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At least 19 recordsLinked to original sources
PubMed1975

[Caffeine as an inhibitor of the conjugation transfer of R-factors. A study of the quantitative effect of caffeine on the conjugation transfer of R-factors].

The effect of caffeine on the conjugation transfer of R-factors was studied using a standartized kinetic conjugation system described earlier. It was shown that caffeine had a pronounced inhibitory effect on R-factor transfer. The inhibition coefficients at a caffeine concentration of 2000 gamma/ml were from 2.5 (when using strain CSH-2 R222 of E. coli as the donor) to 13.8 (when using strain J5-3 RI drd of E. coli as the donor). Higher concentrations of caffeine induced a significant increase in the coefficient. Since R-transfer inhibition was induced by rather high concentrations of caffeine, the effect of equivalent concentrations of some normal metabolites of the purine and pyrimidine series, such as ATP, guanine, cytosine and thymine was studied. It was shown that the substances had no inhibitory effect on R-factor transfer. Inhibition of P-transfer by caffeine did not depend on either the type of R-factor or the microbial host.

Bacteriological Techniques↗
PubMed1975

[Caffeine as an inhibitor of the conjugation transfer of R-factors. A study of certain aspects of the mechanism of action of caffeine on the conjugation transfer of R-factors].

Some aspects of the inhibitory effect of caffeine on conjugation transfer of R-factors described by the authors earlier were studied. The effect of the above substance on the donor and recipient competence was tested in experiments with cultivation of the parent strains for 18 hours in the presence of caffeine. For this purpose the effect of caffeine on reduction of the donor and recipient cell competence after starvation in a physiological solution was investigated. It was shown that caffeine markedly decreased the donor competence of strain 15-3Mdrd of E. coli in the experiments of both types. Caffeine also inhibited reduction of the recipient competence of strain C600 of E. coli after starvation without its changing on 18-hour treatment. For the study of the caffeine effect on formation of the conjugation pairs experiments were carried out with dilution of the conjugation mixture after definite intervals which practically stopped formation of new conjugation pairs and eliminated further effect of caffeine on conjugation. Under such conditions transfer of R-factors may occur in the conjugation pairs after elimination of caffeine by dilution, if they were formed in the presence of caffeine before the mixture dilution. The experiments showed that caffeine inhibited not the formation of the conjugation pairs but the genetic transfer of R-factors. In addition, it was found that the substance insignificantly inhibited the process of phenotypic manifestation of the resistance markers. Inhibition of conjugation R-transfer by caffeine was associated with its eliminating effect, since the concentrations used did not induce elimination of the resistance markers in R+ strains.

Caffeine↗
PubMed1976

Restriction and modification of Shigella flexneri phages by R factors.

Out of 420 R factors derived from Shigella flexneri strains, 50.8% restricted Escherichia coli and S. flexneri phages. Phage restriction was produced both by fi- and fi+ R factors. The R factors were divided into nine groups on the basis of the efficiency of plating of S. flexneri phages. Changes of phage types were produced by transferring R factors of different restrictive types. The changes offered some information concerning the evolution of phage types. Studies on phage modification supported the grouping of R factors determined on the basis of restriction. R factors of different restrictive types were type-specific except for types VII and IX. Modified phages proved to be highly practical for epidemiological purposes. The use of modified phages, as an additional phage-set besides that basic phage-set, was suggested to trace the source of strains which changed their phage types as an effect of R factors.

Bacteriophage Typing↗
PubMed1979

[Mechanisms of R-factor coded resistance (author's transl)].

The prevalence of resistance factors (R-factors) has become a serious threat to the chemotherapeutic armament of modern medicine. These extrachromosomal elements exert their effects by supplying the harbouring bacterial cell with the genetic information for detoxifying enzymes, for the expression of biochemical mechanisms which effectively prevent antibiotic molecules from reaching their target or for the synthesis of resistant target molecules. The genes which are responsible for these effects were recently shown to reside on "transposons", genetic entities which can recombine with various DNA moieties, like plasmids, bacterial chromosomes, or the genome of bacteriophages. The transposon nature of most resistance determinants provide the bacterial world with an enormous flexibility in the response to antibiotic selection pressure. It is an absolute requirement for the future to stop further spread of R-factors by reducing the selection pressure. Doctors will have to apply antibiotics more selectively, and in animal breeding and growth promotion only those drugs should be used which are never prescribed for humans. Moreover, pharmaceutical research should be directed towards the development of compounds acting on R-factors or on their enzyme systems.

Anti-Bacterial Agents↗
PubMed1975

[Transmissivity of the various R factors found among E. coli cultures circulating under natural conditions].

Transmissivity of drug resistance in wild strains of E. coli was shown to be determined not only by the presence of the transmissive factor and r-determinants in the microbial cell, but also by the functional activity of the R-factor. The capacity of the R-factor for transmission depended to a certain extent on the number of the r-determinants in the R-factor and the presence of various r-determinants in the R-factor.

Ampicillin↗
PubMed1975

Denaturation mapping of R factor deoxyribonucleic acid.

The R factor NR1 consists of two components: a resistance transfer factor which harbors the tetracycline resistance genes (RTF-TC) and the r-determinants component which harbors the other drug resistance genes. Using partial denaturation mapping it is possible to distinguish the RTF-TC region from the r-determinants region of the composite R factor NR1 DNA which has a contour length of 37 mum and a density of 1.712 g/ml. The r-determinants region was a relatively undenatured 8.5-mum segment of the molecule when the deoxyribonucleic acid was partially denatured at pH 10.7. An RTF-TC genetic segregant of NR1 which had lost the r-determinants component had a contour length of 28.7 mum and a density of 1.710 g/ml. Characterization of an RTF-TC using partial denaturation mapping at pH 10.7 confirmed that the relatively undenatured 8.5-mum r-determinants segment of the composite R factor had been deleted. Circular, transitioned NR1 DNA molecules (1.716 to 1.718 g/ml), whose contour lengths were consistent with an RTF-TC plus an integral number of tandem copies of r-determinants, were also characterized by denaturation mapping. The relatively undenatured region in these molecules had a length equal to an integral number of copies of r-determinants and was located at the same site in the partially denatured RTF-TC as the single copy of r-determinants in the 37-mum composite NR1. This indicates that there is a unique integration site for r-determinants in the RTF-TC component. The R factor UCR122, a TC deletion mutant of NR1, was also characterized by denaturation mapping. The translocation of the TC resistance gene(s) on the denaturation map permitted the alignment of the denaturation map with the heteroduplex map of Sharp et al. (u073). Linear and circular monomeric and presumed multimeric r-determinants DNA molecules (p = 1.718 g/ml) were partially denatured at a higher pH (11.10). The r-determinants multimers showed a repeating 8.3-mum (monomeric) partial denaturation pattern indicating a head-to-tail arrangement of monomers in these poly-r-determinant molecules.

DNA, Bacterial↗
PubMed1976

The purification and properties of the trimethoprim-resistant dihydrofolate reductase mediated by the R-factor, R388.

The R-factor R388 mediates the production of a trimethoprim-resistant dihydrofolate reductase. This enzyme has a different molecular weight and pH profile to the trimethoprim-sensitive enzyme of the Escherichia coli host. The R-factor mediated enzyme was separated completely from the host E. coli enzyme by DEAE-cellulose ion-exchange chromatography. The purified R-factor enzyme was about 20 000 times less susceptible to trimethoprim than the E. coli enzyme and although it was inhibited competitively by trimethoprim, its inhibitor constant (Ki) was 20 000 times greater than that of the host enzyme. The R388 and E. coli enzymes also differed in their substrate specificity requirements. In addition, the R388 enzyme suprisingly conferred high level resistance to the broad spectrum dihydrofolate reductase inhibitor, amethopterin. The possible origins of the R388 enzyme are discussed.

Drug Resistance, Microbial↗
PubMed1977

Penicillin-binding proteins of Escherichia coli. Comparison of a strain carrying an R-factor and the parent strain.

Both from Escherichia coli K12 W3630 carrying an R-factor, R+75, and from the parent strain at least six penicillin- and cephalosporin-binding proteins were obtained as soluble forms. The molecular weights of the binding proteins of the strain carrying an R-factor were similar to those of the parent strain and not affected by the presence of an R-factor which specified the production of a beta-lactamase. Gel filtration with [14C]benzylpenicillin suggested the equimolar binding of benzylpenicillin to each binding protein. Three binding proteins of E. coli carrying R+75 and two binding proteins of the parent strain were purified by affinity chromatography followed by gel filtration. In fluorescence titration, various penicillins and cephalosporins were shown to bind to the purified binding proteins and their association constants were in the range of 0.4 to 21-10(3) M-1. The binding proteins of both strains did not react with the antibody against the beta-lactamase specified by R+75.

Carrier Proteins↗
PubMed1976

Restriction and modification of typing phages by an R factor in S. typhi.

We have investigated the qualities of one R factor 552 discovered on a strain of S. typhi resistant to A, C, S, T, nontypable, isolated from stool cultures; from the same patient, before starting the treatment we isolated, from his blood sample, the strain S. typhi 221, sensitive to A, C, T, degraded phage-type Vi A. Factor R 552 fi- when infecting strains of S. typhi Vi A and of A degraded 221- leads to the conversion of the respective phage-types into non-typable ones, as a result of the restricting and modifying effect on phage Vi A and on the derivatives resulting from it. Derivative R 552-1 as a resistance marker to ampicilline has a restrictive effect on the phage of S. panama A 47 too. Not taking into account possible causes such as spontaneous mutation, lysogeny, and adsorption of phages, we reach for the conclusion that R factor 552, through is restrictive effect, is the only cause responsible for the existence in the same patient of two strains of S. typhi different from the point of view of phage-type and antibiotype.

Bacteriophage Typing↗
PubMed1975

Further properties of P-2 R-factors of Pseudomonas aeruginosa and their relationship to other plasmid groups.

R-factors of the P-2(prototype R-factor R931) incompatibility group of plasmidsdetected in Pseudomonas are compatible with group P,C,W, and NR-factors which areplasmids that can be transferred to Pseudomonas aeruginosa recipients. Members of the P-2 group (R130,R931) have significant homology by DNA-DNA hybridization. R-factors of the P-group (RP1, RP9) and F-group (R1) exhibited homology with P-2 R-factors but to a lesser extent than R130 with R931. Members of the I, C, and W groups showed no significant homology with P-2 R-factors. Minicircular DNA of strain 931(R931) was not homologous with R931 DNA. The host range of R931 and R130 is limited mainly to certain Pseudomonas species including P. aeruginosa, P. fluorescens, P. putida, and P. stutzeri. These R-factors could not be transferredat detectable frequencies to any member of the Enterobacteriaceae examined. R-factor-specified pili were strongly suggested by the detection of pili by electron microscopyin R-+ but not R- non-piliated mutants of P. aeruginosa strain PA01. The combinedproperties of R-factors 931 and similar R-factors reported before and in this study strongly support our previous contention that this group of R-factors form a significant new group of plasmids. A classification scheme previously proposed for plasmids occurring in Pseudomonas has been modified and four groups have been specified.

Bacteriophages↗
PubMedDate not supplied

Compatibility behaviour of some newly isolated F-like R factor.

The incompatibility reactions of four new R factors have been determined against reference plasmids of the compatibility groups FI, FII, FIII, FIV, FV, FVI and various not F-like groups. Two R factors have been found to belong to group FII, while one of the two other plasmids was incompatible with representatives of the FII and FI groups. The last R factor was incompatible with plasmids of FII and P groups. It seems, therefore, that R factors with incompatibility for more than one group of plasmids occur frequently in nature.

Ampicillin↗
PubMed1975

Gentic properties of an R factor carrying resistance to aminolgycoside antibiotics.

R factor Rms 151 is an fi+ R factor and belongs to a incompatibility group FII. It carries the genes governing resistance to various aminoglycoside antibiotics, i.e., kanamycin (KM), lividomycin (LV), gentamicin C complex (GM), and 3',4'-dideoxykanamycin B (DKB), in addition to those governing to tetracycline (TC), chloramphenicol (CM), sulfanilamide (SA), and ampicillin (APC). Electron microscopy observation disclosed that the Rms151 deoxyribonucleic acid was a circular form with length of 31.2 mum. A probable circular genetic map of Rms151 was proposed by genetic and biochemical studies, the genes being in the order of -tet-tra-amp-aad-sul-aph-cml-, in which aad and aph confer resistance to KM.GM.DKB by adenylytransferase or resistance to KM.LV by phosphotransferase, respectively.

Aminoglycosides↗
PubMed1975

Transposition of R factor genes to bacteriophage lambda.

Transpositions of segments of R factor (antibiotic resistance plasmids) to bacteriophage lambda have been selected and characterized. Cells of Escherichia coli harboring R factors that determine kanamycin resistance were infected with phage lambda, and lambdakan transducing lines were obtained. Each of the three examined is unusual when compared to lambda transducing phages containing E. coli chromosomal genes: the kan insertions (a) occur at several sites, each well removed from the integration region POP', (b) are not associated with deletion of lambda phage DNA, and (c) are separable from the lambda genome during transduction or during lytic growth. Two insertions from the same R factor contain 1.5 kilobase sequences repeated in inverted order. The properties of the lambdakan phage suggest that R factors contain systems capable of mediating genetic exchange in the absence of extensive DNA homology. It is suggested that such systems of exchange may have played important roles in R factor evolution.

Chromosome Mapping↗
PubMed1975

Transduction of various R factors by Plkc phage.

Transduction of R-factors with phage Rlkc was studied. Six of the R-factors controlled resistance to single antibacterial drugs, such as tetracycline, levomycetin, ampicillin, neomycin, streptomycin and nitrofurans. When the donor strains produced bacteriocins, treatment of the transducing lysates with trypsine increased the yield of the R+-transductants. Transduction of the resistance determinants was not in most cases accompanied with lysogenization of the recipient cells. It was confirmed that transduction with phage Rlkc provided division of the R-factors into 2 groups, i. e. those with the resistance determinants possessing transferability after transduction and those with the determinants possessing no such ability. It was supposed that one of the causes of the R+-transductant inability to transferance of the resistance determinants on conjugation was their intergration into the recipient chromosomes on transduction.

Ampicillin↗