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Association of PPLO infection and antibody response in rats and mice

Published online by Cambridge University Press:  15 May 2009

Ruth M. Lemcke
Ruth M. Lemcke
Affiliation:
The Lister Institute of Preventive Medicine, London, S.W. 1
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By means of a complement-fixation test of the sera of laboratory rats and mice, the immunological response of these animals to both naturally occurring and induced PPLO infections was determined, and the presence and extent of infection in the animals determined by culture.

PPLO antibodies specific for the infecting strain were demonstrable in rats and mice from which PPLO were isolated.

The amount of serum antibody rises with the extent and severity of the infection. Thus, young rats with PPLO infections confined to the nasopharynx had little or no antibody whereas the oldest rats with consolidated lungs had the highest titres. In mice too, the sera of those with pneumonia had the highest titres.

The comparatively low titres found in rat bronchiectasis together with the failure to isolate PPLO from the spleen and other organs, suggest that the chronic form of the disease remains localized. This is in contrast to infections with rat polyarthritis and related PPLO in which the organisms can be isolated from the lymph nodes and other organs and in which antibody is present in high titre.

In view of the high degree of correlation between the presence of antibodies to PPLO in the blood and the presence of PPLO in the tissue of rats and mice, it is suggested that specific antibody found in man is a significant indicator of PPLO infection.

Type
Research Article
Information
Journal of Hygiene , Volume 59 , Issue 4 , December 1961 , pp. 401 - 412
Copyright
Copyright © Cambridge University Press 1961

References

Card, D. H. (1959). Brit. J. vener. Dis. 35, 27.Google Scholar
Collier, W. A. (1939). J. Path. Bact. 48, 579.CrossRefGoogle Scholar
Edward, D. G. ff. (1940). J. Path. Bact. 50, 409.CrossRefGoogle Scholar
Edward, D. G. ff. (1947). J. Path. Bact. 59, 209.CrossRefGoogle Scholar
Freundt, E. A. (1953). Acta path. microbiol. scand. 32, 468.CrossRefGoogle Scholar
Findlay, G. M., Klieneberger, E., MacCallum, F. O. & Mackenzie, R. D. (1938). Lancet, ii, 1511.CrossRefGoogle Scholar
Findlay, G. M., Mackenzie, R. D., MacCallum, F. O. & Klieneberger, E. (1939). Lancet, ii, 7.CrossRefGoogle Scholar
Klieneberger, E. & Steabben, D. B. (1937). J. Hyg., Camb., 37, 143.CrossRefGoogle Scholar
Klieneberger, E. & Steabben, D. B. (1940). J. Hyg., Camb., 40, 223.CrossRefGoogle Scholar
Klieneberger-Nobel, E. (1959). Brit. med. J. i, 19.CrossRefGoogle Scholar
Klieneberger-Nobel, E. (1960). Ann. N.Y. Acad. Sci. 79, 615.CrossRefGoogle Scholar
Melèn, B. & Gotthardson, A. (1955). Acta path. microbiol. scand. 37, 196.CrossRefGoogle Scholar
Nelson, J. B. (1937 a). J. exp. Med. 65, 833.CrossRefGoogle Scholar
Nelson, J. B. (1937 b). J. exp. Med. 65, 843.CrossRefGoogle Scholar
Nelson, J. B. (1937 c). J. exp. Med. 65, 851.CrossRefGoogle Scholar
Nelson, J. B. (1950). J. exp. Med. 92, 309.CrossRefGoogle Scholar
Nicol, C. S. & Edward, D. G. ff. (1953). Brit. J. vener. Dis. 29, 141.Google Scholar
Preston, W. S. (1942). J. infect. Dis. 70, 180.CrossRefGoogle Scholar
Sabin, A. (1941). Bact. Rev. 5, 1.CrossRefGoogle Scholar
Stokes, E. J. (1955). Lancet, i, 276.CrossRefGoogle Scholar
Sullivan, E. R. & Dienes, L. (1939). Proc. Soc. exp. Biol, N.Y., 41, 620.CrossRefGoogle Scholar
Woglom, W. H. & Warren, J. (1938). J. exp. Med. 68, 513.CrossRefGoogle Scholar