Tinea corporis in Adult
A severe antifungal-resistant tinea has emerged in South Asia from the rapid spread of a novel dermatophyte species: Trichophyton indotineae. Terbinafine-resistant T indotineae infections have been reported in Asia, Europe, Canada, and the United States, including one case in New York City with no history of recent international travel.
Tinea corporis usually appears as annular, erythematous, scaling plaques. Fungal organisms are transmitted to humans by direct contact (with animals or with humans, such as in tinea corporis gladiatorum, common in wrestlers), or through fomites. Tinea corporis is more prevalent in warm, humid climates and may also result from the spread of infection from other body sites.
Tinea corporis may be itchy, especially in the case of Trichophyton rubrum infections, in which case, secondary lichenification from scratching may obscure its annular configuration. It may also be minimally pruritic or asymptomatic. It may be a superficial infection or it may affect follicular structures. When tinea infects the follicle, the condition may appear as a fungal folliculitis, or it may appear otherwise more deeply situated. Follicular infection is known as Majocchi granuloma.
When a dermatophyte infection occurs in the scalp, it is known as tinea capitis. When on the face, it is known as tinea faciei; in the beard area, it is known as tinea barbae; in the inguinal folds, it is known as tinea cruris; on the feet, it is known as tinea pedis; and when it involves the hands (primarily the palms), it is known as tinea manuum.
Tinea imbricata is a distinct form of tinea corporis caused by Trichophyton concentricum, which is prevalent in tropical locales such as Central and South America, the South Pacific, and Southeast Asia.
Severe tinea capitis and corporis, Majocchi-like granulomas, deep ulcerated fungal infections, and fungal nail involvement occur in an inherited deficiency of CARD9 (caspase recruitment domain-containing protein 9), an inflammatory cascade-associated protein. The disorder is autosomal recessive and is most common in North African countries including Algeria, Morocco, and Tunisia. Infections usually begin in childhood and are caused by T rubrum and Trichophyton violaceum. Lymphadenopathy, high IgE antibody levels, and eosinophilia are common. The disorder may be fatal.
In the immunocompromised patient, infection can be quite similar to that in immunocompetent patients, with superficial scaly plaques, pruritus, and lesions displaying the classic annular, advancing, scaling border. However, infections without pruritus or classic features are seen. Disseminated tinea corporis may be seen in patients with immunosuppression, diabetes, Cushing syndrome, malignancy, and old age. Dermatophyte infections are frequently seen in untreated AIDS and solid organ transplant patients. Renal transplant patients are at even higher risk for tinea corporis.
Tinea indecisiva (tinea pseudoimbricata) is tinea corporis that mimics tinea imbricata. These cases are not caused by Trichophyton concentricum but rather by other Trichophyton or Microsporum species. There is usually underlying immunosuppression in patients with tinea indecisiva.
B35.4 – Tinea corporis
84849002 – Tinea corporis
Differential Diagnosis & Pitfalls
- (round, scaly plaques)
- (ring-like lesions but nonscaly)
- (round patches but nonscaly)
- (usually trunk and neck)
- (in body folds)
- (the distribution of lesions is often a helpful clue in distinguishing this entity)
- (if an adult patient has persistent "eczema" that is not adequately responding to therapy, this entity should be ruled out with skin biopsies)
- (necrolytic migratory erythema)