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)

Phosphoinositide metabolism plays a pivotal role in the regulation of receptor-mediated signal transduction, actin remodelling and membrane dynamics. Phosphoinositides co-ordinate these processes by recruiting protein effectors to distinct cellular membranes in a time- and organelle-dependent manner. Intracellular bacterial pathogens interfere with phosphoinositide metabolism to direct their entry into eukaryotic cells, form replication-permissive vacuoles, modulate apoptosis, or trigger fluid secretion. Gram-negative pathogens such as Legionella pneumophila, Shigella flexneri, or Salmonella enterica employ secretion systems to invade host cells by 'pathogen-triggered phagocytosis' and thereby bypass a requirement for phosphatidylinositol 3-kinases [PI(3)Ks]. Contrarily, 'receptor-mediated phagocytosis' of Yersinia spp., Listeria monocytogenes and other pathogenic bacteria depends on PI(3)Ks. Secreted effector proteins have been found to directly bind to and modify host cell phosphoinositides, thus modulating phagocytosis and intracellular survival of the pathogens. These effectors include L. pneumophila proteins that specifically attach to phosphatidylinositol 4-phosphate [PI(4)P] on the Legionella-containing vacuole, and phosphoinositide phosphatases produced by S. flexneri, S. enterica or Mycobacterium tuberculosis. This review covers current knowledge about subversion of host cell phosphoinositide metabolism by intracellular bacterial pathogens with an emphasis on recently identified secreted effector proteins directly engaging phosphoinositides.
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PMID:Modulation of phosphoinositide metabolism by pathogenic bacteria. 1693 34

Nosocomial pneumonia remains an important infection that warrants continuing investigation. The past year has seen a number of reports further describing risk factors, controversial issues around diagnosis, and potential preventive strategies. For specific infecting organisms such as Legionnaire's disease and tuberculosis, further reports of issues related to water supply in the former and staff preventive programs in the latter have also been reported. Substantive advances in prevention or management have not, however, been identified.
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PMID:Nosocomial pneumonia. 1703 95

Modern, non-industrial workplaces may, because of building techniques, widespread use of synthetic materials and artificial ventilation, create risks for the health and well-being of workers. Indoor air pollution by chemical, biological and sometimes physical agents constitutes a significant risk factor, particularly for the respiratory system. The most common effects of exposure to, and inhalation of, indoor air pollutants include acute and chronic inflammations, acute worsening of pre-existing respiratory symptoms or illnesses and airway sensitization to indoor allergens. Upper airway disturbances with an allergic or irritative aetiology are very frequent; Asthma and Hypersensitivity Pneumonitis are more rarely reported but may become severe and widespread when certain environmental conditions prevail. Respiratory infections may have a human source such as tuberculosis or viral diseases or may originate in ventilation systems such as Legionnaire's disease (Legionella pneumophila pneumonia). As all these pathologies may have high social and economic costs and appropriate therapy is not always available, the specialist in Occupational Medicine plays a pre-eminent role in early diagnosis and prevention of respiratory diseases linked to indoor air pollution in the workplace.
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PMID:[Respiratory diseases in confined non-industrial working environments]. 1714 17

Bacterial killing by autophagic delivery to the lysosomal compartment has been shown for Mycobacteria, Streptococcus, Shigella, Legionella and Salmonella, indicating an important role for this conserved trafficking pathway for the control of intracellular bacterial pathogens.(1-5) In a recent study we found that solubilized lysosomes isolated from bone marrow-derived macrophages had potent antibacterial properties against M. tuberculosis and M. smegmatis that were associated with ubiquitin and ubiquitin-derived peptides. We propose that ubiquitinated proteins are delivered to the lysosomal compartment, where degradation by lysosomal proteinases generates ubiquitin-derived peptides with antimycobacterial properties. This surprising finding provokes a number of questions regarding the nature and trafficking of ubiquitin and ubiquitin-modified proteins in mammalian cells. We discuss the possible role(s) that the multivesicular body (MVB), the late endosome and the autophagosome may play in trafficking of ubiquitinated proteins to the lysosome.
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PMID:Ubiquitin trafficking to the lysosome: keeping the house tidy and getting rid of unwanted guests. 1738 86

Epidemiological vigilance in Navarre (601,874 inhabitants) in 2006 included 34 diseases whose notification is compulsory and epidemic outbreaks. Notification is carried out on a weekly basis by the doctors from paediatrics, primary care and specialised care facing any suspicion of these processes, and is completed with microbiological diagnoses. In 2006 the incidence of influenza reached 16.8 cases per 1,000 inhabitants (Epidemic Index, EI: 0.46), showing a late seasonal peak (March) of low dimensions. The incidence of respiratory tuberculosis was 11.3 cases per 100,000 inhabitants, and that of non-respiratory tuberculosis was 2.3; both at similar levels to recent years. Seven cases of tuberculosis occurred in three aggregates amongst cohabitants, and another 7 in non-cohabiting persons resident in the same municipality. Six percent of the cases were coinfected with HIV, and 37% occurred in immigrants. The incidence of meningococcal disease rose to 19 cases (3.2 cases per 100,000 inhabitants; EI 1.46), all of them sporadic. Neisseria meningitidis serogroup B was isolated in 16 cases. There was one case of serogroup C, in a child who had received 3 doses of combined vaccine. In two cases (11%) death occurred. The incidence of legionnaire's disease rose to 28 cases per 100,000 inhabitants (EI:4.88), due to a community outbreak that affected 146 people. Excluding this outbreak, incidence was similar to previous years (3.3 per 100,000 inhabitants). In August an outbreak of parotitis began, and 911 cases had been counted until the end of 2006; and it has continued during 2007. Eleven cases of malaria were registered, all imported. Notifications of toxic food infections has continued to fall (IE:0.48).
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PMID:[Epidemiology of notifiable diseases in Navarre, 2006]. 1789 19

Viable but non-culturable (VBNC) bacteria concept has been defined in 1982 when it has been shown that there exists bacteria whose metabolic activity continue and which can have the ability to reproduce in suitable conditions although they have lost their capability to reproduce in culture. Recent studies have shown that most of the human pathogens (Campylobacter spp., Escherichia coli, Francisella tularensis, Helicobacter pylori, Legionella pneumophila, Listeria monocytogenes, Mycobacterium tuberculosis, Pseudomonas aeruginosa, Salmonella spp., Shigella spp., Vibrio cholerae, V. parahaemolyticus, V. vulnificus) have VBNC form. The interest on this subject has increased due to the detection of some disinfection procedures such as pasteurization of milk and chlorinization of water, cause bacteria to switch to VBNC form. It is thought that, the bacteria in this form may have an important role in recurrent and drug resistant infections as well as infections of unknown origin. However, advanced studies should be done to clarify the role of VBNC bacteria in the setting of recurrent infections, together with their pathogenity and antibiotic resistance. In this review article, the importance of viable but non-culturable bacteria, their morphology, metabolic and genetic properties, pathogenity, resuscitation and identification have been discussed.
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PMID:[Viable but non-culturable form of bacteria]. 1793 63

In spite of advances in microbiological and serological investigations over the last two decades, etiological attribution remains difficult in community-acquired pneumonia (CAP). Even after exhaustive investigation, the etiology of CAP remains unknown in up to 50% of patients. Common pathogens include Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. In addition, several investigators document the importance of atypical pathogens including Mycoplasma pneumoniae, Chlamydophila pneumoniae and Legionella pneumophila in the etiology of CAP in the GCC region. Increasingly, other etiologies, particularly influenza viruses, varicella zoster virus and Mycobacterium tuberculosis, have been recognized as causative pathogens of CAP within the region. Rates of antimicrobial resistance of S. pneumoniae and other pathogens are rising in the Gulf Corporation Council (GCC) region and susceptibility profiles of antibiotics against intracellular pathogens such as Chlamydophila pneumoniae and Mycoplasma pneumoniae are not routinely performed. Injudicious prescribing and over-use of antibiotics drive much resistance. The GCC CAPWG calls for urgent governmental regulations to limit and monitor antibiotic prescription in the GCC region.
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PMID:Microbiology of community-acquired pneumonia in the Gulf Corporation Council states. 1807 66

Non-pathogenic mycobacteria, like Mycobacterium gordonae, are rarely associated to disease. The analysis of the mechanisms which are successful against them in the human host may provide useful information to understand why they fail against the pathogenic M. tuberculosis. We have developed an infection model to test the ability of human phagocytes to kill two strains of M. gordonae, HL184G and an attenuated variety, HL184Gat. As controls we included a strain of M. tuberculosis (HL186T) and another one of L. pneumophila (ATCC13151). We observed that human phagocytes lack the intrinsic ability to eliminate either M. gordonae or M. tuberculosis, but they can kill the attenuated strain. We found a relationship between pathogenicity and the pattern of cytokine production. Thus, both the pathogenic M. tuberculosis and Legionella pneumophila, but not the non-pathogenic M. gordonae, induced the production of significantly different levels of IL-1beta, IL-6 and TNF-alpha in monocytes and IL-8 in neutrophils. Although both monocytes and neutrophils killed HL184Gat, but not HL184G, the patterns of cytokine production induced by either strain were identical. Addition of INF-gamma and/or TNF-alpha did not enhance the antimycobacterial activity of phagocytes.
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PMID:Human phagocytes lack the ability to kill Mycobacterium gordonae, a non-pathogenic mycobacteria. 1816 Jan 7

Although Legionnaires' disease (LD) is frequently accompanied by pleural effusion, the characteristics of pleural effusions in LD have not been well studied. Levels of adenosine deaminase (ADA) activity in pleural fluid >40 IU/L have a high sensitivity (81-100%) and specificity (83-100%) for tuberculosis. ADA activity in pleural effusions due to LD has not been previously reported. The case of a patient with LD complicated by a pleural effusion with high ADA activity is reported. In countries where the prevalence of tuberculosis is high and pleural fluid ADA activities are frequently measured, LD should be included in the differential diagnosis of an exudative pleural effusion with high ADA activity.
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PMID:High adenosine deaminase activity in the pleural effusion of a patient with Legionnaires' disease. 1839 76

Antimicrobial activity in human monocytes infected with Mycobacterium tuberculosis has been difficult to demonstrate in vitro, and the molecular mechanisms allowing the bacteria to survive intracellularly are unknown. As a means to test the influence of bacterial products in the microbicidal activity of monocytes we have developed an infection model with Legionella pneumophila, which is killed by interferon gamma activated cells. We demonstrate that this model is useful because M. tuberculosis lysates inhibit one hundred fold the interferon gamma induced activity against L. pneumophila. Comparable degrees of inhibition are also detected when we use lysates from the less pathogenic Mycobacterium gordonae and the pathogenic Staphylococcus aureus, suggesting the participation of a common mechanism. This hypothesis is supported by the fact that the pattern of cytokine secretion is similar in all cases. A significant difference is, however, observed when we used lysates from the non-pathogenic Escherichia coli, which resulted in the recovery of low numbers of bacteria, probably because they induce the cell death of infected monocytes.
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PMID:Detection of inhibition of antimicrobial activity by mycobacterial lysates in human monocytes infected with Legionella pneumophila. 1843 33


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