The objectives of this study were to assess the risk factors for metritis, its effects on milk yield and on reproductive performance, and the efficacy of ceftiofur therapy in Holstein dairy cows. Cows (n=303) from a commercial dairy herd in Argentina were studied. Cows were scored for body condition, and blood samples were collected on d -14, 7, 21, 31, 41, and 50 relative to parturition. Cows having a watery, purulent, or brown, and fetid vaginal discharge (VD) and rectal temperature ≤ 39.2°C were diagnosed as having clinical metritis, and those having a similar VD and rectal temperature >39.2°C were diagnosed as having puerperal metritis. Both clinical and puerperal metritis cows were randomly assigned to control (no treatment) or ceftiofur group (2.2mg/kg×3 consecutive days). Cure was declared if clear VD was observed at 21 d in milk (DIM). Blood samples were analyzed for nonesterified fatty acids, β-hydroxybutyrate, and blood urea nitrogen using commercial kits, and for insulin-like growth factor-1, insulin, and leptin by RIA. Data were analyzed with PROC MIXED, GENMOD, PHREG, and LIFETEST from SAS (SAS Institute Inc., Cary, NC). The risk for metritis increased with dystocia, retained fetal membranes, and dead calf [AOR (adjusted odds ratio)=2.58, 95% CI: 1.189-5.559], and as prepartum nonesterified fatty acids levels increased (AOR=1.001, 95% CI: 0.999-1.002). Conversely, risk decreased as prepartum insulin-like growth factor-1 increased (AOR=0.65, 95% CI: 0.349-1.219). Cows having either clinical or puerperal metritis produced less milk by 90 DIM than did healthy cows (2,236 ± 172 vs. 2,367 ± 77 vs. 2,647 ± 82 kg, respectively). Cows with puerperal metritis had lower risk for pregnancy by 100 DIM (AOR=0.189, 95% CI: 0.070-0.479) and a lower hazard rate for pregnancy by 150 DIM (hazard rate: 0.753, 95% CI: 0.621-0.911), and took longer to get pregnant (129 vs. 111 vs. 109 d, for puerperal metritis, clinical metritis, and healthy cows, respectively). Ceftiofur treatment was not associated with cure rate or milk yield but was related to increased risk for pregnancy at timed artificial insemination (AOR=2.688, 95% CI: 0.687-10.832), and for lower risk of reproductive cull (AOR=0.121, 95% CI: 0.014-1.066). In conclusion, abnormal calving and negative energy balance are associated with increased risk for metritis. Metritis, especially puerperal metritis, correlates with reduced milk production and poor reproductive performance. Finally, the likelihood for having a normal VD (indicative of cure) increased 2.6% for every day of increase in postpartum time and was 2 times higher for cows with clinical metritis than for those with puerperal metritis.

The objectives of this study were to assess the clinical and metabolic risk factors for clinical endometritis, the likelihood for having a normal vaginal discharge during postpartum, and the effects of endometritis on milk yield, reproductive efficiency, and metabolic status in Holstein cows. The study was conducted in a commercial dairy herd (Cordoba, Argentina) where 303 Holstein cows were enrolled. Cows were body condition scored (1 to 5) and tail bled on -14, 7, 21, 31, 41, and 50 d relative to parturition. Cows having a vaginal discharge with presence of pus between 21 and 41 d postpartum (dpp) were diagnosed as having clinical endometritis. Plasma blood samples were analyzed for nonesterified fatty acids (NEFA), β-hydroxybutyrate (BHBA), and blood urea nitrogen using commercial kits and insulin-like growth factor 1, insulin, and leptin by RIA. Data were analyzed with PROC MIXED, PROC GENMOD, and PROC PHREG of SAS (SAS Institute Inc., Cary, NC). Abnormal calving and puerperal metritis increased the risk for endometritis [adjusted odds ratio (AOR)=2.21 for both]. High prepartum NEFA and high postpartum BHBA increased the risk for endometritis (AOR=1.003 and 1.001, respectively), whereas high prepartum blood urea nitrogen reduced it (AOR=0.853). Cut-offs of 456.6 μM NEFA and 402.5 μM BHBA had sensitivities of 0.69 and 0.58, and specificities of 0.88 and 0.86, respectively. The likelihood for having normal vaginal discharge increased with time (∼1% × dpp) and with normal calving. Cows with endometritis had higher milk yield than normal herdmates (27.8±0.9 vs. 25.7±0.4 kg/d), lower risk for pregnancy by 100 dpp (AOR=0.10), higher nonpregnancy risk by 200 dpp (AOR=2.87), and higher risk for culling than normal cows (AOR=2.28). Cows with endometritis had a lower hazard rate (0.44) for pregnancy and had approximately 70 d longer calving-to-conception intervals. Finally, endometritis had no effect on metabolic hormones. In conclusion, the risk for clinical endometritis increases with abnormal calving and puerperal metritis, as prepartum NEFA and postpartum BHBA concentrations increase. Prepartum NEFA and postpartum BHBA could be useful for the prediction of endometritis. Last, clinical endometritis has detrimental effects on reproductive efficiency, as affected cows take longer to get pregnant and are at higher risk for culling.

Effects of partially hydrogenated oil on performance, loss of body weight and body condition score, and blood metabolite and hormone concentrations were evaluated in 37 multiparous Holstein cows in grazing conditions during the first 100 d of lactation. Six additional Holstein cows, each fitted with a ruminal cannula, were allocated to a replicated 3 x 3 Latin square to evaluate effects of supplemental fat on rumen environment and pasture digestion. All cows grazed mixed pastures based on alfalfa (Medicago sativa) and orchardgrass (Dactylis glomerata L.) and received 5.4 kg/d of a basal concentrate to which 0, 0.5, or 1 kg/cow per day of partially hydrogenated oil (melting point 58 to 60 degrees C) containing 30.3, 34.9, 21.8, and 3.3% of C16:0, C18:0, C18:1, and C182, respectively, was added. Feeding 1 kg/d of supplemental fat increased fat-corrected milk from 23.4 to 26.3 kg/d, milk fat content from 3.44 to 3.78%, and milk fat yield from 0.87 to 1.03 kg/d compared to control. Milk protein percentage and yield were not affected. Cows fed 1 kg/d of fat increased the content and yield of C16:0 and C18:0 in milk compared with cows fed no added oil. Dry matter intake (DMI) from pasture decreased from 17.8 kg/d for control cows to 13.6 kg/d for cows fed 1 kg of oil, whereas DMI from concentrate was higher for cows fed 1 kg/d of fat (6.0 kg/d) than for controls (5.2 kg/d). Supplemental fat did not affect total dry matter or estimated energy intake and did not change losses of body weight or body condition scores. Plasma concentrations of nonesterified fatty acids, insulin, somatotrophin, and insulin-like growth factor-I did not differ among treatments. Concentration of plasma triglycerides was lowered from 318.5 to 271.2 mg/dl, whereas plasma cholesterol was elevated from 185.0 to 235.8 mg/dl in cows receiving 1 kg/d of supplemental fat compared with controls. Responses to lipolytic or insulin challenges were not affected by feeding oil. Supplemental fat did not affect the digestion of pasture fiber. The addition of energy in the form of partially hydrogenated fat to early lactation dairy cows fed primarily on pasture increased the yield of fat-corrected milk and milk fat content when it represented about 11% of the total metabolizable energy requirement of cows, without affecting milk protein content. The partial hydrogenation of a byproduct of the oil industry apparently prevented detrimental effects of fat supplementation on ruminal digestion.