Sperm release into tubules starts as early as 8 months and occurs in most bulls by 10 months. Therefore tubule impaction with sperm and tubule rupture with escape of sperm into the peritubular space of the testis tissue would not be expected to occur much before 8 months. Because sperm are antigenically foreign, a tissue reaction against escaped sperm could cause fibrosis. Impaction of seminiferous tubules might be due to congenital failure to develop a tubular connection to the rete tubules. Tubule rupture and a tissue reaction against sperm should not occur until testes produce sperm; as production increases, testes lesions would be expected to increase in number and severity.
Bacterial and viral infections are common in early post‐weaning period when maternal immunity has waned and animals of multiple origins intermingle [36]. Thus an infectious process, as a cause of fibrotic lesions, would fit the time period when testis lesions appear in young bulls. Although bacterial or viral infections would be expected to cause testicular swelling and pain, perhaps inflammation is mild and not apparent. Infectious agents could cause inflammation of arterioles and capillaries in the testes, leading to local tissue necrosis and formation of foci of fibrosis [10]. Viral infections may also target specific cells within seminiferous tubules, e.g. Sertoli cells or individual germinal cells, resulting in tubule damage and fibrous tissue infiltration [37, 38].
Two common viral diseases of cattle, bovine herpesvirus (BHV)‐1 and BVDV, have been investigated for their role in male reproductive infections. Both viruses have been isolated from semen [39, 40] and BHV‐1 has been associated with degenerative changes in the seminiferous epithelium, perhaps due to illness and fever [41]; however, there are no reports that associate BHV‐1 or BVDV with lesions in bovine testes.
The association of a greater prevalence of testis fibrosis with occurrence of a severe outbreak of BRSV respiratory disease in the Group 1 bulls in Argentina, combined with a lesser prevalence of testis lesions in Group 2 (vaccinated against BRSV), suggests that BRSV may be involved in etiology of testis fibrosis. However, immunohistochemistry of testis tissues from 10 bulls that were culled and slaughtered from Group 1 failed to detect BRSV antigen. Failure to find evidence of BRSV antigen may indicate that this virus does not multiply in testis tissue or it might be due to the lack of fibrotic lesions in 9 of 10 of the testes from which samples were submitted and because samples were obtained ~12 months after BRSV incident.
Viral agents multiply within the testes of several species. For example, mature male domestic European rabbits were infected with an attenuated strain of myxoma virus. The animals developed symptoms of myxomatosis 7–10 days after infection and had high viral titers in testes. After 20–30 days, testes were 50% of normal size and affected animals had interstitial orchitis and epididymitis [42]. Protein and genomic studies of a porcine paramyxovirus had a close relationship to human mumps virus [43, 44], known to multiply in human testis, causing orchitis in postpubertal men [45]. Furthermore, when 9‐month‐old boars were experimentally infected with porcine paramyxovirus, histopathological epididymal alterations and testicular atrophy associated with degeneration of seminiferous tubules occurred [38]. In another study, colostrum‐deprived pigs were inoculated with porcine circovirus type 2 alone, porcine parvovirus alone, or with both viruses. All pigs that received both viruses became ill; at necropsy (21–26 days after infection), many had hepatomegaly and enlarged kidneys, with granulomatous lesions apparent in many tissues, including testis [46].
Obesity is associated with testicular degeneration and scrotal insulation has been used to produce testicular degeneration; however, scrotal insulation did not induce fibrotic lesions [4]. In one study, deficient, normal, and excessive dietary intakes did not affect prevalence of fibrotic lesions. However, with prolonged abnormal thermoregulation, especially when semen quantity and quality are very severely reduced, with loss of testis tone and size and with severe seminiferous tubular degeneration, scar tissue infiltration and testis fibrosis are plausible.
Trauma to the testes has also been proposed as a cause of testis fibrosis [10]. Trauma caused by a blow to the testes from kicking or butting could occur at any age, but may be more frequent during crowding in pens or handling in chute systems. Therefore appearance of fibrosis in conjunction with postweaning penning and feeding could be considered in the etiology of testis fibrosis. However, one of the authors observed a bull receive an acute blow to the testes with a metal pipe. Ultrasonography the following day and several times over the course of a month did not reveal any damage to the testes. Perhaps testis trauma, although common in penned bulls, does not cause fibrotic lesions.
Interestingly, fibrotic lesions in the testes were not associated with poor semen quality. Even bulls with very severe fibrosis produced semen with up to 94% morphologically normal sperm. Therefore presence of relatively large amounts of scar tissue within testis parenchyma did not prevent remaining unaffected parenchyma from producing normal sperm. Although large amounts of scar tissue would be expected to reduce sperm production, this has apparently not been reported.
References
1 1 Waites, G. (1970). Temperature regulation and the testis. In: The Testis, Vol. I (eds. A.D. Johnson, W.R. Gomes and N.L. VanDemark), 241–279. New York: Academic Press.
2 2 Setchell, B. (1978). The scrotum and thermoregulation. In: The Mammalian Testis, 50–69. Ithaca, NY: Cornell University Press 90–103.
3 3 Kastelic, J., Cook, R., and Coulter, G. (1997). Scrotal/testicular thermoregulation and the effects of increased testicular temperature in the bull. Vet. Clin. North Am. Food Anim. Pract. 13: 271–282.
4 4 Arteaga, A., Barth, A., and Brito, L. (2005). Relationship between semen quality and pixel‐intensity of testicular ultrasound images after scrotal insulation in beef bulls. Theriogenology 64: 408–415.
5 5 Barth, A. and Oko, R. (1989). Abnormal Morphology of Bovine Spermatozoa, 142–143. Ames, IA: Iowa State University Press.
6 6 Ndama, P., Entwhistle, K., and Lindsay, J. (1983). Effect of protected protein supplements on some testicular traits in Brahman cross bulls. Theriogenology 20: 639–650.
7 7 Evans, H. (1932). Testicular degeneration due to inadequate vitamin A in cases where E is adequate. Am. J. Phys. 99: 477–486.
8 8 Rhode, L., Coulter, G., Kastelic, J., and Bailey, D. (1995). Seminal quality and sperm production in beef bulls with chronic dietary vitamin A deficiency and subsequent realimentation. Theriogenology 43: 1269–1277.
9 9 Gomes, W. (1977). Chemical agents affecting testicular function and male fertility. In: The Testis, vol. III (eds. A.D. Johnson, W.R. Gomes and N.L. VanDemark), 241–279. New York: Academic Press.
10 10 McEntee, K. (1990). Reproductive Pathology of Domestic Mammals, 260–261. San Diego, CA: Academic Press.
11 11 Vanyi, A., Timar, I., Szeky, A., and Fusariotoxicoses, I.X. (1980). The effect of F‐2 fusariotoxin (zearalenone) on the spermatogenesis of rams and bulls. Magyar Allatorvosok Lapja 35: 777–780.
12 12 Robinson, J., Tanphaichitr, N., and Bellve, A. (1986). Gossypol‐induced damage to mitochondria of transformed Sertoli cells. Am. J. Pathol. 125: 484–492.
13 13 Chenoweth, P., Chase, C. Jr., Risco, C., and Larson, R. (2000). Characterization of gossypol‐induced sperm abnormalities in bulls. Theriogenology 53: 1193–1203.
14 14 Velasquez‐Pereira, J., Chenoweth, P., McDowell, L. et al. (1998). Reproductive effects of feeding gossypol and vitamin E to bulls. J. Anim. Sci. 76: 2894–2904.
15 15 Panter, K., James, L., and Hartley, W. (1989). Transient testicular degeneration in rams fed locoweed (Astragalus lentiginosus). Vet. Hum. Toxicol. 31: 42–46.
16 16 Deschamps, J., Ott, R., McEntee, K. et al. (1987). Effects of zeranol on reproduction in beef bulls:
