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PubMed1988

Cachectin/TNF production in experimental burns and Pseudomonas infection.

Burn injury and infection result in significant losses of lean tissue. The cytokine cachectin/tumor necrosis factor has been implicated in this process but is not uniformly detected during infection. We sought to determine the relationship between body composition changes and in vivo hepatic levels of pretranslational message for cachectin (messenger RNA) in a burn and infection rodent model. Adult Wistar rats were grouped as follows: (1) freely fed, (2) 30% burn, (3) 30% burn with Pseudomonas aeruginosa infection, (4) pair fed, and (5) 30% burn and infection with recombinant cachectin. Compared with controls or animals only burned, burned and infected rats had a 100% increase in hepatic cachectin messenger RNA content, lost carcass protein, and exhibited muscle loss with sparing of liver mass. Tissue production of cachectin as well as other cytokines may be sufficient to mediate several body composition changes observed in response to injury and infection.

Animals↗
PubMed1972

Effect of vincristine sulfate on Pseudomonas infections in monkeys.

In rhesus monkeys, intravenous challenge with 0.6 x 10(10) to 2.2 x 10(10)Pseudomonas aeruginosa organisms caused acute illness of 4 to 5 days' duration with spontaneous recovery in 13 of 15 monkeys; blood cultures became negative 3 to 17 days after challenge. Leukocytosis was observed in all monkeys. Intravenous or intratracheal inoculation of 2.0 to 2.5 mg of vincristine sulfate was followed by leukopenia in 4 to 5 days. Intravenous inoculation of 4.2 x 10(10) to 7.8 x 10(10) pyocin type 6 Pseudomonas organisms in monkeys given vincristine sulfate 4 days previously resulted in fatal infection in 11 of 14 monkeys, whereas none of four receiving Pseudomonas alone died. These studies suggest that an antimetabolite-induced leukopenia predisposes to severe Pseudomonas sepsis and that such monkeys may serve as a biological model for study of comparative efficacy of antimicrobial agents.

Animals↗
PubMed1999

IL-10 attenuates excessive inflammation in chronic Pseudomonas infection in mice.

Cystic fibrosis (CF) lung disease is characterized by an excessive inflammatory response associated with chronic Pseudomonas aeruginosa endobronchial infection. Compared with bronchoalveolar lavage fluid from healthy subjects, lavage fluid from patients with CF contains elevated proinflammatory cytokines but negligible amounts of the anti-inflammatory cytokine interleukin-10 (IL-10). We sought to determine whether IL-10 deficiency results in increased local and systemic morbidity in mice with chronic endobronchial infection with P. aeruginosa embedded in agar beads and to determine if exogenous IL-10 might reduce these effects. Infected IL-10 knockout mice had more severe weight loss (p = 0.04) and increased area of lung inflammation (28 +/- 4 versus 10 +/- 2%, p < 0.002) but no alterations in bacterial burden compared with wild-type mice. Infected CD-1 mice treated with IL-10 had improved survival (p = 0. 035), less severe weight loss (p < 0.005), fewer bronchoalveolar lavage neutrophils (3 x 10(5)/ml versus 5 x 10(6)/ml, p < 0.02), and decreased area of lung inflammation (11 +/- 2 versus 35 +/- 7%, p < 0.01) but no alterations in bacterial burden compared with placebo-treated mice. These data suggest that IL-10 is an important regulator of the inflammatory response to P. aeruginosa endobronchial infection and that further investigation into the use of IL-10 in CF is warranted.

Animals↗
PubMed1984

Can pseudomonas infection in experimental animals mimic Kawasaki's disease?

Experiments aimed at producing a model of Kawasaki's disease by injecting animals intraperitoneally with Pseudomonas bacilli are described. Injection of large numbers of bacilli into mice caused rapidly fatal sepsis. With appropriate numbers of organisms, some mice died within 3 days, most remained healthy, while in some an inapparent chronic disease developed. Positive blood cultures were occasionally obtained 4-17 weeks after the slow infection. An alcohol-precipitable polysaccharide, which could be measured by Roe's procedure for levan, was found in 20% of the experimentally infected mice. We suggest that this substance was partly responsible for the course of the infection. Severe vasculitis with little acute inflammatory reaction and carditis with coronary aneurysms were often obtained by injecting mice and guinea-pigs with supraliminal doses of bacilli at the same time as their immune system was impaired by treatment with either nitrogen-mustard or cyclophosphamide. We suggest that pseudomonas infection in immunologically deficient animals may mimic Kawasaki's disease and that a similar mechanism may operate in the natural form of the disease in children.

Animals↗
PubMed1981

Infections with Pseudomonas aeruginosa in the compromised host.

A review is given of the role of the various host defences in man against Pseudomonas aeruginosa and the mechanisms by which these are compromised in certain patient categories especially susceptible to serious Pseudomonas infections. The defects of host defences are usually complex and multiple, affecting various sites in the local and the systemic defences. Certain defects are emphasized, e.g. abnormalities of first line defences (skin, mucous membranes), and both quantitative and qualitative defects in polymorphonuclear granulocytes. However, it is also suggested that compromised functions of other components of antimicrobial defences may play a role in Pseudomonas infections, e.g. functional abnormalities in the systems of B cells. T cells and mononuclear phagocytes. Recent data suggesting mechanisms by which P. aeruginosa can exert suppressive effects on host defences, are mentioned, and the possibility of immunopathogenesis in Pseudomonas infections is discussed, particularly processes involving the complement system. Some important clinical features of Pseudomonas infections are described. The clinical peculiarities of bacterial infections in the severely neutropenic patient are emphasized, and exemplified with a brief description of Pseudomonas pneumonia. Finally, Pseudomonas septicaemia is mentioned with a brief discussion of certain important prognostic factors. It is concluded that a better understanding of the complex defense mechanisms against P. aeruginosa and therapeutic regimens by which they can be manipulated, is imperative to achieve any significant advances in the prevention and treatment of these infections.

Antibody Formation↗
PubMed1998

Pseudomonas infections in Tohid Burn Center, Iran.

Burn injury is a major public health problem in many areas of the world. Pseudomonas aeruginosa is one of the most common causes of burn wound infection in burn patients. Septicemia due to this organism is a major cause of mortality among burn patients. This study analyzed P. aeruginosa infections in the Tohid Burn Center in Tehran during 1995-1997 in order to estimate their frequency, antibiotic susceptibility and their role in burn morbidity. Among 2122 patients who were admitted during this study period, 3365 bacterial strains were isolated and the frequency of P. aeruginosa was 73.9%. This was followed by Staphylococcus aureus (9.1%) and other organisms (17%) in frequency. The frequency of P. aeruginosa resistant to gentamicin, carbenicillin, co-trimoxazole, ceftizoxime and tetracycline was over 95% and resistance to amikacin which was 49% in 1995, increased to 90% in 1997. With the introduction of ciprofloxacin at our burn center, the frequency of P. aeruginosa resistance increased from 45% in 1995, to 82% in 1997. P. aeruginosa was found more frequently in the ICU than in the wards. These findings show that P. aeruginosa remains the leading cause of nosocomial infections in our burn center. It is necessary to introduce urgent measures for restriction of the spread of P. aeruginosa infections in our burn center.

Adolescent↗