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Query: UMLS:C0023241 (Legionella)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe the first known case of Legionella longbeachae infection in the Netherlands in a patient with myasthenia gravis. Infection with L. longbeachae relapsed after prolonged therapy with erythromycin. No environmental source of L. longbeachae could be traced.
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PMID:Relapse of Legionella longbeachae infection in an immunocompromised patient. 897 93

Solid-organ transplantation is a therapeutic option for many human diseases. Infections are a major complication of solid-organ transplantation. All candidates should undergo a thorough infectious-disease screening prior to transplantation. There are three time frames, influenced by surgical factors, the level of immunosuppression, and environmental exposures, during which infections of specific types most frequently occur posttransplantation. Most infections during the first month are related to surgical complications. Opportunistic infections typically occur from the second to the sixth month. During the late posttransplant period (beyond 6 months), transplantation recipients suffer from the same infections seen in the general community. Opportunistic bacterial infections seen in transplant recipients include those caused by Legionella spp., Nocardia spp., Salmonella spp., and Listeria monocytogenes. Cytomegalovirus is the most common cause of viral infections. Herpes simplex virus, varicella-zoster virus, Epstein-Barr virus and others are also significant pathogens. Fungal infections, caused by both yeasts and mycelial fungi, are associated with the highest mortality rates. Mycobacterial, pneumocystis, and parasitic diseases may also occur.
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PMID:Infections in solid-organ transplant recipients. 899 60

Legionella pneumophila, the causative agent of legionnaires' disease, is a gram-negative pleomorphic bacillus and fastidious in its growth in artificial medium. These bacteria grow readily intracellularly, including growth in macrophages and other phagocytic cells. Humoral antibodies develop readily to these bacteria not only in infected patients, but also in persons who have had subclinical exposure. High-levels of serum antibodies may also occur in individuals who recover from infection. However, cell-mediated immunity based on lymphocytes reacting with the organisms and cytokines produced by such lymphocytes are important in resistance. Vaccines prepared from killed Legionella or their components readily induce cell-mediated immunity. Immune resistance to disease depends on lymphocyte-based immunity, activating cytokine formation, some of which activate macrophages to resist infection. Resistance to Legionella infection by experimental animals such as mice correlates with activation of macrophages, which can inhibit replication of the bacteria. Much recent experimental work has involved studies using inbred animals, including inbred mice genetically resistant to Legionella versus mice genetically susceptible. Detailed studies show that regulation of macrophage resistance versus susceptibility to infection is mediated by specific genetic mechanisms. Induction of cytokines by Legionella can activate immune cells, especially helper T cells. Th 1 type helper cells that produce type 1 class cytokines, such as interferon gamma and interleukin-2 (IL-2), are known to be important in cellular immunity to Legionella as well as to other opportunistic intracellular bacteria. In contrast, Th 2 type helper cells, which secrete type 2 class cytokines such as IL-4, IL-5, and IL-6, activate B lymphocytes to produce humoral antibodies important in resistance to extracellular bacteria which secrete toxins and extracellular factors as compared to intracellular bacteria such as Legionella. Although Legionella, similar to other ubiquitous opportunistic pathogens, can cause serious infection in immunocompromised individuals, these bacteria have many distinguishing characteristics, such as very rapid replication in macrophages from susceptible individuals. However, activated macrophages restrict the growth of these bacteria. Infection by Legionella, if recognized clinically, can be readily treated with appropriate antibiotics. Currently, many studies are in progress concerning the mechanism of pathogenicity and assessment of the molecular biologic mechanisms of protective immune responses to this bacterium, which causes serious infection in immunocompromised individuals.
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PMID:Immunologic response and pathophysiology of Legionella infection. 964 87

Infections caused by M. pneumoniae, C. pneumoniae, and Legionella spp. are important causes of community-acquired pneumonia (CAP). In the past decade, considerable new information has come to light concerning these organisms. Despite this, debate continues concerning the syndromic approach to CAP and the scientific merit of lumping these pathogens together. Because the etiologic diagnosis of these pathogens is established only in a minority of cases, the true prevalence tends to be underestimated. In clinical practice, these pathogens are often empirically treated. More rapid and cost-effective diagnostic techniques are needed so that the clinical course of patients with these infections can be better characterized.
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PMID:The role of atypical pathogens: Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella pneumophila in respiratory infection. 977 79

The 'atypical' pathogens are important causes of pneumonia, causing illness ranging from mild to life-threatening. The most common atypical pathogens are Mycoplasma pneumoniae and Chlamydia pneumoniae; others include Legionella species, Chlamydia psittaci and viruses such as influenza, adenovirus and respiratory syncytial virus. Infection rates for these agents are difficult to determine because many clinicians and investigators do not routinely test for them, but reported rates are in the range of up to 8% (for C pneumoniae) and 15% to 20% (M pneumoniae) of all cases of pneumonia. Diagnostic testing is very difficult because most of these agents cannot be easily cultured. Diagnosis relies on either high acute antibody titres (quickly available but not very accurate) or paired serology samples (more accurate but requires at least a week). While rapid identification using automated polymerase chain reaction testing may be possible in the future, current management is based largely on empirical treatment.
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PMID:Role of 'atypical' pneumonia pathogens in respiratory tract infections. 1020 27

An open comparative study was undertaken in order to assess the efficacy and safety of a single dose of azithromycin in the treatment of community-acquired atypical pneumonia. A total of 100 adult patients with atypical pneumonia syndrome were randomized to receive 1.5 g of azithromycin as a single dose, or 500 mg once daily for 3 days. The presence of Mycoplasma pneumoniae, Chlamydia pneumoniae, Chlamydia psittaci, Coxiella burnetii, and Legionella pneumophila infection was diagnosed by serological tests. Control clinical examinations were performed 72 h, 10-12 days and 4 weeks after treatment initiation. Among 96 patients (48 in each group) who were evaluable for clinical efficacy M. pneumoniae infection was confirmed in 24, C. pneumoniae in nine, C. psittaci in five, C. burnetii in six, and L. pneumophila in five. Forty-seven patients (97.9%) in each group were cured. Side effects were observed in two patients in the single-dose group, and one patient in the 3-day group. In conclusion, a single 1.5 g dose of azithromycin may be an alternative to the standard 3-day azithromycin regimen in the treatment of outpatients with atypical pneumonia syndrome.
Infection
PMID:Azithromycin: single 1.5 g dose in the treatment of patients with atypical pneumonia syndrome--a randomized study. 1037 32

The gene encoding the green fluorescent protein (GFP) was used as a reporter gene in Legionella pneumophila. To analyze GFP expression in Legionella, transcriptional fusions of gfp with the Legionella-specific mip (Macrophage Infectivity Potentiator) promoter (P(mip)) and the sod (SuperOxide Dismutase) promoter (P(sod)) derived from Listeria monocytogenes were constructed. Following transformation into the virulent L. pneumophila strain JR 32, strong GFP-mediated fluorescence was detected with both plasmids, although the sod promoter was associated with a 1ten-fold higher intensity. No fluorescence was observed in L. pneumophila transformed with the promoterless gfp gene. Comparison of fluorescence yields between various L. pneumophila strains that differ in their virulence characteristics and were transformed with the P(mip)-gfp carrying plasmid revealed no differences in GFP expression. Infection studies using Acanthamoeba castellanii as host and recombinant L. pneumophila strains carrying the P(mip)-gfp and P(sod)-gfp fusions indicated that the mip promoter was expressed when the bacteria replicated intracellularly. GFP expression was also used to monitor, in infected A. castellanii cells, the intracellular survival of, and incidence of host-cell killing by. L. pneumophila strains that vary in their virulence properties. As quantified by flow cytometry the highly virulent L. pneumophila strain Corby was twice as infectious to A. castellanii as the Philadelphia strain JR 32. Using the avirulent Philadelphia derivative 25D invasion but no intracellular multiplication was observed. In addition, we examined by flow cytometry the influence of cytochalasin D, cycloheximide, and methylamine on the uptake of Legionella by A. castellanii. In conclusion, gfp appears to be a convenient reporter gene whose expression in Legionella can be followed in real time and allows analysis of promoter activities in Legionella and monitoring of the infection process.
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PMID:Expression and use of the green fluorescent protein as a reporter system in Legionella pneumophila. 1066 67

Virulent Legionella pneumophila replicate readily in thioglycollate-elicited peritoneal macrophages from genetically permissive A/J mice, but avirulent L. pneumophila do not. The production of cytokines by macrophages infected with L. pneumophila has been studied, but the correlation of bacterial virulence with immune responses of macrophages, such as proinflammatory cytokine production, is not well understood. In this regard, production of the cytokines tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1alpha, IL-1beta, and IL-6 were examined in macrophage cultures infected in vitro with virulent vs. avirulent L. pneumophila. Infection of macrophages from A/J mice with the virulent L. pneumophila up-regulated mRNA expression for these cytokines, whereas avirulent bacteria resulted in only a slight or no detectable increase in cytokine mRNA. Similarly, virulent L. pneumophila induced the macrophages to produce relatively high levels of TNF-alpha, IL-1alpha, IL-1beta, and IL-6 proteins as measured by enzyme-linked immunosorbent assays, whereas avirulent bacteria induced only low or often undetectable amounts of these cytokines. Thus, these results show the murine macrophages from susceptible A/J mice are readily infected with virulent L. pneumophila in vitro and stimulated to produce the proinflammatory acute-phase cytokines TNF-alpha, IL-1alpha, IL-1beta, and IL-6, but avirulent L. pneumophila did not. Such differences in induction of these proinflammatory cytokines by macrophages in response to virulent vs. avirulent L. pneumophila infections may be an important factor in the pathogenesis induced by these intracellular bacteria.
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PMID:Murine macrophages differentially produce proinflammatory cytokines after infection with virulent vs. avirulent Legionella pneumophila. 1085 60

A 10-year-old, previously healthy child with pneumonia caused by Legionella pneumophila diagnosed by polymerase chain reaction (PCR) of serum is presented. Diagnostic methods were PCR of serum using two different primer sets, and the detection of specific antibody in paired sera using an indirect immunofluorescence assay. Legionella DNA was amplified from serum obtained before and on day 6, but not after completion of a 14-day course of oral clarithromycin. The etiologic role of L. pneumophila was confirmed by seroconversion. The report illustrates that L. pneumophila PCR of serum may contribute to the identification of this microorganism as a cause of severe pneumonia in immunocompetent children.
Infection 1999
PMID:Diagnosis by polymerase chain reaction of pneumonia caused by Legionella pneumophila in an immunocompetent child. 1088 45

Infection with Legionella remains an important cause of disease and death. We analyzed our laboratory data from 1993 through 1997, augmented by our 20 years of experience. The incidence of Legionella as a cause of pneumonia varied in our study from 5%-9%, with a slight increase during the winter. Isolation of these microorganisms from different water sources was higher during the summer and ranged from 7%-70%. Special laboratory tests are necessary to diagnose the disease and monitor these bacteria in water samples. The serologic method--indirect immunofluorescent assay--for 41 serogroups of Legionella was the main diagnostic method used. Legionella sg. 1 was the most frequent cause of the disease, with an incidence of 52% in 1993, decreasing to 15% in 1997. An increase in the incidence of seropositivity to "other Legionellae" is characteristic for our country. No correlation was found between the incidence of isolation of a specific strain and exposure. However, it is well known that the disease is overtreated but underdiagnosed, which requires reversal. Larger studies of Legionella colonization in water supplies and in air are needed in order to establish the risk of infection. Water sources are presently under-studied, as are respiratory devices in hospitals, or they are not studied at all in Israel, such as in mist machines in supermarkets, in dental clinics, and in ships and airplanes.
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PMID:[Legionellosis in Israel--a view of the situation]. 1091 11


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