The impact of climate and demographic changes on future mortality in Brussels, Belgium.

OBJECTIVES: City populations are particularly vulnerable to climate change, but it is difficult to reliably estimate the impact on health due to the lack of high-resolution data. We used recently developed regional climate model projections at kilometre resolution combined with demographic projections to estimate the future mortality burden associated with temperatures in the region of Brussels, Belgium. STUDY DESIGN: The study incorporated a time-series analysis. METHODS: Based on quasi-Poisson regression with distributed-lag non-linear models for the historical temperature-mortality relationship, we derive the mortality burden for the near (2020-2044) and mid (2045-2069) future and disaggregated the contributions of demographic and climate changes. RESULTS: The cold-related attributable fraction of deaths is expected to decrease from 6.22% (95% empirical confidence interval: 1.76%; 10.52%) in 1994-2019 to 5.17% (1.08%; 9.09%) in 2045-2069, whereas for heat, this fraction will increase from 1.02% (0.59%; 1.47%) to 1.83% (0.82%; 2.96%), with contributions of both climate and demographic changes. In stratified analyses by age, we found that because of demographic changes, the number of cold-attributable deaths will increase for people aged above 85 years, with 6815 (95% empirical confidence interval: 1424; 12,003) deaths expected in 2045-2069 compared to 5245 (1462; 8867) deaths in 1994-2019. For people aged below 65 years, on the other hand, the number of heat-related deaths will decrease from 456 (265; 658) to 344 (154; 561) deaths. CONCLUSIONS: Public health policies that especially target the elderly and the summer-time period are needed to limit the impact of climate change on health.

[Evaluation of a new and rapid antibiotic sensitivity method testing for Enterobacteriaceae responsible for urinary infections]. / Evaluation d'une nouvelle méthode d'étude rapide de la sensibilité aux antibiotiques des entérobactéries responsables d'infections urinaires.

URIFAST Es et Es Plus (International Microbio, Signes, France) are rapid antimicrobial susceptibility testing method in broth medium without using an automatic reader. A screening assay (URIFAST Quatro 1C ou URIFAST Twin 1C) is performed with a 4 or 9 antimicrobial agents with a concentration c' below the low critical concentration (c) defined by the Comité de l'Antibiogramme de la Société Française de Microbiologie (CA-SFM). When a bacterial strain is presumed resistant, an antimicrobial susceptibility test with the two critical concentrations (CA-SFM) can be performed with 5 or 10 antimicrobial agents antibiotiques (URIFAST Twin ABG ou URIFAST ABG). 140 strains of Enterobacteriaceae from urinary tract infections; E. coli (n = 94), P. mirabilis (n = 13), K. pneumoniae (n = 4), K. oxytoca (n = 6), C. diversus (n = 3), P. vulgaris (n = 1), M. morganii (n = 3), C. freundii (n = 4), E. aerogenes (n = 2), E. cloacae (n = 5) and S. marcescens (n = 5); were isolated with CPS ID2 (bioMérieux, Marcy l'Etoile, France). URIFAST results were compared to Rapid ATB Ur et ATB Ur results obtained after reading with ATB expression (bioMerieux). For each discrepancy, the minimal inhibitory concentration (MIC) by agar dilution was used as the reference method. Agreement obtained were 98.57% with Quatro 1C, 98.40% with Twin 1C, 98.14% with Twin ABG and 98.39% with ABG. 94% of beta-lactams susceptible Enterobacteriaceae were detected by the screening tray with the antimicrobial agent concentration c'. URIFAST Es et Es Plus are standardized and easy-to-use methods. Because of their good performances, the URIFAST methods can be used to test antimicrobial susceptibility for Enterobacteriaceae from urinary tract infections.

Results of passive and active immunization directed against ferric aerobactin in experimental enterobacterial infections in mice and chickens.

Production of aerobactin has been reported to be a virulence factor in members of the family Enterobacteriaceae. To investigate the protection afforded by humoral immunity directed towards aerobactin in infectious diseases caused by aerobactin-producing strains, we tested the efficacy of mAbAERO1, a murine monoclonal antibody directed to ferric aerobactin, which, in vitro, was found to impair the growth of aerobactin-dependent strains of Enterobacteriaceae under iron-limited conditions. The mortality of mice experimentally infected with the aerobactin-producing strains Escherichia coli V2019 (LD50 = 3.5 x 10(5) CFU/mice) or Klebsiella pneumoniae Caroli (LD50 = 1.3 CFU/mice) was not reduced when 1 mg of mAbAERO1 was injected intravenously 1 h before or 1 h after bacterial challenge. Nor was mortality reduced after challenge with either E. coli V2019 or K. pneumoniae Caroli, even though the active immunization of mice with purified FeAero (ferric aerobactin) conjugated with thyroglobulin as followed by a rise in systemic anti-FeAero antibodies. Lastly, chicks born of hens immunized with FeAero showed evidence of antibody transmission towards FeAero, but were not protected when challenged with E. coli MT78, an aerobactin-producing strain highly virulent for chickens. Therefore, under the experimental conditions tested, humoral immunity against aerobactin appeared to play only a minor role in protection against infections caused by aerobactin-producing members of the family Enterobacteriaceae. However, other experimental models should be tested to confirm these observations.