Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023241 (Legionella)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of macrophages with Legionella pneumophila induces formation of interleukin 1 beta (IL-1 beta), but the molecular basis of this is not understood. Binding of bacteria to macrophage surfaces is the first step in an infection process. Therefore, we examined whether this step was sufficient to increase the cellular level of mRNAs for IL-1 beta and other cytokines. To assess the effect of binding of L. pneumophila on the steady-state levels of cytokine mRNAs, cultures of thioglycolate-elicited macrophages from L. pneumophila-susceptible A/J mice were treated with cytochalasin D and infected with L. pneumophila and the total RNA was extracted for analysis by reverse transcription-PCR with primers for IL-1 alpha, IL-1 beta, IL-6, tumor necrosis factor alpha, granulocyte macrophage colony-stimulating factor, and beta interferon (IFN-beta). L. pneumophila treatment increased the cellular steady-state mRNA levels of all cytokines except IFN-beta. To determine the specificity of this effect, macrophage cultures were treated with cytochalasin D and either bacterial lipopolysaccharide, bovine serum albumin-sensitized latex, Salmonella typhimurium, or Escherichia coli. Lipopolysaccharide treatment increased all mRNAs, bovine serum albumin-sensitized latex had no significant effect, and treatment with S. typhimurium or E. coli increased all mRNAs except that of IFN-beta. These results suggested that the binding of gram-negative bacteria to the macrophage surface was sufficient to induce a unique pattern of cytokine mRNAs. Additional studies that examined the characteristics of the bacterial ligands involved indicated involvement of both heat-labile and heat-stable surface ligands.
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PMID:Binding of Legionella pneumophila to macrophages increases cellular cytokine mRNA. 806 12

Legionella pneumophila may subvert monocyte defenses by several mechanisms including the inhibition of phagosome-lysosome fusion or the impairment of oxidative metabolism. We have investigated the effect of L. pneumophila Knoxville 1, a virulent strain that does not inhibit phagosome-lysosome fusion, on the oxidative responsiveness of human monocytes. Infection of monocytes with L. pneumophila for 48 h resulted in marked inhibition of superoxide generation stimulated by phorbol myristate acetate (PMA) but not by zymosan, a particulate agonist. Evidence is provided that L. pneumophila interfered with the transductional pathway (i.e., protein kinase C, PKC) leading to activation of the NADPH oxidase in monocytes. The phosphorylation of 34-, 48-, 62-, 68-, and 80-kDa proteins stimulated by PMA was markedly inhibited in infected monocytes. In addition, the expression of both alpha and beta PKC isotypes was partially inhibited in infected monocytes. Taken together, our data suggest that the down-modulation of PKC isotypes plays a role in the inhibition of PMA-stimulated superoxide generation.
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PMID:Legionella pneumophila inhibits superoxide generation in human monocytes via the down-modulation of alpha and beta protein kinase C isotypes. 812 Apr 47

Pneumonia is a common and important infectious disease in all age groups but especially in the elderly. Mortality and morbidity are quite high when associated with certain risk factors such as comorbid medical conditions and clinical features that implicate more severe disease. In the absence of such features, patients can be treated quite safely out of the hospital, as long as followup and compliance issues are not a problem. Therapy should be directed toward gram-positive and gram-negative aerobic bacteria and, at times, be further expanded to cover atypical organisms such as Legionella sp. Appropriate antimicrobial agents are those that not only cover expected microorganisms but are compatible with each patient's existing medical regimen.
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PMID:Community-acquired pneumonia: new outpatient guidelines based on age, severity of illness. 812 50

The sick building syndrome has been widely discussed from epidemiological perspectives. Although there is considerable difference in opinion regarding the concrete and objective evidence to support a distinct sick building syndrome and/or building-related illness, much data indicates that numerous variables within buildings can potentially influence human health. In this paper, we discuss in detail not only the potential and unique infectious diseases caused by Legionella, Pontiac fever, Q fever, and influenza, but also the data implicating noninfectious etiologies of sick building syndrome and building-related illnesses. In addition, the role of psychological factors, mass hysteria, and indoor pollution is discussed with respect to the nature of associations between exposure and symptoms. Finally, comparisons are made in different building construction types of old versus new buildings to highlight changes in modern construction that may have led to a putative increase in work-related symptomatology.
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PMID:Building components contributors of the sick building syndrome. 817 32

Ten patients from a rehabilitation center were admitted to hospital with serious respiratory infections within ten weeks. An outbreak of Legionnaire's disease was suspected based on the epidemic and atypical manifestation of pneumonia and could be proven microbiologically. Pulmonary and extrapulmonary complications included respiratory failure, lung abscess, transitory renal impairment in five patients and acute renal failure requiring dialysis in one, tetraparesis caused by peripheral neuropathy and acute psychosis. Three patients died despite immediate institution of therapy with erythromycin. Legionella pneumophila serogroup 1 subtype Pontiac was isolated from a bronchial lavage sample of one patient and from the water supply of the rehabilitation center. Monoclonal antibody subtyping and restriction endonuclease analysis were performed on both environmental and patient isolates. Potable water was identified as the source of the outbreak based on identical patterns on restriction endonuclease analysis. Despite thermic and chemical disinfection with chlorination (up to 15 ppm) in the rehabilitation clinic, an eleventh case of Legionnaire's disease was detected 11 months later.
Infection
PMID:Nosocomial outbreak of legionellosis in a rehabilitation center. Demonstration of potable water as a source. 822 27

In most cases of respiratory tract infection, antibiotic therapy has to be initiated before the results of microbiological examination are available. The four most common pathogens of acute exacerbations of chronic bronchitis are pneumococci, Haemophilus influenzae, Moraxella catarrhalis and Staphylococcus aureus. Pneumococci are the predominant pathogens of community-acquired pneumonia, followed by H. influenzae and staphylococci. Legionella, mycoplasma and chlamydia vary in frequency according to the population studied. Staphylococci, Pseudomonas, Enterobacter and Klebsiella spp. as well as H. influenzae are the major pathogens of secondary pneumonia. For reasons of cost and environmental problems, oral antibiotics ought to be used whenever possible considering the severity of the infection and patient circumstance. Parenteral antibiotics are indicated in severe infections in order to provide high therapeutic drug levels. Second generation cephalosporins are appropriate for initial therapy of lower respiratory tract infections. In case of severe infection, cephalosporins should be combined with an aminoglycoside, ureidopenicillin or quinolone. Cefuroxime has shown good clinical efficacy and tolerance in lower respiratory tract infections.
Infection 1993
PMID:[Parenteral cephalosporins for the treatment of lower respiratory tract infections]. 831 90

The ability of an opportunistic intracellular bacterial pathogen, Legionella pneumophila, to induce tumor necrosis factor (TNF) in macrophages from susceptible A/J or resistant BDF1 and BALB/c mice was determined. Cultures of peritoneal elicited macrophages from these mouse strains produced TNF in response to the Legionella. The TNF levels produced by the macrophages stimulated with either heat-killed Legionella vaccine or lipopolysaccharide were similar and dose dependent, although the amount of TNF produced by macrophages from permissive A/J mice was 2- to 4-fold higher than that produced by macrophages from the nonpermissive mice. Similar differences in TNF levels occurred when macrophages from either permissive or non-permissive mice were infected with viable Legionella. The TNF levels produced by the A/J mouse macrophages increased as a function of time after infection, with a peak of activity on Day 1 or 2, depending upon the initial concentration of the bacteria. Infection of the A/J mouse macrophages with avirulent Legionella resulted in induced levels comparable to those induced by a virulent strain. Although it is widely believed that TNF production by mouse macrophages is related to resistance to infections, the results of this study did not show a relationship between TNF production by macrophages in vitro and resistance versus susceptibility of the macrophage donor mouse strain to Legionella infection.
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PMID:Legionella pneumophila induced tumor necrosis factor production in permissive versus nonpermissive macrophages. 847 35

Following an outbreak of Legionnaires disease in a Michigan prison in 1993 (1), which was first recognized at a civilian hospital, the Michigan Department of Public Health (MDPH) recommended that surveillance for acute infectious diseases be established in the Michigan Department of Corrections (MDOC). In April 1994, MDOC and MDPH implemented a pilot system to monitor trends and detect clusters of selected acute infectious diseases and injury in six Michigan state correctional facilities. This report summarizes the findings of injury surveillance during April 1994-March 1995.
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PMID:Injury surveillance in correctional facilities--Michigan, April 1994-March 1995. 854 11

The respiratory diseases produced by the Legionella genus of bacteria are collectively called Legionellosis. Presently more than 34 species of Legionella have been identified, 20 of which have been isolated from both environmental and clinical sources. The diseases produced by Legionella include the pneumonic form, Legionnaires' disease, and the flu-like form, Pontiac fever. Because the vast majority of Legionellosis is caused by the L. pneumophila species, this bacterium is the thrust of the discussion.Legionella is a global bacterium. The relationship of the bacterium to its environment has told us many things about infectious diseases. Not until Legionellosis and the discovery of its etiologic agent, Legionella, has such a successful modern-day marriage been consummated between the agent and its environment. Nearly two decades have passed since the term Legionellosis found its way into the vocabulary of the scientific journals, the popular press, and courtroom proceedings. Too often the scientific development, engineering implementation, and societal acceptance are disconnected. The focus of scientific research sometimes does not reflect engineering or societal needs and thus contributes little to the solution of immediate and important problems. At other times, scientific knowledge that could contribute to solutions is overlooked because of poor communication between the problem holders, the scientific community, regulatory agencies, the problem makers, and the public. The scope of this paper provides insights on the ecological niche of Legionella, describes the organism's ecological relationships in the natural world, and provides wisdom for effective control of the bacterium for the industrial and user communities.
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PMID:Ecology of Legionella: From Data to Knowledge with a Little Wisdom 868 9

We prospectively studied the etiology of community-acquired pneumonia among all patients who were admitted to our hospital from July 1994 to June 1995. Tests for microbial pathogens including Chlamydia spp. and Legionella spp. were performed and diagnoses were made with strict criteria. A total 110 patients with 111 episodes of pneumonia were evaluated, and a pathogen was identified in 61 episodes (55%). The most common pathogen was Streptococcus pneumoniae (18%), followed by Haemophilus influenzae, Klebsiella pneumoniae, Pseudomonas aeruginosa, Mycoplasma pneumoniae, and Chlamydia spp. Infection with Legionella pneumophila was not found. Dual pathogens were identified in five episodes. Few prospective studies of the etiology of community-acquired pneumonia have been done in Japan. To prepare guidelines for the management of community-acquired pneumonia in Japan, a national study of the etiology of pneumonia is necessary.
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PMID:[Prospective study of the etiology of community-acquired pneumonia among patients in a general hospital]. 881 Jul 56


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