susceptibility testing confirmed biological resistance to terbinafine. Treatment was switched to oral itraconazole (100 mg/day for 4 weeks), resulting in complete clinical resolution without relapse. This case illustrates an emerging sexually transmitted dermatophytosis due to terbinafine-resistant TMVII. To our knowledge, no previous cases linked to travel to Turkey have been reported. The report highlights the importance of considering TMVII in patients presenting with inflammatory genital dermatophytosis, particularly when lesions are refractory to standard antifungal therapy. Early recognition, molecular confirmation, appropriate treatment, and partner management are essential to prevent further transmission of this emerging pathogen.