Varicella zoster virus transmission in the vaccine era: unmasking the role of herpes zoster.

Varicella (chickenpox) is a highly contagious disease caused by varicella zoster virus (VZV). After infection, the virus remains dormant in sensory dorsal root ganglia. Reactivation of latent VZV is associated with cutaneous disease occurring in $1 dermatomes, termed herpes zoster (HZ). Historically, HZ has been considered significantly less infectious than varicella and has not been thought to play an important role in person-to-person transmission. Since the licensure of the varicella vaccine in 1995 and the more recent recommendation that a second dose of vaccine be given to children aged 4–6 years [1], the epidemiology of pediatric varicella infection has shifted dramatically [2]. Efforts to quantify the burden of varicella in the community since vaccine licensure have been hindered by the absence of mandatory case-based reporting in most jurisdictions [3]. The article by Viner et al in this issue of the journal [4] provides important new insights into the epidemiology and transmissibility of VZV in a highly immunized, healthy pediatric population. The authors analyzed data obtained through a combination of active and passive surveillance for both varicella and HZ in Philadelphia schools and day care centers during 7 academic years. Cases were linked to the Philadelphia Department of Public Health immunization registry for ascertainment of vaccine status. Through this comprehensive surveillance system, 2296 cases of VZVassociated infection were identified, with 28% categorized as secondary varicella. Much of what is known about VZV transmission dynamics in the community comes from outbreak investigations at elementary schools or day care centers. In these settings, varicella attack rates among children who had previously received a single dose of varicella vaccine ranged from 12%–42% [5–7]. A recent report found that prior receipt of a second dose of vaccine did not appreciably decrease the attack rate during a school outbreak [8]. In contrast, in an elementary school outbreak during which the second dose of vaccine was given as an intervention for outbreak control, the attack rate was reduced from 43% among children who had received only a single vaccination to 5% among 2-dose recipients [9]. Large-scale, school-based varicella outbreaks such as these serve as important sentinel events but may not be representative of the true burden and infectivity of VZV in the community. In the study by Viner et al, .80% of epidemiologically linked transmissions involved ,4 secondary cases and, in the absence of a dedicated varicella surveillance system, would be unrecognized and unreported. Despite the continued documentation of outbreaks among immunized school children, the varicella vaccine epitomizes a public health success story. In the prevaccine era, varicella was an almost universal disease of childhood. After the widespread implementation of pediatric vaccination in the United States, incidences of VZV-related infection, hospitalization, and death have all markedly declined [10, 11]. In the present study, .90% of children who developed secondary varicella had received $1 doses of vaccine before the onset of infection, representing vaccine failures. However, even in these breakthrough cases, the benefits of vaccination are evident. As has been reported elsewhere [12, 13], .70% of breakthrough varicella cases had mild disease characterized by ,50 skin lesions. Vaccinated varicella cases were associated with a significantly lower proportion of secondary cases compared with unvaccinated cases, presumably related to lower virus burden and shorter duration of viral shedding. Finally, there was a significant decline in the incidence of all VZV-related infections in Philadelphia schools beginning in 2007, Received 9 December 2011; accepted 12 December 2011; electronically published 27 March 2012. Correspondence: Karen C. Bloch, MD, MPH, Division of Infectious Diseases, Vanderbilt University Medical Center, A-2200, Medical Center North, Nashville, TN 37232 ([email protected]). The Journal of Infectious Diseases 2012;205:1331–3 The Author 2012. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected] DOI: 10.1093/infdis/jis214