ISSN 2398-2977      

Testis: hypoplasia

pequis

Introduction

  • Failure of the testis to develop to normal size, accompanied by failure of the epididymis to reach normal size.
  • Normally evidenced by failure of pre-pubertal testes to develop at puberty. Sometimes even pre-pubertal testes may be noticeably underdeveloped.
  • Can be unilateral or bilateral.
  • Relatively common pathologic entity in stallions. A number of authors state that hypoplastic testes are predisposed to testicular degeneration.
  • Specific breed predilections have not been studied critically.
  • Causes: suspected causes include abnormal karyotype; in-utero infection or toxins; zinc deficiency; hormonal insufficiency; disrupted testicular descent; vascular disturbances.
  • Signs: one or both testes can be involved with varying degrees of hypoplasia due to reduction in the quantity of seminiferous epithelium. Changes evident on semen evaluation.
  • Diagnosis: full clinical examination; ultrasonography; +/- testicular biopsy; cytogenetic studies may be indicated if chromosomal abnormality suspected.
  • Treatment: none.

Pathogenesis

Etiology

  • Probably a multifactorial disease.
  • Can result from primarily congenital aberrations Reproduction: gonadal dysgenesis.
  • Suspected causes include abnormal karyotype; in-utero infection or toxins; zinc deficiency; hormonal insufficiency; disrupted testicular descent; vascular disturbances.

External influences

  • Infections.
  • Intoxications.
  • Malnutrition.
  • Endocrinologic disturbances.
  • Irradiation.
  • Impaired thermoregulation.
  • Male equine hybrids (mules or hinnies).
  • Abdominal or inguinal cryptorchidism Testis: cryptorchidism.
  • Congenitally short cremaster muscles or excessive intrascrotal fat.

Pathophysiology

  • Characterized by incomplete gonadal development.
  • Accelerated development of testis into a sexually functional organ does not normally begin until puberty → derangement of numerous prepubertal events can result in testicular hypoplasia.

Abnormal primordial germ cell activity during fetal life

  • May be caused by:
    • Inadequate proliferation in the yolk sac.
    • Improper migration en route to the fetal gonad.
    • Insufficient multiplication/inordinate degeneration after arrival at the gonad.

Post-natal disruption of the germinal epithelium

  • Mild forms of testicular hypoplasia, most affected seminiferous tubules exhibit active spermatogenesis that progresses to the primary spermatocyte stage or beyond.
  • Isolated tubules remain completely hypoplastic.
  • Resulting fertility is determined by the degree of hypoplasia.
  • Severe hypoplasia is characterized by a pre-ponderance of completely hypoplastic seminiferous tubules.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Pozor M et al (2017) Relationship between echotextural and histomorphometric characteristics of stallion testes. Theriogenology 99, 134-145 PubMed.
  • Pozor M (2005) Diagnostic applications of ultrasonography to stallion's reproductive tract. Theriogenology 64 (3), 505-9 PubMed.
  • Faber N F & Roser J F (2000) Testicular biopsy in stallions: diagnostic potential and effects on prospective fertility. J Reprod Fertil Suppl (56), 31-42 PubMed.
  • Strong M et al (1997) Monorchidism in two horses. Aust Vet J 75 (5), 333-335 PubMed.
  • Parks A H et al (1989) Monorchidism in the horse. Equine Vet J 21 (3), 215-217 PubMed.
  • Santchi E M et al (1989) Monorchidism in three colts. JAVMA 194 (2), 265-266 PubMed.

Other sources of information

  • Arighi M (2011) Developmental abnormalities of the male reproductive tract. In: Equine Reproduction. 2nd edn. Eds: McKinnon A O, Squires E L, Vaala W E & Varner D D. Wiley Blackwell. pp 1109-1111.
  • Johnson L, Griffin C E & Martin M T (2011) Spermatogenesis. In: Equine Reproduction. 2nd edn. Eds: McKinnon A O, Squires E L, Vaala W E & Varner D D. Wiley Blackwell. pp 1026-1052.

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