The objective of this observational study was to investigate the risk factors for metritis, purulent vaginal discharge, and cytological endometritis. The hypothesis was that purulent vaginal discharge and cytological endometritis would have different risk factors because they represent distinct manifestations of uterine disease. Data generated from 1,363 Holstein cows (3 herds) enrolled in a randomized clinical trial were used. Calving history, periparturient disease incidence, and body condition score at calving and at 63 d in milk (DIM) were recorded. Serum nonesterified fatty acid concentration was measured once during the week before expected calving. Serum nonesterified fatty acid, β-hydroxybutyric acid, and haptoglobin (Hapto) concentrations were measured at 4 ± 3, 11 ± 3, and 18 ± 3 DIM. Serum progesterone concentration was measured at 21 ± 3, 35 ± 3, 49 ± 3, and 63 ± 3 DIM. Metritis was diagnosed by farm managers within the first 20 DIM using a standardized definition. Cows were examined at 35 ± 3 DIM by a veterinarian for purulent vaginal discharge (mucopurulent or worse vaginal discharge; Metricheck device) and cytological endometritis (≥ 6% polymorphonuclear cells on endometrial cytology; cytobrush device). Statistical analyses were performed using multivariable logistic regression models for each disease, accounting for the random effect of herd. Risk factors for metritis included increased nonesterified fatty acid prepartum (≥ 0.6 mmol/L), dystocia, retained placenta, and increased Hapto in the first week postpartum (≥ 0.8 g/L). Risk factors for purulent vaginal discharge included twinning, dystocia, metritis, and increased Hapto (≥ 0.8 g/L) in the first week postpartum. Risk factors for cytological endometritis included low body condition score at parturition (≤ 2.75), hyperketonemia (≥ 1,100 μmol/L), and increased Hapto (≥ 0.8 g/L) in the first week postpartum. These results support the hypothesis that some of the risk factors for purulent vaginal discharge and cytological endometritis are different, which supports that they are distinct manifestations of uterine disease.

The objectives of this observational study were to determine and compare diagnostic criteria for postpartum endometritis in dairy cows. Data generated from 1,044 Holstein cows (6 herds) enrolled in a randomized clinical trial were used. Cows were examined for endometritis at 35±3 d (exam 1) and 56±3 d (exam 2) after parturition, using endometrial cytology (cytobrush technique), vaginal discharge scoring (Metricheck device; Simcrotech, Hamilton, New Zealand), and cervical diameter measurement (transrectal palpation). Reproductive data were recorded until 200 d after parturition. Diagnostic criteria for cytological and clinical endometritis were determined based on detrimental effect on subsequent reproductive performance, using logistic regression and Cox proportional hazard models accounting for the effect of herd clustering. Comparison of diagnostic criteria was performed using endometrial cytology as reference test or by quantifying the agreement between diagnostic approaches. At exam 1, diagnostic criteria were ≥6% polymorphonuclear cells and mucopurulent or worse (purulent or foul) vaginal discharge for cytological and clinical endometritis, respectively. At exam 2, diagnostic criteria were ≥4% polymorphonuclear cells and mucopurulent or worse vaginal discharge for cytological and clinical endometritis, respectively. Cows were classified as having cytological endometritis only, clinical endometritis only, or both cytological and clinical endometritis. Prevalence at exam 1 was 13.5, 9.4, and 5.8% for cytological endometritis only, clinical endometritis only, and both cytological and clinical endometritis, respectively. The detrimental effects of cytological and clinical endometritis on reproductive performance were additive. Among cows with clinical endometritis, only 38 and 36% had cytological endometritis at exam 1 and exam 2, respectively. Combination of diagnostic criteria improved neither the accuracy for predicting cytological endometritis nor the agreement between cytological and clinical endometritis. Overall, these results suggested that cytological and clinical endometritis may represent different manifestations of reproductive tract disease. They also suggested that use of the terminology clinical endometritis may not be accurate and that purulent vaginal discharge may be more descriptive.

The objective was to quantify the effect of postpartum uterine diseases on milk production and culling. Data from 2,178 Holstein cows in 6 herds enrolled in a randomized clinical trial were used. Milk production data from the first 4 Dairy Herd Improvement Association (DHIA) test-days and culling data from farm records were collected. Retained placenta (RP; ≥24 h after parturition) and metritis [≤20 d in milk (DIM)] were diagnosed by farm managers using standardized definitions. Farms were visited weekly and cows were examined at 35 and 56 (±3) DIM using endometrial cytology (cytobrush device), vaginal discharge scoring (Metricheck device), and measurement of cervical diameter by transrectal palpation. Diagnostic criteria for cytological endometritis (CYTO) and purulent vaginal discharge (PVD) were established based on a detrimental effect on subsequent reproduction. Statistical analyses were performed using linear mixed models, logistic regression models, and Cox proportional hazard models, accounting for the effects of experimental treatments and herd clustering. Milk production and culling were the outcomes. Primiparous and multiparous cows were modeled separately for milk production. Milk production of primiparous cows was unaffected by uterine diseases. The effect of metritis on milk production was variable over time in multiparous cows: it decreased production per cow by 3.7 kg at the first DHIA test, but was not different at later tests. Retained placenta decreased milk production by 2.6 kg/d in multiparous cows through the first 4 DHIA tests. The projected effects of metritis and RP in multiparous cows were reductions of 259 kg and 753 kg over 305 DIM, respectively; these effects were additive. Neither CYTO nor PVD affected milk production. Culling risks at 30 and 63 DIM were unaffected by RP and metritis. Culling hazard up to 300 DIM was unaffected by RP, metritis, CYTO, or PVD, whether or not pregnancy status, milk production, and displaced abomasum were accounted for. Uterine disease decreased pregnancy rate, which was a substantial risk factor for culling; however, if affected cows became pregnant they were not at greater risk of culling.

The objectives of this study were to assess the efficacy of antibiotic treatment for preventing postpartum uterine disease among cows at high risk of uterine disease, and to assess the efficacy of PGF(2α) for treating cytological endometritis (CYTO) and purulent vaginal discharge (PVD). A total of 2,178 Holstein cows in 6 herds were enrolled in a randomized clinical trial. Within 24h after parturition, cows were classified at being at high risk of uterine disease (HRUD; n=1,017) if they had twins, dystocia, or retained placenta. All remaining cows were classified as being at low risk of uterine disease (LRUD; n=1,161). Cows in the HRUD group were randomly allocated in a factorial design to receive ceftiofur crystalline free acid (CCFA) at 24h after parturition or be untreated, and to receive dinoprost (PGF(2α)) at 35 and 49 (±3) days in milk (DIM) or to be untreated. Cows in LRUD were randomly allocated to receive PGF(2α) at 35 and 49 (±3) DIM or to be untreated. Serum progesterone was measured at 21, 35, 49, and 63 (±3) DIM. Cows were examined at 35 (±3; exam 1) and 56 (±3; exam 2) DIM for CYTO (by cytobrush device; ≥6% polymorphonuclear cells in endometrial cytology) and for PVD (by Metricheck device; mucopurulent or purulent vaginal discharge). Statistical analyses were performed using multivariable logistic regression models accounting for herd clustering. Treatment with CCFA in HRUD cows was not associated with the probability of metritis overall, but interactions occurred such that CCFA decreased the incidence of metritis among HRUD cows that did not have retained placenta and among cows of parity ≥2. Treatment with CCFA in HRUD cows decreased the probability of PVD at exam 1. Treatment with PGF(2α) did not affect the probability of cure of CYTO or PVD irrespective of progesterone concentration at the time of treatment. Among cows affected by CYTO or PVD at exam 1, 66 and 63%, respectively, had spontaneously cured at exam 2. Cows persistently affected at exam 2 had an increased time to pregnancy and were more likely to have both CYTO and PVD at exam 1. Administration of PGF(2α) at both 5 and 7 wk postpartum did not mitigate the effects of CYTO or PVD on reproductive performance. Clinical approaches to treatment of chronic postpartum reproductive tract infection and inflammation should be reassessed.

Mastitis is a highly prevalent disease, which negatively affects cow performance, profitability, welfare, and longevity. The objectives of this study were (1) to quantify the impact of the first instance of mastitis, at different stages of lactation, on production and economic performance, and (2) to further quantify the impact of the first instance of mastitis when only cows that remain in the herd for at least 100 d in milk (DIM) and those that remain for 305 DIM are included in the analysis. A retrospective longitudinal study was conducted using data from existing animal health record files and Dairy Herd Improvement records. After editing based on selected inclusion criteria and completeness of health records, data consisted of records from first-lactation Holstein cows, from 120 herds, that calved for the first time between 2003 and 2014, inclusive. Mastitic cows were assigned to 1 of 4 groups based on when in the lactation the first event of mastitis occurred: transition (1-21 DIM), early lactation (22-100 DIM), mid lactation (101-200 DIM), or late lactation (201+ DIM). Mid-lactation and late-lactation mastitic cows were also stratified by cumulative milk yield before the mastitis event. Healthy cows (i.e., no recorded mastitis event) were randomly assigned for each lactation stage, with mid-lactation healthy and late-lactation healthy cows similarly stratified. Production performance (cumulative milk, fat, and protein yield) and economic performance [milk value, margin over feed cost (MOFC), and gross profit] were analyzed using a mixed model with herd as a random effect. Significant losses in cumulative milk yield (-382 to -989 kg) and correspondingly lower fat and protein yields were found in mastitic cows, with transition and late-lactation mastitic cows having the highest losses. Drops in production translated to significant reductions in cumulative milk value (-Can$287 to -Can$591; -US$228 to -US$470), MOFC (-Can$243 to -Can$540; -US$193 to -US$429), and gross profit (-Can$649 to -Can$908; -US$516 to -US$722) for mastitic cows at all stages. Differences between mastitic and healthy cows in the early lactation and transition stages remained for all variables in the 100-DIM analysis, but, aside from gross profit, were nonsignificant in the 305-DIM analysis. Gross profit accounted for all costs associated with mastitis and thus continued to be lower for mastitic cows at all stages, even in the 305-DIM analysis in which culled cows were omitted (-Can$485 to -Can$979; -US$386 to -US$779). The research reflects the performance implications of mastitis, providing more information upon which the producer can make informed culling decisions and maximize both herd profitability and cow longevity.

The objectives were to identify risk factors for and to quantify the effect of postpartum anovulation on reproductive performance in dairy cows. Data from 2,178 Holstein cows in 6 commercial herds enrolled in a randomized clinical trial were used. Data on periparturient disease incidence, calving history, and body condition score were collected. Cows were examined at wk 5 postpartum for reproductive tract disease; cytological endometritis was defined as ≥6% polymorphonuclear cells in endometrial cytology, and purulent vaginal discharge was defined as the presence of mucopurulent or purulent vaginal discharge. Cows were followed until 300 d in milk (DIM) for reproductive performance. Serum nonesterified fatty acids (NEFA) concentration was measured once during the week before expected calving. Serum β-hydroxybutyrate, NEFA, and haptoglobin were measured at wk 1, 2, and 3 postpartum. Serum progesterone (P4) was measured at wk 3, 5, 7, and 9 postpartum. The end of the postpartum anovulation period was defined as the first sampling time at which P4 was >1 ng/mL. Statistical analyses were performed using logistic regression models and Cox proportional hazard models. The prevalence of anovulation was 72, 44, 26, and 17% at wk 3, 5, 7, and 9, respectively. Cows were classified according to their ovulatory status as having luteal function at 21 DIM (Cyc21), as having low P4 at 21 DIM but having luteal function at least once at 35 or 49 or 63 DIM (Cyc63), or being anovulatory at 63 DIM (Anov63; no samples with P4 >1 ng/mL). Factors associated with early ovulation (Cyc21) included season, parity, decreased haptoglobinemia, and decreased serum NEFA concentration before and after parturition. Risk factors for prolonged anovulation (Anov63) included cytological endometritis, increased haptoglobinemia, and greater serum NEFA concentrations before and after parturition. Cows classified as Anov63 had an increased median time to first breeding compared with Cyc63 (74.1 vs. 73.2 d). The effect of prolonged postpartum anovulation on median time to pregnancy was conditional on parity group; a detrimental effect was present in cows of parity ≥3 (129 d for Cyc21, 151 d for Cyc63, and 180 d for Anov63), but no effect was observed in cows of parity ≤2. Overall, these findings suggest that postpartum anovulation was associated with indicators of energy balance and uterine inflammation, and with detrimental effects on reproductive performance.