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At least 19 recordsLinked to original sources
PubMed1979

Experimental Pseudomonas infection in mice: effect of single cyclophosphamide administration on Pseudomonas infection.

The kinetic effect of cyclophosphamide (CY) was investigated using the immune response to sheep red blood cells (SRBC), activation of the mononuclear macrophage system and altered susceptibity to pseudomonas infection. The level of delayed type hypersensitivity (DTH) was enhanced with suppressed antibody formation, when antigenic stimulation was given about 3 days after CY administration. In contrast, antibody formation increased markedly when challenged with antigen about 10 days after CY administration. Activity of macrophage system as measured by rate of carbon clearance and spreading of peritoneal macrophage was decreased within 6 days after CY, therefore increased to a peak at the 13th day of CY administration. CY increased a susceptibility to pseudomonas infection at the early time of its administration such as the 3rd day, whereas more increased resistance was observed at the later time such as the 13th day. These results indicated that B-lymphocyte depletion included by administration of sublethal dose of CY (200mg/kg) was followed by vigorous hyperplasia of B-lymphocyte.

Animals↗
PubMed1979

Therapeutic possibilities in Pseudomonas infections.

Acute pseudomonas infections require treatment with antibiotics producing a bactericidal effect. The most useful are gentamicin, tobramycin, sisomicin and polymyxin B. In resistant strains, amikacin is indicated in addition. Carbenicillin, ticarcillin, carfenicillin or azocillin should never be given alone but in combination with some of the above preparations. Other drugs, such as chloramphenicol, tetracycline or streptomycin, though effective in vitro, should be avoided. Chemotherapy may be complemented by passive immunization either with hyperimmune specific gama globulin or hyperimmune plasma. A programmatic item of combined treatment is active immunization, especially with toxoid vaccine. Chronic processes are not, perhaps with the exception of urinary infections, suitable for antibiotic therapy. For this reason effective polyvalent vaccines should be developed from appropriate strains. It is now certain that in infections caused by mucous strains (most frequently encountered in cystic fibrosis) the vaccine should be prepared from these strains, since they have distinct functional and antigenic characteristics.

Acute Disease↗
PubMed1977

Experimental studies on the pathogenesis of infections due to Pseudomonas aeruginosa: direct evidence for toxin production during Pseudomonas infection of burned skin tissues.

Direct evidence is presented for the production of an exotoxin by Pseudomonas aeruginosa multiplying at the burned site in an infected mouse. Pseudomonas toxin was assayed by measurement of its ability to catalyze the transfer of radioactivity from [14C]adenine-labeled nicotinamide adenine dinucleotide to elongation factor 2 (adenosine diphosphate ribosylation activity). This enzyme activity was found in saline extracts of burned infected skin but was not present in similar extracts of burned uninfected skin. It was detected in the serum of infected animals by 26 hr after infection. The level of active elongation factor 2 in the livers of infected mice was reduced significantly after infection. These data suggest that pseudomonas exotoxin, produced by bacteria multiplying at the burn site, enters the circulation and is disseminated to different organs where it acts by depletion of elongation factor 2 and thus causes a reduction in protein synthesis.

Animals↗
PubMed1978

Experimental Pseudomonas infection in mice: acquired resistance against Pseudomonas septicemia and altered susceptibility in BCG infected mice.

Pseudomonas septicemia in mice caused the early death in the first three days of infection without any localized lesions. Localized lesions such as abscess are observed in the kidney and liver after the third day of infection. The early death increased in the BCG infected mice showing an increased level of macrophage activation. It seemed that such early death is due to endotoxin produced by Pseudomonas aeruginosa. However, the BCG infected mice showing an enhanced antibody formation were more resistant to pseudomonas septicemia. Immune serum protected such death, but immune spleen cells did not. Furthermore immune serum also protected the increased death in BCG infected mice.

Animals↗
PubMed1979

[The effect of various steroid hormones on the course of pseudomonas infections in 3rd grade burns].

The effect of hydrocortisone, aldosterone, and estrogen on the course of pseudomonas infection after third-degree burns was examined in animal experiments. The effect of the drugs is represented by different lethality rates. Hydrolytic hydrocortisone reduced the average survival time as well as aldosterone. Estrogen, however, had no statistically ascertained effect on lethality.

Aldosterone↗
PubMed1979

Pseudomonas infections of the lung treated with azlocillin. Microbiology, pharmacokinetics, clinic.

6-[(R)-2-(2-Oxo-imidazolidine-1-carboxamido)-2-phenyl-acetamido]-penicillanic acid sodium salt (azlocillin, Securopen), has a special activity against Pseudomonas species besides is broadspectrum character. We confirmed the high in vitro potency of that antibiotic in 200 clinical Pseudomonas isolates. Good penetration of azlocillin into bronchial secretions was found, especially through the inflamed bronchial mucosa, but also in the post-inflammatory phase. In 16 patients with serious Pseudomonas infections of the respiratory tract the good efficacy of azlocillin was shown. There were no tolerance problems.

Azlocillin↗
PubMed1979

Program of bacteriophage gh-1 DNA transcription in infected Pseudomonas putida.

The program of transcription in phage gh-1-infected Pseudomonas putida was examined. It was found that the host P. putida RNA polymerase transcribes early RNA from the L strand of gh-1 DNA during the initial stages of infection. The host RNA polymerase is also undoubtedly responsible for transcription of complementary RNA late in the infectious cycle because complementary RNA was not transcribed when rifampin was added to the infected cell culture. The gh-1-induced RNA polymerase transcribes late RNA from the L strand of gh-1 DNA late in the infectious cycle. The P. putida RNA polymerase transcribed only early RNA from primarily the L strand of gh-1 DNA in vitro when the molar ratio of enzyme to gh-1 DNA was 0.5. When the molar ratio was 50 the P. putida RNA polymerase transcribed RNA from the H strand of gh-1 DNA as well as complementary RNA. Thgh-1 RNA polymerase transcribed only the L strand of gh-1 DNA in vitro but transcribed both early and late RNA.

Bacteriophages↗
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↗
PubMed1977

Persistence of a specific pseudomonas infection in a large general hospital.

Of at least 37 strains of Pseudomonas aeruginosa distinguishable by their pyocine production, Type 10 is noteworthy for its relative rarity and its virulence to man. Opportunistic infections by this organism occurring in a single hospital over 8 years are described, and its ecology discussed with reference to its possible control.

Cross Infection↗
PubMed1978

Recurrent Pseudomonas infection associated with neutrophil dysfunction.

A 72-year-old male is described with a history of 4 episodes of Pseudomonas aeruginosa sepsis and chronic otitis media caused by pseudomonas species. In vitro testing of the patient's polymorphonuclear leukocytes (PMNs) revealed profoundly abnormal chemotactic responses and defective intracellular killing of Ps. aeruginosa, Staphylococcus aureus and Escherichia coli. Chemiluminescence production by the patient's PMNs in response to opsonized zymosan as well as endotoxin stimulated nitroblue tetrazolium dye reduction were markedly depressed. These data indicate the presence of a profound, apparently acquired, defect in PMN function in an elderly male. Detailed evaluation of adult patients with recurrent infections may reveal similar, apparently acquired defects in PMN function.

Aged↗