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PubMed2005

Severe Pseudomonas aeruginosa infections. Tackling the conundrum of drug resistance.

Pseudomonas aeruginosa infections are a frequent cause of morbidity and mortality in hospitalized patients. Treatment of these infections is complicated by the intrinsic and acquired resistance of this bacterium to many commonly used antimicrobial agents. In this article, Drs Hauser and Sriram argue that careful consideration of the mechanisms by which P. aeruginosa resists the activity of antimicrobial agents is essential for optimal treatment decisions. Although many aspects of treatment of severe P. aeruginosa infections remain controversial, the authors suggest specific treatment options for patients both before and after susceptibilities are known.

Anti-Bacterial Agents↗
PubMed1998

Surfactant protein-A-deficient mice are susceptible to Pseudomonas aeruginosa infection.

To determine the role of surfactant protein-A (SP-A) in host defense, the murine SP-A locus was targeted by homologous recombination to produce mice lacking SP-A. SP-A-/- and wild-type mice were infected with mucoid Pseudomonas aeruginosa by intratracheal instillation. Pulmonary bacterial loads were greater in SP-A-/- than in wild-type mice, with increased numbers of mucoid P. aeruginosa in lung homogenates at 6 and 24 h after infection. Pulmonary infiltration with polymorphonuclear leukocytes (PMN) was similar in both groups; however, an earlier influx of PMN into the lung occurred in the SP-A-/- mice. The number of bacteria phagocytosed by alveolar macrophages was decreased in the SP-A-/- mice at 1 h after infection. Superoxide-radical generation by PMN was similar for the SP-A-/- and wild-type mice, but nitrite levels were increased in SP-A-/- mice. Concentrations of tumor necrosis factor-alpha, interleukin-6, and macrophage inflammatory protein-2 (proinflammatory cytokines) were greater in bronchoalveolar lavage fluid at 2 h after infection in SP-A-/- mice. SP-A plays an important role in the pathogenesis of mucoid P. aeruginosa infection in the lung in vivo by enhancing macrophage phagocytosis and clearance of bacteria, and by modifying the inflammatory response.

Animals↗
PubMed1979

A rat model of chronic respiratory infection with Pseudomonas aeruginosa.

Chronic, nonlethal, pulmonary infection of rats by Pseudomonas aeruginosa can be initiated by intratracheal inoculation of 10(4) bacteria enmeshed in agar beads. The number of bacteria recoverable from the lung increased to approximately 10(6) within 3 days and remained at that number during 35 days of observation. Histologic examination of the infected lungs revealed lesions resembling those seen in lung tissue of humans with acute or chronic nonbacteremic, Pseudomonas aeruginosa pneumonia, including the presence of goblet-cell hyperplasia, focal areas of necrosis, and acute and chronic inflammatory infiltrate. This model should be useful for investigating the interactions between microbial virulence factors and host defense mechanisms.

Animals↗
PubMed2005

[Detection and management of early Pseudomonas aeruginosa infection in patients with cystic fibrosis].

Initial Pseudomonas aeruginosa infection in patients with cystic fibrosis is a key step in pulmonary evolution of the disease. This first infection is most of the time early in life and gives some practical problems to the clinicians. It is important to look for colonisation with Pseudomonas aeruginosa as often as possible, at least every 3 month, by sputum culture when the child is able to or with induced sputum by hypertonic saline nebulisation. Treatment with inhalation of an antibiotic, preferably tobramycin for a 28 days course. Efficacy of the treatment as to be assessed by new culture.

Anti-Bacterial Agents↗
PubMed1993

Mechanism of conversion to mucoidy in Pseudomonas aeruginosa infecting cystic fibrosis patients.

Chronic respiratory infections with mucoid Pseudomonas aeruginosa are the leading cause of high mortality and morbidity in cystic fibrosis (CF). The initially colonizing strains are nonmucoid, but in the CF lung they invariably convert into the mucoid, exopolysaccharide alginate-overproducing form causing further deterioration and poor prognosis. Here we report the molecular basis of conversion to mucoidy. The algU gene is required for expression of the key alginate biosynthetic gene algD and encodes a protein homologous to sigma H, an alternative sigma factor regulating sporulation and other post-exponential-phase processes in Bacillus. The algU gene and the negative regulators mucA and mucB constitute the gene cluster controlling conversion to mucoidy. We demonstrate a critical role of mucA in this process based on (i) the presence of frameshift mutations disrupting the mucA coding region in mucoid cells that were absent in nonmucoid parental strains, (ii) genetic complementation of mucA mutations with the mucA+ gene, (iii) allelic replacements with specific mutant mucA genes causing conversion to mucoidy in previously nonmucoid cells, and (iv) detection of identical and additional mucA mutations in clinical mucoid strains isolated from the lungs of CF patients. These results suggest that the switch from the nonmucoid to mucoid state can be caused by inactivation of mucA, resulting in constitutive expression of alginate biosynthetic genes dependent on algU for transcription and that such mutants may be selected in vivo during chronic infections in CF.

Alginates↗
PubMed1983

Active and passive immunization against Pseudomonas aeruginosa infection of burned patients.

A 16-part polyvalent pseudomonas vaccine, PEV-01 and an immunoglobulin prepared from plasma from human volunteers vaccinated with PEV-01 were tested in a controlled clinical trial in burned patients at Safdarjang hospital, New Delhi. The mortality of the burned patients was reduced four-fold in adults and three-fold in children by the immunological treatments. Both immunoglobulin and vaccine increased the concentration of protective antibody. Patients responded to all 16 components in PEV-01. The vaccine caused no toxic side-effects and enhanced the bactericidal activity of polymorphonuclear leucocytes against Pseudomonas aeruginosa.

Adult↗
PubMed1990

Comparative therapy with cefpirome alone and in combination with rifampin and/or gentamicin against a disseminated Pseudomonas aeruginosa infection in leukopenic mice.

Treatment of disseminated Pseudomonas aeruginosa infection in leukopenic mice was evaluated using cefpirome alone and in combination with gentamicin and/or rifampin. Mice were made leukopenic with cyclophosphamide and infected through a skin incision with an inoculum of 1250 organisms (13 LD50). Antibiotics were administered subcutaneously for 48 h. Although the addition of cefpirome to gentamicin and/or rifampin improved survival significantly at 48 h compared with untreated controls (84.6%-100% vs. 38.5%), therapy with these combinations did not improve survival significantly from that achieved with cefpirome alone. Quantitative blood and tissue (liver, spleen, kidney, lung) cultures in mice treated with cefpirome alone or including rifampin were lower than in infected controls or groups receiving therapy that excluded cefpirome. Highest counts were observed in mice receiving cefpirome plus gentamicin. Except for the cefpirome plus gentamicin group, which demonstrated areas of acute tubular necrosis, the cefpirome group had less tissue pathology than infected controls.

Animals↗
PubMed2006

Regulation of pulmonary Pseudomonas aeruginosa infection by the transcriptional repressor Gfi1.

Pulmonary Pseudomonas aeruginosa infections are characterized by the release of proinflammatory mediators, focal induction of apoptosis in respiratory epithelial cells and internalization of the bacteria. Here, we demonstrate that the transcriptional regulator Gfi1 is critically involved in the regulation of proinflammatory cytokine release and the induction of apoptosis in respiratory epithelial cells and macrophages upon P. aeruginosa infection. Gfi1-deficient mice responded to a pulmonary P. aeruginosa infection with uncontrolled pulmonary release of interleukin (IL)-1 and tumour necrosis factor (TNF)-alpha, sepsis and death, which were delayed by injection of IL-1- and TNF-alpha-neutralizing antibodies. The uncontrolled release of cytokines seems to be caused by a failure of Gfi1-deficient respiratory epithelial cells in large to small bronchi and macrophages to respond to P. aeruginosa infection with an induction of apoptosis. Pharmacological inhibition of apoptosis in wild-type mice by intravenous injection of the broad-spectrum caspase inhibitor zVAD-cmk mimicked the phenotype of Gfi1-deficient mice and resulted in a profound sensitization of mice to P. aeruginosa, an increased release of cytokines, sepsis and death of the animals. Thus, Gfi1 controls apoptosis of respiratory epithelial cells and macrophages upon infection with P. aeruginosa. Inhibition of apoptosis by Gfi1 deficiency or caspase blockers sensitizes mice to P. aeruginosa infections, suggesting that apoptosis functions as a novel defence mechanisms in the regulation of the local innate immune response.

Animals↗
PubMed2004

Chronic Pseudomonas aeruginosa infection in cystic fibrosis airway disease: metabolic changes that unravel novel drug targets.

The cystic fibrosis (CF) airways have an incompletely characterized defect in innate defense that eventually leads to bacterial infection and airway inflammation. Persistent Pseudomonas aerugionsa infection resulting from defective innate immunity and a bacterial phenotypic switch to a more intractable mucoid form inside the airway are now well established as important components of CF pathogenesis. Broad-based factors leading to chronic infection will be discussed with respect to: bacterial virulence in the context of biofilm formation, quorum sensing machinery and alginate overproduction, and failure of innate lung immunity in CF airways. In addition, a controversial question as to whether inflammation or infection comes first during CF airway disease will be addressed. Finally, a new hypothesis, that P. aeruginosa thrives as biofilms within the thickened anaerobic mucus layers, will be developed.

Animals↗
PubMed1996

Usefulness of a computerized expert system associated with systematic O-serotyping for the early detection of outbreaks of hospital acquired infections and for the presumptive antibiotic therapy of Pseudomonas aeruginosa infections.

Over a four-year period, the systematic O-serotyping of all Pseudomonas aeruginosa isolated in Hôpital de Rodez associated with the use of a computerized expert system, facilitated the early detection of two outbreaks of nosocomial infections with multiresistant serotype O:11 and multiresistant serotype O:12 P. aeruginosa respectively involving ten patients over 16 months and six patients over six months. Over this four-year period, serotype O:12 represented 14% of 404 clinical isolates of P. aeruginosa, and most isolates of this serotype were resistant to multiple antibiotics. Combination experiments showed that fosfomycin/amikacin together were active against 86% of O:12 isolates. Fosfomycin/amikacin might be considered as a therapeutic alternative to ceftazime/amikacin for the presumptive antipseudomonal therapy of serotype O:12 infections.

4-Quinolones↗
PubMed1996

Epidemiology of community-acquired Pseudomonas aeruginosa infections in children.

The epidemiology of community-acquired Pseudomonas aeruginosa infections in children during a one-year period (January through December 1993) was evaluated. A total of 6,859 clinical samples, each one representing a separate individual with suspected infection, were cultured. Pseudomonas aeruginosa was isolated from 218 children with various infections occurring in the following order of frequency: chronic suppurative otitis media, 76.3%; appendicitis/peritonitis, 10.3%; osteomyelitis, 8.9%; skin or soft tissue infection, 6.3%; acute conjunctivitis, 3.0%; and urinary tract infection, 0.1%. A variety of O serogroups were identified: O1 (15.2%), O6 (14.7%), O11 (12.4%), O10 (11.5%), O3 (10.6%), O5 (5.1%), and O9 (4.6%). Other serogroups and nontypable strains were recovered at a frequency of 11.2% and 14.7%, respectively. Nontypable strains predominated in chronic otitis media (18.9%), while serogroups O1 (18.3%), O6 (17.5%), and O11 (17.5%) were recovered most frequently among the typable isolates. Susceptibility of Pseudomonas aeruginosa to antipseudomonadal agents was extremely high. The rate of susceptibility to ceftazidime was 99.6%, to azlocillin 98.6%, to piperacillin 98.2%, to aztreonam 97.3%, to gentamicin and netilmicin 97.7%, and to ciprofloxacin 99.1%. All isolates were susceptible to tobramycin, imipenem, and amikacin. The results might suggest that community-acquired Pseudomonas aeruginosa infections in children can be treated successfully with any antipseudomonadal antibiotic.

Age Factors↗
PubMed2006

Pseudomonas fluorescens infections in clinical practice.

Pseudomonas fluorescens was isolated from an elderly immunocompromized patient with fever. Treatment with ceftazidime was successful, after empirical therapy failed. Pseudomonas fluorescens is 1 of the less virulent members of the Pseudomonadaceae family. The epidemiology of the infection and the difficulties in isolation and susceptibility assessment are further discussed.

Aged, 80 and over↗
PubMed2001

Pseudomonas aeruginosa infections in cancer patients: have they gone away?

Pseudomonas aeruginosa infection continues to be a threat to cancer patients, especially if they are neutropenic. As many as 50% of infections are community acquired. Prompt, effective therapy results in cures in about 80% of patients, although the presence of shock or pneumonia indicates a poor prognosis. Antibiotic resistance is an increasing problem.

Bacteremia↗
PubMed1985

Edetate sodium aerosol in Pseudomonas lung infection in cystic fibrosis.

In vitro and animal experimental data suggest the combination of edetate sodium (EDTA) by aerosol plus oral antimicrobials might be effective in the treatment of chronic Pseudomonas infection in patients with cystic fibrosis (CF). For six months we studied the effects of edetate sodium administered by ultrasonic nebulizer to ten children with CF and chronic Pseudomonas aeruginosa infection in a double-blind, placebo-controlled, crossover study. The children had evidence of mild to moderate disease at entry in the study, with a mean (+/- SD) forced expiratory volume in the first second of 85% (+/- 18%) of the predicted value and a mean (+/- SD) Shwachman-Kulczycki score of 83 (+/- 7)/100. Each child was on a three-month regimen of aerosolized edetate sodium plus oral tetracycline twice daily followed by three months of placebo aerosol plus tetracycline or vice versa. Progress was assessed by measurement of pulmonary function, physical examination, and sputum cultures at four weekly intervals, plus chest roentgenograms on entry and after each of the three-month treatment periods. Daily symptoms were assessed using a diary card system. Two patients could not complete the study, one because of severe respiratory relapse, the other because of antibiotic side effects. Of the remaining eight patients, none showed any improvement in pulmonary function, weight gain, or growth acceleration, and none was rendered free of Pseudomonas lung infection. Daily symptom scores and chest roentgenograms were unaltered by edetate sodium. We conclude that the combination of aerosol edetate sodium plus oral tetracycline over a three-month period does not modify the clinical course nor the pulmonary flora in patients with CF with chronic Pseudomonas lung infection.

Administration, Oral↗