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Deep dermatophytosis caused by Trichophyton rubrum
Melanie A Warycha MD, Marie Leger MD PhD, Julia Tzu MD, Hideko Kamino MD, Jennifer Stein MD PhD
Dermatology Online Journal 17 (10): 21

Department of Dermatology, New York University, New York, New York


A 50-year-old man with hepatitis C virus infection and liver cirrhosis, who was awaiting transplantation, was admitted to the Transplant Surgery Service for treatment of a pleural effusion and an elevated ammonia level. Skin examination showed violaceous, firm nodules on the right thigh, which had been present for eight months. A fungal culture showed Trichophyton rubrum. The patient was started on itraconazole with improvement in the eruption.


A 50-year-old man with Crohn disease, hepatitis C virus infection, portal hypertension, esophageal varices, and liver cirrhosis, who was awaiting transplantation, was admitted to the Transplant Surgery Service at Tisch Hospital for increased shortness of breath and muscle aches. A left pleural effusion, an elevated ammonia level, and leukocytosis were present. The Dermatology Service was consulted to evaluate asymptomatic nodules on the anterior aspect of the thigh, which had been present for eight months. The patient reported that the nodules would come and go although he continued to develop new lesions. Medications included furosemide, spironolactone, and rifaximin. Further review of systems disclosed fatigue.

Physical examination

Figure 1

Diffuse yellow skin and grouped, violaceous, firm nodules and plaques with scale were present of the anterior aspect of the right thigh.

Laboratory data

The white-cell count was 17.4 x 109/L, hemoglobin 12 g/dL, and platelet count 7.1 x 109/L, aspartate aminotansferase 80 U/L, alkaline phosphatase 209 U/L, and albumin 2.2 gm/dL. Ammonia level was elevated at 50 mcmol/L. A chest radiograph showed a left pleural effusion. Magnetic resonance imaging of the abdomen with and without contrast showed an interval progression of cirrhosis with portal hypertension, increased ascites, and nonocclusive thrombi in the main portal vein and right posterior branch of the portal vein.


Figure 2Figure 3

There is a hair follicle with epithelial hyperplasia and associated fibrosing granulation tissue and suppurative granulomatous inflammation. A periodic acid-Schiff-diastase stain shows septated and branching filamentous fungi and a few budding spores.


Dermatophytes are typically restricted to infection in the cornified layers of the skin, hair, and nails and penetrate no deeper than the granular layer [1]. There are rare case reports of invasion into the deep dermis, subcutaneous tissue, or internal organs. The classic presentation is Majocchi granuloma, which is characterized by a granulomatous and neutrophilic inflammation of dermal and subcutaneous tissue that is secondary to the rupture of hair follicles [2]. Although not so common, cases of dermal dermatophytosis also can arise in the absence of perifollicular involvement and foreign-body giant cells, which suggests dermatophyte invasion through other modalities [1]. Although several theories as to the pathogenesis of this condition have been generated, which include traumatic implantation, direct extension from an existing superficial dermatophyte infection in the setting of altered host immune response likely plays a role in this disease process [3]. This theory is supported by the fact that the majority of deep dermal dermatophytoses develop in immunocompromised patients, which include organ transplant recipients; those with underlying malignant conditions, such as leukemia or lymphoma; individuals with human immunodeficiency virus infection; or those on chronic immunosuppressive therapy for rheumatologic, dermatologic, or pulmonary conditions. Topical glucocorticoids also have been used prior to the diagnosis of dermatophytosis, which contributes to the invasive potential of this infection [3]. Although our patient was not immunocompromised, he did have a number of underlying medical conditions that predispose to abnormal immune function, which included Crohn disease, hepatitis C virus infection, and liver cirrhosis. A small number of cases of deep dermatophytosis in immunocompetent patients have been reported [4, 5].

Although the clinical presentation of deep dermatophytosis is variable, often it appears as fluctuant-to-firm nodules, abscesses, or ulcers on the extremities, with a few cases with lesions on the face and trunk [2, 6]. Trichophyton rubrum is the most common dermatophyte isolated in deep dermatophytosis although infection with Trichophyton mentagrophytes, Trichophyton violaceum, Microsporum canis, and Trichophyton verrucosum has been documented. An elevated IgE level and hypereosinophilia may be observed [7]. Systemic treatment with itraconazole or terbinafine is advocated although amphotericin B, griseofulvin, and ketoconazole also have been used successfully in isolated reports. Surgical excision should be considered in cases that are unresponsive to systemic therapy.


1. Hay RJ, Baran R. Deep dermatophytosis: rare infections or common, but unrecognized, complications of lymphatic spread? Curr Opin Infect Dis 2004;17:77 [PubMed]

2. Lillis JV, et al. Disseminated dermal Trichophyton rubrum infection – an expression of dermatophyte dimorphism? J Cutan Pathol 2010;37:1168 [PubMed]

3. Smith KJ, et al. Trichophyton rubrum showing deep dermal invasion directly from the epidermis in immunosuppressed patients. Br J Dermatol 2001;145:344 [PubMed]

4. Sentamilselvi G, et al. Deep dermatophytosis caused by Trichophyton rubrum – a case report. Mycopathologia 1998;142:9 [PubMed]

5. Gong JQ, et al. Deep dermatophytosis caused by Trichophyton rubrum: report of two cases. Mycoses 2007;50:102 [PubMed]

6. Sommer S, et al. Microbiological and molecular diagnosis of deep localized cutaneous infection with Trichophyton mentagrophytes. Br J Dermatol 1999;141:323 [PubMed]

7. Chastain MA, et al. Deep dermatophytosis: report of 2 cases and review of the literature. Cutis 2001;67:457 [PubMed]

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