CHAPTER 19 Infertility Due to Noninflammatory Abnormalities of the Tubular Reproductive Tract
Infertility in mares can result from developmental abnormalities or acquired conditions that cause reproductive failure due to inflammation with or without infection in the reproductive tract, abnormal physiologic events, abnormal reproductive tract anatomy, structural alterations resulting in abnormal function, and neoplasia. This chapter will focus on infertility that is due to congenital or acquired problems of the tubular reproductive tract that are noninflammatory in nature.
REPRODUCTIVE TRACT DEVELOPMENT
Abnormal reproductive tract development can arise from an abnormal chromosomal/genetic condition or an abnormal hormonal environment as well as from exogenous factors.1 Many different conditions that result in abnormal development of the reproductive tract in the horse have been reported. The most common genetic condition is X monosomy or (63XO) gonadal dysgenesis, which is the presence of an aneuploid defect of the sex chromosomes.2 The fetus develops into a female with hypoplastic ovaries and a small underdeveloped tubular reproductive tract with hypoplastic endometrial glands. These animals fail to cycle normally even following hormonal treatment and are considered sterile. Attempts to establish pregnancies via embryo transfer into these mares have not been successful enough to consider these animals appropriate recipients. Affected mares are typically small and weak at birth and remain small in stature as adults. The condition is thought to arise from nondisjunction during meiosis and is sporadic in nature rather than hereditary.
The second most common condition is XY sex reversal.3 XY gonadal dysgenesis results in a gonadal female with ovaries or streak gonads and a variability in female phenotype from normal to one with hypoplastic or aplastic tubular genitalia. These animals fail to demonstrate normal cyclic estrous behavior despite hormonal stimulation. This author has seen one Thoroughbred mare with the XY gonadal dysgenesis syndrome. This mare would sporadically display estrous behavior, presumably from adrenal steroid production.
A multitude of other genetic/chromosomal anomalies have been reported in conjunction with hermaphroditic, pseudohermaphroditic, and subfertile conditions including XX sex reversal, XXY, mosaicism, and chimerism. These animals have displayed varying degrees of gender ambiguity, associated with the internal and external portions of the reproductive tract, and infertility.
Other developmental abnormalities will be discussed with regard to the structure that is affected.
Oviducts
Congenital Defects
Although rare, developmental abnormalities involving the oviducts have been reported.4 Segmental aplasia is the condition in which a portion of the oviduct does not develop. Hydrosalpinx may result from the lack of patency of the oviductal lumen depending on the location of the aplastic segment. Some cysts or series of cysts near the caudal portion of the oviduct are thought to be a persistence of accessory oviducts that may develop at the end of the paramesonephric duct. Large cystic structures may be a cause of infertility.
Acquired Abnormalities
Acquired abnormalities of the uterine tube are usually secondary to disease processes occurring around other structures. For example, adhesions involving the oviduct may develop secondary to salpingitis, which typically arises from severe inflammatory/infectious processes in the uterus or abdomen. Adhesions that obstruct the lumen from external pressure may also cause hydrosalpinx.4 Fertilization following ovulation from the ipsilateral ovary would be prevented in cases in which complete occlusion of the oviductal lumen is present.
Although globular collagenous masses have frequently been reported to occur mainly in the ampullar isthmic junction area, the clinical significance of these structures remains controversial. Unfertilized oocytes have been located on the up- and downstream aspects of many of these masses, and large collagenous accumulations appeared to fill and in some cases distend the oviductal lumen. Oviductal blockage could prevent oocyte/embryo migration past the mass. One study demonstrated increased pregnancy establishment following surgical intervention to re-establish oviductal patency of previously blocked tubes in a group of mares with a 2- to 4-year history of infertility.5 Although not easily diagnosed under field conditions, oviductal occlusion should be a consideration in mares in which other causes of infertility have been ruled out.
Uterus
Developmental Defects
Segmental aplasia is the condition in which a portion of the uterine horn or body does not develop. This author has observed cases in which aplasia has involved one entire uterine horn. The mares involved had a history of being difficult to get in foal and subsequently bearing small offspring. Two other mares were reported to establish pregnancies when the ovary ipsilateral to the existing horn had ovulated.6 Segmental aplasia involving one uterine horn prevents sperm from contacting the ovum following ovulation from the ovary of the aplastic side. When the aplastic segment includes the uterine body, sperm are completely prevented from passage into the oviduct and fertilization. Depending on the location of the aplastic segment in one uterine horn, this condition may prevent adequate uterine migration by an embryo conceived from an ovulation by the contralateral ovary. Inadequate uterine migration by an embryo will result in a lack of maternal recognition of pregnancy. Decreased functional uterine space may also limit placental growth and result in smaller offspring, premature delivery, or abortion. One mare with repeated abortions was reported to have a short or absent uterine body.7 Pregnancy loss was attributed to insufficient placental surface.
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