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Investigate the role of wildlife as sources of resistance for domestic animals (and man), and the likely sources and mechanisms of persistence of antibiotic resistance in wildlife in the absence of obvious exposure to antibiotics. <P>
Cross sectional and longitudinal studies of wild rodent populations to determine the epidemiology of antibiotic resistance. This includes a detailed examination of temporal patterns and the relationship between resistance and variables such as age and sex of the rodent host. <P>Investigation of spatial patterns of antibiotic resistance in wild rodents, in-contact farm animals and the environment. <P>Combining molecular studies with information on antibiotic usage to examine the origin and mechanisms of resistance and its transferability to other bacteria and other mammalian hosts. <P>Study of the environment, diet and seasonal variation in the normal enteric flora of wild rodents (including captive colonies of wild rodents) to investigate how antibiotic resistance persists in the absence of antibiotic therapy.
Progress: Antibiotic resistance is an increasingly important problem in farm animal and human medicine. The increased prevalence of resistance is assumed to be largely due to selection through the use of antibiotics. There is considerable ignorance, however, regarding both the original sources of the resistant strains and the genetic elements that encode resistance, and the dynamics and persistence of resistance under different antibiotic-use regimens. Although several groups have produced valuable theoretical models to help understand the ecology of antibiotic resistance, there is an need for detailed, longitudinal, empirical studies, especially of commensal bacteria (rather than pathogens) and in natural populations.
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In this project, we have investigated the role of wildlife as sources of resistance for domestic animals (and man), and the likely sources and mechanisms of persistence of antibiotic resistance in wildlife in the absence of obvious exposure to antibiotics.
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We have indeed demonstrated that antibiotic resistance in common in the normal bacterial flora of wildlife, and that the prevalence varies between individual animals, host species, environment and time of year – but that there is no clear association with contact with livestock or the intensity of farming, both of which might be taken a proxies for exposure to exogenous antibiotics.
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The genes for resistance in wild rodent isolates are most often the same as those most commonly found in domestic animals and, for that matter, human beings. Furthermore, similar resistance genes are found in environmental isolates. This, plus the identification of some resistance strains with identical PFGE profiles, suggests that transfer between wildlife and domestic livestock is possible. However, the ecology of resistance appears to be very dynamic, with evidence for some resistant strains of E. coli having wide mammalian host ranges, but resistance genes also moving regularly between different strains of E. coli.
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Thus it may well be that antibiotic resistance is, and perhaps always has been, common, and even normal in the gut flora of many animals – an hypothesis which would fit well with theories of both antibiotics and resistance having evolved through competition between strains and species. The complex dynamics observed in this study might reflect the complex relationships that might be expected to develop in such systems.
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Alternatively, the prevalence of resistance may have increased recently owing to general and widespread contamination of the environment with antibiotics and their metabolites, many of which are known to have long half lives in the environment. A further possible mechanism of selection identified in this study is a possible link between antibiotic resistance and, for example, mercury resistance. Multiple resistances carried on plasmids could provide a powerful means for the co-selection of all the associated genes through any one selective mechanism.
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