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Infection and Immunity, September 1994, p. 3599-3603, Vol. 62, No. 9
0019-9567/1994/$04.00+0     DOI:

research-article

Local vaccination with killed Streptococcus uberis protects the bovine mammary gland against experimental intramammary challenge with the homologous strain.

J M Finch, A W Hill, T R Field, and J A Leigh

Institute for Animal Health, Compton Laboratory, Newbury, United Kingdom.

ABSTRACT

The ability of killed streptococcus uberis to induce protection against mastitis when administered either into the cistern of the dry mammary gland (intramammary vaccination) without adjuvant or subcutaneously with adjuvant was investigated. Bacteria were never reisolated from vaccinated quarters following challenge with the same strain during the subsequent lactation, and no inflammatory response was detected. In contrast, following subcutaneous vaccination, milk from challenged quarters contained very small numbers of bacteria, but these quarters did exhibit clinical disease, whereas quarters on nonvaccinated control animals produced discolored, clotted secretion with large numbers of bacteria and somatic cells and required antibiotic therapy by 60 h postchallenge. There was a significant increase in the levels of S. uberis-specific immunoglobulin G1 (IgG1), IgG2, and IgM in milk following intramammary vaccination and in the levels of specific IgG1 and IgG2 in milk following subcutaneous vaccination. Levels of specific antibody in serum were also elevated following vaccination by either route. However, despite this, there was no increase in the opsonic activity of serum or milk. Both peripheral blood lymphocytes and dry-period mammary gland lymphocytes showed strong proliferative responses to S. uberis in vitro following subcutaneous vaccination, but only mammary gland lymphocytes responded following intramammary vaccination. It was concluded that the protection seen in vaccinated quarters did not appear to be related to levels of specific antibody or neutrophil function and was possibly brought about by the inhibition of bacterial growth.


Infection and Immunity, September 1994, p. 3599-3603, Vol. 62, No. 9
0019-9567/1994/$04.00+0     DOI:




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