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At least 145 records · Page 8Linked to original sources
PubMed1989

[Local treatment of Pseudomonas infection of the ear. A small clinical study].

Infections of the middle and external ear caused by the problem-micro-organism Pseudomonas aeruginosa can be cured by local therapy with Ciprofloxacin and Tutofusin very quickly and without any complications. Drum ruptures caused by ear secretions close up again spontaneously. Tympanon tubes can be left in situ. Function disturbances of the middle and internal ear clear up and the functions return to normal.

Audiometry, Pure-Tone↗
PubMed2001

Tap water colonization with Pseudomonas aeruginosa in a surgical intensive care unit (ICU) and relation to Pseudomonas infections of ICU patients.

Water faucets on a surgical intensive care ward were examined prospectively as a source of Pseudomonas aeruginosa infections. All water outlets harbored distinct genotypes of P aeruginosa over prolonged time periods. Over a period of 7 months, 5 (29%) of 17 patients were infected with P aeruginosa genotypes also detectable in tap water.

Cross Infection↗
PubMed2004

Corneal response to Pseudomonas aeruginosa infection.

Pseudomonas aeruginosa (P. aeruginosa) is a common organism associated with bacterial keratitis, especially in those who use extended wear contact lenses. Recent advances in our understanding of host innate and adaptive immune responses to experimental infection have been made using a variety of animal models, including inbred murine models that are classed as resistant (cornea heals) vs. susceptible (cornea perforates). Evidence has been provided that sustained IL-12-driven IFN-gamma production in dominant Th1 responder strains such as C57BL/6 (B6) contributes to corneal destruction and perforation, while IL-18-driven production of IFN-gamma in the absence of IL-12 is associated with bacterial killing and less corneal destruction in dominant Th2 responder strains such as BALB/c. The critical role of IL-1 and chemotactic cytokines such as MIP-2 in PMN recruitment and the critical role of this cell in the innate immune response to bacterial infection is reviewed. Regulation of PMN persistence is also discussed and evidence provided that persistence of PMN in B6 cornea is regulated by CD4+ T cells, while macrophages regulate PMN number in the cornea of BALB/c mice. The studies provide a better understanding of the inflammatory mechanisms that are operative in the cornea after P. aeruginosa challenge and are consistent with long-term goals of providing targets for alternative or adjunctive treatment for this disease. Future studies will be aimed at better defining the role of Toll receptors, neuropeptides (as unconventional modulators of the immune response) and exploitation of disease control by new techniques, such as RNA silencing.

Animals↗
PubMed1976

Zinc sulfadiazine for topical therapy of pseudomonas infection in burns.

Zinc sulfadiazine is a new compound which is effective in vitro and in vivo against Pseudomonas aeruginosa infections in burned mice and rats. It contains an important body constituent, zinc, and appears to expedite wound healing, diminish weight loss after infected burns and improve food intake. Like silver sulfadiazine, it prevents the postburn changes in plasma proteins. After topical application, the uptake of the radioactively labeled zinc is significant in the zone of injury and negligible in organs and body fluids. The binding to deoxyribonucleic acid by zinc is similar to, but less than, that by silver. The data indicate that zinc sulfadiazine may be a valuable addition to the therapeutic armamentarium for the control of burn wound sepsis.

Administration, Topical↗
PubMedDate not supplied

A quantitative model of invasive Pseudomonas infection in burn injury.

To evaluate newer therapies for wound infections, it becomes necessary to quantify bacteria that invade from the infected wounds into the adjacent tissues. For example, antibody-targeted photolysis targets the invasive Pseudomonas with antibodies carrying photochemical dyes. A full-thickness burn wound was infected with Pseudomonas aeruginosa with a modification of previous methods. In mice, a skin fold was elevated, and two preheated brass blocks at 92 degrees to 95 degrees C were applied for 5 seconds, producing a 5% total body surface area injury with discrete margins. The eschars were immediately inoculated with Pseudomonas. Survival at 10 days was 100% with burn injury alone and 60% with infected burns. Pseudomonas (10(8)/gm) were recovered from the unburned muscle by 24 hours. The method produced uniform and reproducible quantitative bacteriology within the muscle immediately beneath the burn injury (SL < 0.05). Quantitative comparisons can be used to determine the effectiveness of newer modalities to control Pseudomonas burn wound infections.

Animals↗
PubMed2004

Role for cystic fibrosis transmembrane conductance regulator protein in a glutathione response to bronchopulmonary pseudomonas infection.

The lung maintains an elevated level of glutathione (GSH) in epithelial lining fluid (ELF) compared to serum. The mechanism(s) by which the lung maintains high levels of ELF GSH and factors that modulate them are largely unexplored. We hypothesized that lung cystic fibrosis transmembrane conductance regulator protein (CFTR) modulates GSH efflux in response to extracellular stress, which occurs with lung infections. Mice were challenged intratracheally with Pseudomonas aeruginosa, and on the third day of infection bronchoalveolar lavage fluid was obtained and analyzed for cytokines and antioxidants. Lung tissue antioxidants and enzyme activities were also assessed. P. aeruginosa lung infection increased levels of inflammatory cytokines and neutrophils in the ELF. This corresponded with a marked threefold increase in GSH and a twofold increase in urate levels in the ELF of P. aeruginosa-infected wild-type mice. A twofold increase in urate levels was also observed among lung tissue antioxidants of P. aeruginosa-infected wild-type mice. There were no changes in markers of lung oxidative stress associated with the P. aeruginosa lung infection. In contrast with wild-type mice, the CFTR knockout mice lacked a significant increase in ELF GSH when challenged with P. aeruginosa, and this correlated with a decrease in the ratio of reduced to oxidized GSH in the ELF, a marker of oxidative stress. These data would suggest that the lung adapts to infectious agents with elevated ELF GSH and urate. Individuals with lung diseases associated with altered antioxidant transport, such as cystic fibrosis, might lack the ability to adapt to the infection and present with a more severe inflammatory response.

Animals↗
PubMed1991

[Clinical implications of the O-antigen serovar E and drug resistance in persistent Pseudomonas infection].

We studied bacteriological parameters in patients with persistent Pseudomonas aeruginosa (PA) infection, including distribution of the PA O-antigen serovars, incidence of serovar conversion during treatment and relationship between these serovars and susceptibility to antibiotics. PA was identified using an automated bacterial identification system (Avantage Microbiology Center, Abbot Lab., USA) and the PA O-antigen serovar was performed with a monoclonal serovar diagnostic kit (Mei-Assay Pseudomonas Aeruginosa, Meiji Seika, Tokyo). Antibiotic susceptibility was evaluated by minimum inhibitory concentration according to the NCCLS method. The PA was isolated in 14.7% of the total of 1,900 isolates in our hospital from April, 1987 to March, 1988, and was most frequently isolated from urine specimens (51.9%), followed by sputum (40.0%). The serovar E was isolated in 57 (36.3%) of 157 PA strains tested, followed by the serovar B (21.0%) and G (17.8%). The serovar E was widely distributed in the wards of hematology (55.6%), neurosurgery (54.2%) and urology (42.3%). The serovar E showed high resistance rates to many antibiotics: 62.5% to piperacillin; 58.3%, cefsulodin; 58.3%, cefoperazone; and 70.8%, gentamicin. Serovar conversion during treatment was noticed in 8 of 24 patients with persistent PA infection. Three of 5 patients in whom the serovar had converted to the serovar E died. These results suggest that PA infection with the serovar E, especially with that converting from another serovar is an unfavorable prognostic sign.

Blood Group Antigens↗
PubMed2000

Therapeutic guidelines for Pseudomonas aeruginosa infections.

Pseudomonas aeruginosa nowadays is encountered among the leading pathogen in (i) ICU pneumonia; (ii) nosocomial bacteremia and AIDS primary bacteremia; (iii) iv drug users endocarditis; (iv) exacerbations of cystis fibrosis; (v) malignant external otitis and 'swimmers's ear', and (vi) contact lenses keratitis and traumatic endophthalmitis. The most vulnerable nosocomial hosts are the neutropenics and the mechanically ventilated patients in whom mortality rate exceeds 30%. Virulence of P. aeruginosa is attributed to the elaboration of various enzymes and toxins. There is also worldwide emergence of multiresistant phenotypes to antipseudomonal antibiotics. Therapeutic guidelines should therefore be based on (i) continuous resistance surveillance; (ii) in vitro synergistic interactions of antibacterial agents; (iii) pharmacodynamic properties of antibiotics interpreted by optimal dosing and appropriate frequency of administration; and (iv) current information on the necessity for combination therapy using an aminoglycoside.

Anti-Bacterial Agents↗
PubMed1979

Kawasaki's disease and infantile polyarteritis nodosa: is Pseudomonas infection responsible? Report of a case.

A nineteen-month-old child presented with a febrile illness, skin rash, painful swelling of the joints, lymphadenopathy and hepatosplenomegaly. Pseudomonas was cultured from the blood during life and, subsequently, at autopsy. Autopsy revealed a generalized panarteritis involving the coronary, retroperitoneal and pulmonary arteries with thickening of arterial walls and narrowing of the lumina. Thrombi and foci of necrosis and infarcts were found in many organs. Numerous bacilli were present in fresh lesions, but not in the organizing lesions. Periodic acid-Schiff-positive deposits were found in occasional macrophages, in walls of affected vessels, in the marginal sinuses of lymph nodes and diffusely in epicardial and retroperitoneal adipose tissue. The findings suggest that some or even all cases of Kawasaki's disease and infantile polyarteritis nodosa may be caused by Pseudomonas sepsis. It is also suggested that the vasculitis and paucity of inflammatory reaction in many cases of Pseudomonas sepsis might be related to the fact that many strains of Pseudomonas produce high-molecular-weight levan (or another polysaccharide). This compound is known to inhibit the inflammatory reaction and to increase bacterial pathogenicity.

Arteries↗