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of a mature bull with small hyperechoic foci distributed throughout the testis parenchyma.
Figure 10.3 Sagittal view of a testis with small hyperechoic foci (large arrow) surrounding the mediastinum (small arrow) suggestive of lesions in the straight ducts that drain the seminiferous tubules into the rete testis.
Figure 10.4 Sagittal view of a testis with multiple linear radiating hyperechoic lesions, two of which are highlighted by the smaller arrows. A normal mediastinum testis is shown (large arrow).
Tumors are generally more hyperechoic than the normal testis parenchyma (Figure 10.5), but mixed or hypoechoic echogenicity is also possible [4]. Mineralized lesions are extremely hyperechoic and are usually accompanied by intense or complete shadowing causing a loss of image distal to the lesion (Figure 10.6).
Figure 10.5 Sagittal view of the right ventral testis of an aged beef bull. Histologically, the hyperechoic lesion (arrow) was a Sertoli cell tumor.
Figure 10.6 Sagittal views of the left and right testes of a yearling dairy bull. The left testis is normal, while the hyperechoic areas of the right testis cast prominent dark shadows in the distal tissue and represent areas of mineralization.
Barth et al. [15] have proposed a scoring system for fibrotic lesions in the bull testis based on the size and frequency of hyperechoic lesions detected by ultrasonography in a single transmediastinal plane. They found that the occurrence of fibrotic lesions in young bulls aged between 3 and 20 months was not associated with decreased semen quality. This is consistent with their histologic findings, where seminiferous tubules within the area of fibrosis were generally affected, but immediately adjacent germinal tissue was quite often completely normal. However, bulls that experienced a dramatic increase in fibrosis score at a second examination (≥4 points, 4–13 months later) were more likely to have poor semen quality than bulls that did not experience this degree of change [15]. While bulls in this report with up to 50% of their parenchyma affected were able to produce mostly normal sperm, it is reasonable to suspect that they would have reduced production capacity.
The cause of fibrotic lesions in the testis is unknown. Possible etiologies include infectious or inflammatory conditions, developmental defects of the seminiferous tubules or their connecting ducts, autoimmunity, degenerative conditions, or aging. Ram testes inoculated with Trueperella pyogenes (formerly Arcanobacterium pyogenes) eventually developed hyperechoic lesions that consisted of fibrotic tissue [16]. A severe outbreak of bovine respiratory syncytial virus (BRSV) in a group of bulls was associated with an increased prevalence of fibrotic lesions in one report, though a cause‐and‐effect relationship could not be confirmed [15]. On the other hand, scrotal insulation resulting in a dramatic decrease in semen quality did not cause fibrosis or any other ultrasonically detectable change in the testis within four months [17] or six months [12] after the insulation event. A progressive fibrosis that is more marked in the ventral testis has been described as a histologic feature of aging in the bull [18].
Distinct hypoechoic lesions in the testis parenchyma are seen less commonly (Figure 10.7). Intratesticular inoculation of T. pyogenes in rams caused an initial hypoechoic change associated with edema, neutrophilic infiltration, and degenerative changes in the seminiferous tubules [16]. Tumors may present as hypoechoic areas in some cases. Since an increase in echogenicity is seen at puberty in association with proliferation of the spermatogenic tissue, it seems reasonable to speculate that areas affected by a degenerative process would be more hypoechoic by contrast.
Figure 10.7 Transverse view of the testis containing two discrete hypoechoic wedge‐shaped areas (between arrows) of unknown etiology or significance.
A hypoechoic distension of the rete testis was first reported in Ayrshire cattle [19]. Most of the bulls in this report had bilateral distension and were azoospermic by 16 months of age, suggesting a block to sperm outflow. A genetic predisposition to the condition was suspected. A similar unilateral lesion was reported in a mature Holstein bull in conjunction with agenesis of the ipsilateral seminal vesicle, epididymal body and tail, as well as low semen volume [20]. Figure 10.8 shows an ultrasonogram from a yearling Holstein bull with a history of oligospermia and low semen volume. Note the enlarged hypoechoic appearance of the mediastinum. The contralateral testis and mediastinum appeared normal (not shown). Surgical removal of the affected testis confirmed a diagnosis of agenesis of the body of the epididymis and fluid distension of the rete testis. The distension can also affect the efferent ducts. In our experience, extensive and uniform hypoechoic distension of the rete testis as seen in Figure 10.8 is pathognomonic for sperm outflow obstruction, most often congenital. In unilateral cases, the presenting complaint is usually low sperm numbers and semen volume in an otherwise normal young bull. Congenital cases may be associated with aplasia affecting the epididymis, deferent duct, ampulla, or seminal vesicle.
Figure 10.8 Sagittal view of the left testis of a mature Holstein bull that presented with a complaint of low semen volume and oligospermia. Note the hypoechoic distension of the rete testis (dark linear area between arrows). The distension was secondary to a complete outflow obstruction resulting from the absence of the epididymal body on this side.
The head of the epididymis is best seen in a sagittal view and is found on the dorsocranial aspect of the testis. It is usually less echoic than the parenchyma of the testis. The tail of the epididymis can be readily located by palpation and is found on the ventral aspect of the testis. Acquired lesions of the epididymides can lead to outflow obstruction.