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Associations between activity of arginase or matrix metalloproteinase-8 (MMP-8) and metritis in periparturient dairy cattle. | LitMetric

Metritis, a uterine disease caused by bacterial infection, is highly prevalent in dairy cattle after parturition. Uterine disease has negative effects on milk production and reproductive efficiency. Finding markers or indicators that can predict cows at greater risk for uterine disease could be beneficial to mitigating these deleterious effects. This study investigates the immune-derived enzymes arginase and matrix metalloproteinase-8 (MMP-8) as potential markers for development of metritis in dairy cows. In a retrospective matched case-control study, 53 lactating Holstein cows diagnosed with metritis were matched and paired to 53 lactating Holstein control cows. In addition to examining cows for diagnosis of metritis on d 4, 7, 10, and 14 after parturition, occurrence of retained fetal membranes, gender of the calf, and the event of a stillbirth were recorded. Blood samples were collected 7 ± 3 d before calving, on the day of calving, and 7 ± 3 d after calving and were assayed for activity of arginase and MMP-8. Associations between metritis and activity of arginase or MMP-8 were determined by conditional logistic regression at each individual sampling time point. An interaction between activity of arginase, before and on the day of parturition, and retained fetal membranes tended (P ≤ 0.13) to be associated with metritis. After parturition, activity of arginase and the interaction between activity of arginase and retained fetal membranes were not (P ≥ 0.22) associated with metritis. Activity of MMP-8 was not (P ≥ 0.20) associated with metritis in the periparturient period. Retained fetal membranes were associated with the odds of developing metritis. Activity of arginase before and at the time of parturition might be a potential marker for occurrence of metritis, especially in cows that develop retained fetal membranes. MMP-8 does not seem to be a potential indicator for metritis.

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http://dx.doi.org/10.1016/j.theriogenology.2017.04.025DOI Listing

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