title: Low Prevalence of Carbapenem-Resistant Bacteria in River Water: Resistance Is Mostly Related to Intrinsic Mechanisms.
abstract: Carbapenems are last-resort antibiotics to handle serious infections caused by multiresistant bacteria. The incidence of resistance to these antibiotics has been increasing and new resistance mechanisms have emerged. The dissemination of carbapenem resistance in the environment has been overlooked. The main goal of this research was to assess the prevalence and diversity of carbapenem-resistant bacteria in riverine ecosystems. The presence of frequently reported carbapenemase-encoding genes was inspected. The proportion of imipenem-resistant bacteria was on average 2.24 CFU/ml. Imipenem-resistant strains (n=110) were identified as Pseudomonas spp., Stenotrophomonas maltophilia, Aeromonas spp., Chromobacterium haemolyticum, Shewanella xiamenensis, and members of Enterobacteriaceae. Carbapenem-resistant bacteria were highly resistant to other beta-lactams such as quinolones, aminoglycosides, chloramphenicol, tetracyclines, and sulfamethoxazole/trimethoprim. Carbapenem resistance was mostly associated with intrinsically resistant bacteria. As intrinsic resistance mechanisms, we have identified the blaCphA gene in 77.3% of Aeromonas spp., blaL1 in all S. maltophilia, and blaOXA-48-like in all S. xiamenensis. As acquired resistance mechanisms, we have detected the blaVIM-2 gene in six Pseudomonas spp. (5.45%). Integrons with gene cassettes encoding resistance to aminoglycosides (aacA and aacC genes), trimethoprim (dfrB1b), and carbapenems (blaVIM-2) were found in Pseudomonas spp. Results suggest that carbapenem resistance dissemination in riverine ecosystems is still at an early stage. Nevertheless, monitoring these aquatic compartments for the presence of resistance genes and its host organisms is essential to outline strategies to minimize resistance dissemination.
authors.affiliation: 1 Biology Department and CESAM, University of Aveiro , Aveiro, Portugal .|2 Biology Department and iBiMED, University of Aveiro , Aveiro, Portugal .
authors.forename: Marta
authors.initials: M
authors.lastname: Tacão
authors.affiliation: 1 Biology Department and CESAM, University of Aveiro , Aveiro, Portugal .
authors.forename: António
authors.initials: A
authors.lastname: Correia
authors.affiliation: 2 Biology Department and iBiMED, University of Aveiro , Aveiro, Portugal .
authors.forename: Isabel S
authors.initials: IS
authors.lastname: Henriques
mesh_terms: D000333:Aeromonas / Q000187:drug effects / Q000201:enzymology / Q000235:genetics; D000617:Aminoglycosides / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism; D015780:Carbapenems / Q000494:pharmacology*; D002701:Chloramphenicol / Q000494:pharmacology; D002861:Chromobacterium / Q000187:drug effects / Q000201:enzymology / Q000235:genetics; D004755:Enterobacteriaceae / Q000187:drug effects / Q000201:enzymology / Q000235:genetics; D004784:Environmental Monitoring; D015870:Gene Expression; D008826:Microbial Sensitivity Tests; D010957:Plasmids / Q000737:chemistry / Q000378:metabolism; D011174:Portugal; D011549:Pseudomonas / Q000187:drug effects / Q000201:enzymology / Q000235:genetics; D015363:Quinolones / Q000494:pharmacology; D045483:Rivers / Q000382:microbiology*; D020592:Shewanella / Q000187:drug effects / Q000201:enzymology / Q000235:genetics; D020615:Stenotrophomonas maltophilia / Q000187:drug effects / Q000201:enzymology / Q000235:genetics; D015662:Trimethoprim, Sulfamethoxazole Drug Combination / Q000494:pharmacology; D014871:Water Microbiology; D018440:beta-Lactam Resistance / Q000235:genetics*; D001618:beta-Lactamases / Q000235:genetics* / Q000378:metabolism
chemical_list: D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D015780:Carbapenems; D015363:Quinolones; D002701:Chloramphenicol; D015662:Trimethoprim, Sulfamethoxazole Drug Combination; D001618:beta-Lactamases; C063912:carbapenemase