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PubMed1975

Plasmid-determined resistance to erythromycin: comparison of strains of streptococcus faecalis and streptococcus pyogenes with regard to plasmid hmology and resistance inducibility.

Streptococcus faecalis strains DS-5 and Streptococcus pyogenes strain AC-1 both have a 17 million dalton plasmid that determines resistance to erythromycin, lincomycin, and vernamycin B(alpha). The results of deoxyribonucleic acid-deoxyribonucleic acid hybridization experiments indicate that the two plasmids are about 95% homologous. It was also shown that erythromycin resistance is inducible in AC-1 and constitutive in DS-5.

Drug Resistance, Microbial↗
PubMed1975

Potential for in vivo acquisition of R plasmids by one strain of Vibrio cholerae biotype El tor.

The feces of five patients admitted to a hospital during an outbreak of cholera in Melbourne, Australia, in November 1972, were examined for the presence of tetracycline-resistant coliforms and tetracycline-resistant strains of Vibrio cholerae. Despite the abundance of tetracycline-resistant coliforms able to transfer this resistance to other strains of Escherichia coli, no tetracycline-resistant strains of V. cholerae were detected. In vitro transfer experiments using the V. cholerae strain responsible for the outbreak as recipient revealed that it was a particularly poor host for most R plasmids.

Cholera↗
PubMed1975

Distribution of R plasmids among the O-antigen types of Escherichia coli isolated from human and animal sources.

The O-antigen types of 600 independently isolated Escherichia coli strains from human feces have been determined, and the types have been related to the antibiotic resistance patterns of the strains. The relative abundance of each O-antigen type differed in the susceptible and resistant series of strains. The majority (86%) of the resistant strains carried R plasmids. Resistant E. coli (20.3%) were found associated with O-antigen types 8, 9 and 101, whereas the susceptible strains covered a wide range of O-antigen types. Examination of 174 resistant strains isolated from calf feces also showed a prevalence of O-antigen types 8, 9, 101 (24.1%), and it seems probable that strains expressing these three O-antigen types commonly carry R plasmids in the alimentary tracts of man and calves. The number of strains not typeable with the O sera available were similar in the human (12.5%) and the calf (11.5%) series. There are no grounds for distinguishing "human" from "calf" E. coli on the basis of their O-antigen reactions.

Animals↗
PubMed1975

Plasmid-determined epistatic susceptibility to kasugamycin.

The effect of two representative plasmids, R100 and F8-gal, on the susceptibility of Escherichia coli to kasugamycin was studied. R(+) and F(+) cells were found to be more susceptible to this antibiotic than R(-) and F(-) cells, respectively. Retransfer and curing experiments of these plasmids show that this increased susceptibility of host cells to kasugamycin was conferred by either of the plasmids. At the early stage of growth of R100(+) cells in the presence of kasugamycin, R(-) segregants overgrew the population and then they were replaced by kasugamycin-resistant mutants of the R(+) cells which became the majority cell line of the population. The former phenomenon is assumed to be due to the increased susceptibility of R100(+) cells to kasugamycin, and the latter is probably related to the finding that R100 enhances the spontaneous mutation of host cells to resistance to kasugamycin. The practical and experimental significance of these findings are discussed.

Aminoglycosides↗
PubMed1975

Binding of bacteriocin Clo DF13 to Clo DF13 plasmid deoxyribonucleic acid in vivo and in vitro.

The bacteriocinogenic plasmid Clo DF13 is present in Escherichia coli to the extent of 10 copies per cell. A complex of Clo DF13 plasmid deoxyribonucleic acid (DNA) and protein can be isolated from cells. Treatment of the complex with ionic detergents or proteases dissociates the complex but does not convert any supercoiled Clo DF13 DNA to the open circular form, indicating that this complex is not a relaxation complex. The complex is stable in 0.5 M NaCl and contains one polypeptide species. The protein, present in the complex, appeared to be bacteriocin Clo DF13 for the following reasons: (i) the protein is de novo synthesized in Clo DF13-harboring minicells, indicating that this protein is Clo DF13 specific; (ii) this protein shows bacteriocinogenic activity on a bacteriocin Clo DF13-susceptible indicator strain; (iii) this protein has the same molecular weight (60,000) as bacteriocin Clo DF13. DNA-protein binding experiments, involving QAE-Sephadex column chromatography and nitrocellulose membrane filters, demonstrate that bacteriocin Clo DF13 has also affinity in vitro for Clo DF13 DNA. Membrane filter binding experiments revealed that bacteriocin Clo DF13 does not interact with other DNA species, such as ColE1 DNA, yeast DNA, calf thymus DNA, phiX174 DNA, and also not with denatured Clo DF13 DNA. In addition no binding to Clo DF13 DNA of a related bacteriocin, colicin E3, could be detected. These results indicate that the binding of bacteriocin Clo DF 13 to double-stranded Clo DF13 DNA is very specific.

Bacterial Proteins↗
PubMed1976

Distribution of R plasmids among the Q-antigen types of Escherichia coli isolated from various clinical sources.

A total of 655 Escherichia coli strains from various clinical sources were O-antigen typed, and the serological properties were correlated with R-plasmid carriage. Of the 655 strains, 224 were resistant to one or more antibiotics and 148 of these carried R plasmids. The distribution of O-antigen types among the susceptible strains was similar to that reported previously by others in England. The O-antigen types among the R(+) strains showed some similarities to those found in susceptible strains, but O-antigen types O8, O9, O17, O18 and, perhaps, O101 and O107 were more common in the R(+) than in the susceptible series. There is therefore some overlap between the O-antigen types of E. coli prevalent in R(+) strains from clinical cases and from human and animal fecal sources.

Antigens, Bacterial↗
PubMed1976

Chelocardin-inducible resistance in Escherichia coli bearing R plasmids.

Two plasmid-linked tetracycline resistance characters, tet A and tet B, were distinguishable in part, according to the level of resistance they conferred to minocycline (<3 mug/ml for tet A; >6 mug/ml for tet B). Escherichia coli K-12 strains that harbored the tet B character were also resistant to tetracycline but susceptible to chelocardin. In such tet B strains, subinhibitory concentrations of tetracycline could induce resistance to chelocardin as well as to otherwise inhibitory concentrations of tetracyclines. Chelocardin itself was ineffective as an inducer and therefore could be used to select constitutively resistant mutants. E. coli K-12 strains harboring the tet A character were also resistant to tetracycline and susceptible to chelocardin; tetracycline did not induce resistance to chelocardin in these strains.

Drug Antagonism↗
PubMed1976

R-factor-mediated resistance to sulfonamides by a plasmid-borne, drug-resistant dihydropteroate synthase.

Evidence was found for the existence of an episome-specified variant of the enzyme dihydropteroate synthase involved in folic acid formation. Since the plasmid-borne enzyme showed a decreased susceptibility for sulfonamide inhibition and was transferable together with resistance to this drug, it is proposed that diploidy for the target enzyme in some cases could be the mechanism of R-factor-mediated resistance to sulfonamides. Two types of evidence were obtained. One was the rescue from temperature sensitivity of bacterial mutants with a lesion in the chromosomal dihydropteroate synthase by the R factor R1dr19 mediating sulfonamide resistance. The other evidence was found by the determination of dihydropteroate forming activity in extracts from R(-) and R(+) bacteria. Cells harboring R1dr19 were found to contain an enzyme activity which was far less susceptible to sulfonamide inhibition than the corresponding activity from R(-) cells.

Dihydropteroate Synthase↗
PubMed1976

Plasmid-mediated penicillin beta-lactamases in Pseudomonas aeruginosa.

A penicillin beta-lactamase (PCase) was extracted from Pseudomonas aeruginosa Rms139(+) and purified by means of column chromatography. The isoelectric point of Rms139 PCase was 5.7 and its molecular weight was 22,500 +/- 1,000. The optimal pH for the hydrolysis of benzylpenicillin was 7.0 to 7.5 and the optimal temperature was 45 C, with the PCase also showing high activity against carbenicillin. It is concluded that this enzyme is a new type of penicillin beta-lactamase different from the type I, II, or III R plasmid-mediated PCases reported previously.

Bacterial Proteins↗
PubMed1976

Antibiotic resistance and Hly plasmids in serotypes of Escherichia coli associated with porcine enteric disease.

A total of 359 hemolytic Escherichia coli strains, representing eight pig pathogenic serotypes and isolated from pigs with enteric disease, was tested for transferable resistance to eight antibiotics. The co-transfer of plasmids controlling hemolysin production (Hly) with antibiotic resistance plasmids (R-factors) was evaluated. Transferable resistance to tetracycline, streptomycin, and/or sulfonamides was found in 47% of the total number of strains and 80% of the resistant ones. Chloramphenicol resistance was seldom seen. Co-transfer of Hly with R-factors occurred in 22.5% of the strains, generally to a degree excluding a genetic linkage. Stable coexistence of two R-factors in a cell was indicated by transfer patterns in 29 of the strains.

Animals↗
PubMed1976

Association of a penicillin resistance gene with a tetracycline resistance plasmid (PTP-2) in Staphylococcus aureus.

On transduction with a lysogenic strain of Straphylococcus aureus isolated from a clinical specimen and having tetracycline (TC)-penicillin (PC)-chloramphenicol (CP)-resistant plasmids, the three-drug-resistant strain was frequently obtained. By repeatedly transducing from this strain, a strain (TP-2) having stable resistance to TC and PC could be obtained. In transformation with the deoxyribonucleic acid (DNA) of TP-2 as donor, all of the transformants obtained by selecting with either TC or PC were both TC and PC resistant. According to electron microscopy study of the covalently closed circular DNA of TP-2, the plasmid DNA size was 1.37 +/- 0.03 mum (2.84 x 10(6) daltons). The plasmid (P(TP-2)) is presumed to be a new plasmid in which the PC resistance gene was integrated into the TC-resistant plasmid.

Culture Media↗
PubMed1976

Resistance plasmids of Pseudomonas aeruginosa: change from conjugative to nonconjugative in a hospital population.

Properties of a population of carbenicillin- and gentamicin-resistant, tobramycin-susceptible Pseudomonas aeruginosa at Veteran's Administration Hospital, Cincinnati, Ohio, have been followed during a 16-month period. As originally described, the strains were isolated from patients with urinary tract colonizations and were predominantly Parke-Davis immunotype 7. For the majority of these organisms, antibiotic resistance was correlated with the presence of a self-conjugative plasmid of incompatibility group P-2. The source and relative incidence of multiply resistant isolates have remained constant during the current study, but the immunotype has shifted form type 7 to type 2. Concomitantly, the population has lost the property of conjugative transfer of resistance, and resistant strains are now compatible with P-2 plasmids. A group P-2 R plasmid, pMG5, will mobilize resistance markers, demonstrating that the multiple resistance of the nonconjugative strains is mediated by R plasmids. Additionally, gentamicin resistance due to either conjugative or nonconjugative plasmids is correlated with the presence of similar gentamicin acetyltransferase activity. pMG5-mobilized plasmids are shown to be incompatible with pMG5. pMG5 is also shown to mobilize resistance markers from nontransferring antibiotic-resistant strains representing populations from Parkland Memorial Hospital, Dallas, Texas, and Cleveland Clinic Foundation, Cleveland, Ohio.

Acetyltransferases↗
PubMed1976

Multiresistant plasmids from Pseudomonas aeruginosa highly resistant to either or both gentamicin and carbenicillin.

High-level resistance to gentamicin and carbenicillin was found in 30 and 10.7%, respectively, of Pseudomonas aeruginosa strains, especially in isolates from urine. In 23 out of 25 strains tested, these resistances were R mediated and linked to multiresistant plasmids, carrying genes for resistances to five other aminoglycosides, tobramycin, kanamycin, neomycin, streptomycin, and spectinomycin, and for resistances to chloramphenicol, tetracycline, sulfonamides, and mercury chloride. Carbenicillin resistance was unstable in Pseudomonas, and in its presence the multiresistant plasmids had a host range extended to the Enterobacteriaceae (group I plasmids). Otherwise they were transferable intragenerically only (group II plasmids). The extended host range plasmids were, as a rule, in fi(-) incompatibility class A-C. Segregants incompatible with both class A-C and P plasmids were detected. The beta-lactamase specified by the carbenicillin marker was of the TEM-like type. Multiple linkages of resistance determinants to the aminoglycosides were concomitantly present in most of the plasmids. Results from the bioassay indicated the presence of at least two aminoglycoside-inactivating enzymes.

Anti-Bacterial Agents↗
PubMed1976

Plasmids in Streptococcus lactis: evidence that lactose metabolism and proteinase activity are plasmid linked.

Populations of lactose positive (Lac+) and proteinase positive (Prt+) cells from Streptococcus lactis M18, C10, and ML3 grown at 39 degrees C gave rise to increasing proportions of Lac- Prt- clones. The deficiencies did not appear until after a number of generations at the elevated temperature, and the rate depended on the strain.Lac- Prt+ and Lac+ Prt- mutants were isolated after treatment with ethidium bromide. Plasmid deoxyribonucleic acid was isolated by cesium chloride-ethidium bromide equilibrium density gradient centrifugation from the parent cultures as well as from their Lac- Prt-, Lac- Prt+, and Lac+ Prt- mutants. Five distinct plasmid sizes of approximate molecular weights of 2,4, 8, 21, and 27 million were found in S. lactis C10, whereas the Lac- Prt- derivative lacked the 8- and 21-million-dalton plasmids, but the 8-million-dalton plasmid was present in the Lac-Att mutant. In S. lactis m18 five plasmids possessing molecular weights of about 2, 4, 10, 18 and 27 million were observed. The 10- and 18-million-dalton plasmids were not detected in the Lac- Prt- mutants, whereas the Lac- Prt+ derivative lacked only the 18-million-dalton plasmid and the Lac+ Prt- mutant lacked only the 10-million-dalton plasmid. In S. lactis ML3 five distinct plasmids, with approximate molecular weights of 2, 4, 8, 22, and 30 million, were present. The 8- and 22-million-dalton plasmids were not detected in the Lac- Prt- derivative, but the 8-million-dalton plasmid was present in the Lac- Prt+ mutant. The evidence suggests that lactose-fermenting ability and proteinase activity in these organisms are mediated through two distinct plasmids having molecular weights of 8 x 10(6) to 10 x 10(6) for proteinase activity and 18 x 10(6) to 22 x 10(6) for lactose metabolism.

DNA, Bacterial↗
PubMed1976

Transductional evidence for plasmid linkage of lactose metabolism in streptococcus lactis C2.

A lactose-negative (Lac-), proteinase-negative (Prt-) mutant, designated C145 was isolated from Streptococcus lactis C2 after treatment with nitrosoguanidine and ultraviolet irradiation. The mutant appeared to be cured of the prophage(s) present in S. lactis C2 based on non-inducibility by ultraviolet irradiation or mitomycin C. When cleared lysate material from C145 was subjected, to cesium chloride-ethidum bromide (EB) density gradient centrifugation, no plasmid peak was observed, suggesting that C145 was cured of plasmid deoxyribonucleic and (DNA). A histogram showing distribution of contour lengths of circular molecules of DNA from C145, however, revealed the presence of a greatly diminished number of DNA molecules as compared with the parent culture and indicated the absence of the 30 x 10(6) plasmid. Cesium chloride-ethidium bromide gradient profiles from Lac+, Prt- and Lac+ Prt+ transductants of C145 revealed no plasmid peak, but electron microscopy of the fractions normally possessing the satellite band of DNA showed the presence of a new plasmid species having a molecular weight from 20 x 10(6) to 22 x 10(6). This plasmid was lost when the transductants became Lac-. Examination of a plasmid histogram from a spontaneous Lac- Prt- mutants of S. lactis C2 resembled that of C145, with the absence of the 30 x 10(6) plasmid and the presence of the 22 x 10(6) plasmid in Lac+ Prt+ transductants. The results suggest that lactose metabolism is mediated through the 30 x 10(6) plasmid in S. lactis C2 and that the transducing bacteriophage, which is too small to accommodate the entire plasmid, is transferring about two-thirds of the original plasmid through a process termed transductional shortening.

DNA, Bacterial↗
PubMed2000

A genomic sample sequence of the entomopathogenic bacterium Photorhabdus luminescens W14: potential implications for virulence.

Photorhabdus luminescens is a pathogenic bacterium that lives in the guts of insect-pathogenic nematodes. After invasion of an insect host by a nematode, bacteria are released from the nematode gut and help kill the insect, in which both the bacteria and the nematodes subsequently replicate. However, the bacterial virulence factors associated with this "symbiosis of pathogens" remain largely obscure. In order to identify genes encoding potential virulence factors, we performed approximately 2,000 random sequencing reads from a P. luminescens W14 genomic library. We then compared the sequences obtained to sequences in existing gene databases and to the Escherichia coli K-12 genome sequence. Here we describe the different classes of potential virulence factors found. These factors include genes that putatively encode Tc insecticidal toxin complexes, Rtx-like toxins, proteases and lipases, colicin and pyocins, and various antibiotics. They also include a diverse array of secretion (e.g., type III), iron uptake, and lipopolysaccharide production systems. We speculate on the potential functions of each of these gene classes in insect infection and also examine the extent to which the invertebrate pathogen P. luminescens shares potential antivertebrate virulence factors. The implications for understanding both the biology of this insect pathogen and links between the evolution of vertebrate virulence factors and the evolution of invertebrate virulence factors are discussed.

Animals↗