Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PROTEUS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,063 records · Page 59Linked to original sources
PubMed1986

Induction of beta-lactamase in Proteus vulgaris.

Various beta-lactam antibiotics, including monocyclic beta-lactams, induced the beta-lactamase of Proteus vulgaris; when clinical isolates were induced by benzylpenicillin, each strain produced a single beta-lactamase but the activity per milligram dry weight differed from strain to strain. The beta-lactamases of the P. vulgaris strains were heterogeneous with respect to their isoelectric points, but had almost the same specific activities, substrate specificities and Michaelis constants. The kinetics of beta-lactamase formation were investigated in three strains, each with a different beta-lactamase activity. Differential rates of enzyme synthesis and peak activity depended on the concentration of inducer. The plots of the reciprocals of the differential rates versus the reciprocals of the inducer concentrations were linear, and the maximum rate of enzyme synthesis and the concentration of the inducer giving half-maximum induction were determined from this double reciprocal plot. The maximum rates of enzyme synthesis were different in the three strains. The kinetic analysis of beta-lactamase formation revealed that the beta-lactamase activities in a single bacterial species were determined by differences in the rate of enzyme synthesis and not by differences in the properties of the enzyme.

Cephalosporins↗
PubMed1986

Effect of R-plasmid RP1 on surface hydrophobicity of Proteus mirabilis.

The presence of R-plasmid RP1, as well as the conditions of growth, affected the surface hydrophobicity of a clinical isolate of Proteus mirabilis. However, results depended upon the method of assessment. Stationary phase plasmid-containing cells appeared to be less hydrophobic than plasmid-free cells when hydrophobicity was measured by the contact angle method, but more hydrophobic when measured by bacterial adherence to hydrocarbons or hydrophobic interaction chromatography. Cells growing in a chemostat differed in hydrophobicity from stationary phase cells and results varied with the growth rate. Plasmid-mediated effects were greatest in iron-depleted cells, and differences between plasmid-containing and plasmid-free cells were virtually eliminated by pre-treatment with antiserum.

Chromatography↗
PubMed1987

Cloning and expression in Escherichia coli of Proteus vulgaris genes for 16S ribosomal RNA.

In contrast to the established systems of plasmid-coded homologous ribosomal DNA (rDNA) cistrons in Escherichia coli little is known about the fate of heterologous rRNA. In order to study expression of foreign rDNA, rRNA cistrons from Proteus vulgaris were cloned in phage vector Charon 35, subcloned in pBR322 and transformed in E. coli. The inserts of two clones (pPM2 and pPM14) were characterized by restriction analysis and Southern hybridization. Each of them harboured a complete rrn cistron. The location of rRNA genes of clone pPM2 was also verified by R-loop analysis. The 5' flanking region of the 16S rRNA of pPM2 was sequenced and compared to the E. coli counterparts. High-level homologies exist in the functional parts of this region, e.g. promoters, box A and RNAase III recognition site. The copy number of pPM2 and pPM14 was estimated to be 8 and 10, respectively. Clones showed a markedly reduced growth rate (generation time about 57 to 70 min) as compared to the non-transformed cells (generation time 40 min). rDNA cistrons of P. vulgaris were properly expressed and the transcripts are processed as demonstrated by the presence of 16S rRNA from P. vulgaris in both ribosomes and 30S ribosomal subunits isolated from the transformed E. coli cells. The fraction of heterologous rRNA in ribosomes was about 25%.

Amino Acid Sequence↗
PubMed1990

Restoration of hydrogenase activity in hydrogenase-negative strains of Escherichia coli by cloned DNA fragments from Chromatium vinosum and Proteus vulgaris.

DNA fragments from Proteus vulgaris and Chromatium vinosum were isolated which restored hydrogenase activities in both hydA and hydB mutant strains of Escherichia coli. The hydA and hydB genes, which map near minute 59 of the genome map, 17 kb distant from each other, are not structural hydrogenase genes, but mutation in either of these genes leads to failure to synthesize any of the hydrogenase isoenzymes. The smallest DNA fragments which restored hydrogenase activity to both E. coli mutant strains were 4.7 kb from C. vinosum and 2.3 kb from P. vulgaris. These fragments were cleaved into smaller fragments which did not complement either of the E. coli mutations. The cloned heterologous genes also restored formate hydrogenlyase activity but they did not restore activity in hydE, hupA or hupB mutant strains of E. coli. The cloned genes, on plasmids, did not lead to the synthesis of proteins of sufficient size to be the hydrogenase catalytic subunit. The hydrogenase proteins synthesized by hydA and hydB mutant strains of E. coli transformed by cloned genes from P. vulgaris and C. vinosum were shown by isoelectric and immunological methods to be E. coli hydrogenase. Thus, these genes are not hydrogenase structural genes.

Blotting, Southern↗
PubMed1991

Composition of the outer membrane of Proteus mirabilis in relation to serum sensitivity in progressive stages of cell form defectiveness.

A serum-resistant strain of Proteus mirabilis was used to determine whether changes in the composition of surface components could be detected following induction of progressive stages of cell form defectiveness by beta-lactam antibiotics. The critical stage was the conversion from filaments to the spheroplast form, which was accompanied by increased susceptibility to the bactericidal action of human serum. Inner and outer membranes of the bacterium, its filament form and its spheroplast form were separated by sucrose density-gradient centrifugation after digestion of peptidoglycan, followed by osmotic lysis of the cells. Outer membranes of the bacterial and the filament forms sedimented at the same density, whilst the outer membrane fraction of the spheroplast form sedimented in a region of lesser density. In addition, the amounts of two major outer-membrane proteins as well as the O-polysaccharide content of the lipopolysaccharide were reduced in the spheroplast form. These results indicate a general disorganization in structure and assembly of components in regard to their interactions with one another in the outer membrane of the spheroplast form.

Anti-Bacterial Agents↗
PubMed1992

Recombination and UV resistance of Escherichia coli with the cloned recA and recBCD genes of Serratia marcescens and Proteus mirabilis: evidence for an advantage of intraspecies combination of P. mirabilis RecA protein and RecBCD enzyme.

In Escherichia coli, constituents of the main recombination pathway are provided by the genes recA (RecA protein) and recBCD (RecBCD enzyme). Recombination in conjugation experiments and repair of UV damage of E. coli mutants deleted for recA, for recBCD or for recA plus recBCD were restored, although to different degrees, by the cloned recA and recBCD genes from Serratia marcescens or Proteus mirabilis. When both recombination enzymes were from the same species, repair and recombination efficiencies had the order E. coli greater than S. marcescens greater than P. mirabilis. However, the P. mirabilis recA plus recBCD genes resulted in higher levels of repair and recombination than those obtained with one component from P. mirabilis (recA or recBCD) and the other from E. coli or S. marcescens. The data provide evidence for the similarity of RecABCD pathways of recombination among enteric bacteria and suggest an in vivo advantage of an intraspecies combination of P. mirabilis RecA protein and RecBCD enzyme over interspecies combinations. This could point to a cooperation between these basic recombination enzymes. The molecular processes which could be involved are discussed.

Cloning, Molecular↗
PubMed1993

Dependence of induction of enterobacterial AmpC beta-lactamase on cell-wall peptidoglycan, as demonstrated in Proteus mirabilis and its wall-less protoplast L-form.

The mobilizable plasmid pMD101 (ampR, ampC) was constructed by inserting cloned ampC, the structural gene for the chromosomal AmpC beta-lactamase of Citrobacter freundii, and the closely linked ampR encoding the transcriptional regulator essential for enzyme induction, into the broad host-range plasmid pKT231. Plasmid pMD101 was transconjugated into Proteus mirabilis VI and its isogenic, cell-wall-less protoplast L-form LVI. AmpC beta-lactamase was expressed constitutively from cloned ampR and ampC in bacteria and in some L-form protoplasts. However, induction of the enzyme by beta-lactam antibiotics occurred only in bacterial cells and not in the cell-wall- and peptidoglycan-deficient L-form. In agreement with current models, induction of AmpC beta-lactamase is thought to be initiated by an induction signal arising from the metabolic disturbance of cell-wall peptidoglycan.

Bacterial Proteins↗
PubMed1994

Cloning and sequencing of the Proteus mirabilis gene for a single-stranded DNA-binding protein (SSB) and complementation of Escherichia coli ssb point and deletion mutations.

The gene of Proteus mirabilis coding for a single-stranded DNA-binding protein (SSB) was cloned in Escherichia coli from a genomic library. It restored the UV resistance and the rate of cell division of an E. coli ssb-113 mutant to the same extent as the cloned E. coli ssb+ gene did. An E. coli mutant with deleted ssb was viable with the P. mirabilis ssb+ gene provided on a single-copy-number plasmid and had the same cell division rate as with the E. coli ssb+ gene on the same vector plasmid. The recovery from UV damage of an excision repair deficient (uvrA) mutant deleted for the ssb gene was identical with the ssb+ gene from P. mirabilis or E. coli, suggesting full substitution in recombinational DNA repair of the homologous by the heterologous SSB protein. The nucleotide sequence of the gene revealed that the SSB has 81% amino acid sequence homology with the E. coli SSB and only 58-63% with various plasmid SSBs. The data provide evidence that the bacterial chromosomally coded SSBs and the plasmid encoded SSBs constitute separate groups.

Amino Acid Sequence↗
PubMed2002

Swarming-coupled expression of the Proteus mirabilis hpmBA haemolysin operon.

The HpmA haemolysin toxin of Proteus mirabilis is encoded by the hpmBA locus and its production is upregulated co-ordinately with the synthesis and assembly of flagella during differentiation into hyperflagellated swarm cells. Primer extension identified a sigma(70) promoter upstream of hpmB that was upregulated during swarming. Northern blotting indicated that this promoter region was also required for concomitant transcription of the immediately distal hpmA gene, and that the unstable hpmBA transcript generated a stable hpmA mRNA and an unstable hpmB mRNA. Transcriptional luxAB fusions to the DNA regions 5' of the hpmB and hpmA genes confirmed that hpmB sigma(70) promoter activity increased in swarm cells, and that there was no independent hpmA promoter. Increased transcription of the hpmBA operon in swarm cells was dependent upon a 125 bp sequence 5' of the sigma(70) promoter -35 hexamer. This sequence spans multiple putative binding sites for the leucine-responsive regulatory protein (Lrp), and band-shift assays with purified Lrp confirmed the presence of at least two such sites. The influence on hpmBA expression of the key swarming positive regulators FlhD(2)C(2) (encoded by the flagellar master operon), Lrp, and the membrane-located upregulator of the master operon, UmoB, was examined. Overexpression of each of these regulators moderately increased hpmBA transcription in wild-type P. mirabilis, and the hpmBA operon was not expressed in any of the flhDC, lrp or umoB mutants. Expression in the mutants was not recovered by cross-complementation, i.e. by overexpression of FlhD(2)C(2), Lrp or UmoB. Expression of the zapA protease virulence gene, which like hpmBA is also upregulated in swarm cells, did not require Lrp, but like flhDC it was upregulated by UmoB. The results indicate intersecting pathways of control linking virulence gene expression and swarm cell differentiation.

Amino Acid Sequence↗
PubMed1975

Chromosome transfer in Proteus mirabilis mediated by hybrid plasmid.

A previously-described fused plasmid, P-lacRIdrd19, was found to mediate chromosomal transfer between cells of Proteus mirabilis strain PM5006; PM5006-(P-lacRIdrd19) was usually the donor and various auxotrophs of PM5006 resistant to nalidixic acid and/or streptomycin were recipients. The donor was usually counterselected with nalidixic acid and/or high concentrations of streptomycin. Recombination experiments with single markers indicated a 40-fold variation in recombination frequencies for different markers. Mapping double-auxotrophic markers by their gradient of transmission confirmed this variation and placed each of two independent isolates of eight markers in a linkage group his-ser-ura-pyrB-trp-cys-ade-ilv. Some donor markers did not register. Despite low recombination frequencies, interrupted mating experiments showed a polarity of early marker transfer. The segregation of unselected markers confirmed the order of some markers and showed that genetic material passed from the presumptive donor to the recipient. Recipients with two auxotrophic markers which could not be cotransduced by phage 5006M were converted to prototrophy by conjugation. The plasmid transferred to recipients at high frequency and all recombinants carried it. Recombinants could act as donors in further matings. Recombinants were fully susceptible to phage 5006M, unlike transductants of PM5006 by this phage. Direct involvement of the plasmid was indicated by drastically diminished recombination frequencies in crosses with recipients carrying P-lac as resident. P-lac had previously been shown to reduce the frequency of transfer of the hybrid plasmid to cells harbouring it. The histidine region was the first to register in recipients and recombined at the highest frequency of 5 times 10-6/donor cell. Some temporary association of plasmid and perhaps only the histidine region of the chromosome is favoured as the mechanism of chromosomal transfer. This could explain why not all donor markers could be mapped. Transduction and transformation were excluded as the cause of results.

Chromosome Mapping↗
PubMed1976

Transduction of leucine auxotrophs of Proteus mirabilis to prototrophy or antibiotic resistance by P. mirabilis high frequency transducing bacteriophages.

High frequency transducing (HFT) phages 5006MHFTk and 5006MHFTak for kanamycin or ampicillin plus kanamycin resistance, derived from Proteus mirabilis strains PM5006(R394) and PM5006(R394) respectively, transduced (at low multiplicities of infection, m.o.i.) antibiotic resistance and prototrophy to PM5006 leu-I at high frequency. Simultaneous transduction of these markers occurred at very much lower frequencies. The latter result was correlated with the proportion of multiply-infected bacteria which, due to the great transducing potential of the phage, could register as transductants. Each HFT lysate was thus heterogenous with regard to high frequency transducing phage. Apart from the additional antibiotic resistance marker carried by one phage, no other difference between the two lysates was detected. High segregation frequencies of antibiotic-resistant or prototrophic transductants indicated transduction by lysogenization. Although antibiotic-sensitive segregants of antibiotic-resistant prototrophic transductants occurred at high frequency, no auxotrophic segregants of these transductants were found. This suggests transduction by a double cross-over event in the leucine region. Most transductants, even at low m.o.i., were lysogenically converted to homologous phage non-adsorption as a result of interaction between the transducing phage genome and the resident cryptic prophage. They could, however, be retransduced by appropriate phage lysates; thus, lysogenic conversion to non-adsorption was not absolute. Some prototrophic transductants were non-lysogenic although their segregants liberated low-titre phage. The latter anomaly, and the fact that the leucine marker and antibiotic resistance were not cotransduced, are explained by the mode of integration of the phage into the host chromosome in relation to the resident cryptic prophage and the leucine region.

Adsorption↗
PubMed1976

Intra-species tranduction with Proteus mirabilis high frequency transducing phages.

The properties of three additional Proteus mirabilis hosts for the high frequency transducing (HET) phages 5006MHFTkappa and 5006MHFTak are described. The phages transduce resistance to kanamycin and to ampicillin plus kanamycin, respectively, and were produced by ultraviolet induction of derivatives of P. mirabilis strain PM5006. Strain PM804 could not be shown to adsorb the phages although it yielded a few transductants. All transductants, even those produced at low multiplicities of phage input were lysogenic and segregated markers at high frequency. Ultraviolet induced phage lysates of these transductants transduced PM804 at higher frequencies and PM5006 at lower frequencies than the original phages. Strain PM804 or its derivatives did not adsorb phage from these lysates. Tranmission experiments through PM5006 of phage in the transductant lysates confirmed that PM804 had a host-controlled modification system which modified HFT phage from PM5006. That PM804 also possessed a restriction system was inferred from the greater numbers of transductants obtained with page which bore a compatible modification pattern. Strain N and a restrictionless mutant of it named NHI, adsorbed the HET phages avidly and failed to modify their host range. Transduction frequencies of the phage markers were about 10(-4)/p.f.u. adsorbed to strain NHI and only about tenfold lower to strain N which did not plate the phages. Tranductants also had the features of heterogenotes and those obtained at low multiplicites of infection were non-lysogenic. The latter transductants adsorbed homolgous phage while NHI transductants also plated the HFT lysates. Strain NHI, lysogenized by the parent phage 5006M, did not adsorb the HFT phages. These findings suggest that the HFT phages were most likely defective for lysogenic conversion to homologous phage non-adsorption. The postulated restriction enzymes of PM804 and strain N could not be shown to be thermolabile.

Adsorption↗
PubMed1976

Derivation and properties of Proteus mirabilis systems for high frequency transduction of streptomycin--sulphonamide and streptomycin-sulphonamide--kanamycin resistances.

Properties of two transducing systems with phages capable of high frequency transduction (HFT) of streptomycin and sulphonamide resistance markers of the V group plasmid R905, and of these markers plus the kanamycin resistance marker derived from a previously described HFT phage 5006MHFTak, are described. Transducing particles of the former phage, named 5006MHFTsus, were detected using the replica-plate technique in an ultraviolet-induced lysate of Proteus mirabilis strain PM5006 transduced to streptomycin and sulphonamide resistance by phage 5006M grown on PM5006 carrying R905. Phage 5006MHFTsusk was also detected by the replica-plate technique in ultraviolet-induced lysates of of phage 5006MHFTsus transductants retransduced to ampicillin and kanamycin resistance by phage 5006MHFTak. Both phages were serologically identical to the parent phage 5006M. Ultraviolet-induced lysates transduced their markers to PM5006 at frequencies of about 5 X 10(-2)/plaque-forming unit adsorbed for both the phages. With phage 5006MHFTsusk, this frequency was increased about 10-fold by simultaneous infection of recipients with homologous non-transducing phage, while phage 5006MHFTsus transductions only underwent a twofold increase. Transductants took about 60 min to express complete resistance to 50 mug streptomycin/ml, and resistance to 1600 mug sulphadiazine/ml was complete within 120 min after phage adsorption. Phage 5006MHFTsusk was slightly more resistant to ultraviolet inaction of its transducing potential and reasons are given for the belief that transductants of both phages are heterogenote-like. Both phage lysates were also capable of generalized transduction and, like previously described HFT phages, lysates transduced the leucine marker at increased frequencies. Using previously described extra- and intra-species phages hosts, it was found that the phages could transduce in single infection and were defective in the lysogenic conversion function as well as in a maturation step. Possible modes of formation of the HFT particles are discussed9

Ampicillin↗
PubMed1987

R-plasmid RP1 increases sensitivity of Proteus mirabilis to normal body defences.

The bactericidal action of non-immune whole blood on Proteus mirabilis was increased when the bacteria contained the R-plasmid RP1. This effect was due mainly to increased phagocytosis. Iron-depleted stationary-phase cells were more sensitive than carbon-depleted cells. The contribution of serum was usually negligible but was increased during a minor non-specific infection. Most plasmid-containing phenotypes were more sensitive than were those without plasmids but there were considerable differences between stationary and exponentially-growing cells. The R-plasmid-mediated increase in sensitivity to phagocytosis may be due in part to the presence of additional glycosylated proteins in the outer membrane.

Animals↗
PubMed1989

The haemagglutinins and fimbriae of Proteus penneri.

The haemagglutinins and fimbriae produced by 18 strains of Proteus penneri were studied and compared with those formed by representative strains of other species of Proteeae. After repeated subcultures at 30 degrees C, 12 P. penneri strains formed only MR/K haemagglutinins which were associated with thin, non-channelled, type-3 fimbriae. Two strains formed simultaneously both MS and MR/K haemagglutinins associated with thick, channelled, type-1 fimbriae and type-3 fimbriae, respectively. Four strains formed simultaneously both MR/K and MR/P haemagglutinins. No P. penneri strain formed either MS or MR/P haemagglutinins alone under these conditions. The type-3 fimbriae from P. penneri strain E180 were isolated, purified and found to be protein of 19 Kda. Immunoelectronmicroscopy studies with antibody to the type-3 fimbriae of strain E180 showed that P. penneri strains at least two antigenic types of type-3 fimbriae. The type-3 fimbrial antigen of the vaccine strain E180 was shared by another eight strains of P. penneri. A further eight P. penneri strains and the strains representative of other genera within Proteeae had type-3 fimbriae of a different antigenic type. The formation of these haemagglutinins and fimbriae suggests that this organism is well endowed to be a urinary-tract pathogen.

Antigens, Bacterial↗
PubMed1990

Interactions of Escherichia coli and Proteus mirabilis with mouse mononuclear phagocytes.

Five strains of enterobacteria (three of Escherichia coli and two of Proteus mirabilis) were studied to assess and compare their phagocytic uptake and intracellular killing by mouse macrophages. Each strain was injected intraperitoneally into separate groups of mice and peritoneal exudate cells were harvested after 3 min for phagocytosis to occur in vivo. Acridine orange staining showed that there were approximately 10-fold fewer intracellular P. mirabilis than E. coli cells. The average numbers of viable intracellular bacteria per leucocyte were 0.03 and 0.02 for P. mirabilis strains M13 and H1, respectively, and 0.48, 0.45, and 0.28 for E. coli strains M14, A-D M5 and H40. Thus, both P. mirabilis strains were ingested less readily than any of the three E. coli strains (p less than 0.01). The rates of in-vitro intracellular killing were similar for all five strains of bacteria. The intracellular killing constants (Kk) for the three mouse isolates were 0.017, 0.016 and 0.020 min for E. coli M14 and A-D M5, and P. mirabilis M13, respectively; the Kks for the two human isolates were 0.026 and 0.029/min for E. coli H40 and P. mirabilis H1, respectively. The Kks for all five strains were not significantly different. Assuming that the numbers of viable intracellular bacteria at the beginning of the assay represented 100% viability, 6-17% of the intracellular bacteria remained viable after 2 h, reflecting log10 3.9-5.6 bacteria (6-8) x 10(6) peritoneal exudate cells. Intravenous injection of these five strains into separate groups of mice demonstrated that the P. mirabilis strains were more virulent than the E. coli strains. Injection of each P. mirabilis strain was associated with ruffled fur and death, whereas mice given any of the three E. coli strains remained visibly healthy and none died. Consistent with these observations, quantitation of viable bacteria in the liver and spleen showed that greater numbers of P. mirabilis M13 than of E. coli M14 or A-D M5 persisted in these organs; similarly greater numbers of P. mirabilis H1 than of E. coli H40 persisted in the liver and spleen. Because the rates of intracellular killing of these five strains were similar, the relative virulence of both strains of P. mirabilis appeared to be associated with decreased phagocytic uptake rather than differences in intracellular survival.

Animals↗
PubMed1976

A continuous study of morphological phase in the swarm of Proteus.

Continuous study, at intervals of 1 h, on the advancing edge of the swarm of Proteus vulgaris confirms that this is almost permanently composed of elongated swarmers, and that short, non-swarming forms arise in the interior of the culture where motion has already ceased. Previous errors have probably arisen from inaccurate sampling.

Movement↗
PubMed2005

Role of swarming in the formation of crystalline Proteus mirabilis biofilms on urinary catheters.

The care of many patients undergoing long-term bladder catheterization is frequently complicated by infection with Proteus mirabilis. These organisms colonize the catheter, forming surface biofilm communities, and their urease activity generates alkaline conditions under which crystals of magnesium ammonium phosphate and calcium phosphate are formed and become trapped in the biofilm. As the biofilm develops it obstructs the flow of urine through the catheter, causing either incontinence due to leakage of urine around the catheter or retention of urine in the bladder. The aim of this study was to investigate the role of the surface-associated swarming motility of P. mirabilis in the initiation and development of these crystalline catheter biofilms. A set of stable transposon mutants with a range of swimming and swarming abilities were tested for their ability to colonize silicone surfaces in a parallel-plate flow cell. A laboratory model of the catheterized bladder was then used to examine their ability to form crystalline, catheter-blocking biofilms. The results showed that neither swarming nor swimming motility was required for the attachment of P. mirabilis to silicone. Mutants deficient in swarming and swimming were also capable of forming crystalline biofilms and blocking catheters more rapidly than the wild-type strain.

Bacterial Adhesion↗