Many researchers have reported fertilization rates to be over 90% per cycle in reproductively sound mares and 81 to 92% in subfertile mares. The similarities change however shortly after fertilization. According to Ball and coworkers (1986, 1989), embryonic loss between fertilization and day 14 occurs approximately 9% of the time in young, reproductively sound mares and over 60% in aged, subfertile mares. For the first 40 to 50 days, rate of EED is approximately 20% in fertile mares and over 70% for mares considered to be subfertile. During the 1999 season at ERC, we had 8 cases where EED was diagnosed. In each case the mare was diagnosed pregnant by ultrasound exam at day 14. Mares were then followed with multiple ultrasound exams and embryonic death was seen to occur anywhere from day 16 to day 41.
In 1992, a comprehensive review by Ball outlined many factors that contribute to early embryonic loss. These factors were described as maternal, embryonic or external in origin. Maternal factors pertain to changes that occur within the mare that affect the pregnancy. Alterations in progesterone levels, the uterine and oviductal environment, maternal age and postpartum breeding have all been implicated with causing EED, either directly or indirectly. Progesterone is a hormone produced by differentiated tissue within the ovary called the corpus luteum or CL. The presence of progesterone following ovulation is critical for maintaining a pregnancy. Although this hormone has many functions, its primary purpose is to help sustain a uterine environment that will promote embryonic development. Inadequate progesterone levels will induce abortion allowing the mare to come back into heat. Progesterone levels can be measured and monitored throughout a pregnancy to identify a problem. This will however only tell the practitioner that there is insufficient endogenous progesterone being produced, not that it’s the actual cause for EED. Systemic levels of progesterone can only be maintained if maternal recognition of pregnancy occurs. The embryo needs to signal to the mare that it is present within the uterus. If there is not adequate communication then prostaglandin-F2a , a hormone produced within the uterus, will be released resulting in regression of the CL and a decrease in progesterone production. The embryo helps to communicate by moving throughout the uterus continuously from day 6 to 16 of gestation. Although not fully understood, it is thought that the embryo and/or the uterus is releasing certain proteins that aid in identifying one another. In 1998, Crossett and associates found that the progesterone dependent protein, lipocalin, does travel from the uterine lining to the yolk sac cavity of the developing embryo as early as day 16 or 17 of gestation. Estrogen produced from an early staged embryo has also been postulated to be involved with maternal recognition of pregnancy. According to Sharp and associates (1989), there appears to be a “critical deadline” between days 9 and 14 after ovulation in which recognition of the conceptus occurs. Any restriction or delay in movement during this time may not prevent the release of prostaglandins, thus creating a uterine environment that initiates early embryonic death. Disruption in the uterine environment can
bring death upon the embryo. Endometritis or an inflammation to the uterine lining induced by infection almost always results in premature prostaglandin release, CL regression and embryonic loss. Many researchers, including Ball and associates in 1988, have induced endometritis and subsequent embryonic death by inoculating pregnant mare with infective agents such as pathogenic bacteria or yeast. Fibrous tissue formed around the uterine glands can also create inadequate conditions for sustaining a pregnancy. These periglandular fibrotic lesions limit the ability of the glands to function properly and aid in embryonic development. An early study by Kenney (1978) found that fibrosis is a common cause of embryonic death between 40 and 90 days of gestation. The presence of uterine le