General Characteristics of Testicular Inflammation
Inflammatory involvement of the testes (orchitis) rarely occurs as an isolated, independent process. In the vast majority of cases, the pathology also affects the epididymis, resulting in a combined condition known as epididymo-orchitis. Inflammatory changes may also spread from the prostate to the bulbourethral glands and seminal vesicles, which are rarely affected in isolation.
There are two main pathways for infection to enter testicular tissue:
- Hematogenous pathway. Infection is borne via the bloodstream. This mechanism is typical for viral infections, pyogenic flora (including septicopyemic states), and syphilitic testicular involvement.
- Ascending pathway. The pathogen ascends the urinary tract from the urethra or urinary bladder. This pathway is characteristic of classic sexually transmitted infections (Neisseria gonorrhoeae, Chlamydia trachomatis) and gram-negative enteric bacteria (Escherichia coli, Proteus vulgaris).
Acute Nonspecific and Specific Orchitis
In acute infectious orchitis, bacterial flora triggers a pronounced nonspecific inflammatory response. Pathogenetically, the infection first involves the epididymis and then spreads via lymphatic vessels or tubules into the testicular parenchyma itself. Morphologically, the organ tissue is edematous and hyperemic. A dense cellular infiltration of lymphocytes, macrophages, and neutrophils is observed. The process begins in the stroma but rapidly extends to the seminiferous tubules. Inflammation may culminate in abscess formation or purulent-necrotic breakdown. The outcome of such a condition is dense scarring and fibrosis, which permanently disrupts organ structure and leads to infertility.
Specific acute lesions exhibit distinct morphological features:
- Gonococcal epididymo-orchitis. Characterized by the primary formation of abscesses within the epididymis with destruction of surrounding tissues, after which the purulent process secondarily involves the testis.
- Mumps interstitial orchitis. A systemic viral infection predominantly affecting children. It manifests as an acute unilateral focal lesion approximately one week after parotitis. Microscopy reveals marked stromal edema and abundant infiltration by plasma cells, lymphocytes, and macrophages (neutrophils are exceedingly rare). The primary clinical consequence is a high risk of infertility.
Chronic and Granulomatous Orchitis
Chronic orchitis is most commonly the sequel to acute conditions or a manifestation of specific infections (tuberculosis, syphilis, fungal invasions).
Tuberculous orchitis classically originates in the epididymis, accompanied by concurrent tuberculous vesiculitis and prostatitis.
Syphilitic orchitis (both congenital and acquired) has an important distinguishing feature: epididymal inflammation is typically absent, and the testis is primarily affected. Two variants of tissue changes develop:
- Formation of gummas (foci of necrosis surrounded by a rim of lymphocytes, macrophages, epithelioid cells, and plasma cells with Langhans giant cells).
- Diffuse lymphoplasmacytic infiltration of the interstitium accompanied by obliterating endarteritis.
Testicular malacoplakia is a chronic granulomatous inflammation closely associated with chronic urinary tract infections. Grossly, the enlarged organ reveals brownish-yellow softening foci. Microscopically, the infiltrate consists of plasma cells and large macrophages called Hansemann cells. Their cytoplasm contains laminated, calcified structures known as Michaelis-Gutmann bodies (defective lysosomes containing undigested bacterial remnants).
Non-infectious granulomatous orchitis is autoimmune in nature, affecting men aged 30 to 80 years. Unlike tuberculosis, its granulomas completely lack caseous necrosis, and neutrophils are present within the infiltrate.
Testicular Atrophy
Atrophy of normally descended scrotal testes is a frequent consequence of prior disease. It can develop as the sequel to severe purulent orchitis or trauma. Other contributing factors include:
- Marked atherosclerosis of the internal spermatic artery with impaired trophic supply.
- Cachexia and hypopituitarism.
- Obstruction of the seminal tracts.
- Radiation therapy.
- Prolonged administration of estrogen-based medications (e.g., used in the treatment of prostate adenocarcinoma).