Dairy heifers are a sizable financial investment for producers and therefore should enter first lactation healthy in order to yield good return on investment. Most mammary growth and development occur during a dairy heifer’s first gestation and this initial development determines the number of secretory mammary epithelial cells in the lactating gland. The heifer mammary gland prior to first gestation is primarily composed of the mammary fat pad and contains minimal mammary epithelium. With the initiation of pregnancy, this previously existing mammary fat pad is replaced by secretory mammary epithelium. Unfortunately, coupled at this time is the increased prevalence of intramammary infections (IMI) as a result of pathogenic bacteria entering the mammary gland via the teat canal and establishing an infection. Such IMI are expected to shortchange future mammary maturation and ultimately reduce the number and/or functional capacity of secretory mammary epithelial cells. However, how these IMI affect mammary gland growth and development in rapidly growing and developing mammary glands has not been investigated. Therefore, Dr. Pari Baker explored the effects of IMI on mammary gland growth and development in nulligravid heifers.
The objectives of this study were to histologically compare uninfected and Staphylococcus aureus-infected mammary glands by quantifying tissue areas occupied by mammary epithelium and stromal tissue and determine whether infection status affects the degree of cellular proliferation and apoptosis in rapidly growing mammary glands. Nulligravid dairy heifers were administered estradiol and progesterone for 14 days to stimulate mammary growth and development and 2 quarters of each heifer were either infused with Staphylococcus aureus (CHALL) or served as an uninfected control (UNINF). Heifers were randomly euthanized on either the last day of hormonal injections (GRO), or 13 d post-injections (DEV) and mammary tissues were collected from two different regions in each mammary gland: parenchyma that abuts the mammary fat pad, distal to the teat end (edge parenchyma) and mammary parenchyma located proximal to the teat end, slightly above the gland cistern (center parenchyma).
It was found that in GRO tissues, CHALL quarters had less epithelial tissue area and more intralobular stroma, coinciding with the greater percentage of apoptotic mammary epithelial cells and lower percentage of apoptotic stromal cells observed in CHALL quarters compared to UNINF quarters. However, these tissue area differences observed in GRO tissues were not present in DEV tissues. The only significant observation was that UNINF quarters had more adipose tissue area than CHALL quarters, which suggests that mammary gland development was partially influenced by IMI and extensive epithelial infiltration into the mammary fat pad was prevented in CHALL quarters.
These results indicate that IMI during periods of mammary growth and development can reduce the amount of mammary epithelium and prevent its expansion into the mammary fat pad. These tissue changes prior to calving are expected to negatively impact first lactation milk yields. Continued research into heifer IMI is important for developing and enhancing strategies to mitigate the effects of IMI on the heifer mammary gland.
Pari Baker was born in Mississauga, Ontario, Canada and recently obtained her Master of Science at The Ohio State University in the Mastitis and Mammary Physiology Laboratory under Dr. Benjamin Enger. She now works as a research assistant at Case Western Reserve School of Medicine within the Center for Global Health and Diseases, US under Dr. Stephanie Langel, whose research focuses on mucosal immune protection against viral diseases and the development of vaccines.