S4864 A Viral Twist to a Familiar Flare: HSV Colitis in Inflammatory Bowel Disease

Introduction: Herpes simplex virus (HSV) colitis is a rare infection, mostly documented in immunocompromised individuals, including patients with inflammatory bowel disease. HSV colitis often has associated morbidity and mortality from complications such as bowel necrosis or perforation. The clinical presentation of HSV colitis can be identical to an exacerbation of colonic inflammatory bowel disease, often delaying diagnosis and complicating management. Case Description/Methods: A 26-year-old woman with history of ulcerative pancolitis, previously in clinical remission with vedolizumab, presented with bloody diarrhea, abdominal pain, and weight loss after being off of vedolizumab for 7 months. Laboratory and imaging findings revealed a C-reactive protein of 13.4 mg/L, fecal calprotectin >3000 mg/g, and pancolitis on abdominal computed tomography. Infectious workup including cytomegalovirus, Clostridium difficile and other stool pathogen testing, was negative. Patient was initiated on intravenous corticosteroid therapy, however, had lack of clinical improvement. On day 3 of admission, a flexible sigmoidoscopy revealed continuous, severe mucosal inflammation in the descending colon (graded as Mayo 3) and multiple well-demarcated, punched-out ulcers in the sigmoid colon. Histopathology demonstrated moderate chronic active colitis with HSV viral cytopathic effect confirmed via immunohistochemical staining. Given the HSV colitis diagnosis, intravenous acyclovir was initiated, and intravenous corticosteroids were transitioned to oral prednisone. Her symptoms improved rapidly within 3 days, and she was discharged on a 2-week valacyclovir course. On follow-up, patient continued to do well and was ultimately restarted on vedolizumab and continued suppressive valacyclovir with colonoscopy after 6 months revealing Mayo 0 colon and resolution of HSV changes. Discussion: HSV colitis can be indistinguishable in patients with ulcerative colitis (UC), as it can mimic UC flare symptoms, often requiring endoscopic and histologic confirmation. Deep, well-circumscribed ulcers are a unique feature of HSV colitis. Early initiation of anti-viral therapy and a reduction or temporary cessation of immunosuppressive agents is needed for HSV colitis treatment. In our case, balancing management of a UC flare with the need to treat HSV infection was critical. Withholding immunosuppressives carries the risk of worsening UC, while continued steroids may promote viral dissemination and potential tissue necrosis. This case underscores the importance of considering rare infectious triggers of UC in patients with refractory colitis symptoms.