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Use of cortisone derivatives to inhibit resistance to Nippostrongylus brasiliensis and to study the fate of parasites in resistant hosts

Published online by Cambridge University Press:  10 June 2015

Bridget M. Ogilvie*
Affiliation:
Department of Animal Pathology, School of Veterinary Medicine, Madingley Road, Cambridge

Extract

Acquired resistance to some nematode parasites can be suppressed by daily administration of cortisone acetate to the host. Cortisone treatment completely suppressed previously acquired resistance of mice to Trichinella spiralis (Coker, 1956) and suppressed, at least partially, the acquisition of resistance to T. spiralis by rats during initial infection (Markell & Lewis, 1957).

A previous report (Weinstein, 1955) suggested cortisone acetate treatment was less effective in the suppression of acquired resistance of rats to Nippostrongylus brasiliensis. Weinstein showed that daily treatment with 2 mg cortisone acetate throughout five immunizing infections and continued during the challenge infection increased the number of worms in the intestine and had a marked effect on the cellular response in the skin and lungs. However, there was no significant effect when daily cortisone treatment commenced only on the fifth day before the challenge infection. This result suggested that acquisition of immunity to N. brasiliensis was partially overcome by cortisone treatment, but the same level of drug treatment had no effect on immunity already acquired.

In the experiments reported here, previously acquired resistance to N. brasiliensis was suppressed completely and the initiation of immunity stopped, either completely or at a very early stage, by treatment with the cortisone derivatives prednisolone or betamethasone. The complete suspension of all manifestations of acquired resistance obtained by treatment with these drugs was used to investigate the fate of larvae migrating in an immune host.

The rats and strain of parasite, and the methods of handling them, have been described previously (Ogilvie, 1965).

Type
Research Article
Copyright
Copyright © Cambridge University Press 1965

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References

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