Postpartum metritis in dairy cows is characterized by an enlarged uterus and fetid red-brown or purulent uterine discharge that is typically diagnosed within 7–10 d postpartum. The expectation is that 10–20 % of dairy cows will develop metritis after calving [[1], [2], [3]]. Most cows recover from metritis within the first month postpartum. Cows with metritis are at an increased risk of developing chronic uterine inflammation (endometritis), which can have long-term negative effects on fertility [4,5]. In addition to uterine disease, postpartum cows may experience negative energy balance and associated metabolic disease postpartum that can affect fertility [6,7]. One current hypothesis for infertility in postpartum cows is that the combined effects of uterine and metabolic disease have a negative effect on oocyte quality leading to defects in fertilization or early embryonic development [2,[6], [7], [8]].

Most studies testing the effects of inflammatory molecules or metabolites use oocytes removed from healthy cows and treated in vitro. Fewer studies have performed similar work on the whole animal. Dickson et al. [9] experimentally induced endometritis in nonlactating dairy cows and reported a reduction in embryo development to the morula stage following in vitro fertilization of aspirated oocytes. Ribeiro et al. [10] flushed embryos from postpartum cows and reported a reduction in cleaved, live, and high-quality embryos in cows that previously experienced uterine disease.

In this work, the results of the previous studies [9,10] were extended by specifically working with primiparous postpartum cows with or without metritis, and COC were collected for in vitro embryo production (IVP) during three timepoints: 30, 80, 165 d after parturition. Collectively, this research examines the short-term (oocytes collected at approximately 1 month postpartum) and long-term (oocytes collected at approximately 80–165 d postpartum) effects of early postpartum uterine disease on oocyte developmental capacity. The current study is different from all other previously published work because we worked with early postpartum lactating cows and removed oocytes from cows to separate the biological effect of the oviductal and uterine environment from the capacity of the oocyte to develop. We hypothesized that uterine disease would negatively affect oocyte developmental competence. We also measured the relative importance of systemic factors by measuring an acute phase protein (haptoglobin) and energy metabolites [non-esterified fatty acids (NEFA), beta-hydroxybutyrate (BHB), and glucose] and associating their plasma concentrations postpartum with subsequent developmental competence of the oocyte. Finally, we tested the association between oocyte development and bacterial genera present in the reproductive tract.