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Non-Immune Hydrops Fetalis Caused by Herpes Simplex Virus Type 2 in the Setting of Recurrent Maternal Infection

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Non-Immune Hydrops Fetalis Caused by Herpes Simplex Virus Type 2 in the Setting of Recurrent Maternal Infection Journal of Perinatology (2013) 33, 817–820 & 2013 Nature America, Inc. All rights reserved 0743-8346/13 www.nature.com/jp PERINATAL/NEONATAL CASE PRESENTATION Non-immune hydrops fetalis caused by herpes simplex virus type 2 in the setting of recurrent maternal infection KM Pfister1, MR Schleiss2, RC Reed3 and TN George1 We report a case of non-immune hydrops fetalis (NIHF) caused by herpes simplex virus type 2 (HSV-2) in an infant whose mother had recurrent HSV-2 infection. In spite of prematurity, severe disseminated infection and hydrops, the infant survived and was neurologically intact. HSV-2-induced NIHF is extremely rare, particularly in the setting of recurrent maternal infection, and this case is, to our knowledge, the first report of a surviving infant. HSV-2 should be considered in the differential diagnosis of NIHF and early initiation of empiric acyclovir therapy is recommended in this setting, pending the results of virologic diagnostic tests. Journal of Perinatology (2013) 33, 817–820; doi:10.1038/jp.2013.68 Keywords: neonatal HSV infection; fetal hydrops; HSV-2 infection; placental infection; acyclovir; torch infection INTRODUCTION Following transfer to our neonatal intensive care unit from a Non-immune hydrops fetalis (NIHF), which occurs in 1 in 2500 to referring facility on day of life (DOL) 1, examination was remark- 4000 pregnancies, continues to have a very high perinatal mortality able for a severely hydropic-appearing premature infant with a rate, ranging from 50 to 90%.1,2 Cardiac disorders, genetic distended abdomen and an enlarged, firm liver. Skin examination abnormalities, fetal malformations, hematologic disorders and showed diffuse erythema, non-tense bullae on the chest and infections can all lead to NIHF. Among the infectious etiologies of extremities, as well as superficial erosions and hemorrhagic macules NIHF, the most common causes are cytomegalovirus, toxoplasmosis, and papules. The face and scalp were notably spared (Figure 1). syphilis and parvovirus B19 infection. Herpes simplex virus (HSV) is Initial lab values demonstrated a white blood cell count of only rarely described as a cause of NIHF, typically in the setting of 10.4  109 l À 1, a hemoglobin of 8 g dl À 1, a platelet count of primary maternal infection, and no surviving infants have been 38  109 l À 1, a direct antiglobulin and antibody that were both described in the previous case reports.3–10 We report the case of an negative, an international normalized ratio of 2.87 (reference range, infant with NIHF secondary to intrauterine HSV-type 2 (HSV-2) 0.81 to 1.30), a partial thromboplastin time of 89 s (reference range, infection who survived; notably, this infant was born to a woman 27 to 52 s), a fibrinogen of 198 g dl À 1 (reference range, 200 to with recurrent HSV-2 infection. 420 mg dl À 1) and an aspartate aminotransferase and alanine aminotransferase of 468 (reference range, 20 to 65 U l À 1)and41 (reference range, 0 to 50 U l À 1)UlÀ 1,respectively. CASE The infant required high-frequency oscillatory ventilation for A 24-year-old gravida 1 para 0 woman presented at 27-1/7 weeks’ severe hypoxemic respiratory failure. Initial echocardiogram gestation with preterm labor and spontaneous rupture of showed evidence of pulmonary hypertension with tricuspid membranes for 2 h. Her pregnancy had been uncomplicated to regurgitation and right-to-left shunting through the patent that point, with normal ultrasounds at 12 and 20 weeks. Prenatal foramen ovale and patent ductus arteriosus, as well as severely labs were unremarkable and she was HIV negative. The patient had depressed biventricular function and a small pericardial effusion a history of a primary genital HSV-2 infection approximately 4 years without tamponade. Inhaled nitric oxide (iNO) was initiated, prior to this pregnancy, documented at that time by culture and resulting in a change of the patent ductus arteriosus shunt to type-specific serology (HSV-2 immunoglobulin G positive). She bidirectional status, and subsequent clinical improvement was denied a history of symptomatic recurrent genital HSV infections, noted. Although iNO therapy is not routinely recommended for and she had not received suppressive nucleoside therapy prior to severe respiratory failure and has not been shown to be beneficial or during this pregnancy. At presentation, she was fully dilated, in this setting,11,12 a recently published NIH consensus statement and a hydropic-appearing male infant was spontaneously deli- on iNO therapy for premature infants (http://consensus.nih.gov/ vered several minutes after admission. The infant had no 2010/inofinalstatement.htm) noted that there are clinical spontaneous respiratory effort or movement, with an initial heart situations, including pulmonary hypertension, in which iNO may rate less than 60. Resuscitation included intubation, positive have benefit in preterm infants. Given the clinical presentation pressure ventilation, chest compressions, intravenous epinephrine and the echocardiogram results, we felt that iNO would be and intravenous fluids. Surfactant was administered. Apgar scores beneficial to this infant. Medical therapies included empiric were 4 and 7 at 1 and 5 min, respectively. ampicillin and gentamicin, and pressor support (dopamine, 3 to 1Division of Neonatology, Department of Pediatrics, University of Minnesota Amplatz Children’s Hospital, Minneapolis, MN, USA; 2Center for Infectious Diseases and Microbiology Translational Research, Division of Pediatric Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Amplatz Children’s Hospital, Minneapolis, MN, USA and 3Department of Laboratory Medicine and Pathology, University of Minnesota Amplatz Children’s Hospital, Minneapolis, MN, USA. Correspondence: Dr MR Schleiss, Center for Infectious Diseases and Microbiology Translational Research, Division of Pediatric Infectious Diseases and Immunology, Department of Pediatrics, Minneapolis, MN 55455, USA. E-mail: [email protected] Received 15 April 2013; accepted 8 May 2013 Non-immune hydrops fetalis caused by herpes virus KM Pfister et al 818 Figure 1. Skin findings in intrauterine HSV-2 infection. Multiple bullae and erosions are noted on trunk and extremities. HSV, herpes simplex virus. 20 mcg kg À 1 min À 1, for 3 days with peak dosing at approximately 48 h of life, and dobutamine 3 to 7 mcg kg À 1 min À 1, for 12 h on DOL 2). Corticosteroid therapy for clinical adrenal insufficiency was initiated on DOL 3 (hydrocortisone sodium succinate, 4mgÀ 1 kg À 1 day for 2 days, which was tapered over the follow- ing 5 days). Intravenous immunoglobulin (2 doses of 0.5 g kg À 1 each on DOL 3 and 4), and multiple packed red blood cell, platelets, and fresh frozen plasma transfusions were also administered. Empiric acyclovir therapy was initiated at 8 h of life. Abdominal ultrasound demonstrated diffuse hepatic microcalcifications. Head ultrasound revealed hemorrhage in the left ventricle without ventricular dilation with a small periventricular hemorrhage, as well as right germinal matrix hemorrhage. Diagnostic studies obtained to elucidate the potential etiology of NIHF included parvovirus, toxoplasma and treponema serolo- Figure 2. Herpes simplex viral inclusions in amniotic epithelium gies; blood and urine cytomegalovirus culture and polymerase of fetal membranes. (a) Hematoxylin and eosin (H&E) stain chain reaction (PCR); and blood PCR for HIV and enterovirus, all of showing eosinophilic intranuclear viral inclusion (arrow). (b) H&E which were negative. The total serum immunoglobulin M level stain showing chromatin margination and ground-glass nuclear viral inclusions (arrows). (c) Immunoperoxidase stain for HSV-1 and 2. was 234 mg dl À 1. Blood HSV-2 PCR was positive; in addition, Magnification  400. HSV, herpes simplex virus. HSV-2 was also identified by both conjunctival viral culture and PCR, and from the nasopharynx and rectum by PCR. Ophthalmo- logic exam revealed bilateral herpetic keratitis. A lumbar puncture lesions resolved, although post-inflammatory hypopigmentation was not possible due to clinical instability. Placental pathology was noted. Brain MRI prior to discharge showed moderate atrophy demonstrated viral cytopathic changes in amniotic epithelial cells of the right cerebellar hemisphere and slightly less than expected of the fetal membranes, including chromatin margination and T1 hyperintensity in the corticospinal tracts and posterior limb of eosinophilic intranuclear inclusions. Immunohistochemical stain- the internal capsule on the left. There were no cystic changes. The ing with an HSV-specific monoclonal antibody confirmed the infant was discharged on DOL 114 at 43-2/7 weeks corrected age presence of HSV (Figure 2). There was also evidence of acute and with a plan to continue supplemental low-flow oxygen therapy chronic funisitis and acute chorioamnionitis, but no villitis. and gastrostomy tube feeds. Oxygen therapy was gradually HSV DNA was no longer detected in blood by DOL 10. weaned and discontinued by 6 weeks post-discharge. The infant was treated with high-dose intravenous acyclovir Upon discontinuation of acyclovir, after 6 months of suppres- (40 mg kg À 1 per day) for 30 days and then transitioned to oral sive therapy, the patient had recurrence of skin lesions. He was acyclovir suppressive therapy (300 mg m À 2 three times per day) again treated with intravenous acyclovir for 48 h, and transitioned for 6 months.13 Topical trifluridine was also administered for to oral suppressive therapy for an additional
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