Escherichia coli is increasingly implicated in the pathogenesis of ileal Crohn's disease (ICD), offering a potential therapeutic target for disease management. Empirical antimicrobial targeting of ileal E. coli has advantages of economy and speed of implementation, but relies on uniform susceptibility of E. coli to routinely selected antimicrobials to avoid apparent treatment failure. Therefore, we examined the susceptibility of ileal E. coli to such antimicrobials.
E. coli from 32 patients with ICD and 28 with normal ileum (NI) were characterized by phylogroup, pathotype, antimicrobial susceptibility, and presence of antimicrobial resistance genes.
In all, 17/32 ICD and 12/28 NI patients harbored ≥1 E. coli strain; 10/24 E. coli strains from ICD and 2/14 from NI were nonsuscepti-ble to ≥1 antimicrobial in ≥3 categories (multidrug-resistant). Resistance to amoxicillin/clavulanic-acid, cefoxitin, chloramphenicol, ciprofloxa-cin, gentamicin, and rifaximin was restricted to ICD, with 10/24 strains from 8/17 patients resistant to ciprofloxacin or rifaximin (P < 0.01). Adherent-invasive E. coli (AIEC) were isolated from 8/32 ICD and 5/28 NI, and accounted for 54% and 43% of E. coli strains in these groups. In all, 8/13 AIEC strains from ICD (6/8 patients) versus 2/6 NI (2/5 patients) showed resistance to the macrophage-penetrating antimicrobials ciprofloxacin, clarithromycin, rifampicin, tetracycline, and trimethoprim/sulfamethoxazole. Resistance was associated with tetA, tetB, tetC, bla- TEM , bla oxa-1 , sulI, sulII, dhfrI, dhfrVII, ant(3″)-Ia, and catI genes and prior use of rifaximin (P < 0.01).
ICD-associated E. coli frequently manifest resistance to commonly used antimicrobials. Clinical trials of antimicrobials against E. coli in ICD that are informed by susceptibility testing, rather than empirical selection, are more likely to demonstrate valid outcomes of such therapy.
Article first Published online 16 April 2012
*Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York
†Jill Roberts Center for Inflammatory Bowel Disease, Weill Medical College of Cornell University, New York, New York
‡Department of Population Medicine and Diagnostic Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York
§University of Texas Health Science Center at Houston, School of Public Health, Houston, Texas
‖Department of Pathology and Microbiology, Faculty of Veterinary Medicine, University of Montreal, Montreal, Canada.
Reprints: Kenneth W. Simpson or Belgin Dogan, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY (e-mail: firstname.lastname@example.org or email@example.com).
Supported by a grant from NY Presbyterian/Weill Cornell Medical College and the Jill Roberts Center for Inflammatory Bowel Disease.
Received February 05, 2012
Accepted March 12, 2012