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the minimal inhibitory concentrations (MIC ranging from 0.032 µg
mL-1 to 256 µg mL-1) responsible for the selection of antibiotic-
resistant bacteria, demonstrating the resilience of this water
environment to contamination by antibiotics [OBE 12, LEC 13].
However, possible effects on bacterial physiology have been
described for subinhibitory or sublethal concentrations (0.9x CMI to
0.25x CMI) (Davies et al ., 2006, Kohanski et al ., 2010). Indeed, the
most stable molecules, such as the quinolones, the macrolides and the
sulfonamides, which persist longer in water, could accumulate in
environments such as the biofilms of periphytons or estuary mudflats.
The occurrence of antibiotic-resistant E. coli and Enterococcus
strains released in waters results from the selective pressure exerted on
the intestinal microbiota of humans during antibiotic treatment. In the
water, no relationship between the phenotypes for resistance in fecal
bacteria and contamination by antibiotics exists, since only the most
stable molecules are detectable and the bacteria can harbor integrons
that confer resistance to several antibiotics. However, the abundance
of antibiotic-resistant fecal bacteria decreases during their transfer
from the source to the estuary, mainly due to a more important decay
of hospital strains, that harbor gene implicated in spread of antibiotic
resistance (integrons, erm gene), in favor of strains less resistant to
antibiotic and probably better adapted to the environment. These
results also underline the resilience capacity of this aquatic
environment [BER 13, LEC 13].
However, the estuarine sediments chronically exposed to multiple
chemical contaminants, including antibiotics, to which are added
supplies of antibiotic-resistant bacteria, are vulnerable environments.
If indeed in the sediments exposed to contamination by antibiotics, the
degradation of the organic matter by the denitrifying or sulfate-
reducing communities seems barely affected due to the functional
redundancy of the microbial communities, this effect of exposure to
multiple contamination is not described in the literature. In estuarine
mudflats, the enrichment of the bacterial resistome of the sediments
with antibiotic-resistant genes from fecal bacteria, in an environment
where subinhibiting concentrations of antibiotics could be reached,
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