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 Table of Contents  
CASE REPORT
Year : 2019  |  Volume : 8  |  Issue : 1  |  Page : 54-56

Intrauterine herpes simplex virus type one infection presenting with skin erosions and ulcers: Masking as neonatal sepsis


1 Children's Leeds Congenital Heart Unit, Leeds General Infirmary, UK
2 Department of Dermatovenerology, University Medical Centre Ljubljana, Ljubljana, Slovenia
3 Department of Perinatology, University Medical Centre Ljubljana, Neonatal Intensive Care Unit, Ljubljana, Slovenia

Date of Web Publication29-Jan-2019

Correspondence Address:
Dr. Ines Hribernik
Alder Hey Children's Hospital, Liverpool
UK
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcn.JCN_112_17

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  Abstract 


Neonatal infection with herpes simplex virus (HSV) either type 1 or type 2 can be acquired in utero, intrapartum, and postnatally. We report a case of intrauterine HSV type 1 infection with atypical cutaneous manifestations, misdiagnosed initially as neonatal sepsis. A high index of suspicion with diverse cutaneous manifestations kept in mind is necessary to diagnose infants with intrauterine HSV infection.

Keywords: Herpes simplex virus, herpetic cutaneous manifestations, intrauterine infection, neonate


How to cite this article:
Hribernik I, Dragoš V, Cerar LK. Intrauterine herpes simplex virus type one infection presenting with skin erosions and ulcers: Masking as neonatal sepsis. J Clin Neonatol 2019;8:54-6

How to cite this URL:
Hribernik I, Dragoš V, Cerar LK. Intrauterine herpes simplex virus type one infection presenting with skin erosions and ulcers: Masking as neonatal sepsis. J Clin Neonatol [serial online] 2019 [cited 2019 Jul 22];8:54-6. Available from: http://www.jcnonweb.com/text.asp?2019/8/1/54/250978



Intrauterine herpes simplex virus infection has diverse cutaneous manifestations and can present without typical vesiculobullous lesions. This should be kept in mind when making a differential diagnosis of the skin lesions in the newborns, as atypical clinical presentation can lead to misinterpretation and delay the institution of appropriate treatment. Our case was first misdiagnosed as neonatal sepsis due to the unusual skin lesions; the correct diagnosis was not made until day 15 of life.


  Introduction Top


Neonatal infection with herpes simplex virus (HSV) can be acquired in utero (5% of cases), intrapartum (85%), and postnatally (10%).[1] Transmission to newborns can occur with either genital HSV type 1 (HSV-1) or HSV type 2 (HSV-2). it is estimated that 75% of neonatal HSV cases are caused by HSV-2 and 25% by HSV-1.[2] We present a case of intrauterine HSV-1 infection with atypical cutaneous manifestations, misdiagnosed initially as neonatal sepsis.


  Case Report Top


A 33-year-old Caucasian secundigravida with single gestation of 24 weeks presented with purulent vulvovaginitis and colpitis, without systemic signs of infection. She was treated empirically with antibiotic clindamycin. The vaginal swab culture showed mixed bacterial flora in small amounts (viral cultures were not obtained). After antibiotic treatment, the inflammation gradually regressed. She had negative prenatal laboratory studies for hepatitis B, syphilis, and toxoplasmosis. She had no history of HSV in herself or her sexual partner. In the 25th week of gestation, there was a spontaneous rupture of membranes. She received betamethasone for fetal lung maturation and the antibiotic therapy with clindamycin was continued. In 26-4/7 weeks (2 weeks after the rupture of membranes), labor began with spontaneous contractions. The amniotic fluid was clear. The labor was vaginal and lasted one hour.

The infant (a boy) needed short resuscitation after birth with bag-mask ventilation with room air and upper airway aspiration. The birth weight was 800 g (appropriate for gestational age), birth length was 33 cm, and head circumference was 23 cm. Apgar score was 6–7. He was admitted to the neonatal intensive care unit due to prematurity.

After admission, he had no signs of respiratory distress. The whole body was covered with extensive (somewhere polycyclic) erosions, yellow crusts, and shallow ulcers with an erythematous base; the mucosal surfaces of the mouth and genitals looked intact. There were no vesicular lesions. Apart from skin lesions, the clinical examination was normal. Laboratory results showed elevated C-reactive protein (CRP) (38 mg/L) and a left shift in white blood cell differential (over 20% of immature neutrophils). On suspecting early neonatal sepsis, an empirical antibiotic therapy with ampicillin and gentamicin was started. Bacterial cultures of nasopharyngeal, external auditory canal and skin swabs were sterile, as was blood culture. Swabs cultured for fungi were negative. As CRP was slowly rising, the baby was switched to systemic therapy with metronidazole to cover anaerobes and local skin therapy with clindamycin. There was no progression of skin eruptions, and the erosions showed gradual healing with residual scar formation [Figure 1].
Figure 1: Skin erosions and crusts in intrauterine herpes simplex virus infection (our case)

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The abdominal ultrasound performed on day 7 showed derangement of the liver parenchymal architecture with fine nodular hyperchogenic patterns on the liver surface over the ductus venosus; the remaining part of the liver parenchyma seemed normal. No intrahepatic duct dilatation was seen, and there were no signs of intrahepatic venous congestion. Serum levels of liver transaminases were only minimally elevated and did not rise in the following days.

On day 13 of life, CRP rose to 133 mg/L. Despite unusual clinical presentation, skin swabs from conjunctiva and oral mucosa were taken for HSV-1 and HSV-2 PCR. The swabs were positive for HSV-1. The blood serology showed positive IgM and IgG antibodies to HSV-1. Antiviral therapy with intravenous acyclovir was started. A lumbar puncture was performed on day 23 (after 7 days of antiviral therapy) and showed negative PCR to HSV-1 in cerebrospinal fluid. The boy received 14 days of acyclovir therapy. The laboratory markers of inflammation normalized subsequently. The crusts and erosions underneath were replaced with extensive atrophic scars.

The boy had multiple ophthalmologic examinations which showed no signs of eye involvement. Due to periorbital scarring and subsequent incomplete eye closure, he later developed erosive keratitis, which we treated symptomatically with artificial tears. Regular head ultrasounds were performed, with no signs of intracranial pathology. There were also no clinical signs of the central nervous system (CNS) involvement.

The mother was serologically positive for HSV-1 infection (IgM and IgG antibodies) and negative for HSV-2 infection at the time of diagnosis in her child.


  Discussion Top


Intrauterine HSV infection is typically described as a triad of cutaneous, CNS, and ophthalmologic manifestations. However, a review of reported cases showed that more than two-thirds do not present with the typical triad.[3] Cutaneous findings are the most common clinical manifestation (95% of cases),[3] most typically as vesiculobullous lesions. Neonates can also present with erosions/ulcerations, pustules, erythematous macules, plaques, or hypopigmented patches/scars.[3],[4] Macules and plaques can later progress to form vesicles or pustules.[3],[5] However, cutaneous presentations of intrauterine (congenital) HSV infection with absence of vesicles or vesiculopustules have been reported.[6] Our case never showed vesicular changes. The expected natural progression of herpetic lesions is to evolve from vesicle to ulcer, crust, and then heal; the type of cutaneous presentation in intrauterine infection depends on the stage of the eruption at the time of birth.[3] HSV can also mimic other diseases such as other congenital infections, the bullous form of neonatal lupus, epidermolysis bullosa, aplasia cutis congenita, and incontinentia pigmenti.[3]

Factors that influence transmission of HSV from mother to newborn are type of maternal infection (primary, recurrent), maternal HSV antibody status, duration of rupture of membranes, mucocutaneous barrier integrity, and mode of delivery (vaginal, cesarean).[7] The mother of the boy had signs of vulvovaginitis, which, according to her positive serology testing for HSV-1 (positive IgM and IgG antibodies), was most probably a primary infection with HSV-1. The prolonged duration of rupture of membranes can explain the atypical cutaneous presentation in the child with only secondary changes left.

Mortality and morbidity of intrauterine herpetic infection are extremely high.[8] Antiviral therapy with acyclovir should not be delayed when clinical suspicion of neonatal HSV infection exists. The treatment does not reverse the injury sustained in utero; however, it may prevent the progression of the mucocutaneous disease to CNS and disseminated disease.[3]


  Conclusion Top


We report a premature baby with intrauterine HSV infection who presented with extensive skin lesions with no evidence of the involvement of other organs. The correct diagnosis was not made until day 15 of life, due to the absence of vesicles, and significantly elevated inflammatory markers that suggested neonatal sepsis. After the institution of treatment with intravenous acyclovir, the boy showed no neurologic or ophthalmologic (except for erosive keratitis due to periorbital scars) sequelae. The erosions healed with scarring. A high index of suspicion with diverse cutaneous manifestations kept in mind is necessary to diagnose infants with intrauterine HSV infection.[3]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Kimberlin DW. Neonatal herpes simplex infection. Clin Microbiol Rev 2004;17:1-3.  Back to cited text no. 1
    
2.
Allen UD, Robinson JL; Canadian Paediatric Society, Infectious Diseases and Immunization Committee. Prevention and management of neonatal herpes simplex virus infections. Paediatr Child Health 2014;19:201-12.  Back to cited text no. 2
    
3.
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. 3
    
4.
Salvador A, Meislich D, Tunnessen WW Jr. Picture of the month. Intrauterine herpes simplex virus infection. Arch Pediatr Adolesc Med 1994;148:1311-2.  Back to cited text no. 4
    
5.
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. 5
    
6.
Koch LH, Fisher RG, Chen C, Foster MM, Bass WT, Williams JV, et al. 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. 6
    
7.
Kimberlin DW, Baley J; Committee on Infectious Diseases, Committee on Fetus and Newborn. Guidance on management of asymptomatic neonates born to women with active genital herpes lesions. Pediatrics 2013;131:e635-46.  Back to cited text no. 7
    
8.
Pichler M, Staffler A, Bonometti N, Messner H, Deluca J, Thuile T, et al. Premature newborns with fatal intrauterine herpes simplex virus-1 infection:First report of twins and review of the literature. J Eur Acad Dermatol Venereol 2015;29:1216-20.  Back to cited text no. 8
    


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