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Query: UNIPROT:Q96DG6 (Pseudomonas)
 76,258 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infections with Pseudomonas aeruginosa and Serratia marcescens are often difficult to treat because of the narrow therapeutic ratio of available antimicrobials. Synergistic inhibitory and bactericidal activity for gentamicin and carbenicillin against P. aeruginosa has been documented in vitro. The purpose of this study was to compare 4 methods of determining in vitro synergism between several aminoglycosides and penicillins. The agar dilution method using an inoculum replicator was employed, and a drug combination showing inhibition equal to or less than one-fourth of the individual minimal inhibitory concentrations was termed synergistic. Combinations using amikacin and BL-P1654 showed synergism against a greater per cent of strains of P. aeruginosa and S. marcescens than combinations using gentamicin or carbenicillin. Additionally, the "checkerboard" broth dilution method using both minimal inhibitory concentration and minimal bactericidal concentration as endpoints and killing curves according to the methods of Jawetz was studied. Comparison of the results of these 4 methods showed excellent correlation, verifying the consistency of the 4 techniques for determining in vitro synergism.
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PMID:Comparison of methods for assessing in vitro antibiotic synergism against Pseudomonas and Serratia. 81 May 33

The resistance of Ps. aeruginosa to 100 mug carbenicillin and 30 mug gentamicin was analyzed for all strains originating from hospitalized patients between 1970 and 1973. Eighty per cent of all isolates were inhibited by 100 mug carbenicillin and 90% by 30 mug gentamicin (1973). Most Pseudomonas strains were isolated from the surgerical and pediatric departments, however the two departments seem to show different tendencies. It is concluded from the results obtained that resistant strains normally do not survive for a long time in one unit since the pattern of the resistance shows considerable differences six months later.
Infection 1975
PMID:[Incidence and resistance of pseudomonas aeruginosa 1970-1973 in hospitalized patients at the Bonn University hospital]. 81 46

Among the main aspects to be considered when treating burns, the problem of infection control remains unsolved. Considerable financial resources are needed to prevent the transmission of organisms. To justify such investments in buildings and antiseptic measures, an extensive epidemiological hospital study was carried out from 1970 to 1974, involving 930 patients, and more than 25,000 wound biopsies as well as 10,000 contact cultures and environmental swabs. Bacteria from the environment of severly burned patients were counted every week. Serotyping was used for a specialized study of Pseudomonas aeruginosa. In 200 patients wound organisms were counted. The most important organisms were: Streptococcaceae (pyogenic streptococci, less frequently faecal and salivary streptococci). Pseudomonadaceae, Enterobacteriaceae, and Micrococcaceae (especially Micrococcus aureus). Povidon iodine, gentamicin and silver sulfadiazine were used for local disinfection. Antibiotics used were gentamicin, carbenicillin and polymyxin. Whereas from 1970 to 1972 P. aeruginosa was the predominant organism found in wounds, other gram-positive organisms increased from 1972 on. Wounds were colonized mainly in the course of the first two weeks of treatment. Special studies regarding P. aeruginosa revealed a predominance of serotypes 5 and 13 between 1970 and 1973, whereas types brought into the hospital were dominant from 1973 on. An analysis of furniture and equipment, water faucets and drains showed that Pseudomonas strains found in the water did not coincide with those found in wounds. Therefore, a contamination from this source seems unlikely. Strains found on furniture and equipment, however, also appeared in the wound flora. When the therapeutic routine was changed (to prevent patients passing through common treatment areas such as bathrooms and dressing areas) hospital organisms 5 and 13 could be eliminated almost completely. Thus, it is possible to achieve a considerable reduction in the rate of cross-infection among patients by, for instance, excluding common treatment areas from the therapy programme. Nevertheless, in the majority of cases wounds will still be colonized, in particular by bacteria that were already in the anal region or on the skin before the patient was injured. For this reason, the elimination of such organisms by topical bactericidal agents constitutes an an important factor in efforts to reduce the rate of septicaemic complications. In view of the persisting high mortality due to generalized infections this therapeutic aspect must also be exploited thoroughly in the future. Although in comparative studies of topical therapy using povidon iodine, silver sulfadiazine and gentamicin, organisms did appear in the course of the first two weeks; in the case of the PVP-I the colonization never reached 10(5) organisms per cm2, i.e. the danger threshold for generalized sepsis. There was no evidence of a correlation between number of organisms and depth of burns.
Infection 1977
PMID:[Asepsis and antisepsis in the treatment of burn patients (author's transl)]. 85 28

The emergence of Providencia stuartii as a hospital pathogen in a burn unit was demonstrated by routine infection surveillance. The organism was initially recognized in a burn wound and subsequently in urine or sputum. Compared to controls, those patients harboring P. stuartii were similar in age and percentage of body surface burned and were more likely to have been in one of the two burn unit rooms, (p less than 0.02). Infection with P. stuartii was independent of duration in the Intensive Care Unit or Burn Unit, and of number of visits to hydrotherapy or operating rooms (OR). Once patients were colonized with P. stuartii they had greater morbidity than non-colonized patients as evidenced by longer stays in the unit and increased visits to the OR for debridement. P. stuartii was isolated from air samples (5/14) more commonly than from the hands of personnel. In vitro tests suggested that extensive use of parenteral gentamicin and replacement of the antibacterial topical cream sulfamylon by silver sulfadiazine favored the emergence of P. stuartii over Pseudomonas aeruginosa as the predominant colonizing organism.
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PMID:Providencia stuartii, a hospital pathogen: potential factors for its emergence and transmission. 95 86

Infection of Pseudomonas BAL-31 with the lipid-containing bacteriophage PM2 resulted in no detectable change in the rate of phosphatidylglycerol (PG) or phosphatidylethanolamine (PE) biosynthesis. An increase in the PG content of infected cultures was not seen until the cultures began to lyse, and this increase was in fact only a relative increase resulting from the extensive turnover of PE at the onset of culture lysis. Turnover studies revealed that the glycerol, phosphorus fatty acid, and ethanolamine moieties of PE turned over simultaneously at the time of lysis, and therefore made it unlikely that there was a PE to PG conversion during the latent period of the phage. The lipid found in the bacteriophage did not reflect a preferential selection for lipid synthesized before or after infection, but in fact reflected the composition of the host membrane at the time the phage were assembled. The use of a modified medium that allowed the cultivation of Pseudomonas BAL-31 as a prototroph and resulted in reliable lysis times of infected cultures led us to the conclusion that PM2 infection effects little change in host phospholipid metabolism, and that there is sufficient PG in the host cytoplasmic membrane to account for a full burst of phage. As a result of the reliable lysis times that we have achieved, we concluded that certain metabolic events, i.e., PE turnover, are lytic phenomena and must not be confused with events relevant to the biosynthesis and maturation of the phage.
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PMID:Phospholipid metabolism in Pseudomonas BAL-31 infected with lipid-containing bacteriophage PM2. 95 79

A fatal case of melioidosis, thought to be the third recorded from New South Wales, is presented. Infection probably occurred in Queensland. The patients presented with a subcutaneous abscess complicated by pyaemia, extensive lung involvement and septicaemic shock. The diagnosis was bacteriologically confirmed shortly before death, by isolation of Pseudomonas pseudomallei from blood, pus swabs and tracheal aspirates. There is a need for greater awareness of this disease in persons who have resided in South-East Asia and in North-Eastern Australia.
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PMID:Terminal exacerbation of chronic melioidosis in New South Wales. 99 67

The internationally accepted term septicaemia is used to describe illnesses in which pathogenic microorganisms are present in the blood. Septicaemia should be defined according to the causative organism, the portal of entry and the underlying disease. In the last 16 years the causative organisms in 788 cases of septicaemia in our hospital were found to be gram-positive cocci in 28.1% gram-negative rods in 37.6%, and other organisms in 24.i%. Infections with Psuedomonas in particular have become more frequent in recent years. The range of causative organisms in septicaemia varies considerably with the patient groups involved. Thus patients with myeloid insufficiency contracted primarily gram-negative septicaemia. As in the past, the pathogens in endocarditis today are primarily streptococci. In hemodialysis staphylococci and gram-negative rods are shown to occur with equal frequency. The most important clinical manifestation of septicaemia is fever with rigor. The poor prognosis in gram-negative septicaemia is mainly due to the onset of septic shock. Skin colonisation is often a typical sign of septicaemia and can also sometimes serve as a diagnostic indication. Hemorrhagic pustules surrounded by a zone of inflammation are typical in septicaemia caused by meningococci or gonococci. Skin eruptions are rare in septicaemia caused by streptococci of staphylococci. Whereas skin eruptions are absent in septicaemia due to enterobacteria, they are very often present in septicaemia caused by Pseudomonas. In bacterial endocarditis a wide variety of skin lesions can occur.
Infection 1976
PMID:[Clinical study of septicaemia (author's transl)]. 101 83

The causes of death were investigated in 315 adults with acute leukemia during a 7-year period (1966-1972). Infection alone or in combination was the most common cause (75%), followed by hemorrhage (24%) and organ failure (9%). Most of the infections were either systemic or pulmonary. Seventy-five percent of the systemic infections and 72% of the pneumonias were caused by bacteria. Klebsiella pneumoniae, Escherichia coli and Pseudomonas aeruginosa were the most frequent organisms isolated. After 1968, there was a sharp decrease in the number of fatal infections caused by Pseudomonas aeruginosa and a marked increase in the incidence of fatal infections caused by Klebsiella spp. and E. coli. Infections caused by Gram-positive cocci occurred in only 3% of the cases. The incidence of systemic fungal infections was 13%; most common fungi causing infection were Candida spp. and Aspergillus spp. Eighty-five percent of 159 patients with a terminal neutrophil count of less than 100/mm3 died of infection, compared to 48% of 62 patients with a terminal neutrophil count of greater than 1000/mm3. Hemorrhage was mostly due to thrombocytopenia (61%) and disseminated intravascular coagulation (12%). This study indicates that infection continues to be the most common cause of death in patients with acute leukemia. Although advances in antibiotic therapy have changed the distribution of causative organisms, ultimate control of infection requires further improvements in supportive care measures which rectify impairments in the patients' host defense mechanisms.
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PMID:Causes of death in adults with acute leukemia. 106 11

Infection of Pseudomonas putida by the bacteriophage gh-L-induced the synthesis of a novel DNA-dependent RNA polymerase. This gh-L-induced RNA polymerase was purified to near homogeneity. It was shown to be distinct from the host RNA polymerase (alpha-2 beta beta sigma) physically and in respect to many of its catalytic properties. The gh-L-induced RNA polymerase was composed of a single polypeptide of approximately 98,000 molecular weight. The divalent metal ion requirement for in vitro RNA synthesis by the gh-L-polymerase could be satisified with Mg-2+, but not with Mn-2+. Rna synthesis by the gh-L polymerase was highly resistant to inhibition by rifampicin and streptolydigin but could be inhibited by relatively low concentrations of KCl or the rifamycin derivative AF/013. The structural analog of ATP, 3'-deoxyadenosine 5'-triphosphate, inhibited both the gh-L-induced and the host RNA polymerases by competing for a single binding site with ATP. The phage polymerase was extremely sensitive to this inhibitor, exhibiting an apparent K-i value (2 times 10-8 M) approximately 100 times lower than that for the host RNA polymerase. The gh-L polymerase had a highly specific template requirement for DNA from the homologous gh-L phage. It would not efficiently utilize denatured DNA templates and had only low levels of activity with pyrimidine-containing polydeoxyribonucleotide homopolymers.
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PMID:Purification and characterization of bacteriophage gh-I-induced deoxyribonucleic acid-dependent ribonucleic acid polymerase from Pseudomonas putida. 111 26

Bronchopulmonary infection in cystic fibrosis (CF) patients is associated with chronic progressive lung disease and episodes of acute exacerbation. Infection is predominantly caused by bacteria, although infections with viruses, mycoplasma and fungi may play undervalued roles. Bacteria commonly isolated from CF sputum include Staphylococcus aureus, Haemophilus influenzae and Pseudomonas aeruginosa. Colonisation of the airways by mucoid, alginate-producing variants of P. aeruginosa is recognised as a major cause of pulmonary deterioration. In addition, there is now considerable concern relating to the clinical consequences of colonisation and cross-infection with P. cepacia. This review discusses the microbiology of CF focussing on the pathogenesis and epidemiology of P. aeruginosa and P. cepacia.
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PMID:Microbiology of lung infection in cystic fibrosis. 128 Oct 36


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