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At least 19 recordsLinked to original sources
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↗
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

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↗
PubMed1978

R factors from Enterobacter group.

Twenty-six R factors transmissible to E. coli K12 were derived from 79 strains of Enterobacter species isolated in various clinical specimens (urine, sputum, blood, pus); 71 of 79 strains were Enterobacter cloacae. Fifteen R factors were fi+: 14 belonged to group FII, 1 to group FI. Eleven R factors were fi-: 5 belonged to group M, of the others 6 (all controlling the cloramphenicol-resistance) 1 was recognized of group K, 1 was incompatible with standard plasmids of both groups S and W, and 4 belonged to group S.

Anti-Bacterial Agents↗
PubMed1975

Genetic transfer of Pseudomonas aeruginosa R factors to plant pathogenic Erwinia species.

The R factors RP1, R68 and R91 were freely transmissible to and from Pseudomonas aeruginosa, Salmonella typhimurium, and various plant pathogenic Erwinia spp. The antibiotic resistance spectrum of R+ Erwinia recipients was similar to those of other bacteria harboring these R factors, but maximum resistance levels differed with each recipient. The sponstaneous elimination of these factors from the Erwinia strains and the ability to transfer multiple antibiotic resistance suggest that these exist as plasmids in these hosts. Several, but not all, RP1-carrying Erwinia strains were sensitive to the RP1 specific phage PRR1. The R factor R18-1 was also transferred from P. aeruginosa to Erwinia spp. R18-1 was unstable in all Erwinia strains. Stable strains were isolated in which R18-1 could not be eliminated by sodium dodecyl sulfate and could not be transferred to other strains.

Anti-Bacterial Agents↗
PubMed1977

R factor types found in Salmonella typhimurium and Escherichia coli isolated from calves in a confined environment.

Typing of R factors by genetic properties was done with Salmonella typhimurium and Escherichia coli isolated from calves on a feedlot where epizootics of clinical or subclinical calf salmonellosis had repeatedly occurred during 5 years. Forty-nine R factors from S typhimurium were fi- (no fertility inhibition) and spp- (no restriction against phage lambda vir). Twenty-three (46.9%) of them belonged to compatibility group Ialpha and the remainder were nontypable. Fourteen R factors from E coli belonged to different genetic types: fi+ (11=78.6%) and fi- (3=21.4%); spp+ (1=7.1%) and spp- (13=92.9%); compatibility groups FII (5=35.7%), N (1=7.1%), and nontypable (8=57.2%). In contrast to the R factors of S typhimurium, 9 (64.3%) of the 14 R factors of E coli carried resistance against aminobenzyl penicillin with or without kanamycin resistance. The compatibility groups of R factors of S typhimurium seemed to be useful as a subsidiary epizootiologic marker in this feedlot.

Ampicillin↗
PubMed1975

[Suppresion of the R-factor transduction transmission of antibiotic resistance markers in E. coli by distamycin A].

Some mechanisms of inhibition by distamycin A of transduction of antibiotic resistance markers of R-factors (RI drd and R222) with the moderate phage PI kc in E. coli were studied. The kinetics of the transduction of the R-factor markers was investigated in comparison with the stages of interaction of PI kc phage particles with bacterial cells of E. coli K-12 carrying the R-factors such as RI and R222 -- phage PI kc -- E. coli C6000. Later the effect of distamycin A on transduction of the above R-factors was studied using the same system. It was shown that distamycin A in concentrations of 75 gamma/ml suppressed the transduction of the R-markers when added to the transduction mixture simultaneously with the phage. The transduction rate decreased 15 times if the drug was added 5 minutes after beginning of the phage contact with the recipient culture. Addition of distamycin A at the 20th minute of the experiment induced no inhibition of the transduction of the R-factor markers. Preliminary 18-hour exposure to distamycin A of the recipient culture and phagolysates possessing transduction capacity resulted in decreased rates of the transduction of the antibiotic resistance markers 35 to 40 times. No inhibitory effect of distamycin A on the process of phenotypic manifestation of the antibiotic resistance markers of the R-factors was noted. The experiments showed that distamycin A affected the early stages of interaction of the transducing particles with the recipient culture, possibly the process of penetration of the transducing DNA of the R-factors into the cells of the recipient culture.

Anti-Bacterial Agents↗
PubMed1976

The effect of long term tetracycline treatment for acne vulgaris on the occurrence of R factors in the intestinal flora of man.

R factors are known to be the most important mechanism of antimicrobial resistance of intestinal flora. Short courses with therapeutic doses (1000 mg/day) of tetracycline select for strains containing transferable resistance factors to more than one antimicrobial agent. In this report we show that long term treatment with very low doses (100 mg/day) of tetracycline for acne vulgaris has an equally strong effect favouring establishment of resistent strains and R factors in the intestinal flora of patients.

Acne Vulgaris↗
PubMed1978

R-factor mediated dihydrofolate reductases which confer trimethoprim resistance.

Six different R-factors conferring trimethoprim resistance had been isolated from a variety of sources. The trimethoprim-resistant dihydrofolate reductases (EC 1.5.1.3) from strains containing these R-factors were purified by ammonium sulphate precipitation and DEAE-cellulose ion-exchange chromatography. The enzymes showed no significant differences in molecular weight, pH profile, substrate profile, heat sensitivity, inhibition profile and Michaelis-Menten kinetics. There was, however, considerable variation in the specific activity of these enzymes in the same bacterial host. When two Escherichia coli trimethoprimsensitive dihydrofolate reductases were examined as controls, considerable differences between their properties and those of the enzymes mediated by R-factors were detected. The data suggest that one trimethoprim resistance gene could be spreading through the bacterial population, possibly situated on a transposon.

Escherichia coli↗
PubMed1979

Effect of a Salmonella group H1 R factor on virulence and response of infections to antimicrobial therapy.

A group H1 R factor encoding resistance to chloramphenicol, streptomycin, sulfonamide, and tetracycline was transferred into Salmonella typhimurium LT-2. The virulence of LT-2 for mice, as assessed by intraperitoneal 50% lethal dose and the number of organisms in the spleen, was not affected by the R factor. On the other hand, the R factor conferred resistance in mouse infections to therapy with chloramphenicol and trimethoprim plus sulfamethoxazole.

Animals↗