Understanding unequal ageing: towards a synthesis of intersectionality and life course analyses

Intersectionality has received an increasing amount of attention in health inequalities research in recent years. It suggests that treating social characteristics separately—mainly age, gender, ethnicity, and socio-economic position—does not match the reality that people simultaneously embody multiple characteristics and are therefore potentially subject to multiple forms of discrimination. Yet the intersectionality literature has paid very little attention to the nature of ageing or the life course, and gerontology has rarely incorporated insights from intersectionality. In this paper, we aim to illustrate how intersectionality might be synthesised with a life course perspective to deliver novel insights into unequal ageing, especially with respect to health. First we provide an overview of how intersectionality can be used in research on inequality, focusing on intersectional subgroups, discrimination, categorisation, and individual heterogeneity. We cover two key approaches—the use of interaction terms in conventional models and multilevel models which are particularly focussed on granular subgroup differences. In advancing a conceptual dialogue with the life course perspective, we discuss the concepts of roles, life stages, transitions, age/cohort, cumulative disadvantage/advantage, and trajectories. We conclude that the synergies between intersectionality and the life course hold exciting opportunities to bring new insights to unequal ageing and its attendant health inequalities

The Role of Epidemic Resistance Plasmids and International High-Risk Clones in the Spread of Multidrug-Resistant Enterobacteriaceae

Escherichia coli ST131and Klebsiella pneumoniae ST258 emerged in the 2000s as important human pathogens; have spread extensively throughout the world and are responsible for the rapid increase in antimicrobial resistance among E. coli and K. pneumoniae respectively. E. coli ST131 causes extra-intestinal infections, is often fluoroquinolone resistant and associated with Extend-spectrum β-lactamase production especially CTX-M-15. K. pneumoniae ST258 causes urinary and respiratory tract infections and is associated with carbapenemases most often KPC-2 and KPC-3. The most prevalent lineage within ST131 is named fimH30 because it contains the 2 H30 variant of the type 1 fimbrial adhesin gene and recent molecular studies have demonstrated that this lineage emerged in early 2000‟s and was then followed by the rapid expansion of its sublineages H30-R and H30-Rx. K. pneumoniae ST258 comprises of 2 distinct lineages namely clade I and clade II. Moreover, it seems that ST258 is a hybrid clone that was created by a large recombination event between ST11 and ST442. Epidemic plasmids with blaCTX-M and blaKPC belonging to the incompatiblity group F have contributed significantly to the success of these clones. E. coli ST131 and K. pneumoniae ST258 are the quintessential examples of international multidrug-resistant high risk clones.In part by a research grant from the Calgary Laboratory Services (#10006465).http://cmr.asm.orghb201