UMLS:C0021311 - FACTA Search

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Query: UMLS:C0021311 (Infection)
38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adenovirus is a non-enveloped DNA virus which may lead to severe diseases of the respiratory tract. In order to study the influence of virus infection on primary cultured peribronchial submucosal gland cells, we performed in vitro infection with human adenovirus type 3. Peribronchial submucosal glands are the main source of tracheobronchial mucus and, therefore, play a major pathophysiological role in common pulmonary diseases such as bronchial asthma, chronic obstructive pulmonary disease and cystic fibrosis. The success of infection was verified by means of immunofluorescence and transmission electron microscopy. Infection follows a certain timetable with a climax of paracristalline intranuclear virus inclusions after 48 h of infection. Virus particles could be detected in the nucleus as well as in peripheral and perinuclear cytoplasmatic vacuoles. The release of virus capsids from the nucleus could be visualized using transmission electron microscopy and immunofluorescence with antibodies against hexon proteins. Two different kinds of mechanisms of transition of newly synthesized virus capsids from the nucleus into the cytoplasm could be identified. Due to an increasing cytopathic effect, viruses spread from cytoplasm after longer terms of infection. Cytopathic effects and cytoskeleton aspects under this virus infection could be characterized using immunofluorescence with several monoclonal antibodies against different cytokeratins.
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PMID:Morphology of adenovirus type-3 infection of human respiratory epithelial cells in vitro. 1202 26

Infection of Pseudomonas aeruginosa in cystic fibrosis patients is a major cause of mortality. This organism shows wide ranging antibiotic resistance that is largely attributable to the expression of xenobiotic efflux pump(s). Here, we show a novel mechanism by which the resistance-nodulation-division-type xenobiotic transporter expels potential hazards and protects the interior of the cells. The xenobiotic transporters MexB and MexY preferentially export beta-lactam and aminoglycoside antibiotics, respectively. When two large extramembrane loops of MexY were replaced by the corresponding loops of MexB, the hybrid protein exhibited beta-lactam selectivity (MexB-type), but failed to recognize aminoglycoside. As the transmembrane segment of MexB was replaced with a corresponding transmembrane segment of MexY, one-by-one for all 12 segments, all the hybrid proteins showed MexB-type antibiotic selectivity. These results clearly demonstrated that the resistance-nodulation-division-type efflux pump in P. aeruginosa selects and transports substrates via the domains that largely protrude over the cytoplasmic membrane. The transmembrane segments were unlikely to have been involved in substrate selectivity. These observations led us to propose a novel mechanism by which the xenobiotic transporters in Gram-negative bacteria select and expel substrates from the periplasmic space before potential hazards penetrate into the cytoplasmic membrane.
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PMID:An elegant means of self-protection in gram-negative bacteria by recognizing and extruding xenobiotics from the periplasmic space. 1246 Sep 90

Infection with bacterial species belonging to the Burkholderia cepacia complex contribute significantly to morbidity and mortality in persons with cystic fibrosis (CF). The majority of isolates recovered from CF patients belong to B. cepacia genomovar III and several distinct 'epidemic' strains have been described. This study examined the population structure of B. cepacia genomovar III by using multilocus restriction typing, indexing allelic variation at five chromosomal genes by restriction analysis of PCR-amplified genes. A collection of 375 isolates, recovered from CF and non-CF patients and natural environments in North America, Europe and Australia, was examined. Among these isolates 144 different restriction types were found. Overall, the population is at linkage disequilibrium, indicating that it has a clonal structure. The majority (86.7 %) of restriction types grouped into three major clonal complexes, comprising the epidemic ET12, PHDC and Midwest clonal lineages. The analysis indicates that these complexes are geographically widespread and demonstrate varying degrees of genetic recombination. These differences in population structure among major clonal complexes within the same species are likely related to differences in evolutionary history and ecology. The observation that genetic recombination is frequent within some B. cepacia genomovar III populations has important implications for the biotechnological use of B. cepacia complex species.
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PMID:Population structure analysis of Burkholderia cepacia genomovar III: varying degrees of genetic recombination characterize major clonal complexes. 1257 82

Melioidosis is endemic in South East Asia, Asia and northern Australia. Infection usually follows percutaneous inoculation or inhalation of the causative bacterium, Burkholderia pseudomallei, which is present in soil and surface water in the endemic region. While 20-36% of melioidosis cases have no evident predisposing risk factor, the vast majority of fatal cases have an identified risk factor, the most important of which are diabetes, alcoholism and chronic renal disease. Half of all cases present with pneumonia, but there is great clinical diversity, from localised skin ulcers or abscesses without systemic illness to fulminant septic shock with multiple abscesses in the lungs, liver, spleen and kidneys. At least 10% of cases present with a chronic respiratory illness (sick > 2 months) mimicking tuberculosis and often with upper lobe infiltrates and/or cavities on chest radiography. As with tuberculosis, latency with reactivation decades after infection can also occur, although this is rare. Confirmation of diagnosis is by culture of B. pseudomallei from blood, sputum, throat swab or other samples. Microbiology laboratories need to be informed of the possibility of melioidosis, as those not familiar with it can misidentify the organism. Antibiotic therapy is initial intensive therapy with i.v. ceftazidime or meropenem or imipenem +/- cotrimoxazole for > or = 10 days, followed by eradication therapy with cotrimoxazole +/- doxycycline +/- chloramphenicol (first 4 weeks only) for > or = 3 months. Melioidosis has been increasingly recognised in returning travellers in Europe and recently melioidosis and colonisation with B. pseudomallei have been documented in cystic fibrosis patients visiting or resident in endemic areas.
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PMID:Melioidosis: an important cause of pneumonia in residents of and travellers returned from endemic regions. 1451 49

Infection with Pseudomonas aeruginosa plays a major role in the pulmonary inflammation and injury associated with cystic fibrosis. Lung inflammation may also lead to more widespread systemic effects on other organs. We tested the following hypotheses: (1) ongoing P. aeruginosa lung infection produces diaphragmatic and limb muscle weakness and (2) such muscle dysfunction is directly correlated with the level of pulmonary inflammation. Chronic bronchopulmonary infection with mucoid P. aeruginosa was induced in C57BL/6 mice. At Day 2 after infection, diaphragmatic force was decreased (37%) only in mice infected with a high dose of 1 x 10(6) cfu, whereas by Day 7 after infection, diaphragmatic force was similarly reduced (36%) even at a fivefold lower inoculating dose. No significant correlations were found between diaphragmatic weakness and pulmonary inflammation, as assessed by the number of neutrophils, macrophages, and lymphocytes in bronchoalveolar lavage fluid. Moreover, in marked contrast to the diaphragm, no effects of P. aeruginosa infection on contractile function were observed in prototypical slow- and fast-twitch hindlimb muscles. We conclude that sustained lung infection with P. aeruginosa induces preferential weakness of the diaphragm, which is not directly correlated with the degree of pulmonary inflammation induced under these conditions.
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PMID:Preferential diaphragmatic weakness during sustained Pseudomonas aeruginosa lung infection. 1500 46

Respiratory tract infection with eventual respiratory failure is the major cause of morbidity and mortality in cystic fibrosis (CF). Infective exacerbations need to be treated promptly and effectively to minimize potentially accelerated attrition of lung function. The choice of antibiotic depends on in vitro sensitivity patterns. However, physicians treating patients with CF are increasingly faced with infection with multidrug-resistant isolates of Pseudomonas aeruginosa. In addition, innately resistant organisms such as Burkholderia cepacia complex, Stenotrophomonas maltophilia and Achromobacter (Alcaligenes) xylosoxidans are becoming more prevalent. Infection with methicillin-resistant Staphylococcus aureus (MRSA) is also a problem. These changing patterns probably result from greater patient longevity and increased antibiotic use for acute exacerbations and maintenance care. Multidrug-resistant P. aeruginosa infection may be treated successfully by using two antibiotics with different mechanisms of action. In practice antibiotic choices have usually been made on a best-guess basis, but recent research suggests that more directed therapy can be achieved through the application of multiple-combination bactericidal testing (MCBT). Aerosol delivery of tobramycin for inhalation solution achieves high endobronchial concentrations that may overcome bacterial resistance as defined by standard laboratory protocols. Resistance to colistin is rare and this antibiotic should be seen as a valuable second-line drug to be reserved for multidrug-resistant P. aeruginosa. The efficacy of new antibiotic groups such as the macrolides needs to be evaluated.CF units should adopt strict segregation policies to interrupt person-to-person spread of B. cepacia complex. Treatment of panresistant strains is difficult and often arbitrary. Combination antibiotic therapy is recommended, usually tobramycin and high-dose meropenem and/or ceftazidime, but the choice of treatment regimen should always be guided by the clinical response.The clinical significance of S. maltophilia, A. xylosoxidans and MRSA infection in CF lung disease remains uncertain. If patients show clinical decline and are chronically colonized/infected with either of the former two pathogens, treatment is recommended but efficacy data are lacking. There are defined microbiological reasons for attempting eradication of MRSA but there are no proven deleterious effects of this infection on lung function in patients with CF. Various treatment protocols exist but none has been subject to a randomized, controlled trial. Multidrug-resistant microorganisms are an important and growing issue in the care of patients with CF. Each patient infected with such strains should be assessed individually and antibiotic treatment planned according to in vitro sensitivity, patient drug tolerance, and results of in vitro studies which may direct the physician to antibiotic combinations most likely to succeed.
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PMID:Antibiotic treatment of multidrug-resistant organisms in cystic fibrosis. 1471 98

Reported actuarial one-year survival for patients with cystic fibrosis (CF) after lung transplant is 55-91%. Infection is the most common cause of early death. Colonization with Burkholderia cepacia complex is associated with reduced survival and international lung transplant referral guidelines support individual unit assessment policies for patients colonized with other pan-resistant bacteria. We examined local data on survival after transplant for CF to determine the impact of colonization with pan-resistant bacteria. A retrospective review of all CF patients from Royal Prince Alfred Hospital (RPAH), Sydney, who underwent lung transplantation at St Vincent's Hospital, Sydney, 1989-2002, was performed. Sixty-five patients were listed for lung transplantation with 54 (male: female=29:25) receiving transplants. Of the 11 patients (17%) who died on the waiting list, six were colonized with pan-resistant Pseudomonas aeruginosa. Thirty of the 54 transplanted patients had at least one pan-resistant organism before transplant. In 28 this included P. aeruginosa. Overall one-year survival was 92% with a median survival of 67 months. Overall survival for the pan-resistant group (N = 30) was not significantly different to survival in those with sensitive organisms (N = 24) (Logrank chi square = 1.6, P = 0.2). Three patients colonized with B. cepacia complex pre-transplant survive at 11, 40 and 60 months post-transplant. Infection contributed to 11 of the 18 post-transplant deaths, with pre-transplant-acquired bacterial pathogens responsible in two cases. Patients continued to acquire multiresistant bacteria post-transplantation. Lung transplant survival at St Vincent's Hospital for CF adults from RPAH compares favourably with international benchmarks. Importantly, colonization with pan-resistant bacteria pre-transplant did not appear to adversely affect survival post-transplant.
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PMID:The impact of pan-resistant bacterial pathogens on survival after lung transplantation in cystic fibrosis: results from a single large referral centre. 1506 37

Infections caused by respiratory pathogens such as Burkholderia cepacia and Pseudomonas aeruginosa are associated with an increased morbidity and mortality in people affected by cystic fibrosis, the most common lethal genetic disease in Caucasian populations. Preventing the acquisition of these pathogens is paramount for these patients. The goal of this survey was to assess the distribution and the prevalence of the measures adopted for the prevention and control of infections caused by respiratory pathogens in the 28 italian centres for cystic fibrosis. 21 questionnaires were returned and some important differences can be observed in the adoption of segregation measures. Although results may be influenced by other factors, specific segregation policies appear to be more directly associated than other measures (e.g., intensive disinfection; behavioural rules to minimise patient' contacts) with lower prevalence of Pseudomonas aeruginosa (OR 0.36 CI95% 0.31-0.42), of multidrug-resistant Pseudomonas aeruginosa (OR 0.30 CI95% 0.22-0.40), and of methicillin-resistant Staphylococcus aureus (OR 0.67 CI95% 0.48-0.94).
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PMID:[Prevention and control of respiratory tract infections in the network of Italian Centers for Cystic Fibrosis]. 1515 77

Burkholderia cenocepacia is an opportunistic pathogen that can cause severe lung infections in cystic fibrosis patients. To understand the contribution of B. cenocepacia flagella to infection, a strain mutated in the major flagellin subunit, fliCII, was constructed in B. cenocepacia K56-2 and tested in a murine agar bead model of lung infection. C57/BL6 mice infected with approximately 10(8) wild-type K56-2 bacteria exhibited 40% mortality after 3 days, whereas no mortality was noted in mice infected with the fliCII mutant. Among the mice surviving the infection with either strain, there was no significant difference in the bacterial loads in the lungs and spleen, bacteremia, weight loss, or infiltration of immune effector cells at 3 days postinfection. Similar results were observed at 24 h, prior to expression of the lethality phenotype. KC, a murine interleukin-8 (IL-8) homolog, was elevated in both the bronchoalveolar lavage fluid and serum of mice infected with the wild type compared to the fliCII mutant at 24 h, suggesting that flagella stimulated host cells. To demonstrate that flagella contributed to these responses, the interaction between B. cenocepacia and Toll-like receptor 5 (TLR5) was investigated. Infection of HEK293 cells with heat-killed wild-type K56-2, but not infection with the fliCII mutant, resulted in both NF-kappaB activation and IL-8 secretion that was dependent upon expression of TLR5. Together, these results demonstrate that B. cenocepacia flagella contribute to virulence in an in vivo infection model, and that induction of host immune responses through interaction with TLR5 may contribute to its overall pathogenic potential.
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PMID:Contribution of Burkholderia cenocepacia flagella to infectivity and inflammation. 1532 6

Pseudomonas aeruginosa lung infection is the major cause of morbidity and mortality in patients with cystic fibrosis. Infection usually begins in childhood and is responsible for respiratory failure and death in most patients with cystic fibrosis. The organism triggers an exuberant chronic inflammatory reaction which damages the airways and leads to progressive loss of lung function. Over the last decade significant advances have been made in the understanding of the pathophysiology of cystic fibrosis airways disease. These should assist the development of new and better therapies to treat this pathogen. This review provides an overview of pseudomonal infection in cystic fibrosis, including mechanisms by which the bacteria may colonize the cystic fibrosis airway, persistence of pseudomonal infection and the biofilm mode of growth. Available treatments and possible novel approaches to therapy will be discussed.
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PMID:Pseudomonal infection in cystic fibrosis: the battle continues. 1548 58

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