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)

In acquired immunodeficiency syndrome (AIDS) the pulmonary opportunistic infections are due to the depression of cellular immunity and they are found in more than 50% of patients. Most frequently the infection is due to Pneumocystis carinii, Cytomegalovirus, Cryptococcus neoformans and Mycobacterium avium-intracellulare. Non-opportunistic infections in AIDS are mostly due to the Mycobacterium tuberculosis and Legionella pneumophila. In Kaposi sarcoma in AIDS the lungs may be involved into pulmonary manifestations of the syndrome. In this paper the diagnostics of pulmonary disturbances in AIDS is briefly evaluated together with the therapy of most frequent pulmonary infections.
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PMID:[Pulmonary manifestations in patients with AIDS]. 279 62

Certain types and causes of pneumonia are unique to the immunocompromised host. The most frequent causes are cytomegalovirus, Pneumocystis carinii, varicella zoster virus, Candida species and Aspergillus species. Lymphoid interstitial pneumonia has recently been recognized in children with the acquired immunodeficiency syndrome. With the exception of varicella-zoster pneumonitis, an invasive procedure, such as open lung biopsy, is required to establish a definitive diagnosis. Infrequent causes of pneumonitis in immunocompromised children include Toxoplasma gondii; Cryptosporidium; Herpes simplex; adenovirus, gram-negative bacillary infections (Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli, Legionella pneumophilia); Nocardia spp; zygomycetes, and Cryptococcus neoformans. The discovery of any of the aforementioned pneumonias suggests the patient may have a serious underlying immunodeficiency.
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PMID:Pneumonia in the immunocompromised child. 282 16

The acquired immunodeficiency syndrome (AIDS) is a devastating new disease caused by the human immunodeficiency virus (HIV). This retrovirus causes profound immunoincompetence in its infected hosts, who are thereafter susceptible to develop myriad severe and relapsing protozoal, fungal, bacterial, viral, and arthropodal opportunistic infections, as well as unusual malignancies. The more than 50,000 patients who have developed AIDS in the United States have produced a sudden unexpected deluge of diagnostic dilemmas that are stressing laboratories of pathology everywhere. This paper describes the gross and microscopic pathology of the numerous complications in patients infected by HIV: (a) the prodromal AIDS-related complex with persistent generalized lymphadenopathy, (b) lymphoid infiltration of salivary gland and lung, including the complex of lymphoid interstitial pneumonitis-pulmonary lymphoid hyperplasia, (c) extranodal non-Hodgkin's lymphomas, (d) multifocal mucocutaneous and visceral Kaposi's sarcoma, (e) small cell undifferentiated (oat cell) carcinomas, (f) protozoal infections caused by Pneumocystis carinii, Toxoplasma gondii, Acanthamoeba, Cryptosporidium species (sp.), and Isospora belli, (g) the causes of chronic enteritis, (h) mycotic infections caused by Candida sp., Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis, and Sporothrix schenckii, (i) bacterial infections caused by Mycobacterium avium-intracellulare, M. tuberculosis, M. kansasii, Nocardia sp., Listeria monocytogenes, Legionella sp., Treponema pallidum, and others, (j) viral infections caused by cytomegalovirus, herpes simplex and zoster, polyomavirus (progressive multifocal leukoencephalopathy), hepatitis B, molluscum contagiosum, and papillomavirus, (k) oral hairy leukoplakia, (l) subacute encephalopathy, and (m) Norwegian scabies.
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PMID:The pathology of AIDS. 283 78

We describe 3 patients with simultaneous infection by Cryptococcus neoformans and Legionella pneumophila. Legionnaires' disease (pneumonia) occurred shortly after onset of cryptococcal meningitis in a cardiac transplant patient receiving ciclosporin, a second patient with chronic lymphocytic leukemia and a third patient with Hodgkin's disease and autoimmune hemolytic anemia. Defects in cell-mediated immunity have been identified in patients with hematologic malignancies and in those who have received organ transplants. Clinical and experimental data suggest that the primary host defense mechanism against cryptococcal and Legionella infection involves cell-mediated immunity. Thus, the simultaneous occurrence of cryptococcal and L. pneumophila infection in these 3 patients supports experimental studies which have demonstrated common host defense mechanisms against both pathogens.
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PMID:Simultaneous infection with Cryptococcus neoformans and Legionella pneumophila. In vivo expression of common defects in cell-mediated immunity. 329 33

Pulmonary infections are a significant cause of morbidity after liver transplantation; Gram-negative bacilli, cytomegalovirus, and Pneumocystis carinii were the usual pulmonary pathogens in the earlier studies in liver transplant recipients receiving cyclosporine. We prospectively assessed the impact of pulmonary infection in 101 consecutive liver transplant recipients receiving the new immunosuppressive agent tacrolimus (FK506). Fifteen percent (15/101) of the patients had 19 episodes of pneumonia; 58% (11/19) of the pneumonias were bacterial, 37% (7/19) were fungal, and 5% (1/19) were protozoal (Toxoplasma gondii). Twenty-seven percent of the bacterial pneumonias were due to Legionella. None of the patients had cytomegalovirus or P carinii pneumonia. Seven percent (7/10) of the study patients had fungal pneumonitis; 4% had invasive aspergillosis and 3% had cryptococcosis. Mortality was significantly higher (53%, 8/15) for patients with pneumonia than for patients without pneumonia (10%, 9/86, P = 0.0004). Only fungal pneumonias were the direct cause of death; 63% (5/8) of the deaths were in patients with fungal pneumonitis. Our data suggest a changing pattern of microbial etiologies of pneumonitis in the era of modern immunosuppressive agents. We show that P carinii pneumonia and cytomegalovirus can be effectively curtailed with appropriate prophylaxis. Fungal infections, on the contrary, not only constituted a major proportion of the pneumonia, but also carried the highest pneumonia-associated mortality. Legionella infections can be overlooked unless specialized laboratory methodology (cultured on selective media, urinary antigen) are applied routinely on all cases of pneumonia. We recommend routine culture on the water supply for Legionella in all transplant centers.
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PMID:Pulmonary infections in liver transplant recipients receiving tacrolimus. Changing pattern of microbial etiologies. 861 Mar 49

Mycobacterium tuberculosis is one of the intracellular parasitic bacteria escaping the intracellular killing inside macrophages. The aim of this symposium was to get some insight into the mechanism of pathogenicity and host defense in M. tuberculosis infection, which has not yet been elucidated well, by the presentation of up-to-date knowledge on these aspect in infection with different intracellular parasitic microbes. Dr. Yoshikai (Nagoya Univ.) indicated that TLR is involved in the initial response of host against S. choleraesuis. Among the cytokines contributing to the induction of specific immunity, the importance of IL-15 was emphasized, based on their own experimental data using IL-15 transgenic mice and the application of anti-IL-15 antibody in vivo. Dr. Yoshida (Kyushu Univ.) reviewed the mechanisms of intracellular growth of Legionellae. Several genes so far identified as essential genes in intra-macrophage growth appeared to be similar to those encoding type 3 secretion system observed in Shigellae. There is a significant strain difference in the growth of L. pneumophila inside macrophages and such difference seemed to be under the control of a gene at chromosome 13, Lgn 1. The investigation of difference in the mode of escape among various Legionella. spp. may provide a novel mechansim in bacterial invasion and escape. Dr. Kawamura (Kyoto Univ.) summarized some new reports on the molecular mechanism of the inhibition of P-L fusion by M. tuberculosis. He emphasized the importance of the alteration in phagosomal maturation as indicated by the accumulation of TACO protein. The possible involvement of TLR in the recognition of Mycobacterial cells and its LAM was discussed. Dr. Kawakami (Ryukyu Univ.) first discussed the possibility that Cryptococcus neoformans, a fungal pathogen, could be regarded as one of the intracellular parasitic microbes. His presentation mainly focused on the TH1-Th2 balance in the expression of host defense against C. neoformans in mice. From their experimental infection using attenuated strain TC-13 in various cytokine-knock out mice, the pivotal role of both IL-12 and IL-18 was clearly indicated.
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PMID:[Mechanisms of pathogenicity and host defense in infections by intracellular parasitic microbes]. 1106 72

Damage to local and systemic host defenses of the lung makes the immunocompromised patient vulnerable to inhaled microorganisms. When a pulmonary infiltrate occurs, the array of possibilities is very large including conventional and opportunistic agents. The type of underlying disease and its associated immunodeficiency allow a high degree of accurate pathogen prediction. Neutropenia is associated with Gram-negative bacilli pneumonia. Prolonged neutropenia increases the risk of invasive aspergillosis and other unusual mycotic agents. Cellular immunodeficiency is associated with intracellular microorganisms including Mycobacteria spp., Nocardia spp., Legionella spp., Rhodococcus equi, cytomegalovirus, Strongyloides stercoralis, Toxoplasma gondii, Histoplasma capsulatum, Coccidioides spp., Cryptococcus neoformans and Pneumocystis carinii, parasites such as Toxoplasma gondii and Strongyloides stercoralis, and virus such as cytomegalovirus, Herpes simplex or zoster, adenovirus, respiratory syncitial virus and measles. Humoral immunodeficiency predisposes to infection with encapsulated pathogens such as S. pneumoniae and Haemophilus influenzae. Chest computerized tomography scan and bronchoalveolar lavage are essential procedures for diagnosis. However, despite continuous progress in diagnostic methods, the specific etiology remains often unknown. Successful treatment depends on the type of pathogen, status of host defences and early adequate choice of antibiotic. Enhancement of host defences with growth factors and cytokines may decrease the incidence and improve the final outcome of respiratory infections in the immunocompromised host.
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PMID:[Respiratory infections during chemotherapy-induced aplasia]. 1142 9

Free-living amoebae feed on bacteria, fungi, and algae. However, some microorganisms have evolved to become resistant to these protists. These amoeba-resistant microorganisms include established pathogens, such as Cryptococcus neoformans, Legionella spp., Chlamydophila pneumoniae, Mycobacterium avium, Listeria monocytogenes, Pseudomonas aeruginosa, and Francisella tularensis, and emerging pathogens, such as Bosea spp., Simkania negevensis, Parachlamydia acanthamoebae, and Legionella-like amoebal pathogens. Some of these amoeba-resistant bacteria (ARB) are lytic for their amoebal host, while others are considered endosymbionts, since a stable host-parasite ratio is maintained. Free-living amoebae represent an important reservoir of ARB and may, while encysted, protect the internalized bacteria from chlorine and other biocides. Free-living amoebae may act as a Trojan horse, bringing hidden ARB within the human "Troy," and may produce vesicles filled with ARB, increasing their transmission potential. Free-living amoebae may also play a role in the selection of virulence traits and in adaptation to survival in macrophages. Thus, intra-amoebal growth was found to enhance virulence, and similar mechanisms seem to be implicated in the survival of ARB in response to both amoebae and macrophages. Moreover, free-living amoebae represent a useful tool for the culture of some intracellular bacteria and new bacterial species that might be potential emerging pathogens.
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PMID:Microorganisms resistant to free-living amoebae. 1508 8

The haploid social soil amoeba Dictyostelium discoideum has been established as a host model for several pathogens including Pseudomonas aeruginosa, Cryptococcus neoformans, Mycobacterium spp. and Legionella pneumophila. The research areas presently pursued include (i) the use of Dictyostelium wild-type cells as screening system for virulence of extracellular and intracellular pathogens and their corresponding mutants, (ii) the use of Dictyostelium mutant cells to identify genetic host determinants of susceptibility and resistance to infection and (iii) the use of reporter systems in Dictyostelium cells which allow the dissection of the complex host-pathogen cross-talk. The body of information presented in this review demonstrates that the availability of host cell markers, the knowledge of cell signalling pathways, the completion of the genome sequencing project and the tractability for genetic studies qualifies Dictyostelium for the study of fundamental cellular processes of pathogenesis.
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PMID:Dictyostelium as host model for pathogenesis. 1567 34

Dictyostelium discoideum is a molecularly amenable host model system for several human pathogens, including Legionella pneumophila, Mycobacterium avium, Mycobacterium marinum, Pseudomonas aeruginosa, and Cryptococcus neoformans. Dictyostelium wild-type cells have proven useful in screening and identifying numerous bacterial und fungal virulence factors. Moreover, Dictyostelium mutant cells can be used to identify genetic host determinants of susceptibility and resistance to infections. Marker genes such as the green fluorescence protein (GFP) gene allow the in vivo monitoring of infection-relevant host factors. Here, we present methods that have already contributed to the deciphering of important aspects of the Dictyostelium-Legionella interaction. Moreover, the described phagocytosis assay, infection assay, and the confocal in vivo monitoring of GFP-tagged host factors can easily be adapted to other host-pathogen interactions.
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PMID:Dictyostelium discoideum as a model to study host-pathogen interactions. 1695 11


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