[Downloadedfreefromhttp://www.ijstd.orgonMonday,May02,2011,IP:164.100.1.

206]||ClickheretodownloadfreeAndroidapplicationfort

Case Report

Chronic genital herpes

Kishan Kumar Agarwal, Devinder Mohan Thappa
Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER),
Pondicherry, India

Correspondence:
Dr. Devinder Mohan Thappa, Department of Dermatology and STD, JIPMER, Pondicherry - 605 006, India.
E-mail: dmthappa@gmail.com

Abstract
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.

Key words: Chronic herpes genitalis, HIV infection

INTRODUCTION persons may require increased doses of antiviral

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
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
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

How to cite this article:

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

Indian J Sex Transm Dis 2007; Vol. 28, No. 2 97

 [Downloadedfreefromhttp://www.ijstd.orgonMonday,May02,2011,IP:164.100.1.206]||ClickheretodownloadfreeAndroidapplicationfort
Agarwal and Thappa: Chronic genital herpes
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. Grams
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
Figure 1: Multiple superficial ulcerations of herpes genitalis involving
external genitalia
98
healed after 10 days [Figure 2] and patient was
discharged on ATT and antiretroviral therapy.
DISCUSSION
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 patients 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
Figure 2: Healing of the genital herpes with hypopigmentation
Indian J Sex Transm Dis 2007; Vol. 28, No. 2
 [Downloadedfreefromhttp://www.ijstd.orgonMonday,May02,2011,IP:164.100.1.206]||ClickheretodownloadfreeAndroidapplicationfort
Agarwal and Thappa: Chronic genital herpes

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
1. Centers for Disease Control and Prevention. 1998 guidelines for the
treatment of sexually transmitted diseases. MMWR Recomm Rep
1998;47:1-111.
2. Schomogyi M, Wald A, Corey L. Herpes simplex virus-2 infection:
An emerging disease? Infect Dis Clin North Am 1998;12:47-61.
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.
4. Ball SC. Persistent herpes simplex virus infection. AIDS Read
2001;11:249-51.
5. Maier J, Bergman A, Ross M. Acquired immunodeficiency syndrome
manifested by chronic primary genital herpes. Am J Obstet Gynecol
1986;155:756-8.
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.
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.
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.
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.
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.
Source of Support: Nil, Conflict of Interest: None declared.

Author Help: Sending a revised article

1) Include the referees remarks and point to point clarification to those remarks at the beginning in the revised article file itself. In addition, mark
the changes as underlined or coloured text in the article. Please include in a single file
a. referees comments
b. point to point clarifications on the comments
c. revised article with text highlighting the changes done
2) Include the original comments of the reviewers/editor with point to point reply at the beginning of the article in the Article File. To ensure that
the reviewer can assess the revised paper in timely fashion, please reply to the comments of the referees/editors in the following manner.
There is no data on follow-up of these patients.
Authors Reply: The follow up of patients have been included in the results section [Page 3, para 2]
Authors should highlight the relation of complication to duration of diabetes.
Authors Reply: The complications as seen in our study group has been included in the results section [Page 4, Table]

Indian J Sex Transm Dis 2007; Vol. 28, No. 2 99