We established an international consortium to review and discuss relevant clinical evidence in order to develop expert consensus statements related to cancer management during the severe acute respiratory syndrome coronavirus 2-related disease (COVID-19) pandemic. The steering committee prepared 10 working packages addressing significant clinical questions from diagnosis to surgery. During a virtual consensus meeting of 62 global experts and one patient advocate, led by the European Society for Medical Oncology, statements were discussed, amended and voted upon. When consensus could not be reached, the panel revised statements until a consensus was reached. Overall, the expert panel agreed on 28 consensus statements that can be used to overcome many of the clinical and technical areas of uncertainty ranging from diagnosis to therapeutic planning and treatment during the COVID-19 pandemic.

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BackgroundNosocomial infections due to vancomycin-resistant enterococci (VRE) have become a major problem during the last years. The purpose of this study was to investigate the economic burden of nosocomial VRE infections in a European university hospital.MethodsA retrospective matched case-control study was performed including patients who acquired nosocomial infection with either VRE or vancomycin-susceptible enterococci (VSE) within a time period of 3 years. 42 cases with VRE infections and 42 controls with VSE infections were matched for age, gender, admission and discharge within the same year, time at risk for infection, Charlson comorbidity index (±1), stay on intensive care units and non-intensive care units as well as for the type of infection, using criteria of the Centers for Disease Control and Prevention.ResultsThe median overall costs per case were significantly higher than for controls (EUR 57,675 vs. EUR 38,344; p = 0.030). Costs were similar between cases and controls before onset of infection (EUR 17,893 vs. EUR 16,600; p = 0.386), but higher after onset of infection (EUR 37,971 vs. EUR 23,025; p = 0.049). The median attributable costs per case for vancomycin-resistance were EUR 13,157 (p = 0.036). The most significant differences in costs between cases and controls turned out to be for pharmaceuticals (EUR 6030 vs. EUR 2801; p = 0.008) followed by nursing staff (EUR 8956 vs. EUR 4621; p = 0.032), medical products (EUR 3312 vs. EUR 1838; p = 0.020), and for assistant medical technicians (EUR 3766 vs. EUR 2474; p = 0.023). Furthermore, multivariate analysis revealed that costs were driven independently by vancomycin-resistance (1.4 fold; p = 0.034).ConclusionsThis analysis suggested that nosocomial VRE infections significantly increases hospital costs compared with VSE infections. Therefore, hospital personal should implement control measures to prevent VRE transmission.

DSWI represents an important economic factor for the hospital as they may almost triple the costs for patients undergoing CABG. Thus, appropriate infection control measures for the prevention of DSWI should be enforced.

This guideline is an evidence-based approach to the diagnosis, management and prevention of CRI in cancer patients.

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Quinolone antibiotics constitute a clinically successful and widely used class of broad-spectrum antibiotics; however, the emergence and spread of resistance increasingly limits the use of fluoroquinolones in the treatment and management of microbial disease. In this study, we evaluated the quantitative contributions of quinolone target alteration and efflux pump expression to fluoroquinolone resistance in Pseudomonas aeruginosa. We generated isogenic mutations in hot spots of the quinolone resistance-determining regions (QRDRs) of gyrA, gyrB, and parC and inactivated the efflux regulator genes so as to overexpress the corresponding multidrug resistance (MDR) efflux pumps. We then introduced the respective mutations into the reference strain PA14 singly and in various combinations. Whereas the combined inactivation of two efflux regulator-encoding genes did not lead to resistance levels higher than those obtained by inactivation of only one efflux regulator-encoding gene, the combination of mutations leading to increased efflux and target alteration clearly exhibited an additive effect. This combination of target alteration and overexpression of efflux pumps was commonly observed in clinical P. aeruginosa isolates; however, these two mechanisms were frequently found not to be sufficient to explain the level of fluoroquinolone resistance. Our results suggest that there are additional mechanisms, independent of the expression of the MexAB-OprM, MexCD-OprJ, MexEF-OprN, and/or MexXY-OprM efflux pump, that increase ciprofloxacin resistance in isolates with mutations in the QRDRs.

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