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

The interaction between normal cynomolgus monkey alveolar macrophages and Legionnaires disease bacteria was studied by transmission electron microscopy. After ingestion of Legionnaires disease bacteria, the organisms replicated within macrophages and destroyed the phagocytic cell.
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PMID:In vitro interaction between normal cynolmolgus monkey alveolar macrophages and Legionnaires disease bacteria. 11 92

A high-molecular-weight surface component (F-1 fraction) has been isolated from the four serogroups of Legionella pneumophila. Antibody raised against live organisms was found by microagglutination assay to be specific for the homologous serogroup. Agglutinating activity of antiserum was markedly diminished after absorption with the homologous, but not heterologous, F-1 fraction. In addition, it was found that L. pneumophila organisms were not interiorized by rat alveolar macrophages or mouse peritoneal macrophages in the absence of antiserum, whereas homologous antiserum effectively opsonized the organisms. The opsonizing activity of serogroup-specific antisera was eliminated by absorption of the antisera with the homologous, but not heterologous, F-1 fraction. These data indicate that the serogroup-specific antigen of L. pneumophila resides in the F-1 fraction and that antibody to the F-1 fraction is required for phagocytosis of L. pneumophila by mammalian phagocytes.
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PMID:Serospecificity and opsonic activity of antisera to Legionella pneumophila. 12 Nov 14

We obtained four bacterial isolates from patients with Legionnaires' disease and examined them for in-vitro and in-vivo fine-structure characteristics. All isolates had an outer membrane, cytoplasmic membrane, and intracellular membrane structure. Numerous intracellular inclusions were seen, particularly from in-vivo specimens, and appeared membrane-limited. Fine-structure analysis did not reveal the presence of a definitive peptidoglycan structure. Isolation, purification, and chemical analysis of Legionnaires' disease bacterium pepdoglycan established molar ratios of alanine-glutamic acid and muramic acid-glucosamine. Diaminopimelic acid was absent in the Legionnaires' disease bacterium peptidoglycan. The Kellenberger procedure for fixation appears to be the best method for the fine-structure determination of Legionnaires' disease bacteria.
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PMID:Fine structure of the Legionnaires' disease bacterium. In-vitro and in-vivo studies of four isolates. 21 38

The investigation of Legionnaires' disease was riddled with problems, and as a result, was largely ineffective. But the lesions it taught can be extremely valuable to future public-health efforts if they are heeded. This chapter has attempted to highlight those problems and offer some possible solutions. It is now up to the public-health hierarchy to use what is offered in these pages to spark the building of programs and systems that provide the level of effectiveness the American people have a right to expect from public-health departments. Finally, it was my intent to raise questions about the Center for Disease Control's new organism. The Center may, indeed, have found the responsible agent. We must not, however, allow ourselves to have tunnel vision in the continuing investigation--switching to other possibilities only if the microorganism theory is exhausted. The evidence and remaining questions demand a broader scope of investigation. How tragic it will be if we have not learned from the inflexibility and narrowness of the 1976 investigation of Legionnaires' disease.
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PMID:The "missing" investigation of Legionnaires' disease. 22 64

The susceptibility of the Legionnaires disease bacterium to various antimicrobial agents was determined by inoculation of embryonated eggs via the yolk sac. When administered prophylactically, the minimal dose of drug preventing all deaths due to the infection was as follows: rifampin, 0.02 mg; gentamicin, 0.25 mg; streptomycin, 0.39 mg; erythromycin, 0.62 mg; sulfadiazine, 1.56 mg; chloramphenicol, 2.50 mg; and cephalothin, 20.0 mg. Smaller amounts delayed deaths, and larger or equal amounts rendered the embryos free of infection. Oxytetracycline in the largest tested amount, 5.0 mg, protected 80% of the embryos from death, and as little as 0.31 mg delayed death. Chlortetracycline (0.50 mg) and ampicillin (10.0 mg) were ineffective. The six most effective drugs were studied in an experiment in which they were administered at various times after infection in doses that were twice the minimal prophylactic dose preventing all deaths. In this therapeutic experiment, rifampin, and erythromycin allowed 100% survival when given even 72 h after infection; gentamicin, streptomycin, sulfadiazine, and chloramphenicol did so when given 48 h after infection. All six drugs increased mean survival time when administered 72 h after infection.
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PMID:In vivo susceptibility of the Legionnaires disease bacterium to ten antimicrobial agents. 26 85

Beta-lactam-inactivating activity has been found in all sero-groups of Legionella pneumophila. The beta-lactamase activity could be detected in intact cells and released by ethylenediaminetetraacetic acid treatment, indicating that it is located in the periplasmic space. The enzyme acted primarily as a cephalosporinase hydrolyzing cefamandole, cephalothin, cephaloridine, and also penicillin G and ampicillin. Cefoxitin and cefuroxime were not hydrolyzed. Clavulanic acid and CP-45,899, beta-lactamase inhibitors, prevented the hydrolysis of cephalosporins and penicillins. The beta-lactamase activity appears to be different from that found in Enterobacteriaceae and Pseudomonas.
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PMID:Inactivation of beta-lactam antibiotics by Legionella pneumophila. 31 86

To identify the etiologic agent of Legionnaire's disease, we examined patients' serum and tissue specimens in a search for toxins, bacteria, fungi, chlamydiae, rickettsiae and viruses. From the lungs of four of six patients we isolated a gram-negative, non-acid-fast bacillus in guinea pigs. The bacillus could be transferred to yolk sacs of embryonated eggs. Classification of this organism is incomplete. We used yolk-sac cultures of the bacillus as antigen to survey suspected serum specimens, employing antihuman-globulin fluorescent antibody. When compared to controls, specimens from 101 to 111 patients meeting clinical criteria of Legionnaires' disease showed diagnostic increases in antibody titers. Diagnostic increases were also found in 54 recent sporadic cases of severe pneumonia and, retrospectively, in stored serum from most patients in two other previously unsolved outbreaks of respiratory disease. We conclude that Legionnaires' disease is caused by a gram-negative bacterium that may be responsible for widespread infection.
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PMID:Legionnaires' disease: isolation of a bacterium and demonstration of its role in other respiratory disease. 33 45

A patient with Legionnaires' disease developed consolidated pneumonia with severe hypoxemia and mental confusion; his condition improved with therapy with positive end-expiratory pressure, steroids, and chloramphenicol. The retrospective diagnosis was made by a fourfold rise in indirect fluorescent antibody titers. The chest x-ray films showed bilateral alveolar infiltrates and air bronchograms.
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PMID:Legionnaires' disease. A sporadic case. 34 Jan 53

The first case of Legionnaires' disease recognized in Pennsylvania since the Philadelphia epidemic of 1976 was that of a 53-year-old emphysematous man who had extensive unilateral pneumonia accompanied by high fever, hypoxemia, and disorientation. His illness progressed despite treatment with cephalothin, but he recovered coincident with the administration of gentamicin and erythromycin. The diagnosis was established serologically by a 32-fold rise in antibody titer to the agent of Legionnaires' disease. Similar illness did not affect others in his community, and infection in four family members was excluded clinically and serologically.
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PMID:Sporadic Legionnaires' disease. 34 Jul 16

Thirty-two confirmed and 24 highly probable cases of Legionnaires' disease occurred in Vermont between May 1 and Oct 15, 1977. Confirmed cases had positive results for direct fluorescent antibody testing of lung tissue or fourfold rise in antibody titer. Highly probable cases had one elevated titer (greater than or equal to 1:256) and a compatible illness. Forty-eight (86%) had underlying chronic disease, and 22 (39%) were immunocompromised. Prominent early symptoms were fever, cough, chills, and malaise. All but one patient had verified pneumonia. Courses ranged from a pneumonia not requiring hospitalization to respiratory failure necessitating support with mechanical ventilation. Seventeen patients died. Although the clinical presentation was variable, rapid development of high fever and leukocytosis together with negative cultures of lower respiratory tract secretions strongly suggested the diagnosis in an epidemic setting.
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PMID:Legionnaires' disease in Vermont, May to October 1977. 35 Dec 19


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