Case Presentation: A 65 yo female with fatty liver, IBS, and Gilbert syndrome presented with 3 weeks of persistent, non-bloody, non-mucoid diarrhea. No recent travel, sick contacts, or changes in eating habits prior to onset. Illness began with subjective fever and watery diarrhea, and she sought treatment twice in the ED. Workup included testing for Clostridium Difficile (CD), SARS-Cov-2, stool cultures, and CT abdomen and were all unremarkable. Patient was given fluids and anti-diarrheal medication and was admitted to the hospital with ongoing diarrhea 11 days after symptom onset. Vital signs were stable, physical exam with diffuse abdominal tenderness. GI recommended repeat stool culture, fecal leukocytes, O&P, CD testing, fecal elastase, calprotectin, and celiac antibody testing which were all negative. Colonoscopy with no acute findings. She was discharged 5 days later on ciprofloxacin which she discontinued due to myalgias. She was readmitted 4 days later for similar symptoms. Infectious disease was consulted and found had eaten a bag of lettuce prior to onset of symptoms raising concern for Cyclospora, although acid fast smear for cyclospora was negative. HIV, norovirus, rotavirus, cryptosporidium, and giardia were negative. The suspicion for Cyclospora remained high, PCR testing was sent out and the patient was empirically started on bactrim. PCR testing was positive for Cyclospora and her diarrhea resolved at discharge. She was later diagnosed as having post-infectious irritable bowel syndrome (PI-IBS) due to Cyclospora infection.
Discussion: Here we present a rare, and to our knowledge the first documented case of Cyclospora-induced post-infectious inflammatory bowel syndrome (PI-IBS) in an immunocompetent host. PI-IBS presents as abdominal discomfort, bloating, and diarrhea that continue despite clearance of the pathogen (1). Incidence and prevalence of PI-IBS is variable, with global numbers ranging from 5-32% (1). PI-IBS is typically associated with bacterial pathogens, with other studies showing possible pathogenetic link between IBS and parasites (2,3). However, there are no documented cases of Cyclospora-induced PI-IBS. Cyclospora infection is usually more severe in immunocompromised patients and self-limited in immunocompetent hosts (4). Anorexia, nausea, flatulence, diarrhea, low-grade fever, and weight loss are common (5). Complications include cardiac arrest (6), biliary disease and acalculous cholecystitis in AIDS patients (7-9), Guillain-Barré syndrome (10), and reactive arthritis syndrome (11). Treatment is typically Bactrim, with longer durations or higher doses for immunocompromised hosts (3). PI-IBS has an encouraging prognosis with gradual improvement and remission of symptoms in most patients. (1) Treatment is the same as treatment of IBS as they are clinically difficult to distinguish from one another. Probiotics have been proven effective in preventing or attenuating acute GE (1). No study has yet assessed the efficacy of interventions that modulate gut flora for preventing or treating PI-IBS.
Conclusions: Cyclospora can be an unlikely infection, however suspicion should be maintained even in immunocompetent patients when they have typical presentations. This is possibly the first documented case of Cyclospora-induced PI-IBS in an immunocompetent host. Treatment is the same for PI-IBS as for IBS. Further studies need to be conducted to assess other interventions for treatment and prevention.