Hostname: page-component-78c5997874-m6dg7 Total loading time: 0 Render date: 2024-11-03T00:03:05.519Z Has data issue: false hasContentIssue false

A comparison of virulence of two strains of Legionella pneumophila based on experimental aerosol infection of guinea-pigs

Published online by Cambridge University Press:  19 October 2009

R. I. Jepras
Affiliation:
Experimental Pathology Laboratory, Public Health Laboratory Service, Centre for Applied Microbiology and Research, Porton Down, Salisbury, Wiltshire, U.K.
R. B. Fitzgeorge
Affiliation:
Experimental Pathology Laboratory, Public Health Laboratory Service, Centre for Applied Microbiology and Research, Porton Down, Salisbury, Wiltshire, U.K.
A. Baskerville
Affiliation:
Experimental Pathology Laboratory, Public Health Laboratory Service, Centre for Applied Microbiology and Research, Porton Down, Salisbury, Wiltshire, U.K.
Rights & Permissions [Opens in a new window]

Summary

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Two strains of Legionella pneumophila (LP) serogroup I, of differing virulence, were examined in terms of numbers of viable organisms in tissues, pyrexia and mortality following aerosol infection. The Corby strain was the more virulent, with Pyrexia and deaths of guinea-pigs 3 to 6 days after infection. This strain multiplied very rapidly in the lungs to reach a peak of 5 × 1011 viable organisms/lung. Organisms were present in the blood, liver, spleen and kidney. The Philadelphia-1 strain (NCTC 11192) was unable to replicate in the lung and was cleared between 14 and 21 days after infection. Pyrexia was not observed. No guinea-pigs died and viable LP was not found in any organ other than the lung.

Lung lavages on aerosol infected animals were performed and the virulent Corby strain was found to be mainly intracellular. The avirulent Philadelphia-1 strain was found predominantly in the extracellular location. There were approximately 10 times the number of viable virulent LP in the lung macrophage fraction than in the lung PMNL fraction. In comparison, there were approximately equal numbers of the viable avirulent strain in the macrophages and the PMNL. Experimental evidence suggests that the macrophage preferentially supports the growth of the virulent Corby strain compared with the PMNL. The avirulent strain on the other hand appears to be destroyed by both the macrophages and the PMNL.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1985

References

REFERENCES

Baskerville, A., Dowsett, A. B., Fitzgeorge, R. B., Hambleton, P. & Broster, M. (1983). Ultrastructure of pulmonary alveoli and macrophages in experimental Legionnaires' Disease. Journal of Pathology 140, 7790.CrossRefGoogle ScholarPubMed
Baskerville, A., Fitzgeorge, R. B., Broster, M., Hambleton, P. & Dennis, P. J. (1981). Experimental transmission of Legionnaires' Disease by aerosol infection with Legionella. Lancet ii, 1389.Google Scholar
Bornstein, N., Nowicki, M. & Fleurette, J. (1984). Loss of virulence of Legionella pneumophila serogroup 1 with conversion of cells to long filamentous rods. In: Legionella: Proceedings of the 2nd International Symposium, pp. 7071. Washington, D.C.American Society for Microbiology.Google Scholar
Chandler, F. W., Blackmon, J. A., Hicklin, M. D., Cole, R. M. & Callaway, G. S. (1979). Ultrastructure of the agent of Legionnaires' disease in the human lung. American Journal of Clinical Pathology 71, 4350.CrossRefGoogle ScholarPubMed
Davis, G. S., Winn, W. C., Gump, D. W. & Beaty, H. N. (1983). The kinetics of early inflammatory events during experimental pneumonia due to Legionella pneumophila in guinea pigs. The Journal of Infectious Diseases 148, 823835.CrossRefGoogle ScholarPubMed
Druett, H. A. (1969). A mobile form of the Henderson apparatus Journal of Hygiene 67, 437448.CrossRefGoogle ScholarPubMed
Edelstein, P. H. (1981). Improved semiselective medium for isolation of L. pneumophila from contaminated clinical and environmental specimens. Journal of Clinical Microbiology 14, 298305.CrossRefGoogle ScholarPubMed
Fitzgeorge, R. B., Baskerville, A., Broster, M., Hambleton, P. & Dennis, P. J. (1983). Aerosol infection of animals with strains of Legionella pneumophila of different virulence: comparison with intraperitoneal and intranasal routes of infection. Journal of Hygiene 90, 8189.Google Scholar
Fitzgeorge, R. B. & Dennis, P. J. (1983). Isolation of Legionella pneumophila from water supplies: comparison of methods based on the guinea pig and culture media. Journal of Hygiene 91, 179187.CrossRefGoogle ScholarPubMed
Hambleton, P., Broster, M. G., Dennis, P. J., Henstridge, R., Fitzgeorge, R. & Conlan, J. W. (1983). Survival of virulent Legionella pneumophila in aerosols. Journal of Hygiene 90, 451460.CrossRefGoogle ScholarPubMed
Henderson, D. W. (1952). An apparatus for the study of airborne infection. The Journal of Hygiene 50, 5368.CrossRefGoogle Scholar
Hicklin, M. D., Thomason, B. M., Chandler, F. W. & Blackmon, J. A. (1980). Pathogenesis of acute Legionnaires' Disease pneumonia: immunofluorescent microscopic study. American Journal of Clinical Pathology 73, 480487.CrossRefGoogle Scholar
Horwitz, M. A. & Silverstein, S. C. (1980). The Legionnaires' disease bacterium (Legionella pneumophila) multiplies intracellularly in human monocytes. The Journal of Clinical Investigation 66, 441450.CrossRefGoogle Scholar
Lattimer, G. L. & Ormsbee, R. A. (1981). Legionnaires' Disease, p. 176. New York, Basel: Marcel Dekker.Google Scholar
MRC (1974). The acreditation and recognition schemes for supplies of laboratory animals. Medical Research Council Laboratory Animals Centre, Manual Series No. 1. Carshalton, Surrey.Google Scholar
Watts, J. C., Hicklin, M. D., Thomason, B. M., Callaway, B. S. & Levine, A. J. (1980). Fatal pneumonia caused by Legionella pneumophila, serogroup 3: demonstration of the bacilli in extrathoracic organs. Annals of Internal Medicine 92, 186188.CrossRefGoogle ScholarPubMed