Przegla̜d Gastroenterologiczny | 2021
Herpes simplex virus-2-associated esophagitis in immunocompetent host
Abstract
Herpes esophagitis (HE) is typically caused by herpes simplex virus type 1 (HSV-1), although less frequently, it is caused by HSV type 2 (HSV-2). Most cases of HE occur in immunocompromised hosts, but occasionally immunocompetent patients develop this condition. Thus, HSV-2 esophageal infection in immunocompetent individuals is comparatively rare [1]. Canalejo Castrillero et al. performed a review of published HE cases (English and Spanish language) in immunocompetent patients from 1950 to 2009. The HSV type was identified in only 27 out 56 cases. However, among the identified cases, 96% (26) were due to HSV-1 and only 4% (1) was due to HSV-2 [1]. The overall reported incidence of HE is 1.8% [2]. Common risk factors for HE include a history of HIV, AIDS, malignancy, solid organs transplant, use of steroids, immunosuppressant medications, chemotherapy, and radiation therapy [1, 3–7]. An estimated 10–15% of bone marrow transplant patients and up to 20% of AIDS patients may develop HE [8]. The mode of esophageal infection in immunocompromised individuals is either viral reactivation or new infection, whereas in immunocompetent individuals, new infection is the primary mode [1]. We present a case of HE that is unique because it is due to HSV-2 in an immunocompetent patient who was found to have esophageal lesions, atypical for HSV-2 esophagitis on endoscopic visualization. A 31-year-old woman with a history of intravenous drug use, anemia, and recent hip fracture repair after a motor vehicle accident presented with a right foot infection. She was admitted and initially treated with antibiotics. The hospital course was complicated by an episode of hematemesis and a decline in hemoglobin (HGB) from 7 mg/dl on admission to a nadir of 6.1 mg/ dl (baseline HGB 10 mg/dl). She only noted some throat discomfort. She had no abdominal pain or tenderness on examination. A fecal occult blood test was positive. For the evaluation of a possible upper gastrointestinal bleed, she underwent esophagogastroduodenoscopy (EGD) which demonstrated an erythematous posterior oropharynx. Upper endoscopy also revealed multiple nonbleeding patches of linear ulcers involving the longitudinal folds of the proxima and distal esophagus (Figure 1). No source of active bleeding from the esophagus, stomach or duodenum was identified. Linear esophageal ulcers were thought to be due to cytomegalovirus (CMV) esophagitis on endoscopic visualization. Multiple biopsies of the esophageal ulcers were taken for diagnostic confirmation and she was empirically started on ganciclovir. Biopsy results revealed squamous epithelium with a viral cytopathic effect consistent with herpes simplex virus (Figure 2). Immunohistochemical staining was positive for HSV-2 and negative for Helicobacter pylori, CMV and HSV-1 (Figure 3). Based on the pathology results, ganciclovir was switched to valacyclovir for 2 weeks. A blood test for HIV was negative. The vast majority of HE patients are immunocompromised men with HSV-1 infections. In fact, HE is three times more common in men as compared to women [4–6]. The reason for this uneven distribution is unknown. Only a handful of HE cases due to HSV-2 have been published (Table I). Our patient reported throat discomfort which may have been part of a prodrome. Many patients do not experience prodromal symptoms such as fever, malaise, pharyngitis or respiratory symptoms [1, 3–6]. She was incidentally found to have esophagitis