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14 Vesicular Adenitis
Mike Thompson
Willow Bend Animal Clinic, Holly Springs, MS, USA
The vesicular glands are paired glands located on the floor of the cranial pelvic cavity situated laterally and craniodorsal to the prostate and the origin of the paired ampullae. They have also been described as lateral to the ampullae and dorsal to the neck of the bladder. The size of the vesicles is age related. These glands have a lobar structure and each is normally 2–4 cm wide and 10–15 cm long (Figure 14.1). As bulls age, non‐infected glands may have considerable variation in size. The vesicular glands are easily palpated per rectum; hence an appreciation of the normal variation is important. As the major accessory sex glands in the bull, infection and inflammation of the vesicular glands has a significant impact on bull fertility. The glands secrete a clear fluid containing nutrients and buffers, which is discharged immediately before and during ejaculation through ducts that open into the urethra adjacent to the colliculus seminalis [1].
Figure 14.1 Normal vesicular glands.
Source: Courtesy Maarten Drost VISGAR.
The overall prevalence of vesicular adenitis has been reported to be between 1 and 10%, with the highest incidence occurring in yearling and peripubertal bulls and bulls over nine years old [2]. The prevalence is also higher in bulls that are intensively housed and/or fed high energy diets [3]. The actual prevalence of vesicular adenitis in pre‐mortem bulls is difficult to establish due to the variance in diagnostic criteria.
Multiple microorganisms have been associated with vesicular adenitis. These include bacteria, chlamydia, mycoplasma, and ureaplasma [2, 3]. Bacteria are considered the most common cause with the most common isolates, including Trueperella pyogenes, Histophilus somni, and Brucella abortus (in areas where brucellosis has not been eradicated). Multiple other pathogens have been isolated from infected vesicular glands [4]. Although the precise mechanism and route of infection is not known, suggested routes of infection include ascending, descending, direct invasion from local sources, and hematogenous routes [2, 4, 5]. Association with congenital defects, particularly involving the development of the colliculus seminalis, as well as naval abscesses in calves have been suggested to predispose bulls to vesicular adenitis [6]. Congenital defects leading to retrograde ejaculation or urine reflux can be a source of infection or sterile inflammation [7]. High energy diets that predispose young bulls to rumen acidosis and rumenitis with subsequent bacteremia may lead to hematogenous vesicular gland infection [2, 3, 7, 8].
Although most bulls diagnosed with vesicular adenitis are found during routine breeding soundness examinations without any history suggestive of vesicular adenitis, occasionally bulls will present with a history of subfertility [3]. Rarely, these bulls may present with acute signs mimicking peritonitis, gastritis, tenesmus, or hindlimb lameness [4].
Physical examination findings, with the exception of those identified through transrectal palpation, are usually normal. Transrectal palpation can reveal a range of findings. Some bulls with vesicular adenitis have no palpable abnormalities with either vesicular gland. Abnormal findings can include any or all of the following: loss of symmetry, bilateral enlargement, loss of lobulation, increase in firmness, heat, and pain (Figure 14.2) [2, 3]. In chronically infected bulls, fibrin and adhesions may be palpable [2, 4].
Figure 14.2 Vesicular adenitis with enlargement and loss of lobulation.
Source: Courtesy Maarten Drost, VISGAR.
Bulls suspected of vesicular adenitis should have a thorough examination of the entire reproductive tract. These physical examination findings should be corroborated with semen evaluation. Large numbers of leukocytes with or without flocculi of pus can be found without palpable evidence of vesicular adenitis. Conversely, bulls with palpable signs of vesicular adenitis may have no evidence of infection during semen evaluation. Bulls with transrectal signs of vesicular adenitis but no leukocytes in semen should be further massaged and recollected to ensure proper evaluation and classification of the presence of disease [2–4, 7]. Transrectal ultrasonography can be revealing in subclinical cases. The normal vesicular gland has homogeneously echogenic lobes with small anechoic vesicles and a distinct anechoic collecting duct all surrounded by a distinct capsule. Vesicular adenitis leads to varying degrees of enlargement, loss of lobular structure, thickened walls, and increased echogenicity with fluid‐filled cavities in the gland [9].
Due