Disseminated cutaneous herpes zoster—A frequently misdiagnosed entity

Dear Editors, There are many myths about herpes zoster (HZ) that can affect the diagnosis and treatment of the patient. HZ is described as a localised unilateral infection to one or more contiguous dermatomes. In clinical practice, there are cases of disseminated HZ or its lesions that cross the border line (bilateral HZ). Disseminated cutaneous HZ is misdiagnosed frequently, due to lack of information and rarity of the reports; sparse cases have been described in immunocompromised patients, but in healthy persons is still uncommon. We describe a case of disseminated cutaneous HZ in an apparently healthy non-elderly man, treated with systemic acyclovir and full recovery and review the literature. All cases of disseminated cutaneous HZ should be rapidly recognised and treated, followed by a thorough evaluation of the patient for identifying a hidden immunosuppressive condition. A 67-year-old male patient with a past medical history of arterial hypertension was examined for a dermatomal HZ associated with scattered non-dermatomal herpetic lesions on the trunk, face, and right inferior limb (Figures 1 and 2). He was in very good health condition, completely asymptomatic. Clinical examination and evaluation were not able to discover an underlying immunosuppressive condition. Based on the clinical suspicion of disseminated HZ and very high anti-Varicella-zoster virus (VZV), IgG antibody titre of 1500 (>4.0 is defined as positive) treatment with oral acyclovir was started, expecting the viral culture (which later proved to be positive and finally concluded the diagnosis). Complete recovery of skin lesions was achieved with a 7-day treatment with acyclovir. He was followed up for 6 months with no relapse and still without any immunosuppressive parameter. Recently, rare, but interesting cases of disseminated HZ have been reported, raising the disputes over diagnosis and, most importantly, recognising the clinical entity in daily clinical practice. VZV is a double-stranded DNA virus, from the alpha herpes virus group, that causes varicella-chickenpox (as an acute infection) and HZ-shingles (reactivation of VZV from dorsal root ganglia).1 The risk of HZ rises in the fifth decade of age and continues to increase by age.2 It has been proved that more than 95% of not-vaccinated immunocompetent persons, older than 50, are seropositive for VZV, so at high risk to develop HZ.3 Highest risk of reactivation of VZV is reserved to immunocompromised individuals, especially leukaemia, post-organ, and stem cell transplant.1, 4 The definition of disseminated HZ is, someway, not clear, because debates exist on the number of scattered lesions outside the involved dermatomes. Typical lesions of HZ are represented by cluster of vesicles on an erythematous base associated with pain, paraesthesia, and itch along one or two adjacent dermatomes. In case of disseminated HZ, scattered herpetic lesions are identified on other areas of the body; number of these lesions can vary from a few to more than 20 and the diagnosis of disseminated HZ can be made clinically.5 Diagnosis is made by clinical grounds, but confirmation can be obtained by polymerase chain reaction, viral culture or, rarer, by direct fluorescent antibody analysis.1 Another opinion is that disseminated HZ should/may include diffuse typical rash, encephalitis, hepatitis, and pneumonitis occurring in a compromised individual; this form is named severe disseminated HZ or atypical HZ.6 Typical HZ incidence increases with age due to decreased specific VZV cell-mediated immunity within elderly patients.7 It has been thought that, almost exclusively, disseminated HZ appears with immunosuppression: human immunodeficiency virus infection, due to impaired T cell immune response to VZV, or transplant solid organ and stem cell recipients, who develop a reduced VZV cellular response and specific IgG antibody avidity.8 Being aware of this type of HZ, during last years, more and more cases have been published, raising the susceptibility of the diagnosis especially in 'target group population'. A case of a diabetic patient and disseminated cutaneous VZV infection associated with multiple cerebral infarcts caused by VZV vasculopathy was described.9 Reports of cases of disseminated HZ in non-immunosuppressed patients are, however, rare and raise the question of a neglected immune depression at the moment of diagnosis.5, 10 For clinicians, it is obligatory to recognise disseminated HZ, to impose prevention and treatment especially for immunocompromised patients and to closely monitor apparent immunocompetent individuals. The authors declare no conflicts of interest.