Author Information
Pandey
Indu*, Qureshi Shabnam**, Gupta
AS
(*First
Year Resident, ** Assistant Professor, *** Professor. Department
of Obstetrics and Gynecology, Seth GS Medical College and KEM
Hospital , Mumbai , India
Abstract
Herpes
simplex infection is the most common sexually transmitted infection of
reproductive age group. It is an important cause of intra-uterine fetal and
neonatal infection. We present a case of HSV-2 infection in second trimester of
pregnancy in which the patient developed an IUFD at 26 weeks of gestation.
Introduction
Herpes
simplex virus (HSV) is a DNA virus. Infection is transmitted through mucosal
membranes and grazed skin. It reaches the nerve tissues and rests there in a
dormant state. HSV-1 and HSV-2 are the two subtypes infecting orofacial and
genital area respectively. However crossover infection can happen with both the
subtypes.[1] Genital herpes infection can be primary, non primary,
recurrent or asymptomatic.[1] In our case, patient was infected but
was asymptomatic.
Case
report
A 23 years
old primigravida 26 weeks of gestation was referred from a private hospital in
view of intrauterine fetal death. She had no complaints. She had a
ultrasonography (USG) report at 14 weeks showing a thickened placenta of 4-5
cm in size, liquor pocket of 2-3 cm,
nuchal translucency (NT) of 1.2mm (corresponding to13.5weeks). Patient was
tested for TORCH infection. HSV 2 IgM antibody was detected. She was treated
with tablet Acyclovir in the dose of 200mg 3 times a day for 21 days .After one
month she had a repeat USG at 18 weeks of gestation. It showed placental
thickness of 5-6cm.There were no congenital anomalies seen, fetal biometry was
suggestive of symmetrical intrauterine growth retardation. Patient received
Injection Alamine intravenously thrice a week for three weeks till 5 months of
gestation. The repeat U SG done at 26 weeks showed intrauterine fetal death of
19-20 weeks of gestation, Spalding sign was also seen. There was no history of
fever, of multiple sexual partners, any vaginal discharge or history of rashes
around the genitalia. On examination there was no active lesion or healed
lesion seen on the body. Her vital parameters were stable. Abdominally the
uterus was 20 weeks in size. On speculum examination, there were no genital
lesion seen, cervix and vagina were healthy. On vaginal examination, Os was
closed, uneffaced. Her husband, a textile mill worker was asymptomatic. He had
no history of lesions on his genitalia, or fever or multiple sexual partners.
Her hemogram, DIC profile, urine examination were within normal limits. Consent
to induce labor was obtained. Single dose of 200 micrograms of misoprostol
tablet was administered vaginally. A macerated male abortus of 300 grams and
thickened placenta of 150 grams were expelled spontaneously and completely.
Figure 1.
It shows the large placenta with its fetal surface. M is the fetal membranes.
Arrow indicates the umbilical cord.
Figure 2.
It shows the maternal surface of the thickened placenta and the unhealthy
cotyledons. C is the cotyledon. Arrow indicates the umbilical cord.
Pathological
of the placenta and the umblical cord showed grossly the surface to be
congested with yellowish brown discoloration at places. Cotyledons were
distorted and could not be identified. On cut section the cotyledons appeared
congested and autolytic. On microscopy placenta showed normal villi with sheets
of trophoblastic cells, fibrinoid necrosis, hemorrhage, and presence of
lymphocytes, myeloid precurssor cells with hneutrophils. No evidence of
vilitis. Featrues suggestive of maternal sepsis.
Discussion
Prevalence
of HSV infection increases with age. Factors that facilitate risk of infection
are related to number of sexual partners. HSV has a greater propensity for the
female gender.[2,3] Perinatal
transmission of HSV infection can occur at three periods. One as a vertical
transmission transplacentally or as an ascending infection from the cervix in
the intrauterine period, during labor from the infected birth canal or after
birth due to breast feeding or if the neonate comes in contact with the
infected lesions of the parent. Risk of neonatal infection is in the range of
30%-50%, when HSV infection is acquired in the last trimester, whereas risk is
only 1% when it is acquired in early pregnancy. Late in pregnancy the body does
not have adequate time to develop antibodies against HSV. Viral load increases
as the replication cannot be stopped prior to onset of labor. Affect of genital
herpes on pregnancy is spontaneous abortion, intrauterine growth retardation,
preterm labor and congenital herpes infection [4,5]. Congenital
herpes is a catastrophic infection that affects the CNS in 50% of neonates. Our
patient had no risk factors for HSV-2 infection; she did not have any active
lesion. Yet, she had an acute HSV-2 infection which infected the fetus gravely
resulting in intrauterine fetal death. In our case obviously the infection was
intrauterine in origin most likely transplacental as seen by the thickened
placental membranes, cotyledons and the thickened cord and increased placental
weight. Placenta weighed half that of the fetus. It is most likely that our
patient had a primary type of the HSV infection as the incidence of vertical
transmissions from primary infection is to the tune of 40 to 50 % against 5 %
in the recurrent HSV infections.[6] In primary infections there is
increased maternal viral load and hence greater transplacental transfer of the
virus and severe infection to the fetus in utero leading to its demise as seen
in our patient.
Conclusion:
Primary
Herpes Simplex Virus infection during pregnancy leads to grave intrauterine
consequences for the fetus. Hence it is important to educate about sexually
transmitted diseases and identify pregnant women at risk to prevent the
vertical transmission or congenital herpes infection.
References
1.
Gupta R, Warren T, Wald A. Genital herpes.
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2.
Smith JS, Robinson NJ. Age-Specific prevalence
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3.
Suligoi B, Cusan M , Santopadre P , Palu G ,
Catania S , Girelli G , Pala S , and
Vullo V; HSV-2 specific seroprevalence among various populations in
Rome, Italy. Sex Transm Infect 2000;76:213-214.
4. Arvaja M,
Lehtinen M, Koskela P, Lappalainen M, Paavonen J, Vesikri T. Serological
evaluation of herpes simplex virus type 1 and type 2 infections in pregnancy. Sexully Transmitted Infections , 1999:75(3):168-171.
5. Brown ZA, Selke S, Zeh J, Kopelman J, Maslow A, Ashley
RL, et al.The acquisition of herpes simplex virus during pregnancy. N Engl J
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6.
Katharine H Barefoot AB, George A Little MD and
Kim T Ornvold MD. Fetal Demise Due to Herpes Simplex Virus: An Illustrated Case
Report. J. Perinatol 2002;22:86-88.
Citation
Pandey I,
Qureshi S, Gupta AS.