OBJECTIVE: To define causes of increased susceptibility to coliform mastitis after parturition. ANIMALS: 12 healthy Holstein cows assigned to 2 groups. Group-1 cows (n = 6) had calved between 6 and 10 days earlier. Group-2 cows (n = 6) were in midlactation. PROCEDURE: Cows from each group were paired and challenge exposed with Escherichia coli in 1 mammary gland. Mastitis severity was determined by bacterial concentration in milk, pyrexia, and milk production. Measures of host defense were neutrophil chemotaxis, adhesion molecule expression, leukocyte recruitment, and cytokine production. RESULTS: After challenge exposure, group-1 cows had more rapid E coli growth, higher peak bacterial concentration, and higher fever. Leukocyte recruitment was poor in 1 group-1 cow that had peracute mastitis. In contrast, leukocyte recruitment in 5 other group-1 cows began sooner than that in group-2 cows. In these group-1 cows, prechallenge-exposure milk somatic cell counts (SCC) were significantly lower than those in group-2 cows. Prechallenge-exposure SCC were correlated to stimulated CD18 expression (R2 = 0.79), and both measures correlated inversely with bacterial growth rate (R2 = -0.75). Values for tumor necrosis factor alpha, interleukin 1, and interleukin 8 in group-1 cows after challenge exposure were greater than or equal to those in group-2 cows. CONCLUSIONS: Weak leukocyte recruitment to the mammary gland is associated with increased severity of coliform mastitis. Impaired production of cytokines measured is not a cause of increased susceptibility to coliform mastitis in early lactation. CLINICAL RELEVANCE: Low milk SCC after calving may increase susceptibility to severe coliform mastitis.
OBJECTIVE: To define causes of increased susceptibility to coliform mastitis after parturition. ANIMALS: 12 healthy Holstein cows assigned to 2 groups. Group-1 cows (n = 6) had calved between 6 and 10 days earlier. Group-2 cows (n = 6) were in midlactation. PROCEDURE: Cows from each group were paired and challenge exposed with Escherichia coli in 1 mammary gland. Mastitis severity was determined by bacterial concentration in milk, pyrexia, and milk production. Measures of host defense were neutrophil chemotaxis, adhesion molecule expression, leukocyte recruitment, and cytokine production. RESULTS: After challenge exposure, group-1 cows had more rapid E coli growth, higher peak bacterial concentration, and higher fever. Leukocyte recruitment was poor in 1 group-1 cow that had peracute mastitis. In contrast, leukocyte recruitment in 5 other group-1 cows began sooner than that in group-2 cows. In these group-1 cows, prechallenge-exposure milk somatic cell counts (SCC) were significantly lower than those in group-2 cows. Prechallenge-exposure SCC were correlated to stimulated CD18 expression (R2 = 0.79), and both measures correlated inversely with bacterial growth rate (R2 = -0.75). Values for tumor necrosis factor alpha, interleukin 1, and interleukin 8 in group-1 cows after challenge exposure were greater than or equal to those in group-2 cows. CONCLUSIONS: Weak leukocyte recruitment to the mammary gland is associated with increased severity of coliform mastitis. Impaired production of cytokines measured is not a cause of increased susceptibility to coliform mastitis in early lactation. CLINICAL RELEVANCE: Low milk SCC after calving may increase susceptibility to severe coliform mastitis.