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Perinatal/Neonatal Case Presentation Perinatal/Neonatal Case Presentation &&&&&&&&&&&&&& Severe Intrauterine Herpes Simplex Disease with Placentitis in a Newborn of a Mother with Recurrent Genital Infection at Delivery Archana Chatterjee, MD, PhD We present a case of fatal neonatal HSV-2 infection in a Stephen A. Chartrand, MD premature infant delivered by cesarean section to a mother who at Christopher J. Harrison, MD delivery had recurrent HSV-2 infection, based on history and Anna Felty-Duckworth, MD maternal antibody titers. It was clinically evident at birth, and Chhanda Bewtra, MD subsequently confirmed by laboratory studies, that the infant was infected before delivery, likely from the previous maternal episode during pregnancy. This case illustrates an uncommonly documented, We present a case of fatal herpes simplex type 2 (HSV-2) in a premature but known complication in a mother with primary disease during infant born to a mother diagnosed with recurrent HSV-2, based on history pregnancy and recurrent genital herpes at delivery — intrauterine and HSV serology results. It was clinically evident at delivery, and transmission to the fetus. subsequently confirmed by laboratory studies that the infant was infected before delivery. There was histopathologic evidence of placentitis and CASE REPORT chorioamnionitis upon examination of the placenta and fetal membranes. This case illustrates a relatively uncommon complication of recurrent A 27-weeks’ gestation male was delivered by caesarean section due to genital herpes at delivery — intrauterine transmission to the fetus from a failed tocolysis and deteriorating biophysical profile. Twelve hours primary episode during pregnancy. before delivery, the mother developed active genital herpes simplex Journal of Perinatology 2001; 21:559 – 564. lesions over her labia. The obstetrician reported that her membranes were intact at the time of delivery. The mother had labial lesions 2 months prior (her first known clinical infection), which were culture positive for HSV-2. At that time, a diagnosis of primary INTRODUCTION genital herpes infection was made by the obstetrician, based on an HSV-2 IgM of 3.5 EIA units (normal <0.9) and HSV-2 IgG of 0.9 The most serious complication of maternal genital herpes simplex EIA units (normal 0.9, Specialty Laboratories, Los Angeles, CA). She virus (HSV) infection is neonatal HSV disease, which occurs due to did not receive antiviral therapy during her primary infection. She either ascending infection or, more commonly, by delivery through was also noted to have genital condylomata at about 15 weeks’ an infected birth canal.1,2 The estimated incidence of neonatal HSV gestation. infection is approximately one case in 2000 to 5000 deliveries per At the time of delivery the infant was noted to have multiple year.3 Thus, each year, 1500 to 2000 cases of neonatal herpes vesiculobullous lesions over the entire body (Figure 1A–C). His infection occur in the United States.4 The outcome of these infections Apgar scores were 7 and 7 at 1 and 5 minutes, respectively. He was can be devastating, including death or severe neurodevelopmental immediately intubated, given surfactant, and admitted to the disability.5 Four percent of these cases are acquired prenatally, 86% neonatal intensive care unit. Broad-spectrum antibiotics plus natally, and 10% postnatally.2 In the largest case series on acyclovir (10 mg/kg every 8 hours) were administered intra- intrauterine HSV infections (13 infants), there was clinical evidence venously. A direct fluorescent antibody (DFA) examination of of primary genital HSV infection in 4 of the 13 mothers, and only 1 scrapings from the lesions was positive for HSV-2. An initial chest mother had a history compatible with recurrent genital HSV infection radiograph showed no infiltrates. Serologic tests for syphilis, HIV, and during pregnancy.6 hepatitis B were negative. Liver enzymes were elevated, with AST of 428 U/l (normal 17 to 59) and ALT of 81 U/l (normal 3 to 45), while total serum bilirubin was 5.1 mg/dl (normal 1.3 to 11.3) on Combined Division of Pediatric Infectious Disease ( A.C., S. A.C. ) , Creighton University and the day 3 of life. Subsequently, cultures of the vesicular fluid and blood University of Nebraska Medical Center, Omaha, NE; Department of Pediatrics ( C.J.H. ) , obtained shortly after birth grew HSV-2. Culture of the amniotic fluid University of Louisville, Louisville, KY; and Department of Pathology ( A.F.-D., C.B. ) , Creighton University, Omaha, NE. taken at delivery was also positive for HSV-2. Polymerase chain reaction (PCR) on the blood was positive for HSV-2 using the Address correspondence and reprint requests to Archana Chatterjee, MD, PhD, Department of Pediatrics, Creighton University, 2500, California Plaza, Room 409, Criss II, Omaha, NE 68178. procedure of Kimura et al.7 A lumbar puncture was not performed Journal of Perinatology 2001; 21:559 – 564 # 2001 Nature Publishing Group All rights reserved. 0743-8346/01 $17 www.nature.com/jp 559 Chatterjee et al. Fatal Neonatal HSV-2 Infection Figure 1. A, B, C, Multiple vesiculobullous lesions seen all over the body of the infant. initially due to the infant’s instability, but on day 15 (day 14 of 28% monocytes. There were 10,000 red blood cells/cmm (normal 0 acyclovir), the CSF contained 189 white blood cells (WBCs) /cmm to 10/cmm), with 527 mg/dl protein (normal 15 to 45 mg/dl), (normal 0 to 5/cmm), with 55% neutrophils, 17% lymphocytes, and and 32 mg/dl glucose (normal 60 to 80 mg/dl). Cerebrospinal 560 Journal of Perinatology 2001; 21:559 – 564 Fatal Neonatal HSV-2 Infection Chatterjee et al. Figure 1. (continued). fluid cultures were negative for bacteria and viruses, and PCR was The child’s hospital course was complicated by seizures, bilateral negative for HSV-1 and HSV-2. intraventricular hemorrhage (IVH), and sepsis with Candida The placenta was discoid and small, measuring 16.3Â14.7Â1.2 parapsilosis on day 14 and Klebsiella pneumoniae on day 16. Blood cm, and weighing 229.8 g ( <25th percentile for estimated cultures remained positive for both organisms despite adequate gestational age). The umbilical cord inserted approximately 2.8 cm antibacterial and antifungal therapy. Due to his severe IVH and from the nearest margin. The fetal surface of the placenta was progressively deteriorating status, he was taken off life support on day smooth and had no vesicular lesions. The maternal surface was 21, following consultation with the family. An autopsy was requested, grossly unremarkable and all cotyledons appeared intact. The but refused by the family. umbilical cord was boggy, but no other gross abnormalities were identified. The membranes were somewhat discolored, but not friable or foul smelling. LITERATURE REVIEW AND DISCUSSION Microscopic examination of the placenta showed several necrotic Genital HSV infection can be acquired primarily or recur during abscesses in the intervillous spaces with an intense neutrophilic pregnancy. Several studies have suggested associations between HSV infiltrate, marked karyorrhexis and degeneration (Figure 2A). There infection acquired during pregnancy and preterm labor, intrauterine were varying degrees of neutrophilic infiltration in both intact and growth retardation, and spontaneous abortion.2,8 Specific maternal degenerating peripheral villi. No intranuclear inclusions were IgG against the relevant HSV serotype appears to provide relative identified in these areas on H&E stain and an immunoperoxidase protection against intrauterine infection, but this protection is not stain for HSV was negative. Gram stain for bacteria was also negative. absolute. Hutto et al.6 described 13 cases of intrauterine HSV-2 Microscopic examination of the membranes showed foci of acute infection, with only 1 of the mothers having recurrent disease. inflammation with frank necrosis in the decidua basalis and HSV-2 infects nearly 50% of infants whose mothers have primary chorionic plate (Figure 2B). Foci of increased chronic inflammation genital herpes at delivery, whereas <5% of infants exposed to were also present in these areas, containing a predominantly recurrent maternal infection at the time of delivery become infected. lymphocytic population. Gram stain was negative in these areas as Prober et al.9 reported no cases of neonatal herpes among 34 exposed well. The amnion was not directly involved in the acute or chronic babies in mothers with recurrent HSV infection who were shedding inflammatory process. Small nests of somewhat columnar, more virus at the time of delivery. Brown et al.10 documented infection in 1 reactive cells were observed, but no intranuclear inclusions or of 33 similarly exposed infants. Even with recurrent disease, multinucleated giant cells were identified on H&E sections. symptomatic HSV in the mother poses a greater risk than Immunoperoxidase staining of these reactive cell populations in the asymptomatic.11 Other risk factors for acquisition of neonatal HSV amnion was positive for HSV (Figure 2C). infection include: (1) cervical (as opposed to vulvar or buttock) Journal of Perinatology 2001; 21:559 – 564 561 Chatterjee et al. Fatal Neonatal HSV-2 Infection Figure 2. A, Necrotic abscess in the intervillous space with an intense neutrophilic infiltrate, marked karyorrhexis and degeneration. B, Acute inflammation with frank necrosis in the decidua basalis and chorionic plate. C, Immunoperoxidase staining of reactive cell populations in the amnion positive for HSV. lesions, which result in more virus being shed into vaginal secretions;
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