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SUMMARY
Zosteriform Herpes simplex infection is a very rare
clinical entity. This was reported in a HIV seropositive
married woman. Here CD4 count was 313 cells/
cmm. She had multiple small localized ulcerations
in both labia majora contiguously spread to the
perineum and perianal region. Tzanck's smear test
was positive for giant epithelial cells. She was
positive for HSVI IgG and HSV2 IgM by type specific
antibody test for HSV. She responded to Acyclovir
therapy for Herpes infection. Oral candidiasis
responded to both Ketoconazole, Fluconazole
therapy. Now, she is in follow – up.
KEY WORDS
HSV - II - Zosteriform - Female Genital - HIV
Seropositive
INTRODUCTION
Zosteriform Herpes Simplex virus infection is an
uncommon presentation of HSV. In 1923 Teague
and Good Pasture observed a band like ipsilateral
lesion several days later akin to the eruption of
Shingles in rabbits1. This distinct type of cutaneous
herpes is called Zosteriform Herpes Simplex. HSV
replicates in the epithelium, gains access to axonal
terminae and is retrogradely transported to sensory
ganglia. A short period of viral replication within
infected sensory ganglia is concomitant with the
establishment of the non–productive latent infection.
HSV may reemerge from the nervous system and
cause disease within the same dermatome, at a
location distal from the initial site of infection. This
phenomenon is termed as Zosteriform spread.
Zosteriform spread usually occurs after the primary
inoculation in the skin of both outbred and inbread.
Zosteriform skin lesions result from anterograde
spread of the virus following invasion of the nervous
ZOSTERIFORM HERPES IN THE FEMALE
GENITAL OF A HIV SEROPOSITIVE
Williams Jayakumar*, Ravichandran V**, Thirunavukkarasu*, Suganya S**, Sri Ram S*
* Professor and Head of the Department of STD
** Assistant Professor of STD
*Asstistant Professor of Microbiology
**Pre Final Year M.B.B.S.Student,
*Final Year M.B.B.S. Student
Address for Correspondence :
Dr. Jeyakumar Williams, B.Sc., MD, Venereaology, MNAMS, 4/169, Immanuel Cottage, Tahsildar Nagar,
Madurai-625020
system2. This spread requires an intact nerve supply
and the virus must traverse the nervous system
during viral reactivation to cause this type. Normal
skin becomes infected via nerve endings. Viral
growth at any peripheral side may have a zosteriform
component superimposed on initial local replication.
The assumption has been suggested that the
immune mechanism were mediating their effect,
rapidly destroying infected epidermal or other
peripheral cells, and thereby inhibiting cell to cell
spread, which is a modification of the Zosteriform
component3. This effect is T cell dependent. The
reason for this apparent failure of immunity is not
clear. It could be that the transferred immune cells
are diverted to sites other than those associated with
the Zosteriform lesion, thereby diluting their
effectiveness. Alternatively, immune cells may fail
to recognize the virus as it first. These lesions used
to subside within a week. Usually this attack was
precipitated by prolonged exposure to sunlight5. This
disease cannot be diagnosed without laboratory
help. This lesion is usually misdiagnosed as zoster.
Clinicians should be aware of HSV infection in
patients with Zosteriform appearance.
Multiple, herpetiform ulcerations of labia majora and
contiguous spread to perineal and perianal regions.
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CASE REPORT
Mrs. S. aged 35 years, an urban married lady who
is a mill worker attended the STD Department,
Government Mohan Kumarmangalam Medical
College Hospital, Salem, on 17-02-2004, for the
complaints of ulcer genitalia for 15 days, pain in the
upper abdomen, cough with expectoration, fever on
and off for 3 months duration. She was referred from
the Obstetrics and Gynaecology Out-Patient
Department of the same Hosptial.
She had married twice and she demied any sexual
contact other than these two husbands. First
husband left her six years before. Now she is living
with her second husband.
She was a well built woman. On February 17, 2004,
here weight was 50 kgs. Pulse 72/mt, regular B.P.
120/80m.m. of Hg.
CVS, RS, CNS, and abdominal exammations were
normal. Oral examination showed extensive
pseudomembranous oral candidiasis over the
dorsal. ventral and lateral aspect of tongue, hard
palate, soft palate, inner aspect of cheek, fauces,
and uvula. She also had oral blisters on the lips and
tongue.
Genital examination showed multiple, tiny superficial
ulcers on both labia majora, perineum and perianal
region. Cervix appeared normal. Vaginal vault was
free. Inguinal glands were enlarged, discrete and
tender on left side. Right side inguinal glands were
just palpable.
Blood total count was 8,700 cells/cmm. Differential
count was P68, L30 and E2. ESR was 20 mm/hour.
Blood sugar, urea and serum creatnine  were  with
in normal limits. Blood VDRL was non reactive.
Blood  TPHA was negative. ELISA for HIV was
reactive. Blood TPHA was negative. ELISA for HIV
was reactive. Her CD4 count was 313 cells/cmm.
ELISA for Hepatitis -B was nonreactive. Type specific
antibody test for HSV showed HSVI lgG positive
and HSV 2 lgM positive. Dark field examination was
negative for T.P. Smear for haemophilus Ducreyi was
negative. Smear for calymato bacterium was
negative. X-ray chest PA view was normal. Sputum
for AFB was negative. Purified protein derivative for
mantoux method '0' mm. Cervical culture for
Gonococcus was negative. Vaginal culture for
trichomoniasis and candidiasis was negative.
Histopathological examination of the lesion showed
non specific inflammatory changes. Ophthalmic
screening showed both fundi were normal. There
was no evidence of retinopathy.
Mrs. S was treated with t. Acyclovir 200 mg 5 times
daily along with Tab Nimesulide. Ulcer healed
completely within 2 weeks time. For oral candidiasis,
she was treated with tablet ketoconazole 200 mg.
12th hourly for four weeks and clotrimazole oral paint
5 times daily for 6 weeks.
She had reported with the recurrence of herpes in a
month interval for two times and was treated by same
line of management. Afer 5 months, oral candidiasis
had relapsed for which she was treated with oral
fluconazole 200mg daily for 2 weeks. She responded
to the therapy.
Parallel examination of her second husband revealed
that he was a HIV positive. His blood VDRL was
non reactive. All the other investigations were normal
for the second husband. He had a bunch of genital
warts. He was treated with 10 per cent tincture
podophyllin external application.
Now she and her husband are in follow– up.
DISCUSSION
Zosteriform herpes of the genitals is a very rare
presentation of herpes simplex infection which made
us to present this case.
In HIV infected patients, lesions typically start as
small, localized ulcerations and can spread
contiguously to cover large areas of perineum and
buttocks. This Zosteriform appearance of HSV can
occur in persons with high CD4 cell counts6. Our
patient was also a known HIV seropositive with the
CD4 counts of 313 cells/cmm. She had also showed
small, localized multiple ulcerations contiguously
spread to the perineum and perianal simulated the
literature. In this case, herpetic ulcers around the
perineum and perianal region may be taken as
Zosteriform herpes.
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Giant epithelial cells were demonstrated from the
tiny, superficial ulcers of the labia majora by Giemsa
smear test. They also showed negative results to
Treponema pallidum. Haemophilus Ducreyi and
Calymato bacterium. The presence of giant
epithelial cells in TZANCK's smear test evidenced
for Herpes.
Type specific lgG and lgM antibody test for HSV 1
and HSV 2 showed that she was positive for HSV 1
lgG antibody and HSV 2 lgM antibody. It clearly
indicated the evidence for Herpes simplex virus
infection.
At any time in the course of HSV/HIV/AIDS patients
are at high risk of developing a debilitating herpetic
infection and there is a possibility of transmitting
both HSV and HIV to health care perosnals who
handle these type of patients.
ACKNOWLEDGEMENT
1. Our thanks are due to the Dean, Government
Mohan Kumaramangalam Medical College
Hospital for giving permission to publish this
case report.
2. Our thanks are due to Medical Officers and
paramedical workers of Microbiology
Department for providing us ELISA results.
3. Our thanks are due to the Pathologist,
Government Mohan Kumaramangalam Medical
College, Salem for the HPE results.
4. Our thanks are due to the patient who was co-
operative for this study.
REFERENCES
1. Teague O. Goodpasteur F.W. Experimental herpes
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2. Summers BC, Mavgetis T.P., Lerb DA. Herpes
simplex virus Type 1 corneal infection results in
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of Virology 2001, PP. 5069-5075.
3. Simmons A, Nash AA, Zosteriform spread of
Herpes simplex virus as a model of recrudescence
and itruse to investigate the role of Immune cells
in prevention of recurrent disease, J. viral, 1984,
53 frownface 3 : 816-821.
4. Spruance SL, overall Jr., Kern ER, Kreuger GC,
Plain V Miller W. The natural history of recurrent
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5. Inamador CA, Yatgiri RV, Recurrent Zosteriform
Herpes simplex 1992, Vol-58, Issue 5, PP 289-291.
6. Schacker T, Corey L, Herpes virus infections in
human Immunodeficiency Virus-infected persons.
In De Vita VT Jr, Hellman S, Rosanberg SA; eds,
AIDS, Etiology, Diagnosis, Treatment and
Prevention Lippincott-Raven Publishers, 4th
edition, chapter 14.5, PP 267-280.
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