Gradual Immunologic Decline Explains Frequency of Herpes Zoster Among the Elderly
John M Conly, MD,CCFP, FRCPC, FACP
Consultant, Infectious Diseases
Director, Infection Prevention and Control
University Health Network (Toronto General,
Toronto Western and Princess Margaret Hospitals)
Professor of Medicine, University of Toronto
Introduction
Although it is now understood that varicella-zoster virus (VZV) is the etiologic agent for both varicella and herpes zoster, it is of historical interest to note that in the early medical literature, the clinical illnesses of varicella and herpes zoster were considered separate entities. Just six decades ago it was still taught at Harvard University that these viruses were unrelated.1 In 1943, a pediatrician named Garland suggested that zoster may be due to the reactivation of a latent varicella virus,2 but it was not until 1958 that VZV was definitively recognized as the etiologic agent for both varicella and zoster.3,4 The VZ virus is a DNA virus and is a member of the Herpesviridae family bearing many distinct similarities to other members of this group of viruses. The virus is spread by direct contact, by droplet and airborne routes from vesicular fluid of skin lesions, or from secretions from the respiratory tract.5 Transplacental transmission has also been documented.
