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Testicular Hypoplasia in Male Animals
Testicular hypoplasia is a congenital condition in male animals where one or both testes fail to develop to normal size and function due to incomplete or defective development of germ cells.
Testicular hypoplasia may be partial or total due to a failure of germinal cells to develop in the yolk sac, failure to migrate to the gonad, failure to multiply in the gonad or extensive degeneration of early germinal cells after they have entered the gonad.
Testicular hypoplasia is congenital hereditary in origin is caused by a marked lack of or reduction in spermatogonia in the gonads during fetal life.
It is observed as a unilateral or bilateral condition at the time of the puberty or later in all of our domestic animals. Most commonly seen in bulls, rams, boars and stallions.

Swedish Highland breed with white coat colour is commonly affected. Cattle with black ears were not affected.
In these cattle hypoplasia of left testis occurred about 25 percent of all bulls, in the right testis 1 percent and in both testes 4-5 percent.
This condition in cattle is due to a single autosomal recessive gene with incomplete penetrance.
Symptoms
In most cases-sexual desire is excellent and coitus is prompt. Therefore owners may not suspect the infertility for sometime
The degree of either unilateral or bilateral testicular hypoplasia varies from complete hypoplasia causing sterility to only slight softer unsuspected hypoplasia.
Lowered conception rates are often evident in bilaterally affected males.
Severe testicular hypoplasia is usually observed in young bulls of 1-2 years of age.

In sterile bull with bilateral hypoplasia, the semen is usually clear, and watery with few or no spermatozoa.
Centrifugation of the ejaculate and staining of the sediment revealed the presence of giant cells and medusa cells or ciliated cells from the efferent tubules.
Giant cells or multinucleated cells with 6-8 nuclei apparently result from incomplete maturation division of the primary spermatocytes. These cells are seen in testicular hypoplasia and severe degeneration.
Sexual organ develop normally except the affected testis.
The consistency of the testes was soft, flabby or hard, indurated and fibrotic.
Males which are severally affected are nearly sterile, but an occasional conception may occur in females bred to them.
The semen picture shows a lower concentration of spermatozoa usually less than 70,000 per cmm, low motility, many abnormal spermatozoa and the possible presence of a few giant cells.
In some bulls with a moderate to slight amount of testicular hypoplasia the conception rate is low, about 20-40%. The testicles may appear nearly normal in size and consistency. The spermatozoa concentration is from 1,00,000 to 5,00,000 per cmm. The motility is usually low and the number of pathological or abnormal spermatozoa is high about 30% or greater.
Epididymis
Depending on the degree of hypoplasia, affected bulls will have a small, firm epididymis—especially in the tail region—indicating reduced spermatogenesis and low gonadal sperm reserves.
Spermatic cords of hypoplasia testicles are shorter as the testes are less heavy and the scrotum smaller than in normal males.
Slight or mild cases of testicular hypoplasia may predispose to testicular degeneration.
Diagnosis
Diagnosis is done based on the above described symptoms.
The diagnosis of testicular hypoplasia should not be made before 2 years of age in the bull and horse or before one year of age in the boar, ram, dog or cat unless the hypoplasia is marked and the male is well grown.
The testicular hypoplasia may be erroneously diagnosed in young immature males that are underdeveloped or are retarded in growth at the generally accepted time of puberty for the species.
Prognosis
Prognosis is poor. Affected animals should not be used for breeding because the condition may be hereditary.
Severally affected animals are sterile or highly infertile. Mildly to moderately affected animals may have only a lowered fertility but are more prone to early testicular degeneration.
Treatment
Treatment of testicular hypoplasia in animals has been unsuccessful. The germinal epithelium of the affected animals apparently cannot respond to gonadotropic therapy because spermatogonia are reduced in numbers or lacking in hypoplasia of testis.