The transmission dynamics of antibiotic–resistant bacteria: the relationship between resistance in commensal organisms and antibiotic consumption

Abstract

We propose a mathematical model of the transmission dynamics of colonization by commensal bacteria within a human community subject to varying levels of antibiotic use designed to control morbidity induced by pathogenic strains of the normally commensal organisms. Colonization is assumed not to induce morbidity in the majority of cases, and antibiotic use is assumed to be related to the arrival and growth of pathogenic strains that give rise to infections including clinical symptoms of disease. In the absence of antibiotic resistance, the model shows how the pattern of antibiotic prescription and use can eliminate the non-pathogenic commensal strains from the host community if the fraction of people taking antibiotics with a defined efficacy exceeds some critical level. The model is extended to take account of the evolution of antibiotic resistance in the commensal population. We assume resistance may be either plasmid-mediated or conferred by selection of low-level pre-existing mutants, and that resistant organisms may experience reduced reproductive fitness. Invasion of the host community by drug-resistant commensals is possible if certain antibiotic prescribing patterns pertain. We calculate these conditions in terms of the transmission parameter of the organism and the level of antibiotic prescription and use. The model is employed to address the issues of how best to use antibiotics in populations harbouring resistant organisms, and when resistant bacteria will out-compete sensitive strains.

Impact of antimicrobial usage on the transmission dynamics of antimicrobial resistant bacteria among pigs

“…This clear-cut dis- It has previously been observed that so long as antimicrobial resistant mutations are present in host, drug resistance will always emerge once a new drug is introduced (Austin et al, 1997;Rong et al, 2007). In our study, it was demonstrated that this depends in turn on the recovery rate and on the magnitude of the transmission parameters.…”

“…However the models by Austin et al (1997) and Kavanagh et al (2005) assumed that the treatment effect was constant whereas in our model, a more realistic time-varying treatment effect was assumed. Our model can be adapted to study the transmission dynamics of a commensal bacteria such as E. coli as well as a zoonotic bacteria such as Salmonella in animals following the models proposed by Austin et al (1997) and Kavanagh et al (2005) respectively.…”

“…The model is similar in formulation to those of Austin et al (1997) and Kavanagh et al (2005). However the models by Austin et al (1997) and Kavanagh et al (2005) assumed that the treatment effect was constant whereas in our model, a more realistic time-varying treatment effect was assumed.…”

“…The few studies that have characterized the dynamics of resistant genes and bacteria and the effect of antimicrobial usage have been in human populations in Intensive Care Units or closed communities. For example, Austin et al (1997) proposed a mathematical modeling framework for studying the relationship between resistance in commensal organisms and antibiotic consumption. Their model characterized the colonization of a human host population (in an intensive care unit) by commensal bacteria in the presence of antimicrobial agents.…”

“…It was assumed that drug-resistant pigs recovered spontaneously faster than drug-sensitive pigs although they have a lower transmission rate. The energy burden associated with mutations and plasmid transfer thus rendered drug-resistant bacteria less competitive (Austin et al, 1997;Banhoeffer et al, 1997;Lenski, 1998).…”