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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new polyvalent, cell wall extract, Pseudomonas aeruginosa vaccine (PEV-01), was evaluated by using a guinea pig model of experimental Pseudomonas pneumonia. Guinea pigs routinely developed fourfold rises in serum hemagglutinating Pseudomonas antibodies after four vaccine injections given over 2 weeks. Vaccinated animals survived an intratracheal Pseudomonas challenge (1 X 10(8) colony-forming units) significantly better (13 of 14 survived) than did a control group (5 of 14 survived) (P less than 0.01). Clearance of viable Pseudomonas from lung tissue was significantly better in vaccinees than controls at both 3 h (P less than 0.02) and 6 h (P less than 0.05) after infection. Both gross and histological examinations of lung tissue revealed less pulmonary tissue damage in vaccinated animals following Pseudomonas infection. Thus, PEV-01 Pseudomonas vaccine appears capable of eliciting a specific protective response in the guinea pig respiratory tract.
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PMID:Evaluation of a new polyvalent Pseudomonas vaccine in respiratory infections. 11 86

In comparison with polyvalent immunoglobulins, Pseudomonas immunoglobulin (Psomaglobin) is enriched several times in antibodies to Ps. lipopolysaccharide antigens and exotoxin A as well as lipid A. The resulting protective action which is superior to polyvalent immunoglobulins in infections with Pseudomonas, was demonstrated both in cell culture (protection against cytotoxicity of Ps. exotoxin A in heart muscle cells) and in animal models of sepsis. In patients suffering from Ps. pneumonia and Ps.-sepsis clinical improvement is seen after application of this immunoglobulin and also in quantifiable by scoring systems, the unequivocal proof of lowering lethality by using this specific immunoglobulin in Pseudomonas infection is to be shown however.
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PMID:[Use of pseudomonas immunoglobulin. Indications and results]. 250 71

In 1985, at the University of Arizona, Tucson, two attempts were made to "bridge" patients from impending death to heart transplantation, using orthotopically positioned total artificial hearts. The first attempt, using an unapproved device on an emergency basis, failed after transplantation because of severe pulmonary edema and Pseudomonas pneumonia and the apparent transmission of a Pseudomonas infection from donor to recipient. The second experience, using a Jarvik-7 device, led to stable support for nine days with one major complication, a reversible neurologic deficit with no associated computed tomographic scan abnormality. This patient survived cardiac transplantation and, after being successfully treated for complications, has made a full recovery and returned to full-time work.
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PMID:The total artificial heart as a bridge to transplantation. A report of two cases. 353 40

Pseudomonas aeruginosa has emerged as an important pathogen during the past two decades. It causes between 10% and 20% of infections in most hospitals. Pseudomonas infection is especially prevalent among patients with burn wounds, cystic fibrosis, acute leukemia, organ transplants, and intravenous-drug addiction. P. aeruginosa is a common nosocomial contaminant, and epidemics have been traced to many items in the hospital environment. Patients who are hospitalized for extended periods are frequently colonized by this organism and are at increased risk of developing infection. The most serious infections include malignant external otitis, endophthalmitis, endocarditis, meningitis, pneumonia, and septicemia. The likelihood of recovery from pseudomonas infection is related to the severity of the patient's underlying disease process. The introduction of the antipseudomonal aminoglycosides and penicillins has improved substantially the prognosis of these infections. Ticarcillin and carbenicillin have been especially beneficial in neutropenic patients; however, prompt institution of therapy is mandatory for optimal benefit. Many new drugs with antipseudomonal activity, including penicillins, cephalosporins, and other beta-lactams, have been introduced in recent years and offer the potential for new approaches to therapy for these infections.
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PMID:Infections caused by Pseudomonas aeruginosa. 640 75

Carbenicillin and ticarcillin are penicillins which were initially developed as agents to treat serious Pseudomonas infections in the seriously ill hospitalized patient. These drugs have made a major contribution to improved survival in the neutropenic patients with Pseudomonas infection, the burn patient and to the care of the patient with cystic fibrosis. Areas of use for the compounds have enlarged to include aspiration pneumonitis in hospitalized patients, intra-abdominal and pelvic sepsis, and infections due to Proteus and Enterobacter species. Careful attention to the pharmacology of the agents is necessary to achieve clinical and bacteriologic success and to avoid the toxic side-effects such as bleeding and hypokalemia associated with the use of these agents. A decade of use has shown that the agents have remained effective agents in institutions in which their use has not been abused. It is too early to clearly position azlocillin, mezlocillin, and piperacillin. In the next few years the role of these potent compounds will be established. As noted in this review, these three agents have been used with success to treat all of the aforementioned infections. With these drugs it is also essential that the physician closely correlate in vitro data and the human pharmacology of the drugs if he or she wishes to achieve the most effective response from the agents.
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PMID:Carbenicillin and ticarcillin. 703 41

Pseudomonas aeruginosa septicemia rarely occurs in non-immunocompromised adults. We present a case of septic shock following Pseudomonas aeruginosa pneumonia in a previously healthy 48-year-old woman. The onset was sudden, with back pain, pyrexia and shock. Chest radiographs revealed pneumonia, and Pseudomonas aeruginosa was identified from blood and sputum cultures. Therapy with dopamine, piperacillin and fluid replacement led to a prompt recovery. Laboratory tests failed to reveal any immunological deficits. Including this case, only five cases of Pseudomonas aeruginosa septicemia in patients though to be non-immunocompromised have been reported. Two remarkable features of this type of Pseudomonas infection are apparent: i) it commonly develops from pneumonia and ii) it has a better prognosis than that in immunocompromised hosts.
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PMID:Septic shock due to Pseudomonas aeruginosa in a previously healthy woman. 779 Jun 8

Pseudomonas aeruginosa infection is unusual in individuals with human immunodeficiency virus infection, and it most often occurs in the setting of other risk factors, such as neutropenia or cytotoxic drug use. We noted an increasing number of pulmonary isolates of this organism in our clinic population and sought to describe the clinical correlates of this finding. Our study consisted of a retrospective review of the microbiology, radiology, and clinical records of 1,852 HIV-seropositive adults seen at a university-based outpatient AIDS clinic. We identified 16 individuals with Pseudomonas bronchopulmonary infection. All subjects had advanced HIV disease with prior AIDS diagnoses, and mean CD4 counts of 25/mm3 (0.025 x 10(9)/L). Pseudomonas was the sole pulmonary pathogen in 14 of 16 patients and was associated with new chest X-ray abnormalities in 14 cases. Four individuals had acute pseudomonal pneumonia with sepsis; this presentation was associated with hospitalization and other known risk factors for Pseudomonas infection. In contrast, 12 patients had more indolent, community-acquired infection, which had a low mortality rate and occurred in the absence of other risk factors. Survivors of the initial bout of Pseudomonas infection had an 86% relapse rate despite a median survival of only 4.5 months. This pattern of pseudomonal disease is reminiscent of cystic fibrosis and suggests a role for maintenance therapy.
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PMID:Pseudomonas aeruginosa bronchopulmonary infection in late human immunodeficiency virus disease. 821 56

Neonatal sepsis is a life-threatening emergency and any delay in treatment may cause death. Initial signs of neonatal sepsis are slight and nonspecific. Therefore, in suspected sepsis, two or three days empirical antibiotic therapy should begin immediately after cultures have been obtained without awaiting the results. Antibiotics should be reevaluated when the results of the cultures and susceptibility tests are available. If the cultures are negative and the clinical findings are well, antibiotics should be stopped. Because of the nonspecific nature of neonatal sepsis, especially in small preterm infants, physicians continue antibiotics once started. If a baby has pneumonia or what appears to be sepsis, antibiotics should not be stopped, although cultures are negative. The duration of therapy depends on the initial response to the appropriate antibiotics but should be 10 to 14 days in most infants with sepsis and minimal or absent focal infection. In infants who developed sepsis during the first week of life, empirical therapy must cover group B streptococci, Enterobacteriaceae (especially E. coli) and Listeria monocytogenes. Penicillin or ampicillin plus an aminoglycoside is usually effective against all these organisms. Initial empirical antibiotic therapy for infants who developed sepsis beyond the first days of life must cover the organisms associated with early-onset sepsis as well as hospital-acquired pathogens such as staphylococci, enterococci and Pseudomonas aeruginosa. Penicillin or ampicillin and an aminoglycoside combination may also be used in the initial therapy of late-onset sepsis as in cases with early-onset sepsis. In nosocomial infections, netilmicin or amikacin should be preferred. In cases showing increased risk of staphylococcal infection (e.g. presence of vascular catheter) or Pseudomonas infection (e.g. presence of typical skin lesions), antistaphylococcal or anti-Pseudomonas agents may be preferred in the initial empirical therapy. In some centers, third-generation cephalosporins in combinations with penicillin or ampicillin have been used in the initial therapy of early-onset and late-onset neonatal sepsis. Third-generation cephalosporin may also be combined with an aminoglycoside in places where aminoglycoside-resistance to this antibiotic is high. However, third-generation cephalosporins should not be used in the initial therapy of suspected sepsis, because 1) extensive use of cephalosporins for initial therapy of neonatal sepsis may lead to the emergence of drug-resistant microorganisms (this has occurred more rapidly as compared with the aminoglycosides), 2) Antagonistic interactions have been demonstrated when the other beta-lactam antibiotics (e.g. penicillins) were combined with cephalosporins. Infections due to gram-negative bacilli can be treated with the combination of a penicillin-derivative (ampicillin or extended-spectrum penicillins) and an aminoglycoside. Third-generation cephalosporins in combination with an aminoglycoside or an extended-spectrum penicillin have been used in the treatment of sepsis due to these organisms. Piperacillin and azlocillin are the most active of extended-spectrum penicillins against Pseudomonas aeruginosa. Among the third-generation cephalosporins, cefoperazone and ceftazidime possess anti-Pseudomonas activity. Ceftazidime was found to be more active in vitro against Pseudomonas than cefoperazone or piperacillin. New antibiotics for gram-negative bacteria resistant to other agents are carbapenems, aztreonam, quinolones and isepamicin. Enterococci can be treated with a cell wall-active agent (e.g. penicillin, ampicillin, or vancomycin) and an aminoglycoside. Staphylococci are susceptible to penicillinase-resistant penicillins (e.g. oxacillin, nafcillin and methicillin). Resistant strains are uniformly sensitive to vancomycin. A penicillin or vancomycin and an aminoglycoside combination result in a more rapid bacteriocidal effect than is produced by either dr
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PMID:Antibiotic use in neonatal sepsis. 972 68

We examined the role of redox signaling generated by NADPH oxidase in activation of NF-kappaB and host defense against Pseudomonas aeruginosa pneumonia. Using mice with an NF-kappaB-driven luciferase reporter construct (HIV-LTR/luciferase (HLL)), we found that intratracheal administration of P. aeruginosa resulted in a dose-dependent neutrophilic influx and activation of NF-kappaB. To determine the effects of reactive oxygen species generated by the NADPH oxidase system on activation of NF-kappaB, we crossbred mice deficient in p47(phox) with NF-kappaB reporter mice (p47(phox-/-)HLL). These p47(phox-/-)HLL mice were unable to activate NF-kappaB to the same degree as HLL mice with intact NADPH oxidase following P. aeruginosa infection. In addition, lung TNF-alpha levels were significantly lower in p47(phox-/-)HLL mice compared with HLL mice. Bacterial clearance was impaired in p47(phox-/-)HLL mice. In vitro studies using bone marrow-derived macrophages showed that Toll-like receptor 4 was necessary for NF-kappaB activation following treatment with P. aeruginosa. Additional studies with macrophages from p47(phox-/-) mice confirmed that redox signaling was necessary for maximal Toll-like receptor 4-dependent NF-kappaB activation in this model. These data indicate that the NADPH oxidase-dependent respiratory burst stimulated by Pseudomonas infection contributes to host defense by modulating redox-dependent signaling through the NF-kappaB pathway.
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PMID:p47phox deficiency impairs NF-kappa B activation and host defense in Pseudomonas pneumonia. 1473 63

Pseudomonas aeruginosa is a leading cause of hospital-acquired pneumonia, and approximately 80% of patients with cystic fibrosis are infected with this bacterium. To investigate the overall role of complement and the complement activation pathways in the host defense against P. aeruginosa pulmonary infection, we challenged C3-, C4-, and factor B-deficient mice with P. aeruginosa via intranasal inoculation. In these studies, C3(-/-) mice had a higher mortality rate than C3(+/+) mice. Factor B(-/-) mice, but not C4(-/-) mice, infected with P. aeruginosa had a mortality rate similar to that of C3(-/-) mice, indicating that in this model the alternative pathway of complement activation is required for the host defense against Pseudomonas infection. C3(-/-) mice had 6- to 7-fold more bacteria in the lungs and 48-fold more bacteria in the blood than did C3(+/+) mice at 24 h postinfection. In vitro, phagocytic cells from C3(+/+) or C3(-/-) mice exhibited a decreased ability to bind and/or ingest P. aeruginosa in the presence of C3-deficient serum compared to phagocytic cells in the presence of serum with sufficient C3. C3(-/-) mice displayed a significant increase in neutrophils in the lungs and had higher levels of interleukin-1beta (IL-1beta), IL-6, IL-10, KC, and MIP-2 in the lungs at 24 h postinfection than did C3(+/+) mice. Collectively, these results indicate that complement activation by the alternative pathway is critical for the survival of mice infected with P. aeruginosa and that the protection provided by complement is at least in part due to C3-mediated opsonization and phagocytosis of P. aeruginosa.
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PMID:The alternative activation pathway and complement component C3 are critical for a protective immune response against Pseudomonas aeruginosa in a murine model of pneumonia. 1510 2


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