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

The Infectious Diseases Society of America (IDSA) has published guidelines for the treatment of community-acquired pneumonia (CAP). Although Streptococcus pneumoniae remains the most common etiologic agent, Chlamydia pneumoniae and Legionella pneumophila are also important causes. For all suspected CAP patients, particularly those requiring hospitalization, chest radiographs are strongly recommended to confirm the diagnosis. The IDSA guidelines, in contrast to those published by the American Thoracic Society, emphasize the use of sputum Gram's stain and culture in all patients, whenever possible, to establish etiology. This information can be used not only to guide therapy but also to track trends in the etiologic pathogens for CAP and their antibiotic susceptibility. In light of the better outcomes with the earliest possible interventions, the IDSA recommends initial empiric antimicrobial therapy until laboratory results can be obtained to guide more specific therapy. Macrolides, doxycycline, and fluoroquinolones are suggested for primary empiric therapy, since each has activity against common bacterial pathogens and atypical agents. Detailed antibiotic recommendations are made for various pathogens. For inpatients, attempts should be made to cover Legionella and other common pathogenic bacteria. Alternative antibiotics are recommended for patients with structural diseases of the lung, penicillin allergy, or suspected aspiration pneumonia. Switch to an appropriate oral antibiotic is recommended as soon as the patient's condition is stable and he or she can tolerate oral therapy, often within 72 h.
 ...
PMID:Treatment of community-acquired pneumonia--IDSA guidelines. Infectious Diseases Society of America. 1008 53

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.
 ...
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.
 ...
PMID:Expression and use of the green fluorescent protein as a reporter system in Legionella pneumophila. 1066 67

Macrolide antibiotics (Mac) consist of a 12- to 16-membered lactone ring combined with a sugar moiety, and they inhibit protein synthesis via binding to 23S ribosomal RNA in bacteria. The 14- and 16-membered Mac are used for treating infectious diseases caused by Gram-positive and other bacteria; e.g., Haemophilus influenzae, Bordetella pertussis, Legionella pneumophila, Campylobacter, Treponema pallidum and Mycoplasma. Resistance to macrolide, lincosamide, and streptogramin-B (MLS) antibiotics in staphylococci is known to have the following mechanisms: 1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the erm gene, and consequently a decrease in binding of MLS antibiotics; 2) inactivation of streptogramin-B (STG-B) and lincosamide by the products of the sbh (encoding streptogramin B hydrolase) and linA' (encoding 3-lincomycin 4-clindamycin O-nucleotidyltransferase) genes, respectively; and 3) active efflux of Mac and STG-B antibiotics determined by the msrA and msrB genes in Staphylococcus epidermidis and Staphylococcus xylosus, respectively, both of which appear to act as an ATP-dependent efflux pump. I have shown that Staphylococcus aureus 8325(pEP2104) exhibits inducible resistance to PMS (partial macrolide and streptogramin B)-antibiotics [the 14-membered macrolides, erythromycin (EM), and oleandomycin (OL), and the 16-membered macrolide mycinamicin (MCM) and STG-B]. The sequence of the N-terminal amino acid residues of a 63 kDa protein (MsrSA) that appeared in the membrane of PMS-resistant strains was identical to that of an MsrA polypeptide related to enhanced efflux of [14C]EM. Ribosomes from PMS-resistant strains showed a similar affinity for EM to those from the PMS-sensitive host strain NCTC8325, and no inactivation of EM by 8325(pEP2104) was observed. In the present study, I showed the DNA sequence of the msrSA region on the constitutive PMS-resistant plasmid pMC38, PMS-inducible resistant plasmid pEP2104 and PMS-sensitive mutant plasmid pSP6, and the region that is essential for inducible expression in PMS resistance. In addition, I investigated the relationship between PMS resistance and intracellular accumulation of EM.
 ...
PMID:[Study of macrolide, lincosamide, and streptogramin B antibiotics resistance in Staphylococcus aureus]. 1077 59

Lower respiratory tract infections are the major cause of death due to infectious disease in the developed and developing world. Despite substantial progress in defining pathogens and in therapeutic options, there continues to be major controversies in the clinical management of these infections. This report reviews the guidelines for community-acquired pneumonia from the Infectious Diseases Society of America (IDSA), updated from the initial publication. Diagnosis should include a chest X-ray to differentiate acute bronchitis from pneumonia. The decision for hospitalization should be based on social factors and evaluation of severity of illness. Identification of an etiological agent for inpatients should include two pretreatment cultures, one pretreatment sputum specimen, with seriously ill patients requiring studies for Legionella spp. Recommendations for empiric treatment of outpatients are doxycycline, a macrolide or a fluoroquinolone. Recommendations for empiric treatment of hospitalized patients are a cephalosporin plus a macrolide, or a fluoroquinolone alone. Recommendations for ICU patients are a beta-lactam combined with either a macrolide or a fluoroquinolone. While concern has arisen about increasing resistance to fluoroquinolones, arguments in favor of these agents include the fact that they have good in vitro activity against nearly all treatable pathogens except some anaerobes. Clinical trials have shown equivalence or superiority compared to other standard agents. They are well tolerated, and can be administered intravenously or orally, once daily. A recent retrospective review has shown superior outcome with fluoroquinolone treatment compared to cephalosporins, including a 36% reduction in mortality.
 ...
PMID:Treatment of community-acquired pneumonia. 1081 Feb 10

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.
 ...
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.
 ...
PMID:[Legionellosis in Israel--a view of the situation]. 1091 11

Infection of BALB/c mice with a sublethal concentration of Legionella pneumophila causes an acute disease that is resolved by innate immune responses. The infection also initiates the development of adaptive Th1 responses that protect the mice from challenge infections. To study the early responses, cytokines induced during the first 24 h after infection were examined. In the serum, interleukin-12 (IL-12) was detectable by 3 h and peaked at 10 h, while gamma interferon was discernible by 5 h and peaked at 8 h. Similar patterns were observed in ex vivo cultures of splenocytes. A transient IL-4 response was also detected by 3 h postinfection in ex vivo cultures. BALB/c IL-4-deficient mice were more susceptible to L. pneumophila infection than were wild-type mice. The infection induced higher serum levels of acute-phase cytokines (tumor necrosis factor alpha [TNF-alpha], IL-1beta, and IL-6), and reducing TNF-alpha levels with antibodies protected the mice from death. Moreover, the addition of IL-4 to L. pneumophila-infected macrophage cultures suppressed the production of these cytokines. Thus, the lack of IL-4 in the deficient mice resulted in unchecked TNF-alpha production, which appeared to cause the mortality. Monocyte chemoattractant protein-1 (MCP-1), a chemokine that is induced by IL-4 during Listeria monocytogenes infection, was detected at between 2 and 30 h after infection. However, MCP-1 did not appear to be induced by IL-4 or to be required for the TNF-alpha regulation by IL-4. The data suggest that the early increase in IL-4 serves to regulate the mobilization of acute phase cytokines and thus controls the potential harmful effects of these cytokines.
 ...
PMID:Induction of interleukin-4 (IL-4) by legionella pneumophila infection in BALB/c mice and regulation of tumor necrosis factor alpha, IL-6, and IL-1beta. 1094 49


<< Previous 1 2 3 4 5 6 7 8 9 10