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PubMed1975

Pseudomonas aeruginosa infection in hospital: a comparison between 'infective' and 'environmental' strains.

One hundred and fifty-six infections or episodes of infection associated with Pseudomonas aeruginosa in six hospitals over 14 months were investigated. Pyocine typing and serotyping suggested that 145 distinct episodes had occurred, caused by 78 different strains. During this period 15 distinct strains were isolated from the environment at one of the hospitals; 12 of these were apparently unassociated with infection in the same ward during the period, and 4 were of types not encountered in infective processes at any hospital. There appeared to be a rather higher proportion of unclassifiable pyocine inhibition patterns among the environmental strains; in general these strains also produced smaller amounts of haemolysin. If failure to produce haemolysin in vitro is correlated with lack of virulence in vivo, this may partially explain the sporadic nature of hospital infection with Ps. aeruginosa, despite the prevalence of strains of this species in the environment.

Child↗

PubMed1990

Typing of Pseudomonas aeruginosa ear infections related to outcome of treatment.

Of 142 patients with Pseudomonas aeruginosa (PSA) ear infections, 88 (62 per cent) had chronic otitis media and 54 (38 per cent) external otitis. Following serotyping and pyocin typing of their bacteria, and relating the type to outcome, patients could be divided into three groups: (1) 120 patients who had no recurrence with isolation of only one PSA strain, (2) 13 patients who had recurrent infections and in whom the same PSA strain was isolated in repeated cultures, and (3) nine patients who had recurrent disease, but who had a change in their PSA strains. Most of the PSA strains isolated from patients in groups (1) and (2) were stable to pyocin, and resistent to gentamicin. Patients in the first group were all cured initially by medical management. Of the nine patients in group (3) who had a different serotype on repeated cultures, medical treatment was successful in eight (89 per cent), but of the 13 patients in group (2) who had the same Pseudomonas aeruginosa serotype cultured, medical therapy failed in six (46 per cent) and mastoid surgery was required. Serotyping of Pseudomonas aeruginosa otitis may be helpful in predicting the type of management in patients who have recurrent infections.

Adolescent↗

PubMed1981

Lytic enzyme produced by Pseudomonas aeruginosa concomitantly with bacteriophage PS17. Purification, characterization, and comparison with PR1-lysozyme.

A bacteriolytic enzyme was found to be produced, concomitantly with the progeny phage, in Pseudomonas aeruginosa P14 infected with phage PS17. The enzyme, named PS17-lysozyme, was purified by acrinol treatment, two cycles of Amberlite CG-50 chromatography, and SP-Sephadex C-50 chromatography. Homogeneity of the preparation was demonstrated by three electrophoretic techniques. PS17-lysozyme behaved like a basic protein (pI, 9-10) consisting of a single polypeptide chain (molecular weight, 24,500) and showed the substrate specificity as hen egg-white lysozyme. The enzyme exhibited much higher specific activity than the egg-white enzyme when assayed with chloroform-killed P. aeruginosa P14 as a substrate. These characteristics, as well as the amino acid composition, were very similar to those of PR1-lysozyme; a bacteriolytic enzyme produced in mitomycin C-induced P. aeruginosa P15 concomitantly with a phage-tail-like bacteriocin, pyocin R1 (Ochi et al. (1978) J. Biochem. 83, 727-736). However, the behavior of these two lysozymes from P. aeruginosa in Amberlite CG-50 chromatography and some other properties indicated that they were not identical, though they were similar. The results are in accord with the view that pyocin R1 may be a defective form of a bacteriophage closely related to but not identical with phage PS17.

Amino Acids↗

PubMed1974

Susceptibility of 1,500 isolates of Pseudomonas aeruginosa to gentamicin, carbenicillin, colistin, and polymyxin B.

A series of 1,500 strains of Pseudomonas aeruginosa was collected from a variety of sources to provide a group of strains which would truly represent the species. All of them were pyocine typed, and a wide range of types was included among the isolates from each source. The gentamicin, carbenicillin, colistin, and polymyxin minimal inhibitory concentration of each strain was measured by the agar dilution method employing the Steers inocula replicator. Over 99% of strains were inhibited by 8 mug of gentamicin per ml, by 256 mug of carbenicillin per ml, and by 4 mug of colistin per ml. The small number of strains more resistant to each antibiotic comprised a variety of different pyocine types. Few strains were found to be susceptible to tetracycline, chloramphenicol, kanamycin, or streptomycin at the single concentration tested.

Carbenicillin↗

PubMed1976

Emergence of gentamicin- and carbenicillin-resistant Pseudomonas aeruginosa in a hospital environment.

Strains of Pseudomonas aeruginosa resistant to either gentamicin or carbenicillin have been noted since their introduction into clinical use. During a 6-month period, twice-weekly cultures were obtained from all patients treated with either gentamicin or carbenicillin and from all patients with a positive culture for P. aeruginosa. Susceptibility testing to gentamicin and carbenicillin and pyocine typing were performed on all isolates. Organisms with a minimal inhibitory concentration greater than 12.5 mug of gentamicin per ml or greater than 100 mug of carbenicillin per ml were defined as resistant. P. aeruginosa was cultured from 238 patients. One patient was initially infected with a gentamicin-resistant isolate. In 11 other patients, serial cultures revealed the emergence of resistance to gentamicin. All but one of these resistant isolates occurred in patients treated with gentamicin. In eight instances the pyocine and/or serological types before and after the change in sensitivity pattern were the same. Gentamicin-resistant P. aeruginosa emerged significantly more often in patients treated with gentamicin than in those who did not receive gentamicin. Carbenicillin-resistant P. aeruginosa emerged in four of 14 patients treated with carbenicillin. Seventeen of the 238 patients were infected de novo with carbenicillin-resistant P. aeruginosa. Carbenicillin-resistant P. aeruginosa emerged significantly more often in patients treated with carbenicillin than in those who did not receive carbenicillin. No evidence was found for in-hospital spread of resistant P. aeruginosa.

Adult↗

PubMed1970

Plaquelike Clearings Induced by Antimicrobial Agents on Lawns of Pseudomonas aeruginosa.

Plaques similar in appearance to those induced by phage were observed adjacent to chloramphenicol and tetracycline discs on Pseudomonas aeruginosa lawns used for the determination of antibiotic susceptibility. Thirteen strains were selected for study, 10 of which exhibited the plaquing phenomenon. The ability to form plaques induced by tetracycline was not related to any of the biochemical properties of the strains studied, their overall antimicrobial susceptibility pattern, or their pathological source. Some pseudomonad strains were capable of pyocin production; however, the relationship between plaque formation and pyocin production was not apparent. Supernatant fluids of resuspended plaque contents of eight strains originally demonstrating clearings could induce plaques on sensitive indicator lawns only when collected from tetracycline-induced plaque areas; supernatant fluids of the same strains could not produce clearings without previous exposure to the drug. Of the eight supernatant fluids capable of plaque induction, three were active on their homologous indicator lawns. In a subsequent survey of 95 P. aeruginosa strains, it was found that 28 isolates exhibited plaques. Of these, 17 were associated with tetracycline, 7 were associated with chloramphenicol, 3 were associated with triple sulfa; and 1 was associated with nalidixic acid.

Journal Article↗

PubMed1972

Protection of normal, lysogenic, and pyocinogenic strains against ultraviolet radiation by bound acriflavine.

The presence of bound acriflavine protects bacteria against the lethal effects of ultraviolet (UV) light, presumably because pyrimidine dimer formation is inhibited. Although acriflavine present in plating medium usually results in reduced viable counts from irradiated bacteria, no enhancement of lethal effects is observed when acriflavine is added to irradiated bacteria left in suspending buffer for 45 min before plating. Acriflavine remaining bound to the deoxyribonucleic acid of irradiated bacteria at the time they are plated likewise does not affect their survival. Protection is precisely dose-modifying unless some killing of bacteria by UV results from induction of prophage, against which bound acriflavine is less protective, or from induction of pyocin, against which there is no protection at all. It is inferred that prophage induction proceeds in part, and pyocin induction wholly, by virtue of effects of UV other than pyrimidine dimerization. The response of Escherichia coli strain B to radiation has been postulated to be attributable in part to induction of a prophage or a lethal protein; but exact dose modification was observed for this strain, to about the same extent, whether or not the irradiated organisms were grown in conditions thought to enhance the expected contribution to killing if such a mechanism were involved. Our results support the hypothesis that the inhibition by acriflavine of dimer formation is attributable to energy transfer mechanisms. They fail to support the hypothesis that shapes of survival curves (in particular the manifestation of "shoulders") can be attributed to inactivation by radiation of repair enzymes.

Acridines↗

PubMed1996

Identification and characterization of the tolQRA genes of Pseudomonas aeruginosa.

The tolQ, tolR, and tolA genes from Pseudomonas aeruginosa PAO were cloned using degenerate oligonucleotide PCR primers designed based on conserved transmembrane regions of Escherichia coli TolQ and TolR and E. coli and Pseudomonas putida ExbB and ExbD. The resulting PCR product was used as a probe to isolate a 6.5-kb DNA fragment containing P. aeruginosa tolQ, tolR, and tolA. The nucleotide sequence of a 2.9-kb DNA fragment containing the tolQ, tolR, and tolA genes was determined. The DNA sequence predicts TolQ to be a 25,250-Da protein exhibiting 53% identity to E. coli TolQ. TolR is predicted to be a 15,788-Da protein, sharing 38% identity with the E. coli TolR protein. The P. aeruginosa tolA sequence predicts a 37,813-Da protein with 27% identity to the E. coli TolA. The P. aeruginosa TolQRA proteins were expressed in E. coli minicells. Analysis of plasmid-encoded tolQ::lacZ and tolA::lacZ promoter fusions in E. coli indicated that these genes are expressed at different levels, suggesting transcription from different promoters. Transcriptional analysis of the tol genes in P. aeruginosa revealed that the tolQ and tolR genes are cotranscribed as an approximately 1.5-kb transcript and that tolA is transcribed from its own promoter as an approximately 1.2-kb transcript. The P. aeruginosa Tol proteins were functionally unable to complement E. coli tol mutants, although P. aeruginosa TolQ was able to complement the iron-limited growth of an E. coli exbB mutant. Introduction of the tolQRA genes in the tol-like mutant PAO 1652 restored pyocin AR41 killing, indicating that the Tol proteins are involved in the uptake of pyocin AR41 in P. aeruginosa. Attempts to inactivate the chromosomal copy of the tolA or tolQ gene in the parent strain PAO proved to be unsuccessful, and we propose that inactivation of these genes in P. aeruginosa results in a lethal phenotype.

Amino Acid Sequence↗

PubMed1989

Oropharyngeal and fecal carriage of Pseudomonas aeruginosa in hospital patients.

This prospective study was designed to determine the incidence of rectal and/or oropharyngeal colonization rates of patients with Pseudomonas aeruginosa upon admission to a general hospital and the risk of becoming colonized while hospitalized. Consecutive 186 admissions (180 patients) to one medical ward, one surgical ward, and the intensive care unit were studied over a period of 5 months. Rectal and oropharyngeal swabs for P. aeruginosa were obtained on admission, weekly thereafter, and/or upon discharge. Forty-two patients (22.6%) were colonized on admission, 20 patients (10.8%) acquired P. aeruginosa during hospitalization. Colonization on admission was observed twice as frequently on the surgical ward and in the intensive care unit as on the medical ward. Positive rectal cultures were more frequent than oropharyngeal cultures throughout the study (P less than 0.01). For patients admitted culture positive or culture negative, the probabilities of remaining culture positive or culture negative, respectively, remained at 44 and 72% after 35 days of hospitalization. The most common P. aeruginosa serotypes were 1, 6, and 10, and pyocin types 1, 3, and 10 were predominant. There was no statistical difference in the serotypes or pyocin types detected on admission or acquired during hospitalization. Except for two hospital-acquired first isolates which were resistant to moxalactam, all first isolates were susceptible to the four antibiotics tested. During the study, one isolate became resistant to azlocillin, gentamicin, and tobramycin, while two isolates became resistant to moxalactam. A statistical analysis was performed for 13 risk factors for all colonized and noncolonized patients. Colonization detected at the time admission was positively associated with age ( > 65 years), previous surgery of the gastrointestinal tract for neoplasm, and anemia ( P< 0.05). In contrast, for patients who entered the study culture negative, none of the analyzed 13 risk factors was associated with an increased probability for colonization. This observation included the administration of antimicrobial agents singly or in combination or both.

Carrier State↗

PubMed1976

Fluorescent pseudomonads capable of growth at 41 degrees C but distinct from Pseudomonas aeruginosa.

One hundred and twenty-seven apyocyanogenic fluorescent Pseudomonas strains capable of growth at 41 degrees C, but differing from Pseudomonas aeruginosa, were typed serologically and tested for pyocin production, antibiotic susceptibility, selected biochemical reactions, and utilization of selected substrates. Results were compared with those from 40 apyocyanogenic and 14 pyocyanin-producing strains of P. aeruginosa. Unidentified fluorescent Pseudomonas (UFP) strains generally were not agglutinated by P. aeruginosa antisera and showed little or no pyocin activity. In contrast to P. aeruginosa strains, UFP strains usually failed to oxidize D-gluconate or reduce nitrate to nitrogen gas. They could not use D-gluconate or D-mannitol as sole carbon source and were susceptible to kanamycin. The cellular fatty acid compositions of major UFP groups resembled those of the alcaligenes-stutzeri groups.

Anti-Bacterial Agents↗

PubMed1979

Bactericidal activity of the tail of Pseudomonas aeruginosa bacteriophage PS17.

The tail of bacteriophage PS17 of Pseudomonas aeruginosa was shown to be bactericidal, and its properties were compared with those of pyocin R1. Temperature-sensitive mutants were isolated from PS17, and the products at nonpermissive temperature were morphologically characterized. Bactericidal substances were found in the lysates of such mutants that were defective in the head formation but not in the tail formation. Phage tails were purified from the lysate of one such mutant, and its chemical and biological properties were studied. Isolated tails killed sensitive cells by a single-hit process and repressed the uptake of leucine in sensitive cells. These results were consistent with the previous findings on the serological and morphological relationship between PS17 and pyocin R1. However, certain differences were also shown between them in shape and protein composition.

Antigens, Viral↗

PubMed1994

Polyagglutinable Pseudomonas aeruginosa from cystic fibrosis patients. A survey.

Chronic Pseudomonas aeruginosa lung infection is responsible for most of the mortallity and morbility observed in cystic fibrosis patients. During the course of the disease, the bacteria change from being O-serogroup typable (monoagglutinable), non-mucoid, resistant to normal human serum and motile, to become O-serogroup non-typable (polyagglutinable), serum-sensitive and non-motile. In spite of high levels of antibodies produced by the patient, and intensive antibiotic therapy it is not possible to eradiate the polyagglutinable bacteria from the lungs of the patients. The bacteria will reappear and it is not fully understood if it is the same strain which reappears, or it is a super-infection with a new strain which takes place. A reliable and stable typing method is needed to clarify this question. In the present study, the conventional typing methods, such as serotyping, phage typing and pyocin typing were compared with the newer DNA typing methods, such as, restriction fragment length polymorphism (RFLP) in combination with pulsed field gel electrophoresis (PFGE) and typing with a specific DNA probe. Typability, reproducibility and discriminatory power using the different typing methods were investigated. The conventional typing methods have proved to be adequate when typing P. aeruginosa isolates from non cystic fibrosis sources, but because the majority of cystic fibrosis P. aeruginosa isolates are polyagglutinable or non typable, serotyping is not useful. Phage typing also lacks discriminatory power as it lumps up to 40% of the isolates in the same phage group. Pyocin typing has the disadvantage of low reproducibility. Most of the conventional typing methods are based on receptors on the bacterial surface, which on exposure to the environmental conditions in the lung, are likely to provoke phenotypic changes of the bacteria. The obvious advantage of the newer DNA typing methods is that these methods are based on internal properties of the bacteria, as part of the bacterial genome is investigated. The present study has revealed that for the time being, restriction fragment length polymorphism (RFLP) and pulsed field gel electrophoresis (PFGE) in combination with phage typing is the best method of typing P. aeruginosa isolates from cystic fibrosis patients for epidemiological purposes.

Agglutination Tests↗

PubMed1993

Epidemiological study of Pseudomonas aeruginosa isolated from clinical specimens.

The epidemiology of Pseudomonas aeruginosa infection was studied in Siriraj Hospital. During April 1989-June 1990, P. aeruginosa 436 strains were isolated from clinical specimens of 260 patients, ie blood (19 strains), pus (192 strains), sputum (159 strains) and urine (66 strains). By using a combination of serogroups and pyocin types as epidemiological markers, it was found that there were 10 serogroups and 8 pyocin types which can be differentiated into 33 serogroup/pyocin types or patterns. The most common pattern was E 211111 (26.3%) followed by B 121614 (24.5%), G 373112 (13%) and L 888888 (7.1%), respectively.

Bacterial Typing Techniques↗

PubMed1998

[Imipenem resistance in Pseudomonas aeruginosa].

In 1997 in western Austria, 9.9% of Pseudomonas aeruginosa strains from patients of general practitioners were resistant to imipenem as well as 18.2% of the isolates from hospitals and 20.2% of the strains at a university teaching hospital. Within the hospital the imipenem resistance varied from 9.9% among out-patients to 28.7% in isolates from intensive care units. In medical/surgical words, up to 15.1% of P. aeruginosa strains were resistant to imipenem. The incidence of imipenem-resistant P. aeruginosa strains correlates to the use of carbapenems. In June 1997, 10 consecutive isolates from 8 patients were obtained and typed using restriction fragment length polymorphism analysis (RFLP) and Pyocin typing. All 10 isolates were resistant to meropenem as well as to imipenem. The finding (by RFLP and Pyocin typing) of individual bacterial types in each isolate strongly contradicts the spread of infection by cross infection. However, all patients were proven to have been treated with imipenem during the 3 months prior to testing. In 1997, 13,880 g of imipenem were used at the university hospital in Innsbruck. The use of carbapenems appears to be the main cause for the increased incidence of imipenem-resistant P. aeruginosa strains.

Austria↗

PubMed1990

Structural models for the cell surface lipooligosaccharides of Neisseria gonorrhoeae and Haemophilus influenzae.

A structural model is proposed for the surface glycolipids, or lipooligosaccharides (LOS), of gram-negative pathogenic bacteria that colonize human mucosae, e.g. Neisseria gonorrhoeae and Haemophilus influenzae. The development of this model has involved analysis of a series of pyocin-resistant mutants with altered LOS and other recent immunochemical and structural data. A comprehensive approach to determining the necessary structural data has been constructed that utilizes liquid secondary ion mass spectrometry, tandem mass spectrometry, methylation analysis and nuclear magnetic resonance. To prepare purified oligosaccharides for these analyses, chromatographic and chemical techniques have been developed that include high-pH anion-exchange chromatography of underivatized oligosaccharides and reverse-phase chromatography after derivatization with hydrazino alkyl benzoates. The proposed LOS model has several unique features that distinguish it from models developed for the lipopolysaccharides of enteric bacteria. This information should lead to an understanding of the unique structure/function relationship of LOS and to the development of carbohydrate-based vaccines.

Chromatography, Gel↗

PubMed1995

Short-chain lipopolysaccharide mutants of serogroup B Neisseria meningitidis of potential value for production of outer membrane vesicle vaccines.

Four lipopolysaccharide (LPS) mutants (Mu-1 to Mu-4) were isolated after exposing Neisseria meningitidis strain 44/76 to pyocins from Pseudomonas aeruginosa. Parent strain LPS contained one major SDS-PAGE band expressing the immunotype determinants of L3, L3,7 and L3,7,9 and a minor band of higher mobility expressing the immunotype determinants of L8, L8a, L1,8,10 and L11. Each mutant LPS appeared as one SDS-PAGE band of higher mobility than the bands of the parent strain. None of these LPSs expressed the immunotype determinants of the parent strain, except Mu-4 LPS which reacted with the L11-specific MAb 4C4. Strain 44/76 LPS was found to contain galactose (Gal), glucose (Glc), heptose (Hep), glucosamine (GlcN), and 2-keto-3-deoxy-octulosonic acid (Kdo) in the molar ratios of 1.9:1.3:1.7:3.5:2.1. The corresponding ratios of the mutants were: Mu-4, 0:1.7:1.7:2.8:2.0; Mu-3, 0:0:1.7:2.4:1.6; Mu-2, 0:0:2.1:1.8:2.0, Mu-1, 0:0:1.8:1.9. Thus, all mutant LPSs lacked Gal and possessed less GlcN as compared to strain 44/76 LPS. Consequently, these mutants do not express the lacto-N-neo-tetraose (Gal1-4GlcN1-3Gal1-4Glc) commonly found as a part of meningococcal LPS and also on structures of human erythrocytes. These LPS mutants will be considered for use in production of OMV vaccines without host-like antigens, which might favour induction of antibodies to more conserved epitopes of meningococcal LPS.

Antibodies, Bacterial↗

PubMed1983

Construction of recombination-deficient strains of Pseudomonas aeruginosa.

The rec-102 mutation had pleiotropic effects in Pseudomonas aeruginosa: low recombinational proficiency in conjugation and transduction; high UV sensitivity; inability to induce pyocin R2 by mitomycin C; and increased susceptibility to mitomycin C and nalidixic acid. The rec-102 locus was mapped by R68.45-mediated conjugation in the 45 min region of the PAO chromosome, between argF and thr-9001. By selection for a marker in this region, rec-102 can be introduced into a P. aeruginosa strain of interest using an R68.45 rec-102 donor. The recombination-deficient strains constructed in this way were phenotypically similar to Escherichia coli recA mutants.

Chromosome Mapping↗

PubMedDate not supplied

Selective procedure to isolate haemophilus influenzae from sputa with large quantities of Pseudomonas aeruginosa.

The identification of respiratory pathogens (e. g. Haemophilus influenzae, Streptococcus pneumoniae) is impaired by the presence of large quantities of Pseudomonas aeruginosa, as is the case in the sputum specimens of cystic fibrosis patients. A procedure has been evaluated whereby the selective inhibition of the proliferation of P. aeruginosa is achieved by a broad spectrum pyocin, whereas the growth of H. influenzae is not influenced. This technique has been tested over a two year period resulting in a significantly augmented rate of identification of H. influenzae.

Bacteriocins↗