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At least 739 records · Page 41Linked to original sources
PubMed1996

How mutant CFTR may contribute to Pseudomonas aeruginosa infection in cystic fibrosis.

Patients with cystic fibrosis (CF) have a pronounced hypersusceptibility (80 to 90%) to Pseudomonas aeruginosa infection. We hypothesized that airway epithelial cell ingestion of bacteria followed by cellular desquamation may protect the lung from infection, and epithelial cells expressing mutant forms of the cystic fibrosis transmembrane conductance regulator (CFTR) may be defective in this function. We found that transformed human airway epithelial cells homozygous for the delta F508 allele of CFTR were significantly defective in uptake of P. aeruginosa compared with the same cell line complemented with the wild-type allele of CFTR. Partial membrane expression of the delta F508 CFTR protein occurs in cells grown at 26 degrees C, and under these conditions uptake of P. aeruginosa occurred at levels comparable to cells with a wild-type allele of CFTR. Epithelial cell ingestion assays using isogenic bacterial strains differing in lipopolysaccharide (LPS) phenotype, along with inhibition studies, identified the LPS-core oligosaccharide as the bacterial ligand for epithelial cell invasion. Inhibition of epithelial cell ingestion of P. aeruginosa in a neonatal mouse lung infection model led to increased levels of bacteria in the lungs 24 and 48 h after infection. Defective epithelial cell internalization of P. aeruginosa may be a critical factor in hypersusceptibility of CF patients to chronic lung infections.

Animals↗
PubMed1997

Excessive inflammatory response of cystic fibrosis mice to bronchopulmonary infection with Pseudomonas aeruginosa.

In cystic fibrosis (CF), defective function of the cystic fibrosis transmembrane conductance regulator (CFTR) in airway epithelial cells and submucosal glands results in chronic pulmonary infection with Pseudomonas aeruginosa. The pulmonary infection incites an intense host inflammatory response, causing progressive suppurative pulmonary disease. Mouse models of CF, however, fail to develop pulmonary disease spontaneously. We examined the effects of bronchopulmonary infection on mice homozygous for the S489X mutation of the CFTR gene using an animal model of chronic Pseudomonas endobronchial infection. Slurries of sterile agarose beads or beads containing a clinical isolate of mucoid P. aeruginosa were instilled in the right lung of normal or CF mice. The mortality of CF mice inoculated with Pseudomonas-laden beads was significantly higher than that of normal animals: 82% of infected CF mice, but only 23% of normal mice, died within 10 d of infection (P = 0.023). The concentration of inflammatory mediators, including TNF-alpha, murine macrophage inflammatory protein-2, and KC/N51, in bronchoalveolar lavage fluid in CF mice 3 d after infection and before any mortality, was markedly elevated compared with normal mice. This inflammatory response also correlated with weight loss observed in both CF and normal littermates after inoculation. Thus, this model may permit examination of the relationship of bacterial infections, inflammation, and the cellular and genetic defects in CF.

Animals↗
PubMed1997

Epidemiology of chronic Pseudomonas aeruginosa infections in the airways of lung transplant recipients with cystic fibrosis.

BACKGROUND: The source of airway colonisation with Pseudomonas aeruginosa is not well defined in patients with cystic fibrosis after lung transplantation. Using a DNA-based typing system a study was undertaken to investigate whether lung transplant recipients acquired new strains of P aeruginosa or retained those they had before transplantation. METHODS: Seventy four P aeruginosa isolates taken before and after transplantation were analysed from 11 patients with cystic fibrosis who had undergone lung transplantation in the Medical School of Hannover between 1988 and 1994. The genetic relatedness of the 74 P aeruginosa strains was evaluated from macrorestriction fragment pattern similarity. RESULTS: Each of the 11 lung transplant recipients harboured one identical P aeruginosa clone before and after transplantation. The airways of four of the 11 patients were preoperatively colonised by two or three different clones, but six months after transplantation only one clone was detectable. CONCLUSIONS: These results show that there is no change in the P aeruginosa population in the airways of lung transplant recipients before and after transplantation and it is assumed that the chronic drainage of P aeruginosa into the lung allografts is caused by the bacterial reservoir in the paranasal sinuses and the trachea.

Adolescent↗
PubMed1989

[Pseudomonas aeruginosa infection of the sternum and costal cartilages in cardiosurgery. Therapeutic experience using aztreonam].

Clinical effectiveness of Aztreonam was studied. This new monobactam antimicrobial agent was tasted in the treatment of post-operative infectious complications of cardiac surgical sternal wounds. Ten patients (4 men and 6 women, age range 20 to 68 years) were entered into the study. All had a Pseudomonas aeruginosa infection of sternum or sternum and ribs and all underwent an extensive regional surgery of the infection wound and received a topical and/or IV treatment with Aztreonam. In all cases we obtained a satisfactory result, with complete eradication of the infection. Both local and systemic tolerance to the drug were excellent and no side-effect was registered. Therefore Aztreonam can be considered an active and safe antibiotic for the treatment of sternal and/or costal postsurgical infections by Pseudomonas aeruginosa.

Adult↗
PubMed1998

The effect of Pseudomonas aeruginosa infection on clinical parameters in steady-state bronchiectasis.

STUDY OBJECTIVE: To investigate the effect of Pseudomonas aeruginosa infection on clinical parameters in Chinese patients with noncystic fibrosis and steady-state bronchiectasis. DESIGN: Prospective, cross-sectional clinicomicrobiological study with informed consent. SETTING: Consecutive outpatient recruitment from a specialist bronchiectasis respiratory clinic. PATIENTS: Outpatients (n = 100; 62 women; 55.1+/-16.7 years old; FEV1/FVC 1.4+/-0.7/2.1+/-0.9 L), who had stable respiratory symptoms for more than 3 weeks. MEASUREMENTS AND RESULTS: Respiratory pathogens isolated from the sputum were: Pseudomonas aeruginosa (33), Haemophilus influenzae (10), Moraxella catarrhalis (2), other Gram-negative bacilli (5), Streptococcus pneumoniae (6), Staphylococcus aureus (5), mycobacteria (3), and yeast (1). Clinical parameters in patients with positive isolation of P aeruginosa were compared with those without the organism in the sputum culture (non-P aeruginosa). In the P aeruginosa group, the FEV1/FVC ratio and sputum volume were lower (p < 0.005) and higher (p < 0.0001), respectively, than those of the non-P aeruginosa group. The FEV1/FVC ratio (< 60%) and sputum volume (grading > 5) were independently associated with a positive sputum isolation of P aeruginosa with odds ratios of 3.1 (confidence interval [CI] 1.2 to 8.4; p < 0.01) and 4.7 (CI 1.6 to 13.3; p < 0.001), respectively. CONCLUSIONS: P aeruginosa is the predominant respiratory pathogen isolated in the sputum of Chinese patients with steady-state bronchiectasis, and its isolation is associated with high sputum output (> or = 75th quartile) and moderately severe airflow obstruction (FEV1/FVC < 60%).

Adult↗
PubMed2003

Current and future perspectives for levofloxacin in severe Pseudomonas aeruginosa infections.

The question of whether levofloxacin includes Pseudomonas aeruginosa in its spectrum of clinical activity is discussed by reviewing the major findings on this issue, mainly those published in Italy. The in vitro activity of levofloxacin against P. aeruginosa is now documented on thousands of strains worldwide. The pharmacodynamic properties of levofloxacin allow for the treatment of pseudomonal infections. The levofloxacin clinical results extrapolated from published studies document the efficacy of levofloxacin in the treatment of infections sustained by P. aeruginosa.

Anti-Bacterial Agents↗
PubMed1986

Evaluation of ciprofloxacin in the treatment of Pseudomonas aeruginosa infections.

The efficacy and safety of ciprofloxacin in the treatment of Pseudomonas aeruginosa infections was evaluated in 72 patients suffering from upper urinary tract infection (19 patients), deep soft tissue infection (16), chronic osteomyelitis (12), abscess (7), chronic otitis media (6), otitis externa (3) and bronchopneumonia (9). Forty-eight patients received an oral dose of 500 mg or 750 mg b.i.d. and five patients an i.v. dose of 200 mg b.i.d., while 19 patients were given both oral and parenteral doses. The duration of therapy ranged from seven days to more than four months. The MICs of ciprofloxacin for the Pseudomonas aeruginosa strains isolated were in the range less than 0.06-2 mg/l; 36% of the strains were resistant to all other available antibiotics. At follow-up after a minimum of six months the clinical success rate was 75% and the infecting organism was permanently eradicated in 49% of the patients. In nine patients the organism developed resistance, particularly when the initial MIC was higher than 0.5 mg/l. No significant adverse reactions were observed. Ciprofloxacin is the first antipseudomonal antimicrobial agent which can be administered orally and therefore fulfills a need in chemotherapy.

Abscess↗
PubMed1975

Rabbit corneal damage produced by Pseudomonas aeruginosa infection.

Gross, light microscopic, and electron microscopic examination of the rabbit corneal destruction produced by experimental Pseudomonas aeruginosa infections revealed a combination of acute inflammation and liquefaction necrosis of the cornea. Degeneration of the epithelial cells and the start of polymorphonuclear leukocyte infiltration of the cornea occurred initially. These changes were followed by loss of the epithelium, degeneration and loss of the keratocytes and endothelium, loss of the characteristic weblike pattern of the proteoglycan ground substance, dispersal of ultrastructurally normal collagen fibrils, extensive accumulation followed by degeneration of polymorphonuclear leukocytes, and accumulation of plasma proteins and fibrin in the necrotic cornea. Histochemical examination of the cornea suggested a loss of the proteoglycan ground substance but not of collagen. Rabbit corneas injected with Clostridium histolyticum collagenase showed gross and cellular changes similar to those observed during the pseudomonal infections; however, histochemical examination suggested a loss of collagen, and electron microscopy revealed ultrastructurally abnormal collagen fibrils. The results support the idea (i) that a bacterial or host-derived collagenase is not required for extensive corneal damage during a P. aeruginosa corneal infection, and (ii) that a P. aeruginosa corneal infection may severly damage the cornea by producing extensive corneal edema and by causing the loss of the corneal proteoglycan ground substance, thus resulting in dispersal of undamaged collagen fibrils, weakening of the cornea, and subsequent descemetocele formation and corneal perforation by the anterior chamber pressure.

Clostridium↗
PubMed1995

Endobronchial inflammation following Pseudomonas aeruginosa infection in resistant and susceptible strains of mice.

The early endobronchial inflammation induced by Pseudomonas aeruginosa infection varies in resistant and susceptible strains of mice. Mice of the DBA/2 strain are severely afflicted by the infection, with a high bacterial burden accumulating rapidly following inoculation and a high mortality rate occurring. Mice of the BALB/c strain are resistant to infection and clear the bacteria within 3 to 7 days. Infection of (BALB/c x DBA/2)F1 hybrid mice showed that the resistance to lung P. aeruginosa infection is inherited as a dominant trait. Mice of the A/J and C57BL/6 strains were found to have an intermediate phenotype to Pseudomonas aeruginosa infection when compared with BALB/c and DBA/2 strains. The decrease in the bacterial load seen early after infection coincided with a steady and strong recruitment of inflammatory cells to the bronchoalveolar spaces of mice of the resistant BALB/c strain. On the other hand, the recruitment of inflammatory cells to the lungs of mice of the susceptible DBA/2 strain was deficient, resulting in the failure to control bacterial multiplication. Chemotactic factors, proinflammatory cytokines, and the number and function of recruited inflammatory cells may play major roles in the determination of the genetic resistance to lung infection with P. aeruginosa in a normal immunocompetent host.

Animals↗
PubMed1987

A mouse model of chronic pulmonary infection with Pseudomonas aeruginosa and Pseudomonas cepacia.

A mouse model of chronic pulmonary infection with either Pseudomonas aeruginosa or Pseudomonas cepacia was developed to compare bacteriologic and pathologic features of these infections. Experimental pneumonia was established in Swiss mice by transoral intratracheal inoculation of 10(3)-10(4) colony-forming units of mucoid P. aeruginosa or P. cepacia enmeshed in agarose beads. Unilateral infection with either strain was tolerated without morbidity. By 10 days postinoculation, the mean colony-forming units per infected lung was 3.8 X 10(5) for P. aeruginosa and 1.0 X 10(5) for P. cepacia. Bacterial counts remained stable through 21 days with no significant difference between organisms. Acute and chronic inflammatory histopathologic changes similar to many found in the lungs of cystic fibrosis patients were present in 95% of lung specimens. The changes occurred with both organisms but were more extensive with mucoid P. aeruginosa. This model represents an important tool for study of the contribution of complement, antibody, and adoptive transfer of T cell-mediated immunity to the pathogenesis of chronic pneumonia with Pseudomonas species, and represents the first successful model of chronic pulmonary infection with P. cepacia.

Animals↗
PubMed2006

Evaluating the "Leeds criteria" for Pseudomonas aeruginosa infection in a cystic fibrosis centre.

Four separate categories of chronic Pseudomonas aeruginosa (Pa) infection in children with cystic fibrosis (CF) have been previously defined, based on airway cultures taken over the previous year. The aim of the present study was to evaluate this definition in the current authors' paediatric and adult CF clinic using clinical, immunological and lung function parameters. During follow-up, out of 193 patients, 55 (34%) CF patients had never been infected with Pa, 27 (17%) were free of Pa, 29 (18%) were intermittently infected and 51 (31%) were chronically infected. Disease severity markers, such as lung function, were significantly worse in the chronic group, especially in the paediatric population. Differences in adult patients were smaller and no longer significant. Pa antibodies differed strongly between the groups, and were very high (mean+/-sd 55.4+/-5.5) and highly statistically significant from all other groups in the chronic group. They were low and different from all other groups in the never group (1.8+/-0.6). Pa antibodies did not differ between the free of Pa and the intermittent group. In conclusion, the current authors confirmed an agreement between Pseudomonas aeruginosa status according to the new definition and clinical status, as well as with the level of Pseudomonas aeruginosa antibodies.

Adolescent↗
PubMed1996

In vivo oral efficacy of levofloxacin for treatment of systemic Pseudomonas aeruginosa infections in a murine model of septicemia.

The in vivo efficacies of levofloxacin and ciprofloxacin in lethal, systemic Pseudomonas aeruginosa infections in mice were compared. MICs of levofloxacin and ciprofloxacin ranged from 0.5 to 2.0 micrograms/ml and from 0.12 to 1.0 microgram/ml respectively. Infecting doses ranged from 5.0 x 10(1) to 3.2 x 10(3) CFU per mouse, depending on the isolate. Test fluoroquinolones were administered orally at 1 h (single dose) or at 1 and 3 h (divided dose) postinfection, with 10 infected mice used for each of six concentrations of each fluoroquinolone tested (1 to 40 mg/kg of body weight) in each dosing regimen. Whether given in a single or a divided dose, the total daily dose was the same for each fluoroquinolone. For mice treated 1 h postinfection with levofloxacin and ciprofloxacin, the effective doses for 50% of the infected mice ranged from 2.09 to 13.80 mg/kg and from 2.34 to 11.22 mg/kg, respectively, and for those treated 1 and 3 h postinfection, the effective doses for 50% of the infected mice ranged from 3.71 to 16.98 mg/kg and from 2.95 to 13.18 mg/kg, respectively. Although the potency varied for both levofloxacin and ciprofloxacin among all strains of P. aeruginosa tested, there were small differences within the same strain for levofloxacin and ciprofloxacin when given in the same dosing regimen. Levofloxacin proved nearly as effective as ciprofloxacin against a systemic P. aeruginosa infection in mice.

Administration, Oral↗
PubMed1985

Protective effect of Lactobacillus casei on Pseudomonas aeruginosa infection in mice.

The protective effect of heat-killed Lactobacillus casei YIT9018 (LC 9018) against Pseudomonas aeruginosa infection in mice was compared with that of Corynebacterium parvum. Survival of mice after intraperitoneal (i.p.) infection with P. aeruginosa was augmented in mice that had been pretreated i.p. with LC 9018 5 days previously. Similar treatment of mice with C. parvum, however, was not effective at all. Moreover, mice became more susceptible to infection with P. aeruginosa after such treatment. Growth of P. aeruginosa in the peritoneal cavity and spleen was markedly inhibited in LC 9018-pretreated mice, whereas such inhibition of bacterial growth was not observed in C. parvum-treated mice. The protective effect of LC 9018 was observed in mice subjected to 800 rads of whole body irradiation but was abrogated when mice were treated with carrageenan. These results suggest that augmentation of the resistance of mice to P. aeruginosa was caused by the induction of activated macrophages. The number of macrophages detectable in the peritoneal cavity was almost the same in LC 9018- and C. parvum-treated mice. Growth of Listeria monocytogenes was inhibited by pretreatment with LC 9018. Inhibition of L. monocytogenes was also observed after the same pretreatment with C. parvum. It was suggested that macrophages activated with LC 9018 were involved in the protective immunity to P. aeruginosa.

Animals↗