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Further studies on the mechanism of mosquito transmission of myxomatosis in the European rabbit

Published online by Cambridge University Press:  15 May 2009

M. F. Day ,
Frank Fenner ,
Gwendolyn M. Woodroofe  and
G. A. McIntyre
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Proof of the existence of multiplication of myxoma virus in mosquitoes has been sought by a variety of experiments with Aedes aegypti and Anopheles annulipes. All were completely negative. All features of transmission are compatible with a purely mechanical and none is compatible with a ‘biological’ mechanism.

In mechanical transmission important features of the infected animal host are the number and accessibility of viruliferous skin lesions, and the location and concentration of virus in these lesions.

By inducing mosquitoes to probe through infectious skin lesions and subsequently permitting them to make many successive probes on marked skin sites on the backs of susceptible rabbits, it has been possible to obtain quantitative information on the median minimum virus load of probing mosquitoes, and the rates of loss due to probing and the passage of time.

A preparation of myxoma virus suspended in normal rabbit serum had a half-lifetime of 11 days at 4° C., 5 days at 18–20° C., and 31 hr. at 27–28° C. Apart from losses due to probing (about 12% of the virus load per probe) viable virus on the proboscis of the mosquito probably disappears at about the same rates.

Type
Research Article
Information
Journal of Hygiene , Volume 54 , Issue 2 , June 1956 , pp. 258 - 283
Copyright
Copyright © Cambridge University Press 1956

References

REFERENCES

Andrewes, C. H. (1936). J. exp. Med. 63, 157.CrossRefGoogle Scholar
Bennett, S. J. C., Horgan, E. S. & Haseeb, M. A. (1944). J. comp. Path. 54, 131.CrossRefGoogle Scholar
Bernhard, W., Bauer, A., Harel, J. & Oberling, Ch. (1955). Bull. Cancer, 41, 423.Google Scholar
Brody, A. L. (1936). Mem. Cornell Agric. exp. Sta. 195, 1.Google Scholar
Coons, A. H. & Kaplan, M. H. (1950). J. exp. Med. 91, 1.CrossRefGoogle Scholar
Day, M. F. (1955). Exp. Parasitol. 4, 387.CrossRefGoogle Scholar
Epstein, B., Reissig, M. & De Robertis, E. (1952). J. exp. Med. 96, 347.CrossRefGoogle Scholar
Fenner, F., Day, M. F. & Woodroofe, G. M. (1952). Aust. J. exp. Biol. & med. Sci. 30, 139.CrossRefGoogle Scholar
Fenner, F., Day, M. F. & Woodroofe, G. M. (1956). J. Hyg., Camb., 54, 284.CrossRefGoogle Scholar
Fenner, F. & McIntyre, G. A. (1956). J. Hyg., Camb., 54, 246.CrossRefGoogle Scholar
Hurst, E. W. (1937). Brit. J. exp. Path. 18, 15.Google Scholar
Jacotot, H., Toumanoff, C., Vallée, A. & Virat, B. (1954). Ann. Inst. Pasteur, 87, 477.Google ScholarPubMed
Kilham, L. & Dalmat, H. T. (1955). Amer. J. Hyg. 61, 45.Google Scholar
Kilham, L. & Fisher, E. R. (1954). Amer. J. Hyg. 59, 104.Google Scholar
Kilham, L. & Woke, P. A. (1953). Proc. Soc. exp. Biol., N.Y., 83, 296.CrossRefGoogle Scholar
Lloyd, B. J. & Kahler, H. (1955). J. Nat. Canc. Inst. 15, 991.Google Scholar
McLean, D. M. (1955). Aust. J. exp. Biol. med. Sci. 33, 53.CrossRefGoogle Scholar
Moses, A. (1911). Mem. Inst. Osw. Cruz, 3, 46.CrossRefGoogle Scholar
Mykytowycz, R. (1953). Nature, Lond., 172, 448.CrossRefGoogle Scholar
Philip, C. B. (1942). J. Parasit. 28, 395.CrossRefGoogle Scholar
Shope, R. E. (1940). Arch. ges. Virusforsch. 1, 457.CrossRefGoogle Scholar
Mather, K. (1949). Biometrics, 5, 127.CrossRefGoogle Scholar