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Year : 2016  |  Volume : 5  |  Issue : 3  |  Page : 205-208

Congenital herpes simplex type-2 infection; challenges and solutions

Department of Pediatric, Neonatal Intensive Care, Latifa Hospital, Dubai, United Arab Emirates

Date of Web Publication28-Sep-2016

Correspondence Address:
Dr. Khaled Mahmoud El-Atawi
Department of Pediatric, Neonatal Intensive Care, Latifa Hospital, P.O. Box 29793, Dubai
United Arab Emirates
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2249-4847.191269

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Congenital herpes simplex virus (HSV) Type-2 infection is a rare but life-threatening condition that usually results from vertical transmission from mother to her fetus. This case report presents a rare case of a preterm born with congenital HSV with the classical triad of cutaneous, central nervous system (CNS), and ophthalmologic disease. The infant had mild respiratory distress at the time of birth but otherwise appeared normal. On day 3 of birth, the child presented with classical symptoms of HSV. The child was given antiviral therapy for HSV infection; however, the infection was progressive and adversely affected the CNS, eyes, and overall development of the child. This paper highlights the importance of prenatal screening in women at risk to reduce the incidence of congenital HSV. Since most of the congenital HSV cases camouflage as other congenital, infectious, or developmental disorders of neonates, proper antenatal and postnatal screening is required to identify such cases.

Keywords: Chorioretinitis, congenital herpes simplex Type-2 infection, encephalitis, hydrocephalus

How to cite this article:
El-Atawi KM, Elhalik MS, Farid AR. Congenital herpes simplex type-2 infection; challenges and solutions. J Clin Neonatol 2016;5:205-8

How to cite this URL:
El-Atawi KM, Elhalik MS, Farid AR. Congenital herpes simplex type-2 infection; challenges and solutions. J Clin Neonatol [serial online] 2016 [cited 2023 Feb 2];5:205-8. Available from: https://www.jcnonweb.com/text.asp?2016/5/3/205/191269

  Introduction Top

Congenital herpes simplex virus (HSV) Type-2 infection is a rare but life-threatening condition of neonates that occurs in 1:3200-1:15,000 pregnancies.[1] Clinically, it is manifested as vesicular lesions on the skin, eye, and mouth, neonatal encephalitis, and disseminated infection involving liver, lung, spleen, or adrenals.[2] Drug therapy for HSV infection includes antiviral drugs such as acyclovir, valacyclovir, foscavir, and penciclovir. Although the prognosis of HSV is good after antiviral therapy, there are evidences of patients developing resistance after therapy and not responding to the treatment.[3],[4]

Most fetal infection from HSV is fatal and results in abortion. If fetus survives, it is born with a rare triad of cutaneous, ophthalmological, and central nervous system (CNS) manifestations.[2] This case report presents a preterm infant with congenital HSV-2.

  Case Report Top

A premature male child born at 31 weeks of gestation to an unbooked primipara mother at a government hospital in Dubai, United Arab Emirates, was admitted to the Neonatal Intensive Care Unit for respiratory distress and prematurity. Antenatal scan at 30 weeks of gestation showed severe hydrocephalus, with dangling choroid plexus and severely compressed cerebellum with vermian hypoplasia and retro-cerebellar cyst [Figure 1]a and b. On the 1st day of life, orbital and brain ultrasound scan revealed advanced hydrocephalus along with cerebellar and vermian hypoplasia and retro-cerebellar cystic formation [Figure 2], chalky white discs, bilateral retinal detachment with fibrosis, and choroidal thickness [Figure 3]a and b. On day 3 of life, vesicular bullous rashes erupted on the upper limb and scapula [Figure 4], and the child experienced multifocal clonic seizures, for which phenobarbitone (two loading doses of 15 mg/kg followed by maintenance of 5 mg/kg daily) was given. Later on, it was replaced by levetiracetam 10 mg/kg/dose bd. The child continued to be lethargic and hypotonic.
Figure 1: Findings of antenatal scan done at 31 weeks of gestation (a) Antenatal scan demonstrating severe hydrocephalus, (b) retrocerebellar cyst

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Figure 2: Advanced hydrocephalus along with cerebellar and vermian hypoplasia as demonstrated in brain ultrasound scan (BUSS) on day 1 of life

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Figure 3: Findings of orbital scan done on day 1 of life (a) bilateral retinal detachment with fibrosis and choroidal thickness (b) bilateral retinal detachment with fibrosis and choroidal thickness

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Figure 4: Vesicular bullous rashes on the left hand on day 3 of life

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Subsequent brain MRI on the 7th day of age showed severe dilatation of lateral, third and fourth ventricles, and the cisterna magna which left very thin portion of mantle of cerebral and cerebellar tissues and chalky white discs, bilateral retinal detachment with fibrosis, and choroidal thickness [Figure 5]a-c; the case was discussed with a neurosurgeon who advised for conservative management at this stage.
Figure 5: Findings of brain magnetic resonance imaging on day 7 of life (a) severe dilatation of lateral ventricles, third and fourth ventricles; (b) severe dilatation of lateral ventricles, third and fourth ventricles, and the cisterna magna; (c) bilateral retinal detachment with fibrosis and choroidal thickness

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Based on the above findings, intrauterine infection was suspected, and the child was screened for TORCH titers (toxoplasmosis, rubella, cytomegalovirus, and HSV), titer was positive for HSV2. Polymerase chain reaction (PCR) DNA from vesicles swab was positive. The cerebrospinal fluid (CSF) examination done on day 9 of life showed the presence of HSV infection. The child was started on intravenous (IV) acyclovir (20 mg/Kg/8 hourly), and the PCR HSV DNA and CSF examinations were repeated on a weekly basis to track improvements. The child continued to be HSV-positive even after 6 weeks of acyclovir. Hence, it was replaced by foscarnet sodium IV 40 mg/kg/dose tds for 2 weeks and then it was discontinued after negative CSF examination. Eye examination revealed active chorioretinitis for which he received fluorometholone drops 0.1% tds and bilateral intravitreal ganciclovir injection without any improvement.

Three days after stopping the antiviral therapy, other crops of vesicular rash erupted on the right hand, arm, and forearm. PCR HSV2 from vesicles swab was positive, so IV acyclovir was re-started. Two weeks later, repeated tests for HSV2 were negative, and the baby was shifted to oral acyclovir and was decided to be continued for 1 year or to shift to IV form if new vesicular crops appear. On day 80, as the child was stable on room air and on full orogastric feed, he was discharged on oral acyclovir 20 mg/Kg/8 hourly, levetiracetam 10 mg/kg/dose bd, and tobramycin eye drops, and was given all concerned appointments for follow-up, however, the child did not attend future follow-up.

  Discussion Top

HSV infection in neonates can be acquired during uterine, intrapartum, or postnatal exposure to the infectious agent.[5] Intrauterine transmission represents only 4-5% of neonatal HSV disease but leads to catastrophic events such as death, developmental anomalies, and disabilities.[6]

CNS manifestations are responsible for mortality and morbidity.[7] Other clinical manifestations include purpura, microphthalmia, cataract, and chorioretinitis.[5],[6]

This case demonstrates a classical triad of congenital HSV2 clinical symptoms. This infant presented with respiratory distress at birth and developed seizure on day 3 followed by vesicular rashes on the body. Diagnostic tests confirmed congenital HSV2 infection, for which he received antiviral therapy. Despite the initiation of the therapy, the child continued to deteriorate resulting in developmental delay and hydrocephalus with visual impairment. All therapeutic measures taken were for symptomatic relief and did not provide definitive treatment. Koch et al. and Low et al. independently presented two similar cases of congenital HSV but without CNS and ophthalmological manifestations.[8],[9]

Therapeutic measures in congenital HSV are not sufficient to resolve the damage. Efforts to identify risk factors and to develop prevention and risk management strategies are essential. Identification of risk factors and prenatal screening of women of childbearing age and their sexual partners can reduce the chances of congenital HSV. Neonates born to mothers <21 years or had the first episode of HSV infection during the third trimester and neonates born before 38 weeks of gestation are at a high risk of developing HSV infection.[10],[11]

Prenatal TORCH screening and proper treatment of women with existing infection can also reduce the chances of vertical transmission of HSV. A prenatal counseling in high-risk women or in those with a history of HSV infection is also beneficial in reducing the chances of transmission to their newborn.[12] Immunization of pregnant women for HSV may reduce the chances of HSV transmission to fetus; however; no approved vaccine is available so far.[12]

Acyclovir and vidarabine have remained the mainstay of congenital HSV infection treatment till date.[8],[10]

  Conclusion Top

Congenital HSV infection is a rare clinical presentation in neonates. Antenatal ultrasonography scan is beneficial for the early detection of intrauterine fetal infection. Early management of congenital HSV infection with antiviral drugs is efficient in reducing morbidity. The primary focus of preventing congenital HSV infection should be prevention in the antenatal period along with prompt and adequate treatment in the postnatal period.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Wald A, Corey L. Persistence in the population: Epidemiology, transmission. Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Ch. 36. In: Arvin A, Campadelli-Fiume G, Mocarski E, Moore PS, Roizman B, Whitley R, et al. editors. Cambridge: Cambridge University Press; 2007.  Back to cited text no. 1
Kesson AM. Management of neonatal herpes simplex virus infection. Paediatr Drugs 2001;3:81-90.  Back to cited text no. 2
James SH, Prichard MN. A possible pitfall in acyclovir prophylaxis for recurrent herpetic keratitis? J Infect Dis 2013;208:1353-5.  Back to cited text no. 3
van Velzen M, van de Vijver DA, van Loenen FB, Osterhaus AD, Remeijer L, Verjans GM. Acyclovir prophylaxis predisposes to antiviral-resistant recurrent herpetic keratitis. J Infect Dis 2013;208:1359-65.  Back to cited text no. 4
Russell-Eggitt I, Lightman S. Intrauterine infection and the eye. Eye (Lond) 1992;6(Pt 2):205-10.  Back to cited text no. 5
Marquez L, Levy ML, Munoz FM, Palazzi DL. A report of three cases and review of intrauterine herpes simplex virus infection. Pediatr Infect Dis J 2011;30:153-7.  Back to cited text no. 6
Sanchez P, Demmler-Harrison G. Viral infections of the foetus and neonate. In: Feigin R, Cherry J, Demmler-Harrison G, Kaplan SL, editors. Textbook of Paediatric Infectious Diseases. 6 th ed. Philadelphia: WB Saunders Co.; 2009. p. 918-24.  Back to cited text no. 7
Koch LH, Fisher RG, Chen C, Foster MM, Bass WT, Williams JV. Congenital herpes simplex virus infection: Two unique cutaneous presentations associated with probable intrauterine transmission. J Am Acad Dermatol 2009;60:312-5.  Back to cited text no. 8
Low LC, Carton J, Walker M, Tudor-Williams G, Hardman C. Intrauterine herpes simplex virus infection presenting with hypopigmented lesions. Pediatr Dermatol 2012;29:515-8.  Back to cited text no. 9
Corey L, Wald A. Maternal and neonatal herpes simplex virus infections. N Engl J Med 2009;361:1376-85.  Back to cited text no. 10
Whitley RJ. Neonatal herpes simplex virus infections. J Med Virol 1993;41 Suppl S1:13-21.  Back to cited text no. 11
Anzivino E, Fioriti D, Mischitelli M, Bellizzi A, Barucca V, Chiarini F, et al. Herpes simplex virus infection in pregnancy and in neonate: Status of art of epidemiology, diagnosis, therapy and prevention. Virol J 2009;6:40.  Back to cited text no. 12


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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