Читать книгу Bovine Reproduction - Группа авторов - Страница 211

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 to likely contamination of samples with environmental microorganisms and normal flora, Parsonson et al. described a technique to obtain vesicular gland secretions for microbiologic examination [10]. After clipping preputial hair, the penis is extended by transrectal massage of the urethralis muscle. The glans penis is restrained by grasping it manually with sterile gauze sponges and wearing sterile gloves. After washing and disinfecting the end of the penis, the urethra is irrigated with sterile saline utilizing a sterile teat cannula. A 25‐ to 30‐cm sterile Silastic tube is passed up the urethra to a point leaving 2.5–5 cm protruding from the penis. The vesicular glands are then massaged and the secretions are collected into a sterile container.

Several treatment modalities for vesicular adenitis have been utilized. These include multiple systemic antimicrobials given at several different dosages and frequencies. Intraglandular antibiotics and intraglandular chemical ablation have shown some success. Surgical removal of chronically infected glands has been described.

Many systemic, parenteral antibiotics have been used in the past to attempt treatment of vesicular adenitis. Since spontaneous recovery commonly occurs in younger bulls, evaluation of treatment methods is complicated [4]. Earlier antimicrobials utilized include penicillin, oxytetracycline, chloramphenicol (no longer legal), sulfamethazine, florfenicol, and cetiofur [2]. These medications all produced poor treatment success rates, even though the bacterial isolates from the vesicular glands are usually sensitive to most antibiotics [2, 11]. Success was improved when increased dosages of these agents was used. Unfortunately, even at twice the recommended dose, these antibiotics often do not reach inhibitory concentrations in vesicular gland tissue [2]. Antibiotics that are highly lipid soluble and low protein binding possess a pH higher than vesicular gland fluid along with a favorable pKa, and should be chosen [4, 12]. Due to the varying clinical signs of vesicular adenitis, establishing whether treatment is successful can be difficult. Treatment can be considered successful when the ejaculate contains less than one neutrophil per five high‐powered fields (1000×) [4].

More recently, tilmicosin and tulathromycin have shown efficacy for treatment of vesicular adenitis [13]. The author has treated multiple older bulls successfully using subcutaneous tulathromycin. There is evidence these antimicrobials accumulate in macrophages and neutrophils, which carry the antibiotics into sites of infection to be released slowly [14, 15]. Recovery rates were higher for bulls treated with tulathromycin than tilmicosin in all age groups; thus tulathromycin at this time appears to be the drug of choice [2].

Intraglandular injection of antimicrobials or chemical ablation agents is another option for treatment of refractory vesicular adenitis. Multiple antimicrobial agents have been utilized in this technique, all with varying results. Success has been achieved in some cases utilizing a single intraglandular injection of ceftiofur or penicillin. In one study, bulls were treated with intraglandular penicillin or intraglandular ceftiofur. Bulls that did not recover were treated with whichever antibiotic was not used initially. Approximately half of the bulls receiving the second treatment responded. Bulls that did not recover after intraglandular treatment with ceftiofur and penicillin recovered after three treatments of tilmicosin [13].

Chemical ablation of chronically infected vesicular glands utilizing 4% formalin has been described [16]. The success of parenteral tulathromycin as an initial treatment has substantially reduced the usage of chemical ablation in the author's practice. Resolution of vesicular adenitis after intraglandular formalin ablation approached 100% when utilized by the author. The procedure requires the bull to be restrained in a chute with epidural anesthesia. After clipping and prepping an area lateral to the anus, a 14‐gauge needle is placed through the skin directly caudal to the affected vesicular gland (Figure 14.3). The affected gland is grasped transrectally to stabilize it for injection and a 30‐cm, 18‐gauge needle is introduced through the 14‐gauge needle (Figure 14.4). This needle is advanced pararectally to achieve penetration of the affected vesicular gland. When sure the needle is within the gland, inject 10–15 ml of saline to ensure proper needle placement. Gland enlargement verifies proper needle placement. At this point, inject 4% formalin to a volume where the gland is enlarged with a smooth surface (Figure 14.5). In the author's experience, this will be approximately 50 ml. After injection, the bull should be treated with flunixin meglumine for three days, as most bulls show signs of abdominal discomfort. The proper authorities should be consulted regarding current legal use and withdrawal time prior to the extra label use of formalin for chemical ablation.

Figure 14.3 Placement of a 14‐gauge needle through the skin.

Source: Courtesy Josh Thompson.

Figure 14.4 Passing a 30‐cm, 18‐gauge needle through the 14‐gauge needle into the vesicular gland.

Source: Courtesy Josh Thompson.

Figure 14.5 After removing the stylus from the needle, the proper solution is injected into the vesicular gland.

Source: Courtesy Josh Thompson.

Surgical removal of the vesicular glands may be considered in bulls that do not spontaneously recover or do not respond to antimicrobial treatment or ablation. A subrectal approach has been described that provides better visualization of the vesicular glands and improved postsurgical fertility than traditional pararectal approaches. None of the described techniques for surgical gland removal has provided uniform success in returning a bull to function [1].

Any specific plan for prevention of vesicular adenitis is limited by the lack of a definitive pathogenesis. Proper herd health and husbandry may play an important role in reducing the prevalence of vesicular adenitis. Proper vaccination and deworming help support the overall health and general disease resistance of bulls. Proper nutrition and bunk management to reduce the incidence of rumen acidosis may reduce the possibility of hematogenous bacteria reaching the vesicular gland. Monitoring the genetic lines of bulls with vesicular adenitis may reveal a genetic basis for the disease. Although early detection, with or without medical intervention, has not shown a significant reduction in the incidence of clinical vesicular adenitis [17], herds with a high prevalence of adenitis may benefit from early transrectal palpation and treatment [2].