PMC:3266646 / 27344-30120 JSONTXT

{"project":"2_test","denotations":[{"id":"22303296-20707672-36966609","span":{"begin":177,"end":181},"obj":"20707672"},{"id":"22303296-18487337-36966610","span":{"begin":614,"end":618},"obj":"18487337"},{"id":"22303296-15855499-36966611","span":{"begin":1680,"end":1684},"obj":"15855499"},{"id":"22303296-18273063-36966612","span":{"begin":2044,"end":2048},"obj":"18273063"},{"id":"22303296-21368907-36966613","span":{"begin":2254,"end":2258},"obj":"21368907"}],"text":"Integrons\nSeveral studies have highlighted the crucial role of integrons, particularly class 1 integrons, in the evolution of antibiotic resistances in clinics (Cambray et al., 2010). Indeed, class 1 integrons are not only platforms for genes aggregation, leading to the establishment of multi-drug resistance, but their localization on mobile genetic elements such as plasmids and transposons favor the spread of several genes in a unique transfer event. Recently, studies on environmental microbial communities have demonstrated that integrons of class 1 are largely present in the environment. Gillings et al. (2008) have provided evidences that the clinical class 1 integrons originated from environmental bacterial communities. The authors observed that class 1 integrons isolated from environmental samples do not carry any antibiotic resistance gene and harbored the qac gene cassettes, which is responsible for the bacterial resistance to quaternary ammoniums by efflux. Clinical class 1 integrons would have arisen from environmental ones by integration on a Tn402-like transposon, which then disseminated in human commensals and pathogens. The presence of the qac gene has conferred a selective advantage to adapt in clinical environments, where bacteria are often challenged by disinfectants. The establishment of class 1 integrons in clinical strains has later on enabled the acquisition of antibiotic resistances positively selected by the usage of drugs. This hypothesis is also supported by the fact that clinical class 1 integrons demonstrated similar structures among them, in terms of integrases and recombination site, inferring a common ancestor. Gaze et al. (2005) have demonstrated how pollution of water bodies and their sediments with quaternary ammonium compounds, directly select for bacteria harboring qacE gene cassettes, located on the class 1 integrons. Furthermore, evidence of selection of bacteria harboring class 1 integrons in water bodies contaminated by industrial waste has been provided by Wright et al. (2008). The authors demonstrated that the contamination of freshwater with heavy metals correlated positively with a higher abundance of class 1 integrons in the bacterial community. More recently, Gaze et al. (2011) showed in sewage sludge and pig slurry that the prevalence of class 1 integrons and of qac genes was higher in bacteria exposed to detergents and/or antibiotic residues. All these studies demonstrate that pollution of water bodies with different agents increases the risk of selection and spread of integron structures. These genetic structures may be acquired by bacterial species that play role as shuttle between environment and clinics, constituting gene vectors for further dissemination in nosocomial bacteria."}