I. Male
The male reproductive system in the horse consists of testes and the accessory genital organs that include penis and prepuce. The testes of the sexually mature stallion assume a double complementary function: the production of sperm and the secretion of steroid hormones, mainly testosterone to produce the male phenotype. In domestic animals the testes descend into the scrotum shortly before or after birth and need to remain in this position permanently for regulated optimal spermatogenesis at a temperature lower than that of the body. In the horse, testicular descent is completed at birth or shortly after birth (10–14 days) considering average gestation of 300 days.
1. Morphology of the normal mature equine testis
The stallion testis is enveloped by a protective fibrous tunica albuginea with the epididymis loosely attached to the testis. On cross section, the pigmented testicular parenchyma should bulge indicating functional maturity. It also should present the mediastinum testis as a band of connective tissue passing from pole to pole. The mediastinum testis contains blood vessels, lymphatics, and the rete tubules.
Testicular tissue requires a fixative for optimal preservation of the seminiferous tubules and the interstitium containing the interstitial or Leydig cells. The preferred fixative is Bouin’s solution.
The seminiferous tubules containing germ cells and Sertoli cells are extremely sensitive to a variety of exogenous and endogenous adverse influences. Structural integrity and prevention of breakdown of the immunologically protective blood–testis barrier is another point of consideration for certain pathologic immune-deranged processes in the testis.
Sperm development and maturation are complex processes following integrated influences of hormones, nutritional factors, temperature, photoperiod, and genetically determined rate of spermatogenesis (49 days in the stallion).
Figure 12.1. Horse. Testis. Normal. Sexually Mature Stallion. The cross section shows a slightly bulging red parenchyma and the mediastinum testis as a regular gray band in the center (arrows). The amount of lipopigment wthin the interstitial cells determines the color of the testicular surface. (Courtesy Dr. M. Pozor, University of Florida.)
Figure 12.2. Horse. Juvenile. Testes and Epididymes. The epididymis normally is loosely attached to the maturing testis.
2. Testicular hypoplasia
Testicular hypoplasia is a pathologic condition at puberty. It needs to be differentiated from testicular atrophy. Cryptorchidism is an example of a condition that leads to testicular hypoplasia. It is the result of failure of testicular descent whereupon one or both testes may be arrested in the abdomen or inguinal ring. Usually testicular descent is completed by the time of birth. Rarely it occurs days after birth.
Figure 12.3. Horse. Testes. Unilateral Hypoplasia. Cryptorchidism. There is asymmetry in the testicular size with the smaller testis being hypoplastic from failing to descend into the scrotum.
3. Testicular degeneration/atrophy
The seminiferous epithelium is very susceptible to a variety of adverse influences, and injury to the germ cell layers interfering with the spermatogenic cycle frequently induces degeneration with progression to testicular atrophy as end phase of the process.
Figure 12.4. Horse. Testis. Unilateral Atrophy. The stallion had a unilateral inguinal hernia. The testis on the left is unaffected from the trauma. The testis on the right is small and dark. The red brown color is typical of atrophy. (Courtesy Dr. R. Foster, University of Guelph.)
The literature surprisingly contains very little information about primary testicular degeneration in the horse despite the obvious importance of reproductive health, particularly in breeding stallions. In general, testicular degeneration has a variety of exogenous and endogenous etiologies. It needs to be differentiated from testicular hypoplasia because diffuse, chronic degeneration results also in reduction of testicular size.
4. Testicular inflammation
Orchitis may start as periorchitis from a preceding, descending peritonitis, or it may ascend from an epididymitis, spread hematogenously, or develop secondary to trauma to the scrotum.
Figure 12.5. Horse. Testis. Chronic Verminous Orchitis. The parenchyma has a mottled white appearance indicating fibrosis and does not bulge on cut section. Causes for orchitis in the horse are bacteria such as Actinobacillus equuli, Streptococcus sp., Staphylococcus sp., and parasites such as migrating Strongylus edentatus larvae as has been the case in this image. (Reprinted with permission from Color Atlas of Reproductive Pathology of Domestic Animals, Buergelt, Figure 3-41, Page 40, Copyright Elsevier, 1997.)
5. Testicular neoplasia
Primary testicular neoplasms affect aged stallions. They are either sex cord (gonadal-stromal) tumors including Leydig cell (interstitial cell) and Sertoli cell tumors, or germ cell tumors to include seminomas and teratomas. Sex cord-stromal tumors are rare with individual case reports in the literature as is the case with mixed germ cell-sex cord-stromal tumors. Cryptorchid testicles in particular should be examined for hidden tumors.
Figure 12.6. Horse. Testis. Seminoma. A multilobulated bulging mass has replaced the testicular parenchyma and has caused testicular enlargement. Seminomas are usually unilateral and malignant in horses.
Figure 12.7. Horse. Testis. Benign Teratoma. This usually small tumor affects young individuals, deriving from various embryonic germ layers. The tumor may contain visible hair or bone. On occasion it is malignant with local invasion.
Figure 12.8. Horse. Testis. Leiomyosarcoma. This mesenchymal tumor arose from the tunica albuginea and spread into the space between epididymis and vaginal cavity.
6. Accessory male sex organs
Seminal Vesiculitis. Gram-negative bacteria such as Pseudomonas aeruginosa can be isolated from this uncommon inflammatory disorder.
7. External genitalia
Figure 12.9. Horse. Penis. Paraphimosis. This condition is defined as the inability to withdraw the penis into the sheath. The opposite condition, the inability of the penis to extend from the sheath, is defined as phimosis. Paraphimosis occurs congenitally or is acquired after treatment with tranquilizing drugs. Postmortem paraphimosis occurs in conjunction with severe decomposition. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 12.10. Horse. Penis. Coital Exanthema. Equine herpesvirus (EHV)-3 causes pustular and ulcerative balanoposthitis. Differential etiologies should include habronemiasis, early squamous cell carcinoma, frostbite, trauma, and infection with Trypanosoma equiperdum (equine dourine) in regions where this disease is endemic.
Figure 12.11. Horse. Penis. Ulcerative, Pyogranulomatous Balanitis. Habronemiasis. Severe, ulcerative, pyogranulomatous inflammation of the tip of the penis and prepuce (posthitis) can result from infestation of larvae of Habronema sp. that have a tissue preference for the urethral process. Immediate differential diagnosis should be squamous cell carcinoma.
Figure 12.12. Horse. Tip of Penis. Habronemiasis. Hebronema larval nodules are present at the urethral orifice, a typical site of deposition. (Courtesy P. Isenbarg, Henderson, NV.)
Figure 12.13. Horse. Prepuce. Squamous Cell Carcinoma. This neoplasm typically presents as a cauliflower-like ulcerative malodorous growth on the glans penis or prepuce with local invasion and metastasis to regional lymph nodes. Equine papilloma virus has been detected via molecular techniques in equine genital squamous cell carcinomas. Another neoplasm with similar biologic behavior at this penile site is melanoma in aged gray stallions.
8. Miscellaneous
Figure 12.14. Horse. Testis. Unilateral Torsion with Ischemic Hemorrhagic Necrosis. This very painful condition is characterized by severe hemorrhagic infarction of the testis and its soft tissues as it twists around its longitudinal axis. The right testis depicted has twisted, with infarction, congestion, and mild atrophy being the principal changes. (Courtesy Dr. A. King, Drost Project, University of Florida.)
Figure 12.15. Horse. Testis. Tunica Albuginea. Ectopic Cortical Adrenal Tissue (arrow). Small discrete nodules on the surface are present.
Figure 12.16. Horse. Testis. Nodules on Tunica Albuginea. Small discrete nodules on the surface of the gonad and adjacent to the head of the epididymis may be appendix testis (double arrow), a paramesonephric duct vestige.
Figure 12.17. Horse. Reproductive Tract. Intersex. Intersexes are defined as individuals equivocal as to gender differentiation and phenotype. They are typically sterile and can be appropriately classified according to genotype by sex chromosomal analysis via karyotyping. This reproductive tract has been diagnosed as male pseudohermaphrodite with intra-abdominal testes, epididymes, spermatic cords, and thin tubular structures resembling a juvenile uterus. Externally, prepuce-like and penis-like structures can be expected in equine male intersexes.
Figure 12.18. Horse. External Genitalia. Intersex. Externally, prepuce-like and/or penis-like structures can be expected in equine intersexes.
II. Female (nonpregnant)
The equine female reproductive tract consists of ovaries, oviducts, uterus, cervix, and vagina representing accessory female sex organs. The function of the ovaries is to produce mature eggs and steroid hormones for the regulation of the reproductive tract in nonpregnant and pregnant conditions. The gametogenic and endocrine functions of the ovary work in a cyclic pattern.
1. Morphology of the normal mature equine ovary
The mare’s ovary has unique morphologic and functional features. The medulla is external to the cortex. Ovulation occurs at the site of the ovulation fossa. The Graafian follicles become quite large prior to ovulation measuring up to 6 cm and more in diameter and should not be confused with cystic follicles. The texture of the equine ovary is firm due to a very fibroblastic stroma and should not be mistaken for a mesenchymal tumor during gross and/or microscopic evaluations.
Figure 12.19. Horse. Ovary. Normal Configuration. The shape of the ovary is oval with the ovulation fossa being the concave portion adjacent to the fimbriae. The ovary is covered by a fibrous capsule.
Figure 12.20. Horse. Cycling Ovary. On cross section, follicles and a corpus luteum are visible. (Courtesy Dr. J. Roberts, National Zoo, Washington, DC.)
2. Anomalies
Figure 12.21. Horse. Genital Tract. Turner Syndrome. This chromosomal abnormality characterized by an XO karyotype leads to noncycling ovaries and a juvenile female reproductive tract.
X monosomy appears to be a relatively common cytogenetic disorder in mares. Affected animals appear normal externally but with smaller than normal vulva. The uterus is also small, the cervix usually open and flaccid. The ovaries range in size from small to very small. Most XO mares fail to cycle, although some show sporadic or indistinct periods of estrous behavior.
3. Ovarian cysts
These are either next to the ovary, defined as parovarian cysts and congenital in origin (remnants of the mesonephric ducts or tubules), or intraovarian and depending on the histologic features, also congenital or acquired. Appropriate classification requires histologic examination of cyst lining and wall composition.
Figure 12.22 Horse. Left Ovary. Corpus Hemorrhagicum. Hemorrhage occurring into the cavity of the follicle after ovulation produces a corpus hemorrhagicum. Right Ovary. Parovarian Cyst. The cysts are lined by a single layer of cuboidal epithelium and contain clear fluid. About ten morphologic different parovarian and intraovarian cysts may occur. These have to be differentiated by microscopic examination.
4. Ovarian inflammation
Inflammation of the ovaries is extremely rare in horses. If present, it results from an adjacent peritonitis.
5. Ovarian neoplasia
Typically in the mare these would be sex cord-stromal tumors known as granulosa cell tumors. The tumors are usually unilateral and benign, and they may reach the size of a grapefruit. They are hormonally active, produce inhibin, estrogens, or androgens, and consequently interfere with the estrous cycle. The contralateral ovary may undergo atrophy. Surgical removal is curative. Germ cell tumors such as dysgerminoma or teratoma are very rare.
Figure 12.23. Horse. Ovary. Granulosa Cell Tumor. The typical appearance on cross section is characterized by multiple cystic spaces separated by dense stromal tissue. Differential diagnoses should consider the infrequent germinal inclusion cyst and cystadenomas.
Figure 12.24. Horse. Ovary. Cystadenoma. Very rare. This is an example of benign neoplastic intraovarian cysts progressively occupying the entire ovary. (Reprinted with permission from Color Atlas of Reproductive Pathology of Domestic Animals, Buergelt, Figure 9-36, Page 109, Copyright Elsevier, 1997.)
The case was diagnosed as cystadenoma. Cystadenomas are rare, mostly unilateral polycystic tumors that do not metastasize or are not hormonally active. The differential diagnosis is germinal inclusion cysts when peritoneal cells become entrapped in the ovary after ovulation to fill with fluid and to expand within the ovary.
Figure 12.25. Horse. Ovary. Papillary Carcinoma of Ovulation Fossa. This shaggy tumor arose from the surface epithelial cells of the ovary. Its occurrence is extremely unique in the horse. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 12.26. Horse. Ovary. Benign Teratoma. On cross section an encapsulated cystic growth contains packaged hair in the center. This type of usually benign tumor is composed of multiple tissues foreign to the organ in which they arise.
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