Substantial evidence indicates that innate and acquired defense mechanisms are lowest from 3 wk precalving to 3 wk postcalving. This lowered responsiveness includes aspects of systemic and mammary gland immunity that may account, at least in part, for the increased incidence of peripartum disease. The physical and metabolic stresses of pregnancy, calving, and lactation may contribute to this decrease in host resistance and the subsequent increase in disease incidence. However, variation among cows in their host resistance mechanisms suggests that genotype and phenotype may possibly be used to identify cows that are able to mount beneficial immune responses over the periparturient period. Our own studies suggest that cows may be categorized as high or low responders based on the peripartum antibody responses to ovalbumin and Escherichia coli J5. Low responders were hyporesponsive to these test antigens and had a higher incidence of peripartum diseases, particularly mastitis. In many species, a functional link exists between the immune and endocrine systems, and, during periods of stress or physical injury, neuropeptides and neuroendocrine hormones function as immunomodulators. Initial investigations of peripartum cows reveal positive relationships between growth hormone kinetics and profiles of antibody response. Whether hormone fluctuations during the periparturient period are responsible for the alterations observed in immune responsiveness remains uncertain.
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