No abstract

Uterine infections (i.e., endometritis) can have a major economic impact on dairy production. Identifying cows that are susceptible to endometritis and improving the diagnosis of endometritis could lead to a reduction in the impact of such infections. Thus, we used Holstein cows to determine whether postpartum changes in 13, 14-dihydro-15-keto-PGF2alpha (PGFM), a metabolite of PGF2alpha, could be used to identify cows that are susceptible to endometritis and to improve the diagnosis of endometritis. Cows were assigned to three treatments. 1) Control (n = 10) had no clinical or bacteriological signs of endometritis during the study. 2) Treated (n = 11) developed endometritis spontaneously and were treated i.m. with 25 mg of PGF2alpha immediately after clinical diagnosis (d 17.6 +/- 0.8 postpartum; mean +/- SEM). 3) Untreated (n = 10) developed endometritis spontaneously and were not treated after diagnosis (d 20.0 +/- 0.5). Examinations of external and internal genitalia and bacteriological data were used to diagnose endometritis. From d 0 (calving) until approximately d 63 postpartum, jugular blood was collected three times weekly. Progesterone and PGFM were quantified in plasma. For PGFM, the treatment x day interaction was significant (P < 0.01). Overall PGFM profiles for Control and Treated differed (P < 0.05), but the Untreated profile did not differ from either Control or Treated. To better understand the interaction, PGFM data from d 0 to 35 postpartum were partitioned into consecutive 7-d periods, and d-36 and greater data were partitioned into one period. Effects of treatment, day, and the treatment x day interaction were then evaluated within period. Except for the d-15 to -21 period, PGFM was greater (P < 0.03) in Control than in Treated and Untreated. In Treated and Untreated, PGFM increased during the d-15 to -21 period. For progesterone, treatment did not affect the profiles, but day was significant (P < 0.001). Progesterone concentrations were basal from d 0 until approximately d 12, and they generally increased after d 12. Onset of endometritis was associated with increased progesterone concentrations. Treatment did not affect the interval from calving to first detected estrus (29.5 +/- 4.9 d) or from calving to AI (73.3 +/- 8.7 d). We conclude that PGFM measures have the potential to be used to identify cows that are more likely to develop endometritis and that PGFM may aid in the diagnosis of endometritis.

No abstract

Synchronization of estrus and ovulation is essential for AI of ewes during a predetermined time frame, and progestogen-eCG treatments are typically used to prepare the ewes. However, eCG is not readily available in the United States, but P.G. 600 (400 IU of eCG and 200 IU of hCG) is available. Thus, we conducted a study to determine the effects of eCG and P.G. 600 on the timing of estrus and ovulation after progestogen withdrawal. Ewes were assigned to two replicates of an experiment with the following treatments: 1) 3-mg norgestomet implant (i.e., one-half of a Syncro-Mate-B [SMB] implant) for 10 d, plus 2 mL of saline i.m. at SMB removal (n = 11); 2) 3-mg SMB implant for 10 d, plus 400 IU of eCG i.m. at SMB removal (n = 13); and 3) 3-mg SMB implant for 10 d, plus P.G. 600 i.m. at implant removal (n = 9). On d 6 after SMB insertion, PGF2alpha was used to induce luteolysis. Beginning 12 h after implant removal, vasectomized rams were used at 12-h intervals to check for estrus. When a ewe was detected in estrus, each ovary was evaluated ultrasonically. Ovaries were evaluated again 16 h later and then at 8-h intervals until ovulation. Treatment altered the interval from implant removal to estrus (less [P < 0.05] in SMB + eCG than in the other two groups) and to ovulation (greatest [P < 0.05] in SMB). However, the treatment x replicate interaction was significant for the intervals from implant removal to estrus (P < 0.03) and from implant removal to ovulation (P < 0.05). An inconsistent response in the SMB-treated ewes seemed to be primarily responsible for the interaction. The intervals to estrus and to ovulation for the SMB-treated ewes were shorter (P < 0.05) in Replicate 1 than in Replicate 2. Also, both intervals seemed to be less consistent between replicates for the SMB + P.G. 600- than for the SMB + eCG-treated ewes; that is, eCG seemed to increase the predictability of the intervals to estrus and to ovulation. Neither the main effects of treatment and replicate nor their interaction were significant for the interval from estrus to ovulation (38.4 /- 3.3 h), size of the ovulatory follicle (7.7 +/- 0.8 mm), or ovulation rate (1.6 +/- 0.2). We concluded from this experiment that eCG is a better choice than P.G. 600 as the gonadotropin to use at the time of progestogen withdrawal to prepare ewes for AI during a predetermined interval.

In cattle and sheep, a progestogenated uterus is susceptible to infections, but this is not well documented for pigs. Therefore, the effects of day of the estrous cycle and progesterone on the susceptibility to uterine infections were evaluated. Gilts (n = 5 per group) were assigned to treatments in 2 x 2 factorial arrays. In Exp. 1, day of cycle and bacterial challenge were main effects. On d 0 or 8, uteri were inoculated with either 70 x 10(7) cfu of Escherichia coli and 150 x 10(7) cfu of Arcanobacterium pyogenes in PBS or with PBS. In Exp. 2, ovariectomy (OVEX) and progesterone treatment were main effects. On d 0, gilts were ovariectomized or a sham procedure was performed. After surgery, gilts received i.m. injections of progesterone (10 mg/5 mL) or 5 mL of safflower oil diluent twice daily. On d 8, gilts were inoculated with the same doses of bacteria as in Exp. 1. In Exp. 1 and 2, vena caval blood was collected for 4 d, after which uteri were collected. Sediment and ability to culture E. coli and A. pyogenes from uterine flushings were used to diagnose infections. Differential white blood cell counts and lymphocyte response to concanavalin A (Con A) and lipopolysaccharides (LPS) were used to measure lymphocyte proliferation. Progesterone, estradiol-17beta, prostaglandin F2alpha, (PGF2alpha), and prostaglandin E2 (PGE2) were measured in vena caval blood. In Exp. 1, d-8 gilts receiving bacteria developed infections, but d-0 gilts receiving bacteria did not. Daily percentages of neutrophils and lymphocytes changed (P < 0.05) with cycle day and bacterial challenge. Basal- and Con A-stimulated lymphocyte proliferation were greater (P < 0.05) for d-0 than for d-8 gilts. Concentrations of PGF2, (P < 0.01) and PGE2 (P < 0.05) increased after bacterial challenge, regardless of stage of the estrous cycle at the time of inoculation. In Exp. 2, OVEX decreased (P < 0.001) and progesterone treatment increased (P < 0.001) progesterone concentrations, and OVEX decreased (P < 0.01) estradiol-17beta. Gilts with ovarian and/or exogenous progesterone developed infections. Daily percentages of neutrophils and lymphocytes changed in response to OVEX, and neutrophils changed (P < 0.05) in response to endogenous and exogenous progesterone. Lymphocyte proliferation in response to Con A and LPS increased (P < 0.05) with OVEX and decreased (P < 0.05) with progesterone treatment. We conclude that endogenous and exogenous progesterone reduce the ability of the uterus in gilts to resist infections.