Bovine Reproduction. Группа авторов

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Bovine Reproduction - Группа авторов


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R., and Coulter, G. (2001). Relationship among scrotal and testicular characteristics, sperm production, and seminal quality in 129 beef bulls. Can. J. Vet. Res. 65: 111–115.

      32 32 Barth, A. (2000). Bull Breeding Soundness Evaluation, 2e, 6–7. Saskatoon: Western Canada Association of Bovine Practitioners.

      33 33 Blockey, M. (1979). Observations on group mating of bulls at pasture. Appl. Anim. Ethol. 5: 15–34.

      34 34 Barth, A., Alisio, L., Aviles, M. et al. (2008). Fibrotic lesions in the testis of bulls and relationship to semen quality. Anim. Reprod. Sci. 106: 274–288.

      35 35 Curtis, S. and Amann, R. (1981). Testicular development and establishment of spermatogenesis in Holstein bulls. J. Anim. Sci. 53: 1645–1657.

      36 36 Nagaraja, T., Galyean, M., and Cole, N. (1998). Nutrition and disease. Vet. Clin. North Am. Food Anim. Pract. 14: 257–277.

      37 37 Bouters, R. (1964). A virus with enterogenic properties causing degeneration of the germinal epithelium in bulls. Nature 201: 217–218.

      38 38 Ramirez‐Mendoza, H., Hernandez‐Jauregui, P., Reyes‐Leyva, J. et al. (1997). Lesions in the reproductive tract of boars experimentally infected with porcine rubulavirus. J. Comp. Pathol. 117: 237–252.

      39 39 Kupferschied, H., Kihm, U., Bachmann, P. et al. (1986). Transmission of IBR/IPV virus in bovine semen: a case report. Theriogenology 25: 439–443.

      40 40 McClurkin, A., Coria, M., and Cutlip, R. (1979). Reproductive performance of apparently healthy cattle persistently infected with bovine viral diarrhea virus. J. Am. Vet. Med. Assoc. 174: 1116–1119.

      41 41 French, E. (1962). Relationship between infectious bovine rhinotracheitis (I.B.R.) virus and a virus isolated from calves with encephalitis. Aust. Vet. J. 38: 555.

      42 42 Fountain, S., Holland, M., Hinds, L. et al. (1997). Interstitial orchitis with impaired steroidogenesis and spermatogenesis in the testes of rabbits infected with an attenuated strain of myxoma virus. J. Reprod. Fertil. 110: 161–169.

      43 43 Berg, M., Bergvall, A., Svenda, M. et al. (1997). Analysis of the fusion protein gene of the porcine rubulavirus LPMV. Comparative analysis of paramyxovirus F proteins. Virus Genes 14: 55–61.

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      46 46 Kennedy, S., Moffett, D., McNeilly, F. et al. (2000). Reproduction of lesions of postweaning multisystemic wasting syndrome by infection of conventional pigs with porcine circovirus type 2 alone or in combination with porcine parvovirus. J. Comp. Pathol. 122: 9–24.

       Mike Thompson

       Willow Bend Animal Clinic, Holly Springs, MS, USA

Photo depicts normal vesicular glands. Source: Courtesy Maarten Drost VISGAR.

      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].

Photo depicts vesicular adenitis with enlargement and loss of lobulation.

      Source: Courtesy Maarten Drost, VISGAR.

      Due


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