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Bullous Viral Eruptions

»What do herpes simplex (HSV) virus and varicella-zoster virus (VZV) have in common?
»What happens during primary HSV infection?
»What about recurrent infection?
»What is the difference between a primary and an initial HSV infection?
»How is HSV transmitted?
»How long is incubation period for HSV (i.e., the time from initial infection to appearance of vesicles)?
»Define asymptomatic shedding.
»Can you be infected with HSV and not know it?
»How do HSV-1 and -2 differ?
»How do you diagnose HSV infection?
»How is a Tzanck smear performed?
»What are the drugs of choice for treatment of HSV?
»When is chronic suppressive therapy indicated?
»Are patients with genital herpes at greater risk for becoming infected with the human immunodeficiency virus (HIV)?
»What recommendations can you make to a patient with genital herpes to reduce the risk of transmission to his or her partner?
»Can HSV infect the skin in areas other than around the mouth or anogenital areas?
»How does a baby get herpes? Is it a serious problem?
»Describe the natural history of varicella.
»What is shingles?
»Can herpes zoster be recurrent?
»What is disseminated zoster?
»Is herpes zoster contagious?
»What is postherpetic neuralgia?
»How do you diagnose VZV infection?
»What is the treatment for varicella?
»How about herpes zoster?
»Should I be concerned about the patient with herpes zoster involving the tip of the nose?
»Who should get the herpes zoster vaccine?
»What is hand, foot, and mouth disease?
»What is orf?

 
 
 

What are the drugs of choice for treatment of HSV?

There are three systemic antiviral agents routinely used for the treatment of HSV: acyclovir, valacyclovir, and famciclovir (Table 25-1). Valacyclovir is the L-valyl ester of acyclovir with a bioavailability 3 to 5 times greater than acyclovir. Famciclovir is the diacetyl-6-deoxy analog of penciclovir. It is well absorbed and has a long intracellular half-life. Both valacyclovir and famciclovir offer the advantage of less frequent dosing compared to acyclovir. All three drugs are generally safe and highly effective because of their very specific antiviral activity. The antiviral drug is preferentially taken up by infected cells, where it must be converted to its active form by the viral enzyme thymidine kinase. The active form preferentially inhibits viral DNA synthesis, with little impact on host cell metabolism.

Cernik C, Gallina K, Brodell RT: The treatment of herpes simplex infections: an evidence-based review, Arch Intern Med 168: 1137–1144, 2008.