Resident Physician ZUCKER SCHOOL OF MEDICINE, NORTHWELL HEALTH AT MATHER HOSPITAL Port Jefferson, New York, United States
Introduction:
Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized by inflammation of the colonic mucosa. This case highlights the interplay between rotavirus infection and UC flare-up, underscoring the importance of considering infectious causes in patients presenting with IBD exacerbations. Current literature suggests that viral infections can mimic IBD symptoms and trigger flares, complicating management strategies.
Case Presentation:
A 23-year-old man diagnosed with ulcerative colitis (UC) in August 2024 and treated with mesalamine, visited the hospital after experiencing nausea, vomiting, and bloody diarrhea for six days. He had no history of coming into contact with sick individuals or recent antibiotic use. Initially, he believed his symptoms were due to anxiety related to starting a new job. However, upon examination, he appeared dehydrated and had a rapid heartbeat. Laboratory tests revealed an elevated white blood cell count (20,000/µL), abnormal liver function, and high inflammatory markers (CRP 248 mg/L, ESR 84 mm/hr). Imaging showed pancolitis. He was initially treated for a UC flare with intravenous hydrocortisone, but his symptoms persisted. Further investigation revealed that he had a positive rotavirus PCR in stool cultures, while bacterial and protozoal cultures were negative. Serologic and autoimmune tests, including tests for cytomegalovirus (CMV), Epstein-Barr virus (EBV), and autoimmune hepatitis, were negative, except for mildly elevated α1- antitrypsin levels. Stool tests confirmed a rotavirus infection. His treatment was changed to oral budesonide, along with pantoprazole and probiotics for supportive care. His symptoms improved, with reduced diarrhea and normalization of lab markers. He continued budesonide and mesalamine upon discharge. It was later demonstrated that continuing mesalamine during the UC flare, even in the presence of a rotavirus infection, was clinically effective. After the infection resolved, mesalamine remained a reliable treatment for long-term management, eliminating the need to switch to a biological agent such as infliximab. This approach proved successful in controlling both the acute flare and maintaining remission.
Conclusion:
Patients with UC are at risk of disease exacerbations triggered by both endogenous and exogenous factors, including infections. Viral infections, particularly with pathogens like rotavirus, have been implicated in triggering UC flares by exacerbating the underlying inflammation. This case illustrates the interaction between infectious processes and UC exacerbations, emphasizing the need for comprehensive evaluation in patients with IBD experiencing flare-ups. The interplay between rotavirus infection and UC highlights the complexity of managing IBD exacerbations in the context of concurrent infections.
