Indian J Sex Transm Dis Indian J Sex Transm Dis
Official Publication of the Indian Association for the Study of Sexually Transmitted Diseases
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Year : 2007  |  Volume : 28  |  Issue : 2  |  Page : 97-99

Chronic genital herpes

Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry, India

Correspondence Address:
Devinder Mohan Thappa
Department of Dermatology and STD, JIPMER, Pondicherry - 605 006
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0253-7184.39014

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A 30-year-old, previously healthy, nulliparous married woman presented with painful genital ulceration of 1 month duration. She was admitted with a diagnosis of chronic genital herpes with oral thrush and pulmonary tuberculosis. ELISA test for antibodies against HIV was positive for both the partners. She was treated in isolation ward with four-drug regimen of antituberculous therapy (ATT), oral cloxacillin oral fluconazole and acyclovir 400 mg three times daily. The genital lesions completely resolved after treatment with acyclovir.

Keywords: Chronic herpes genitalis, HIV infection

How to cite this article:
Agarwal KK, Thappa DM. Chronic genital herpes. Indian J Sex Transm Dis 2007;28:97-9

How to cite this URL:
Agarwal KK, Thappa DM. Chronic genital herpes. Indian J Sex Transm Dis [serial online] 2007 [cited 2022 Sep 28];28:97-9. Available from:

   Introduction Top

Genital herpes is the most common cause of genital ulceration worldwide and its association with human immunodeficiency virus (HIV) was noted as early as 1981. While approximately 90% of recurrent genital herpes is caused by herpes simplex virus (HSV)-2, an increasing number of primary cases, up to 30%, are suspected to be caused by HSV-1. [1],[2] Genital herpes typically presents as erythematous papules that progress to vesicles that ulcerate and then heal over a period of approximately 1 week. Primary infection tends to cause most severe symptoms and recurrences are less painful and of a shorter duration than the primary infection. Genital herpes is a potential portal of entry of HIV. In HSV-infected HIV-seropositive individuals, genital lesions may not only be the source of transmission of HSV, but may also be a focus of shedding of HIV due to the infected CD4 cells infiltrating the herpetic lesions. [3]

Clinical presentations are frequently severe and atypical. The HSV-2 infection is common in HIV-1 infected subjects and generally causes classical vesicular herpetic genital lesions [2] with several recurrent episodes, sometimes severe and associated with extensive genital ulcerations and prolonged viral shedding. [4] Bacterial or fungal super infections may occur. Treatment of HSV infection in HIV-seropositive persons may require increased doses of antiviral medications. [3] In the treatment of refractory patients, susceptibility testing is warranted. Additionally, suppressive therapy for HSV appears to improve significantly survival in HIV-positive patients. [3] We herewith report a case of chronic genital herpes which subsequently was found to have HIV infection and responded well to acyclovir therapy.

   Case Report Top

A 30-year-old, previously healthy, nulliparous married woman presented with painful genital ulceration of 1 month duration. Initially, she developed a painful labial vesicle, which ulcerated over the next few days. Similar lesions appeared in the ensuing weeks. Three weeks after the initial lesion, she developed extensive ulcerations over the external genitalia. She also complained of fever and night sweat of 1-month duration and had recently lost 2 to 3 kg of weight. She also had burning sensation in the oral cavity. She denied previous episodes of herpes infection or other sexually transmitted disease and had no history of blood transfusion and premarital or extramarital sexual contact. Her husband had history of multiple heterosexual extramarital contacts, but denied having similar genital lesions.

Physical examination revealed pallor and generalised lymphadenopathy. Lungs had scattered basilar rales. Cheesy white deposits were present in the oral cavity. Numerous 0.5 to 3 cm confluent ulcerations were present throughout the external genitalia [Figure - 1]. They were shallow with an erythematous base, exquisitely tender and covered with purulent exudate. Regional inguinal lymphadenopathy was tender. Her cutaneous examination was otherwise unremarkable.

The patient was admitted with a diagnosis of chronic genital herpes with oral thrush and pulmonary tuberculosis. Her haemogram revealed white blood cell count of 3900/cmm with 72% neutrophils, 22% lymphocytes and 6% eosinophils. Erythrocyte sedimentation rate was 64 at first hour. Chest X-ray revealed non-homogenous opacities in bilateral lower lobes of lungs. Scraping from oral cavity for KOH examination was positive for candida. Gram's stain from genital lesion showed plenty of pus cells with Gram-positive cocci and culture grew staphylococcus aureus. Tzanck smear was negative for multinucleated giant cells. Mantoux test was negative. ELISA test for antibodies against HIV was positive for both the partners. VDRL test was non-reactive.

The patient was treated in isolation ward with four-drug regimen of antituberculous therapy (ATT), oral cloxacillin oral fluconazole and acyclovir 400 mg three times daily. Oral and genital hygiene was maintained. Over 5 days, the patient had a moderate improvement, the exudates cleared and the lesions began to epithelialise. Acyclovir was continued for another 5 days. Fever and burning sensation in oral cavity also improved. The genital lesions completely healed after 10 days [Figure - 2] and patient was discharged on ATT and antiretroviral therapy.

   Discussion Top

Patients with acquired immunodeficiency syndrome (AIDS), lymphoma, leukaemia or organ transplants exemplify immunocompromised persons who may experience an excessive number and size of lesions in both primary and reactivated HSV infections as compared with immunocompetent patients. [5] The vesicles and ulcers are more necrotic, painful and heal slowly because of an ineffective cell-mediated immune response compared with immunologically normal hosts. [1],[3] As CD4 cell count drops and immunosuppression worsens, recurrent outbreaks increase in frequency and severity until there is no period of complete healing between outbreaks. Non-healing ulcers of the anogenital region in immunocompromised patients should elicit a high index of suspicion of chronic herpes simplex infection. Chronic HSV ulcers of more than 1 month duration are an AIDS defining illness in HIV-infected patients. [1] Atypical HSV presentations occur relatively often in HIV patients. In particular, severe lesions have been reported on patient's lower back, buttocks or perianal region and these lesions may expand to 20 cm in diameter. [1],[3] Such ulcers commonly become impetiginised and require intensive long-term therapy. Tong and Mutasim [6] reported a case that described HSV-2 presenting as hyperkeratotic verrucous lesions resembling condyloma in severely immunocompromised patient.

Mole et al. documented increased plasma HIV viral load in HIV patients experiencing an outbreak of HSV. [7] By reducing or attenuating the occurrences of HSV outbreaks, acyclovir therapy may help reduce the deleterious effects of these infections. Studies suggest that chronic suppressive acyclovir therapy prolongs survival in AIDS patients with extensive HSV infections. [8]

Herpes simplex virus should be considered in the differential diagnosis of chronic genital ulcer in HIV-seropositive persons. When in doubt or whenever a non-healing ulcer has been present for more than 4-6 weeks, investigation should be carried out with a biopsy and herpes culture. A Tzanck preparation offers less sensitivity. Nucleic acid amplification detection techniques, such as polymerase chain reaction, may enhance sensitivity of HSV detection in the future. A chronic HSV ulcer of more than 1-month duration is an AIDS defining illness in HIV-infected patients. [9],[10]

   References Top

1.Centers for Disease Control and Prevention. 1998 guidelines for the treatment of sexually transmitted diseases. MMWR Recomm Rep 1998;47:1-111.  Back to cited text no. 1    
2.Schomogyi M, Wald A, Corey L. Herpes simplex virus-2 infection: An emerging disease? Infect Dis Clin North Am 1998;12:47-61.  Back to cited text no. 2  [PUBMED]  
3.Czelusta A, Yen-Moore A, Vander Straten M, Carrasco D, Tyring SK. An overview of sexually transmitted diseases (STDs) Part III: STDs in human immunodeficiency virus-infected patients. J Am Acad Dermatol 2000;43:409-32.  Back to cited text no. 3    
4.Ball SC. Persistent herpes simplex virus infection. AIDS Read 2001;11:249-51.  Back to cited text no. 4  [PUBMED]  
5.Maier J, Bergman A, Ross M. Acquired immunodeficiency syndrome manifested by chronic primary genital herpes. Am J Obstet Gynecol 1986;155:756-8.  Back to cited text no. 5    
6.Tong P, Mutasim D. Herpes simplex virus infection masquerading as condyloma acuminata in a patient with HIV disease. Br J Dermatol 1996;134:797-800.  Back to cited text no. 6    
7.Mole L, Ripich S, Margolis D, Holodniy M. The impact of active herpes simplex virus infection on human immunodeficiency virus load. J Infect Dis 1997;176:766-70.  Back to cited text no. 7  [PUBMED]  
8.Stein DS, Graham NM, Park LP, Hoover DR, Phair JP, Detels R, et al . The effect of the interaction of acyclovir with zidovudine on progression to AIDS and survival: Analysis of data in the Multicenter AIDS Cohort Study. Ann Intern Med 1994;121:100-8.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Centers for Disease Control. 1993 revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. MMWR Recomm Rep 1992;41:1-19.  Back to cited text no. 9    
10.Tayal SC, Pattman RS, McLelland J, Sviland L, Snow MH. An indolent penile herpetic ulcer in a patient with previously undiagnosed human immunodeficiency virus infection. Br J Dermatol 1998;138:334-6.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]


  [Figure - 1], [Figure - 2]


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