Herpes simplex esophagitis (HSE) is commonly identified in immunosuppressed patients. It is rare among immunocompetent patients and almost all of the reported cases are due to HSV-1 infection. HSV-2 esophagitis is extremely rare. We report the case of a young immunocompetent male who presented with dysphagia, odynophagia, and epigastric pain. Endoscopy showed multitudes of white nummular lesions in the distal esophagus initially suspected to be candida esophagitis. However, classic histopathological findings of multinucleated giant cells with eosinophilic intranuclear inclusions and positive HSV-2 IgM confirmed the diagnosis of HSV-2 esophagitis. The patient rapidly responded to acyclovir treatment. Although HSV-2 is predominantly associated with genital herpes, it can cause infections in other parts of the body previously attributed to only HSV-1 infection.
Herpes simplex virus (HSV) has been recognized with increased frequency as an opportunistic invader of the esophagus in immunosuppressed or severely ill patients as a result of primary infection or more commonly viral reactivation [
We present a case of a 28-year-old gentleman who presented to the hospital with four days of progressive dysphagia, odynophagia, and epigastric pain and two days of subjective fever. He was unable to tolerate oral intake and had lost approximately 8 pounds over the last several days. He had been in a sexual relationship with one partner for six months and was unaware of any potential exposure to HSV. His past medical history is significant for asthma controlled without steroids. At admission he was febrile with a temperature of 102.8 and tachycardia of 110/min. There were no oral or pharyngeal lesions. He had tenderness in the epigastric area, but no palpable masses or hepatosplenomegaly. Laboratory workup was significant only for atypical lymphocytes noted on smear. Esophagogastroduodenoscopy (EGD) revealed small ulcers with overlying exudate with normal intervening mucosa with some areas of confluence in the lower and middle third of the esophageal mucosa (Figure
Endoscopy shows multitudes of small ulcers with normal intervening mucosa (a) and areas of confluent plaque-like lesions (b) in the distal esophagus.
(a) H&E of the esophagus showing mucosal necrosis with smudgy nuclear chromatin and multinucleation, highly characteristic of HSV infection (400x). (b) Showing positive immunohistochemistry for HSV (400x).
HSE is common in immunosuppressed patients. HSE is rare, but distinct entity in immunocompetent patients. [
HSV-1 is most commonly associated with HSE, although HSV-2 infections were reported rarely [
This case also presented with a unique challenge for endoscopic diagnosis of HSE. Initially, due to the white-plaque-like raised appearance of the lesions, candida esophagitis was suspected. There were more characteristic discrete nummular lesions hidden around the large plaque-like lesions. HSV-2 was ultimately diagnosed by immunohistochemistry for HSV and IgM antibodies for HSV-2. IgM/IgG antibodies were not detected for HSV-1. Although tissue immunohistochemistry and PCR for HSV-2 would have been alternate methods to confirm the diagnosis, due to the technical difficulties, we were not able to perform them. However, we believe that the evidence is compelling in this case to confirm the diagnosis of HSV-2 esophagitis.
The authors have no conflict of interests to disclose.