Loss In Mares Research Articles

Analysis of some factors associated with pregnancy rates of frozen semen: a multi-center study

A potential source of fertility loss in mares is oviductal dysfunction, potentially caused by masses or debris in the lumen, that may prevent either sperm from reaching the fertilization site or the embryo from reaching the uterus. Recently a novel therapeutic method leading to increased pregnancy results was described by infusing misoprostol, a synthetic prostaglandin E1, in the uterus of mares with unexplained fertility problems. In this study, we aimed, after examining the compatibility of misoprostol with semen, to evaluate the pregnancy rate after routine preovulatory deep uterine horn application of misoprostol in clinically normal oestrous mares, which were inseminated in the same cycle. In experiment 1, ejaculates of 10 stallions diluted with INRA 96™ were mixed with different concentrations of misoprostol (0.01 mg/mL, 0.001 mg/mL, 0.0001 mg/mL, and 0.00001 mg/mL) and total semen motility was evaluated immediately, 12, 24, 48, and 72 h later, and compared with a control sample (mixed with NaCl 0.9%). In experiments 2 and 3, 33 privately-owned clinically normal oestrous mares were each allocated to a treatment or control group. Ovulation was then induced with intramuscularly 2.25 mg deslorelin acetate. At the moment of ovulation induction (experiment 2) and 24 h earlier (experiment 3), 0.2 mg misoprostol diluted in 2 mL NaCl 0.9% were applied deep in the uterine horn (treatment groups) and pure 2 mL NaCl 0.9% in the mares of the control groups. Mares were then inseminated 24 h after deslorelin administration and prior to ovulation with commercial chilled-warmed or frozen-thawed semen, as well as immediately after ovulation detection (both types of semen) maximally 48 h after ovulation induction. In experiment 1, regardless of time and compared with the control groups, all solutions with different concentrations of misoprostol had a negative effect on total motility of semen, which was significant for the highest concentrations (0.01 mg/mL: 18.0% reduction, CI = 22–13%, p = < 0.01). We found no beneficial effect of preovulatory uterine treatment with misoprostol on pregnancy rate (OR = 0.45, CI = 0.15–1.31, p = 0.14): in experiment 2, 2/11 (18.2%) mares of the treatment group became pregnant vs. 12/22 (54.5%) mares in the control group (OR = 0.19, CI = 0.03–1.06, p = 0.07), in experiment 3, 5/14 (35.7%) mares in the treatment group vs. 7/19 (36.8%) mares in the control group (OR = 0.95, CI = 0.23–4.02, p = 0.95), respectively. In conclusion, pregnancy rate was not increased in reproductively normal mares with routine preovulatory deep uterine horn application of misoprostol.

Incidence of embryo loss in mares inseminated before or after ovulation

Incidence of embryo loss in mares inseminated before or after ovulation

Lack of correlation between exposure to lyme disease (Borrelia burgdorferi) and pregnancy loss in mares

Exposure to Borrelia burgdorferi, the agent of Lyme disease, has been incriminated as causing an increased incidence of reproductive failure in mares. To test this hypothesis, B. burgdorferi (Lyme) antibody concentrations and incidence of early embryonic death (loss of embryo <45 days gestation, EED) and abortion (loss of fetus >45 days gestation) were determined in mares on two farms, one with a high (66% in November, 1990) incidence of Lyme exposure (Farm A, n=78 mares) and one with a low (<3%) incidence of positive Lyme results (Farm B, n=47 mares). Broodmare management practices and nutrition were similar on the two farms. All mares were bred by artificial insemination and checked by ultrasound for pregnancy at 12-20 days and again at 34-45 days after breeding. Blood samples for ELISA determination of B. burgdorferi antibody concentrations were taken prior to thebreeding season (November, 1990) and at the 34-45 day pegnancy check (February - June, 1991). Farm A had a high incidence of Lyme exposure with 23 seroconversions recorded at the time of the second pregnancy check. Only one of the mares exhibited clinical signs of Lyme disease. There was no difference in the incidence of EED between the two farms (Farm A: 12.8%; Farm B: 7.3%; P=.25) though abortions after 45 days tended to be higher on Farm A (10%) than on Farm B (2%, P=.09). There was no correlation (P=.5) with the Lyme status of mares and occurrence of EED or abortion, however, on Farm A, Early embryonic loss (but not abortion) tended to be correlated with longer residence on Farm A(EED: 31±3 mo; no EED: 17±3 mo, P=.10) though length of residence did not affect Lyme status of the mares at the time of breeding (P=.85) nor was age of the mare correlated in the incidence of EED (P=.85). Exposure to B. burgdorferi does not significantly increase the risk of EED in mares. The effect of chronic exposure to B. burgdorferi on risk of abortion and resistance to clinical signs of the disease warrants further investigation.

Relationship of progesterone to early pregnancy loss in mares

Exogenous progestins are often given to pregnant mares but many questions remain unanswered as to the relationship between concentrations of progesterone and embryo survival. Thus, embryos were collected 7 days after ovulation and transferred into either ovarian-intact recipients (I,n=15) or ovariectomized recipients which were given 100 mg progesterone (L,n=15) or 1,500 mg progesterone (H,n=15) daily. Concentrations of progesterone were determined in all mares from days 0 to 13. Recipients were examined for pregnancy with ultrasonography during days 11 through 25. Between days 28 and 100, twelve ovarian-intact, pregnant recipients were monitored for follicular and luteal changes and bled for determination of progesterone concentrations for 4 days at 2-week intervals. Twelve ovariectomized pregnant recipients were taken off injectable progesterone days 25-30 and pregnancy maintained to day 100 with an oral progestin, altrenogest. Concentrations of progesterone in these mares were determined every 3 days. Progesterone treatment had no effect on maintenance of pregnancy to day 100 or size of embryonic vesicle (P>0.05). Levels of progesterone during days 1 to 13 were 1.3 to 3.0 ng/ml, >25 ng/ml and 7 to 9 ng/ml for groups L, H and I, respectively. Concentrations of endogenous progesterone in ovariectomized pregnant mares became >1 ng/ml by day 91 of gestation indicating placental progesterone secretion. Increased concentrations of progesterone from days 60 to 100, seen in ovarian-intact, pregnant mares, were primarily due to secretions from corpora lutea. There was, in fact, a correlation between the number of 2°CL and progesterone level (r2=0.74). Initial formation of secondary CL's (2°CL) occurred from 28 to 51 days, with peak formation of 2°CL on days 55 to 70 of gestation.

Role of the embryonic vesicle and progesterone in embryonic loss in mares.

Characteristics of spontaneous embryonic loss in 21 mares were compared with those of 52 contemporary mares that maintained pregnancy. Embryonic losses were, in retrospect, grouped according to day of loss and length of the interovulatory interval, respectively, as follows: group 1, less than or equal to day 20 and less than or equal to 30 days (n = 10); group 2, less than or equal to day 20 and greater than 30 days (n = 3); and group 3, greater than day 20 and greater than 30 days (n = 8); ovulation was day 0. Mean diameter of the embryonic vesicle in group 1 was smaller (P less than 0.05) on days 12-18 than in the pregnancy-maintained group, but among the pregnancy-maintained group and the embryonic-loss groups, the mean individual growth rates of vesicles was similar (no significant difference). A more frequent (P less than 0.05) location of the vesicles in the uterine body on day 13 in group 1 was due to a greater proportion of small vesicles and for day 18 was due to a greater incidence of fixation failure. Luteal regression occurred at the expected time in 77% of the mares with loss sooner than day 20. Low concentration of progesterone on days 12, 15 and 18, a detected decrease in diameter of the corpus luteum on days 15 and 18, and an interovulatory interval of less than or equal to 30 days indicated that luteolysis was not prevented by the embryonic vesicle in group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Embryonic Loss in Mares: Incidence, Possible Causes, and Diagnostic Considerations

Fertilization rates were similar for normal and subfertile mares, and much of the difference in fertility between normal and subfertile mares was due to embryonic loss. Fertilization rate estimates for mares ranged from 71 to 96 per cent. The incidence of embryonic loss detected by ultrasonography between Days 11 and 50 was approximately 9 per cent for normal mares, and the estimated incidence of embryonic loss before Day 14 was also 9 per cent. Therefore, the estimated incidence of embryonic loss in normal mares between fertilization and Day 50 is approximately 18 per cent (Fig. 1). In subfertile mares, the corresponding estimate for embryonic loss between fertilization and Day 50 is 80 per cent, with most embryonic losses occurring before Day 14 in subfertile mares (Fig. 1). The high rate of early embryonic loss in subfertile mares could be related to embryonic defects, oviductal environment, or uterine environment. Oviductal embryos from subfertile mares were less viable than embryos from normal mares; therefore, embryonic defects were important in early embryonic losses in subfertile mares. These defects might be inherent within the embryo or might arise from the early oviductal environment. The uterine environment of subfertile mares was adequate to support normal embryos in early gestation; however, the relationship between the uterine environment and the increased metabolic demands of the conceptus in the late embryonic or early fetal periods requires further study. The uterine environment is also altered in mares with endometritis; therefore, endometritis may also be an important factor in embryonic loss in some mares. Uterine-induced luteolysis, as well as the effect of the pathogen or the resulting inflammation, may lead to embryonic loss. An increased susceptibility of some subfertile mares to endometritis could result in embryonic loss secondary to a postcoital endometritis that persists until the embryo reaches the uterus at Days 5 or 6 postovulation. Although progesterone is critical to embryonic survival, the cause-and-effect relationship between progesterone and spontaneous embryonic loss remains unclear. Reduced progesterone concentrations could be related to endometritis, failure of maternal pregnancy recognition, or luteal insufficiency. Progesterone supplementation may be indicated for some mares, but the value of exogenous progesterone for prevention of spontaneous embryonic loss has not been critically tested. A number of other factors have been associated with embryonic loss in mares.(ABSTRACT TRUNCATED AT 400 WORDS)

Embryonic loss in pony mares induced by intrauterine infusion of [formula omitted][formula omitted

Pony mares which were detected pregnant by transrectal ultrasonography received a single intrauterine infusion of either sterile saline (control, n = 12 mares) or 10 6 Candida parapsilosis (treated, n = 12 mares) between Days 11 to 14 postovulation. Subsequent embryonic loss was studied by daily ultrasonography of the mare's uterus, by serum progesterone levels, by endometrial swabs for cytologic and microbiologic examination and by endometrial biopsies that were taken after embryonic loss was detected. Significantly fewer (P<0.01) embryonic losses occurred in control than in treated mares ( 4 12 vs 12 12 ). The mean interval from intrauterine infusion until embryonic loss was 5.8 ± 2.8 d for control mares (n = 4) and 2.1 ± 0.2 d for treated mares (n = 12). Prior to embryonic loss, moderate to marked edema of the endometrial folds in 12 of 12 treated mares and free fluid in the uterine lumen of 5 of 12 treated mares were detected by ultrasonography. After embryonic loss, Candida parapsilosis was cultured from the uteri of 8 of 12 treated mares, and E . coli was cultured from the uteri of 2 of 4 control mares. Postloss endometrial smears had cytologic evidence of inflammation in 10 of 12 treated mares and 3 of 4 control mares. Intrauterine inoculation of C. parapsilosis consistently induced embryonic loss and may provide a basis to further study the relationship between endometritis and embryonic loss in mares.

Embryonic loss in mares: Pregnancy rate, length of interovulatory intervals, and progesterone concentrations associated with loss during days 11 to 15

Pregnancy rates, length of interovulatory intervals, and progesterone concentrations were examined in mares which had ultrasonically detected collections of fluid in the uterine lumen and in mares which lost the embryonic vesicle during Days 11 to 15 and did not become pseudopregnant. In mares with embryonic loss, the loss rate for mares with re-established pregnancies ( 9 18 ) was greater (P<0.05) than the loss rate for all pregnancies ( 38 154 ), indicating repeatability. Pregnancy rates were higher (P<0.01) in controls ( 100 177 ) than in mares with intrauterine fluid collections ( 2 34 ) or mares with embryonic loss ( 10 33 ), excluding the pregnancy associated with embryonic loss. The mean length (days) of the interovulatory interval was reduced (P<0.05) in mares with intrauterine fluid collections (20.4 ±0.9) and in mares with embryonic loss both for the intervals in which loss occurred (19.6 ±0.7) and for intervals in which pregnancy was not detected (21.0 ±1.0; controls, 23.5 ±0.6). Mean progesterone concentration (ng/ml) on Day 7 was lower (P<0.05) in mares with intrauterine fluid collections (8.8 ±1.8) and in mares with embryonic loss (12.1 ±1.1) than in pregnant controls (17.2 ±0.9) and nonpregnant controls (17.5 ±0.1). The embryonic loss seemed attributable to uterine-induced luteolysis in association with uterine inflammation, but the possibility of involvement of a primary luteal inadequacy or other factors in at least some of the mares was not eliminated.

Embryonic loss in mares: Nature of loss after experimental induction by ovariectomy or prostaglandin F 2α

Twenty-one pregnant pony mares were assigned to one of the following groups: 1) controls, 2) ovariectomy at Day 12, 3) ovariectomy at Day 12 plus daily progesterone treatment on Days 12 to 40, 4) PGF 2α on Day 12, 5) PGF 2α on Day 21, and 6) PGF 2α on Day 30. Based on daily examinations by ultrasound, the embryonic vesicle was maintained to Day 40 in all control mares and in mares that were ovariectomized on Day 12 and given progesterone. The embryonic vesicle was lost in all mares of the other four groups. Administration of progesterone prevented the embryonic loss associated with ovariectomy at Day 12, indicating that progesterone may be the only ovarian substance required for survival of the early embryo. The mean number of days to embryonic loss was greater for mares treated with PGF 2α on Day 12 (6.8 days) than for mares ovariectomized on Day 12 (3.0 days). In the PGF 2α-treated group, the vesicles did not become fixed at the expected time (Day 15), and mobility continued until the day of loss. In the mares treated with PGF 2α on Day 21 and in one of the mares treated on Day 30, the vesicle was lost within one to three days without prior indication. Loss may have occurred by expulsion through the cervix, since the cervix was patent on the day of loss in these mares and in the mares ovariectomized or treated with PGF 2α on Day 12. In the remaining mares treated on Day 30, the intact embryonic vesicle was dislodged on Day 31 or 32. The dislodged vesicle was mobile within the uterus and was frequently found in the uterine body. The fluid volume of the dislodged vesicle gradually decreased, and the fluid was no longer detected by Day 38 to 42. Some of the placental fluids may have been eliminated by resorption since the cervix remained closed while the fluid volume decreased.

Embryonic loss in mares: Incidence and ultrasonic morphology

Pregnancy was determined by ultrasound on Days 11, 15, 20, 25, 30, 35, 40, 45, and 50 in 154 ponies and 27 horses. In ponies, the embryonic loss rate for Days 11 to 15 ( 28 154 , 18.2%) was greater (P<0.01) than for any of the subsequent five-day intervals (0% to 3.3%). There were no losses during Days 11 to 15 in horses ( 0 27 ), and the difference between ponies and horses was significant. The loss rates for the seven periods encompassing Days 15 to 50 were not significantly different among periods. Pseudopregnancy occurred more frequently (P<0.01) following embryonic loss after Day 20 (Days 11 to 15, 26%; Days 15 to 20, 33%; after Day 20, 100%). Embryonic vesicles that were lost during Days 11 to 15 were smaller on the average than control vesicles. However, most of the vesicles grew at an apparently normal rate. Two of five vesicles that were lost between Days 15 and 20 and three of four that were lost between Days 20 and 25 were undersized during preceding examinations. Undersized vesicles were found during 13 415 (3%) examinations during Days 11 to 20 in mares that maintained the embryo and in 21 106 (20%) in mares that lost the embryo. Embryonic vesicles that were lost during Days 11 to 15 usually disappeared without previous indications, except in three mares in which the vesicle was floating in a small collection of fluid. Ultrasonic indications of impending loss at later stages included failure of fixation, an echogenic ring (vesicle) or mass floating in a collection of fluid, an echogenic area in the dead embryo, absence of heart beat, and a gradual decrease in volume of placental fluids with disorganization of the placental membranes. The solid remnants and at least some of the fluids resulting from late embryonic and early fetal death were retained sometimes for weeks or months until the debris was apparently expelled through an open cervix.

Embryonic loss in mares: Incidence, time of occurrence, and hormonal involvement

Embryonic loss in mares: Incidence, time of occurrence, and hormonal involvement