Prevalence of Klebsiella pneumoniae strains producing carbapenemases and increase of resistance to colistin in an Italian teaching hospital from January 2012 To December 2014

The aim of this study was to characterize the spread of carbapenemase-producing Klebsiella pneumoniae (CPKP) in a tertiary level hospital using ongoing active surveillance with rectal swab cultures. Furthermore, this study analyzed the presence of CPKP in the clinical samples (CS) of a single patient as well as the evolution of Colistin-sensitive strains (CoS) to Colistin-resistant strains (CoR)

Prevalence of Klebsiella pneumoniae strains producing carbapenemases and increase of resistance to colistin in an Italian teaching hospital from January 2012 To December 2014

Background: The aim of this study was to characterize the spread of carbapenemase-producing Klebsiella pneumoniae (CPKP) in a tertiary level hospital using ongoing active surveillance with rectal swab cultures. Furthermore, this study analyzed the presence of CPKP in the clinical samples (CS) of a single patient as well as the evolution of Colistin-sensitive strains (CoS) to Colistin-resistant strains (CoR). Methods: This study was performed from January 1, 2012 to December 31, 2014. In 2012, a survey was conducted in the Intensive Care Department. In autumn 2013, active monitoring was extended to the Surgery Department, and since mid-2014, the surveillance has included the Medical Department as well. Only the first isolated strain from each patient was included. Antimicrobial susceptibility testing was performed on CPKP isolates: Klebsiella pneumoniae carbapenemase, oxacillinase-48, Verona integron-encoded metallo-beta-lactamase and New Delhi metallo-beta-lactamase were detected using a validated in-house PCR method, and multilocus sequence typing (MLST) was used to investigate the clonal transmission of strains. Results: A total of 15,104 patients were included in the study, and 496 consecutive non-replicated strains of CPKP were collected: 149 strains were collected in 2012 (39 [26.2 %] from surveillance rectal swabs [SRS]), 133 strains were collected in 2013 (70 [52.6 %] from SRS) and 214 strains were collected in 2014 (164 [76.6 %] from SRS). We observed a significant increase in the percentage of positive SRS cases in 2014 relative to 2013 and 2012 (p = 0.0001 and p = 0.0172, respectively) and in the proportion of CPKP first isolated by SRS relative to those identified by CS (p < 0.0001). Among all available samples, the number of CoR isolated from SRS was higher in 2013 and 2014 compared with 2012 (p = 0.0019 and p = 0.008, respectively). ST-258 and ST-512 were more prevalent in the tested specimens, and a new single locus variant (SLV) of ST-512 (ST-745) was isolated. Conclusions: The results of this 3-year study of 15,104 patients highlight the clinical relevance of antimicrobial resistance as well as the drug-selection pressure of colistin therapy. The active surveillance in the three different departments increased the level of CPKP cases isolated by SRS

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases.

Dysfunction of the gastrointestinal neuromuscular apparatus (including interstitial cells of Cajal) is presumed to underlie a heterogeneous group of disorders collectively termed gastrointestinal neuromuscular diseases (GINMDs). There is increasing experimental and clinical evidence that some GINMDs are immune-mediated, with cell-mediated dysfunction relatively well studied. Humoral (antibody)-mediated autoimmunity is associated with several well-established acquired neuromuscular diseases and is now implicated in an increasing number of less well-characterised disorders, particularly of the central nervous system. The role of autoimmunity in GINMDs has been less studied. Whilst most work has focused on the presence of antibodies directed to nuclear antigens, particularly in the context of secondary disorders such as paraneoplastic intestinal pseudo-obstruction, the possibility that 'functional' anti-neuronal antibodies directed to membrane-bound ion channels may cause disease (channelopathy) is now also being realised. The evidence for humoral autoimmunity as an etiologic factor in primary (idiopathic) and secondary GINMDs is systematically presented using the original paradigms previously applied to established autoimmune neuromuscular disorders. The presence of anti-enteric neuronal antibodies, although repeatedly demonstrated, still requires the identification of specific neuronal autoantigens and validated evidence of pathogenicity