Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PSEUDOMONAS INFECTIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources

Cost effectiveness of magnetic resonance imaging in diagnosing Pseudomonas aeruginosa infection after puncture wound.

This study was performed to determine the cost effectiveness of radiologic imaging studies in diagnosing Pseudomonas aeruginosa infections after puncture wounds and the respective comparison of imaging and scintigraphy. Using retrospective medical record review, we studied 12 patients with culture-proven Pseudomonas infections of bone, cartilage or joint, or soft tissues. Attention was paid to radiographic presentation, scintigraphic studies, and magnetic resonance imaging results. All available imaging studies were reviewed. A survey of the costs of each imaging study was conducted. All patients underwent surgery. Three patients had magnetic resonance imaging studies that provided definitive diagnosis of osteomyelitis and precise localization of involved bones, soft tissue edema, and periosteal abscess. Eight patients had bone scans, one of which was consistent with cellulitis; seven, with osteomyelitis; and two with no abnormalities. All patients had radiographs of the involved foot. Case 4 had three series of radiographs. Nine of the twelve patients (75%) had normal findings on radiographs, with only soft tissue swelling or osteoporosis. Five patients had evidence of osteomyelitis. Magnetic resonance imaging is a cost-effective method in diagnosing Pseudomonas osteomyelitis. Early use of magnetic resonance imaging can provide definitive diagnosis and more precise anatomic localization necessary for surgical intervention.

Child↗

Characterization of the inflammatory response induced by corneal infection with Pseudomonas aeruginosa.

In order to characterize the inflammatory response to corneal infection by Pseudomonas aeruginosa, ocular cytokine and arachidonic acid metabolite levels were determined in the C57BL/6J strain of mice. The effects of topical anti-inflammatory drugs on the ability of the mice to clear viable P. aeruginosa from the eyes during the 12 day infection period was also examined. Ocular IL-1 alpha, IL-6, and TNF-alpha were detected over an 11 day time period. Little or no bacteria, as determined by quantitative plate counts, was detected after this time period. The kinetics of the cytokine production varied from one another, with an immediate release of peak levels of IL-1 alpha within 24 hours after infection which did not begin to approach baseline until 9 to 11 days after infection. Five to ten-fold lower concentrations of IL-6 and TNF-alpha were detected. IL-6 levels were induced at 24 hours after infection but there was essentially no distinct peak time-point. Peak levels of TNF-alpha were detected at 6 days post-infection. The kinetics of arachidonic acid metabolite release from infected eyes were also examined. Peak levels of PGE2 and TxB2 were observed at 6 days post-infection whereas peak LTB4 levels were determined at 3 days post-infection. Topical treatment of infected eyes with the two anti-inflammatory drugs, prednisolone or quercetin, resulted in higher ocular bacterial levels throughout the infection.

Animals↗

Severity and predicted outcome of postoperative Pseudomonas aeruginosa infections.

The severity and predicted outcome of postoperative Pseudomonas aeruginosa (P. aeruginosa) infections (PPAI) was evaluated using a severity scoring system based on a simplification and modification of the APACHE II system. A total of 86 patients in whom P. aeruginosa was isolated from various sources were examined. PPAI developed in 50 patients, resulting in an overall mortality rate of 24%. An increased severity score (SS) correlated with an increased risk of developing PPAI. Thus, PPAI developed in 33% of the patients with an SS of 0-1, in 66.7% of those with an SS of 2-3, and in 100% of those with an SS of 6 or higher. Moreover, the mortality rate of the patients with an initial score of 6 or higher was 50%. The mean (+/- SD) initial severity score was 5.4 +/- 2.9 for survivors and 2.9 +/- 2.6 for nonsurvivors (P < 0.01). In the patients who subsequently died, the SS remained high throughout the clinical course despite therapy, whereas in the survivors the SS decreased progressively, reflecting a favorable clinical course. These results suggest that our severity scoring system was useful for predicting outcome and monitoring the response of PPAI to therapy.

Adult↗

Emergence of resistance to imipenem during therapy for Pseudomonas aeruginosa infections.

We studied the mechanism of resistance to imipenem in three clinical isolates of Pseudomonas aeruginosa. Two of these isolates arose from imipenem-susceptible strains isolated during therapy with imipenem and were associated with treatment failure. One of these two strains had previously been broadly resistant to beta-lactams; the second acquired resistance to imipenem alone. One isolate of the third strain was resistant to imipenem but susceptible to other antipseudomonal beta-lactams. No isolate contained beta-lactamase activity capable of hydrolyzing imipenem at a detectable rate. Studies of the penicillin-binding proteins of all isolates revealed no differences in the number of proteins, molecular weight of, affinity for penicillin, or affinity for imipenem in any isolate. In each case the resistant isolate lacked one or more outer membrane proteins that were present in a susceptible isolate of the same strain. The observed alterations in outer membrane proteins may be associated with diminished permeability of the bacterial outer membrane to imipenem and may be the major factor responsible for resistance in these isolates.

Adult↗

[Hospital infections with pseudomonas aeruginosa: I. Technical devices and wet areas as sources of infection in intensive care units (author's transl)].

In an intensive care unit system comprising three surgical intensive care wards bacteriologic investigations on the presence of Pseudomonas aeruginosa were carried out over a period of 7 months (as an example for the aetiology of hospital infections). Centers of contaminations were found to exist in wet areas and in technical devices (ultrasonic nebulizers, respirators etc.). In many cases, the bacterial strains isolated from patients were found by means of phage-typing to be identical with strains isolated from devices and wet areas. Additional experimental investigations showed the predominant role of ultrasonic nebulizers for germ dissemination. On the basis of the results obtained a patient oriented scheme of probable infection chains was tried to establish. Hereby the wet areas play a central role as reservoirs of germs and therapeutical devices as vectors. The results obtained were evaluated in order to define a catalogue of practical measures for interruption of infection chains.

Bacteriophage Typing↗

Regular three monthly oral ciprofloxacin in adult cystic fibrosis patients infected with Pseudomonas aeruginosa.

In 31 adult patients with cystic fibrosis (CF) who were chronically infected with Pseudomonas aeruginosa we examined the effect of giving regular three monthly oral ciprofloxacin. Patients received ciprofloxacin or placebo for 10 days every 3 months for 1 yr in a randomized, double-blind, placebo-controlled study. During each course of treatment patients receiving ciprofloxacin reported an improvement in cough, sputum production and peak expiratory flow (PEF) P = < 0.005. During the year of study patients receiving ciprofloxacin showed an improvement in PEF when compared with those receiving placebo (P = < 0.05) but the changes in FEV1 and FVC were not statistically different in either group. Regular oral ciprofloxacin was well tolerated but did not prevent hospital admissions or reduce the number of courses of intravenous antibiotics throughout the year. The median MIC to ciprofloxacin in the active treatment group rose from 0.5 mg l-1 to 0.75 mg l-1 during treatment. We conclude that CF patients are likely to benefit from oral ciprofloxacin for exacerbations of respiratory symptoms. However, regular treatment with ciprofloxacin over 1 yr improves PEF but does not reduce the rate of hospital admissions with acute exacerbations of respiratory symptoms.

Administration, Oral↗

Treatment of pulmonary Pseudomonas aeruginosa infection in cystic fibrosis with cefsulodin.

20 patients with cystic fibrosis and chronic pulmonary Pseudomonas aeruginosa infection underwent a total of 23 courses of treatment with a new cephalosporin, cefsulodin. The patients were given 100-150 mg/kg/day in 3 divided doses for 14 days, alone or in combination with tobramycin. Maximum serum levels were around 150 microgram/ml and 6-h levels above 5 micrograms/ml. 90% of the infecting strains were sensitive to 5 micrograms/ml in vitro. Apart from discomfort in direct relation to intravenous bolus injection the drug was well tolerated. Clinical improvement was pronounced, and in 5 cases. P. aeruginosa disappeared from bronchial secretions. Patients allergic to carbenicillin tolerated cefsulodin without signs of allergy. Cefsulodin thus appears to be an effective alternative to carbenicillin in the treatment of severe P. aeruginosa infections.

Adolescent↗

Aprotinin treatment of pseudomonal corneal infection.

Pseudomonas aeruginosa produces proteolytic enzymes capable of causing severe corneal degradation. In this study we tested aprotinin, a broad-spectrum protease inhibitor, on rabbit corneas infected with P. aeruginosa to determine whether any benefit could be derived. Corneas treated with aprotinin and tobramycin topically and subconjunctivally were not clinically better than corneas treated with tobramycin alone.

Administration, Topical↗

The importance of extracellular antigens in Pseudomonas cepacia infections.

A clinical isolate of Pseudomonas cepacia from a cystic fibrosis patient was examined for its ability to produce extracellular toxic material. The organism was grown to stationary phase in a defined medium and toxic material was isolated by ultrafiltration, ion-exchange chromatography on DEAE-Sephacel and gel-filtration chromatography on Sepharose 4B. It consisted of a surface carbohydrate antigen, lipopolysaccharide and protein, and had an LD50 (when injected intraperitoneally into mice) of 395 +/- 20 micrograms. The toxicity appeared to be associated with the lipopolysaccharide portion of the complex, because boiling for 15 min and exposure to proteolytic enzymes had no effect on toxicity. However, saponification destroyed the toxicity of the compound. Studies employing radial immunodiffusion with the sera of mice infected with this organism demonstrated production of the complex in vivo at levels approaching those sufficient to produce death. When sublethal amounts of this complex were placed in the lungs of specific-pathogen-free rats, the lung pathology observed after 12, 24, 36 and 48 h was extensive. However, antibody generated in rabbits against this material could protect mice against the complex, as well as against challenge by the homologous organism. These data indicate that extracellular toxic material produced by P. cepacia may be responsible for the lethality and lung tissue destruction normally associated with an active pneumonia caused by this organism.

Animals↗

Substance P regulates natural killer cell interferon-gamma production and resistance to Pseudomonas aeruginosa infection.

Studies have shown that after Pseudomonas aeruginosa (P. aeruginosa) corneal infection, BALB/c mice that are capable of resolving the disease, locally produce IFN-gamma. As T cells are not detected in the infected cornea of these mice, antibody depletion was used to test whether NK cells produce the cytokine. After depletion, decreased corneal IFN-gamma mRNA and increased disease severity, bacterial load, and PMN infiltrate resulted. Further work determined if substance P (SP), a pro-inflammatory neuropeptide, participated in regulation of this response. To this end, mice were treated with the SP antagonist, spantide I that blocks SP interaction with neurokinin-1, its major receptor. The treatment significantly decreased corneal IFN-gamma and IL-18 protein levels and corneal perforation resulted. In vitro experiments using isolated splenic NK cells confirmed their ability to respond to IL-18 and SP and to secrete IFN-gamma protein. We conclude: that for development of the BALB/c resistance response, NK cells are required to produce IFN-gamma; that the cells express the neurokinin-1 receptor; and that SP directly regulates IFN-gamma production through this receptor. The data suggest a unique link between the nervous system and development of innate immunity in the cornea.

Analgesics↗

Expression of cathepsins B, D and L in mouse corneas infected with Pseudomonas aeruginosa.

C57BL/6J naïve and immunized mice were intracorneally infected with Pseudomonas aeruginosa. Semi-quantitative RT-PCR was performed to detect cathepsin gene expression and the results were further confirmed by immunoblot analysis. The enzymatic activities of cathepsins B, D and L were measured by peptidase assays. Immunohistochemical staining was carried out to localize the expression of the cathepsins. Cathepsins B, D and L were detected in the normal cornea by RT-PCR. A peptidase assay revealed activities of all three cathepsins under normal physiological conditions. In naïve mice, enzymatic activities of cathepsins B, D and L were all significantly enhanced when the corneas were infected with P. aeruginosa and the peak of the induction appeared around day 6 postinfection. Immunoblot analysis showed increased expression of cathepsins B, D and L. The infected corneal samples from immunized mice exhibited much lower induction of enzymatic activities compared to those from naïve mice. Immunohistochemistry showed that the expression of cathepsins in the normal cornea was restricted to the epithelial tissue while the induced expression of cathepsins was predominantly in the substantia propria. Our data revealed up-regulated enzymatic activities of cathepsins B, D and L in the naïve corneas infected with P. aeruginosa, which correlated well with the inflammatory response. Immunization of mice against P. aeruginosa attenuated the inducing effect on cathepsin expression caused by infection. The time sequence for induction of cathepsin proteins and enzymatic activities suggests a mechanism of host proteolytic degradation of the extracellular matrix resulting in corneal destruction after P. aeruginosa infection.

Animals↗