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Varicella zoster virus (VZV) causes two distinct clinical entities: varicella or chickenpox, and herpes zoster or shingles. Chickenpox, a ubiquitous and extremely contagious infection, is usually a benign illness of childhood characterized by an exanthematous vesicular rash. With reactivation of latent VZV (which is most common after the sixth decade of life), herpes zoster presents as a dermatomal vesicular rash, usually associated with severe pain.(1)
Primary infection with varicella is most likely to take place via the respiratory tract. It is thought that the virus begins to replicate in the nasopharynx, eventually invading the reticuloendothelial system, ultimately leading to the development of the viremia and the appearance of the characteristic lesions of chickenpox. The mechanism of reactivation of VZV that results in herpes zoster is unknown. It is postulated that the virus infects the dorsal root ganglia during chickenpox infection, and remains latent until reactivated.
Most patients presenting with herpes zoster have no history of recent exposure to individuals with VZV infection. Herpes zoster, more commonly known as shingles, can occur at any age, but seems to occur with the greatest frequency in the sixth to eighth decade of life. It has also been suggested that approximately 2 percent of patients who suffer from herpes zoster will suffer a second episode of infection. The prevalence of zoster in HIV-infected individuals appears higher than in other age-matched immunocompetent persons and seems to reliably herald the loss of cell-mediated immunity and progression to AIDS.(2, 3)
The onset of the disease is often heralded by the presence of pain within a dermatome. The pain is often quite severe, and may continue throughout disease progression. The typical history is one of several days of itching, tingling, burning, or pain in a dermatomal distribution that is followed by a vesicular eruption consisting of clear vesicles on an erythematous base. The vesicles become cloudy, dry, and crust over in about one to two weeks.(4) Most frequently found in the thoracic dermatomes, fully two-thirds of cases are found in T-5 to T-10. The lesions are generally few in number and form only for a period of three to five days. The total duration of the disease is generally between 7-10 days; however, it may take as long as two to four weeks for the skin to return to normal.
Approximately 45 percent of patients over 50 who develop shingles will experience pain persisting for more than six weeks after vesicles clear. This is known as postherpetic neuralgia, and is intense, burning, hyperpathic, and unrelenting. It is almost never seen in children who develop zoster, and is a rarity among adults less than 50 years old. When branches of the trigeminal nerve are affected, lesions may appear on the face, in the mouth, in the eye, or on the tongue. In a syndrome known as Ramsay-Hunt syndrome, which affects the geniculate ganglion of the facial nerve, pain and vesicles occur in the external auditory canal, and patients lose the sense of taste in the anterior two-thirds of the tongue and develop ipsilateral facial palsy.
Like chickenpox, herpes zoster is more severe in the immunocompromised host, with vesicles continuing to form for over a week. Scabbing is often not complete until three weeks into the illness. Patients with Hodgkin's disease and non-Hodgkin's lymphoma are at greatest risk for the development of shingles. Cutaneous dissemination occurs in about 40 percent of the patients affected, and of these patients, the risk of serious complications is increased by 5-10 percent.
Another population at much greater risk of developing shingles are individuals who have received a bone marrow transplant. Thirty percent of cases of post-transplantation VZV infection occur within one year (50 percent of these within nine months); 45 p
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