Herpes zoster (shingles) results from an inadequate cell-mediated immune response to latent VZV reactivation (see chapter 21). Zoster occurs only by reactivation of the patient’s own virus; it is not acquired from other patients with zoster or varicella.1
HZ presents clinically as a unilateral vesicular rash in a dermatomal distribution in the majority of cases. The dermatomal distribution of the rash is the key diagnostic feature. In 70–80 percent of HZ cases in older adults, prodromal pain and/or itching occurs three to four days before the appearance of the rash.2 In the majority of patients, HZ is an acute and self-limiting disease, with the rash lasting 10 to 15 days. However, complications can occur, especially with increasing age.
The majority of zoster cases occur in adults aged 40 years or older. Herpes zoster does occur in infants and children, but it is uncommon. When it occurs in those aged under 2 years it may reﬂect in utero chickenpox, with the greatest risk arising following exposure between 25 and 36 weeks’ gestation, with reactivation in early life.
A common complication of zoster is post-herpetic neuralgia, a chronic, often debilitating pain condition that can last months or even years. The risk for post-herpetic neuralgia in patients with zoster is 10–18 percent, although it is uncommon in healthy children and young people and the risk rises with age. Another complication of zoster is eye involvement, which occurs in 10–15 percent of zoster episodes and can result in prolonged or permanent pain, facial scarring and loss of vision.
Herpes zoster occurs more commonly in immunosuppressed individuals (eg, cancer treatment or organ transplant patients) and those with human immunodeficiency virus (HIV). Up to 10 percent of children treated for a malignant neoplasm may develop herpes zoster. In immunosuppressed patients, extensive viraemia in the absence of a vigorous immune response can result in a disseminated form of HZ that includes severe multi-organ disease.2