BackgroundSurveillance for healthcare-associated infections (HAI) is a priority in the neonatal intensive care unit (NICU), given the critical immune status of patients. The aim of this study was to assess surface bacterial contamination before and after improving cleaning and disinfection practices.Materials and methodsThis was a cross-sectional study conducted in March 2018. Surface samples were taken from the same areas in three steps: after cleaning, after "improved" cleaning, and after terminal disinfection using hydrogen peroxide vapor (VHP). Sampling and culture was carried out according to standard ISO14698-1: 2004. Results interpretation was based on the thresholds defined by good hospital pharmacy practice. Statistical analysis was performed by SPSS 21.0 and a P-value < 0.05 was considered to be significant.ResultsIn total, 290 samples were taken from different zones: fixed equipment (69%), aseptic washbasins (12%), pneumatic system (9%), computer equipment (6%) and mobile equipment (4%). Prevalence of non-compliances after cleaning and disinfection was 75%, 10% after “improved” cleaning, and 0% after automated VHP (P < 0.0001). Median of CFU was 24[EI (0–625)] after standard cleaning, 2[EI (0–35)] after “improved” cleaning and 0 [EI (0–3)] after VHP (P < 0.0001). Isolated germs werecoagulase-negative Staphylococcus (31.2%), Acinetobacter baumannii (26%), Staphylococcus aureus (19.5%), Pseudomonas aeruginosa (9%), Klebsiella pneumoniae (9%), E. coli (4%) and Enterobacter sp (1.3%).ConclusionImproved cleaning and disinfection practices associated to VHP give microbiological satisfactory results. It is important to educate cleaning staff for effective surface cleaning and disinfection operations to control HAI.

Nonalcoholic fatty liver disease (NAFLD) refers to the pathologic buildup of extra fat in the form of triglycerides in liver cells without excessive alcohol intake. NAFLD became the most common cause of chronic liver disease that is tightly associated with key aspects of metabolic disorders, including insulin resistance, obesity, diabetes, and metabolic syndrome. It is generally accepted that multiple mechanisms and pathways are involved in the pathogenesis of NAFLD. Heredity, sedentary lifestyle, westernized high sugar saturated fat diet, metabolic derangements, and gut microbiota, all may interact on a on genetically susceptible individual to cause the disease initiation and progression. While there is an unquestionable role for gene-diet interaction in the etiopathogenesis of NAFLD, it is increasingly apparent that epigenetic processes can orchestrate many aspects of this interaction and provide additional mechanistic insight. Exciting research demonstrated that epigenetic alterations in chromatin can influence gene expression chiefly at the transcriptional level in response to unbalanced diet, and therefore predispose an individual to NAFLD. Thus, further discoveries into molecular epigenetic mechanisms underlying the link between nutrition and aberrant hepatic gene expression can yield new insights into the pathogenesis of NAFLD, and allow innovative epigenetic-based strategies for its early prevention and targeted therapies. Herein, we outline the current knowledge of the interactive role of a high-fat high-calories diet and gene expression through DNA methylation and histone modifications on the pathogenesis of NAFLD. We also provide perspectives on the advancement of the epigenomics in the field and possible shortcomings and limitations ahead.

Introduction Leclercia adecarboxylata is a ubiquitous aerobic, motile, gram-negative bacilli. The human gastro-intestinal tract is known to harbor this rarely opportunistic microorganism. We describe a rare case of invasive infection with a gastrointestinal starting point due to L. adecarboxylata in a patient with Hirschsprung disease. Case report It is about a newborn female who was admitted on the 3rd day of life to the neonatal intensive care unit for intestinal obstruction. On the 9th day of life, while managing the neonatal obstruction, the patient developed febrile peaks. Cytobacteriological examination of cerebrospinal fluid, blood cultures and culture of umbilical vein catheter allowed the exclusive isolation of Leclercia adecarboxylata . It was producing extended spectrum beta-lactamase and was treated with intravenous imipenem . After favourable evolution, the patient was transferred to the pediatric surgery department. There, she was diagnosed with Hirschsprung disease. Discussion Knowledge of the route of transmission of L. adecarboxylata is limited and the possible source of the infection is unclear. However, the authors describe three hypotheses of contamination of our propositus. In our patient, one or more of these routes of contamination would be possible. Indeed, bacteremia could occur as a result of a bacterial translocation across the mucosal barrier of the colon altered by Hirschsprung disease, antibiotic use and feeding practices. Conclusion Infection with L. adecarboxylata revealed a wide range of infection. It has only recently been acknowledged as an emerging pathogen. Further studies of the pathogenesis and risk factors are required.

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