Dissemination of the tetM tetracycline resistance determinant to Ureaplasma urealyticum

Roberts, Marilyn C.; Kenny, George E.

doi:10.1128/aac.29.2.350

Cited by 123 publications

(81 citation statements)

References 22 publications

(9 reference statements)

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“…Koutsky et al 1983). Tetracycline-resistant strains of U. urealyticum and M. hominis have recently been shown to contain DNA sequences homologous to the streptococcal tetracycline-resistance determinant tet M (Roberts et al 1985;Roberts & Kenny, 1986 (Hudson, 1971), for 12 bovine strains of mycoplasma. The susceptibility of these strains showed marked variation with MICs ranging from 0-06-60 4tsg ml-'; those strains with the lowest MIC (0-06 ,tg ml-') required the greatest number of passages (16-18) in antibiotic-containing medium to acquire a high level of resistance (100 lg ml-').…”

Section: Discussionmentioning

confidence: 99%

Antibiotic sensitivity and mutation rates to antibiotic resistance inMycoplasma mycoidesssp.mycoides

Lee

Milès

Inal³

1987

Epidemiol. Infect.

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SUMMARYThe antibiotic resistance ofMycoplasma mycoidesssp.mycoidesstrain T1was investigated. This strain was resistant to high levels ( > 100 μg ml−1) of rifampicin and nalidixic acid. It was sensitive to streptomycin, spectinomycin and novobiocin; however, single step mutants with high levels of resistance ( > 100 μg ml−1) were readily isolated. With erythromycin and tylosin for which the minimum inhibitory concentration (MIC) for the parent strain was < 0·1 μg ml−1, mutants resistant to > 100 μg ml−1were obtained in two and three steps respectively. The MIC of tetracycline in single step resistant mutants (0·6 μg ml−1) was tenfold higher than the parent strain, but could not be increased further. There was only a twofold increase in resistance to chloramphenicol in single step mutants. The frequency of resistant mutants varied with the antibiotic and was between 4× 10minuss;6and 2× 10−8. The mutation rate to antibiotic resistance to streptomycin, spectinomycin, novobiocin, erythromycin and tylosin was between 3× 10−8and 5× 10−9per cell per generation. There was a fivefold decrease in mutation rate to resistance to 60 μg ml−1streptomycin compared to that to 20 μg ml−1.

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Section: Discussionmentioning

confidence: 99%

Antibiotic sensitivity and mutation rates to antibiotic resistance inMycoplasma mycoidesssp.mycoides

Lee

Milès

Inal³

1987

Epidemiol. Infect.

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“…Most work on bacterial resistance has either been conducted with pathogenic bacteria, which usually cause disease when present, or opportunistic bacteria, which occasionally cause disease (145,146,157,160,223,229,230,(232)(233)(234)(235)(236)(237)(238)(239)(240)(241)(242)(243)(244). Opportunistic bacteria are often part of the host's normal flora and can cause disease when they leave their normal sites.…”

Section: Incidence Of Tetracycline Resistancementioning

confidence: 99%

Tetracycline Antibiotics: Mode of Action, Applications, Molecular Biology, and Epidemiology of Bacterial Resistance

Chopra

Roberts

2001

Microbiol Mol Biol Rev

3,572

2,643

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Tetracyclines were discovered in the 1940s and exhibited activity against a wide range of microorganisms including gram-positive and gram-negative bacteria, chlamydiae, mycoplasmas, rickettsiae, and protozoan parasites. They are inexpensive antibiotics, which have been used extensively in the prophlylaxis and therapy of human and animal infections and also at subtherapeutic levels in animal feed as growth promoters. The first tetracycline-resistant bacterium, Shigella dysenteriae, was isolated in 1953. Tetracycline resistance now occurs in an increasing number of pathogenic, opportunistic, and commensal bacteria. The presence of tetracycline-resistant pathogens limits the use of these agents in treatment of disease. Tetracycline resistance is often due to the acquisition of new genes, which code for energy-dependent efflux of tetracyclines or for a protein that protects bacterial ribosomes from the action of tetracyclines. Many of these genes are associated with mobile plasmids or transposons and can be distinguished from each other using molecular methods including DNA-DNA hybridization with oligonucleotide probes and DNA sequencing. A limited number of bacteria acquire resistance by mutations, which alter the permeability of the outer membrane porins and/or lipopolysaccharides in the outer membrane, change the regulation of innate efflux systems, or alter the 16S rRNA. New tetracycline derivatives are being examined, although their role in treatment is not clear. Changing the use of tetracyclines in human and animal health as well as in food production is needed if we are to continue to use this class of broad-spectrum antimicrobials through the present century

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“…Five of these determinants, Tet A to Tet F, are found only in gram-negative bacteria (11,12,14), while Tet K, Tet L, Tet N, and Tet P have previously been described only for gram-positive species (1,4,7,23). Tet M has been found in gram-positive (3)(4)(5)(6)20), gram-negative (8,13,20,23), and cell-wall-free species (18,19), whereas Tet 0 has been associated with Streptococcus spp., Enterococcus spp. (23), and Campylobacter spp.…”

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confidence: 99%

“…A number of species of urogenital bacteria, including anaerobic, aerobic, gram-positive, and gram-negative species, are tetracycline resistant, and many carry the Tet M determinant (8,9,13,18,19). The aim of the present study was to investigate whether other genera found in the urogenital tract, such as Lactobacillus spp., were tetracycline resistant and whether they carried any of the previously described tetracycline determinants.…”

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confidence: 99%

Genetic basis of tetracycline resistance in urogenital bacteria

Roberts

Hillier

1990

Antimicrob Agents Chemother

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The distributions of the nucleotide sequences related to the tetracycline resistance determinants Tet K, Tet L, Tet M, and Tet 0 were studied by dot blot hybridization with randomly chosen clinical urogenital tract isolates of viridans group streptococci, Streptococcus agalactiae, Enterococcus faecalis, Gardnerella vaginalis, Lactobacillus spp., Fusobacterium nuckatum, Peptostreptococcus spp., and Veilonella parvula. Among the Peptostreptococcus spp., 79% of the isolates hybridized with one (64%) or more (36%) of the probes for Tet K (27%), Tet L (30%), Tet M (75%) and Tet 0 (13%). Of the viridans group streptococci, 82% of the strains hybridized with one (34%) or more (66%) of the four probes. The distribution of the four determinants in this group was as follows: Tet K, 36%; Tet L, 31%; Tet M, 43%; Tet 0, 61%. Twenty-nine percent of the enterococci and forty-six percent of the group B streptococci hybridized with the probes; however, the Tet K, Tet L, and Tet 0 determinants were found in only a few strains, while the Tet M determinant predominated. A total of 29% of the F. nucleatum isolates, 55% of the G. vaginalis isolates, and 26% of the V. parvula isolates hybridized with the Tet M determinant. In contrast, 43% of the Lactobacillus spp. hybridized with the Tet 0 determinant. The data indicate that tetracycline resistance determinants are common to many of the microorganisms isolated from the urogenital tract.

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Dissemination of the tetM tetracycline resistance determinant to Ureaplasma urealyticum

Cited by 123 publications

References 22 publications

Antibiotic sensitivity and mutation rates to antibiotic resistance inMycoplasma mycoidesssp.mycoides

Antibiotic sensitivity and mutation rates to antibiotic resistance inMycoplasma mycoidesssp.mycoides

Tetracycline Antibiotics: Mode of Action, Applications, Molecular Biology, and Epidemiology of Bacterial Resistance

Genetic basis of tetracycline resistance in urogenital bacteria

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