- Primary varicella infection (chickenpox) and herpes zoster are both caused by varicella zoster virus (VZV).
- Herpes zoster (shingles) represents activation of varicella zoster virus from cranial or dorsal root ganglion, thus affecting the skin in a dermatomal distribution. It can disseminate and can have internal organ involvement.
- The hallmark lesion of primary varicella and herpes zoster is a vesiculopustule. In zoster, multiple lesions are grouped and/or present within a dermatomal distribution.
- A potential complication of herpes zoster is post-herpetic neuralgia (PHN), the development of persistent pain and/or dysesthesia at the sites previously affected by herpes zoster. There is limited evidence to support a definitive intervention to prevent the development of PHN. Management of PHN includes nerve-directed therapies.
- Primary varicella infection and disseminated zoster can be a dermatologic emergency in patients who are immunocompromised, including pregnant women.
Varicella zoster virus (VZV) is a herpes family virus that causes primary varicella infection and herpes zoster. Prior to the introduction of varicella vaccination, the lifetime prevalence of primary varicella was approximately 90%, with most cases occurring during childhood. This highly contagious virus is spread through respiratory and salivary secretions and results in nonspecific symptoms (fever, headache, malaise) followed by a generalized pruritic vesiculopustular eruption. Infection with primary varicella leads to lifelong immunity in approximately 90% of cases; the lifetime prevalence of having additional infections with primary varicella is estimated at 13%. Since the introduction of childhood varicella vaccination, the rates of primary varicella infection have been dramatically reduced. Typically, primary varicella infection is self-limited and requires only symptomatic treatment. However, infection of adults may be severely debilitating, requiring systemic antiviral medication and possibly hospitalization. Primary varicella infection of pregnant individuals may result in intrauterine infection (especially in the first or second trimesters of pregnancy), resulting in congenital varicella syndrome, a syndrome marked by significant morbidity and mortality to both mother and child.
Herpes zoster represents the reactivation of VZV from the cranial or dorsal root ganglion with presentation of a painful vesicular rash in a dermatomal distribution. Prior to the development of the zoster vaccine, the lifetime prevalence of zoster in the adult American population was 10-20% with increased risk with advancing age; the prevalence of zoster approached 50% in individuals over the age of 85. Zoster vaccination, generally recommended for individuals over the age of 60, is safe and significantly reduces the risk of zoster reactivation. Patients with cranial nerve V1 involvement require ophthalmic evaluation to rule out the possibility of ocular involvement. In very severe cases, herpes zoster may be systemically disseminated, resulting in a generalized vesicular eruption with possible internal organ involvement; immunocompromised and immunosuppressed individuals are at high risk for disseminated zoster. Cases of disseminated zoster with central nervous involvement may be fatal. Patients with disseminated zoster are highly contagious, and shed virus through respiratory and salivary secretions in addition to skin, requiring both contact and respiratory isolation.
In localized (single dermatome involvement) herpes zoster, treatment with systemic antivirals is the standard of care, especially in patients presenting with early lesions; early intervention with systemic antivirals may thwart the development of vesicular lesions. Patients are considered infectious through direct viral shedding from skin lesions until these lesions crust over and thus require strict contact precautions (especially from immunocompromised, pregnant patients, and patients who have never had varicella before). Although there is excellent data that systemic antivirals reduce the duration of zoster lesions, reduce associated pain, and reduce viral shedding, there is limited evidence to support a definitive intervention to prevent the development of post-herpetic neuralgia (PHN), including zoster vaccination. PHN is the development of persistent pain and/or dysesthesia at the sites previously affected by herpes zoster. In one study, the incidence of PHN at 9 years (defined by pain within the past 12 months at the site affected by herpes zoster) following herpes zoster was 21%, and risk factors associated with the development of PHN included: pain preceding the development of cutaneous rash by >72 hours, moderate to severe pain with rash, severity of rash, and female gender. Management of PHN includes nerve-directed therapies.