Case Presentation: A 29-year-old woman with a past medical history of mild intermittent asthma treated with albuterol and morbid obesity status post gastric sleeve surgery presented to the emergency department with sharp epigastric pain of two days duration. The patient was initially seen at an urgent care center and empirically treated for gastritis with omeprazole, however her pain progressively worsened and was accompanied by vomiting, prompting her presentation to the emergency department.  The physical examination revealed an uncomfortable but healthy-appearing woman with normal vital signs. Abdomen was soft with epigastric tenderness. Oropharyngeal, cardiac, pulmonary, extremity, integumentary, and neurologic exams were normal. Laboratory tests were all within normal range. HIV rapid screen was also negative and viral load undetectable. The patient underwent esophagogastroduodenoscopy, which revealed white plaque lesions extending from gastroesophageal junction to mid-esophagus. Biopsy was taken with cold forceps. The patient was initially treated with intravenous fluconazole for possible Candidaesophagitis, however she did not clinically improve. The endoscopic biopsy revealed ulcerating esophagitis and marked atypia. Immunostains for herpes simplex virus (HSV) 1 and 2 were strongly positive in the squamous lining cells. In addition, PAS/Alcian blue stain was negative for fungal organisms or goblet cells. The patient was diagnosed with HSV esophagitis; intravenous acyclovir was initiated. The patient’s symptoms resolved by the third day of antiviral treatment, and she was discharged home. She completed 14-day course of antiviral therapy with valacyclovir. Serum HSV-1 IgG was undetectable during the hospitalization; lab work obtained 4 weeks after discharge revealed positive HSV-1 IgG, confirming HSV-1 seroconversion.

Discussion: Typical endoscopic findings of HSV esophagitis include multiple discrete or coalescent ulcerations of mid-distal esophagus. White mucosal plaques involving the esophagus are a classic endoscopic finding in Candida esophagitis, however HSV esophagitis may have a similar endoscopic appearance. White exudate may be present in 40% of HSV esophagitis cases. HSV esophagitis in the immunocompetent host is an uncommon entity that presents a diagnostic challenge—it may occur in absence of oral lesions or prior HSV infection. This diagnosis may be considered in patients treated for Candidaesophagitis who do not improve with antifungal therapy. Definitive diagnosis of HSV esophagitis may be achieved through endoscopic biopsy.

Conclusions: White mucosal plaques in the esophagus typically lead to diagnosis of Candida esophagitis, however when confronted with this manner of esophageal lesion, clinicians should maintain suspicion for entities other than Candida esophagitis to avoid misdiagnosis.