Testicular Histology and Conditions Quiz

Male Genital System Pathology

• The presentation covers the pathology of the male genital system, encompassing anatomy, histology, developmental abnormalities, inflammation, and neoplasms.

Anatomy of the Male Genital System

• The diagram displays the key structures: Vas deferens, Scrotum, Ureter, Urinary Bladder, Seminal Vesicles, Prostate Gland, Epididymis, and Testicles.

Testicle Histology

• Seminiferous tubules are the primary structures within the testicle.
• Sertoli cells support spermatogenesis.
• Spermatids, primary spermatocytes, and secondary spermatocytes are crucial stages in sperm development.
• Spermatozoa are mature sperm cells.
• Leydig cells produce testosterone.

Developmental Abnormalities of Intersexes

• Hermaphrodites possess both testicular and ovarian tissues.
• These tissues can appear in separate structures or be mixed (ovotestis).
• Variations of hermaphroditism include bilateral (ovotestis on both sides), unilateral (ovotestis on one side), and lateral (testis on one side, ovary on the other).
• The remainder of the genital tract might be indeterminate.
• Mechanisms for intersex conditions are currently unknown.
• In most cases, the chromosomal constitution is normal but more individuals are female than male.

Developmental Abnormalities: Cryptorchidism

• Cryptorchidism (retained testes) is the failure of the testes to descend into the scrotum by birth.
• More often a unilateral condition than bilateral.
• Undescended testes can be located anywhere along the path from the caudal region to the kidney to the scrotum.
• The most common condition in the dog affecting 13% of males.
• Genetic and endocrine considerations are potential predisposing factors, along with testicular hypoplasia and estrogen exposure.

Cryptorchidism Appearance

• Before puberty, the undescended testicle appears normal.
• After puberty, the testicle often becomes smaller and fibrotic.
• Microscopically, atrophy occurs associated with interstitial collagen deposition, hyaline thickening of tubular basement membrane, and germinal epithelium atrophy, but also an increase in interstitial cells.

Testicular Hypoplasia

• Characterized by incomplete development of the testes.
• Often not apparent until after puberty.
• Unilateral hypoplasia is more common than bilateral hypoplasia.
• Difficult to distinguish from testicular degeneration.
• Associated with incomplete or improper descent into the scrotum.
• Causes include cryptorchidism, vitamin A deficiency, zinc deficiency, and hormonal issues.

Histopathology of Testicular Hypoplasia

• Severe hypoplasia shows abnormalities in nearly all tubules, small in diameter, uniform microscopic appearance with occasional vacuolation of Sertoli cells.
• Moderate hypoplasia features fewer small tubules with differentiation in some normal-sized tubules.
• Mild hypoplasia presents few small tubules lined by Sertoli cells. Most are active, producing sperms, with multinucleated giant cells noted in the tubules.

Testicular Degeneration

• Can be unilateral or bilateral depending on the cause.
• Local factors: Fever, localized scrotal heat, obstruction of sperm flow, vascular issues, or age-related issues.
• Systemic factors: Nutritional deficiencies (vitamin A and zinc), hormonal imbalances, space-occupying lesions in the pituitary gland or hypothalamus or testicular tumors like Sertoli cell tumor.
• Toxicities and irradiation are also factors.
• Grossly, the testes are reduced in size, are soft and flabby in early stages, and can develop wrinkles in the tunica albuginea. In later stages, they become small and firm, sometimes with calcification.
• Histopathology shows vacuolation of spermatogenic cell layers, germinal cell desquamation, decreased thickness of the germinal epithelium and the pyknosis of spermatocyte nuclei.

Intratubular giant cell formation is also possible. Also possible is inflammation and granulomas following death of sperms, and infiltration of the connective tissue. Sertoli cells may become the only cellular component of the testes after the conclusion of the degeneration process, and calcification can exist within the debris.

Inflammation

• Causes include viral (like malignant catarrhal fever and blue tongue), bacterial (Brucellosis, mycobacterial infection, and pyogenic bacteria), and autoimmune triggers.
• Orchitis: Inflammation of the testicular tissues.
• Types include: autoimmune, interstitial, intratubular, necrotizing, granulomatous.
• Often arises from ascending urinary infections in intratubular cases.
• Cryptorchidism predisposes to inflammation.

Blood-Testis Barrier

• A physical barrier between blood vessels and seminiferous tubules, formed by tight junctions between Sertoli cells.

Autoimmune orchitis Features

• Disruption of the blood-testis barrier leads to autoimmune orchitis.
• Sequestration, or the release of small sperm antigens from sertoli cell tight junctions, can activate suppressor lymphocytes, ultimately reducing inflammation..

Types of epididymitis

• Focal, multifocal, diffuse
• Inflammation of the epididymis.
• Usually associated with ascending urinary tract infections.

Epididymitis: Gross Appearance

• Acute inflammation: Soft and swollen
• Chronic inflammation: Firm and swollen due to fibrous tissue deposition; possibly nodular due to duct enlargement or presence of spermatic granulomas or abscesses.

Spermatocele

• Local distension of the epididymis filled with accumulated sperms.
• Follows congenital or acquired blockage in the lumen.
• Sperms might leak out from the duct into the connective tissue.

Spermatic Cord and Varicocele

• Varicocele: Local dilation of the spermatic vein.
• Can lead to affected vessel thrombosis and testicular atrophy.
• Torsion happens when the testicle is undescended.
• Vascular occlusion of the spermatic vein or arteries can cause vascular infarction in the testicle.
• Possible necrosis in the testicle.

Testicular Tumors

• Germ cell neoplasms: Seminoma, teratoma
• Gonadal stromal tumors: Leydig cell tumor, Sertoli cell tumor

Scrotum Structure and Dermatitis

• The scrotum is a skin outpouching that contains the tunica dartos and scrotal fascia.
• The parietal layer of the tunica vaginalis has a connection with the scrotal fascia.
• Dermatitis: Common inflammatory condition of the scrotal skin; can be non-specific trauma or infection.
• Sequelae can be damage to thermoregulation in the scrotum.

Tunica Vaginalis Inflammation

• Non-infectious inflammation: Could be due to trauma, often mild and focal.
• Infectious inflammation: Can be an extension from orchitis or epididymitis.
• Common infectious agents include Brucella ovis, Actinobacillus seminis, Trypanosoma brucei.
• Hydro, pyo, hemato, and spermacoeles might be present due to fluid, pus, or sperms accumulating in the vaginal tunic.

Seminal Vesiculitis

• Significant cause of male infertility, particularly in bulls.
• Inflamed seminal vesicles are a recognized source of inflammatory cells in bovine semen.
• Causes include viral, protozoal, chlamydial, mycoplasmal, and bacterial infections such as Brucella abortus and Mycobacterium bovis in bulls; and Brucella abortus and Pseudomonas pseudomallei in boars.
• Chronic form is the usual appearance.
• The gland is enlarged and firm, with a loss of lobulation, collagen deposits between the acini.
• Mixture of lymphocytes, plasma cells, macrophages, and few neutrophils and eosinophils in the interstitium.
• Desquamated epithelial cells and debris are visible in the gland.
• Metaplasia of the glandular epithelium into stratified type is common.

Prostate Hyperplasia

• Hyperplasia of the prostate is commonly seen in aged bulls and dogs.
• Etiology encompasses constipation, interference with urination, and hormonal imbalance (as seen in adrenocortical tumors in castrated dogs).
• Excess androgen causes acinar hyperplasia, and excess estrogen causes fibromuscular hyperplasia.
• Gross appearance shows enlargement up to four times the normal size and presence of cysts often at the capsule of the gland..
• Histopathologic findings are characterized by adenomatous and stromal hyperplasia.

Prostatitis

• Common in aged dogs, caused by urinary pathogens like E. coli, proteus and staph
• Grossly:
  • Focal: Minute, multiple, or large abscesses.
  • Diffuse: Enlarged, congested and boggy gland; oozes pus in cut section.
• Microscopically:
  • Acute: Acinar with ordinary catarrhal signs, neutrophilic infiltration throughout gland structure, often with abscess formation.
  • Chronic: Aggregation of lymphocytes in the fibromuscular stroma.

Penis and Prepuse Abnormalities

• Developmental abnormalities include hypospadias (abnormal urethral opening on ventral side), epispadias (abnormal opening on the dorsal side), phimosis (inability to retract the penis due to a tight prepuce), and paraphimosis (inability to retract the penis due to swelling).

Inflammation of the Penis-- Balanitis and Posthitis

• Inflammation of the glans penis and prepuce, respectively. Both terms are combined as balanoposthitis.
• Etiology:
  • Viral: Bovine herpes virus (infectious pustular balanoposthitis), equine herpes, equine pox, and canine herpes.
  • Bacterial: Many bacteria, possibly those in the urinary tract, are implicated.
  • Trauma
  • Parasitic.
• Specific details related to the etiologies of the different types are detailed in specific lesion descriptions.

Neoplasms of the Male Genitalia

• Transmissible venereal tumors and fibropapilloma are common.

This quiz focuses on various testicular conditions, histological features, and the anatomy of the male genital system. Test your knowledge about testicular degeneration, intersex conditions, and related developmental abnormalities. Perfect for students studying urology or reproductive biology.