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At least 1,279 records · Page 71Linked to original sources
PubMed1992

[Pseudomonas aeruginosa infection in cystic fibrosis: predominance of a single strain and the influence of antibiotic therapy and the environment].

We analysed the implantation pattern and persistence of Pseudomonas aeruginosa in the tracheobronchial tracts of patients with cystic fibrosis, and investigated the relation of this bacterium with the environment and antibiotic therapy. We used four different techniques to ensure the precise and detailed identification of isolates. In particular, chromosomal differences were assessed by pulsed field electrophoresis (pulsotype determination). Sputum samples were collected from 8 patients, from 6 to 22 years-old, over a period of 19 to 24 months. Only a single strain was isolated from samples from each five patients taken at different times, and there was a predominant strain in the samples from two others. Patient 8, aged 14, was free of infection throughout the study. None of the infections was eradicated by antibiotic therapy (an association of two antibiotics for 15 days at one or two months interval). The strains isolated from two patients became resistant to imipenem: 3 out of the 4 resistant strains were the result of mutation in the resident, susceptible strain. Swabs were taken from the environments of infected patients and were tested for P. aeruginosa: this bacteria was found in three sites, and two of these contained an isolate with the same pulsotype as the strain responsible for the infection, whereas no P. aeruginosa was detected in the environment of an uninfected patient. The detailed and accurate identification of the isolates (by pulsotyping) enabled us--to show that each infected patient was infected by a single or predominant strain,--to investigate the relationship of these strains with those in the environment and the effects of antibiotic therapy.

Adolescent↗
PubMed1989

Antibody-independent protection against Pseudomonas aeruginosa infection in mice after treatment with a homologous strain vaccine.

Formalin-killed cells of Pseudomonas aeruginosa strain M-24 elicited an antibody-independent protective effect against P. aeruginosa infection in mice. The effect was observed as early as 6 h after administration and 100% protection was obtained by 48 h. The protective effect could not be attributed to the production of specific antibody. In M-24-treated mice, the bacteria in the peritoneal cavity, blood and liver were eliminated 12 h after P. aeruginosa infection. This suggested that the protective effect was due to enhanced bacterial elimination. The percentage of macrophages in the peritoneal cavity was increased after M-24 administration. Furthermore, the enhanced bacterial elimination was abrogated by treatment of mice with 60Co-irradiation or carrageenan. These findings suggest the involvement of macrophages in the enhanced bacterial elimination observed. The chemiluminescence of peritoneal exudate cells from M-24-treated mice was markedly increased when compared with that of cells from untreated mice. The ability to kill P. aeruginosa in vitro was also greater in macrophages from mice treated with killed M-24 than in cells from proteose-peptone-treated mice. The M-24-treated mice showed enhanced nonspecific protection against infection with lethal doses of P. aeruginosa, Escherichia coli or Listeria monocytogenes. However, susceptibility to LPS in mice was not increased by M-24 treatment. These results suggest that macrophage activation without increasing LPS susceptibility was responsible for the antibody-independent protection induced by killed M-24.

Animals↗
PubMed2004

Inhaled diesel engine emissions reduce bacterial clearance and exacerbate lung disease to Pseudomonas aeruginosa infection in vivo.

Despite experimental evidence supporting an adverse role for air pollution in models of human disease, little has been done in the way of assessing the health effects of inhalation of whole mixtures from defined sources at exposure levels relevant to ambient environmental exposures. The current study assessed the impact of inhaled diesel engine emissions (DEE) in modulating clearance of Pseudomonas aeruginosa (P.a.) and the adverse effects of infection to the pulmonary epithelium. At DEE concentrations representing from high ambient to high occupational exposures, mice were exposed to DEE continuously for one week or six months (6 h/day), and subsequently infected with P.a. by intratracheal instillation. At 18 h following P.a. infection, prior exposure to DEE impaired bacterial clearance and exacerbated lung histopathology during infection. To assess the airway epithelial cell changes indicative of lung pathogenesis, markers of specific lung epithelial cell populations were analyzed by immunohistochemistry. Both ciliated and non-ciliated airway epithelial cell numbers were decreased during P.a. infection by DEE exposure in a concentration-dependent manner. Furthermore, the lung transcription regulator, thyroid transcription factor 1 (TTF-1), was also decreased during P.a. infection by prior exposure to DEE concordant with changes in airway populations. These findings are consistent with the notion that environmental levels of DEE can decrease the clearance of P.a. and increase lung pathogenesis during pulmonary bacterial infection.

Animals↗
PubMed1998

[Study on pathogenetic role of myeloperoxidase, tumor necrosis factor alpha, interferon gamma in chronic airway infection with Pseudomonas aeruginosa].

This study was performed to demonstrate the pathogenetic role of mucoid-alginate produced by Pseudomonas aeruginosa in relation to immuno-interaction in host cells. The obtained results are as follows. 1. Clinical Observation The concentration of MPO, TNF alpha, and IFN gamma in peripheral blood of 37 cases of chronic airway infection were observed. The cases were divided into the groups with mucoid strain positive (21 cases) and negative (16 cases), and each group was also divided into subgroups with active clinical symptom and without. High concentration of serum IFN gamma was shown in the group of mucoid strain positive cases (0.10 +/- 0.08 IU/ml in healthy volunteers group, 0.54 +/- 0.56 IU/ml in mucoid group with symptom: p < 0.01, 0.09 +/- 0.15 IU/ml in mucoid group without symptom, 0.13 +/- 0.13 IU/ml in non-mucoid group with symptom, 0.09 +/- 0.13 IU/ml in non-mucoid group without symptom). But plasma concentrations of MPO and serum concentrations of TNF alpha were not increased in all groups, except MPO in non-mucoid group with symptom. It indicates that IFN gamma has a characteristic role in chronic airway infection with mucoid Pseudomonas aeruginosa (P. aeruginosa). 2. Experimental Observation One hundred twenty-two of alginate-immunized mice were made by 5 times of intraabdominal injection with purified alginate extracted from mucoid P. aeruginosa PT-1252. 4 x 10(6) CFU/body of mucoid P. aeruginosa PT-1252 or 20 micrograms/body of purified alginate was intubated per trachea into the immunized mice, and changes in mean fluorescence intensity (MFI) of MPO and TNF alpha on neutrophils and IFN gamma on CD3 positive lymphocytes in BALF were observed. MFI of MPO (99.7 +/- 16.5-->177.0 +/- 23.1: p < 0.001) and TNF alpha (59.2 +/- 13.3-->197.0 +/- 62.0: p < 0.001) were increased on day 2 and they were kept up till on day 30 in P. aeruginosa group. But in alginate group they were temporally decreased on day 2, and they were gradually increased (MPO: 99.7 +/- 16.5-->212.6 +/- 12.1: p < 0.001, TNF alpha: 59.2 +/- 13.3-->162.4 +/- 30.9: p < 0.01). The temporally decrease of MPO and TNF alpha on day 2 in alginate group may suggest that a large amount of alginate inhibits neutrophils chemotaxis. MFI of IFN gamma in P. aeruginosa was also increased (110.0 +/- 32.9-->198.3 +/- 23.0: p < 0.01) on day 2 and it was gradually decreased on day 30 (156.0 +/- 13.8). In alginate group, MFI of IFN gamma in BALF was increased on day 5 (110.0 +/- 32.9-->201.0 +/- 49.3: p < 0.001) and kept a high level till day 30 (223.0 +/- 57.5: p < 0.01). In morphological, the moderate grade of lymphocytes infiltration observed in intersitial area of lung tissue on both groups of P. aeruginosa and alginate intubation mice. The findings was continuously seen from day 5 through day 30. The lymphocytes infiltration appeared in lung tissue can be though as an result of immuno-interaction with IFN gamma positive lymphocytes and mucoid-alginate. Inferences are drawn from the clinical results and the experimental ones that the CD3 positive IFN gamma lymphocytes expressed by immunological interaction with mucoid-alginate and the IFN gamma lymphocytes (Th1 like cells) plays an important role on advancement of chronic airway infection with mucoid P. aeruginosa.

Alginates↗
PubMed1980

Evidence for the role of toxin A in the pathogenesis of infection with Pseudomonas aeruginosa in humans.

Levels of antibody to toxin A of Pseudomonas aeruginosa were determined by a solid-phase radioimmunoassay. Mean (+/- SEM) peak levels of IgG in 24 normal soldiers were 2.6 +/- 0.5 microgram/ml, white mean peak levels in 12 patients colonized with and 13 patients infected in sites other than the blood with toxin A-producing strains were 16.7 +/- 7.0 and 17.1 +/- 4.4 microgram/ml, respectively. Levels of IgG were determined in 52 patients with pseudomonas bacteremia, and those surviving and those dying of bacteremia due to toxin A-producing strains had mean peak levels of 25.8 +/- 5.5 and 4.6 +/- 2.0 microgram/ml, respectively. The antitoxin response in sequential bacteremic sera began shortly after onset of bacteremia and decreased gradually, but antitoxin could be recalled promptly upon reinfection with Pseudomonas. Death from pseudomonas bacteremia was significantly associated with infection by a toxin A-producing strain, presence of underlying disease, hypotension, and antitoxin level of < 2 microgram/ml.

Adult↗
PubMed2002

Nosocomial infections caused by multidrug-resistant isolates of pseudomonas putida producing VIM-1 metallo-beta-lactamase.

Successful carbapenem-based chemotherapy for the treatment of Pseudomonas infections has been seriously hindered by the recent appearance of IMP- and VIM-type metallo-beta-lactamases, which confer high-level resistance to carbapenems and most other beta-lactams. Recently, multidrug-resistant Pseudomonas putida isolates for which carbapenem MICs were >/=32 micro g/ml were recovered from cultures of urine from three inpatients in the general intensive care unit of the Ospedale di Circolo, Varese, Italy. Enzyme assays revealed production of a metallo-beta-lactamase activity, while molecular analysis detected in each isolate a bla(VIM-1) determinant carried by an apparently identical medium-sized plasmid. Conjugation experiments were unsuccessful in transferring the beta-lactamase determinant to Escherichia coli or Pseudomonas aeruginosa. Macrorestriction analysis by pulsed-field gel electrophoresis demonstrated that the isolates were of clonal origin. PCR mapping and sequencing of the variable region of the plasmid-borne class 1 integron carrying the bla(VIM-1) determinant (named In110) showed that the bla(VIM-1)-containing cassette was identical to that previously found in strains of different species from other Italian hospitals and that the cassette array of In110 was not identical but clearly related to that of In70 (a bla(VIM-1)-containing plasmid-borne integron from an Achromobacter xylosoxidans isolate), pointing to a common origin of this cassette and to a related evolutionary history of their cognate integrons.

Aged↗
PubMed2005

External otitis caused by infection with Pseudomonas aeruginosa or Candida albicans cured by use of a topical group III steroid, without any antibiotics.

CONCLUSIONS: Irrespective of the microbial agent, group III steroid solution cured external otitis efficiently in a rat model. The addition of antibiotic components to steroid solutions for the treatment of external otitis is of questionable validity. OBJECTIVE: External otitis, caused by infection with either Pseudomonas aeruginosa or Candida albicans, was established in a rat model and the treatment efficacy of a group III steroid solution was studied. MATERIAL AND METHODS: Three treatments were studied: (i) a group III steroid solution; (ii) a group I steroid combined with two antibiotic components; and (iii) a saline solution. A scoring scale was used to evaluate the characteristics of the ear canal skin. Bacteriological and fungal samples were collected for culturing and ear canal skin biopsies were taken for structural analyses. RESULTS: It was possible to cause P. aeruginosa and C. albicans infections in an animal model. In the P. aeruginosa-infected animals, only the group III steroid treatment cured all the animals. In the C. albicans-infected animals, group III steroid treatment resolved external otitis faster than the other treatment modalities.

Administration, Topical↗
PubMed1998

Effect of inhibition of nitric oxide synthase on Pseudomonas aeruginosa infection of respiratory mucosa in vitro.

We studied the effect of the nitric oxide synthase (NOS) inhibitor asymmetric dimethyl arginine (ADMA) and the inactive enantiomer N G-methyl-D-arginine (D-NMMA) on Pseudomonas aeruginosa infection of the respiratory mucosa in nasal turbinate organ cultures. We also investigated the effect of P. aeruginosa culture filtrate on the expression of inducible NOS (iNOS) messenger RNA (mRNA) by an epithelial cell line (A549). Organ cultures were preincubated with ADMA (0.1 to 4 x 10(-4) M) or D-NMMA (2 x 10(-4) M) for 30 min prior to bacterial infection. Infected organ cultures (8 h) had significantly (P <= 0.05) greater epithelial damage and fewer ciliated and unciliated cells than did control cultures. There was an increased level of nitrite in the medium feeding infected organ cultures as compared with control cultures. ADMA significantly (P <= 0.05) reduced both bacterially induced epithelial damage and loss of ciliated cells in a concentration-dependent manner. D-NMMA did not influence the effect of P. aeruginosa infection of the mucosa. ADMA, but not D-NMMA, significantly (P <= 0.04) reduced total bacterial numbers adherent to the respiratory mucosa. P. aeruginosa culture filtrates (24 h and 36 h) significantly (P = 0.02) increased iNOS with respect to glyceraldehyde-3-phosphate dehydrogenase mRNA expression. These results show that P. aeruginosa stimulates iNOS expression by a cell line and NO production by an organ culture. ADMA reduces mucosal damage and loss of ciliated cells, which suggests that NO may be a mediator of epithelial damage caused by P. aeruginosa.

Arginine↗
PubMed2006

Regulation of systemic and local neutrophil responses by G-CSF during pulmonary Pseudomonas aeruginosa infection.

Granulocyte colony-stimulating factor (G-CSF) regulates the production, maturation, and function of neutrophils. Its expression is often induced during infection, resulting in high concentrations of G-CSF in inflammatory exudates and in the blood, suggesting that it may regulate both local and systemic neutrophil responses. Herein, we characterize the neutrophil response in G-CSFR(-/-) mice following intratracheal injection with Pseudomonas aeruginosa-laden agarose beads, modeling the pulmonary infection observed in many patients with cystic fibrosis. G-CSFR(-/-) mice are markedly susceptible to bronchopulmonary P aeruginosa infection, exhibiting decreased survival and bacterial clearance as well as extensive damage to lung tissue. The systemic neutrophil response was mediated primarily by enhanced neutrophil release from the bone marrow rather than increased neutrophil production and was attenuated in G-CSFR(-/-) mice. Despite normal to increased local production of inflammatory chemokines, neutrophil accumulation into the infected lung of G-CSFR(-/-) mice was markedly reduced. Moreover, the percentage of apoptotic neutrophils in the lung was elevated, suggesting that G-CSF signals may play an important role in regulating neutrophil survival at the inflammatory site. Collectively, these data provide new evidence that G-CSF signals play important but specific roles in the regulation of the systemic and local neutrophil response following infection.

Animals↗
PubMed1986

Cefsulodin in treatment of Pseudomonas urinary tract infection in patients with spinal cord injury. Comparison with aminoglycosides.

Male patients with spinal cord injury and urinary tract infection with Pseudomonas aeruginosa were treated with cefsulodin (1.0 or 1.5 Gm) every six hours or an aminoglycoside (amikacin 5 mg/Kg or tobramycin 1 mg/Kg) every eight hours for seven days. The study was discontinued after treating 6 patients with aminoglycosides because of the poor results with these antibiotics. At five to nine days after completing treatment P. aeruginosa was eliminated from the urine of 12 to 15 patients (80%) treated with cefsulodin and 3 of 6 patients (50%) treated with an aminoglycoside. When examined at four to six weeks 5 of 15 (33%) of the cefsulodin group had persistent infection or relapse, while 5 of 6 (83%) infections treated with an aminoglycoside either persisted or relapsed. Cefsulodin was discontinued in 1 patient, known to be allergic to penicillin, because of hypersensitivity resulting in periorbital edema and rash. No other serious side effects were noted with cefsulodin or the aminoglycosides. These results indicate that cefsulodin is an effective antibiotic in the treatment of urinary tract infection with P. aeruginosa in patients with neurogenic bladder resulting from spinal cord injury and confirmed previous observations of a poor response of Pseudomonas urinary tract infection to aminoglycosides in this group of patients.

Adult↗