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At least 19 recordsLinked to original sources
PubMed1986

Cloning of urease gene sequences from Providencia stuartii.

Providencia stuartii was the most prevalent isolate recovered from urine specimens taken weekly over a 1-year period from 51 nursing home patients with urinary catheters in place. Thirty percent of the isolates were urease positive. Urease, which is implicated in renal stone formation, was shown to be transmissible on an 82-kilobase conjugative plasmid in one isolate. Plasmid DNA isolated from this strain was digested with EcoRI, ligated into the EcoRI site of pBR322, and used to transform Escherichia coli HB101. Ampicillin-resistant clones were replica plated onto urea segregation agar, and a urease-positive clone, designated pMID101, was isolated. Recombinant and native urease from cell lysates had identical electrophoretic mobilities on nondenaturing polyacrylamide urease activity gels. The native enzyme was induced fourfold when cells were grown in the presence of 0.1% urea and had a km of 9.4 mM and a Vmax of 3.2 mumol of NH3 per min per mg of protein. Its molecular weight was estimated to be 375,000 +/- 35,000 by Sephacryl S-300 chromatography. The enzyme was cytoplasmic in P. stuartii, was inhibited in vitro by hydroxyurea, acetohydroxamic acid, and EDTA, and appears to have a complex subunit structure and a unique molecular size within genera of the Proteeae tribe.

Cell Compartmentation↗
PubMed1998

Identification and characterization of aarF, a locus required for production of ubiquinone in Providencia stuartii and Escherichia coli and for expression of 2'-N-acetyltransferase in P. stuartii.

Providencia stuartii contains a chromosomal 2'-N-acetyltransferase [AAC(2')-Ia] involved in the O acetylation of peptidoglycan. The AAC(2')-Ia enzyme is also capable of acetylating and inactivating certain aminoglycosides and confers high-level resistance to these antibiotics when overexpressed. We report the identification of a locus in P. stuartii, designated aarF, that is required for the expression of AAC(2')-Ia. Northern (RNA) analysis demonstrated that aac(2')-Ia mRNA levels were dramatically decreased in a P. stuartii strain carrying an aarF::Cm disruption. The aarF::Cm disruption also resulted in a deficiency in the respiratory cofactor ubiquinone. The aarF locus encoded a protein that had a predicted molecular mass of 62,559 Da and that exhibited extensive amino acid similarity to the products of two adjacent open reading frames of unknown function (YigQ and YigR), located at 86 min on the Escherichia coli chromosome. An E. coli yigR::Kan mutant was also deficient in ubiquinone content. Complementation studies demonstrated that the aarF and the E. coli yigQR loci were functionally equivalent. The aarF or yigQR genes were unable to complement ubiD and ubiE mutations that are also present at 86 min on the E. coli chromosome. This result indicates that aarF (yigQR) represents a novel locus for ubiquinone production and reveals a previously unreported connection between ubiquinone biosynthesis and the regulation of gene expression.

Acetyltransferases↗
PubMed2006

Functional characterization of Escherichia coli GlpG and additional rhomboid proteins using an aarA mutant of Providencia stuartii.

The Providencia stuartii AarA protein is a member of the rhomboid family of intramembrane serine proteases and required for the production of an extracellular signaling molecule that regulates cellular functions including peptidoglycan acetylation, methionine transport, and cysteine biosynthesis. Additional aarA-dependent phenotypes include (i) loss of an extracellular yellow pigment, (ii) inability to grow on MacConkey agar, and (iii) abnormal cell division. Since these phenotypes are easily assayed, the P. stuartii aarA mutant serves as a useful host system to investigate rhomboid function. The Escherichia coli GlpG protein was shown to be functionally similar to AarA and rescued the above aarA-dependent phenotypes in P. stuartii. GlpG proteins containing single alanine substitutions at the highly conserved catalytic triad of asparagine (N154A), serine (S201A), or histidine (H254A) residues were nonfunctional. The P. stuartii aarA mutant was also used as a biosensor to demonstrate that proteins from a variety of diverse sources exhibited rhomboid activity. In an effort to further investigate the role of a rhomboid protein in cell physiology, a glpG mutant of E. coli was constructed. In phenotype microarray experiments, the glpG mutant exhibited a slight increase in resistance to the beta-lactam antibiotic cefotaxime.

Agar↗
PubMed1984

Characterization of endemic Providencia stuartii isolates from patients with urinary devices.

Providencia stuartii has emerged as a significant nosocomial urinary tract pathogen. An increase in the number of Providencia isolates from urine cultures prompted an investigation into the possibility of an outbreak due to this organism. A high proportion of patients studied had urinary devices. Four wards were screened at two time periods to ascertain the prevalence of Providencia stuartii in urine cultures. Biotype, serotype, antibiogram and plasmid content were determined for each Providencia isolate. Of 129 patients initially sampled 22.5% were found to harbor Providencia stuartii. Biotyping, serotyping and antibiograms indicated an epidemic strain was not present. Similar results were obtained when the wards were screened a second time, with 25.4% of urine cultures found to contain Providencia stuartii. By plasmid analysis the isolates could be grouped into one of ten profiles. A correlation could be made between urease activity and the presence of a large plasmid. No association however could be made between a particular plasmid profile and antibiogram. The data indicate that an epidemic strain of Providencia stuartii was not present. The source(s) of the endemic Providencia stuartii strains remain unknown.

Bacteriuria↗
PubMed1987

Inducible expression of an aminoglycoside-acetylating enzyme in Providencia stuartii.

Strains of Providencia stuartii were collected from a chronic-care geriatric ward of a large Veteran's Administration hospital. Two strains of P. stuartii, and one of Escherichia coli isolated from the same ward, were transferred five times in the presence of gentamicin or netilmicin. At the fifth transfer the MICs of both gentamicin and netilmicin for the two P. stuartii strains had increased at least ten-fold. The MICs for the E. coli remained essentially unchanged. Enzyme assay demonstrated increased activity of an aminoglycoside-2'-acetylating enzyme in P. stuartii during the period of the transfers. Five subsequent transfers in the absence of aminoglycosides resulted in return of enzyme activity to the initial level. Neither of the P. stuartii strains tested contained any detectable plasmid DNA. The 2'-acetylating enzyme in some strains of P. stuartii can be induced to high levels of activity by exposure to gentamicin or netilmicin.

Acetyltransferases↗
PubMed1981

Three episodes of nosocomial urinary tract infections caused by one O-serotype of Providencia stuartii.

The results of O-serotyping Providencia stuartii isolates in a general hospital showed that 43 isolates were the same serotype (063) and were from 15 patients located in 1 or 2 adjacent wards. On retrospective examination it was found that the series of infections occurred during a 9-month period and could be separated into 3 episodes, involving 7, 6 and 2 patients. All patients who acquired the Providencia stuartii 063 strain were catheterized. The introduction of the strain into the hospital was attributed to a patient catheterized before admission from an institution in which the 063 strain had been identified previously. Antibiotic irrigation was not successful in eliminating Providencia stuartii from the urine and the procedure may be a predisposing factor in preferentially selecting strains of this species.

Cross Infection↗
PubMed1977

Nosocomial urinary tract infections caused by two O-serotypes of Providencia stuartii in one hospital.

Providencia stuartii nosocomial urinary tract infections occurring in the same hospital over an 18-month period of retrospective study were shown, by serotyping and biotyping, to have been caused by two endemic strains. Two episodes, involving 38 patients in one ward and 11 patients in another, were caused by a mannitol-positive strain of serotype O55. Transmission of the strain through the movements of one patient appeared to have been the basis for the introduction of the agent from one ward to the other. In another episode, involving two patients in a third ward, the infections were caused by a mannitol-negative strain of serotype O49. The study demonstrated the usefulness of serotyping and biotyping in epidemiological studies of infections caused by P. stuartii.

Bacteriuria↗
PubMed1974

Phosphorylation of kanamycin, lividomycin A, amd butirosin B by Providencia stuartii.

The isolation of Providencia stuartii resistant to multiple aminoglycoside antibiotics prompted an investigation into the mechanism of their resistance. Crude enzyme extracts of a strain of P. stuartii inactivated kanamycin, lividomycin A, and butirosin B in the presence of adenosine 5'-triphosphate (ATP), as measured by a microbiological assay. The occurrence of inhibitory concentrations of 500 mug or greater per ml against kanamycin, lividomycin A, and butirosin B, coupled with the inactivation of these antibiotics in the presence of ATP, suggested enzymatic phosphorylation. This was documented by the transfer of the gamma-phosphate of [gamma-(32)P]ATP. In contrast, the inability to inactivate gentamicin or tobramycin by the crude enzyme extracts in the presence of ATP suggests another enzymatic mechanism of resistance for these antibiotics, such as adenylation or acetylation. Of importance is the fact that amikacin, a semisynthetic analogue of kanamycin A which is resistant to inactivation by most resistance transfer factor enzymes, was found to inhibit the growth of P. stuartii at low concentrations.

Aminoglycosides↗
PubMed1995

Contribution of gentamicin 2'-N-acetyltransferase to the O acetylation of peptidoglycan in Providencia stuartii.

A collection of Providencia stuartii mutants which either underexpress or overexpress aac(2')-Ia, the chromosomal gene coding for gentamicin 2'-N-acetyltransferase (EC 2.3.1.59), have been characterized phenotypically as possessing either lower or higher levels of peptidoglycan O acetylation, respectively, than the wild type. These mutants were subjected to both negative-staining and thin-section electron microscopy. P. stuartii PR100, with 42% O acetylation of peptidoglycan compared with 52% O acetylation in the wild type, appeared as irregular rods. In direct contrast, P. stuartii strains PR50.LM3 and PR51, with increased levels of peptidoglycan O acetylation (65 and 63%, respectively), appeared as coccobacilli and chain formers, respectively. Membrane blebbing was also observed with the chain-forming strain PR51. Thin sectioning of this mutant indicated that it was capable of proper constriction and separation. P. stuartii PM1, when grown to mid-exponential phase, did not have altered peptidoglycan O-acetylation levels, and cellular morphology remained similar to that of wild-type strains. However, continued growth into stationary phase resulted in a 15% increase in peptidoglycan O acetylation concomitant with a change of some cells from a rod-shaped to a coccobacillus-shaped morphology. The fact that these apparent morphological changes were directly related to levels of O acetylation support the view that this modification plays a role in the maintenance of peptidoglycan structure, presumably through the control of autolytic activity.

Acetylation↗
PubMed1989

Usefulness of trehalose fermentation and L-glutamic acid decarboxylation for identification of biochemically aberrant Providencia stuartii strains.

A total of 849 Providencia isolates were collected during a 4-year period when an increased incidence of nosocomial Providencia stuartii infection was noted in urologic wards. Of these isolates, 630 were identified as P. stuartii, 206 were identified as Providencia rettgeri, and 1 was identified as Providencia alcalifaciens. Twelve inositol-positive isolates from 10 patients (10 strains) resembled P. stuartii in fermenting trehalose but resembled P. rettgeri in fermenting D-arabitol or meso-erythritol or both. The latter traits, however, were not stable in all cases. These aberrant strains were identified as P. stuartii on the basis of their O antigens and DNA hybridization experiments. All isolates were tested for L-glutamic acid decarboxylase activity by a qualitative thin-layer chromatography method. All P. stuartii isolates, including the aberrant ones, were trehalose positive and L-glutamic acid decarboxylase negative. None of the P. rettgeri isolates fermented trehalose, while 99.0% of them and the single P. alcalifaciens strain were L-glutamic acid decarboxylase positive. Thus, trehalose fermentation and L-glutamic acid decarboxylation are more useful for separating P. stuartii from P. rettgeri than are D-arabitol and meso-erythritol fermentation.

DNA, Bacterial↗
PubMed1981

Transferable urease activity in Providencia stuartii.

Six urea-positive Providencia stuartii strains were tested for transmissible urease determinants. Two strains, when implanted with "helper" conjugative plasmids, were found to be capable of transferring urease genes to Escherichia coli or urea-negative P. stuartii. Recombination of the urease genes with the helper plasmid in P. stuartii was noted in one case. One of the urea-positive P. staurtii strains was found to harbor a conjugative plasmid which mediated both urease activity and ampicillin resistance. This large plasmid (molecular weight, approximately 140 x 10(6)) was transmissible to and stably maintained in E. coli strains. The demonstration of transmissible genes for urease activity in P. stuartii is significant in that it accounts for previous problems associated with classifying urea-positive strains of this species.

Anti-Bacterial Agents↗
PubMed1979

Chlorhexidine resistance and the lipids of Providencia stuartii.

The lipid composition of Providencia stuartii has been shown to resemble closely that of Proteus mirabilis. The ability of some Pv, stuartii strains to survive exposure to high concentrations of the antiseptic chlorhexidine could not be explained in terms of differences in lipid content between sensitive and resistant strains. In addition, resistance could not be attributed to either reduced adsorption of the antiseptic or to its gross enzymic degradation.

Adsorption↗
PubMed2001

Role of SspA in the density-dependent expression of the transcriptional activator AarP in Providencia stuartii.

The AarP protein in Providencia stuartii encodes a small transcriptional activator which activates the chromosomal aminoglycoside acetyltransferase aac(2')-Ia gene. In addition, AarP activates genes involved in a multiple antibiotic resistance (Mar) phenotype. Expression of an aarP-lacZ fusion increased in a density-dependent manner and reached peak levels at stationary phase. The expression of an aarP-lacZ fusion could be prematurely activated in cells at early to mid-exponential phase by the addition of spent culture supernatants from stationary phase cultures or by ethyl acetate extracts of these supernatants. Nutrient starvation had a negligible effect on aarP expression. In a search for mutations that block aarP activation at stationary phase, a mini-Tn5Cm insertion has been identified within a gene whose product was 77% identical to SspA, a regulatory protein involved in stationary phase gene expression and virulence. An unmarked sspA null allele (sspA2) was created by allelic replacement to further examine the role of sspA in P. stuartii. The sspA2 allele resulted in substantial decrease in aarP mRNA accumulation at various phases of growth. Furthermore, in an sspA mutant background, the aarP-lacZ fusion was no longer activated by an extracellular signal.

Adhesins, Bacterial↗
PubMed1987

Survey of multiply resistant Providencia stuartii in a chronic care unit.

Providencia stuartii was cultured over a 4-year period from the urinary tract, throat, perineum, axilla and stools of patients in a long-term chronic care unit, the most common site of colonization being the urinary tract. A total of 17 patients had Prov. stuartii bacteraemia and manipulation of the urinary tract preceded bacteraemia in 10 cases. Eighty-two per cent of the patients had long-term urinary tract colonization from 1 month to 4 years. Although most isolates were resistant to all aminoglycosides except amikacin, the organisms were all susceptible to thienamycin, ceftazidime, cefotaxime, ceftizoxime and moxalactam.

Adult↗
PubMed1982

[Effectiveness of the combined use of tobramycin with carbenicillin or cephalosporins in experimental infection in mice caused by Providencia stuartii].

Antibacterial activity of tobramycin in combination with carbenicillin or cephalosporins against 20 strains of Providencia stuartii was studied. The combinations of tobramycin with carbenicillin (1 : 2.5) or cephaloridine (1 : 1) were most active. The MIC of tobramycin used in combination with carbenicillin or cephaloridine decreased 3-30 times. In treatment of albino mice with sepsis caused by Providencia stuartii it was possible to lower 2-8 times the dose of tobramycin used in combination with carbenicillin or cefazolin.

Animals↗
PubMed1987

Uropathogenicity in rats and mice of Providencia stuartii from long-term catheterized patients.

Providencia stuartii, a frequent and persistent isolate from the urinary tract of chronically catheterized elderly patients, is multiply antibiotic resistant and may cause fatal bacteremia in those patients. We studied P. stuartii strains in rats and mice to determine differences in uropathogenicity. Strains studied varied in expression of factors which contribute to pathogenicity of other bacterial species. Urinary tract responses following challenge with P. stuartii strain HO (factors expressed) were similar to responses reported for uropathogenic E. coli strains both in bacterial persistence and histologic change. In animals similarly challenged with P. stuartii strain RO (factors not expressed), responses were similar to those reported for non-uropathogenic E. coli strains. Results indicate that: a) animal model studies may be useful in differentiating P. stuartii strains based on uropathogenicity, b) P. stuartii uropathogenicity may be related to identifiable factors associated with virulence in other species, and c) the CBA mouse model appears to be the most suitable for studies of P. stuartii uropathogenicity.

Animals↗
PubMed1987

Modifications of DNA-gyrase and of permeability in a norfloxacin-resistant clinical isolate of Providencia stuartii.

We obtained a clinical isolate of Providencia stuartii showing a high level of resistance to norfloxacin and to other 4-quinolones, whose target is the enzyme DNA-gyrase. This strain showed resistance also to beta-lactam and aminoglycoside antibiotics. In order to detect modification of DNA-gyrase, we performed supercoiling assays in vitro in presence of norfloxacin and ciprofloxacin. Furthermore, outer membrane proteins, which are involved in permeability mechanisms, were analyzed on SDS-polyacrylamide gels. Results showed that both modifications in DNA-gyrase and changes in outer membrane proteins can be held responsible for resistance to 4-quinolones; moreover, these modification are probably supported by a third mechanism of resistance.

Bacterial Outer Membrane Proteins↗
PubMed1985

Providencia stuartii: a search for its natural habitat.

A selective differential medium has been used to search for Providencia stuartii in sewage, sewage contaminated natural waters and the faeces and skin of a small population of healthy non-hospitalized males. Colonization of 12 male patients with long-term indwelling bladder catheters and the general environment of the spinal injury unit was also examined. Providencia stuartii was not isolated from the non-hospital samples, but colonization of the urine (two patients) faeces (five patients) and skin (eight patients) was observed. Apart from equipment that had been in contact with patients urine or skin there was no general contamination of the ward environment suggesting that colonized patients were the main reservoir of this multiply antibiotic-resistant nosocomial pathogen.

Bacteriuria↗