Department of Animal Sciences, University of Florida, Gainesville 32611.
Institute of Life Science, Swansea University Medical School, Swansea, SA2 8PP, United Kingdom.
J Dairy Sci. 2019 Mar;102(3):2686-2697. doi: 10.3168/jds.2018-15595. Epub 2019 Jan 26.
Bacterial infection of the uterus causes clinical endometritis in 15 to 20% of postpartum dairy cows and reduces fertility, even after the resolution of disease. However, it is difficult to disentangle the mechanisms linking reduced fertility with endometritis because cows have multiple confounding postpartum conditions. The aim of the present experiment was to develop an in vivo model of clinical endometritis in Holstein heifers using pathogenic Escherichia coli and Trueperella pyogenes. Estrous cycles of heifers were synchronized using a 5-d Co-Synch protocol, and subsequently received exogenous progesterone to elevate circulating progesterone at the time of uterine infusion. Endometrial scarification was performed before uterine infusion of live pathogenic Escherichia coli and Trueperella pyogenes, or sterile vehicle. Effects of infusion were evaluated by measuring rectal temperature, plasma haptoglobin, hematology, grading pus in the vaginal mucus, quantifying 16S rRNA in vaginal mucus, and transrectal ultrasonography. Bacterial infusion increased the median vaginal mucus to grade 2 by d 3 postinfusion, and to grade 3 from d 4 to 6 postinfusion. Control heifers maintained a median vaginal mucus grade ≤1 from d 1 to 6. Transrectal ultrasound revealed the accumulation of echogenic fluid in the uterus of heifers following bacterial infusion, which was absent in control heifers. Total 16S rRNA in vaginal mucus was elevated in bacteria-infused heifers compared with control heifers at d 5. Rectal temperature was increased in bacteria-infused heifers. Plasma haptoglobin, general health, and appetite did not differ between groups. As indicated by increased vaginal mucus grade after bacterial infusion and absence of systemic signs of illness, this model successfully induced symptoms resembling clinical endometritis in virgin Holstein heifers. The model allows the isolation of effects of uterine disease on fertility from confounding factors that can occur during the postpartum period in dairy cows.
细菌感染子宫会导致 15%至 20%的产后奶牛出现临床子宫内膜炎，并降低其生育能力，即使疾病得到治愈也是如此。然而，由于奶牛在产后有多种混杂因素，因此很难理清将生育力降低与子宫内膜炎联系起来的机制。本实验的目的是使用致病性大肠杆菌和腐生真杆菌在荷斯坦小母牛体内建立临床子宫内膜炎的体内模型。小母牛的发情周期通过 5 天的 Co-Synch 方案同步，并随后接受外源性孕酮，以在子宫输注时提高循环孕酮水平。在子宫输注活致病性大肠杆菌和腐生真杆菌或无菌载体之前，对子宫内膜进行划痕。通过测量直肠温度、血浆触珠蛋白、血液学、阴道黏液中脓性物质评分、阴道黏液中 16S rRNA 定量和经直肠超声检查来评估输注的效果。细菌输注使阴道黏液中位数在输注后第 3 天增加到 2 级，并从第 4 天到第 6 天增加到 3 级。对照小母牛在第 1 天至第 6 天期间阴道黏液中位数保持在 1 级以下。经直肠超声显示细菌输注后小母牛子宫内有回声液体积聚，而对照小母牛则没有。与对照小母牛相比，细菌输注小母牛的阴道黏液中总 16S rRNA 在第 5 天升高。细菌输注小母牛的直肠温度升高。血浆触珠蛋白、一般健康状况和食欲在两组之间没有差异。细菌输注后阴道黏液等级增加，且没有奶牛产后期间常见的全身疾病迹象，表明该模型成功地诱导了处女荷斯坦小母牛出现类似于临床子宫内膜炎的症状。该模型可以将子宫疾病对生育力的影响与奶牛产后可能出现的混杂因素隔离开来。
