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Vesicular adenitis of bulls: A review
THERIOGENOLOGY
VESICULAR
ADENITIS
OF BULLS:
A REVIEW
D.A. Dargatz, R.G. Mortimer, L. Ball Department of Clinical Sciences School of Veterinary Medicine Colorado State University Fort Collins. CO 80524 Received
for publication: Accepted<
November
3,
June 8,
1987
1986
ABSTRACT The prevalence of inflammatory disease of the vesicular glands can be as high as 49% in some groups of bulls under common management conditions. Since these bulls are classified as questionable or unsatisfactory potential breeders, this disease can cause significant economic loss to the producer. The current knowledge of the etiology, pathogenesis, diagnosis, treatment, and prevention are discussed. Key words:
bull, vesiculitis,
vesicular
adenitis,
breeding
soundness
examination
INTRODUCTION The accessory sex glands of the bull include the prostate, bulbourethral, and vesicular glands (1). The vesicular glands are paired structures that lie on the floor of the pelvis lateral to the ampullae and the neck of the bladder (2). The vesicular glands are lobular structures measuring 10 to 15 cm in length and 2 to 4 cm in diameter (2). The average weight of both vesicular glands of bulls is 75 g, or approximately 0.0142% of bodyweight (1,3). Vesicular gland weight is highly correlated with bull age (r = 0.4462) (3). The glands are lobular with a branched tubular architecture (1). A prominent layer of smooth muscle is present in the interstitium of the glands (1). The ducts of the vesicular glands share a common orifice into the urethra with the ipsilateral ductus deferens (1). The accessory sex glands’ function is regulated by testosterone levels; these levels in turn are governed by the anterior pituitary through the action of luteinizing hormone (LH ; 3.4). The accessory sex glands secrete fluid that acts as a transport medium for spermatozoa during ejaculation (1). The volume and composition of the fluid varies between species (4). The predominant components of the vesicular gland secretions of the bull are fructose and citric acid (5). Fructose is used as an energy source by the sperm and the citric acid acts as a reducing agent in the semen (4). The term vesicular glands is preferred to the older name seminal vesicles. as the glands do not act as reservoirs for sperm as that name would imply (6). Congenital defects of the vesicular glands have been reported (2). These defects are usually unilateral and include aplasia, hypoplasia, cysts, and duplication of the gland (2). These lesions are often associated with segmental aplasia of the mesonephric duct system which gives rise to the epididymis, ductus deferens, ampullae, and vesicular glands (2,3).
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THERIOGENOLOGY
The most common disease of the vesicular glands is inflammation (2). Vesicular adenitis has been reported in bulls in Belgium, Britain, Canada, Denmark, France, Germany, India, Italy, the Netherlands, South Africa, Switzerland, Sweden, and the United States (7). Vesicular adenitis probably occurs in all areas where cattle are raised (7). Beef or dairy bulls may be affected (6,7). Bos indicus cattle as well as Bos taurus breeds are affected (8). The incidence of vesicular adenitis is variable. incidences up to 49% of a population (9-18).
Researchers
have
reported
ETIOLOGY Vesicular adenitis is an infectious process (19). Many organisms have been isolated from semen or genitalia of bulls with vesicular adenitis, including bacteria, chlamydia, and viruses (3,6,7,15,20). Where brucellosis has not been controlled, Brucella abortus is the primary cause of vesicular adenitis (6,7). The bacterium most frequently isolated from lesions of the vesicular glands in Western Europe and North America (where brucellosis has been controlled) is Corvnebacterium pvonenes (6,15,21). Gram-negative anaerobes and Corvnebacterium pvoaenes have been cultured together from the semen of bulls with vesicular adenitis (D.A. Dargatz, unpublished data, 1986). PATHOGENESIS Inflammatory lesions of the vesicular glands are due to infection (19). The predisposing factors leading to infection are unknown. Infection of the vesicular glands could potentially occur by one of four routes: by ascending the genito-urinary tract, by descending from the upper urinary tract or reproductive tract, by hematogenous spread, or by direct invasion of the glands from Iocal sources. The ascending route is unlikely as the distal genito-urinary tract is flushed frequently with micturition. However, Roberts describes this as the most likely route of infection (2). Pseudomonas aeruainosa has been reported as a cause of vesicular adenitis in bulls, albeit rarely (2,22,23). In a survey of the bacterial flora of the male genitalia, Pseudomonas aeruninosa was cultured from the urethra of normal animals (24). In the above survey Corvnebacterium pvoeene$ was not isolated from the urethra of normal animals at any level (24). Attempted creation of vesicular adenitis by reoeated instillation of Corvnkbacterium bvoeenes into the penile urethra was unsuccessful (7). The descending route of infection is more likely. Vesicular adenitis is noted to occur secondary to epididymitis or orchitis (6). Vesicular adenitis and ampullitis occurs ipsilateral to orchitis induced by Brucella abortus (25). In cases of vesicular adenitis caused by Corvnebacterium pvoaenes there is frequently involvement of other parts of the reproductive system (3,15,16,26,27). The temporal relationship between these lesions has not been clearly identified but some feel that many bulls with vesicular adenitis subsequently develop epididymo-orchitis (3). Pyelonephritis has only rarely been reported in conjunction with vesicular adenitis (26). The hematogenous route of infection has been suggested as a probable pathogenesis in vesicular adenitis cases (2,7,26,28). Multiple portions of the reproductive tract are frequently involved (3,15,16,26,27). In a postmortem study, 50% of bulls with vesicular adenitis had concurrent lesions outside the reproductive tract, including vegetative endocarditis, chronic bronchopneumonia, polyarthritis, and traumatic gastritis (26). As stated earlier, the most common
514
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1987 VOL. 28 NO. 4
THERIOGENOLOGY
bacterial agent associated with vesicular adenitis in areas where brucellosis is controlled is Corvnebacterium ovoaenes. A recurrent periodic bacteremia frequently occurs in cattle and is known to occur commonly following rumenitis (29). Liver abscesses in feedlot cattle result from the hematogenous spread of organisms from the forestomachs of cattle to the liver (30). The bacteremia is secondary to rumenitis due to acidosis in these animals (30). The most common isolates from liver abscesses of feedlot cattle are Corvnebacterium ovoaenes and gram-negative anaerobic bacteria (30). Young bulls in performance tests or being fitted for sale are commonly fed rations similar to those fed in feedlots (15). The incidence of vesicular adenitis is higher among bulls under this form of management than among range bulls (6,15,27). Bulls in performance tests or being fitted for sale are often housed together and homosexual activity is high among these groups (15). This homosexual activity may increase the likelihood of the organism’s penetrating the mucous membranes to be spread hematogenous1~ (6). The association of a history of omphalophlebitis with vesicular adenitis stimulated a researcher to inoculate Corvnebacterium ovonenes into the periNone of the calves developed toneal cavity of calves at the umbilicus (7). vesicular adenitis, though one calf developed periepididymitis (7). Factors other than infection have been associated with vesicular adenitis. Stressors such as shipment have been reported to contribute to the development of vesicular adenitis (6,31,32). Rare congenital anomalies of the mesonephric duct system have been noted with increased frequency in bulls with vesicular adenitis (31). These may act as a locus minorus resistentiae (31). CLINICAL
SIGNS
Overt abnormal clinical signs are often lacking in bulls with vesicular adenitis (6). When these signs are present, they resemble those seen in cases of traumatic reticulitis (6). Bulls may be febrile, stand with their back arched, and be reluctant to move (6,7). Varying degrees of hypophagia may be present (6). Bulls may show evidence of pain on defecation or ejaculation (6,7). The vesicular glands can be examined by palpation per rectum. Unilateral and bilateral cases of vesicular adenitis are reported, but unilateral cases are most common (7). Asymmetry of the glands is often present in unilateral cases of adenitis (6,27). Some asymmetry is normal, however, and this should be interpreted with care (6,26,27). Affected glands are often enlarged with a loss of the normal distinct lobulation (6,27). Bulls may show evidence of pain when the affected glands are palpated per rectum; however, this response is lacking in chronically affected bulls (6,154. Enlarged glands often contain abscesses (26). A single large abscess may form and fluctuate when palpated (26). As the lesions become chronic, fibrosis develops and results in a gland that is much firmer than normal (26). Following abscess of the gland(s), adhesions frequently form and involve other pelvic or abdominal organs near the glands (6,15). Fistula formation from abscessed glands to the rectum, urinary bladder, peritoneal cavity, or skin surface has been reported (6). Frequently, pathologic changes are present in other reproductive organs of bulls with vesicular adenitis (16,27). These lesions may not be grossly evident in all cases (16,27).
are
The semen of bulls with vesicular adenitis is usually virtually always seen when the semen is examined
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1987 VOL. 28 NO. 4
abnormal. Floccules grossly (6,32). The
515
THERIOGENOLOGY
ejaculate may have a brownish discoloration due to blood pigments or may be blood-tinged (26,32). Microscopic evaluation of the semen generally reveals an admixture of white blood cells (usually polymorphonuclear leukocytes) with the sperm (6,7,27,32). In normal bulls, when white blood cells are present in the semen, they are usually present in small numbers (7). In bulls with vesicular adenitis, more than 1 white blood cell per 100 sperm cells are commonly seen (7). Leukocytes are present in aggregates or are dispersed evenly (26). Agglutination of sperm cells to clumps of leukocytes also has been reported (7). The volume of the ejaculate from infected bulls is not always decreased even if both glands are affected (7). The effect of vesicular adenitis on semen quality is variable. Carroll et al. report that as many as 80% of bulls with vesicular adenitis have semen of substandard quality, usually as a result of decreased motility (27). Morphological abnormalities of sperm have been reported to be within normal limits in bulls with vesicular adenitis when there is not concomitant disease of the testicles (33). When morphologic abnormalities are present, they are mostly secondary; many of the other genital organs of bulls with vesiculitis had subclinical inflammatory changes when examined microscopically (27). In other studies a high percentage of loose heads have been reported in semen from bulls with vesicular adenitis (7). There appears to be no correlation between the degree of severity of inflammatory lesions of the genitalia and the number of primary or secondary morphologic abnormalities in the semen (16). Biochemical changes in the semen of bulls with vesicular adenitis have been noted. The seminal pH is usually increased (7,32,34). An average pH of semen from normal bulls of 6.1 vs an average for bulls with vesicular adenitis of 7.2 is reported (34). The total solids in the seminal plasma as measured with a refractometer may be abnormally low (<5g/dl) in acute cases of vesicular adenitis (32). The fructose content of the semen from diseased bulls is often reduced, although this is an inconsistent finding (34). Citric acid content of the semen of bulls with vesicular adenitis is decreased. Alkaline phosphatase activity in semen of bulls with vesicular adenitis is sometimes decreased (35). The reported fertility of bulls with vesicular adenitis is variable. Decreased conception rates have been reported (2,25,28,35). However, others report “fair” conception rates when bulls with vesicular adenitis are used for either natural service or for artificial insemination (6,26). In the case of artificial insemination, a number of ejaculates must be discarded periodically due to poor quality (26). DIAGNOSIS Diagnosis of vesicular adenitis is usually based on clinical signs. While many bulls with chronic inflammatory disease of the vesicular gland show no outward abnormal signs, palpation of the glands per rectum is usually diagnostic (26). An abnormal amount of asymmetry between the glands, glandular enlargement with loss of lobulation, fibrosis, or periglandular adhesions are all reasonably reliable indicators of vesicular adenitis (2,6). The most practical and reliable laboratory test for vesicular adenitis is examination of the semen for leukocytes (32). This is accomplished by evaluating a Giemsa-stained smear of the semen (32). Increased numbers of leukocytes in the semen shouid be interpreted with caution because other sites such as the prepuce are potential sources of inflammation. An increase above 7.0 in the pH of semen can be regarded as compatible with lesions of the vesicular glands (7). Decreased
516
OCTOBER 1987 VOL. 28 NO. 4
THERIOGENOLOGY
citric acid concentration in semen is also a reliable indicator of pathologic changes in the vesicular glands (34). However, this test is not easily performed and is probably not very practical for routine or large-scale use. An etiologic diagnosis of vesicular adenitis can be obtained by culturing the semen. Care should be taken to avoid contamination of the semen sample Catheterization of the penile urethra and during the collection process. collection of the fluid expressed by massage of the vesicular glands is the most desirable method of obtaining a sample for culture (7). Once a sample is obtained, it should be transported anaerobically until it can be transferred to a medium for growth. Samples should be cultured both aerobically and anaerobicAttempts at virus isolation are of doubtful value. The potential for ally. Brucella pbortus infection should be considered and serum and seminal plasma should be evaluated for titers to the organism (6). THERAPY Bulls with vesicular adenitis may be treated medically or surgically. Antibiotic therapy when used should be based on antibiotic sensitivity patterns of the etiologic agent. Vesicular adenitis due to Brucella abortus should not be treated and the animal should be slaughtered. Response to antibiotic therapy is generally poor (6,31) but spontaneous cures are reported (6). Even when inflammation appears to have been resolved, the disease may recur (31). Infected vesicular glands can be removed surgically if adhesions are not extensive and the size of the gland is moderate (2,31). Epidural and local anesthesia with tranquilization is used and an elliptical incision is made in the iscchiorectal fossa on the side of the affected gland. Blunt and sharp dissection is used to isolate the affected gland. The duct of the gland is ligated near the attachment to the urethra and the gland is removed (2). The effect of vesicular adenectomy on fertility and semen quality is variable (2,26,36,37). Volume of the ejaculate, sperm motility, percentage of live cells in the ejaculate, and number of primary morphologic abnormalities of the sperm cells decrease following removal of the vesicular glands (37). Concentration of the ejaculate and the number of secondary morphologic abnormalities of sperm cells in the ejaculate may increase postoperatively (37). Vesicular adenectomy has no apparent effect on libido (36). Bulls are able to mate naturally after the operation with acceptable fertility (37). Sperm cell tosses during freezing are increased after vesicular adenectomy; however, the vitality of the remaining cells is not affected and it appears that enough sperm cells survive for normat fertility levels (36). Since there is a propensity for concomitant involvement of other parts of the male genital tract in cases of vesicular adenitis, othe reproductive organs should be carefully evaluated prior to the decision to remove the vesicular glands (31). Congenital anomalies of the mesonephric duct system appear with increased frequency in bulls with vesicular adenitis. In one report of 32 bulls determined to have vesicular adenitis, 22 were of one breed and 10 were closely related to a single sire (31). Segmental aplasia of the mesonephric duct system is heritable (31). The possibility that bulls developing vesicular adenitis may have a heritable predisposition for the disease should be considered before surgical or medical treatment of the condition is undertaken.
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l-HERIOGENOLOGY
PROGNOSIS The prognosis in cases of vesicular adenitis is guarded to poor (15). Occasionally spontaneous cures occur (6,27); however, this process may take many months (27). The response to medical therapy is poor (6). Few cases meet the criteria necessary for surgical treatment (i.e.; size, degree of adhesions) and justify the economic investment. In most instances, affected animals are slaughtered (3 1). DISCUSSION Inflammatory disease of the vesicular glands has been a prevalent disease among young beef bulls with up to 49% of some groups examined being affected either clinically or subclinically histologically (16). Bulls with vesicular adenitis are classified as questionable potential breeders and are usually slaughtered. Bulls with vesicular adenitis frequently have concurrent pathologic conditions of other parts of the reproductive tract such as orchitis or epididymitis. These animals must be classified as unsatisfactory potential breeders and should be slaughtered. Slaughter of affected bulls represents an economic Performancetested bulls in the western and genetic loss to the producer. states sell for an average of $1200.00 per head. Slaughtered bulls usually bring $40.00 per hundredweight. Bulls at the end of performance test would average 1100 lb; therefore, a loss of $760.00 per affected bull would be anticipated. The genetic loss cannot be quantitated; however, producers usually place their best potential breeding bulls on performance test so the loss is no doubt substantial. The current prevalence of vesicular adenitis is unknown; consequently, its economic impact is also unknown. The route of infection and predisposing causes for vesicular adenitis have not been determined. Hematogenous spread from a gastrointestinal source has been postulated in those cases of vesicular adenitis caused by Corvnebacterium The presence of gram negativeanaerobes in these infections is pvoaenes. suspected. Concurrent infections with these organisms have been shown in the case of ovine infectious bulbar necrosis, bovine liver abscessation, and bovine pyometra (38,39). The gram- negative anaerobes produce a leukocidal toxin Protective for Corvnebacterium pvoaenes as well as for themselves (39). stimulating factor for the Corvnebacterium pvoaeneg produces a growthevidence supports the hypothesis of hematogenous anaerobes (39). Circumstantial spread of the organism(s). The disease is most common in young bulls on performance test receiving feedlot rations. The most common organism involved is the same as that seen most commonly in liver abscesses of feedlot cattle, a disease known to be due to hematogenous spread of the organism from the forestomachs subsequent to acidosis and rumenitis. Corvnebacterium ovoaenes is not a normal inhabitant of the urethra of bulls. The disease cannot be recreated by repeated instillation of the organism into the penile urethra of normal bulls. A descending route of infection cannot be demonstrated except in the case of vesicular adenitis due to Brucella abortus. This organism infects the testicle and/or epididymis by the hematogenous route prior to metastasis to the vesicular glands. More work needs to be done to define the current extent and significance of the problem and to determine the pathogenesis of the disease so that measures to prevent the condition can be developed and implemented.
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Price, D. and Williams-Ashman, H.G. The accessory reproductive glands of mammals. In: Sex and Internal Secretions. Young, W.C. (ed.). Williams and Wilkins Co, Baltimore. 1961, pp. 366-448.
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Carroll, E.J., Ball, L. and Scott, summary of 10, 940 examinations. (1963).
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Blom, E. and Christensen, N.O. Studies on pathological conditions in the testis, epididymis and accessory sex glands in the bull. I. Normal anatomy, technique of the clinical examination and a survey of the findings in 2000 Danish slaughter bulls. Skand. VetTidskr 12:1-49 (1947).
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Van Der, Sluis, L. Experiences with the examination into herd Proc. 1st World Congr. Fertil. Steril., NY. 1953, pp. 703-716.
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Van Der, Sluis L. The systematic examination of bulls on the grounds of fertility and recording of the results in the pedigree herdbooks. Proc. 4th Int. Congr. Anim. Reprod. The Hague. 1961, pp. 116-131.
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R.C., Hancock, J.L. and Walton, A. Semen in the bull. J. Agric. Sci. 44:227-248 (1954). Corvnebacterium
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Ball, L., Young, lesions in genital (1968).
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Vanderplassche, M, Laing, J.A., Melrose, D.R., Reed, H.C.B. and Smith, G.F. Male abnormalities. b Laing, J.A. (ed.). Fertility and Infertility in Domestic Animals. Bailliere Tindall, London. 1979, pp. 100-101.
20.
Storz, J., Carroll, E.J., Ball, L. and Faulkner, L.C. Isolation of a psittacosis agent (Chlamydia) from semen and epididymis of bulls with seminal vesiculitis syndrome. Am. J. Vet. Res. a549-555 (1968).
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McEntee, K. Seminal vesiculitis in the bull. Proc. United Sanitary Assoc., Washington, DC, &160-167 (1962).
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Carroll, E.J., Ball, L., Young, S. Seminal vesiculitis J. Am. Vet. Med. Assoc. 152:1749-1757 (1968).
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Williams, W.W. Diseases of the bull interfering Vet. Med. Assoc. 11:29-47 (1920).
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Jensen, R., Flint, J.C. and Griner, L.A. Experimental in beef cattle. Am. J. Vet. Res. B5-14 (1954).
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Blom, E. Studies on seminal vesiculitis in the bull. methods and post mortem findings. Nord. Vet. Med.
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Seminal vesiculitis in the bull Nord. Vet. Med. 17:435-445 (1965).
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Causes of sterility in bulls in southern 114-126 143-150 200-206 (1949). F.C. Sperma en aadndoeningen v Diergeneesk =28-47 (1949).
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on seminal vesiculitis in the bull. II. Malformation as a possible predisposing factor in the pathogenesis Nord. Vet. Med. L1:241-250 (1979).
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33.
Lagerlof, N., Hedstrom, H. and Hoflund, S. Infektiosa lidanden i sadesblasorna hos djur som orsak till sterilitet. Svensk. VetTidskr 47:602-630 (1942).
34.
Juneja, N.L., Faulkner, L.C. and Hopwood, M.L. Biochemical aspects semen in bovine seminal vesiculitis. Fertil. Steril. 16:361-369 (1965).
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King, G.J.. and MacPherson, J.W. Influence of seminal bovine semen. J. Dairy Sci. 21837-1842 (1969).
37.
Faulkner, L.C., Hopwood, ML. and Wiltbank, J.N. Seminal vesiculectomy in bulls. II. Seminal characteristics and breeding trials. J. Reprod. Fertil. al79-182 (1968).
38.
Blood, D.C., Radostits, OM._ and Henderson, Bailliere Tindall, London, 1983, ~~269, 669.
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Olson, J.D., Ball, L., Mortimer, R.G., Farin, P.W., Adney, W.S., Huffman, E.M. Aspects of bacteriology and endocrinology of cows with pyometra and retained fetal membranes. Am. J. Vet. Res. 45:2251-2255 (1984).
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OCTOBER 1987 VOL. 28 NO. 4
J.A.
vesiculectomy
Veterinary
on
Medicine.
521
VESICULAR
ADENITIS
OF BULLS:
A REVIEW
D.A. Dargatz, R.G. Mortimer, L. Ball Department of Clinical Sciences School of Veterinary Medicine Colorado State University Fort Collins. CO 80524 Received
for publication: Accepted<
November
3,
June 8,
1987
1986
ABSTRACT The prevalence of inflammatory disease of the vesicular glands can be as high as 49% in some groups of bulls under common management conditions. Since these bulls are classified as questionable or unsatisfactory potential breeders, this disease can cause significant economic loss to the producer. The current knowledge of the etiology, pathogenesis, diagnosis, treatment, and prevention are discussed. Key words:
bull, vesiculitis,
vesicular
adenitis,
breeding
soundness
examination
INTRODUCTION The accessory sex glands of the bull include the prostate, bulbourethral, and vesicular glands (1). The vesicular glands are paired structures that lie on the floor of the pelvis lateral to the ampullae and the neck of the bladder (2). The vesicular glands are lobular structures measuring 10 to 15 cm in length and 2 to 4 cm in diameter (2). The average weight of both vesicular glands of bulls is 75 g, or approximately 0.0142% of bodyweight (1,3). Vesicular gland weight is highly correlated with bull age (r = 0.4462) (3). The glands are lobular with a branched tubular architecture (1). A prominent layer of smooth muscle is present in the interstitium of the glands (1). The ducts of the vesicular glands share a common orifice into the urethra with the ipsilateral ductus deferens (1). The accessory sex glands’ function is regulated by testosterone levels; these levels in turn are governed by the anterior pituitary through the action of luteinizing hormone (LH ; 3.4). The accessory sex glands secrete fluid that acts as a transport medium for spermatozoa during ejaculation (1). The volume and composition of the fluid varies between species (4). The predominant components of the vesicular gland secretions of the bull are fructose and citric acid (5). Fructose is used as an energy source by the sperm and the citric acid acts as a reducing agent in the semen (4). The term vesicular glands is preferred to the older name seminal vesicles. as the glands do not act as reservoirs for sperm as that name would imply (6). Congenital defects of the vesicular glands have been reported (2). These defects are usually unilateral and include aplasia, hypoplasia, cysts, and duplication of the gland (2). These lesions are often associated with segmental aplasia of the mesonephric duct system which gives rise to the epididymis, ductus deferens, ampullae, and vesicular glands (2,3).
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1987 VOL. 28 NO. 4
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THERIOGENOLOGY
The most common disease of the vesicular glands is inflammation (2). Vesicular adenitis has been reported in bulls in Belgium, Britain, Canada, Denmark, France, Germany, India, Italy, the Netherlands, South Africa, Switzerland, Sweden, and the United States (7). Vesicular adenitis probably occurs in all areas where cattle are raised (7). Beef or dairy bulls may be affected (6,7). Bos indicus cattle as well as Bos taurus breeds are affected (8). The incidence of vesicular adenitis is variable. incidences up to 49% of a population (9-18).
Researchers
have
reported
ETIOLOGY Vesicular adenitis is an infectious process (19). Many organisms have been isolated from semen or genitalia of bulls with vesicular adenitis, including bacteria, chlamydia, and viruses (3,6,7,15,20). Where brucellosis has not been controlled, Brucella abortus is the primary cause of vesicular adenitis (6,7). The bacterium most frequently isolated from lesions of the vesicular glands in Western Europe and North America (where brucellosis has been controlled) is Corvnebacterium pvonenes (6,15,21). Gram-negative anaerobes and Corvnebacterium pvoaenes have been cultured together from the semen of bulls with vesicular adenitis (D.A. Dargatz, unpublished data, 1986). PATHOGENESIS Inflammatory lesions of the vesicular glands are due to infection (19). The predisposing factors leading to infection are unknown. Infection of the vesicular glands could potentially occur by one of four routes: by ascending the genito-urinary tract, by descending from the upper urinary tract or reproductive tract, by hematogenous spread, or by direct invasion of the glands from Iocal sources. The ascending route is unlikely as the distal genito-urinary tract is flushed frequently with micturition. However, Roberts describes this as the most likely route of infection (2). Pseudomonas aeruainosa has been reported as a cause of vesicular adenitis in bulls, albeit rarely (2,22,23). In a survey of the bacterial flora of the male genitalia, Pseudomonas aeruninosa was cultured from the urethra of normal animals (24). In the above survey Corvnebacterium pvoeene$ was not isolated from the urethra of normal animals at any level (24). Attempted creation of vesicular adenitis by reoeated instillation of Corvnkbacterium bvoeenes into the penile urethra was unsuccessful (7). The descending route of infection is more likely. Vesicular adenitis is noted to occur secondary to epididymitis or orchitis (6). Vesicular adenitis and ampullitis occurs ipsilateral to orchitis induced by Brucella abortus (25). In cases of vesicular adenitis caused by Corvnebacterium pvoaenes there is frequently involvement of other parts of the reproductive system (3,15,16,26,27). The temporal relationship between these lesions has not been clearly identified but some feel that many bulls with vesicular adenitis subsequently develop epididymo-orchitis (3). Pyelonephritis has only rarely been reported in conjunction with vesicular adenitis (26). The hematogenous route of infection has been suggested as a probable pathogenesis in vesicular adenitis cases (2,7,26,28). Multiple portions of the reproductive tract are frequently involved (3,15,16,26,27). In a postmortem study, 50% of bulls with vesicular adenitis had concurrent lesions outside the reproductive tract, including vegetative endocarditis, chronic bronchopneumonia, polyarthritis, and traumatic gastritis (26). As stated earlier, the most common
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bacterial agent associated with vesicular adenitis in areas where brucellosis is controlled is Corvnebacterium ovoaenes. A recurrent periodic bacteremia frequently occurs in cattle and is known to occur commonly following rumenitis (29). Liver abscesses in feedlot cattle result from the hematogenous spread of organisms from the forestomachs of cattle to the liver (30). The bacteremia is secondary to rumenitis due to acidosis in these animals (30). The most common isolates from liver abscesses of feedlot cattle are Corvnebacterium ovoaenes and gram-negative anaerobic bacteria (30). Young bulls in performance tests or being fitted for sale are commonly fed rations similar to those fed in feedlots (15). The incidence of vesicular adenitis is higher among bulls under this form of management than among range bulls (6,15,27). Bulls in performance tests or being fitted for sale are often housed together and homosexual activity is high among these groups (15). This homosexual activity may increase the likelihood of the organism’s penetrating the mucous membranes to be spread hematogenous1~ (6). The association of a history of omphalophlebitis with vesicular adenitis stimulated a researcher to inoculate Corvnebacterium ovonenes into the periNone of the calves developed toneal cavity of calves at the umbilicus (7). vesicular adenitis, though one calf developed periepididymitis (7). Factors other than infection have been associated with vesicular adenitis. Stressors such as shipment have been reported to contribute to the development of vesicular adenitis (6,31,32). Rare congenital anomalies of the mesonephric duct system have been noted with increased frequency in bulls with vesicular adenitis (31). These may act as a locus minorus resistentiae (31). CLINICAL
SIGNS
Overt abnormal clinical signs are often lacking in bulls with vesicular adenitis (6). When these signs are present, they resemble those seen in cases of traumatic reticulitis (6). Bulls may be febrile, stand with their back arched, and be reluctant to move (6,7). Varying degrees of hypophagia may be present (6). Bulls may show evidence of pain on defecation or ejaculation (6,7). The vesicular glands can be examined by palpation per rectum. Unilateral and bilateral cases of vesicular adenitis are reported, but unilateral cases are most common (7). Asymmetry of the glands is often present in unilateral cases of adenitis (6,27). Some asymmetry is normal, however, and this should be interpreted with care (6,26,27). Affected glands are often enlarged with a loss of the normal distinct lobulation (6,27). Bulls may show evidence of pain when the affected glands are palpated per rectum; however, this response is lacking in chronically affected bulls (6,154. Enlarged glands often contain abscesses (26). A single large abscess may form and fluctuate when palpated (26). As the lesions become chronic, fibrosis develops and results in a gland that is much firmer than normal (26). Following abscess of the gland(s), adhesions frequently form and involve other pelvic or abdominal organs near the glands (6,15). Fistula formation from abscessed glands to the rectum, urinary bladder, peritoneal cavity, or skin surface has been reported (6). Frequently, pathologic changes are present in other reproductive organs of bulls with vesicular adenitis (16,27). These lesions may not be grossly evident in all cases (16,27).
are
The semen of bulls with vesicular adenitis is usually virtually always seen when the semen is examined
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abnormal. Floccules grossly (6,32). The
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THERIOGENOLOGY
ejaculate may have a brownish discoloration due to blood pigments or may be blood-tinged (26,32). Microscopic evaluation of the semen generally reveals an admixture of white blood cells (usually polymorphonuclear leukocytes) with the sperm (6,7,27,32). In normal bulls, when white blood cells are present in the semen, they are usually present in small numbers (7). In bulls with vesicular adenitis, more than 1 white blood cell per 100 sperm cells are commonly seen (7). Leukocytes are present in aggregates or are dispersed evenly (26). Agglutination of sperm cells to clumps of leukocytes also has been reported (7). The volume of the ejaculate from infected bulls is not always decreased even if both glands are affected (7). The effect of vesicular adenitis on semen quality is variable. Carroll et al. report that as many as 80% of bulls with vesicular adenitis have semen of substandard quality, usually as a result of decreased motility (27). Morphological abnormalities of sperm have been reported to be within normal limits in bulls with vesicular adenitis when there is not concomitant disease of the testicles (33). When morphologic abnormalities are present, they are mostly secondary; many of the other genital organs of bulls with vesiculitis had subclinical inflammatory changes when examined microscopically (27). In other studies a high percentage of loose heads have been reported in semen from bulls with vesicular adenitis (7). There appears to be no correlation between the degree of severity of inflammatory lesions of the genitalia and the number of primary or secondary morphologic abnormalities in the semen (16). Biochemical changes in the semen of bulls with vesicular adenitis have been noted. The seminal pH is usually increased (7,32,34). An average pH of semen from normal bulls of 6.1 vs an average for bulls with vesicular adenitis of 7.2 is reported (34). The total solids in the seminal plasma as measured with a refractometer may be abnormally low (<5g/dl) in acute cases of vesicular adenitis (32). The fructose content of the semen from diseased bulls is often reduced, although this is an inconsistent finding (34). Citric acid content of the semen of bulls with vesicular adenitis is decreased. Alkaline phosphatase activity in semen of bulls with vesicular adenitis is sometimes decreased (35). The reported fertility of bulls with vesicular adenitis is variable. Decreased conception rates have been reported (2,25,28,35). However, others report “fair” conception rates when bulls with vesicular adenitis are used for either natural service or for artificial insemination (6,26). In the case of artificial insemination, a number of ejaculates must be discarded periodically due to poor quality (26). DIAGNOSIS Diagnosis of vesicular adenitis is usually based on clinical signs. While many bulls with chronic inflammatory disease of the vesicular gland show no outward abnormal signs, palpation of the glands per rectum is usually diagnostic (26). An abnormal amount of asymmetry between the glands, glandular enlargement with loss of lobulation, fibrosis, or periglandular adhesions are all reasonably reliable indicators of vesicular adenitis (2,6). The most practical and reliable laboratory test for vesicular adenitis is examination of the semen for leukocytes (32). This is accomplished by evaluating a Giemsa-stained smear of the semen (32). Increased numbers of leukocytes in the semen shouid be interpreted with caution because other sites such as the prepuce are potential sources of inflammation. An increase above 7.0 in the pH of semen can be regarded as compatible with lesions of the vesicular glands (7). Decreased
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citric acid concentration in semen is also a reliable indicator of pathologic changes in the vesicular glands (34). However, this test is not easily performed and is probably not very practical for routine or large-scale use. An etiologic diagnosis of vesicular adenitis can be obtained by culturing the semen. Care should be taken to avoid contamination of the semen sample Catheterization of the penile urethra and during the collection process. collection of the fluid expressed by massage of the vesicular glands is the most desirable method of obtaining a sample for culture (7). Once a sample is obtained, it should be transported anaerobically until it can be transferred to a medium for growth. Samples should be cultured both aerobically and anaerobicAttempts at virus isolation are of doubtful value. The potential for ally. Brucella pbortus infection should be considered and serum and seminal plasma should be evaluated for titers to the organism (6). THERAPY Bulls with vesicular adenitis may be treated medically or surgically. Antibiotic therapy when used should be based on antibiotic sensitivity patterns of the etiologic agent. Vesicular adenitis due to Brucella abortus should not be treated and the animal should be slaughtered. Response to antibiotic therapy is generally poor (6,31) but spontaneous cures are reported (6). Even when inflammation appears to have been resolved, the disease may recur (31). Infected vesicular glands can be removed surgically if adhesions are not extensive and the size of the gland is moderate (2,31). Epidural and local anesthesia with tranquilization is used and an elliptical incision is made in the iscchiorectal fossa on the side of the affected gland. Blunt and sharp dissection is used to isolate the affected gland. The duct of the gland is ligated near the attachment to the urethra and the gland is removed (2). The effect of vesicular adenectomy on fertility and semen quality is variable (2,26,36,37). Volume of the ejaculate, sperm motility, percentage of live cells in the ejaculate, and number of primary morphologic abnormalities of the sperm cells decrease following removal of the vesicular glands (37). Concentration of the ejaculate and the number of secondary morphologic abnormalities of sperm cells in the ejaculate may increase postoperatively (37). Vesicular adenectomy has no apparent effect on libido (36). Bulls are able to mate naturally after the operation with acceptable fertility (37). Sperm cell tosses during freezing are increased after vesicular adenectomy; however, the vitality of the remaining cells is not affected and it appears that enough sperm cells survive for normat fertility levels (36). Since there is a propensity for concomitant involvement of other parts of the male genital tract in cases of vesicular adenitis, othe reproductive organs should be carefully evaluated prior to the decision to remove the vesicular glands (31). Congenital anomalies of the mesonephric duct system appear with increased frequency in bulls with vesicular adenitis. In one report of 32 bulls determined to have vesicular adenitis, 22 were of one breed and 10 were closely related to a single sire (31). Segmental aplasia of the mesonephric duct system is heritable (31). The possibility that bulls developing vesicular adenitis may have a heritable predisposition for the disease should be considered before surgical or medical treatment of the condition is undertaken.
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l-HERIOGENOLOGY
PROGNOSIS The prognosis in cases of vesicular adenitis is guarded to poor (15). Occasionally spontaneous cures occur (6,27); however, this process may take many months (27). The response to medical therapy is poor (6). Few cases meet the criteria necessary for surgical treatment (i.e.; size, degree of adhesions) and justify the economic investment. In most instances, affected animals are slaughtered (3 1). DISCUSSION Inflammatory disease of the vesicular glands has been a prevalent disease among young beef bulls with up to 49% of some groups examined being affected either clinically or subclinically histologically (16). Bulls with vesicular adenitis are classified as questionable potential breeders and are usually slaughtered. Bulls with vesicular adenitis frequently have concurrent pathologic conditions of other parts of the reproductive tract such as orchitis or epididymitis. These animals must be classified as unsatisfactory potential breeders and should be slaughtered. Slaughter of affected bulls represents an economic Performancetested bulls in the western and genetic loss to the producer. states sell for an average of $1200.00 per head. Slaughtered bulls usually bring $40.00 per hundredweight. Bulls at the end of performance test would average 1100 lb; therefore, a loss of $760.00 per affected bull would be anticipated. The genetic loss cannot be quantitated; however, producers usually place their best potential breeding bulls on performance test so the loss is no doubt substantial. The current prevalence of vesicular adenitis is unknown; consequently, its economic impact is also unknown. The route of infection and predisposing causes for vesicular adenitis have not been determined. Hematogenous spread from a gastrointestinal source has been postulated in those cases of vesicular adenitis caused by Corvnebacterium The presence of gram negativeanaerobes in these infections is pvoaenes. suspected. Concurrent infections with these organisms have been shown in the case of ovine infectious bulbar necrosis, bovine liver abscessation, and bovine pyometra (38,39). The gram- negative anaerobes produce a leukocidal toxin Protective for Corvnebacterium pvoaenes as well as for themselves (39). stimulating factor for the Corvnebacterium pvoaeneg produces a growthevidence supports the hypothesis of hematogenous anaerobes (39). Circumstantial spread of the organism(s). The disease is most common in young bulls on performance test receiving feedlot rations. The most common organism involved is the same as that seen most commonly in liver abscesses of feedlot cattle, a disease known to be due to hematogenous spread of the organism from the forestomachs subsequent to acidosis and rumenitis. Corvnebacterium ovoaenes is not a normal inhabitant of the urethra of bulls. The disease cannot be recreated by repeated instillation of the organism into the penile urethra of normal bulls. A descending route of infection cannot be demonstrated except in the case of vesicular adenitis due to Brucella abortus. This organism infects the testicle and/or epididymis by the hematogenous route prior to metastasis to the vesicular glands. More work needs to be done to define the current extent and significance of the problem and to determine the pathogenesis of the disease so that measures to prevent the condition can be developed and implemented.
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