Lymphadenitis caused by infection with varicella or herpes zoster virus.

The viruses isolated from patients with varicella (chickenpox) or herpes zoster (shingles) are physically and immunologically identical (1). The varicella-zoster virus (VZV) is a DNA herpes virus that multiplies only in the nucleus of permissive cells and has developmental stages similar to those of the herpes simplex virus (1). Herpesviruses are the etiologic agents of various afflictions, from localized lesions to severe generalized diseases; the latter develop in persons with inadequate immunity, either congenital or acquired as a result of therapeutic immunosuppression or HIV infection. The varicella-zoster virus is relatively unstable in culture; however, the vesicle fluid from patients is highly infectious for a long time (1). The annual incidence of varicella in the United States of about 4 million cases and the average varicella-related deaths of 145 per year have declined dramatically since the introduction of universal childhood vaccination in 1995 (2,3). However, “breakthrough varicella,” often in the form of a very mild disease, may occur in previously immunized persons (2).

Varicella, the primary disease produced in a host without specific immunity, is usually a mild, self-limited illness of young children. Herpes zoster is the recurrent form of the disease, developing in adults who were previously infected with VZV and possess circulating antibodies. It results from the reactivation of latent virus that persisted in the sensory ganglia of the cranial nerves and the spinal dorsal-root ganglia and spreads centrifugally along sensory nerves. The reactivation occurs mainly in elderly persons after decades of latency due to decreasing memory T-cell immunity to VZV (4,5). During the primary disease, the virus enters the respiratory tract and multiplies locally and in the regional lymph nodes; it is then disseminated to the blood, skin, and other organs. Herpes zoster results from the reactivation of latent virus in a susceptible adult with incomplete immunity caused by old age, trauma, infection, cancer, or immunosuppressive therapy. The incidence and severity of herpes zoster increases with advancing age; more than half of patients are older than 60 years. Recently, a vaccine to prevent reactivation of VZV has been developed (6). In immune-deficient persons, the infection may spread from the skin lesions through sensory nerves to the spinal cord or cranial nerves and cause paralysis or fatal disease (3).

In varicella (chicken pox), the onset is sudden and mild; malaise, anorexia, and slight fever are followed in 24 to 48 hours by a maculopapular eruption. The cutaneous lesions of herpes zoster (shingles) resemble those of varicella but are usually limited to one or several sensory dermatomes (4). The involvement varies from a few small vesicles to massive spread of large bullae accompanied by intense pain. The rash has a centripetal distribution and is usually more extensive and severe in older patients. The vesicular skin lesions in both varicella and herpes zoster contain high concentrations of infectious VZV (5). On rare occasions, probably as a result of immune deficiency, atypical, generalized zoster develops. The disseminated lesions are usually preceded by localized dermatomal eruptions, which in turn are preceded by an occult phase of primary viremia (7). In a 20–year-old woman presenting with a prostrating febrile illness and generalized lymphadenopathy, varicella-zoster virus was demonstrated in the lymph nodes 2.5 weeks before the appearance of characteristic skin lesions (7).