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PubMed1983

The role of Pseudomonas aeruginosa in infections.

Pseudomonas aeruginosa, an organism ubiquitous in nature, has assumed an increasingly prominent role as the aetiological agent in serious infections in hospitalized patients. Pseudomonas has a number of pathogenic properties, which include its capsule, exotoxin A and various proteases. Although normal individuals infrequently carry this organism as part of their flora, patients with burns, malignancy, and after surgery often are colonized and subsequently infected with Pseudomonas. Infections produced by Pseudomonas include bacteraemia, respiratory infection, urinary tract infection, osteomyelitis, and infections of burns and soft tissues. Because of the resistance properties of Pseudomonas, therapy has been difficult. However, the development of highly effective antipseudomonas penicillins has brightened the picture. Nonetheless great progress can still be made in control and prevention of serious Pseudomonas infection.

Burns↗
PubMed2003

The complete genomic sequence of lytic bacteriophage gh-1 infecting Pseudomonas putida--evidence for close relationship to the T7 group.

The genome of the lytic Pseudomonas putida bacteriophage gh-1 is linear double-stranded DNA containing 37,359 bp with 216-bp direct terminal repeats. Like other members of the T7 group, the gh-1 genome contains regions of high homology to T7 interspersed with nonhomologous regions that contain small open reading frames of unknown function. The genome shares 31 genes in common with other members of the T7 group, including RNA polymerase, and an additional 12 unique putative genes. A major difference between gh-1 and other members of this group is the absence of any open reading frames between the left direct terminal repeat and gene 1. Sequence analysis of the gh-1 genome also revealed the presence of 10 putative phage promoters with a consensus sequence similar to the promoters of T3 and phiYeO3-12 (consensus: TAAAAACCCTCACTRTGGCHSCM). P. putida mutants resistant to gh-1 were demonstrated to have an altered lipopolysaccharide structure, indicating that members of this group use lipopolysaccharide as their cellular receptor.

Amino Acid Sequence↗
PubMed1971

Passive immunization against experimental pseudomonas infection: correlation of protection to verder and evans "o" serotypes.

Passive-protection tests were conducted in mice with antisera from rabbits immunized with formalinized or heat-killed cells or with an alcohol-precipitated fraction from the slime layer. Protection was conferred by antisera against the heatstable antigens and correlated well with agglutinin levels. Specificity was found to relate closely to the heat-stable "O" serotypes as defined by Verder and Evans.

Journal Article↗
PubMed1987

Comparison of the activity of antibiotic combinations in vitro with clinical outcome and resistance emergence in serious infection by Pseudomonas aeruginosa in non-neutropenic patients.

Techniques for demonstrating synergy in vitro were compared in testing different beta-lactam-aminoglycoside combinations against 30 isolates of Pseudomonas aeruginosa. Poor concordance was noted among the results from chequerboard and 6 h and 24 h time-kill methods. Comparison of in-vitro synergy results with clinical outcome in 14 patients with pseudomonas infection showed that antagonism in the 24 h time-kill method was the most reliable prognostic indicator of clinical and bacteriological outcome. Although more than 70% of patients were cured clinically with cefsulodin or ticarcillin with tobramycin or amikacin, pseudomonas resistant to the beta-lactam emerged in 7 of 14 patients (50%); of those seven, three had poor clinical outcome. The rationale of adding aminoglycoside to beta-lactams against P. aeruginosa to prevent emergence of resistance needs closer examination.

Adult↗
PubMed1998

Role of flagella in pathogenesis of Pseudomonas aeruginosa pulmonary infection.

Pseudomonas aeruginosa strains are opportunistic pathogens associated with infections in immunocompromised hosts and patients with cystic fibrosis. Like many other mucosal pathogens, P. aeruginosa cells express flagella which provide motility and chemotaxis toward preferred substrates but also provide a ligand for clearance by phagocytic cells. We tested the role of flagella in the initial stages of respiratory tract infection by comparing the virulence of fliC mutants in a neonatal mouse model of pneumonia. In the absence of fliC, there was no mortality, compared with 30% mortality attributed to the parental strain PAK or 15% mortality associated with infection due to a pilA mutant PAK/NP (P < 0.0001). The fliC mutants caused pneumonia in only 25% of the mice inoculated, regardless of whether there was expression of the pilus, whereas the parental strain was associated with an 80% rate of pneumonia. Histopathological studies demonstrated that the fliC mutants caused very focal inflammation and that the organisms did not spread through the lungs as seen in infection due to either PAK or PAK/NP. Purified flagellin elicited an intense inflammatory response in the mouse lung. 125I-labeled flagellin bound to the glycolipids GM1 and GD1a and to asialoGM1 in an in vitro binding assay. However, flagellin-mediated binding to epithelial gangliosides was a relatively unusual event, as quantified by binding assays of wild-type or fliC mutant organisms to CHO Lec-2 cells with membrane-incorporated GM1. Fla+ organisms but not fliC mutants were efficiently taken up by murine macrophages. P. aeruginosa flagella are important in the establishment of respiratory tract infection and may act as a tether in initial interactions with epithelial membranes. This function is offset by the contribution of flagella to host clearance mechanisms facilitating phagocytic clearance and the role of flagellar genes in mucin binding and clearance.

Animals↗
PubMed2006

The role of CXC chemokine receptor 2 in Pseudomonas aeruginosa corneal infection.

Pseudomonas is one of the leading causes of contact lens-related microbial keratitis. Despite the use of antibiotics, the host inflammatory response continues to cause damage to the cornea, which may lead to blindness. CXCR2-binding chemokines have been implicated in the pathogenesis of Pseudomonas keratitis, and the exact role of this receptor remains to be elucidated. Corneas of CXCR2 knockout and wild-type mice (Cmkar 2-/- and Cmkar 2+/+) were scratched, and 2x10(6) CFU/mL Pseudomonas 6294 or 6206 was added to corneas. Twenty-four hours postinfection, mice were killed, and eyes were harvested for enumeration of bacteria, myeloperoxidase (MPO) levels, and inflammatory mediators. Cmkar 2-/- had 20- to 100-fold more bacteria than Cmkar 2+/+ mice. There were no differences in MPO levels between gene knockout and Cmkar 2+/+ mice. Histology revealed PMN were restricted to the limbal area. Levels of CXCR2 chemokines (keratinocyte-derived chemokine and MIP-2) were elevated significantly in gene knockout mice. A lack of CXCR2 leads to an inability to control bacterial numbers as a result of the inability of PMN to reach the site of infection in the avascular cornea. These results imply that CXCR2 is critical to the extravasation of neutrophils into the avascular cornea.

Animals↗
PubMed2000

Role of the cystic fibrosis transmembrane conductance regulator in innate immunity to Pseudomonas aeruginosa infections.

Chronic Pseudomonas aeruginosa infection occurs in 75-90% of patients with cystic fibrosis (CF). It is the foremost factor in pulmonary function decline and early mortality. A connection has been made between mutant or missing CF transmembrane conductance regulator (CFTR) in lung epithelial cell membranes and a failure in innate immunity leading to initiation of P. aeruginosa infection. Epithelial cells use CFTR as a receptor for internalization of P. aeruginosa via endocytosis and subsequent removal of bacteria from the airway. In the absence of functional CFTR, this interaction does not occur, allowing for increased bacterial loads in the lungs. Binding occurs between the outer core of the bacterial lipopolysaccharide and amino acids 108-117 in the first predicted extracellular domain of CFTR. In experimentally infected mice, inhibiting CFTR-mediated endocytosis of P. aeruginosa by inclusion in the bacterial inoculum of either free bacterial lipopolysaccharide or CFTR peptide 108-117 resulted in increased bacterial counts in the lungs. CFTR is also a receptor on gastrointestinal epithelial cells for Salmonella enterica serovar Typhi, the etiologic agent of typhoid fever. There was a significant decrease in translocation of this organism to the gastrointestinal submucosa in transgenic mice that are heterozygous carriers of a mutant DeltaF508 CFTR allele, suggesting heterozygous CFTR carriers may have increased resistance to typhoid fever. The identification of CFTR as a receptor for bacterial pathogens could underlie the biology of CF lung disease and be the basis for the heterozygote advantage for carriers of mutant alleles of CFTR.

Animals↗
PubMed2006

Susceptibility testing of clinical isolates of pseudomonas aeruginosa to levofloxacin, moxifloxacin, and gatifloxacin as a guide to treating pseudomonas ocular infections.

PURPOSE: Pseudomonas aeruginosa ocular infections most frequently originate from an environmental source; successful treatment with various ocular antibiotics is well established. However, emergence of resistant clones to available antibiotics poses a real threat to successful treatment. The purpose of this study was to evaluate the antibiotic susceptibilities of 100 random clinical isolates of P. aeruginosa to levofloxacin, moxifloxacin, and gatifloxacin, potential agents for the treatment of ocular infections caused by this microorganism. METHODS: One hundred consecutive strains of P. aeruginosa were isolated from clinical specimens submitted to the clinical microbiology hospital laboratory. Duplicate isolates were not included. The minimum inhibitory concentrations (MICs) of these isolates were determined by using Etests, performed according to the manufacturer's instructions. American Type Culture Collection (ATCC) strains of Escherichia coli, P. aeruginosa, and Staphylococcus aureus served as reference controls. RESULTS: Although most isolates were susceptible to levofloxacin, moxifloxacin, and gatifloxacin and the MICs were not significantly different, significant numbers were resistant. The standardized controls rendered expected MICs. The susceptibility of the isolates varied with regard to source, and resistant strains showed increased resistance. CONCLUSIONS: Based on the data, the treatment of ocular infections caused by P. aeruginosa with levofloxacin, moxifloxacin, and gatifloxacin still has a high likelihood of success. However, six of the isolates collected were resistant to all three of the fluoroquinolones tested. Based on the data, clinicians must be aware that clinical resistance can occur even with the newer fluoroquinolones.

Anti-Bacterial Agents↗
PubMed1981

The role of proteases and exotoxin A in the pathogenicity of Pseudomonas aeruginosa infections.

Most Pseudomonas aeruginosa strains produce exotoxin A and two extracellular proteases (elastase and alkaline protease). Exotoxin A is a lethal toxin that inhibits protein synthesis in mammalian cells by the same mechanism as diphtheria toxin. It is generated in clinical and experimental animal infections. Passive or active immunization against this toxin gives significant protection against experimental infections with exotoxin-producing strains. The proteases have tissue-damaging activity and are capable of degrading various plasma proteins such as complement and coagulation factors. Proteases probably play a part in localized pseudomonas infections such as keratitis, pneumonia and burn infection. When invasion and colonization have occurred and septicemia is established, these enzymes probably are less important.

ADP Ribose Transferases↗
PubMed1976

Evidence for suppressor cell activity associated with depression of contact sensitivity in Pseudomonas aeruginosa infected mice.

Pseudomonas aeruginosa infection depresses contact sensitivity to 2-phenyl-4-ethoximethylene-oxazolone (oxazolone), and enhances the antibody response to sheep erythrocytes (SRBC) in the mouse. Anti-oxazolone antibody titres were found not to be significantly different in infected and uninfected animals; thus, the major circulating classes of antibodies do not seem to be responsibile for the observed depression of skin reactivity. Low dose (20 mg/Kg) cyclophosphamide (CY) pretreatment induced a further potentiation of antibody response to SRBC, and prevented depression of contact sensitivity in infected mice. On the other hand, when infected animals were pretreated with high doses (200 mg/Kg) of CY, antibody production was completely suppressed, whereas contact sensitivity was unaffected. Since CY treatment is known to selectively inhibit B lymphocytes, and since it can abrogate the infection-induced depression of reactivity to oxazolone, it is suggested that suppressor cells, which may have B-cell characteristics, are stimulated during P. aeruginosa infection in the mouse.

Animals↗
PubMed1995

Bronchopulmonary infection with Pseudomonas aeruginosa in patients infected with human immunodeficiency virus.

BACKGROUND: Pseudomonas aeruginosa infection is uncommon in HIV infected patients and is usually nosocomially acquired and associated with risk factors such as neutropenia or central lines. We have recently noted an increase in the number of respiratory isolates of Ps aeruginosa in hospitalised HIV positive patients and sought to describe the clinical correlates of this observation. METHODS: A retrospective case notes review of HIV positive patients admitted to a specialist unit for respiratory investigations from January 1989 to December 1993 was undertaken in order to identify those with Ps aeruginosa respiratory infection and to describe associated risk factors, patterns of presentation and radiographic abnormalities. RESULTS: Of 617 patients admitted 38 (6%) had Ps aeruginosa respiratory infection (notes were incomplete in 1 patient). All patients had advanced HIV disease; median CD4 = 0.02 x 10(9)/l. Two distinct presentations were seen; 9 patients had a fulminant course as part of a sepsis syndrome, 28 patients had an indolent presentation (18 had a single episode and 10 relapsed on one or more occasions, despite successful treatment of the initial episode). Infection was community acquired in 24 patients. Many patients had risk factors traditionally associated with Ps aeruginosa including neutropenia or indwelling central venous catheters, but 13 had no obvious risk factor. Most patients were receiving systemic pneumocystis prophylaxis and/or broad spectrum antibiotics; 20 had co-existent symptomatic sinus disease. A wide variety of chest radiographic abnormalities were seen including interstitial shadowing, mimicking pneumocystis pneumonia in 12 patients, lobar pneumonia in 2 and bronchial wall thickening in 13 patients. CONCLUSIONS: Ps aeruginosa respiratory infection occurs with increased frequency in patients with advanced HIV disease; in a significant proportion infection is community acquired. Although recognised risk factors were present in two thirds of patients it appears that advanced HIV immunosuppression, use of systemic pneumocystis prophylaxis and/or broad spectrum antibiotics and sinus disease are important risk factors. The diagnosis should be considered in patients with advanced HIV disease who present with new respiratory symptoms.

Adult↗
PubMed2002

TOBI: reducing the impact of pseudomonal infection.

Pseudomonas aeruginosa infection is associated with impaired lung function and reduced life expectancy in cystic fibrosis patients. Tobramycin nebulizer solution (TOBI, Chiron Corporation Ltd, Hounslow) has been specifically formulated for use against P. aeruginosa infection in the lung.

Administration, Inhalation↗
PubMed1978

Role of nonagglutinating antibody in the protracted immunity of vaccinated mice to Pseudomonas aeruginosa infection.

Effective immunization against infection with Pseudomonas aeruginosa is difficult to evaluate because agglutinin levels decline rapidly. Because fractionation of hyperimmune sera often yields more specific antibody than can be accounted for by direct agglutination tests, an immunoglobulin-specific assay based on antiglobulin augmentation was used to characterize antibody responses of C3H/HeJ mice vaccinated with P. aeruginosa type 2 lipopolysaccharide. Nonagglutinating antibodies, initially detected at 2 weeks post-primary vaccination, were predominantly immunoglobulin G after 5 weeks, and they remained elevated at levels usually 32-fold higher than the direct titer throughout the 4-month study period. The sequential production of immunoglobulin M, then immunoglobulin G, followed that found in orthodox immunological responses. Sera that contained nonagglutinating antibodies but not direct agglutinins (14 to 16 weeks) enhanced phagocytosis of P. aeruginosa type 2 by macrophages from unimmunized mice and passively immunized mice against lethal challenge doses; bactericidal activity of these sera was not demonstrated in the presence or absence of complement. When challenged with 1, 10, and 100 50% lethal doses at 16 weeks, survival rates of actively immunized mice were significantly higher than those of unvaccinated mice (P < 0.001). Thus, at a time when no direct agglutinins were detectable, the augmented system detected nonagglutinating antibodies that could confer protracted resistance in vaccinated mice to pseudomonas infection.

Agglutinins↗
PubMed1987

[Pseudomonas aeruginosa as a pathogen in opportunistic infections].

Pseudomonas aeruginosa, in spite of being an ubiquitous microorganism, rarely colonizes healthy individuals. Hospitalization, as well as the length of time spent in hospital, significantly increase the rate of colonization, especially in immunocompromised patients. Antibacterial chemotherapy or prophylaxis together with invasive diagnostic procedures favour colonization and infection with P. aeruginosa. Immune deficiencies and adverse interactions of P. aeruginosa with the immune system facilitate infection. Thus, a number of exogenous as well as endogenous factors and their interactions favour infection of patients with P. aeruginosa.

Anti-Bacterial Agents↗