Читать книгу Bovine Reproduction - Группа авторов - Страница 206

Factors involved in pathogenesis of testicular degeneration include abnormal testicular thermoregulation, nutritional excess or deficiency, toxicity, inheritance, congenital blockage of sperm outflow from testes, infectious disease, severe trauma, and senile atrophy.

Testes of scrotal mammals function normally when testis temperature is 2–6 °C below body temperature [1]. Scrotal insulation is a classic model to induce temporary testicular degeneration [2, 3]. In one study, the scrotum was insulated for 10 days; there were reductions in semen quality, but no fibrotic lesions within 6 months after insulation [4]. Therefore abnormal testicular thermoregulation that is reversible (e.g. obesity) may not be a common cause of permanent damage. Other less common causes of chronic abnormal thermoregulation that may lead to temporary or permanent testicular degeneration include severe chronic scrotal dermatitis, heat and swelling due to orchitis, trauma, chronic illness with prolonged fever, endotoxins (potent gonadotropin inhibitors), a congenitally short scrotum, severe scrotal frostbite leading to adhesions, and incomplete descent of a testis into the scrotum.

Obesity is a leading cause of testicular degeneration in bulls. It is common to fatten bulls for livestock shows and sales. Many bulls become obese and fat accumulates in the scrotum, chronically increasing testicular temperatures [2]. However, after a reduction in body condition, including loss of fat from the scrotum, regeneration of seminiferous tubules may occur with return to normal sperm production [5].

Nutritional deficiencies seldom cause testicular degeneration in bulls. Naturally occurring deficiencies are usually multiple and deficiency of any single nutrient as a cause of bull infertility is rare. Similarly, vitamin deficiencies are also rare as a cause of infertility in larger male domestic animals if forages are normal in quality and quantity. However, reductions in feed quality and/or quantity causing weight loss may depress spermatogenesis via an endocrine effect on developing germ cells rather than by vitamin or mineral deficiencies. In one study, protein supplementation of bulls on poor‐quality forage significantly increased dry matter intake, enabling maintenance of live weight, whereas in control (unsupplemented) bulls, weight loss was accompanied by a significant decrease in scrotal circumference and daily sperm production per gram of testis. However, histologically, seminiferous tubule activity was apparently not different between bulls with or without protein supplementation [6]. Vitamin A deficiency can cause testicular degeneration in laboratory rats [7], but in bulls under practical feeding conditions, diets that result in long‐term marginal vitamin A deficiency or a relatively short‐term absence of vitamin A intake probably have minimal effects on spermatogenesis [8]. There is little evidence that deficiencies of vitamins B, C, D, or E cause infertility in domestic animals [9]. Although vitamin E is essential for reproduction in rats, naturally occurring deficiencies resulting in testicular degeneration in livestock have apparently not been reported. Mineral deficiencies may affect male reproduction, but reports are rare. Deficiencies of calcium, manganese, zinc, iodine, potassium, and selenium have not been proven to cause testicular degeneration. Deficiencies of phosphorus, cobalt, iron, zinc, and copper may cause anemia, lack of appetite, and weight loss, with adverse effects on reproduction. Deficiencies of these minerals are often associated with inadequate protein and vitamin A.

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 (Ralgro^TM) 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].