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At least 19 recordsLinked to original sources
PubMed1986

Characterization and mapping of regions encoding clindamycin resistance, tetracycline resistance, and a replication function on the Bacteroides R plasmid pCP1.

The Bacteroides drug resistance plasmid pCP1 encodes clindamycin resistance (Clr) and a cryptic tetracycline resistance (Tcr) determinant that is expressed in Escherichia coli cells grown aerobically, but not anaerobically, and is not expressed phenotypically in Bacteroides spp. Localization of genetic functions on pCP1 was facilitated by the construction of hybrid shuttle plasmids containing portions of pCP1 ligated to pDG5, a pBR322 derivative carrying the RK2 transfer origin. pDP1 delta 4 is a BglII deletion derivative of pCP1 linked to pDG5 and can be maintained in both E. coli and Bacteroides fragilis. By using Tn5 mutagenesis and subcloning, we localized the Clr and Tcr regions on the EcoRI B fragment between the 1.2-kilobase direct repeats of pCP1. The Clr and Tcr determinants are distinct and appear to be transcribed separately. Control of the Tcr phenotype is unusual in that expression is constitutive and is enhanced by a region encompassing the adjacent direct repeat. In addition, a region of pCP1 required for replication in Bacteroides spp. has been identified in the neighboring EcoRI A fragment.

Bacteroides↗
PubMed1997

High-level tetracycline-resistant Neisseria gonorrhoeae in Ontario, Canada--investigation of a cluster of isolates, showing chromosomally mediated resistance to penicillin combined with plasmid-mediated resistance to tetracycline.

Between 1991 and 1994, plasmid-mediated, tetracycline-resistant Neisseria gonorrhoeae (TRNG) increased from 61.8% to 85.96% of all resistant isolates in Ontario, Canada. Ninety-nine isolates with tetracycline MICs >32 mg/L were characterized by auxotype/serovar (A/S) class, plasmid profile, hybridization with eight tetracycline-resistant probes, and pulsed-field gel electrophoresis (PFGE) of genomic DNA after digestion with NheI and SpeI restriction endonucleases. A cluster of 82 isolates with penicillin MICs of 2-4 mg/L and tetracycline MICs of 128 mg/L (chromosomally mediated resistance) belonged to A/S class NR/IB-1 and had identical or closely related PFGE profiles. Seventeen isolates, TRNG (10) and penicillinase-producing TRNG (7), with tetracycline MICs of 64-256 mg/L, belonged to eight A/S classes and displayed 12 different PFGE profiles. The 99 isolates hybridized only with the TetM probe. Phenotypic and molecular characterization indicated a diverse population throughout the Province of Ontario.

Chromosomes, Bacterial↗
PubMed2006

Inactivation of the putative tetracycline resistance gene HP1165 in Helicobacter pylori led to loss of inducible tetracycline resistance.

Tetracycline has been used with other antibiotics in treatment of Helicobacter pylori infection. However, tetracycline resistance has developed in H. pylori clinical isolates, rendering treatment failure. Mutations in 16S rRNA genes have been reported to mediate tetracycline resistance in some isolates. The diversity of tetracycline resistance cases suggests multiple genes are involved. HP1165, a putative tetracycline resistance gene in H. pylori 26695, displays 49.8% identity to the tetracycline efflux gene tetA (P) from Clostridium perfringens. To determine the function of the HP1165 gene in H. pylori, the tetracycline resistance phenotype was investigated, transcription of HP1165 was examined by RT-PCR, and a DeltaHP1165 mutant was generated by insertion of the pBCalpha3 plasmid. The results showed that strains harboring HP1165 were induced to intermediate level resistance in the laboratory (minimum inhibitory concentration=4-6 microg/ml). No mutation was found at or near the tetracycline binding sites of the 16S rRNA gene. The gene was transcribed both in the induced tetracycline resistant and wild type strains, indicating translational or posttranslational control of gene function. Mutation of HP1165 gene resulted in increased tetracycline susceptibility and loss of inducible tetracycline resistance, suggesting that the HP1165 gene is involved in the inducible tetracycline resistance in H. pylori.

Bacterial Proteins↗
PubMed1981

Resistance to tetracycline, erythromycin, and clindamycin in the Bacteroides fragilis group: inducible versus constitutive tetracycline resistance.

The transferability of plasmid-mediated tetracycline, erythromycin, and clindamycin resistance was studied in 63 clinical isolates of the Bacteroides fragilis group. Of 48 strains which were tetracycline resistant (Tcr), the regulation of both the expression of Tcr and its transferability was shown to be under inducible control by tetracycline. In 29 of the strains, Tcr was transferable; in the majority of these (26 strains), transferability was inducible (Trai) and it was constitutive (Trac) in only 3 strains. All four possible phenotypes were found (Tci Trai, Tci Trac, Tcc Trai, and Tcc Trac), which indicates independent control of both Tcr expression and its transferability. Resistance to erythromycin and clindamycin was cotransferred with Tcr in 14 of the 48 Tcr strains and transferred independently of Tcr in only 1 strain.

Bacteroides Infections↗
PubMed2003

Influence of tetracycline exposure on tetracycline resistance and the carriage of tetracycline resistance genes within commensal Escherichia coli populations.

AIMS: To assess the influence of incremental tetracycline exposure on the genetic basis of tetracycline resistance within faecal Escherichia coli. METHODS AND RESULTS: Through the adoption of a novel combination of multiple breakpoint selection, phenotypic characterization and the application of a polymerase chain reaction based gene identification system it proved possible to monitor the influence of antibiotic exposure on resistance gene possession. Using tetracycline as a case study a clear hierarchy was revealed between tet genes, strongly influenced by host antimicrobial exposure history. CONCLUSIONS: The antimicrobial exposure regime under which an animal is produced affects both the identity and magnitude of resistance gene possession of a selected bacterial population within its enteric microflora. Among the ramifications associated with such resistance gene selection is the degree of resistance conferred and the carriage of linked resistance determinants. This selection is applied by exposure to antibiotic concentrations well below recognized minimum inhibitory tetracycline concentration breakpoints widely adopted to characterize bacterial 'susceptibility'. SIGNIFICANCE AND IMPACT OF THE STUDY: This study confirms the ability of minimal antibiotic exposure to select for the continued persistence of resistance genes within the enteric microflora. It is clearly demonstrated that different antimicrobial regimes select for different resistance genes, the implications of which are discussed.

Animals↗
PubMed1999

Reversal of tetracycline resistance mediated by different bacterial tetracycline resistance determinants by an inhibitor of the Tet(B) antiport protein.

Active efflux is a useful strategy by which bacteria evade growth inhibition by antibiotics. Certain semisynthetic tetracycline (TC) analogs, substituted at the 13th carbon at C-6 on ring C of the TC molecule, blocked TC efflux as revealed in everted membrane vesicles from class B TC-resistant (Tcr) Escherichia coli (M. L. Nelson, B. H. Park, J. S. Andrews, V. A. Georgian, R. C. Thomas, and S. B. Levy, J. Med. Chem. 36:370-377, 1993). A representative C-13-substituted analog, 13-cyclopentylthio-5-OH-TC (13-CPTC), was shown to competitively inhibit TC translocation by the Tet(B) protein, blocking the uptake of TC into vesicles and therefore the efflux of TC from whole cells. Against Tcr E. coli, 13-CPTC, when used in combination with doxycycline, produced synergistic inhibition of growth. 13-CPTC was shown to increase the uptake of [3H]TC into the resistant cells. 13-CPTC alone was a potent growth inhibitor against TC-susceptible (Tcs) and Tcr Staphylococcus aureus and enterococci specifying class K or class L efflux-dependent TC resistance mechanisms or, unexpectedly, the class M ribosomal protection mechanism. These findings indicate that derivatives of TC, identified by their ability to block the Tet(B) efflux protein, can restore TC activity against Tcr bacteria bearing either of the two known resistance mechanisms. Blocking drug efflux and increasing intracellular drug concentrations constitute an effective approach to reversing TC resistance and may be generally applicable to other antibiotics rendered ineffective by efflux proteins.

Bacteria↗
PubMed2002

Toxicity of tetracyclines and tetracycline degradation products to environmentally relevant bacteria, including selected tetracycline-resistant bacteria.

Tetracyclines used in veterinary therapy invariably will find their way as parent compound and degradation products to the agricultural field. Major degradation products formed due to the limited stability of parent tetracyclines (tetracycline, chlortetracycline, and oxytetracycline) in aqueous solution were theoretically identified at various environmental conditions, such as pH, presence of chelating metals, and light. Their potency was assessed on sludge bacteria, tetracycline-sensitive soil bacteria, and tetracycline-resistant strains. Several of the degradation products had potency at the same concentration level as tetracycline, chlortetracycline, and oxytetracycline on both the sludge and the tetracycline-sensitive soil bacteria. Further, both 5a,6-anhydrotetracycline and 5a,6-anhydrochlortetracycline had potency on tetracycline-resistant bacteria supporting a mode of action different from that of the parent compounds.

Bacteria↗
PubMed1981

Minocycline treatment of tetracycline-resistant and tetracycline-responsive acne vulgaris.

The purpose of the study presented herein was to determine the safety and efficacy of minocycline in patients whose acne vulgaris failed to respond adequately to tetracycline therapy and to confirm continued improvement in tetracycline-responsive patients when minocycline was substituted for tetracycline. Thirty-six acne vulgaris patients were given oral tetracycline (250 mg four times a day) for six weeks, followed by oral minocycline (50 mg three times a day) for six weeks. An analysis of the increase or decrease in total lesion counts obtained at biweekly intervals revealed that minocycline caused statically significant improvement both in patients who did not respond to tetracycline and in patients who did respond to tetracycline. Patients who did not respond to tetracycline therapy achieved a mean decrease of 54 percent in lesions after after six weeks of minocycline treatment. In tetracycline-responsive patients, six weeks' treatment with tetracycline caused a 33.5 percent mean decrease in the lesion count. When these patients received minocycline for a subsequent six-week period, the mean lesion count decreased by an additional 60 percent. Only one patient developed a side effect: severe itching and urticaria in a minocycline-treated subject warranted discontinuance of therapy. Minocycline was a safe and effective agent in the treatment of acne both in tetracycline-resistant and in tetracycline-responsive patients.

Acne Vulgaris↗
PubMed1990

Transport of divalent cations with tetracycline as mediated by the transposon Tn10-encoded tetracycline resistance protein.

Tetracycline uptake into inverted membrane vesicles from Tn10-bearing Escherichia coli cells required divalent cations. The degree of the stimulation of tetracycline uptake by various divalent cations showed the following decreasing order: Co2+ greater than Mn2+ greater than Mg2+ greater than Cd2+ greater than Ca2+. This order is consistent with the increasing order of the dissociation constants for metal chelate complexes of tetracycline. The Hill constants for the tetracycline uptake rate with various divalent cation concentrations were one. These observations strongly suggested that a 1:1 complex of tetracycline and a divalent cation was transported by a tetracycline resistance protein. This notion was confirmed by our observations that 60Co2+ was actively taken up with tetracycline by the membrane vesicles prepared from resistant cells. In the absence of tetracycline, no uptake of 60Co2+ was observed. It is clear that the 60Co2+ uptake was mediated by the tetracycline resistance protein, because the membrane vesicles from tetracycline-sensitive cells did not show the uptake of 60Co2+ and tetracycline. The 60Co2+ uptake was inhibited in the presence of other divalent cations, without any significant effect on tetracycline uptake, indicating that these cations are also transported with tetracycline by the tetracycline resistance protein.

Biological Transport↗
PubMed2001

Molecular ecology of tetracycline resistance: development and validation of primers for detection of tetracycline resistance genes encoding ribosomal protection proteins.

Phylogenetic analysis of tetracycline resistance genes encoding the ribosomal protection proteins (RPPs) revealed the monophyletic origin of these genes. The most deeply branching class, exemplified by tet and otrA, consisted of genes from the antibiotic-producing organisms Streptomyces rimosus and Streptomyces lividans. With a high degree of confidence, the corresponding genes of the other seven classes (Tet M, Tet S, Tet O, Tet W, Tet Q, Tet T, and TetB P) formed phylogenetically distinct separate clusters. Based on this phylogenetic analysis, a set of PCR primers for detection, retrieval, and sequence analysis of the corresponding gene fragments from a variety of bacterial and environmental sources was developed and characterized. A pair of degenerate primers targeted all tetracycline resistance genes encoding RPPs except otrA and tet, and seven other primer pairs were designed to target the specific classes. The primers were used to detect the circulation of these genes in the rumina of cows, in swine feed and feces, and in swine fecal streptococci. Classes Tet O and Tet W were found in the intestinal contents of both animals, while Tet M was confined to pigs and Tet Q was confined to the rumen. The tet(O) and tet(W) genes circulating in the microbiota of the rumen and the gastrointestinal tract of pigs were identical despite the differences in animal hosts and antibiotic use regimens. Swine fecal streptococci uniformly possessed the tet(O) gene, and 22% of them also carried tet(M). This population could be considered one of the main reservoirs of these two resistance genes in the pig gastrointestinal tract. All classes of RPPs except Tet T and TetB P were found in the commercial components of swine feed. This is the first demonstration of the applicability of molecular ecology techniques to estimation of the gene pool and the flux of antibiotic resistance genes in production animals.

Animal Feed↗
PubMed1992

A Bacteroides tetracycline resistance gene represents a new class of ribosome protection tetracycline resistance.

The ribosome protection type of tetracycline resistance (Tcr) has been found in a variety of bacterial species, but the only two classes described previously, Tet(M) and Tet(O), shared a high degree of amino acid sequence identity (greater than 75%). Thus, it appeared that this type of resistance emerged recently in evolution and spread among different species of bacteria by horizontal transmission. We obtained the DNA sequence of a Tcr gene from Bacteroides, a genus of gram-negative, obligately anaerobic bacteria that is phylogenetically distant from the diverse species in which tet(M) and tet(O) have been found. The Bacteroides Tcr gene defines a new class of ribosome protection resistance genes, Tet(Q), and has a deduced amino acid sequence that was only 40% identical to Tet(M) or Tet(O). Like tet(M) and tet(O), tet(Q) appears to have spread by horizontal transmission, but only within the Bacteroides group.

Amino Acid Sequence↗
PubMed1982

A multifunctional gene (tetR) controls Tn10-encoded tetracycline resistance.

The tetracycline resistance regulatory gene (tetR) of transposon Tn10 was analyzed by a combination of methods involving gene fusion and cloning. This gene is located on a 695-base pair HincII DNA fragment near the center of Tn10. The direction of transcription is opposite to that of neighboring gene tetA, which encodes the TetA protein. The gene product of the tetR gene (the TetR protein) has a molecular weight of 23,000. tet-R-lacZ gene fusions encode fusion beta-galactosidases that are membrane bound, indicating that the TetR protein itself is membrane associated. Mutants defective in tetR result in constitutive tetracycline resistance, but the level of resistance is reduced. Expression of the tetR gene is induced by tetracycline; in the absence of tetracycline, the TetR protein turns off its own synthesis.

Bacterial Proteins↗
PubMed1989

Nomenclature for tetracycline resistance determinants.

Tetracycline resistance determinants are widespread and distinguishable genetically and biochemically. The nomenclature for this increasing number of determinants has been varied and inconsistent. This communication suggests ways of naming these determinants and their genes and gene products consistent with current genetic terminology.

Bacteria↗