Notes from the Field: Trichophyton mentagrophytes Genotype VII — New York City, April–July 2024

Investigation and Outcomes

During April–July 2024, four additional patients received a clinical diagnosis of tinea. Samples were collected for fungal culture; following growth, TMVII was identified using Sanger sequencing of the internal transcribed spacer region of the ribosomal gene. Antifungal susceptibility testing was performed using previously described methods (3). For each patient’s isolate, the minimum inhibitory concentrations of terbinafine and itraconazole were 0.0039 mg/mL and <0.03 mg/mL, respectively, suggesting susceptibility to these drugs. Patients were treated for presumed TMVII infection before laboratory confirmation and antifungal susceptibility results were available. Data on demographic characteristics, potential exposures, clinical course, and current infection status were obtained as part of clinical care. This activity was reviewed by CDC, deemed not research, and was conducted consistent with applicable federal law and CDC policy.^§

All four patients were cisgender men aged 30–39 years who reported recent sexual contact with other men. Patients A and D reported sexual contact with each other; patients B and C had no known epidemiologic link to anyone with known TMVII infection. Patient D was a sex worker. Patient B reported travel to Europe; the other patients reported no recent international travel history. Each patient was screened for other concomitant sexually transmitted infections and received negative test results.

Patient A had no underlying medical conditions and was taking HIV preexposure prophylaxis. He was initially evaluated for a rash on his buttocks. He completed 2 weeks of topical clotrimazole followed by 1 week of topical terbinafine with no improvement. He then was prescribed oral terbinafine (250 mg daily) for a planned 2–4-week course. At last follow-up, the rash was improving.

Patient B had HIV infection and had inconsistent adherence to antiretroviral therapy. He was initially evaluated for a pruritic rash on the corner of his mouth. He completed 1 week of topical clotrimazole with complete resolution of his rash.

Patient C had HIV infection that was well-controlled on antiretroviral medication. He was initially evaluated for a rash on his knee, buttocks, and groin and was prescribed oral terbinafine (250 mg daily) with a planned 4-week course. The rash was improving at last follow-up.

Patient D was taking HIV preexposure prophylaxis and dabrafenib/trametinib for a history of cancer. He was initially evaluated for a pruritic rash on his knee, trunk, arm, and penile shaft (Figure). He completed <1 week of oral terbinafine (250 mg daily) and was switched to itraconazole (200 mg twice daily), topical luliconazole, and topical ketoconazole. The rash was improving at last follow-up.

Preliminary Conclusions and Actions

Health care providers should be aware that TMVII can spread through sexual contact and cause lesions on the genitals, buttocks, face, trunk, or extremities.^¶,** Point-of-care testing with direct microscopy can help confirm tinea (4); however, TMVII identification requires fungal culture and DNA sequencing. Clinicians should initiate empiric therapy based on epidemiologic and clinical features, especially given the insensitivity of fungal cultures (5) and that confirmation of TMVII infection might take weeks. Current evidence suggests that oral terbinafine (250 mg daily) is an effective first-line option for TMVII infections. Some patients have also been successfully treated with itraconazole with adjuvant topical antifungal therapy. Patients might require oral antifungal therapy for up to 3 months and should take the treatment until lesions have fully resolved (1,3). Some patients might respond to topical antifungals alone, but these are not recommended as monotherapy for tinea involving hair follicles (4).

Health care providers should advise patients with TMVII infection about the importance of avoiding skin-to-skin contact with affected areas and not sharing personal items until symptom resolution. Topical corticosteroid products, including combination antifungal-corticosteroid products, can worsen tinea infection and should be avoided in treating TMVII and other dermatophyte infections (4). Public health surveillance, health care provider and patient education and awareness, and increased access to dermatophyte identification and antifungal susceptibility testing could help detect, monitor, and prevent the spread of TMVII.