scholarly journals Evidence that there are two types of determinant for tetracycline resistance among R-factors

1978 ◽  
Vol 31 (1) ◽  
pp. 75-84 ◽  
Author(s):  
E. C. R. Reeve

SUMMARYA series of derepressed mutants of the tetracycline resistance (T) determinant in R-factor R57 have been found to be repressor-negative and recessive to the T determinant in R6. It is shown that these (Tdr) mutants are dominant to the inducible T determinant in RPl, indicating that the T determinants in R57 and RP1 code for different repressors of the resistance gene. The same Tdr determinants are unstable in cells carrying both the R57 mutant and RP1, probably due to selection against the dominant Tdr gene because it depresses the growth rate of the host cell compared with its T+homologue. It is suggested that the T determinants giving high-level resistance in R57, R6 and R100 form one homologous group, probably disseminated by the transposon TnlO, while T determinants giving a much lower level of resistance, such as that in RP1, form a separate group, which may include those in R46, and R199. It is proposed that the gene responsible for tetracycline resistance should be designatedtetAand the repressor genetetI. The R57 Tdr mutants then have the genotypetetI−tetA+.

1974 ◽  
Vol 24 (3) ◽  
pp. 333-343 ◽  
Author(s):  
T. J. Foster ◽  
Áine Walsh

SUMMARYThe tetracycline-resistance determinants of R-factors from different compatibility groups have been tested inEscherichia coliK12 and phenotypically classified into two major classes. Class I determinants confer high-level resistance to tetracycline (> 100 μg/ml) and moderate resistance to minocycline (5–25 μg/ml) while those of Class II gave moderate resistance to tetracycline (50–70 μg/ml) and low resistance to minocycline. Each class was subdivided because of variation in resistance profiles and in the abilities of tetracycline and minocycline to induce increased resistance. Strains carrying two compatible TetrR-factors of the same or different phenotypic groups did not show increased tetracycline resistance.


1972 ◽  
Vol 20 (2) ◽  
pp. 239-252 ◽  
Author(s):  
J. M. Robertson ◽  
E. C. R. Reeve

SUMMARYThe resistance levels conferred by the T-determinants in four R-factors to Tetracycline and Minocycline in cells ofEscherichia coliK 12, before and after induction of maximum resistance by treatment with sub-inhibitory concentrations of the drugs, are measured by simple growth-and-challenge tests. The effect of a plasmid TKwhich confers tetracycline resistance on its hostKlebsiella aerogenesis tested in the same way. The five T-determinants fall into a high-level and a low-level group for resistance, the former giving 3- to 4-fold higher resistance in both induced and uninduced cells than the latter. The T-determinants all confer much lower resistance to Minocycline (a tetracycline molecule modified at the C-6 and C-7 positions) than to Tetracycline. The main cause of this difference is that cells carrying a T-determinant exclude Minocycline much less efficiently than Tetracycline, but in addition Minocycline is less effective than Tetracycline in inducing increased resistance. These results are discussed in the light of a model put forward to explain the inducible nature of R-factor resistance to the tetracyclines.


2007 ◽  
Vol 190 (4) ◽  
pp. 1491-1494 ◽  
Author(s):  
Ricardo E. de Cristóbal ◽  
Paula A. Vincent ◽  
Raúl A. Salomón

ABSTRACT Previously, we demonstrated that Escherichia coli tolC mutations reduce the high-level resistance to tetracycline afforded by the transposon Tn10-encoded TetA pump from resistance at 200 μg/ml to resistance at 40 μg/ml. In this study, we found that the addition of an sbmA mutation to a tolC::Tn10 mutant exacerbates this phenotype: the double mutant did not form colonies, even in the presence of tetracycline at a concentration as low as 5 μg/ml. Inactivation of sbmA alone partially inhibited high-level tetracycline resistance, from resistance at 200 μg/ml to resistance at 120 μg/ml. There thus appears to be an additive effect of the mutations, resulting in almost complete suppression of the phenotypic expression of Tn10 tetracycline resistance.


2001 ◽  
Vol 45 (11) ◽  
pp. 3246-3249 ◽  
Author(s):  
Claire M. Melville ◽  
Karen P. Scott ◽  
Derry K. Mercer ◽  
Harry J. Flint

ABSTRACT A novel tetracycline resistance gene, designatedtet(32), which confers a high level of tetracycline resistance, was identified in the Clostridium-related human colonic anaerobe K10, which also carries tet(W).tet(32) was transmissible in vitro to the rumen anaerobeButyrivibrio fibrisolvens2221R. The predicted gene product oftet(32) has 76% amino acid identity with Tet(O). PCR amplification indicated that tet(32) is widely distributed in the ovine rumen and in porcine feces.


1975 ◽  
Vol 25 (3) ◽  
pp. 297-311 ◽  
Author(s):  
E. C. R. Reeve ◽  
J. M. Robertson

SUMMARYEleven mutants of R-factor R57 have been isolated which show constitutive expression of resistance to tetracycline (Tc). These derepressed (Tdr) mutants all gave a much greater resistance to Tc and to its analogue, minocycline, than could be obtained by optimal induction of cells carrying the wild-type (T+) determinant. Cells carrying each of the Tdr mutants together with T+of either R6-S or of a plasmid found inEscherichia colimi19 showed inducible Tc resistance, indicating that the Tdr mutants were all recessive, i.e. of repressor-negative type. Tdr1 was not recessive to the T-determinant of RP1, suggesting that the repressor gene products of the T-determinants in R57 and RP1 have different specificities.


1966 ◽  
Vol 7 (2) ◽  
pp. 281-286 ◽  
Author(s):  
E. C. R. Reeve

Six one-step Chloramphenicol (Cm)-resistant mutants of Escherichia coli K12 were graded for resistance to Cm, Tetracycline (Tc) and Puromyein (Pm) by streaking on minimal agar plates containing antibiotic. They fell into at least three distinct groups on the basis of their resistance patterns. One mutant showed increased sensitivity to Pm. Most of the mutants expressed their effect on resistance to Cm and Tc in the presence of R-factors carrying resistance genes for these antibiotics, but one mutant with a relatively high level of resistance to Cm had its resistance effect completely masked in the presence of R-mediated resistance. Similar cases were found among mutants selected for Cm-resistance in another strain of K12.


2021 ◽  
Author(s):  
Kai Zhou ◽  
Yingying Cheng ◽  
Yang Liu ◽  
Yong Chen ◽  
Fuman Huang ◽  
...  

The emergence of plasmid-borne tet(X) genes mediates high-level resistance of tigecycline largely threatening its clinical effectiveness. Currently, the dissemination pattern of plasmid-borne tet(X) genes remains unclear. In this study, 684 fecal and environmental samples were collected at six livestock farms, and 15 tet(X)-positive Acinetobacter isolates were recovered, mainly including 9 tet(X3)- and 5 tet(X6)-positive A. towneri strains. A clonal dissemination of tet(X3)-positive A. towneri was detected in a swine farm, while the tet(X6)-positive A. towneri strains mainly sporadically disseminated in the same farm. A tet(X3)-carrying plasmid (pAT181) was self-transmissible from a tigecycline-susceptible A. towneri strain to A. baumannii ATCC17978, causing a 128-fold and 64-512-fold increase in the MIC values of tigecycline and the other tetracyclines, respectively. Worrisomely, pAT181 was stably maintained and increased the growth rate of ATCC17978. Further identification of tet(X)s in 10,680 Acinetobacter genomes retrieved from GenBank revealed that, tet(X3) (n=249) followed by tet(X5)-like (n=61) and tet(X6) (n=53) are the prevalent alleles mainly carried by four species, and most of them are livestock associated. Phylogenetic analysis showed that most of tet(X3) and tet(X6)-positive isolates disseminate sporadically. The structures of tet(X3) and tet(X6) plasmidomes are highly diverse and no epidemic plasmids have emerged yet. However, cross-species and cross-region transmissions of tet(X3) might have been mediated by several plasmids in a small proportion of strains. Our study evidence that tet(X3) and tet(X6) currently disseminate sporadically in Acinetobacter. Continuous surveillance for tet(X)s in the context of One Health is necessary to prevent them from transmitting to humans.


2019 ◽  
Vol 64 (3) ◽  
Author(s):  
Sae Aoki ◽  
Keisuke Nakase ◽  
Hidemasa Nakaminami ◽  
Takeaki Wajima ◽  
Nobukazu Hayashi ◽  
...  

ABSTRACT Antimicrobial-resistant Cutibacterium acnes strains have emerged and disseminated throughout the world. The 23S rRNA mutation and erm(X) gene are known as the major resistance determinants of macrolides and clindamycin in C. acnes. We isolated eight high-level macrolide-clindamycin-resistant C. acnes strains with no known resistance determinants, such as 23S rRNA mutation and erm(X), from different acne patients in 2008 between 2013 and 2015. The aim of this study was to identify the novel mechanisms of resistance in C. acnes. Whole-genome sequencing revealed the existence of a plasmid DNA, denoted pTZC1 (length, 31,440 bp), carrying the novel macrolide-clindamycin resistance gene erm(50) and tetracycline resistance gene tet(W). pTZC1 was detected in all C. acnes isolates (eight strains) exhibiting high-level macrolide-clindamycin resistance, with no known resistance determinants (MIC of clarithromycin, ≥256 μg/ml; clindamycin, ≥256 μg/ml). Transconjugation experiments demonstrated that the pTZC1 was horizontally transferred among C. acnes strains and conferred resistance to macrolides, clindamycin, and tetracyclines. Our data showed, for the first time, the existence of a transferable multidrug-resistant plasmid in C. acnes. Increased prevalence of this plasmid will be a great threat to antimicrobial therapy for acne vulgaris.


2020 ◽  
Vol 8 (8) ◽  
pp. 1240
Author(s):  
Sangjukta Roy ◽  
Meiji Soe Aung ◽  
Shyamal Kumar Paul ◽  
Salma Ahmed ◽  
Nazia Haque ◽  
...  

Enterococcus faecalis is one of the major causes of urinary tract infection, showing acquired resistance to various classes of antimicrobials. The objective of this study was to determine the prevalence of drug resistance and its genetic determinants for E. faecalis clinical isolates in north-central Bangladesh. Among a total of 210 E. faecalis isolates, isolated from urine, the resistance rates to erythromycin, levofloxacin, and gentamicin (high level) were 85.2, 45.7, and 11.4%, respectively, while no isolates were resistant to ampicillin, vancomycin and teicoplanin. The most prevalent resistance gene was erm(B) (97%), and any of the four genes encoding aminoglycoside modifying enzyme (AME) were detected in 99 isolates (47%). The AME gene aac(6′)-Ie-aph(2”)-Ia was detected in 46 isolates (21.9%) and was diverse in terms of IS256-flanking patterns, which were associated with resistance level to gentamicin. Tetracycline resistance was ascribable to tet(M) (61%) and tet(L) (38%), and mutations in the quinolone resistance-determining region of both GyrA and ParC were identified in 44% of isolates. Five isolates (2.4%) exhibited non-susceptibility to linezolide (MIC, 4 μg/mL), and harbored the oxazolidinone resistance gene optrA, which was located in a novel genetic cluster containing the phenicol exporter gene fexA. The optrA-positive isolates belonged to ST59, ST902, and ST917 (CC59), while common lineages of other multiple drug-resistant isolates were ST6, ST28, CC16, and CC116. The present study first revealed the prevalence of drug resistance determinants of E. faecalis and their genetic profiles in Bangladesh.


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