Intergenerational cycle of disease: Maternal mastitis is associated with poorer daughter performance in dairy cattle

Adverse prenatal environments, such as maternal stress and infections, can influence the health and performance of offspring. Mastitis is the most common disease in dairy cattle, yet the intergenerational effects have not been specifically investigated. Therefore, we examined the associations between the dam's mammary gland health and daughter performance using somatic cell score (SCS) as a proxy for mammary health. Using data obtained from Dairy Records Management Systems (Raleigh, NC), we linked daughter records with their dam's records for the lactation in which the daughter was conceived. Linear and quadratic relationships of dam mean SCS with the daughter's age at first calving (AFC; n = 15,992 daughters, 4,366 herds), first- (n = 15,119 daughters, 4,213 herds) and second-lactation SCS (n = 3,570 daughters, 1,554 herds), first- and second-lactation mature-equivalent 305-d milk yield, and milk component yields were assessed using mixed linear regression models. We uncovered a phenomenon similar to those found in human and mouse models examining prenatal inflammation effects, whereby daughters born from dams with elevated SCS had poorer performance. Dam mean SCS was positively associated with daughter's AFC and first- and second-lactation mean SCS. Furthermore, for every 1-unit increase in dam mean SCS, daughter's first- and second-lactation mature-equivalent fat yield declined by 0.34% and 0.91% (−1.6 ± 0.49 kg, −4.0 ± 1.0 kg, respectively), although no effect was found on first- or second-lactation milk or milk protein yield. When accounting for genetics, daughter SCS, and AFC (first lactation only), dam mean SCS was associated with reduced second-lactation milk fat yield (−3.5 ± 1.8 kg/unit SCS), and a tendency was found for first-lactation milk fat yield (−1.9 ± 1.0 kg/unit SCS). Taken together, the association of greater dam mean SCS with lesser daughter milk fat yield is likely due to a few underlying mechanisms, in particular, a predisposition for mastitis and alterations in the epigenome controlling milk fat synthesis. As such, future studies should examine epigenetic mechanisms as a potential underpinning of this phenomenon.