Visceral dissemination of varicella zoster virus (VZV) may follow cutaneous infection
in immunocompromized patients (e. g. bone marrow transplant recipients) [1]. However, involvement of the upper gastrointestinal tract is rare [1]
[2]
[3]
[4].
An 81-year-old man underwent upper endoscopy for heartburn, nausea, and vomiting.
There was no prior history of clinically overt immunodeficiency. Endoscopy revealed
multiple small, superficial ulcers in the esophagus, the gastric corpus and antrum,
and the duodenum ([Fig. 1 a – c]). A few days prior to endoscopic evaluation, the patient had developed a few vesicular
eruptions over his head and trunk ([Fig. 1 d]).
Fig. 1 Small superficial ulcers in the: a esophagus, b antrum, c duodenum. d Encrusted vesicular skin eruption on the patient’s neck.
Histological examination of the biopsy specimens revealed acantholysis and ballooning
of keratinocytes in the esophagus ([Fig. 2 a]). Gastric and duodenal ulcerations were surrounded by a prominent histiocytic infiltrate.
Epithelial and stromal cells showed viral cytopathic changes including enlarged hyperchromatic
nuclei with uneven borders. Nuclei appeared molded with chromatin margination and
a “ground glass” appearance. Single viral inclusions were present ([Fig. 2 b]). Polymerase chain reaction of samples from esophageal and gastric biopsies showed
positive amplification of VZV DNA (44 kDa protein gene).
Fig. 2 a Acantholysis and ballooning degeneration (arrow heads) of keratinocytes with hyperchromatic
enlarged nuclei in the esophagus (× 200). b Cytoplasmic vacuolation and ground-glass nuclei (arrow heads) of antral epithelia
(× 600). Singular “owl eye” nuclei were present (inset).
The patient improved considerably after the initiation of treatment with acyclovir
10 mg/kg three times daily for 10 days.
Multifocal gastrointestinal involvement with VZV following cutaneous dissemination
is uncommon even in immunocompromized hosts, and has not been reported in apparently
immunocompetent patients up to now [1]. After initial infection has occurred, the virus enters a latent stage in the dorsal
root ganglia [1]. Posterior sensory nerve roots contain nerve fibers from both the skin and the inner
organs [1]
[5]. Reactivation of latent VZV may thus lead to a centrifugal spread toward the skin,
as well as a centripetal spread towards the visceral organs [1]
[5]. The present case illustrates the potential visceral dissemination of herpes zoster,
causing multiple ulcers throughout the upper gastrointestinal tract of an apparently
immunocompetent individual.
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