Browse
Submit Data
Databases
API
Help

Dataset Information

20 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Presence of tetracycline resistance determinants and susceptibility to tigecycline and minocycline.

ABSTRACT: No relation between the presence of tetracycline resistance determinants tet(A) to tet(E) and the MICs of tigecycline was observed for Enterobacteriaceae, although tetracycline-susceptible isolates were more susceptible overall to tigecycline, whereas the presence of tet(M) in Staphylococcus aureus was associated with higher MICs of minocycline.

SUBMITTER: Fluit AC

PROVIDER: S-EPMC1068614 | biostudies-literature | 2005 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Presence of tetracycline resistance determinants and susceptibility to tigecycline and minocycline.

Fluit Ad C AC Florijn Alice A Verhoef Jan J Milatovic Dana D

Antimicrobial agents and chemotherapy 20050401 4

No relation between the presence of tetracycline resistance determinants tet(A) to tet(E) and the MICs of tigecycline was observed for Enterobacteriaceae, although tetracycline-susceptible isolates were more susceptible overall to tigecycline, whereas the presence of tet(M) in Staphylococcus aureus was associated with higher MICs of minocycline. ...[more]

PMID: 15793159

Similar Datasets

Comparative pharmacokinetics of chlortetracycline, tetracycline, minocycline, and tigecycline in broiler chickens.

Project description:Tetracyclines continue to be important antimicrobials in veterinary medicine. However, the pharmacokinetics (PK) of tigecycline (TIG) and minocycline (MIN) in broiler chickens has not been investigated to date, and the PK of chlortetracycline (CTC) and tetracycline (TET) remains insufficiently researched, especially in terms of absorption. These antimicrobials have never been compared in a single setting in a single species; therefore, the aim of the present study was to compare the PK of TIG, MIN, CTC, and TET in broiler chickens. Each drug (10 mg/kg) was administered intravenously (IV) and orally (PO). The plasma concentrations of each drug were determined by liquid chromatography-tandem mass spectrometry, and the results were analyzed using compartmental and non-compartmental PK models. Despite the fact that all of the studied antimicrobials were administered at an identical IV dose, the area under the concentration-time curve between zero and the last sampling point (AUC0→t) for MIN (35,014 ± 3,274 μg × hour/mL) and CTC (41,851 ± 10,965 μg × hour/mL) differed significantly from that determined for TIG (18,866 ± 4,326 μg × hour/mL) and TET (17,817 ± 4,469 μg × hour/mL). After IV administration, the values of AUC0→t were also directly related to total body clearance values which were significantly higher for TIG (0.56 ± 0.14 L/hour × kg) and TET (0.60 ± 0.14 L/hour × kg) than for CTC (0.25 ± 0.05 L/hour × kg) and MIN (0.29 ± 0.03 L/hour × kg). In turn, after PO administration, TIG was absorbed in only 1.55% ± 0.82, and CTC in 30.54% ± 6.99, whereas the bioavailability of MIN and TET was relatively high at 52.33% ± 3.92 and 56.45% ± 9.71, respectively. The differences in PK parameters between these drugs, despite their structural similarities, suggest that active transport mechanisms may play a role in their absorption and distribution.

| S-EPMC7598109 | biostudies-literature

Potential of Tetracycline Resistance Proteins To Evolve Tigecycline Resistance.

Project description:Tigecycline is a glycylcycline antibiotic active against multidrug-resistant bacterial pathogens. The objectives of our study were to examine the potential of the Tet(A), Tet(K), Tet(M), and Tet(X) tetracycline resistance proteins to acquire mutations causing tigecycline resistance and to determine how this affects resistance to earlier classes of tetracyclines. Mutations in all four tet genes caused a significant increase in the tigecycline MIC in Escherichia coli, and strains expressing mutant Tet(A) and Tet(X) variants reached clinically relevant MICs (2 mg/liter and 3 mg/liter, respectively). Mutations predominantly accumulated in transmembrane domains of the efflux pumps, most likely increasing the accommodation of tigecycline as a substrate. All selected Tet(M) mutants contained at least one mutation in the functionally most important loop III of domain IV. Deletion of leucine 505 of this loop led to the highest increase of the tigecycline MIC (0.5 mg/liter) among Tet(M) mutants. It also caused collateral sensitivity to earlier classes of tetracyclines. A majority of the Tet(X) mutants showed increased activity against all three classes of tetracylines. All tested Tet proteins have the potential to acquire mutations leading to increased MICs of tigecycline. As tet genes are widely found in pathogenic bacteria and spread easily by horizontal gene transfer, resistance development by alteration of existing Tet proteins might compromise the future medical use of tigecycline. We predict that Tet(X) might become the most problematic future Tet determinant, since its weak intrinsic tigecycline activity can be mutationally improved to reach clinically relevant levels without collateral loss in activity to other tetracyclines.

| S-EPMC4750697 | biostudies-literature

Tetracycline resistance and presence of tetracycline resistance determinants tet(V) and tap in rapidly growing mycobacteria from agricultural soils and clinical isolates.

Project description:Rapidly growing mycobacteria (RGM) inhabit soil and water but certain strains represent a health risk for human and animals. Both clinical and soil RGM may be under selection pressure for resistance to tetracycline (TET) antibiotics, since tetracyclines are administrated to humans and farm animals, and TET residues enter soil through manuring; however, resistance to TET and the presence of TET-resistance genes have been assessed only in clinical isolates. We were therefore interested in comparing soil and clinical RGM in terms of TET resistance and the presence of TET-resistance genes. We used 44 RGM from grasslands with different exposure to animal manure, and 38 clinical RGM from Czech hospitals. There was no difference between the clinical and soil isolates in TET resistance, with >50% resistant isolates in both groups. otr(A), otr(B), tet(K), tet(L) or tet(M) were not detected in any soil or clinical isolate. In contrast, most isolates harbored tet(V) and tap, both encoding mycobacterial efflux pumps, including species where these genes have never been evidenced before. The phylogeny of tet(V) correlated with isolates' BOX-PCR profiles, suggesting that this gene evolved along with mycobacterial genomes as a part of the intrinsic resistome. In certain cases, tet(V) and/or tap were found in TET-sensitive isolates, or inversely, were not found in resistant strains. Concluding, intrinsic efflux pumps may be more important for TET resistance than horizontally transferred genes in both soil and clinical RGM. Their simple presence, however, does not attest to resistance, and therefore their diversity, function and expression merit further research.

| S-EPMC4103549 | biostudies-literature

Nomenclature for new tetracycline resistance determinants.

Project description:Letters of the English alphabet have heretofore been used to name tetracycline resistance determinants. Since all 26 letters have now been used, a nomenclature employing numerals is recommended for future determinants, and one laboratory has offered to coordinate the assignment of numerals.

| S-EPMC89314 | biostudies-literature

Genetic Determinants of Tigecycline Resistance in Mycobacteroides abscessus

Project description:Mycobacteroides abscessus (formerly Mycobacterium abscessus) is a clinically important, rapid-growing non-tuberculous mycobacterium notoriously known for its multidrug-resistance phenotype. The intrinsic resistance of M. abscessus towards first- and second-generation tetracyclines is mainly due to the over-expression of a tetracycline-degrading enzyme known as MabTetX (MAB_1496c). Tigecycline, a third-generation tetracycline, is a poor substrate for the MabTetX and does not induce the expression of this enzyme. Although tigecycline-resistant strains of M. abscessus have been documented in different parts of the world, their resistance determinants remain largely elusive. Recent work on tigecycline resistance or reduced susceptibility in M. abscessus revealed the involvement of the gene MAB_3508c which encodes the transcriptional activator WhiB7, as well as mutations in the sigH-rshA genes which control heat shock and oxidative-stress responses. The deletion of whiB7 has been observed to cause a 4-fold decrease in the minimum inhibitory concentration of tigecycline. In the absence of environmental stress, the SigH sigma factor (MAB_3543c) interacts with and is inhibited by the anti-sigma factor RshA (MAB_3542c). The disruption of the SigH-RshA interaction resulting from mutations and the subsequent up-regulation of SigH have been hypothesized to lead to tigecycline resistance in M. abscessus. In this review, the evidence for different genetic determinants reported to be linked to tigecycline resistance in M. abscessus was examined and discussed.

| S-EPMC9137676 | biostudies-literature

Tetracycline resistance determinants in Mycobacterium and Streptomyces species.

Project description:Two of seven tetracycline-resistant (Tcr) Mycobacterium fortuitum group isolates and six Tcr clinical Streptomyces isolates carried gram-positive Tcr determinants (Tet K and Tet L) and Streptomyces resistance determinants (Otr A, Otr B, and Otr C). This represents the first documentation of the acquisition by mycobacteria of determinants coding for antibiotic resistance and suggests the potential for the spread of antibiotic resistance determinants within mycobacterial species.

| S-EPMC188220 | biostudies-other

Genetic determinants of tetracycline resistance in Vibrio harveyi.

Project description:Isolates of Vibrio harveyi, a prawn pathogen, have demonstrated multiple antibiotic resistance to commonly used antimicrobial agents, such as oxytetracycline. In this paper, we describe the cloning and characterization of two tetracycline resistance determinants from V. harveyi strain M3.4L. The first resistance determinant, cloned as a 4,590-bp fragment, was identical to tetA and flanking sequences encoded on transposon Tn10 from Shigella flexneri. The second determinant, cloned as a 3,358-bp fragment in pATJ1, contains two open reading frames, designated tet35 and txr. tet35 encodes a 369-amino-acid protein that was predicted to have nine transmembrane regions. It is a novel protein which has no homology to any other drug resistance protein but has low levels of homology (28%) to Na(+)/H(+) antiporters. Transposon mutagenesis showed that tet35 and txr were required for tetracycline resistance in a heterologous Escherichia coli host. Tetracycline accumulation studies indicate that E. coli carrying tet35 and txr can function as an energy-dependent tetracycline efflux pump but is less efficient than TetA.

| S-EPMC127092 | biostudies-literature

Genetic basis of tetracycline and minocycline resistance in potentially probiotic Lactobacillus plantarum strain CCUG 43738.

Project description:The potentially probiotic strain Lactobacillus plantarum CCUG 43738, which displayed atypical phenotypic resistance to tetracycline (MIC, 512 microg/ml) and minocycline (MIC, 256 microg/ml), was found to contain a tet(S) gene located on a plasmid of approximately 14 kb. Plasmid curing with novobiocin eliminated this plasmid and restored the tetracycline-susceptible phenotype of the host strain.

| S-EPMC1426919 | biostudies-literature

Characterization of tetracycline and erythromycin resistance determinants in Treponema denticola.

Project description:Treponema denticola isolates were evaluated for the presence of known tetracycline and erythromycin resistance determinants by Southern blot hybridization of whole-cell DNA and PCR assays. We examined all isolates available, which included 12 clinical and 4 American Type Culture Collection isolates. Two isolates carried the Tet B determinant, five isolates carried both the Tet B and Erm F determinants, seven isolates carried the Erm F determinant, and two did not carry any of the Tet or Erm determinants tested. Both the Tet B and Erm F determinants appeared to be associated with the chromosome. Neither of the two T. denticola donors tested could transfer the Tet B determinant, but three of four T. denticola tested transferred the Erm F determinant to an Enterococcus faecalis recipient. This extends the host range of both the tetB and ermF genes into the genus Treponema.

| S-EPMC163396 | biostudies-other

Tigecycline susceptibility and the role of efflux pumps in tigecycline resistance in KPC-producing Klebsiella pneumoniae.

Project description:KPC-producing Klebsiella pneumoniae isolates have emerged as important pathogens of nosocomial infections, and tigecycline is one of the antibiotics recommended for severe infections caused by KPC-producing K. pneumoniae. To identify the susceptibility profile of KPC-producing K. pneumoniae to tigecycline and investigate the role of efflux pumps in tigecycline resistance, a total of 215 KPC-producing K. pneumoniae isolates were collected. The minimum inhibitory concentration (MIC) of tigecycline was determined by standard broth microdilution tests. Isolates showing resistance to tigecycline underwent susceptibility test with efflux pump inhibitors. Expression levels of efflux pump genes (acrB and oqxB) and their regulators (ramA, marA, soxS and rarA) were examined by real-time PCR, and the correlation between tigecycline MICs and gene expression levels were analysed. Our results show that the tigecycline resistance rate in these isolates was 11.2%. Exposure of the tigecycline-resistant isolates to the efflux pump inhibitor NMP resulted in an obvious decrease in MICs and restored susceptibility to tigecycline in 91.7% of the isolates. A statistically significant association between acrB expression and tigecycline MICs was observed, and overexpression of ramA was found in three tigecycline-resistant isolates, further analysis confirmed ramR mutations existed in these isolates. Transformation of one mutant with wild-type ramR restored susceptibility to tigecycline and repressed overexpression of ramA and acrB. These data indicate that efflux pump AcrAB, which can be up-regulated by ramR mutations and subsequent ramA activation, contributed to tigecycline resistance in K. pneumoniae clinical isolates.

| S-EPMC4348519 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data