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Passive immunity in myxomatosis of the european rabbit (Oryctolagus cuniculus): the protection conferred on kittens born by immune does*

Published online by Cambridge University Press:  15 May 2009

Frank Fenner
Affiliation:
The Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra
I. D. Marshall
Affiliation:
The Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra
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1. The existence of passive immunity to myxomatosis was demonstrated by the inoculation of normal young rabbits with either myxoma-immune serum or saline, and their subsequent inoculation with the standard laboratory strain of myxoma virus. All the passively immunized animals lived longer than the control animals and a few survived.

2. Passive immunity could also be demonstrated in the offspring of myxoma-immune mothers. When these were challenged by mosquito bite inoculation with the standard laboratory strain of myxoma virus they either failed to become infected, or survived infection for several days longer than the progeny of normal does. When challenged by the intradermal inoculation of a slightly attenuated strain of myxoma virus 25 % of the progeny of immune does survived the infection, whereas none of the normal kittens survived.

3. The survival times of young rabbits in both the normal and passively immunized groups was influenced by their age, very young animals dying several days earlier than rabbits 4 and 6 weeks old.

4. The possible epidemiological consequences of passive immunity in the behaviour of myxomatosis in populations of wild rabbits are discussed.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1954

References

REFERENCES

Andersen, O. (1937). Z. ImmunForsch. 90, 459.Google Scholar
Anderson, S. G. & Hamilton, J. (1949). Med. J. Aust. 1, 308.CrossRefGoogle Scholar
Bodian, D. (1953). Amer. J. Hyg. 58, 81.Google Scholar
Brambell, F. W. R. (1944). Proc. Zool. Soc. Lond. 114, 1.Google Scholar
Brambell, F. W. R., Hemmings, W. A. & Henderson, M. (1951). Antibodies and Embryos. University of London: The Athlone Press.Google Scholar
Dixon, F. J., Talmage, D. W., Maurer, P. H. & Deichmiller, M. (1952). J. exp. Med. 96, 313.CrossRefGoogle Scholar
Fenner, F. (1948). Brit. J. exp. Path. 29, 69.Google Scholar
Fenner, F. (1949). Aust. J. exp. Biol. 27, 45.CrossRefGoogle Scholar
Fenner, F. (1953). Nature, Lond., 172, 228.CrossRefGoogle Scholar
Fenner, F., Marshall, I. D. & Woodroofe, G. M. (1953). J. Hyg., Camb., 51, 225.CrossRefGoogle Scholar
Fenner, F. & Woodroofe, G. M. (1953). Brit. J. exp. Path. 34, 400.Google Scholar
Fenner, F. & Woodroofe, G. M. (1954). Aust. J. exp. Biol. (In the Press).Google Scholar
Glenny, A. T. & Hopkins, B. E. (1923). J. Hyg., Camb., 22, 37.CrossRefGoogle Scholar
Hurst, E. W. (1937). Brit. J. exp. Path. 18, 15.Google Scholar
Hyde, K. E. (1936). Amer. J. Hyg. 23, 278.Google Scholar
Hyde, R. R. & Gardner, R. E. (1939). Amer. J. Hyg. 30, 57.Google Scholar
Lush, D. (1939). Aust. J. exp. Biol. 17, 85.CrossRefGoogle Scholar
Marshall, I.D., Dyce, A., Poole, W.E. & Fenner, F. (1955). J. Hyg., Camb. (In the Press).Google Scholar
Martin, C. J. (1936). Bull. Coun. sci. industr. Res. Aust., no. 96.Google Scholar
Myers, K., Marshall, I. D. & Fenner, F. (1954). J. Hyg., Camb., 52, 337.CrossRefGoogle Scholar
Mykytowycz, R. (1953). Nature, Lond., 172, 448.Google Scholar
Reed, L. J. & Muench, H. (1938). Amer. J. Hyg. 27, 493.Google Scholar
Stephens, M. N. (1952). Proc. Zool. Soc. Lond. 122, 417.Google Scholar