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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 with this disease.

Ultrasonographic examinations in some groups of bulls in western Canada were done monthly from 3 to 15 months of age. In other groups in Canada and Argentina, ultrasonography was done after weaning at 5–8 months of age and repeated at 12–14 months of age in Canada and 18–20 months of age in Argentina. Testis assessment was done by orienting the transducer vertically on the scrotum and moving it 180° around the testis (both dorsal and ventral portions). Testes were scored for fibrosis from none to very severe, based on number and size of fibrotic lesions (Figures 13.1 and 13.2).

Figure 13.1 An ultrasonogram of testis scored as having mild fibrosis.

Figure 13.2 An ultrasonogram of testis scored as having very severe fibrosis.

Immunohistochemistry was performed on testis tissues of 10 bulls from the group affected by BRSV. Only one of these bulls had fibrotic lesions in testes. Testis tissue was submitted to a diagnostic laboratory for immunohistochemistry for BVDV and BRSV.

Fibrotic lesions scored as slight or mild were very common (31.3%) in testes of a group of bulls raised under intensive rearing conditions in western Canada. Only 2.5% had moderate scores and none had severe scores for fibrosis. In the more extensive management in Argentina, in a group not affected by respiratory disease associated with BRSV, fibrotic lesions were also mainly slight or mild, but incidence was higher (48.6%). In that group, 1.9% were scored moderate and 0.95% severe. In the Argentine group affected by BRSV, fibrotic lesion scores were higher and more frequent. Scores for slight to mild, moderate, and severe to very severe were 58.3, 17.1, and 5.7%, respectively.

Fibrotic lesions appeared as early as 5–6 months of age and number of cases continued to increase until at least 12–14 months. Lesion severity increased in some cases during this period, although it appears that lesion development occurred during a finite interval. There were indications that during fibrosis formation, spermatogenesis was adversely affected; however, presence of a large number of fibrotic lesions that may occupy as much as approximately half of testis parenchyma did not preclude production of a high percentage of morphologically normal sperm. In bulls with no, mild, moderate, or severe testis fibrosis, median percentages of normal sperm were 88, 87, 86, and 90% respectively. Lesion prevalence was not influenced by breed or testis size.

Histologically, lesions consisted of masses of fibrous tissue with fine fibrillation, or heavy bundles of wavy tissue seminiferous tubules. Usually there were fewer germinal cells in seminiferous tubules within masses of fibrous tissue. In some tubules, germinal cells and Sertoli cells were missing entirely and hyaline material was present in the lumen. Similar abnormalities were evident in seminiferous tubules adjacent to fibrous tissue masses; however, completely normal tubules were often beside or very close to fibrous tissue masses. Inflammatory cells were consistently absent. Therefore we inferred that neither the insult that caused fibrosis nor proximity of fibrous tissue to seminiferous tubules affected function of adjacent tubules.

With real‐time ultrasonography, many lesions appeared to extend from the rete testis toward the periphery of the testis and appeared to involve the entirety of one or more tubules at specific sites within the testis. This pattern was apparent in both gross sections (Figure 13.3) and in ultrasonograms (Figure 13.4). It appeared that entire tubules may be destroyed with replacement by fibrotic tissue. In other cases, there were isolated lesions in central or peripheral parts of testis parenchyma without extension to rete testis, implying tubular destruction occurred only at a specific site.

Figure 13.3 Cross‐section of a bull testis with fibrotic lesions that appeared to radiate from rete testis toward the periphery, suggesting individual tubules were destroyed and replaced by scar tissue.

Figure 13.4 Ultrasonogram of a testis with fibrotic lesions radiating from the rete testis toward the periphery.

The cause of the testicular fibrosis is uncertain. Potential causes are disrupted development of embryonic tubule‐to‐rete connections, an infectious disease process affecting tubule health and development, abnormal testes thermoregulation, and trauma.

Developmental changes of testes may be involved in development of fibrotic lesions. Tubularization of seminiferous cords within the testis tissue begins at ~4 months of age and is complete in nearly all bulls by 6 months [35]. 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.