Small Vessel Vasculitis in Herpes Zoster—Discussion of Current Aspects of Varicella Zoster Virus Vasculopathy

Abstract: Varicella zoster virus (VZV) vasculopathy was initially described as herpes zoster ophthalmicus with contralateral hemiplegia in 1896. VZV is able to infect endothelial cells directly, leading to a thickened intima and vascular remodeling due to inflammation. Therefore, a spectrum of vasculopathies is induced, ranging from a discrete capillaritis-to-granulomatous vasculitis and obliterative angiitis. Cutaneous vasculitic changes sui generis with leukocytoclasia, cell debris, vascular damage, and endothelial swelling are very rare feature of herpetic infections in skin biopsies. We report an immunocompetent patient who presented with a rare form of cutaneous VZV infection of the upper leg characterized by vasculitic changes of the small vessels without typical herpetic epidermal features or neural involvement. Intriguingly, the vasculitis appeared prior to the characteristic vesicular rush without any pain symptoms. Because VZV can cause vasculopathic damage mainly within the central nervous system in immunocompetent and immunosuppressed patients, we recommend continuous clinical controls to recognize central symptoms that are related to VZV vasculopathy or giant cell arteriitis.

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