Equis ISSN 2398-2977

Testis: hypoplasia

Contributor(s): Graham Munroe, Elaine Watson

Introduction

  • 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: incomplete gonadal development primarily from congenital factors; variety of possible congenital and acquired causes, eg chromosomal abnormalities   →   infection.
  • Signs: one or both testes can be involved with varying degrees of hypoplasia and changes evident on semen evaluation.
  • Diagnosis: full clinical examination; 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  .
  • Genetic and teratogenic causes are suspected.

  • 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 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.
  • Strong Met al(1997)Monorchidism in two horses.Aust Vet J75(5), 333-335 PubMed.
  • Parks A Het al(1989)Monorchidism in the horse.Equine Vet J21(3), 215-217 PubMed.
  • Santchi E Met al(1989)Monorchidism in three colts.JAVMA194(2), 265-266 PubMed.


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