Testis

Developmental abnormalities

Testicular hypoplasia

The most common form of testicular hypoplasia (Fig. 1) occurs with cryptorchidism. Cryptorchidism is characterized by retention of one or both testes along the natural course of descent to scrotum. The testis developed from the mesodermic genital fold in the lumbar region and descends downwards forwards and medially toward the scrotum.

There are some factors responsible for the normal descent of testis:

1. The gabernacu1um which is a   fibromuscu1ar band attached to the bottom of the scrotum below and to the lower pole of the testis above. As the gabernaculurn contracts and become shorter it will pull the testis down and it will guide it through the inguinal canal and the neck of the scrotum.

2. The intra-abdominal pressure, which squeeze the testis out through the internal, then the external inguinal ring then the neck of the scrotum.

3. The size of the testis if it is very small or very large it fail to engage in the internal  inguinal ring.

4. Chorionic gonadotropic hormones of the anterior pituitary reaching the fetus from the mother’s blood.

Causes of undescended testis (cryptorchidism):

The predisposing factors for incomplete descent of the testis are:

1. Any of the above mentioned factors when deficient.

2. Shortness of the spermatic vessels or the vas deferens.

3. Adhesions and short fibrous band fixing the testis in a higher place.

Pathology:

The testis usually stops at one of the following sites

1. The neck of the scrotum or the external ring: the commonest.

2. The internal canal or the internal ring: less common.

3. The iliac fossa: rare

4. The lumbar region: rarest.

This mean that arrest of descent of the testis can occur any where along the normal line of descent, more commonly lower than higher.

The testis remain normal in size and function until puberty where:

1. The size does not enlarge enough to reach the size of an adult testis (Figure 2).

Fig. 1:Testes showing hypoplasia characterized by the seminiferous tubules are rudimentary and have rare or no spermatogenesis. The leydig cells may be numerous. H&E

Fig. 2: Gross picture of testes showing hypoplastic small tetes.

2. The spermatogenic function does not, develop as the temperature of the abdomen is higher than in the scrotum and it is well known that a lower temperature is required for active spermatogenesis. So this testis become almost sterile and if both testes are undescended sterility is usually the rule.

3. The hormonal function of the testis is on the other hand almost normal so that the secondary sexual characters develop normally, erection occur and the patient is potent.

Microscopic picture:

The seminiferous tubules are rudimentary and have rare or no spermatogenesis. The leydig cells may be numerous (Fig. 3).

There have been instances where the  cryptorchid testis proved to be no more than a modified vas deferens with many tributary tubules.

Fig. 3: Testes suffered from cryptorshidism have rare or no spermatogenesis. The leydig cells may be numerous.

Complications:

1. Sterility if the condition is bilateral.

2. An associated oblique inguinal hernia.

3. The undescended testis is more liable to trauma, torsion and malignant diseases.

Atrophy

It is a decrease in the size of testis after reaching its mature size of mature individual due to adverse systemic or environmental influences as

1. Deprivation of pituitary gonadotropins

2. Administration of exogenous androgens or estrogens

3. Ionizing radiation

4-Genarlized malnutrition

5. Deficiency of vitamin A and E

6. Prolonged fever or hyperthermia

7. Certain infectious diseases

8. Occulosion of spermatic vessels

9. Certain neoplasms

Spermatic cells are most susceptible to the forementioned adverse effect

Leydig cells may undergo atrophy due to hormonal imbalance

Sertoli cells may resist the atrophic changes

Atrophy of all principal cellular components of the testis including germinal cells, sertoli and leydig cells may be result from loss of testicular blood supply due to vascular occlusion or from torsion of spermatic cord or massive dose of ionizing radiation.

Torsion of the testis:

It is actually torsion of the spermatic cord and the testis twists accordingly.

Causes:

This is an uncommon condition which can occur at any age. The predisposing, causes are:

1. Imperfect descent of the testis (undescended testis or ectopic testis).

2. Long mesorchium.

3. Anteversion of the testis especially transverse anteversion.

4. Sirius of the epididymis when the testis is separated from the epididymis by a sort of mesentery. Here the torsion occur in the body of the testis and not the spermatic cord.

5. Long or relaxed spermatic cord.

Pathological features:

1. The testis usually rotates, from outside inwards. It may be one, two, three...etc. turns. At first it becomes congested and edematous, then its co1or changes into dark and finally gangrene and sloughing occurs when the blood supply completely cut off.

2. The spermatic cord shows the twists and the greater the number of twists the shorter will became the cord and the higher will the testis. Thrombosis of the vessels is the ultimate result if the torsion is not reduced quickly.

3. The tunica vaginalis shows hydro or haematoceles.

4. The scrotal skin becomes reddened and edematous.

Hypertrophy and hyperplasia

Testicular hypertrophy and hyperplasia occur rarely due to endocrine imbalance. Unilateral orchiectomy leads to increase in the weight of remaining testis due to  hypertrophy and hyperplasia of leydig cells.

Degeneration

Testicular degeneration is a relatively common lesion, which can be unilateral or bilateral (Figs 4 & 5 The distinction between testicular degeneration and hypoplasia is difficult. A degenerate testes is initially swollen and softer than normal followed by progressive shrinkage. The consistency become firmer after the acute phase. Microscopically, the seminiferous tubules become small with thickened basement membrane, decreased number of seminiferous epithelial cells, intertubular giant cells and interstitial fibrosis (Fig. 6). At the end stage of testicular degeneration, sertoli cells may be the only lining cells remaining. Calcification may occurs.

Fig. 4: Bull showing unilateral testicular degeneration.

Fig. 5:  Testes showing gross picture of testicular degeneration.

Fig. 6:  Testecular degeneration showing degenerating spermatogenic cells and presence of giant cells. H&E

Orchitis and epididymitis

Orchitis: inflammation of the testis.

Epididymitis: inflammation of the epididymis.

Inflammation of the testis (orchitis) is usually associated with inflammation of the epididymis (epididymo-orchitis) or with the spermatic cord and epididymis (funiculo-epididymo-orchitis). The condition may be acute or chronic, the chronic may be specific or non specific.

Acute inflammation: Can occur at any age but commonest at adult life.

Causes:

1. Traumatic as kicks, instrumentation.

2. Infections: The organisms reach the testis, epididymis cord either through ascending route via the urethra or through the blood stream.

The most important organisms are:

- Brucella: Brucella abortus in bulls, Brucella ovis in rams, Brucella suis in boars

- Salmonella abortus equi. The orchitis in horse was accompanied by fever and general body reactions during its, acute stage.

-Pasteurella pseudotuberculosis (corynebacterium-pseudotuberculosis rodeptium) causes a severe purulent orchitis in rams.

-Pseudomonas  aerogenes or bacillus pyocyaneus: This organism of blue-green pus has been identified in diseased male genital tracts, apparently without being responsible for marked 1esions.

- Secondary to some specific fever in man as mumps. They are usually catarrhal inflammation and don’t proceed to     suppuration.

- In a diagnostic test known as straus reaction, male guinea pigs developed periorchitis and a necrotising and a destructive suppurative orchitis a few days subsequent to intraperitoneal inoculation of small doses of         glanders bacilli as well as the organisms which causes epizootic lymphangitis, ulcerative lymphangitis and       ovine caseous lymphadenitis.

Pathological features:

• There is usually focal or diffuse suppurative inflammation, often with abscess (Figures 7& 8).

• The skin of the scrotum shows variable degree of redness, edema. The cord is matted together thickened. The epididymis is enlarged and may show an abscess. The testis is enlarged but the testicular swelling is limited by the tunica vaginalis.

• The cut surface is hyperemic, moist and presents yellowish foci of necrosis or suppuration.

Fig. 7: Testes showing suppurative orchitis.

Fig. 8: Testes of pig showing orchitis.

Chronic inflammation:

These usually result in chronic masses of the cord, epididymis or testis.

The type of the masses are:

a. Non-specific: When a bad management of acute cases, chronicity will supervene (Figures 9 &10). The mass may occur in the cord or epididymis and is irregular and firm and a secondary small hydrocoele is usually present.

Fig. 9: Testes showing chronic orchitis showing irregular swelling of testis.

Fig. 10: Testes showing chronic diffuse orchitis. The parenchyma is infiltrated with chronic inflammatory cells and fibrous tissue. H&E.

1. Tuberculosis.

2. Filarial infestation: Common in Egypt. They may follow acute funiculoepididymitis or may begin as chronic.

Pathological features:

Chronic inflammation is characterised by fibrous connective proliferation in the cord, epididymis and the testis. Once the germinal epithelium is completely destroyed, regeneration doesn’t occur.

Sequelae:

1. The more severe    form of orchitis lead to destruction of the testis, marked pain and in some case a generalized febrile disease with fatal septicemia.

2. The mildest form lead to temporary aspermatogenesis.

3. The disorder is slight, some spermatogenesis will continue.

4. A high percentage of deformed and imperfect spermatozoa supervenes upon injury       to the germinal epithelium.

Neoplasms of testis

Benign tumour of the testis are almost unknown and once a tumour is detected it is considered malignant.

The types of tumours arising from the testis are:

1.  Teratoma (Fig. 11)

2.  The seminoma: It arises from the seminiferous tubules (Fig. 12 ).

3. The Leydig-cell or interstitial-cell tumor secretes the male hormone (masculinizing tumour) (Figs 13 & 14).

4) The sartoli cell or sustantacular-cell tumor secretes the female hormone (feminising tumor) (Figs 15 & 16 ).

Fig. 11: Testes showing teratoma represented by presence of skin and its appendage in testicular parenchyma. H&E

Fig. 12: Dog testes showing seminoma. H&E.

Fig. 13: Testes showing leydige cell tumor. H&E.

Fig. 14: Testes showing leydige cell tumor.

Fig. 15: Testes showing sartoli cell tumor.

Fig. 16: Testes showing sartoli cell tumor. H&E.

Diseases of the tunica vaginalis

The tunica vaginalis is a serous coat originally derived from the peritoneum and covers the front and sides of testis but not epididymis. During intrauterine life it was connected to the peritoneal cavity by the processus vaginalis which later become obliterated completely. The tunica vaginalis has two layers one stick to the testis and called the visceral layer and one free the parietal layer. In between the two there is a thin film of fluid for lubrication during movements of the testis.

Hydrocele

Definition:

It is the accumulation of watery fluid inside the scrotal cavity between layers of tunica (Fig. 17).

Fig. 17: Testes showing hyrocele.

Causes:

1. Congenital due to patency of the processus vaginalis.

2. In hydroperitoneum and there is a communication between the peritoneal cavity and the cavity of tunica vaginalis.

3. Exudate from suppurative peritonitis.

4. T.B of the tunica vaginalis. It is the most frequent result of tuberculosis of the peritoneum. The lesion are typical of pearl disease.

5.  Periorchitis which is due to brucella. It may be serous, or sero-fibrinous or purulent.

6. Parasites as strongylus edematous are found in the cavity of the tunica vaginalis.

7. Inguinal or scrotal hernia.

8. Cyst either acquired or congenital.

Complication:

1.  Infection especially after aspiration lead to opyocele.

2. Hemorrhage in the tunica either spontaneous or traumatic lead to hematocele (Figure18).

Fig. 18: Testes of horse showing hematocele.

3.  Rupture is usually traumatic and is rare.

4. Hernia of the hydrocele sac due to herniation of the parietal tunica at a weak point giving an outside bulge.

5. Traction of the scrotum downwards and invagination of the penis especially in bilateral large masses. This will interfere with the act of micturation.

6. Atrophy of the testis doesn’t occur unless infection or hematocele is present.

Spermatic cord

Varicose is  the local dilatation of the spermatic vein in the pampiniform plexus due to insufficiency of the valves of the vein. The fertility is reduced due to interference with thermoregulation of the testis. It is common in rams.

Torsion. Torsion of the spermatic cord can occur when the testis is undescended. Vascular occlusion lead to testicular necrosis (Fig 19 ).

Fig. 19 :Testes and spermatic cord are congested due to torsion of spermatic cord.

Funiculitis:

It is the inflammation of the spermatic cord. It shares with the process of epididymitis and orchitis (Fig. 20).

Scirrhous cord:

It is an excessive granulation tissue formed on the stump of the spermatic cord following castration.

Causes:

Staphylococcus aureus, Fusiform necrophorum, Actinomyces bovis, Actinobacillus ligniersi and Mycobacterium tuberculosis, Spirochetes may be the etiological factors in many cases in swine.

Lesions

The excessive granulation tissue formed at the stump of the spermatic cord constitutes a mass (Fig. 21). This mass is the result of a chronic hyperplastic proliferative inflammation resulted from operative injury and infection. The mass attain large size in a few weeks. Its consistency is firm at the beginning but later on f1uctuating areas develop and rupture to form fistulous tracts which omit a bad smelling odor.

The mass consists usually of dense fibrous tissue alternating irregularly with areas of more youthful and more active fibroblastic growth. Some areas contain much leucocytic infiltration. There are often thick walled chronic abscesses.

Fig. 20: Spermatic cord showing funculitis.

Fig. 21: Spermatic cord showing scirrhous cord.

Seminal vesicles and bulbo-urethral glands

Seminal vesiculitis or spermatocystitis = inflammation of the seminal vesicles.

The seminal vesicles and bulbo-urethral glands tend to harbor infections because of their complicated structure and poor drainage. They are thus of severe importance as sites of localizations of brucellosis, vibriosis and trichomoniasis as well as for the locally less destructive Pseudomonas aerogenes.

The affected glands are enlarged and cystic (Fig. 22) . The cyst spaces are filled with a thick purulent exudate particularly in brucellosis. The seminal vesicles may be only slightly altered by the tissue reaction, they may contain abscess or the organ may be distended with pus. In the   more severe alteration of the gland there is excessive destruction of the glandular epithelium.

The ability of the affected males to copulate is usually not affected but fertility is reduced or completely suppressed and transmit the infection to the female where it can cause vaginitis, cervicitis and metritis.

Vitamin A deficiency in bulls lead to squamous metaplasia of the columnar epithelial lining of their seminal vesicles.

Fig. 22: Seminal vesiculitis characterized by enlarge an congested.

The prostate

Prostate of cattle, sheep and swine is almost of a rudimentary size. Much of its glandular tissue is disseminated in the wall of the upper urethra. The equine prostate is small. That of the dog is well developed as if it is compensatory to the absence of the seminal vesicles and bulbo-urethral glands. The larger the prostate, the more it is liable to diseases.

Hypertrophy of the prostate:

Causes:

The true causes of enlargement of the prostate is unknown. Theories are:

1. Hormonal imbalance: This theory is proved by the following evidences:

a.  Experimental injection female hormones     in rats resulted in hypertrophy of the prostate.

b. It believed that prostatic enlargement is due to excessive androgenic stimulation.

c. Male hormone injection in patients with hypertrophy of the prostate improve the condition.

2. Chronic inflammation: The lymphocytic infiltration, fibrosis and other evidences of chronic inflammation are the results rather than the causes.

3. A benign tumour as adenoma.

Macroscopic appearance:

The gland is enlarged three times the normal size (Fig. 23) . The enlargement is often pronounced just at the neck and the surface of the bladder with the formation of a “middle lobe”, which actually project into the cavity of the bladder and carries the urethral entrance with it.

Fig. 23: Enlarged prostate gland suffered from prostatic hypertrophy.

The surface is smooth or nodular, cysts may be seen. The urethra may be compressed by the enlarged.

Microscopic appearance:

Hypertrophy of all the 3 elements of the prostate in varying ratios the glandular, the muscular, and the fibrous elements. If the glandular hypertrophy predominates, the gland feel soft, if the fibrous elements predominates, it will feel firm. Epithelial lining of the gland may form papillary projections inside the lumen  or may be atrophied due to pressure atrophy of the secretions (Figs 24 & 25 ) . The secretion of the glandular element may be abundant (corpora amylacea) (Fig. 26) and may even get calcified.

At time, the glandular tubules become greatly dilated (cysts) and fuse with other dilatation to form large cysts. The cysts are lined with atrophied epithelium. The glandular secretion contained within the cyst frequent1y has a brown color due to blood, pigments contained within it.

The cellular exudate in these areas consists primarily of neutrophils and less number of plasma cells, lymphocytes and macrophages.

In other tubules, the epithelium hyperplasia results into papillomatous projections into the1umen of the tubules, which may cause the tubules to become greatly distended. This hyperplasia of the epithelium is frequently confused with neoplasm.

Fig. 24: Prostate hyperplasia showing increase in the number of lining epithelium forming papillomatous projections into the1umen of the tubules. H&E.

Fig. 25: Prostate hyperplasia showing increase in the number of lining epithelium forming papillomatous projections into the1umen of the tubules. H&E.

Fig. 26: Testes showing corpora amylacea.

Complications:

1) In the prostate

a.   Infection and abscess formation.      

 b. Secondary carcinoma.

c. Calculus formation.

2. The urethra

a. Elongation of the urethra

b.  Narrowing of the urethra due to encroachment on its lumen.

c. Complete obstruction of the internal meatus.

d. The internal sphincter is widened by the emmerging middle lobe so that it cannot contract adequately.

3) In the bladder

a.  At first hypertrophy then dilatation, then trabeculation then diverticulum.

b.  Atony of the bladder.

c.  Stasis of the urine resulting in infection and stones.

d. Hemorrhage from the mucosa.

e. Acute and chronic retention of urine.

4) In the ureters and kidneys

a. Dilatation due to back pressure, hydroureter and hydronephrosis.

b. Infection:    bi1ateral pyonephritis or pyonephrosis.

c. Stone formation.

d. Gradual affection of the kidneys function, which may lead to uremia.

B. Sexual complication:

a.  At first there is increase sexual desire. False erection occurs due to engorgement of the penis from impairment of its venous drainage by the enlarged prostate. As the prostate enlarge the prostatic venous plexus is compressed and so it cannot drain the veins of the penis resulting in distension of the erectile tissue of the penis with blood.

b.  Later, new veins form in the prostatic venous plexus which can however accommodate for drainage of the penis and so the erection are lost and the desire is lost.

c.  All the time, the sexual ability is diminished.

C. General complications:

General weakness and loss of weight.

Prostatitis

It is the inflammation of the prostate. It may be acute or chronic.

Acute prostatitis:

Causes:

Pyogenic microorganisms.

The infection reach the prostate by ascending along the urethra or by descending from the bladder.

Lesions

The prostate is enlarged, congested and edematous . There may be a number of abscesses, small or microscopic in size or they may be one or two of large size a maximum diameter of 11 cm (Figure 27 ).

With high resistance of the body’s patients, the abscess or abscesses become heavily encapsulated.

A purulent exudate open or discharge into the urethra. Microscopically, prostatitis usually start as catarrhal and later become purulent (Figs 28 & 29).

Fig. 27: Prostate gland showing acute prostatitis.

Fig. 28: Prostatitis characterized by infiltration of the prostatic parenchyma by neutrophils. H&E.

Fig. 29: Prostate glands showing suppurative inflammation. H&E.

Complications:

a) Rupture of the abscess or abscesses through the urethra or rectum leading to a fistula

b)Spread of inflammation upwards to the bladder and downwards to the seminal vesicles and epididymis.

Prostatic calculi:

It is present in man and dogs, such calculi arise from corpora amylecea. They were smooth discoid, modified hard concretions. Their colour was variable, white mottled or streaked with brown. They consist chiefly of phosphates and carbonates of calcium. The central nucleus is organic material indicating desquamated or other dead cells. They arise in connection with chronic prostatitis and hypertrophy of the prostate. Small collections of stones are asymptomatic, others are irritant and obstructive.

Neoplasms of the prostate:

Prostatic neoplasms are found in aged dogs and are uncommon in most domestic animals. They are: Benign tumours: adenomas, Fibromas, leiomyoma. Malignant tumours: adenocarcinoma (Fig. 30 ).

Fig. 30: Prostate showing adenocarcinoma. H&E.

Metastasis to internal iliac lymph nodes and lungs. Multiple implants are frequently present on the serous surfaces of the peritoneum.

The urethra, penis and prepuce

Hypospadias:

It is a congenital anomaly of the urethra, where the external meatus is situated behind its normal site.

Epispadias:

It is a congenital anomaly of the urethra, where the external meatus is situated in front its normal site.

Stricture of the urethra:

Narrowing of the lumen of the urethra.

Phimosis:

This is narrowing of the preputal orifice prevents extension of the penis from the sheath.

Paraphimosis:

 It is the swelling of the prepuce when the penis protruded and impossible to withdraw (Fig. 31).

Fig. 31: Horse penis showing paraphimosis.

Fig. 32: Penis showing balanoposthitis.

Fig. 33 Penis showing traumatic hematoma.

Fig. 34: Penis  showing fibropapilloma. H&E.

Fig. 35: Penis showing squamous cell carcinoma.