Another single center study analyzed the outcome of UC patients with and without CDI over a period of one 12 months. of among UC patients reported in a nation wide data analysis by Nguyen et al. between 1998 and 2004 were 3.73% as compared to 1.09% for Crohn’s disease and 0.45% MDRTB-IN-1 for general inpatient admissions. They also found that the incidence of CDI in UC patients had doubled from MDRTB-IN-1 2.66% to 5.12% over those 7 years . A study based on a larger cohort of IBD patients in the United States reported similar results and found that CDI was more common in UC patients (2.8%) as compared to the general inpatient populace (0.4%) . There was no significant increase in the overall prevalence of CDI in all Crohn’s disease patients over the study period (1993C2003), but there was an increase in cases of CDI in CD patients with large bowel disease from 1.22% to 2.31% . Rodemann et al. around the same time period (1998C2004) reported adjusted odds ratio of all IBD, UC, and CD admission with CDI as 2.9 (95% CI, 2.1C4.1), 4.0 (95% CI, 2.4C6.6), and 2.1 (95% CI, 1.3C3.4), respectively with doubling of CDI admissions in patients with CD and tripling in those with UC . More recent data from a retrospective observational study by Issa et al. found that the rate of CDI in IBD patients increased from 1.8% in 2004 to 4.6% in 2005. The majority of cases reported in 2005 were colonic IBD (91%) and outpatient acquired infections (76%) . It was argued by Powell et al. that this relative increase in CDI in UC compared to CD was due to the extent of colonic involvement in UC rather than the difference in nature of the two diseases . Their preliminary data suggests a much higher incidence of CDI in left sided and extensive disease as compared to distal disease. Hence, the incidence of CDI has not only increased in the general populace but also to a greater extent in IBD patients. 3. Pathogenicity of [18, 19]. These cytokines account for enhanced permeability, diarrhea, epithelial apoptosis, and ulceration. Genes encoding toxin A (by genes in the same loci. The local effect of these toxins is usually mediated by internalization of toxin via an endosome in epithelial cells leading to a sequence of conformational changes that release the TcdB toxins catalytic-DXD glycosyltransferase domain name. Subsequent glycosylation of the target RhoGTPase disrupts the MDRTB-IN-1 cellular cytoskeleton and causes cell death [20C22]. Most strains of produce both toxin A and B. The proinflammatory mediators induced by these toxins are Rabbit Polyclonal to OR10A5 responsible for the formation of pseudomembrane. It is interesting to note that the classical pseudomembrane is not a frequent obtaining in IBD-associated CDI . One possible explanation is that the weakened intestinal lymphoepithelial environment of a chronically active IBD patient is unable to mount an adequate inflammatory response to form a pseudomembrane. Immunomodulating drugs may also contribute by altering mucosal inflammatory responses. A third toxin called binary toxin is usually produced by some strains though the exact role is not well comprehended . 4. Hypervirulent NAP1/B1/027 Strain The emergence of a hypervirulent strain NAPI/B1/027 at the beginning of the last decade coincided with the increase in CDI cases . In early 2000, an atypical strain that was group B1 (restriction-endonuclease analysis REA), type NAP1 (North American PFGE type1) and ribotype 027 (polymerase chain reaction PCR) was isolated from outbreaks and found to exhibit hypervirulent features that caused more severe disease . The atypical NAP1/B1/027 strain has several features that contribute to MDRTB-IN-1 its clinical presentation. It is resistant to fluoroquinolones. It has mutated that negatively regulates Contamination in IBD 6.1. Clinical Features and Outcome An episode of CDI is usually characterized by.