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

The presumed route of human infection by Legionella pneumophila is inhalation. We investigated possible oral transmission of legionellosis in guinea pigs. Fifty-six guinea pigs (group 1) were given virulent L. pneumophila, serogroup 1, in drinking water. Fifty-nine guinea pigs (group 2) were inoculated with L. pneumophila via gastric intubation. Nineteen guinea pigs (group 3) were given heat-killed L. pneumophila in drinking water. Twenty-four guinea pigs (group 4, positive control) were inoculated intraperitoneally with L. pneumophila. Twenty-seven guinea pigs (group 5, negative control) were either intubated gastrically with phosphate-buffered saline or given drinking water without L. pneumophila. Sixty-six of 115 (57%) of the guinea pigs orally inoculated with viable L. pneumophila (groups 1 and 2) had a temperature greater than or equal to 103 degrees F and 8 of 115 (7%) had diarrhea, compared with 0 of 19 (0%) and 0 of 19 (0%), respectively, in group 3 and 1 of 27 (4%) and 0 of 27 (0%), respectively, in group 5. There were no fatalities in groups 1, 2, 3, and 5 compared with 15 of 24 (63%) in group 4. Groups 1, 2, and 4 consistently showed pneumonitis and splenitis. The pneumonitis of groups 1 and 2 was mild, predominantly interstitial, and mainly composed of macrophages; neither gross nor microscopic evidence of aspiration was seen. In group 1, 4 of 29 (14%) guinea pigs tested seroconverted to L. pneumophila compared with 0 of 7 (0%) in group 3 and 0 of 10 (0%) in group 5. In groups 1 and 2 combined, L. pneumophila was isolated from the lung of 5 of 57 (11%) guinea pigs and spleen of 5 of 47 (11%) guinea pigs compared with 0 of 14 guinea pigs in group 5. We conclude that viable L. pneumophila administered orally produces a self-limited febrile illness in guinea pigs.
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PMID:A self-limited febrile illness produced in guinea pigs associated with oral administration of Legionella pneumophila. 318 81

The guinea pig is the most widely used animal model in the study of Legionellosis. The hamster should also be considered, since it acquires virtually no spontaneous epidemic lung infection, possesses similar cellular immune components observed in other mammals, has a normal body temperature identical to that of man, and is readily available for laboratory investigation. We studied the pathologic findings of four 12 week old inbred London School of Hygiene (LSH) hamsters inoculated intraperitoneally with 0.2 ml of 10(9) organisms per ml suspension of a viable Philadelphia 1 strain of Legionella pneumophila. Four LSH hamsters (control group) received 0.2 ml of sterile phosphate buffered saline, intraperitoneally. All animals of the test group became clinically ill and two of the four spontaneously expired on days 1 and 2 after inoculation. The remainder were sacrificed on day 3. In three out of four animals of the test group, a suppurative peritonitis and an interstitial pneumonitis were observed. It was characterized by infiltrates of neutrophils and macrophages. The test group also exhibited acute splenitis, including microabscesses, and two of four test animals showed hepatic congestion, vacuolization of hepatocytes, and microabscesses. None of the controls appeared sick or died after three days, and neither gross nor microscopic lesions were found at autopsy. Culture results documented L pneumophila in lung and spleen of all test animals and the absence of organisms in the control group. Hence, the LSH hamster is rapidly infected with the Philadelphia 1 strain of L pneumophila given intraperitoneally, and pathological changes can be readily observed. The findings of our study add hamsters to the list of animals susceptible to intraperitoneal infection by L pneumophila.
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PMID:Susceptibility of LSH hamsters to intraperitoneal inoculation with Legionella pneumophila. 394 31

We have described the ultrastructural morphology of splenic and pulmonary exudates from guinea pigs infected intranasally and intraperitoneally by Legionella pneumophila. Legionella pneumophila produced pneumonia and splenitis by both routes of inoculation. The microbe was also disseminated to other organs. Within neutrophils, Legionella pneumophila typically displayed degenerating forms, suggesting that this intracellular environment is somewhat hostile to the bacterium. By contrast, macrophages tended to contain intact forms, located within organelles morphologically identical with rough endoplasmic reticulum. Some bacteria were replicating at this site. In macrophages containing greater than 25 microbes per section, Legionella pneumophila was usually dispersed within the cytoplasm outside of organelles, and many of the heavily infected macrophages exhibited ultrastructural features of injury. Neutrophils phagocytosed Legionella pneumophila, but we found no ultrastructural evidence of either ingestion of Legionella pneumophila by macrophages or of localization of the microbe to primary or secondary phagosomes of macrophages. Our findings support the contention that Legionella pneumophila is an intracellular parasite of macrophages. The homing of Legionella pneumophila to cytoplasmic organelles morphologically indistinguishable from rough endoplasmic reticulum has no bacteriologic parallel. It remains to be determined how Legionella pneumophila enters this organelle, whether this structure is, in fact, functional rough endoplasmic reticulum and whether this site is actively involved in replication of the bacterium. The animal models used herein seem suitable for further delineation of these questions.
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PMID:Electron microscopic examination of the inflammatory response to Legionella pneumophila in guinea pigs. 705 88