Although experimental exposure to various drugs, chemicals, and heavy metals causes testicular degeneration (mainly in rats and mice), there are very few reports of naturally occurring cases in bulls [9, 10]. Ingestion of plant toxins may cause testicular degeneration. Fusarium mold in grain crops is common; one of the toxins produced is zearalenone. It has an estrogenic effect, with potential to reduce semen quality and cause testicular degeneration. In one report [11], 23 young rams became infertile after eating grain containing zearalenone (5–20 mg/kg) for several months. Furthermore, two bulls fed maize containing zearalenone (20 mg/kg) for 72 days had poor semen quality after 21 days [11]. Histologically, rams' testes had complete destruction of germinal epithelium and aspermia, whereas in bulls, degeneration of the germinal epithelium was marked only in certain areas of the testes, although >75% of sperm were degenerate [11]. Cottonseed meal may cause gossypol toxicity; it alters mitochondrial structure and function and causes abnormalities of spermatocytes, spermatids, and mature sperm [12], although it did not appear to cause testicular degeneration [13, 14]. Locoweed (Astragalus lentiginosus) may cause temporary testicular degeneration, as reported in mature rams [15]. Growth‐promoting implants have potential to impair testicular development [16, 17]. When bulls were implanted with zeranol (RalgroTM) at birth and at 3 and 6 months of age, or every 3 months from birth to 18 months of age, scrotal circumference was reduced but tended to recover with increasing age. However, implanting bulls with zeranol after 7 months of age had limited effects on reproductive organs.
Congenital and inherited disorders of testes and epididymis may be involved in testicular degeneration. Young bulls with testicular hypoplasia may produce semen with satisfactory quality, but are more prone to develop testicular degeneration at two to three years of age [10]. In young bulls, small scrotal circumference has been associated with a lack of germinal epithelium within seminiferous tubules [18, 19]. Hypoplasia may be unilateral or bilateral, although most cases are unilateral and the left side is more frequently affected [10]. There appears to be no clear definition for testicular hypoplasia based on physical measurement. Histologically, testicular hypoplasia is defined based on cell populations in seminiferous tubules. Testicular hypoplasia is congenital and possibly hereditary. For example, in Swedish Highland cattle, it appears to be caused by an autosomal recessive gene with incomplete penetrance [20]. This condition occurs in many breeds, albeit at very low frequency [21]. Double muscling (myofiber hyperplasia), inherited as an autosomal recessive, is associated with a high incidence of bilateral testicular hypoplasia [22].
The embryo needs to connect its gonads with the mesonephric urinary system to develop its excurrent duct system. The connection comes via the rete tubules that develop between the fetal gonad and mesonephros. The ureter for the mesonephros, the mesonephric duct, will become the epididymis. Efferent ductules develop from the mesonephric tubules and join to the mesonephric duct via rete tubules during embryonic development. Failure of some efferent ductules to join with the rete may later (at puberty) result in sperm impaction of blind‐ending ductules; their subsequent rupture causes sperm granulomas. If all efferent ductules are obstructed, seminiferous tubule fluid and sperm cannot leave the testes, resulting in testicular enlargement, edema, and degeneration.
Infectious organisms may be involved in testicular degeneration. Eperythrozoon infection caused anemia, scrotal and hindlimb edema, and soft testes in young bulls. Loss of scrotal thermoregulation was likely the main cause of testicular degeneration and poor semen quality [23]. In another report, testicular degeneration and loss of libido occurred in beef bulls experimentally inoculated with Anaplasma marginale [24]. Testicular degeneration was confirmed by histopathology and semen evaluation. Picornavirus and bovine enterovirus isolated from semen and feces of a bull were implicated as a cause of orchitis, testicular degeneration, aspermatogenesis, and loss of libido [25].
Diagnosis
During clinical evaluations, it may be difficult to distinguish between disturbances of testis function that reduce sperm output and increase sperm abnormalities compared to more severe disturbances of testis function that cause degeneration. Therefore a clinical diagnosis of degeneration is arbitrary. Degeneration does not necessarily reduce sperm concentration in the ejaculate, due to sperm accumulation in ampullae during sexual rest.
Ultrasonography is not necessarily clinically useful for distinguishing between normal testis tissue and tissue that has lost germinal epithelium [26]. When considerable fibrous tissue is present, testes may become more firm; however, a diagnosis of fibrosis is best accomplished with ultrasonography. Echographic anatomy of abattoir‐derived bull testes has been reported [27] and ultrasonography of testes does not affect semen quality [28]. Ultrasonography has been used to examine effects of testicular degeneration induced by scrotal insulation in bulls [4, 29, 30]; however, there were no evident visible changes in ultrasonograms after induced testicular degeneration. Furthermore, some studies failed to demonstrate significant correlations between computer analysis of ultrasonogram pixel intensity and semen quality, either during breeding soundness evaluations or after scrotal insulation [29, 31]. In other studies, echogenic changes induced by scrotal insulation preceded increased sperm abnormalities [4]; changes in pixel intensity accounted for 13–25% of variation in semen quality of ejaculates collected two to four weeks after ultrasonographic examination.
Prognosis
Recovery of normal testis tone and spermatogenesis is possible in most cases of testicular degeneration if the cause can be removed. Obese bulls may be fed restricted diets or put on pasture for weight loss, although it often takes three to four months for sufficient weight loss and seminiferous epithelium regeneration to restore semen production. When breeding seasons are short and bull to female ratio is ~1 : 35, there is sufficient breeding overlap to prevent an infertile dominant bull from making a significant impact on herd fertility [32, 33].
Testicular Fibrosis
Focal testicular fibrosis is common in some groups of bulls after weaning. Diffuse fibrosis is much less common and in aged bulls it occurs more commonly in ventral parts of testes [10]. Routine ultrasonography of the testes of bulls may reveal presence of a few to many foci of fibrosis, with or without production of elevated percentages of abnormal sperm. In one study [34], ultrasonography of the testes was done in bulls at three locations in western Canada (n = 325) and one in Argentina (n = 387) to determine prevalence of fibrotic lesions and relationships between fibrotic lesions and location, age, breed, testis size, and semen quality. Bulls in western Canada are typically fed forage and grain‐based rations after weaning, whereas in Argentina, weaned calves did not receive grain supplementation until 18 months of age. Bulls used in the study ranged in age from 3 to 20 months and ultrasonography was done at varying ages.
Bulls in all groups in Canada and Argentina had been vaccinated at weaning with clostridial vaccines and vaccines for bovine viral diarrhea virus (BVDV), infectious bovine rhinotracheitis, and parainfluenza 3 (some bulls also received Mannheimia and Histophilus somni vaccines). In all groups, there were no unexpected health issues except in Group 1 in Argentina. In that group, there was a severe outbreak of respiratory disease with high morbidity and 6% mortality, attributed to bovine respiratory syncytial virus (BRSV). In the following year, bulls at this location were vaccinated for BRSV, preventing problems