Role of microbial translocation, inflammation and intestinal damage in the development of nosocomial bloodstream infections following Clostridium difficile infection.
C. difficile infection (CDI) may be complicated by the development of nosocomial bloodstream infections (n-BSI). Nevertheless, whether CDI predisposes subjects to subsequent BSI is still controversial and neither the clinical link between CDI and n-BSI nor its exact pathogenesis have been demonstrated yet. Given that the observed n-BSIs following CDI were mostly caused by fungi and bacteria belonging to the enteric flora, a possible role of alteration of the normal gut integrity as the pathogenetic trigger for the development of n-BSI was hypothesized. Microbial translocation (MT), defined as the migration of bacteria or their products from the gut to the systemic circulation, might be promoted by the increased intestinal permeability and the intestinal damage (ID) present during CDI.
The hypotheses of the project are that a certain degree of inflammation, intestinal injury and microbial translocation occur during the course of CDI and that these alterations might play a role in the development of n-BSI after CDI.
Thus, primary endpoints are: i) to evaluate the dynamic changes of circulating levels of LPS-binding protein (LBP) and EndoCab IgM (markers of MT), IL-6 (marker of inflammation, IN) and Intestinal Fatty Acid Binding Protein (I-FABP, marker of ID) in patients with CDI and ii) to analyze whether these biomarkers are specifically modified in subjects developing n-BSI within 60 days after the onset of CDI compared with those not developing n-BSI.
This is a single-center, prospective study including subjects with documented CDI hospitalized at the Department of Public Health and Infectious Diseases, Sapienza University of Rome. For each subject, blood samples will be collected at T0 (i.e. before therapy or within 24h from the onset of CDI-specific therapy) and T1 (within 48h from the end of CDI-specific therapy), respectively. Circulating levels of LBP, EndoCab IgM, IL-6 and I-FABP will be analyzed by ELISA assays.