Cutaneous Scedosporiosis with Generalized Tinea Corporis in a Patient with Chronic Heavy Alcohol Use: A Case Report

Abstract

We report a case of Scedosporium boydii (S. boydii)-induced cutaneous infection combined with generalized tinea corporis in a male patient with a long history of heavy alcohol consumption. The clinical presentation, diagnostic findings, treatment course, and outcome are described, together with a review of the relevant literature. A 63-year-old man presented with a 3-week history of generalized erythematous papules, plaques, scaling, and pain. The diagnosis was established through skin biopsy and mycological examination. Following systemic azole therapy, topical antifungal treatment, and supportive care, the patient’s skin lesions and associated symptoms improved substantially. Cutaneous S. boydii infection is rare and may be difficult to distinguish from other infectious or inflammatory skin disorders. Voriconazole is generally considered a preferred systemic treatment, although therapeutic decisions should be guided by species identification, susceptibility data when available, and the patient’s clinical condition. Chronic heavy alcohol consumption may have contributed to increased susceptibility in this patient, but a causal relationship cannot be established from a single case. Early tissue sampling and mycological evaluation are important for timely diagnosis and appropriate treatment.

Introduction

Scedosporium species are environmental opportunistic pathogenic fungi. Scedosporium boydii (S. boydii) can infect individuals across different immune statuses and cause multi-site infections. Because of its natural resistance to multiple antifungal drugs, diagnosis and treatment become very difficult. With a high fatality rate, it can infect immunocompetent or immunocompromised hosts, thereby inducing infections in multiple parts of the body such as the skin, respiratory tract and central nervous system.^1–3 Meanwhile, infectious dermatitis caused by this fungus is rare in clinical practice, and its presentation does not significantly differ from that of common bacterial or fungal dermatitis. This similarity often leads to misdiagnosis, missed diagnosis and delayed treatment.⁴

Here, we report a rare case of cutaneous S. boydii infection combined with generalized tinea corporis in a patient with a long history of heavy alcohol consumption. By describing the diagnostic findings, treatment course, and clinical outcome, this report aims to highlight the diagnostic challenges and clinical management of concurrent cutaneous and superficial fungal infections.

Case Presentation

A 63-year-old man with a history of heavy alcohol consumption for more than 20 years was admitted with a 3-week history of erythema, papules, and pain involving the jaw, extremities, and buttocks. Physical examination revealed scattered and partially confluent erythematous lesions on the jaw, trunk, and extremities, accompanied by papules, crusting, scaling, and tenderness. Well-demarcated annular or polycyclic erythematous lesions were also observed on the trunk, extremities, and buttocks, raising suspicion of a concurrent superficial dermatophyte infection. Cardiopulmonary, abdominal, and neurological examinations revealed no remarkable abnormalities.

Laboratory investigations revealed a red blood cell count of 2.56 × 10¹²/L, hemoglobin of 87.10 g/L, ketone bodies of 3+, bicarbonate of 21.9 mmol/L, total calcium of 2.09 mmol/L, fasting blood glucose of 3.55 mmol/L, fibrinogen of 5.15 g/L, D-dimer of 460 ng/mL, high-sensitivity C-reactive protein of 19.2 mg/L, erythrocyte sedimentation rate of 90 mm/h, interleukin-6 of 29.00 pg/mL, and total cholesterol of 0.82 mmol/L. CA125 was mildly elevated at 58.00 U/mL (laboratory reference range: 0–35 U/mL). Liver and kidney function tests, autoantibody testing, other tumor markers, and routine infection screening showed no clinically significant abnormalities. Electrocardiography showed sinus rhythm with T-wave changes. Imaging examinations indicated an infectious lesion in the submental region, reactive cervical lymphadenopathy, and thyroid nodules. Abdominal ultrasonography demonstrated hepatic steatosis, a hepatic cyst, and a gallbladder polyp. Superficial ultrasonography further demonstrated a submandibular infectious lesion and reactive lymphadenopathy.

The initial diagnoses included infectious dermatitis, submental space infection, chronic apical periodontitis, suspected alcohol-related liver injury, fatty liver disease, hepatic cyst, and benign prostatic hyperplasia. The differential diagnoses for the extensive cutaneous lesions included bacterial skin infection, generalized dermatophytosis, atypical mycobacterial infection, other cutaneous fungal infections, and inflammatory dermatoses. Because of the atypical and extensive skin lesions, a skin biopsy and tissue culture were performed using specimens obtained from a lesion on the dorsum of the right hand on March 2, 2026. Histopathological examination showed fragmented skin tissue, full-thickness dermal edema, diffuse mixed inflammatory-cell infiltration, and multinucleated giant cells, consistent with infectious granulomatous inflammation. The available H&E-stained sections at 4×, 10×, and 20× objective magnification demonstrated the overall distribution and cellular features of the inflammatory reaction (Figure 1). Fungal elements were not definitively identified on H&E staining. PAS and GMS staining were not performed; therefore, fungal tissue invasion could not be confirmed histologically.

Figure 1.

Histopathological findings of the skin biopsy obtained from the dorsum of the right hand. (A) Low-power view showing fragmented skin tissue with extensive inflammatory-cell infiltration (H&E staining, 4× objective). (B) Intermediate-power view showing diffuse mixed inflammatory-cell infiltration within the dermis (H&E staining, 10× objective). (C) Higher-power view showing the cellular features of the inflammatory infiltrate and multinucleated giant cells, consistent with infectious granulomatous inflammation (H&E staining, 20× objective).

Fungal culture of the right-hand tissue specimen yielded an isolate phenotypically identified as Scedosporium boydii on the basis of colony morphology on potato dextrose agar and Sabouraud dextrose agar and microscopic examination of the fungal structures (Figure 2). Molecular confirmation by gene sequencing or matrix-assisted laser desorption/ionization time-of-flight mass spectrometry was not performed. Direct microscopic examination and fungal culture of scrapings obtained from the gluteal lesions demonstrated fungal elements and yielded Trichophyton interdigitale (Figure 3). Formal antifungal susceptibility testing, including minimum inhibitory concentration determination for voriconazole, itraconazole, and amphotericin B, was not performed. The concordance among the clinical presentation, infectious granulomatous inflammation, and recovery of Scedosporium from a tissue specimen obtained from the same lesion supported the diagnosis of cutaneous scedosporiosis caused by an isolate phenotypically identified as S. boydii, together with generalized tinea corporis caused by T. interdigitale.

Figure 2.

Fungal culture and phenotypic identification of an isolate consistent with Scedosporium boydii from the right-hand tissue specimen. (A) Slide culture on potato dextrose agar (PDA) after incubation at 25°C for 5 days, showing septate hyphae and conidial structures (unstained, ×1000). (B) Fluorescence-stained preparation showing fungal hyphae and conidia (×1000). (C) Sexual structures showing dark brown cleistothecia and unicellular fusiform or elliptical ascospores (lactophenol cotton blue staining, ×400). (D) Higher-power view of the sexual structures and ascospores (lactophenol cotton blue staining, ×1000). (E) Obverse colony morphology on PDA after incubation at 25°C for 5 days. (F) Obverse colony morphology on Sabouraud dextrose agar (SDA) after incubation at 25°C for 5 days. Species identification was based on conventional colony and microscopic morphology; molecular confirmation was not performed.

Figure 3.

Mycological examination and culture of Trichophyton interdigitale from the gluteal skin lesions. (A) Fluorescence-stained preparation showing fungal hyphae and conidial structures after culture on SDA at 25°C for 7 days (×400). (B) Higher-power view of the fungal structures (fluorescence staining, ×1000). (C) Obverse colony morphology on PDA after incubation at 25°C for 7 days. (D) Obverse colony morphology on SDA after incubation at 25°C for 7 days.

Oral itraconazole was initially administered at 0.2 g twice daily during the first 3 days of hospitalization as empirical antifungal therapy while the mycological results were pending. Because the skin lesions continued to progress and tissue culture indicated Scedosporium species, itraconazole was discontinued on day 4. Oral voriconazole was subsequently initiated with a loading dose of 0.4 g on day 4, followed by a maintenance dose of 0.2 g twice daily. Voriconazole was administered for 5 days during hospitalization, including the loading-dose day. Piperacillin–tazobactam was administered intravenously at 4.5 g every 8 hours for 3 days for suspected concomitant bacterial infection. Topical mupirocin and ketoconazole creams were applied to the affected areas. Ozone water baths and red-light irradiation were used as adjunctive wound-care and symptom-relief measures rather than as primary antifungal treatments. Additional supportive treatment included gastric protection, correction of anemia and electrolyte disturbances, lipid management, and nutritional support. The patient was also advised to abstain from alcohol.

Given the presence of fatty liver disease and suspected alcohol-related liver injury, serial alanine aminotransferase, aspartate aminotransferase, and total bilirubin measurements were obtained during systemic antifungal treatment to monitor potential hepatotoxicity. Serum voriconazole trough concentrations were not measured. After 17 days of comprehensive treatment, the skin lesions became darker and decreased in size, while the pain and pruritus were substantially relieved (Figure 4). Because systemic antifungal treatment, topical treatment, antibacterial therapy, supportive care, and alcohol abstinence were implemented concurrently, the clinical improvement could not be attributed to voriconazole alone.

Figure 4.

Clinical appearance of the skin lesions before and after treatment. (A) Skin lesions on the dorsum of the right hand before treatment. (B) Clinical appearance after 17 days of comprehensive treatment, showing darkening and reduction of the lesions.

At discharge, the patient was advised to continue oral voriconazole and topical ketoconazole, abstain from alcohol, improve his nutritional status, and attend regular follow-up. However, the actual duration of outpatient voriconazole treatment and the long-term post-discharge outcome were not available in the medical records.

Clinical timeline: The patient developed generalized skin lesions approximately 3 weeks before admission. On March 2, 2026, a skin biopsy and tissue culture were performed using specimens obtained from the dorsum of the right hand. Oral itraconazole was administered during hospital days 1–3 as empirical antifungal treatment. On hospital day 4, itraconazole was discontinued because of continued lesion progression and the tissue-culture findings, and oral voriconazole was initiated. Voriconazole was administered for 5 days during hospitalization. By treatment day 17, the skin lesions had become darker and smaller, with substantial relief of pain and pruritus. At discharge, continued oral voriconazole and topical ketoconazole were recommended; however, the actual duration of outpatient voriconazole treatment and the long-term post-discharge outcome could not be determined from the available medical records.

Discussion

Scedosporium boydii is an opportunistic environmental fungus that may cause infections involving the skin, subcutaneous tissues, respiratory tract, central nervous system, and other organs. The anatomical terminology used to describe scedosporiosis should be precise. Cutaneous scedosporiosis refers to infection primarily involving the skin, whereas subcutaneous scedosporiosis extends into the deeper soft tissues and may present with nodules, abscesses, granulomatous lesions, or mycetoma-like changes. Disseminated or invasive scedosporiosis generally refers to infection involving internal organs or multiple noncontiguous sites. In the present case, the biopsy showed dermal infectious granulomatous inflammation, and Scedosporium was recovered from a tissue specimen obtained from the same right-hand lesion. However, PAS and GMS staining were not performed, fungal elements were not definitively identified on H&E staining, and subcutaneous or visceral involvement was not demonstrated. Therefore, the more conservative term “cutaneous scedosporiosis” was used instead of “deep” or “subcutaneous” scedosporiosis.

The patient had a history of heavy alcohol consumption for more than 20 years. Chronic alcohol exposure may impair host defense through altered neutrophil recruitment and chemotaxis, reduced phagocytic killing, impaired macrophage function, disruption of epithelial barriers, and broader abnormalities in innate and adaptive immunity.⁵ These effects provide a biologically plausible explanation for increased susceptibility to infection. Nevertheless, chronic alcohol consumption cannot be regarded as the established cause of the concurrent fungal infections in this patient. The available immune evaluation was incomplete, and the patient also had anemia, electrolyte and metabolic abnormalities, inflammatory activation, and suspected alcohol-related liver injury. Thus, alcohol consumption should be considered one potential contributing factor among several possible host-related abnormalities rather than the principal causal factor. Previous reports have shown that Scedosporium infections can occur in both immunocompromised and apparently immunocompetent hosts and may range from localized disease to severe disseminated infection.^6–8 Generalized dermatophyte infection involving several noncontiguous body sites may also indicate impaired local or systemic host defense.^9–11 The coexistence of cutaneous scedosporiosis and generalized tinea corporis in this patient is therefore clinically unusual, but a single case cannot establish that the two infections resulted directly from alcohol-related immune dysfunction.

The diagnosis of cutaneous scedosporiosis can be challenging because the skin lesions are nonspecific and may resemble bacterial infection, dermatophytosis, or inflammatory dermatoses. In this case, the diagnosis was supported by the combination of compatible clinical lesions, infectious granulomatous inflammation on skin biopsy, and recovery of Scedosporium from tissue obtained from the same lesion. The use of a tissue specimen rather than a superficial swab reduced, but did not completely eliminate, concern regarding environmental contamination or colonization. Species identification was based on conventional colony morphology and microscopic fungal structures. Molecular sequencing and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry were not performed; therefore, the isolate was described more cautiously as being phenotypically identified as S. boydii. Similarly, the diagnosis of generalized tinea corporis was supported by the clinical distribution of the annular and polycyclic lesions and the mycological findings from the gluteal lesions. These findings emphasize the importance of obtaining appropriately selected specimens for histopathological and mycological examination when extensive or atypical skin lesions fail to respond to empirical treatment.

Voriconazole has substantial antifungal activity against Scedosporium species and is generally regarded as a preferred systemic treatment for scedosporiosis.^12–14 In the present case, itraconazole was initially administered empirically while the mycological results were pending. Because the lesions continued to progress and tissue culture subsequently indicated Scedosporium, treatment was changed to oral voriconazole. Formal antifungal susceptibility testing and minimum inhibitory concentration determination were not performed; therefore, the change in treatment was based on the clinical course, the culture findings, and the known susceptibility profile of Scedosporium species rather than patient-specific susceptibility results. Because the patient had fatty liver disease and suspected alcohol-related liver injury, serial liver function tests were monitored during voriconazole treatment. Serum voriconazole trough concentrations were not measured, which limited assessment of drug exposure in the setting of possible hepatic dysfunction.

The patient’s skin lesions and associated symptoms improved during hospitalization. However, systemic voriconazole, topical ketoconazole and mupirocin, antibacterial therapy, supportive treatment, wound care, nutritional support, and alcohol abstinence were implemented during overlapping periods. Consequently, the observed clinical improvement cannot be attributed solely to voriconazole or topical ketoconazole. Ozone water baths and red-light irradiation were used only as adjunctive measures for wound care and symptom relief and should not be interpreted as established treatments for eradication of S. boydii. The treatment response in this case therefore represents the outcome of a comprehensive therapeutic approach rather than evidence of the independent efficacy of any single intervention.

Several limitations should be acknowledged. First, PAS and GMS staining were not performed, and fungal elements within the tissue were not demonstrated histologically. Consequently, tissue invasion by Scedosporium could not be confirmed directly. Second, species identification relied on conventional phenotypic methods without molecular sequencing or mass spectrometric confirmation, which limits confidence in differentiation from closely related Scedosporium species. Third, formal antifungal susceptibility testing and voriconazole therapeutic drug monitoring were unavailable. Fourth, the immune evaluation was incomplete, and the contribution of chronic alcohol consumption and other metabolic abnormalities to infection susceptibility could not be determined. Fifth, the actual duration of outpatient voriconazole treatment and the long-term post-discharge outcome were unavailable, preventing assessment of complete resolution or recurrence.

Despite these limitations, this case highlights several clinically relevant points. In patients with atypical, extensive, or treatment-resistant skin lesions, especially when superficial and deeper fungal infections are suspected to coexist, early skin biopsy and fungal culture should be considered. Histopathological findings, microbiological results, clinical manifestations, and treatment response should be interpreted collectively, while the limitations of morphology-based species identification should be acknowledged. Chronic heavy alcohol consumption may represent a contributing susceptibility factor, but causal conclusions should be avoided without comprehensive immunological evaluation. Accurate diagnosis, appropriate systemic antifungal treatment, safety monitoring, supportive care, and management of underlying host-related abnormalities remain central to the clinical management of cutaneous scedosporiosis.

Funding Statement

This work was supported by the Guangxi Health Commission Scientific Research Project (No. GXHCFM2023003).

Data Sharing Statement

All data generated or analysed during this study are included in this published article. No additional data are available.

Ethics Approval

Institutional approval was required for publication of this case report and was obtained from the Research Ethics Committee of The First Affiliated Hospital of Guangxi Medical University (No. 2026-E0667). Written informed consent was obtained from the patient for publication of the case details and accompanying images. The reporting of this case followed the CARE guidelines.

Disclosure

Chengxiang Lian and Jiaguang Su report no conflict of interest.