Herpes Zoster Neonatorum

Herpes zoster occurs because of the reactivation of a latent infection of varicella zoster virus (VZV) from the sensory ganglia. It is rare in childhood, and a truly rare occurrence is herpes zoster Neonatorum. Only 10 cases have been reported (1). The expected rate of zoster during the first decade has been estimated at only 0.74 cases per thousand per annum (2). Immunocompromised states and primary VZV infection at less than one year of age increase the risk of acquiring herpes zoster (3). To the best of our knowledge, this is the first case of herpes zoster in a neonate reported from India. We present here a 16-day-old female neonate, the result of a normal pregnancy in a woman who had never had varicella. The infant was brought to the dermatology outpatient department of Government Medical College and Hospital, Faridkot, Punjab, India, with a blistering eruption on the left side of the face of four days duration. Physical examination disclosed an afebrile, comfortable neonate with no systemic findings. Cutaneous examination revealed grouped vesicles on an erythematous and edematous base with overlying crusts at places on the left side of the face extending to involve the parietal region of the scalp (Fig. 1). There were no lesions beyond the midline. Both eyes and the oral mucosa were spared. Tzanck smear demonstrated multinucleated giant cells. There was no previous history of varicella in the mother. During the sixth month of pregnancy, mother had been exposed to a person who had varicella, but there were no signs or symptoms suggestive of chickenpox. The birth history was normal. ELISA for HIV I & II of both mother and child was non-reactive. Only symptomatic treatment was given, and the neonate was kept under observation. The lesions healed within three weeks. Herpes zoster in neonates and children may represent the result of an attenuated response to intrauterine or neonatal infection. There is a definite relationship between childhood zoster and prenatal exposure to varicella. Weller noted that the length of time between the primary infection and the reactivated infection is influenced by host-dependent factors and that maternal infection with varicella during pregnancy is often followed by zoster in the offspring during infancy. He postulated that, in such cases, the shortened time between the primary infection and the reactivation reflects the response of an immature immune system (4). The unique features of the present case are the absence of varicella in the immediate neonatal period and the exposure of the mother to a person who had varicella during the sixth month of pregnancy. The pregnancy itself was not complicated by chickenpox. The possibility of a subclinical infection of the mother which was then transferred to the fetus remains. Because the infant was an otherwise clinically healthy child, some occult triggering factor probably had a role in the development of the herpes zoster. Perhaps because her immune system was not fully developed, she could not produce adequate VZV antibodies, and she developed herpes zoster. Although zoster involving the first branch of the trigeminal nerve is an indication for treatment with acyclovir (5), the child was not offered any specific treatment The Journal of Dermatology Vol. 30: 346–347, 2003