The armA (aminoglycoside resistance methylase) gene, which confers resistance to 4,6-disubstituted deoxystreptamines and fortimicin, was initially found in Klebsiella pneumoniae BM4536 on IncL/M plasmid pIP1204 of ca. 90 kb which also encodes the extended-spectrum -lactamase CTX-M-3. Thirty-four enterobacteria from various countries that were likely to produce a CTX-M enzyme since they were more resistant to cefotaxime than to ceftazidime were studied. The armA gene was detected in 12 clinical isolates of Citrobacter freundii, Enterobacter cloacae, Escherichia coli, K. pneumoniae, Salmonella enterica, and Shigella flexneri, in which it was always associated with bla CTX-M-3 on an IncL/M plasmid. Conjugation, analysis of DNA sequences, PCR mapping, and plasmid conduction experiments indicated that the armA gene was part of composite transposon Tn1548 together with genes ant3؆9, sul1, and dfrXII, which are responsible for resistance to streptomycinspectinomycin, sulfonamides, and trimethoprim, respectively. The 16.6-kb genetic element was flanked by two copies of IS6 and migrated by replicative transposition. This observation accounts for the presence of armA on self-transferable plasmids of various incompatibility groups and its worldwide dissemination. It thus appears that posttranscriptional modification of 16S rRNA confers high-level resistance to all the clinically available aminoglycosides except streptomycin in gram-negative human and animal pathogens.
Objectives Data on antibiotic consumption in the community were collected from 30 EU/EEA countries over two decades. This article reviews temporal trends, seasonal variation, presence of change-points and changes in the composition of the main antibiotic groups. Methods For the period 1997–2017, data on consumption of antibiotics, i.e. antibacterials for systemic use (ATC group J01), in the community, aggregated at the level of the active substance, were collected using the WHO ATC/DDD methodology (ATC/DDD index 2019). Consumption was expressed in DDD per 1000 inhabitants per day and in packages per 1000 inhabitants per day. Antibiotic consumption was analysed based on ATC-3 groups, and presented as trends, seasonal variation, presence of change-points and compositional changes. Results In 2017, antibiotic consumption in the community expressed in DDD per 1000 inhabitants per day varied by a factor 3.6 between countries with the highest (Greece) and the lowest (the Netherlands) consumption. Antibiotic consumption in the EU/EEA did not change significantly over time. Antibiotic consumption showed a significant seasonal variation, which decreased over time. The number of DDD per package significantly increased over time. The proportional consumption of sulphonamides and trimethoprim (J01E) relative to other groups significantly decreased over time, while the proportional consumption of other antibacterials (J01X) relative to other groups significantly increased over time. Conclusions Overall, antibiotic consumption in the community in the EU/EEA did not change during 1997–2017, while seasonal variation consistently decreased over time. The number of DDD per package increased during 1997–2017.
The ant(4)-IIb gene of Pseudomonas aeruginosa BM4492, which encodes an aminoglycoside 4-O-adenylyltransferase, was identified as a coding sequence of 756 bp corresponding to a protein with a calculated mass of 27,219 Da. Analysis of the deduced sequence indicated that the protein was related to aminoglycoside 4-O-adenylyltransferases IIa and Ia found in P. aeruginosa and gram-positive bacteria, respectively. The enzyme conferred resistance to amikacin and tobramycin but not to dibekacin, gentamicin, or netilmicin. The ant(4)-IIb gene had a chromosomal location in five of six clinical isolates of P. aeruginosa tested and was plasmid borne in the remaining strain. The ant(4)-IIb gene was detected by PCR in some clinical strains of P. aeruginosa from the same hospital but not in members of other bacterial genera.Aminoglycosides, in particular, amikacin, are antibiotics of major importance in the treatment of infections due to Pseudomonas aeruginosa. Since the introduction of these antibiotics in clinical practice, numerous strains of P. aeruginosa have developed resistance to this class of drugs. Although efflux has recently been shown to be involved in resistance to aminoglycosides in this bacterial species (11,13,18), the main resistance mechanism remains enzymatic modification of the drugs (16). In P. aeruginosa resistance to amikacin is due to production of either 6Ј-N-acetyl- The ANT(4Ј)-II enzyme is mediated in P. aeruginosa by the ca. 450-kb plasmid pMG77, and in Escherichia coli and Klebsiella pneumoniae it is mediated by plasmids of the IncM incompatibility group (4). The modifying enzyme confers resistance to amikacin, isepamicin, tobramycin, and other aminoglycosides with a 4Ј-hydroxyl group but not to dibekacin (4). In contrast, the ANT(4Ј)-I enzyme of gram-positive microorganisms has been shown to modify both the 4Ј-and 4Љ-hydroxyl groups, and therefore also confers resistance to dibekacin (7, 9, 12). We have studied P. aeruginosa strains isolated in Bulgaria which were resistant to amikacin and susceptible to netilmicin and which did not harbor the ant(4Ј)-IIa gene (15). We have characterized the determinant involved in this resistance, ant(4Ј)-IIb, and studied its dissemination in P. aeruginosa clinical isolates.(An initial report of this work was presented at the 41st Interscience Conference on Antimicrobial Agents and Chemotherapy [S. Sabtcheva et al., Abstr. 41st Intersci. Conf. Antimicrob. Agents Chemother., abstr. C1-166, 2001].). MATERIALS AND METHODSStrains, plasmids, and growth conditions. Seven epidemiologically unrelated clinical strains of P. aeruginosa isolated between 1992 and 1998 at the National Oncology Center in Sofia, Bulgaria, were selected for this study (Table 1). Five isolates (isolates BM4492, BM4529, BM4530, BM4532, and BM4533) that exhibited the unusual phenotype of resistance to amikacin and susceptibility to netilmicin were detected in routine laboratory testing with a Vitek apparatus (bioMérieux). The two remaining strains were BM4531, which was susceptible to amikacin, ge...
bAmong five American Type Culture Collection (ATCC) Citrobacter strains, qnrB60 in Citrobacter freundii ATCC 6879, an isolate from the preantibiotic era, and qnrB61 in Citrobacter braakii ATCC 51113 T , a type strain belonging to the C. freundii complex, were identified. Meanwhile, a truncated qnrB-like pseudogene was identified in C. freundii ATCC 8090 T and ATCC 43864. No qnrB-like sequence was found in Citrobacter koseri ATCC 27028 T . These findings underscore the close relationship between this species and qnrB.A n increasing number of plasmid-mediated quinolone resistance (PMQR) determinants have been reported (1,2). In most studies, PMQR determinants have been found among multiple-drug-resistant bacteria, especially among extended-spectrum -lactamase producers. Despite its only recent discovery, qnrB is one of the most prevalent PMQR determinants among clinical isolates of Enterobacteriaceae (3-7). Interestingly, the distribution of qnrB is uneven among species; most new variants of qnrB have been found in Citrobacter spp., and the prevalence of qnrB seems high among certain populations of Citrobacter spp. strains, a substantial part of which were not multidrug resistant (8). One possible explanation is that qnrB was originally present among some populations of Citrobacter bacteria irrespective of quinolone exposure. More recently, the association between qnrB and clinical isolates of Citrobacter spp. has been well documented by Jacoby et al. (8). In the present study, to clarify this linkage more generally and robustly, reference Citrobacter strains of the American Type Culture Collection (ATCC), including type strains, nonclinical isolates, and a strain from the preantibiotic era, were subjected to detection and characterization of the qnrBlike gene (9)(10)(11).(This work was presented in part at the 49th Interscience Conference on Antimicrobial Agents and Chemotherapy, San Francisco, CA, 2009.) Five Citrobacter strains of the ATCC, including three type strains, were subjected to qnr detection by PCR, i.e., Citrobacter freundii ATCC 8090 T , C. freundii ATCC 43864, C. freundii ATCC 6879, Citrobacter braakii ATCC 51113 T , and Citrobacter koseri ATCC 27028T (see Table S1 in the supplemental material). Two strains, namely, C. freundii ATCC 6879 and C. braakii ATCC 51113 T , were positive for qnrB with two different primer pairs. qnrA and qnrS were not amplified in any strain. In order to perform cloning of qnrB, a BamHI-digested genomic DNA fragment containing the qnrB-like gene and BamHI-digested, bacterial alkaline phosphatase (BAP)-treated pUC119 (TaKaRa Bio Inc., Otsu, Japan) were ligated with TaKaRa Ligation Mighty Mix (TaKaRa Bio Inc.) and chemically transformed into Escherichia coli TOP10 (Invitrogen, Carlsbad, CA). Transformants were selected on LB-agarose plates containing 0.016 g/ml of levofloxacin to screen for strains with elevated quinolone resistance and thereafter on plates containing 100 g/ml of ampicillin (Sigma-Aldrich, St. Louis, MO) to confirm that the resultant clones were truly tr...
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