General characteristics of testicular inflammation
Inflammatory involvement of the testes (orchitis) extremely rarely occurs as an independent isolated process. In the vast majority of cases, the pathology also affects the epididymis, forming a combined disease—epididymo-orchitis. Inflammatory changes may also spread from the prostate gland to the bulbourethral glands and seminal vesicles, which are rarely affected in isolation.
There are two main pathways for infection to penetrate the testicular tissue:
- Hematogenous route. The infection is brought in via the bloodstream. This mechanism is typical for viral infections, pyogenic flora (including states of septico-pyemia), and syphilitic involvement of the testes.
- Ascending route. The causative agent ascends through the urinary tract from the urethra or urinary bladder. This route is characteristic of classic sexually transmitted infections (Neisseria gonorrhoeae, Chlamydia trachomatis), as well as Gram-negative enteric bacteria (Escherichia coli, Proteus vulgaris).
Acute non-specific and specific orchitis
In acute infectious orchitis, bacterial flora causes a pronounced non-specific inflammatory process. Pathogenetically, the infection first involves the epididymis and then spreads via lymphatic vessels or tubules to the testicular tissue itself. Morphologically, the organ's tissue is edematous and hyperemic. There is a dense cellular infiltration composed of lymphocytes, macrophages, and neutrophils. The process starts in the stroma but rapidly extends to the seminiferous tubules. Inflammation may culminate in abscess formation or purulent-necrotic liquefaction. The outcome of such a condition is severe scarring and fibrosis, which irreversibly disrupts the organ's structure and leads to infertility.
Specific acute lesions have distinctive morphological features:
- Gonococcal epididymo-orchitis. Characterized by the primary formation of abscesses in the epididymis with destruction of surrounding tissues, after which the purulent process secondary involves the testis.
- Interstitial orchitis in mumps. A systemic viral infection primarily affecting children. It manifests as an acute unilateral focal lesion approximately a week after inflammation of the salivary glands. Microscopic examination reveals marked stromal edema and abundant infiltration by plasma cells, lymphocytes, and macrophages (neutrophils are extremely rare). The main clinical consequence is a high risk of infertility.
Chronic and granulomatous orchitis
Chronic orchitis is most frequently the outcome of acute conditions or a manifestation of specific infections (tuberculosis, syphilis, fungal invasions).
Tuberculous orchitis traditionally starts in the epididymis, accompanied by simultaneous tuberculous vesiculitis and prostatitis.
Syphilitic orchitis (both congenital and acquired) has an important distinguishing feature: inflammation of the epididymis is usually absent, and the testis is affected primarily. Two variants of changes develop in the tissues:
- Formation of gummas (foci of necrosis surrounded by a ring of lymphocytes, macrophages, epithelioid cells, and plasma cells with Langhans giant cells).
- Diffuse lymphoplasmacytic infiltration of the interstitium, accompanied by obliterating endarteritis.
Testicular malakoplakia is a chronic granulomatous inflammation closely associated with chronic urinary tract infections. Macroscopically, brownish-yellow softening foci are found in the enlarged organ. Microscopically, the infiltrate consists of plasma cells and large macrophages—von Hansemann cells. Their cytoplasm harbors laminated calcified structures—Michaelis–Gutmann bodies (defective lysosomes containing residues of undigested bacteria).
Non-infectious granulomatous orchitis is of autoimmune origin and affects men aged 30 to 80 years. Unlike tuberculosis, caseous necrosis is completely absent in its granulomas, and neutrophils are present in the infiltrate.
Testicular atrophy
Atrophy of normally descended testes is a frequent consequence of past illnesses. It can develop as an outcome of severe purulent orchitis or trauma. Other provoking factors include:
- Pronounced atherosclerosis of the internal spermatic artery with impaired trophism.
- Cachexia and hypopituitarism.
- Obstruction of the seminal ducts.
- Exposure to radiation therapy.
- Prolonged use of estrogen-based drugs (e.g., used in the treatment of prostate adenocarcinoma).
Briefly: answers to topical questions
What macroscopic and microscopic changes are characteristic of tuberculous orchitis?
Tuberculous orchitis is characterized by the fact that the process almost always begins with involvement of the epididymis, subsequently spreading to the testis. In most cases, it occurs simultaneously with tuberculous prostatitis and vesiculitis.
Macroscopic changes: tuberculous involvement of the epididymis is described as a dense, enlarged epididymis; the vas deferens is thickened, sometimes beaded in appearance. In tuberculous involvement of the male genital system, palpation of the prostate and epididymis may reveal painless nodular indurations.
Microscopic changes are represented by typical granulomatous tuberculous inflammation:
- epithelioid cell granulomas;
- foci of caseous necrosis in the center;
- the granuloma is composed of epithelioid cells, lymphocytes, macrophages, and plasma cells;
- multinucleated Langhans giant cells may be found among the epithelioid cells.
Unlike non-infectious granulomatous orchitis, tuberculous inflammation is not characterized by the presence of neutrophils and plasma cells within the inflammatory infiltrate, which serves as a differential diagnostic sign indicated for non-infectious granulomatous orchitis.
Class and exam questions
How to distinguish non-infectious granulomatous orchitis from tuberculous orchitis under a microscope?
In autoimmune non-infectious orchitis, the center of the granulomas lacks the caseous necrosis characteristic of tuberculosis, and the cellular infiltrate contains plasma cells and neutrophils.
What are Michaelis–Gutmann bodies?
These are concentric lamellar structures (calcified degenerating lysosomes containing bacterial residues) that are identified inside large macrophages in malakoplakia.
What else to study on this topic
- Cryptorchidism: morphological changes in the ectopic and normally descended testis.
- Morphology of prostate adenocarcinoma and the Gleason grading system.
- Testicular tumor pathologies (including the risk of malignant transformation in cryptorchidism).
- TNM classification of prostate cancer and pathways of metastasis.
- Diseases of the seminal vesicles and bulbourethral glands (cysts, fibromuscular hyperplasia, rare tumors).
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