Due to ecological effect, it is expected that population exposures to antimicrobial drugs may lead to microorganisms’ modifications, occasionally leading to resistance emergence. The present review was based on previ...Due to ecological effect, it is expected that population exposures to antimicrobial drugs may lead to microorganisms’ modifications, occasionally leading to resistance emergence. The present review was based on previous empirical data and on related literature search for quantitative empirical models exploring the human-bacterial interactions. Our previous studies have shown the emergence of ciprofloxacin resistant (CIP-R) Escherichia coli significantly related to previous specific levels of ciprofloxacin consumption and to urban clusters of CIP-R E. coli. The evidence of significant spatial clustering of antimicrobial resistance (ciprofloxacin resistance E. coli) reinforces the ecological effect hypothesis as a major drive in resistance emergence. In other words, human populations submitted to a certain ciprofloxacin or quinolone usage level may affect neighbours within certain geographical areas, not necessarily due to individual antimicrobial intake, but as a driving pressure over a modified circulating E. coli population. Apparently quantitative spatial-temporal analytical frameworks may be better for understanding human-bacterial interactions based on any of their epiphenomena (antimicrobial consumption, antimicrobial resistance, geno/phenotypic characteristics).展开更多
基金supported by a FAPESP Research Grant:2006/53922-9(http://www.fapesp.br/english/).
文摘Due to ecological effect, it is expected that population exposures to antimicrobial drugs may lead to microorganisms’ modifications, occasionally leading to resistance emergence. The present review was based on previous empirical data and on related literature search for quantitative empirical models exploring the human-bacterial interactions. Our previous studies have shown the emergence of ciprofloxacin resistant (CIP-R) Escherichia coli significantly related to previous specific levels of ciprofloxacin consumption and to urban clusters of CIP-R E. coli. The evidence of significant spatial clustering of antimicrobial resistance (ciprofloxacin resistance E. coli) reinforces the ecological effect hypothesis as a major drive in resistance emergence. In other words, human populations submitted to a certain ciprofloxacin or quinolone usage level may affect neighbours within certain geographical areas, not necessarily due to individual antimicrobial intake, but as a driving pressure over a modified circulating E. coli population. Apparently quantitative spatial-temporal analytical frameworks may be better for understanding human-bacterial interactions based on any of their epiphenomena (antimicrobial consumption, antimicrobial resistance, geno/phenotypic characteristics).
