Yuri Hanada1, Sahil Khanna2, Edward V Loftus2, Laura E Raffals2, Darrell S Pardi3. 1. Department of Medicine, Johns Hopkins Hospital, Baltimore, Maryland (formerly with Mayo Clinic School of Medicine, Mayo Clinic College of Medicine and Science, Rochester, Minnesota). 2. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. 3. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. Electronic address: scipubs@mayo.edu.
Abstract
BACKGROUND & AIMS: Clostridium difficile infection (CDI) causes flares in patients with inflammatory bowel disease (IBD). We investigated the frequency and outcomes of non-CDI bacterial enteric infections in symptomatic patients with IBD. METHODS: We performed a retrospective study of patients with ulcerative colitis (UC) or Crohn's disease (CD) from whom stool samples were collected and analyzed by PCR or culture for bacterial pathogens (Campylobacter jejuni or C coli, Salmonella species, Shigella species, enteroinvasive Escherichia coli, shiga toxin-producing E coli, or Yersinia species) from November 19, 2011, through June 30, 2014. Patients were excluded if they had nonbacterial infections or no symptoms. Data were collected from medical records on IBD duration, treatment, age at diagnosis, and presence of concurrent CDI. Patients were followed for 1 year after the date of infection resolution or until date of last follow-up in the health record. Each patient with an enteric infection was matched with 2 patients with IBD flares and negative results from stool tests (non-infected control) and 2 patients with IBD and CDI (CDI control), adjusted for age (within 5 years at the time of stool test), sex, and IBD subtype. Outcome measures included IBD therapy escalation and hospitalization. RESULTS: Of 9247 patients with IBD seen during the study period, stool samples were tested from 1345 patients (50% with UC and 50% with CD). There were 3 positive results (detection of bacterial pathogens) from 339 PCR analyses of stool samples from 296 patients with UC (0.88%) and 12 positive results from 486 cultures of stool samples from 418 patients with UC (2.5%). There was 1 positive result from 355 PCR analyses of stool samples from 311 patients with CD (0.28%) and 9 positive results from 496 cultures of stool samples from 413 patients with CD (1.8%). Of the 19 patients followed beyond infection, 9 patients required escalation of their IBD therapy (47%)-most commonly addition of an immunomodulator (5 patients) or a biological agent (3 patients)-compared with 34% of CDI controls and 66% of non-infected controls (P < .001). Higher proportions of patients with non-CDI bacterial infections were in remission 1 year after their infection (89%) than patients with CDI (55%) or negative results of stool tests (63%; P = .04). We did not observe differences in hospitalization, emergency department visits, or surgical interventions among groups. CONCLUSIONS: In a retrospective study of patients with an IBD flare, we detected non-CDI bacterial infections in fewer than 3% of those who were tested. Higher proportions of patients with non-CDI bacterial infections were in remission in the year after their infection than patients with CDI.
BACKGROUND & AIMS:Clostridium difficileinfection (CDI) causes flares in patients with inflammatory bowel disease (IBD). We investigated the frequency and outcomes of non-CDI bacterial enteric infections in symptomatic patients with IBD. METHODS: We performed a retrospective study of patients with ulcerative colitis (UC) or Crohn's disease (CD) from whom stool samples were collected and analyzed by PCR or culture for bacterial pathogens (Campylobacter jejuni or C coli, Salmonella species, Shigella species, enteroinvasive Escherichia coli, shiga toxin-producing E coli, or Yersinia species) from November 19, 2011, through June 30, 2014. Patients were excluded if they had nonbacterial infections or no symptoms. Data were collected from medical records on IBD duration, treatment, age at diagnosis, and presence of concurrent CDI. Patients were followed for 1 year after the date of infection resolution or until date of last follow-up in the health record. Each patient with an enteric infection was matched with 2 patients with IBD flares and negative results from stool tests (non-infected control) and 2 patients with IBD and CDI (CDI control), adjusted for age (within 5 years at the time of stool test), sex, and IBD subtype. Outcome measures included IBD therapy escalation and hospitalization. RESULTS: Of 9247 patients with IBD seen during the study period, stool samples were tested from 1345 patients (50% with UC and 50% with CD). There were 3 positive results (detection of bacterial pathogens) from 339 PCR analyses of stool samples from 296 patients with UC (0.88%) and 12 positive results from 486 cultures of stool samples from 418 patients with UC (2.5%). There was 1 positive result from 355 PCR analyses of stool samples from 311 patients with CD (0.28%) and 9 positive results from 496 cultures of stool samples from 413 patients with CD (1.8%). Of the 19 patients followed beyond infection, 9 patients required escalation of their IBD therapy (47%)-most commonly addition of an immunomodulator (5 patients) or a biological agent (3 patients)-compared with 34% of CDI controls and 66% of non-infected controls (P < .001). Higher proportions of patients with non-CDI bacterial infections were in remission 1 year after their infection (89%) than patients with CDI (55%) or negative results of stool tests (63%; P = .04). We did not observe differences in hospitalization, emergency department visits, or surgical interventions among groups. CONCLUSIONS: In a retrospective study of patients with an IBD flare, we detected non-CDI bacterial infections in fewer than 3% of those who were tested. Higher proportions of patients with non-CDI bacterial infections were in remission in the year after their infection than patients with CDI.
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