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Studies in the epidemiology of infectious myxomatosis of rabbits: I. Recovery of Australian wild rabbits (Oryctolagus Cuniculus) from myxomatosis under field conditions

Published online by Cambridge University Press:  15 May 2009

Frank Fenner ,
I. D. Marshall  and
Gwendolyn M. Woodroofe
Frank Fenner
Affiliation:
Department of Microbiology, John Curtin School of Medical Research, The Australian National University, Canberra, Australia
I. D. Marshall
Affiliation:
Department of Microbiology, John Curtin School of Medical Research, The Australian National University, Canberra, Australia
Gwendolyn M. Woodroofe
Affiliation:
Department of Microbiology, John Curtin School of Medical Research, The Australian National University, Canberra, Australia
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1. Australian wild rabbits which had recovered from myxomatosis acquired in the field contained in their serum antibodies which could be detected by complement-fixation or neutralization tests for a long period (more than 18 months) after their recovery. The titre of complement-fixing antibody fell fairly rapidly during the first few months, and remained at a steady level thereafter. No change could be detected in the titre of neutralizing antibodies throughout the observation period.

2. Inoculation of such rabbits with myxoma virus was sometimes followed by the development of a local lesion at the inoculation site, and in these rabbits the titre of complement-fixing antibody rose, but there was no alteration in the neutralizing power of the serum. In other animals no lesion developed and there was no change in the antibody titre.

3. Serum was collected from a total of 824 wild rabbits from seventeen localities in eastern Australia with varying histories of myxomatosis since December 1950. Examination of 135 of these sera by both neutralization and complement-fixation tests showed that the results obtained by the two methods were in close agreement.

4. In many areas in which the disease was absent in the summer of 1950–1 and produced a violent epizootic in 1951–2, the majority (70–90 %) of the sera collected from rabbits 2–5 months after the height of the epizootic contained antibody to myxoma virus, i.e. the majority of the survivors had recovered from the disease.

5. Counts of the rabbit population before and after a violent epizootic in the summer of 1951–2, and the proportion of immune animals amongst the survivors in these areas showed that the case-mortality rate was between 99·4 and 99·8%.

6. Consideration of the results obtained in the serological surveys showed that the case-mortality rate was probably of this order (about 99·5%) in all areas in which there had been no disease or a negligible outbreak in 1950–1, whether they had a grade I or grade II kill in 1951–2.

7. In certain other areas, in which a grade I outbreak in 1950–1 was followed by a grade II or poorer kill in 1951–2, the observed immune rate was considerably higher than would be expected if the case-mortality rate (assuming that the whole rabbit population was susceptible) was 99·5%. The possible causes of this are discussed. Survival of immune survivors from the first epizootic through the second may be a factor of some importance, but it is probably not the only factor involved.

8. The areas just mentioned were exceptional. In most places there was either no build-up of population after the 1950–1 epizootic, or a second effective epizootic destroyed the majority of rabbits in the small population which had developed by reproduction of the survivors of the first outbreak.

Type
Research Article
Information
Journal of Hygiene , Volume 51 , Issue 2 , June 1953 , pp. 225 - 244
Copyright
Copyright © Cambridge University Press 1953

References

Anderson, S. G. & Eagle, M. (1953). Med. J. Aust. 1, 478.CrossRefGoogle Scholar
Berry, G. P. (1937). Proc. Amer. phil. Soc. 77, 473.Google Scholar
Bull, L. B. & Mules, M. W. (1944). J. Coun, sci. Industr. Res. Aust. 17 (2), 1.Google Scholar
Butler, B. E. (1950). Aust. J. agric. Res. 1, 231.CrossRefGoogle Scholar
Donnelley, M. (1951). Aust. J. exp. Biol, med. Sci. 29, 137.CrossRefGoogle Scholar
Fenner, F. (1949 a). Aust. J. exp. Biol, med. Sci. 27, 1.CrossRefGoogle Scholar
Fenner, F. (1949 b). Aust. J. exp. Biol. med. Sci. 27, 45.CrossRefGoogle Scholar
Fenner, F., Day, M. F. & Woodroofe, G. M. (1952). Aust. J. exp. Biol. med. Sci. 30, 139.CrossRefGoogle Scholar
Fenner, F., Woodroofe, G. M. & Marshall, I. D. (1953). In preparation.Google Scholar
Fisk, R. T. & Kessel, I. F. (1931). Proc. Soc. exp. Biol., N.Y., 29, 9.CrossRefGoogle Scholar
French, E. L. (1952). Med. J. Aust. 1, 100.CrossRefGoogle Scholar
Ginder, D. R. & Friedewald, W. F. (1952). Proc. Soc. exp. Biol., N.Y., 79, 615.CrossRefGoogle Scholar
Hills, E. S. (1940). Physiography of Victoria. Whitcombe and Tombs.Google Scholar
Hobbs, J. R. (1928). Amer. J. Hyg. 8, 800.Google Scholar
Hurst, E. W. (1937). Brit. J. exp. Path. 18, 15.Google Scholar
Hyde, R. R. (1939). Amer. J. Hyg. (B), 30, 37.Google Scholar
Jawetz, E. & Coleman, V. R. (1952). J. Immunol. 68, 645.CrossRefGoogle Scholar
Lush, D. (1937). Aust. J. exp. Biol. med. Sci. 15, 131.CrossRefGoogle Scholar
Lush, D. (1939). Aust. J. exp. Biol. 17, 85.CrossRefGoogle Scholar
Martin, C. J. (1936). Fourth Rep. Univ. Cambridge Inst. Animal Path.Google Scholar
Parker, R. F. & Thompson, R. L. (1942). J. exp. Med. 75, 567.CrossRefGoogle Scholar
Ratcliffe, F. N., Myers, K., Fennessy, B. V. & Calaby, J. H. (1952). Nature, Lond., 170, 7.CrossRefGoogle Scholar
Shaffer, J. G. (1941). Amer. J. Hyg., Sec. B, 34, 102Google Scholar