Herpes Simplex Virus Infection in Pregnancy

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.)


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.


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.


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.


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.


1.      Gupta R, Warren T, Wald A. Genital herpes. Lancet, 2007;370(9605):2127-2137.
2.      Smith JS, Robinson NJ. Age-Specific prevalence of infection with herpes simplex virus types 2 and 1: a global view. Journal of Infectious Diseases. 2002:186(supplement 1):S3-S28.
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 Med. 1997;337(8):509-15.
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.


Pandey I, Qureshi S, Gupta AS. Herpes Simplex Virus Infection in Pregnancy. JPGO 2014 Volume 1 Number 6 Available from: http://www.jpgo.org/2014/06/herpes-simplex-virus-infection-in.html