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Dairy Husbandry Research Foundation, University of Sydney, University Farms, Camden, N.S.W., 2570, Australia.
Department of Physiology, University of Western Australia, Nedlands, W.A., 6009, Australia.
Division of Animal Health, CSIRO, Parkville, Victoria, Australia
ABSTRACT
In a recent review Norcross and Stark (12) have discussed various methods of enhancing the immunological resistance of the dairy cow to mastitis. In the light of this review we wish to draw attention to several points from our investigations which apparently require clarification.
In principle it is assumed that the mammary gland would be more resistant to bacterial mastitis if it were possible to sustain sufficient concentration of appropriate antibodies in the secretion. Clearly the rate of transfer of immunoglobulins from the interstitial fluid across the secretory epithelium must be a basic factor in determining whether sufficient antibody of systemic origin will be secreted.
It is well established that a majority of immunoglobulins in ruminant colostrum are transferred into the secretion from the serum (2, 3) and that immunoglobulins transferred belong practically exclusively to a single class referred to as IgG1 or fast IgG (11, 13). In contrast, negligible amounts of IgG2 (slow IgG) which has a similar molecular weight to, and shares many antigenic characteristics with, IgG1 are transferred.
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