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)

Two different monoclonal antibodies directed against Legionella micdadei and L. dumoffii (Genetic Systems Corp., Seattle, Wash.) were evaluated for their specificity and ability to detect L. micdadei and L. dumoffii in human and animal clinical samples and bacterial isolates in an indirect immunofluorescence assay. All three frozen sputum samples and all three Formalin-fixed sputum and liver samples from patients with culture-documented L. micdadei pneumonia were positive when tested with the L. micdadei monoclonal antibody. A Formalin-preserved lung sample from a patient with culture-documented L. dumoffii pneumonia was positive with its homologous monoclonal antibody. No cross-staining reactions were found with either monoclonal antibody on any of 25 human sputum samples tested from patients without Legionella infections. A total of 66 Legionella strains and 56 non-Legionella strains including 22 Pseudomonas strains and 34 other bacterial strains were studied. No cross-staining reactions were found except in Staphylococcus aureus Cowan 1 ATCC 12598. The lower limit of detection in seeded sputum samples was about 7 X 10(4) cells per ml for both monoclonal antibodies. Lung and tracheal lavage specimens from L. micdadei- or L. dumoffii-infected guinea pigs showed specific staining only with their respective monoclonal antibodies. The monoclonal antibodies stained homologous bacteria slightly less intensely than did the polyclonal antisera, but the signal-to-noise ratio was considerably higher for the monoclonal antibodies. No differences in sensitivity of staining of clinical specimens or bacterial isolates were noted between the monoclonal antibodies and the polyclonal reagents for L. micdadei and L. dumoffii (Centers for Disease Control, Atlanta, Ga., and BioDx, Denville, N.J. These monoclonal antibodies ae sensitive and specific, making them good candidates for laboratory diagnostic purposes.
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PMID:Legionella micdadei and Legionella dumoffii monoclonal antibodies for laboratory diagnosis of Legionella infections. 332 84

Nosocomial pneumonia caused by legionella is an increasingly recognized entity. Legionella sp responsible for documented nosocomial disease include Legionella pneumophila, Tatlockia micdadei, Legionella bozemanii, Legionella dumoffi and Legionella oakridgensis. The clinical presentation is nonspecific although diarrhea occurs frequently. Hyponatremia occurs significantly more frequently in legionnaires' disease than pneumonias caused by other agents. Chest roentgenographic findings are nonspecific, although cavitation can be seen in immunosuppressed patients. Laboratory methods require the use of direct fluorescent antibody (DFA) stains, culture using selective media, serologic testing, and detection of antigen in urine. The DFA test is not sensitive; however, it does correlate with the severity of disease. Culture from sputa is now feasible. Bronchoalveolar lavage is a promising technique for obtaining specimens. The ideal specimen for culture is that obtained by transtracheal aspiration, which bypasses oropharyngeal contamination. Combination therapy of erythromycin and rifampin is recommended for selected patients. Because the source of the organism is the hospital water distribution system, we recommend routine environmental surveillance, especially in hospitals in which organ transplants are performed. The role of cooling towers as a vector for dissemination of the organism is disputed. Disinfection of the water supply can be accomplished by using heat eradication. Chlorination has generally proven unsatisfactory because of organism persistence as well as corrosive damage to the plumbing system from the chlorine. Both physician awareness and availability of specialized laboratory testing are necessary for the detection of cases.
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PMID:Legionella species as hospital-acquired respiratory pathogens. 332 Dec 65

Of the Legionellaceae family, Pittsburgh pneumonia agent (Tatlockia micdadei, Legionella micdadei) is second only to Legionella pneumophila in causing human pneumonia. In nosocomial infection, the patients tend to be immunosuppressed. The clinical presentation is nonspecific, although in immunosuppressed hosts the presentation may mimic that of pulmonary embolus (pleuritic chest pain, nonproductive cough, pleural-based densities on chest rontgenogram). The reservoir for the organism is water, and prevention of nosocomial infections can be accomplished by disinfection of the water supply. Diagnosis is best established by isolation of the organism from respiratory secretions by using selective, dye-containing buffered charcoal-yeast extract agar. The organisms can be acid-fast when clinical specimens are stained. Erythromycin is the antibiotic of choice, although tetracyclines, trimethoprim-sulfamethoxazole, and rifampin have also proved to be efficacious.
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PMID:Infections caused by the Pittsburgh pneumonia agent. 332 96

Guinea pigs develop a lethal pneumonia after intratracheal infection with Legionella micdadei, and the lung displays pathological changes similar to those observed in humans. To investigate the role of the resident alveolar macrophage in the pathogenesis of L. micdadei pneumonia, guinea pig alveolar macrophages obtained by bronchoalveolar lavage were cultured in vitro and infected with L. micdadei. In the absence of opsonins L. micdadei was phagocytized by, and multiplied within, alveolar macrophages with greater than a 100-fold increase in cell-associated colony forming units over 20 h. L. micdadei opsonized with complement or antibody multiplied within alveolar macrophages at the same rate as unopsonized bacteria. Guinea pigs which were treated with antimicrobials after infection with L. micdadei and recovered from the pneumonia were immune to challenge with an otherwise lethal inoculum of L. micdadei. However, the growth curve of both unopsonized and opsonized L. micdadei in the alveolar macrophages from immune animals was essentially identical to that in macrophages from susceptible animals. Thus, the resident alveolar macrophage is not capable of limiting the growth of Legionella. Rather, the alveolar macrophages appear to be the primary site of Legionella multiplication within the lung. Although alveolar macrophages may participate in other aspects of pulmonary immunity to the legionellae, these data indicate that the alveolar macrophage alone does not act as an effector cell in cell-mediated immunity to Legionella.
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PMID:Role of the alveolar macrophage in host defense and immunity to Legionella micdadei pneumonia in the guinea pig. 350 55

This study was undertaken to determine the frequency of Legionella infection in a dental clinic setting. Serum samples from 270 dental clinic personnel were evaluated using an enzyme-linked immunosorbent assay to detect Legionella-specific IgM and IgG antibodies. The pooled-species whole-cell-antigen preparation used in these assays was derived from six Legionella pneumophila strains and one strain each from Legionella bozemanii and Legionella micdadei. Significant levels of IgG and IgM antibodies were found in 20% and 16%, respectively, of the samples. This compares with 8% and 10%, respectively, for a randomly selected non-clinical group from the region (P less than 0.005). Samples from clinic personnel with significant IgG titers (greater than 1:128) were also evaluated for activity to each of the eight single-species antigens, with the following results: L. pneumophila, 45% (combined six strains); L. micdadei, 37%; and L. bozemanii, 18%. Comparing individuals' "years spent in the clinic environment" with the incidence of significant antibody levels strongly suggests that the risk of Legionella infection increases proportionately with increased clinic exposure time (P less than 0.05). Analysis of these data implies that Legionella may be present in the dental clinic environment, thus creating an increased risk for clinical personnel or patients.
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PMID:Prevalence of Legionella-specific IgG and IgM antibody in a dental clinic population. 386 49

Genetic exchange mechanisms, to our knowledge, have not been reported for Legionella pneumophila, and consequently, studies on the genetic organization of L. pneumophila have not appeared in the literature. Here, we describe gene transfer mediated by broad host range conjugative plasmids in Legionella spp. Escherichia coli strains carrying plasmids RP1 and R68.45 (IncP1), S-a (IncW), and R40a (IncC), but not plasmids of incompatibility groups FI, FII, and FV, served as donors in matings with L. pneumophila Knoxville 1 (LPK-1). Transconjugants selected by resistance to kanamycin (RP1, R68.45, and S-a) and carbenicillin (R40a) were observed at frequencies of 6.6 X 10(-3), 4.7 X 10(-3), 2.2 X 10(-4), and 5.4 X 10(-5), respectively. Plasmid transfer was not affected by DNase added to the mating medium. After plasmid transfer, LPK-1 stably maintained RP1, R68.45, and S-a, but not R40a. Plasmid-containing LPK-1 isolates also served as donors in agar plate matings with E. coli W1485-1 and naladixic acid-resistant mutants of LPK-1, Legionella micdadei, and Legionella longbeachii. Recombinational exchange of a chromosomal trait was demonstrated when a thymidine auxotroph of L. pneumophila was repaired by R68.45-mediated chromosomal mobilization of a prototrophic donor strain.
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PMID:Conjugation-mediated genetic exchange in Legionella pneumophila. 388

Specimens from 490 patients with suspected legionellosis from many parts of New Zealand were studied. Most of these were sera, but 36 specimens including material from lungs, pleural fluid and sputa were also examined. The sera were tested for the presence of antibodies to Legionella pneumophila serogroups 1 to 6 and Legionella micdadei. Serological evidence of legionellosis was found in 49 patients. Antibodies to L. pneumophila serogroup 6 predominated, while those to L. micdadei and L. pneumophila serogroup 1 were noted in smaller numbers. Antibodies to serogroups 2, 3, 4 and 5 of L. pneumophila were not often encountered.
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PMID:Serological studies on patients with suspected legionellosis in New Zealand. 389 43

Sediment and indigenous microflora taken from water distribution systems has been shown to promote the survival of Legionella pneumophila. The effect of sediment and indigenous microflora on Tatlockia micdadei (Pittsburgh pneumonia agent, PPA) was evaluated by growth curve experiments. Symbiosis between PPA and environmental bacteria was demonstrated by satellitism experiments. Unlike L. pneumophila, the concentration of PPA remained stationary in test tube suspensions containing both microflora and sediment. The difference in the ecology between the two organisms may explain the infrequent environmental recovery of PPA and, ultimately, the epidemiologic differences between Legionnaires disease and Pittsburgh pneumonia.
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PMID:Tatlockia micdadei (Pittsburgh pneumonia agent) growth kinetics may explain its infrequent isolation from water and the low prevalence of Pittsburgh pneumonia. 401 89

Mild diarrhea of poorly documented volume is common early in the course of Legionella infection. We report massive diarrhea of 1.8 to 3 liters per day in a patient with pneumonia in whom Legionella micdadei was isolated from pleural fluid and infection was confirmed serologically. The large volume of diarrhea, not previously associated with Legionella infection, remained unexplained despite clinical evaluation and postmortem study of the gastrointestinal tract. This case expands the clinical spectrum of Legionnaires' disease to include massive diarrhea, which in our patient constituted the chief complaint.
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PMID:Massive diarrhea in Legionella micdadei pneumonitis. 408 49

Both legionnaires' disease and pneumonia caused by Pittsburgh pneumonia agent (PPA) are endemic in the Veterans Administration Medical Center, Pittsburgh. 85% of cases of legionnaires' disease and 100% of the cases of PPA were acquired in hospital. A selective dye-containing medium which allows visual discrimination of Legionella pneumophila and PPA has been used in a large-scale environmental survey of the hospital. Samples from 53 sites, including hot-water storage tanks, showerheads, mixing valves, and taps from 19 wards, were cultured. PPA was isolated from 2 sites and L. pneumophila from 33 sites. Water from a tap in the surgical intensive-care unit yielded 6 colony-forming units (CFU) of PPA/0.1 ml and 300 CFU of L. pneumophila/0.1 ml after centrifugation. Water from the outlet valve of a hot-water storage tank yielded 10 CFU of L. pneumophila/0.1 ml and when concentrated by centrifugation also yielded 2 CFU of PPA/0.1 ml. PPA and L. pneumophila share the same environmental niche, but isolation of PPA is more difficult. It seems that the reservoir for PPA in the VA Medical Center is the hot-water distribution system. PPA and L. pneumophila were simultaneously isolated from the lung tissue of a patient in this hospital who died of hospital-acquired pneumonia; this finding supports the hypothesis of a common reservoir and mode of transmission for the two organisms.
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PMID:Potable water supply as the hospital reservoir for Pittsburgh pneumonia agent. 612 Nov 39


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