The patient was a 34-year old, asymptomatic Zimbabwe-born woman with a positive HIV IgG ELISA on immigration screening in 2002. There was no prior history of sexually transmitted infections, genital or perianal ulceration, and syphilis serology was negative. Her absolute CD4+ T cell count at diagnosis was 156/mm3, with an HIV-1 RNA plasma viral load of more than 100 000 copies/mL. Antiretroviral therapy was initiated one month later, in October 2002, with combivir one tablet twice daily and nevirapine 200 mg twice daily, together with trimethoprim/sulfamethoxazole as primary prophylaxis against P. jiroveci pneumonia. By January 2003, her CD4+ T cell count had increased to almost 500/mm3, and her HIV viral load remained persistently undetectable after March 2003, at which point trimethoprim/sulfamethoxazole was discontinued. In April 2003, she noted multiple painful papules on the left labia, with subsequent superficial ulceration. She had no reported sexual contacts for over a year. Her family physician prescribed empiric therapy with acyclovir 400 mg three times daily and keflex 500 mg three times daily, followed by oral valacyclovir 500 mg twice daily.
In July 2003, nine months after starting HAART, the shallow ulcerations had resolved but a pruritic 1 x 3 cm granulomatous lesion developed on the left labia. This was associated with surrounding tissue edema, and shotty left inguinal lymphadenopathy, and progressed over the subsequent two months (Figure 1(a)). There was no response to azithromycin 1 gram weekly for 4 weeks, as empiric therapy for granuloma inguinale. Both a superficial swab and a punch biopsy of the hypertrophic lesion demonstrated HSV-2, with glassy nuclear chromatin, multinucleation and surrounding severe acute and chronic inflammation (Figure 1(b)). Topical therapy was initiated with trifluridine, together with oral valacyclovir 1 gram twice daily. There was no clinical response, although valacyclovir discontinuation was followed by an outbreak of painful, scattered shallow ulcerations that were culture positive for HSV-2. From November 2003 and December 2005 she was treated with 4 one-month courses of intravenous foscarnet; despite a near total clinical response to the first course, the response waned progressively and the fourth course was complicated by Staphylococcus aureus cellulitis at the line site. Lesion cultures were repeatedly positive for HSV-2, and a repeat labial biopsy in February 2006 showed only chronic granulation tissue. There was no response to a trial of topical protopic (tacrolimus) in August 2006.
In September 2006 there was a prompt clinical response to topical imiquimod 5%, applied 3 times weekly, with resolution of the lesion within eight weeks. She remains asymptomatic on oral valacyclovir 1 gram twice daily combined with topical imiquimod 5% as needed (approximately one topical application every two weeks) with minor residual labial scarring.