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Resistance to tetracycline, macrolides and streptomycin was measured for a period of 8 months in soil bacteria obtained from farmland treated with pig manure slurry. This was done by spread plating bacteria on selective media (Luria Bertani (LB) medium supplemented with antibiotics). To account for seasonal variations in numbers of soil bacteria, ratios of resistant bacteria divided by total count on nonselective plates were calculated. Soil samples were collected from four different farms and from a control soil on a fifth farm. The control soil was not amended with animal manure. The occurrence of tetracycline-resistant bacteria was elevated after spread of pig manure slurry but declined throughout the sampling period to a level corresponding to the control soil. Higher load of pig manure slurry yielded higher occurrence of tetracycline resistance after spreading; however, the tetracycline resistance declined to normal occurrence defined by the tetracycline resistance occurrence in the control soil. Concentrations of tetracycline in soil and in pig manure slurry were measured using HPLC. No tetracycline exceeding the detection limit was found in soil samples. Manure slurry concentrations of tetracycline for three of the farms were 42, 81 and 698 microg/l, respectively. For streptomycin and macrolides, only minor variations in resistance levels were detected. Results obtained in this study thus indicate that tetracycline resistance levels in soil are temporarily influenced by the addition of pig manure slurry. The results indicate also that increased amount of pig manure slurry amendment may result in increased levels of tetracycline resistance in the soil.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12504155&dopt=Abstract antibiotics, tetracycline




Antimicrob Agents Chemother. 1987 Nov;31(11):1739-43.
Cryptic tetracycline resistance determinant (class F) from Bacteroides fragilis mediates resistance in Escherichia coli by actively reducing tetracycline accumulation.

Park BH, Hendricks M, Malamy MH, Tally FP, Levy SB.

Department of Molecular Biology, Tufts University School of Medicine, Boston, Massachusetts 02111.

Escherichia coli bearing a cryptic tetracycline resistance determinant from Bacteroides fragilis expressed low-level constitutive resistance to tetracycline under aerobic, but not anaerobic, growth conditions and accumulated less tetracycline aerobically than did isogenic susceptible cells. This decreased uptake was energy dependent and reversible by increased concentrations of tetracycline, suggesting a saturable carrier-mediated active efflux mechanism. Decreased uptake was not seen when the cells were grown and assayed anaerobically. Other tetracycline resistance determinants (classes A to E) isolated from gram-negative enteric bacteria expressed resistance and generated active efflux of tetracycline under anaerobic as well as aerobic conditions. When the Bacteroides determinant was placed in the same cell with any of the class A to E tetracycline resistance determinants, there was an increase in resistance under aerobic conditions of as much as 48% more than was projected by adding the resistances expressed by the determinants individually. In cells bearing the class A determinant together with the Bacteroides determinant, saturation of the active efflux system required over twofold more exogenous tetracycline than did cells bearing the class A determinant alone. We have designated this new tetracycline resistance determinant class F.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3324960&dopt=Abstract antibiotics, tetracycline




East Afr Med J. 1993 May;70(5):255-8.
Acquired tetracycline resistance genes in nosocomial Salmonella typhimurium infection in a Kenyan hospital.

Kariuki S, Olsvik O, Mitema E, Gathuma J, Mirza N.

Centre for Microbiology Research, Kenya Medical Research Institute, Nairobi.

Tetracyclines have been among the most widely used antibiotics worldwide. Plasmid-mediated tetracycline resistance among hospital strains of bacteria has continued to rise and of major concern has been the transfer of resistance to pathogenic organisms. Bacteraemia due to hospital acquired S. typhimurium has been a major cause of morbidity at Kenyatta National Hospital (KNH), hence the need to study drug susceptibility pattern of this organism. This study also characterized the tetracycline resistance genes using oligonucleotide probes. Ninety seven S. typhimurium strains isolated from patients at KNH were used. Agar dilution method was used to determine minimum inhibitory concentration (MIC). Plasmids were isolated from each strain and the different plasmid profiles were grouped by their molecular weights into 6 patterns. Out of 97, 87 (88%) strains were resistant. MIC ranged from 1 microgram/ml to 128 micrograms/ml. Genes encoding for tetracycline resistance were located on plasmids of molecular weights 65 MDa, 5.2 or both. Plasmid-encoded antimicrobial resistance is likely to spread to other pathogenic organisms, reduce our ability to treat the infection and increase the cost and duration of treatment.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8306897&dopt=Abstract antibiotics, tetracycline




Ann Med Interne (Paris). 1977 Jun-Jul;128(6-7):521-6.
[Current importance of resistance of group A streptococci to tetracyclines]

[Article in French]

Frottier J.

The resistance of group A streptococci to tetracyclines is a long-standing phenomenon, observed in numerous countries. Sixty strains of group A streptococcus, isolated in 1975 and 6976 at the Claude Bernard Hospital, were tested against natural and semi-synthetic tetracyclines and penicillin G. Whilst sensitivity to the latter was constant, approximately 30% of strains were resistant to tetracyclines. Amongst them, minocycline was nevertheless a little more active than natural tetracycline and doxycycline. The mechanism of this resistance would seem to be extra-chomosomal.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=335943&dopt=Abstract antibiotics, tetracycline




Antibiotiki. 1979 Mar;24(3):193-7.
[Streptococcus group A resistance to tetracycline: its spread and transduction]

[Article in Russian]

Bulgakova TN.

The study on antibiotics resistance of group A streptococci isolated in 1977 showed that the number of the antibiotic resistant strains had significantly increased as compared to the data of 1960. High percentage (53%) of the cultures with multiple resistance was noted. It was observed that the number of the streptococcal cultures resistant to erythromycin and chloramphenicol decreased while the number of the strains resistant to tetracyclines increased. The level of resistance to tetracycline increased more than 2 times from 1960 and in some cases reached 125 and 250 gamma/ml. The wide spread of tetracycline resistance was evident of the presence of the mechanism of the marker transduction. Possible transduction of this feature was studied. Microbe-free phagolysates obtained by induction with UV-light from the strains with multiple antibiotic resistance were used as the donor material in the experiment on transduction. Principal possibility of transducing resistance to tetracycline from 2 donors to 4 recipients at a frequency of 10(-6) was shown.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=375816&dopt=Abstract antibiotics, tetracycline




J Clin Microbiol. 2000 Jun;38(6):2103-7.
High rate of tetracycline resistance in Streptococcus pyogenes in Iran: an epidemiological study.

Jasir A, Tanna A, Noorani A, Mirsalehian A, Efstratiou A, Schalen C.

Department of Infectious Diseases and Medical Microbiology, University of Lund, Lund, Sweden.

Streptococcus pyogenes, a major human pathogen, is still considered susceptible to beta-lactams, but for other relevant antibiotics, highly variable resistance rates have been reported. Since no data were available from Iran, we tested 1,335 throat isolates from two different regions of the country for their antibiotic susceptibilities and, for comparison, a collection of 80 strains isolated from 1989 to 1991. Erythromycin resistance was uncommon (0.6%), whereas an overall high rate of tetracycline resistance was found, increasing between 1989-1991 and 1995-1997 from 23 to 42%. The tetracycline-resistant strains belonged to more than 10 different T types, the majority being types 4, 11, and B3264. By conventional M typing of 406 tetracycline-resistant isolates, more than 20 different M types were found. Approximately 50% of the strains were nontypeable by T agglutination as well as serological M typing; however, by genotyping by a combined PCR-capture-enzyme-linked immunosorbent assay, many of these strains were successfully emm typed. We conclude that the high rate of tetracycline resistance among Iranian S. pyogenes isolates is due to multiclonal dissemination of resistance within the streptococcal population rather than epidemic spread of single clones.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10834960&dopt=Abstract antibiotics, tetracycline




J Clin Pathol. 1975 Mar;28(3):195-7.
Detection of tetracycline resistance in Streptococcus pneumoniae.

Stewart SM, Anderson ME, Malcolm MG.

Bacteriological details are given of a patient with chronic purulent bronchitis, who was being followed up during a survey of relapse in chronic bronchitis. A strain of Streptococcus pneumoniae, serotype 10, was isolated from the sputum over a period of six months, followed by a type 47A strain and later a type 28 strain. The patient was receiving prophylactic treatment with tetracycline throughout. The type 10 strain was sensitive to tetracycline in vitro by both the disc diffusion and doubling dilution sensitivity tests and mice infected with this strain were protected by tetracycline. In contrast, both the type 47A and type 28 strains were sensitive by the disc diffusion technique, but showed a low degree of tetracycline resistance by the doubling dilution method; mice infected with both these strains were not protected by tetracycline.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1123446&dopt=Abstract antibiotics, tetracycline




Antimicrob Agents Chemother. 2002 Dec;46(12):3940-6.
Emergence of tetracycline resistance in Helicobacter pylori: multiple mutational changes in 16S ribosomal DNA and other genetic loci.

Dailidiene D, Bertoli MT, Miciuleviciene J, Mukhopadhyay AK, Dailide G, Pascasio MA, Kupcinskas L, Berg DE.

Department of Molecular Microbiology, Washington University Medical School, St. Louis, Missouri 63110, USA.

Tetracycline is useful in combination therapies against the gastric pathogen Helicobacter pylori. We found 6 tetracycline-resistant (Tet(r)) strains among 159 clinical isolates (from El Salvador, Lithuania, and India) and obtained the following four results: (i) 5 of 6 Tet(r) isolates contained one or two nucleotide substitutions in one part of the primary tetracycline binding site in 16S rRNA (AGA(965-967) [Escherichia coli coordinates] changed to gGA, AGc, guA, or gGc [lowercase letters are used to represent the base changes]), whereas the sixth (isolate Ind75) retained AGA(965-967); (ii) PCR products containing mutant 16S ribosomal DNA (rDNA) alleles transformed recipient strains to Tet(r) phenotypes, but transformants containing alleles with single substitutions (gGA and AGc) were less resistant than their Tet(r) parents; (iii) each of 10 Tet(r) mutants of reference strain 26695 (in which mutations were induced with metronidazole, a mutagenic anti-H. pylori agent) contained the normal AGA(965-967) sequence; and (iv) transformant derivatives of Ind75 and of one of the Tet(r) 26695 mutants that had acquired mutant rDNA alleles were resistant to tetracycline at levels higher than those to which either parent strain was resistant. Thus, tetracycline resistance in H. pylori results from an accumulation of changes that may affect tetracycline-ribosome affinity and/or other functions (perhaps porins or efflux pumps). We suggest that the rarity of tetracycline resistance among clinical isolates reflects this need for multiple mutations and perhaps also the deleterious effects of such mutations on fitness. Formally equivalent mutations with small but additive effects are postulated to contribute importantly to traits such as host specificity and virulence and to H. pylori's great genetic diversity.

Source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12435699&dopt=Abstract antibiotics, tetracycline