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ONLINE ONLY ARTICLES - CASE REPORT
Year : 2022  |  Volume : 6  |  Issue : 2  |  Page : 151

Herpes zoster ophthalmicus in an healthy infant with intrauterine infection


1 Department of Dermatology, SDM College of Medical Sciences and Hospital, Dharwad, Karnataka, India
2 Department of Pediatrics, SDM College of Medical Sciences, Dharwad, Karnataka, India

Date of Submission11-Oct-2020
Date of Decision15-Mar-2021
Date of Acceptance21-May-2021
Date of Web Publication26-Aug-2022

Correspondence Address:
R Megha
Department of Dermatology, SDM College of Medical Sciences and Hospital, Dharwad, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cdr.cdr_127_20

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  Abstract 


Herpes zoster (HZ) or shingles is a viral infection with segmental eruption due to reactivation of varicella zoster virus (VZV) from the dorsal root ganglion. HZ is uncommon in immunocompetent children and early adult life. Incidence increases in individuals over the age of 50 years. However, zoster can occur in childhood following intrauterine infection or exposure to VZV at an early age. We report this case, as HZ is rare in infants, especially HZ ophthalmicus due to both intrauterine infection and exposure after birth.

Keywords: Herpes zoster, infant, varicella zoster virus


How to cite this article:
Megha R, Prabhu SR, Naveen K N, Athanikar S B, Kulkarni V. Herpes zoster ophthalmicus in an healthy infant with intrauterine infection. Clin Dermatol Rev 2022;6:151

How to cite this URL:
Megha R, Prabhu SR, Naveen K N, Athanikar S B, Kulkarni V. Herpes zoster ophthalmicus in an healthy infant with intrauterine infection. Clin Dermatol Rev [serial online] 2022 [cited 2022 Oct 7];6:151. Available from: https://www.cdriadvlkn.org/text.asp?2022/6/2/151/354737




  Introduction Top


Varicella is a febrile illness characterized by generalized pruritic vesicular rash caused by the varicella zoster virus (VZV) which has a high infectivity. It is commonly seen in childhood with a worldwide prevalence. However, herpes zoster (HZ) is a localized disease characterized by unilateral radicular pain and vesicular eruption along a dermatome innervated by a single spinal or cranial sensory ganglion. It is caused by reactivation of dormant VZV in sensory ganglia. The disease incidence increases beyond 50 years of age, in immunocompromised states, malignancy, and transplant recipients.


  Case Report Top


An 8-month-old female infant presented with a history of rash over the left side of the face for 3 days and history of fever for 2 days. Infant was born out of full term normal vaginal delivery with no prior history of varicella. Mother gave a history of exposure of the infant to a household contact with a case of HZ 10 days before the onset of the rash. On further enquiry, there was a history of vesicular rash in the mother at 34 weeks of gestation. No history of atopy in mother and the infant. Tzanck smear examination of the lesion demonstrated multinucleate gaint cells, and a diagnosis of varicella was made.

On cutaneous examination, baby had multiple grouped vesicles on an erythematous base involving the left side of the forehead extending to the frontal area of the scalp, left upper eyelid, and left side of the nose with few lesions involving tip of the nose [Figure 1]. These lesions were confined to the midline corresponding to the distribution of ophthalmic division of trigeminal nerve. There was left periorbital edema with serous discharge from left eye.
Figure 1: Multiple grouped vesicles on erythematous base over left side of forehead, left upper eyelid, left side of nose with left periorbital edema

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The diagnosis of HZ ophthalmicus (HZO) was made based on clinical features and Tzanck smear from the base of the vesicle which showed multinucleate giant cells. Ophthalmologic examination suggested mild conjunctival congestion and a clear cornea on slit-lamp microscopy. Pupilary reaction was normal. Corneal sensation could not be elicited. Serology and viral culture was not done. The patient was treated with oral acyclovir 120 mg (20 mg/kg) four times a day for 5 days with mupirocin ointment for local application, 3% acyclovir eye ointment TID, and tobramycin eye drops TID following which the baby had complete resolution of lesions without any sequelae.


  Discussion Top


VZV is a DNA virus belonging to the α subgroup of the Herpesvirus family. It is the causative agent for both varicella (chicken pox) and HZ (shingles). Disease spreads as an airborne infection or due to direct contact with the lesion. After the primary infection with VZV, it leads to viremia and a wide spread vesicular eruption. The virus then enters the sensory nerves in mucocutaneous sites and travels through retrograde axonal transport to the sensory dorsal-root ganglion adjacent to the spinal cord. Here, the virus establishes permanent latency in neuronal cell bodies. HZ is caused due to the reactivation of this persistent VZV from the posterior root ganglion.

Primary varicella is a disease of the childhood, whereas zoster occurs in old age. The incidence of HZ is only 0.45/1000 in children below 14 years of age. The incidence increases in advancing age, in cases of underlying malignancy, transplant recipients, and immunocompromised states. Approximately 3% of HZ cases occur in children with malignancies. Rising incidence of HZ in healthy children may be due to acquisition of primary varicella infection in utero, or in infancy, wherein the immunity is not fully developed. Vaccination with live attenuated virus may be a contributory factor in the development of HZ. Tereda et al. stated that the immunological status at the time of acquiring the primary infection is the most important factor in childhood HZ. A low level of lymphocytes, natural killer cells, and cytokines are seen in infants along with virus-specific immunoglobulins that may result in an inability to maintain the latency of VZV, leading to early appearance of zoster in children.[1]

Primary infection with VZV confers lasting immunity and second attacks are uncommon, especially in immunocompetent individuals. Women in the reproductive age group who have not developed immunity to varicella have a small but finite risk of developing chicken pox during pregnancy (0.05%–0.07%). The highest risk was observed between 13 and 20 weeks of gestation. Incidence of varicella in pregnancy is found to be 2–3/1000 pregnancies.[2] The risk of severe illness is greatest after mid pregnancy for the mother due to relative immunocompromised status. Whereas, the risk of congenital infection is greatest when maternal infection occurs during the first or second trimester.[3] When women have the disease later in pregnancy, the fetus can develop asymptomatic congenital infection and subsequently present clinically with HZ within the 1st year of life. Newborns of VZV-immune mothers can also develop subclinical varicella within the first 6 months of life. In these cases, maternal VZV antibodies passively transferred to the infant may modify the disease into a subclinical form. In general, infants with primary varicella infection are at high risk for HZ within the 1st year of life.[4] In the above case, there was intrauterine infection during 34 weeks of gestation followed by exposure in late infancy 10 days before the onset of lesions.

HZO is due to reactivation of virus along the ophthalmic division of trigeminal nerve. Sometimes, it is preceded by the presence of zoster vesicles on the nose (Hutchinson sign). Keratitis occurs in approximately two-thirds of patients with HZO, often causing corneal ulceration. Other complications include conjunctivitis, uveitis, episcleritis and scleritis, retinitis, choroiditis, optic neuritis, lid retraction, ptosis, and glaucoma.[5]

In general, HZ runs a milder course in children than adults lasting for 1–3 weeks. In children between the age group of 2 and 12 years, acute neuropathic pain was not observed which is the hallmark of HZ in adults. Although lesional pruritus and pain may be present, the incidence of postherpetic neuralgia is negligible which is the most common complication of HZ in adults. Systemic reactions include fever, headache, and lymphadenopathy. Secondary bacterial infections and ophthalmic HZ have been reported. Cranial, cervical, and thoracic segments are the most frequently involved dermatomes.[4]

A diagnosis of HZ is made by detailed clinical examination and confirmed by lab diagnosis by doing a Tzanck smear. The scrapings are taken from the floor of the vesicles that reveal multinucleated giant cells on light microscopy. The other methods are by direct fluorescent antibody tests, presence of high or rising titers of antibodies to VZV, or by culture studies. Direct fluorescent monoclonal antibody test or detection of serum-specific IgM by the indirect fluorescent antibody method is also used to confirm HZ.[1]

The first line of therapy in childhood HZ is antivirals. Oral acyclovir, given at a dose of 20–40 mg/kg body weight, four times a day. The main aim of treatment for HZ is to reduce pain, to promote faster healing, and avoid complications. Treatment should be initiated within 72 h of onset of lesions.

Famciclovir is shown to have superior action compared to valciclovir. Oral acyclovir suspension is available for pediatric age group. Analgesics and appropriate topical management is added to prevent complications.[6]


  Conclusion Top


Although HZ is an uncommon condition in infants, it can occur. The main cause for zoster in an immunocompetent child being intrauterine infection and exposure to VZV after birth. Due to milder presentation in children compared to adults, a high degree of suspicion should be kept in case of children presenting with dermatomal distribution of vesicular lesions. However, children tolerate HZ better than adults with lesser incidence of postherpetic neuralgia.

Declaration of patient consent

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

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Katakam BK, Kiran G, Kumar U. A prospective study of herpes zoster in children. Indian J Dermatol 2016;61:534-9.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Enders G, Miller E, Cradock-Watson J, Bolley I, Ridehalgh M. Consequences of varicella and herpes zoster in pregnancy: Prospective study of 1739 cases. Lancet 1994;343:1548-51.  Back to cited text no. 2
    
3.
Ghosh S, Chaudhuri S. Pregnancy and varicella infection: A resident's quest. Indian J Dermatol Venereol Leprol 2013;79:264-7.  Back to cited text no. 3
  [Full text]  
4.
Kurlan JG, Connelly BL, Lucky AW. Herpes zoster in the first year of life following postnatal exposure to varicella-zoster virus: Four case reports and a review of infantile herpes zoster. Arch Dermatol 2004;140:1268-72.  Back to cited text no. 4
    
5.
Mali S. Herpes zoster: Etiology, clinical features and treatment options, and case report. Egypt J Oral Maxillofac Surg 2012;3:91-100.  Back to cited text no. 5
    
6.
Koshy E, Mengting L, Kumar H, Jianbo W. Epidemiology, treatment and prevention of herpes zoster: A comprehensive review. Indian J Dermatol Venereol Leprol 2018;84:251-62.  Back to cited text no. 6
[PUBMED]  [Full text]  


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