Discussion
The FecA immunization reduced clinical severity of mastitis. The reductions in clinical signs were associated with an increase in antibody titers against FecA in serum and mammary secretion. However, immunizing cows with FecA did not prevent bacterial multiplication in the mammary gland as had been hypothesized. A basic question relative to the observed efficacy of FecA is whether the abatement of clinical signs was due to iron restriction? Apparently immunoglobulin directed against FecA was present in mammary secretion at the time of challenge. However, an inhibitory effect of IgG directed against FecA on the growth of coliform has not been categorically substantiated. We have earlier shown that bovine IgG directed against FepA suppressed the growth of coliform isolates from naturally occurring mastitis in vitro. The concentration of IgG tested was 4 mg/ml, although normal bovine milk contains less than 1 mg/ml of IgG. Therefore, the increase in antibody titers by FecA immunization might not have been sufficient to suppress the growth of E. coli 727 in the mammary gland.
Escherichia coli 727 may not have been the most appropriate choice of challenge strain to test the effects of immunization of dairy cows with FecA. Antibody titers against E. coli 727 cultured to induce FecA did not differ among treatments.
Escherichia coli 727 produce rather mild clinical mastitis. The reason may be partially due to limited FecA production by E. coli 727 compared with other virulent strains (unpublished data). Most E. coli can utilize multiple iron transport systems as an adaptive trait to secure iron in tissue. For example, coliform isolates from naturally occurring mastitis, including E. coli 727, utilize the enterobactin and FepA based system in iron restricted conditions. Therefore, E. coli 727 may have utilized the another iron acquisition system instead of the ferric citrate transport system functionally compromised by antibody directed against FecA.
Despite the total inhibition of bacterial growth in FecA immunized cows, use of the vaccine reduced peak bacterial counts, rectal temperature, and severity and duration of clinical signs following intramammary challenge with E.coli 727. The FecA was immunogenic in cows and the increased antibody responses were related to reduced clinical signs of coliform mastitis. The reduction in clinical signs in FecA immunized cows was similar to previous results of E. coli J5 experimental challenge trials. The abatement of clinical signs in E. coli J5 vaccinated cows was reported due to enhanced opsonization. The immune response to FecA may reduce clinical signs of mastitis by a combination of altering iron acquisition and enhancing phagocytosis of coliform bacteria.