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Abstract Background The emergence of KPC-producing K. pneumoniae has now become a global concern. KPC beta-lactamases are plasmid-borne and, like extended spectrum beta lactamases (ESBLs), can accumulate and transfer resistance determinants to other classes of antibiotics. Therefore, infection control guidelines on early identification and control of the spread of organisms carrying these resistant determinants are needed. Findings Klebsiella pneumoniae carbapenemase (KPC) was detected in two isolates of carbapenem-resistant K. pneumoniae obtained from patients at an Italian teaching hospital. The first strain was isolated from a culture drawn from a central venous device (CVC) in a patient with Crohn's disease who was admitted to a gastroenterology ward. The second was isolated from a urine sample collected from an indwelling urinary catheter in an intensive care unit (ICU) patient with a subdural haematoma. The patients had not travelled abroad. Both isolates were resistant to all β-lactams and were susceptible to imipenem and meropenem but resistant to ertapenem. Isolates also showed resistance to other classes of non-β-lactam antibiotics, such as quinolones, aminoglycosides (with the exception for amikacin), trimethoprim-sulfamethoxazole (TMP-SMX) and nitrofurantoin. They were determined to contain the plasmid encoding the carbapenemase gene bla-KPC and were also positive in the Hodge test. Conclusions This is the second report of KPC-producing isolates in Italy, but the first concerning KPC type 2 gene, and it may have important implications for controlling the transmission of microorganisms resistant to antibiotics.

Abstract Background Coagulase-negative staphylococci (CoNS) are a major cause of nosocomial blood stream infection, especially in critically ill and haematology patients. CoNS are usually multidrug-resistant and glycopeptide antibiotics have been to date considered the drugs of choice for treatment. The aim of this study was to characterize CoNS with reduced susceptibility to glycopeptides causing blood stream infection (BSI) in critically ill and haematology patients at the University Hospital Tor Vergata, Rome, Italy, in 2007. Methods Hospital microbiology records for transplant haematology and ICU were reviewed to identify CoNS with elevated MICs for glycopeptides, and isolates were matched to clinical records to determine whether the isolates caused a BSI. The isolates were tested for susceptibility to new drugs daptomicin and tigecycline and the genetic relationship was assessed using f-AFLP. Results Of a total of 17,418 blood cultures, 1,609 were positive for CoNS and of these, 87 (5.4%) displayed reduced susceptibility to glycopeptides. Clinical review revealed that in 13 cases (7 in haematology and 6 in ICU), CoNS with reduced susceptibility to glycopeptides were responsible for a BSI. Staphylococcus epidermidis was the causative organism in 11 instances and Staphylococcus haemolyticus in 2. The incidence of oxacillin resistance was high (77%), although all isolates remained susceptible to linezolid, daptomycin and tigecycline. Fingerprinting of CoNS identified one clonal relationship between two isolates. Conclusion Multi-resistant CoNS with reduced susceptibility to glycopeptides, although still relatively infrequent in our hospital, are emerging pathogens of clinical concern. Surveillance by antibiotyping with attention to multi-resistant profile, and warning to clinicians, is necessary.

Abstract Background The nosocomial infections surveillance system must be strongly effective especially in highly critic areas, such as Intensive Care Units (ICU). These areas are frequently an epidemiological epicentre for transmission of multi-resistant pathogens, like Acinetobacter baumannii. As an epidemic outbreak occurs it is very important to confirm or exclude the genetic relationship among the isolates in a short time. There are several molecular typing systems used with this aim. The Repetitive sequence-based PCR (REP-PCR) has been recognized as an effective method and it was recently adapted to an automated format known as the DiversiLab system. Methods In the present study we have evaluated the combination of a newly introduced software package for the control of hospital infection (VIGI@ct) with the DiversiLab system. In order to evaluate the reliability of the DiversiLab its results were also compared with those obtained using f-AFLP. Results The combination of VIGI@ct and DiversiLab enabled an earlier identification of an A. baumannii epidemic cluster, through the confirmation of the genetic relationship among the isolates. This cluster regards 56 multi-drug-resistant A. baumannii isolates from several specimens collected from 13 different patients admitted to the ICU in a ten month period. The A. baumannii isolates were clonally related being their similarity included between 97 and 100%. The results of the DiversiLab were confirmed by f-AFLP analysis. Conclusion The early identification of the outbreak has led to the prompt application of operative procedures and precautions to avoid the spread of pathogen. To date, 6 months after the last A. baumannii isolate, no other related case has been identified.

Background: Bloodstream infections (BSI) due to Gram negative bacilli (GNB) represent a major concern among nosocomial infections, since they are noticeably associated with a high mortality rates, increase of healthcare costs and prolongation of hospital stay. Methods: Over a 12-month period (2014-2015) all the adult patients admitted to a university-based Italian hospital were monitored for development of BSIs due to GNB. Multiple logistics regression models were performed to assess the impact of patients' risk factors on the in-hospital and 14-day mortality. Results: During the study period 208 patients were diagnosed with at least a BSI due to a Gram negative species for an incidence rate of 12.8 cases/1,000 admissions (95%CI: 11.2-14.7). Multivariate analyses showed that multiple organ dysfunctions along with immune deficit and inadequate therapy in the first 48hrs were associated with a higher risk of death. Conclusions: A thorough evaluation of both immune status and organ dysfunction at the onset of septic events, along with adequate antimicrobial therapy appear to be the most reliable factors in predicting the outcome in these infections. SOFA score can be efficaciously substituted to the single organ dysfunctions analysis in predicting mortality after these events. [ABSTRACT FROM AUTHOR]

Background: The emergence of KPC-producing K. pneumoniae has now become a global concern. KPC betalactamases are plasmid-borne and, like extended spectrum beta lactamases (ESBLs), can accumulate and transfer resistance determinants to other classes of antibiotics. Therefore, infection control guidelines on early identification and control of the spread of organisms carrying these resistant determinants are needed. Findings: Klebsiella pneumoniae carbapenemase (KPC) was detected in two isolates of carbapenem-resistant K. pneumoniae obtained from patients at an Italian teaching hospital. The first strain was isolated from a culture drawn from a central venous device (CVC) in a patient with Crohn's disease who was admitted to a gastroenterology ward. The second was isolated from a urine sample collected from an indwelling urinary catheter in an intensive care unit (ICU) patient with a subdural haematoma. The patients had not travelled abroad. Both isolates were resistant to all β-lactams and were susceptible to imipenem and meropenem but resistant to ertapenem. Isolates also showed resistance to other classes of non-β-lactam antibiotics, such as quinolones, aminoglycosides (with the exception for amikacin), trimethoprim-sulfamethoxazole (TMP-SMX) and nitrofurantoin. They were determined to contain the plasmid encoding the carbapenemase gene bla-KPC and were also positive in the Hodge test. Conclusions: This is the second report of KPC-producing isolates in Italy, but the first concerning KPC type 2 gene, and it may have important implications for controlling the transmission of microorganisms resistant to antibiotics. [ABSTRACT FROM AUTHOR]

Introduction: Patients with atrial fibrillation (AF) receiving non-vitamin K oral anticoagulants (NOAC) have a slower decline in renal function than those taking warfarin. Moreover, a warfarin-related nephropathy has been described., Aim: We assessed variation of estimated glomerular filtration rate (eGFR) and occurrence of contrast-induced nephropathy (CIN) after percutaneous coronary intervention (PCI) in patients with AF taking warfarin compared with NOAC., Material and Methods: We retrospectively enrolled consecutive patients taking oral anticoagulation for AF undergoing PCI. The primary endpoint was variation in eGFR and serum creatinine levels within 48-72 h after PCI. The secondary endpoint was occurrence of CIN, defined as a ≥ 25% relative increase, or a ≥ 0.5 mg/dl absolute increase, in serum creatinine levels within 48-72 h., Results: We enrolled 420 patients (mean age: 75.0 ±5.5 years, 272 (64.7%) male), 124 (29.5%) treated with NOAC and 296 (70.5%) with warfarin. NOAC patients showed a reduced decline in renal function (eGFR change: -2.8 ±7.9 ml/min/1.73 m 2 vs. -4.5 ±6.5 ml/min/1.73 m 2 , respectively, p = 0.02) and a smaller increase in serum creatinine levels (0.026 ±0.112 vs. 0.055 ±0.132, p = 0.032) after PCI compared with warfarin. In the multivariate linear regression model independent predictors of eGFR changes were diabetes, baseline eGFR ≤ 60 ml/min/1.73 m 2 and warfarin use. Occurrence of CIN did not differ between NOAC and warfarin patients (13 (10.5%) vs. 46 (15.5%), p = 0.22)., Conclusions: Patients with AF taking NOAC have a reduced decline in renal function after PCI compared with warfarin. The NOAC may be a reasonable option for patients with a high risk of developing CIN., Competing Interests: The authors declare no conflict of interest.

The introduction of coronary stents into clinical practice has revolutionized the treatment of coronary artery disease. However, in-stent restenosis (ISR) and stent thrombosis represent the main adverse reactions following stent implantation. Along with procedural and technical factors, individual susceptibility, in particular the inflammatory response, play an important role in the development of these complications. C-reactive protein, one of the most extensively studied inflammatory biomarkers, was found to predict the risk of ISR but not of stent thrombosis in bare-metal stent (BMS)-treated patients. On the contrary, C-reactive protein failed to predict the occurrence of ISR in drug-eluting stent (DES)-treated patients, but it appeared to predict the risk of stent thrombosis. Important differences in the pathophysiological mechanisms of adverse reactions to BMS and DES account for the differences in the prognostic value of inflammatory biomarkers. Moreover, DES polymers are responsible for late hypersensitivity allergic reactions that may lead to late ISR and stent thrombosis. Notably, a correct employment of inflammatory biomarkers may become a useful tool for identification and management of high-risk patients. In this review, the evolving role of inflammatory biomarkers in predicting adverse reactions after stent implantation is discussed, underlying therapeutic and clinical consequences for the management of patients receiving a BMS or a DES.

Early revascularization of the infarct-related artery by primary percutaneous coronary intervention (PPCI) has become the gold standard therapy in ST-segment elevation myocardial infarction (STEMI). However, in a number of patient undergoing PPCI, epicardial coronary artery reperfusion: does not translate into myocardial reperfusion: a phenomenon called as no-reflow. The no-reflow phenomenon has a multifactorial pathogenesis, including: distal embolization, ischemia-reperfusion injury, and individual predisposition of coronary microcirculation to injury. Angiographic and electrocardiographic indexes may be used for the diagnosis. Also, lack of ST-segment elevation resolution is considered an established marker of no-reflow. Importantly, the no-reflow phenomenon provides prognostic information in STEMI patients because it is associated with low ventricular ejection fraction, adverse left ventricular remodelling and mortality at follow-up. Various mechanical devices and pharmacological approaches have been proposed to prevent and to treat the phenomenon: the assessment of mechanisms of no-reflow might guide the development of personalized form of treatment. This paper will be focused on the postulated mechanisms of the phenomenon, modalities for the diagnosis, and the main treatment options.