Microbiological contamination of ear, nose and throat (ENT) units.

Aim: In ENT (Ear, Nose and Throat) treatment units, medical devices for examination are commonly stored on open trays. The aim of this study is to investigate whether open storage is a relevant cause for microbiological contamination of ENT instruments during a working day. Methods: Qualitative and quantitative tests, such as imprints and swabs, were performed on the instruments and the surfaces of the treatment units in an ENT outpatient clinic at the beginning and at the end of consultation hours. The microbiological analysis of the samples focused on potential pathogens, e.g., Staphylococcus aureus or Pseudomonas aeruginosa, bacteria of skin and oral microbiota, as well as the number of colony forming units (CFU). The samples were collected at three distinct ENT treatment units over five working days. Results: The samples taken at the beginning of consultation hours showed a low number of CFU and no pathogens. Overall, 5% of the instruments were contaminated with bacteria of skin microbiota. At the end of a working day, this rate increased significantly to 17.5% (p<0.01). At the beginning of the working day, the mean number on the instrument trays was 4 CFU/25 cm², which increased to 34 CFU/25 cm² at the end of the working day. In some cases of the imprints taken at the end of the working day showed that a bacterial lawn had formed. In two cases, the pathogens Ralstonia picketii and Enterobacter cloacae were detected; in another case Bacillus spp. was identified. The contamination of ENT instruments and the ENT treatment unit increased significantly (p<0.01) over the duration of consultation hours. Conclusion: The results show that the current hygiene requirements for storage und reprocessing are not sufficient to conform to the mandatory guidelines of the German Commission on Hospital Hygiene and Infection Prevention. Although we could not find a pressing risk for the patients, we also cannot exclude it in the long term. Thus, new concepts are needed.

Dialysis drains as a possible source for carbapenem-resistant pathogens causing an ICU outbreak.

OBJECTIVE DESIGN: We describe a case series of patients colonized with KPC-producing Enterobacteriaceae related to dialysis drains at patient's bedside. SETTING: The study was set at the intensive care unit (ICU) of a tertiary referral hospital. PATIENTS: In March 2016, we discovered four ICU patients to be colonized with KPC-producing Enterobacteriaceae in routine screening. All of these patients had already received contact isolation, and all of them were treated with continuous veno-venous dialysis. Environmental examinations showed KPC-producing Enterobacteriaceae in dialysis drains in different ICU rooms and even in rooms not hosting KPC-colonized patients. INTERVENTIONS: Based on our findings, we suspected the dialysis drains as a reservoir of KPC-producing Enterobacteriaceae with a potential risk for the patients. Therefore, we decided to change the dialysis waste management. RESULTS: As a result, no KCP-producing Enterobacteriaceae were detected during the following weekly screening of the patients. CONCLUSIONS: Installation of dialysis connection units including a drain system at the patient's bedside is a comfortable way to provide water supply. In many ICUs, such dialysis drains are installed near the patients' head and directly besides the infusion systems. When the drains are not used properly, in our opinion, they pose a risk of transmission of pathogens from the drain to the patient. Our findings support the need of specific precautions.

Increased resistance of gram-negative urinary pathogens after kidney transplantation.

BACKGROUND: Urinary tract infection is the most common complication after kidney transplantation. It can cause severe sepsis and transplant loss. Emergence of drug resistance among gram-negative urinary pathogens is the current challenge for urinary tract infection treatment after kidney transplantation. METHODS: This study analyzes the antimicrobial susceptibility of gram-negative urinary pathogens after kidney transplantation from 2009 to 2012 at the Transplant Outpatient Clinic of the University Hospital Essen, Germany. Kidney transplant patients at the University Hospital Essen receive regular follow up examinations after transplantation. Midstream urines were examined for bacteriuria at each follow up visit. RESULTS: From 2009 to 2012 15.741 urine samples were obtained from 859 patients. In 2985 (19%) samples bacterial growth was detected. The most frequently detected gram-negative bacteria were E.coli 1109 (37%), Klebsiella spp. 242 (8%) and Pseudomonas aeruginosa 136 (4.5%). Klebsiella spp. showed a significant increase of resistance to trimethoprim-sulfamethoxazole by 19% (p = 0.02), ciprofloxacin by 15% (p = 0.01) and ceftazidime by 17% (p = 0.004). E.coli and P. aeruginosa isolates presented no significant differences of antimicrobial susceptibility to the analyzed antibiotics. CONCLUSIONS: Antimicrobial resistance of Klebsiella spp. increased significant to trimethoprim-sulfamethoxazole, ciprofloxacin and ceftazidime from 2009 to 2012.

Transiently reduced PI3K/Akt activity drives the development of regulatory function in antigen-stimulated Naïve T-cells.

Regulatory T-cells (Tregs) are central for immune homeostasis and divided in thymus-derived natural Tregs and peripherally induced iTreg. However, while phenotype and function of iTregs are well known, a remarkable lack exists in knowledge about signaling mechanisms leading to their generation from naïve precursors in peripheral tissues. Using antigen specific naïve T-cells from mice, we investigated CD4+ CD25+ FoxP3- iTreg induction during antigen-specific T-cell receptor (TCR) stimulation with weak antigen presenting cells (APC). We show that early signaling pathways such as ADAM-17-activation appeared similar in developing iTreg and effector cells (Teff) and both initially shedded CD62-L. But iTreg started reexpressing CD62-L after 24 h while Teff permanently downmodulated it. Furthermore, between 24 and 72 hours iTreg presented with significantly lower phosphorylation levels of Akt-S473 suggesting lower activity of the PI3K/Akt-axis. This was associated with a higher expression of the Akt hydrophobic motif-specific phosphatase PHLPP1 in iTreg. Importantly, the lack of costimulatory signals via CD28 from weak APC was central for the development of regulatory function in iTreg but not for the reappearance of CD62-L. Thus, T-cells display a window of sensitivity after onset of TCR triggering within which the intensity of the PI3K/Akt signal controls entry into either effector or regulatory pathways.