Herpse simplex virus 2_1111DermDx
Herpes simlex virus 2_1111DermDx_2
A 23-year-old female presents to the ED with a 6-month history of exquisitely painful genital ulcers. The patient reports that she initially developed a small white pustule that broke and then formed ulcers around her labia minora. She continued to have multiple ulcers around her genital region that would heal and reappear. During the past month the ulcerations became quite extensive and involved her vulva, inguinal folds, thighs, perianal skin and buttocks. According to the patient, she has seen multiple doctors who had treated her for syphilis with intramuscular penicillin, but did not see clinical improvement. One month prior to presentation, the patient was diagnosed with HIV/AIDS. On physical exam the patient is afebrile and has extensive polycyclic ulcerations in her vulva, which extended to her buttocks and thighs. The patient’s CD-4 T-cell count is 16. Rapid plasma reagin and Treponema pallidum antibodies test results are negative. Both chlamydia and gonorrhea urine polymerase chain reaction (PCR) assays are negative. She is not currently taking any medication. What’s your diagnosis?Submit your answer, and then read the full explanation below. If you like this activity or have a suggestion, tell us about it in the comment box at the bottom of the page.
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Genital herpes is one of the most common STDs and the main cause of genital ulceration in the United States and most regions of the world. Genital herpes is mainly due to herpes simplex virus 2 (HSV-2), with a small percentage of cases due to herpes simplex virus 1 (HSV-1).
In developed countries, the percentage of the population estimated to have been exposed to HSV-2 is between 15% and 25%. However HSV-2 infection is significantly more prevalent in patients with HIV, with infection rates ranging from 50% to 90%.1
Genital herpes is transmitted through sexual contact. Patients can contract HSV either through contact with an active herpes lesion, or from infected secretions from an individual without a clinically apparent HSV infection.
The impaired mucosal barrier that occurs during an active genital herpes outbreak also facilitates HIV viral transmission. After the initial HSV infection, the virus remains in a latent state in the dorsal root ganglia of the sacral sensory nerves and can become reactivated during periods of physiological stress or immunosuppression.
The initial infection is frequently asymptomatic, but may be accompanied by a prodromal period with painful or burning sensations followed by subsequent vesicle eruptions, which progress to painful erosions and ulcerations.
In immunocompetent patients, recurrences are usually of shorter duration and less intense than the initial infection. However, patients with HIV/AIDS, such as our patient, who have a very low CD-4 T-cell count, genital herpes recurrences are more frequent, chronic and severe. 1,2
Genital herpes can frequently be suspected with history and physical exam. Diagnostic tests include scrapings of the ulcer edge for direct fluorescent antibody (DFA) assay, Tzanck smear, viral culture and HSV PCR. Additionally, a skin punch or shave biopsy can be used to diagnose herpes infection.
In the case presented above, diagnosis was established by punch biopsy. Given the high seroprevalence of HSV in the general population and in those with HIV, blood tests are generally not helpful in establishing a diagnosis.1,2
Treating patients with HIV and genital herpes is similar to treating patients without HIV, except that longer treatment duration may be necessary.
Therapeutic options for active infections in patients with HIV include:
- Acyclovir (Zovirax, GlaxoSmithKline): 400 mg po 3x/d; 200 mg PO po 5x/day; or 5-10 mg/kg iv q8 h × 7-14 days
- Famciclovir (Famvir, Novartis): 500 mg po bid
- Valacyclovir (Valtrex, GlaxoSmithKline): 1 g po bid
In HIV patients, it is generally recommended that treatment continue until all mucocutaneous lesions are healed. For patients with HSV resistant to acyclovir (in which case the virus is also resistant to famiciclovir and valacyclovir), IV foscarnet, or topical or IV cidofovir are options.
For chronic suppression to prevent recurrences in patients with HIV, proposed regimens include acyclovir: 400 to 800 mg po bid-tid; famciclovir: 500 mg po bid; and valacyclovir: 500 mg po bid.1,2
Adam Rees, MD, is a graduate of the UCLA School of Medicine and a resident in the Department of Dermatology at Baylor College of Medicine.
1. Martin J. “Update on the Treatment of Genital Herpes.” Actas Dermo-Sifiliográficas (English Edition) 100.1. 2009: 22-32.
2. Bolognia J, Jorizzo JL, Rapini RP. Dermatology. 2nd Ed. Elsevier; 2008: Chapters 77, 79.