Nonspecific Epididymitis and Orchitis

Slide 1 · Nonspecific Epididymitisand Orchitis

Etiology · spread · morphology · functional consequences

Pathology teaching lecture

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Map the routes by which urinary tract infection reaches the epididymis and testis.

Relate age-associated pathogens to nonspecific epididymitis.

Recognize interstitial inflammation, tubular extension, abscess and suppurative necrosis.

Explain scarring-associated fertility loss with relative Leydig-cell preservation.

Distinguish nonspecific inflammation from selected infectious, granulomatous and vascular lesions.

Slide 3 · Epididymis is the common initial site

Epididymis

Testis

Inflammatory lesions occur more frequently here.

Several infections originate in, or first reach, this structure.

Acute infection can later extend into testis.

Testicular inflammation may be secondary to epididymitis.

Some etiologies—mumps and syphilis—primarily involve testis.

The first affected site helps frame the differential.

Context from the parent section: Inflammation and Infections.

Slide 4 · Route-relevant anatomy of the male genital tract

Testis

Epididymis

Vas deferens

Simplified topology; Infection may travel through the vas deferens or lymphatics of the spermatic cord.

Slide 5 · Three common upstream infection sites

Urethritis

An upstream genital-tract infection that may extend toward the epididymis.

Cystitis

A urinary bladder infection that can be associated with epididymal infection.

Prostatitis

A prostatic infection included among the recognized sources.

Source identifies each as a common associated urinary tract infection.

Slide 6 · Ascending infection through the vas deferens

Urinary / genitaltract infection

Vas deferens

Epididymis

Possible testisinvolvement

This route helps explain why epididymitis often precedes orchitis.

Slide 7 · Spread through spermatic-cord lymphatics

Urinary tractinfection

Cord lymphaticpathway

Epididymalinflammation

Possible orchitis

Lymphatic spread is a second route.

Slide 8 · Epididymitis may be followed by orchitis

Epididymalinfection

Acute epididymalinflammation

Spread to testis

Orchitis

The testis may show an inflammatory reaction similar to that in the epididymis.

Slide 9 · Age-associated microbiologic pattern

Population

Clinical context

Frequent organisms

Children

Uncommon; congenital genitourinary abnormality often present

Gram-negative rods

Sexually active males <35 years

Sexually transmitted infection

Chlamydia trachomatis; Neisseria gonorrhoeae

Males >35 years

Common urinary tract organisms

Escherichia coli; Pseudomonas

Slide 10 · Childhood epididymitis: Look for congenital context

Nonspecific epididymitis is uncommon in children.

The textbook associates pediatric cases with a congenital genitourinary abnormality.

The commonly described infecting organisms are gram-negative rods.

Age and anatomic context must be interpreted together.

Slide 11 · Sexually active males younger than 35 years

Chlamydia trachomatis

Neisseria gonorrhoeae

Recognized sexually transmitted pathogen.

One of the most frequent agents in this age group.

Belongs in age-pattern differential.

Recognized sexually transmitted pathogen.

One of the most frequent agents in this age group.

May produce severe suppurative disease.

Slide 12 · After age 35: Ordinary urinary pathogens

Escherichia coli

Pseudomonas

Common urinary tract pathogen.

One of the characteristic organisms in older males.

Supports urinary-source model.

Another pathogen named for older males.

Associated with urinary tract infection.

May participate in nonspecific inflammation.

Slide 13 · What age stratification does—and does not—show

Predominant associations rather than mutually exclusive pathogen lists.

Childhood, young adulthood and later adulthood represent differing etiologic contexts.

Age is therefore an organizing clue; The tissue reaction remains an acute inflammatory pattern.

Avoid equating a pathogen prediction with confirmed microbiologic identification.

Slide 14 · Core tissue response to bacterial infection

Bacterialinfection

Vascularcongestion

Interstitialedema

Neutrophilinflux

The same basic acute inflammatory components occur at other infected sites.

Slide 15 · Congestion: An early vascular component

Congestion is a defining morphologic feature of acute bacterial inflammation in this setting.

Vascular engorgement accompanies the inflammatory response.

The process initially involves epididymal interstitial connective tissue.

Congestion should be read in combination with edema and neutrophils.

Slide 16 · Edema expands the inflammatory interstitium

Edema is part of the acute bacterial inflammatory pattern.

It occurs in the same interstitial compartment as initial inflammation.

Edema contributes to expansion of inflamed tissue before and during tubular extension.

Edema alone is less specific than the full acute inflammatory pattern.

Slide 17 · Neutrophils identify suppurative inflammation

Neutrophilic infiltration is characteristic of bacterial epididymitis.

Neutrophils are present with congestion and edema.

Marked neutrophilic accumulation may culminate in an abscess.

The dominant inflammatory-cell type helps distinguish bacterial and viral patterns.

Slide 18 · Acute inflammation begins in interstitial connective tissue

Tubular lumina

Acute inflammatory cells occupy interstitial spaces before rapidly extending into tubules.

Schematic · not microscopy

Slide 19 · Tubular involvement follows interstitial inflammation

Interstitialconnective tissue

Inflammatorycell accumulation

Extension intoepididymal tubules

Possible tubulardestruction

Robbins specifically describes rapid extension from interstitium to tubules.

Slide 20 · Tubular extension marks advancing disease

The inflammation starts interstitially but can involve tubular structures rapidly.

An inflammatory infiltrate limited to stroma and one involving tubules represent different extents of injury.

The tubules lie directly in the tissue compartment threatened by suppuration.

Severe extension can progress to destructive abscess formation.

Slide 21 · An abscess is a focal outcome of severe suppuration

Purulent center

Surrounding inflamed epididymal tissue

Schematic · not a gross specimen

Slide 22 · Suppurative necrosis: The destructive extreme

Acute inflammation can produce suppurative necrosis of the entire epididymis.

The term denotes more extensive destruction than a localized abscess.

A spectrum: Interstitial inflammation → tubular involvement → suppurative destruction.

Severe tissue loss helps explain the possibility of subsequent scarring.

Slide 23 · Gonococcal epididymitis may replace tissue with abscess

Figure 21.16 is described as acute gonococcal epididymitis.

The figure caption reports replacement of epididymal tissue by an abscess.

The adjacent testis is described as normal in that particular specimen.

This example demonstrates that severe epididymitis need not imply simultaneous orchitis.

Slide 24 · Secondary orchitis follows local spread

Infection can extend from the epididymis into the testis.

Once involved, the testis exhibits a similar acute inflammatory response.

Presence of inflammation in both organs is more extensive than epididymitis alone.

The expected morphologic vocabulary remains congestion, edema and inflammatory infiltration.

Slide 25 · Epididymitis versus epididymo-orchitis

Feature

Epididymitis

Epididymo-orchitis

Initial involvement

Epididymal tissue

Epididymis with secondary testicular inflammation

Inflammatory reaction

Interstitial neutrophils; may extend into tubules

Similar acute inflammation also involves testis

Severe morphologic pattern

Abscess / suppurative necrosis possible

Testicular damage may accompany epididymal injury

Late consequence

Fibrous scarring may impair fertility

Scarring and fertility effects may involve both sites

Slide 26 · Sequence from inflammation to fibrosis

Acute infection

Interstitial andtubular damage

Resolution withfibrous scarring

Potentialsterility

Fibrosis is a recognized late outcome of inflammation involving epididymis and testis.

Slide 27 · Fibrous scarring can follow acute inflammation

Inflammation of epididymis and testis is often followed by fibrosis.

The late scar may reflect healing after destructive inflammatory tissue injury.

Tissue scarring is distinct from the congestion, edema and neutrophils of the acute phase.

Recognizing the phase of injury is important when interpreting pathology.

Slide 28 · Why fibrosis may cause infertility

Inflammatoryinjury

Fibrousreplacement

Disruption ofreproductive tissue

Possiblesterility

The text explicitly links postinflammatory fibrosis with sterility; Not every infection causes it.

Slide 29 · Leydig cells are usually preserved

Leydig cells usually are not destroyed by this inflammation.

Preservation provides a morphologic explanation for maintained androgen production.

Relative endocrine preservation can coexist with damage to sperm-bearing structures.

The qualifier “usually” is important: Preservation is not presented as universal.

Slide 30 · Reproductive and endocrine consequences can differ

Aspect

Pathologic basis

Typical implication

Fertility

Inflammation and fibrous scarring of epididymis/testis

Sterility may occur

Androgen production

Leydig cells usually not destroyed

Testicular androgen output relatively unaffected

Interpretation

Different structures mediate different functions

Do not equate fertility loss with obligatory androgen failure

Slide 31 · Mechanism-to-outcome synthesis

Urinary tractorganisms

Ascending orlymphatic spread

Acutesuppuration

Scarring /possible sterility

Leydig-cell preservation helps explain relatively retained androgen synthesis.

Slide 32 · Gonococcal infection can extend sequentially

Posteriorurethra

Prostate

Seminalvesicles

Epididymis

This sequence as a complication of neglected gonococcal infection.

Slide 33 · Severe gonorrhea may destroy epididymal tissue

Gonococcal infection is among the major sexually transmitted causes in younger males.

Severe involvement can produce epididymal abscesses.

Abscess formation may be accompanied by extensive destruction.

The healing process can leave fibrous scarring.

Slide 34 · Gonococcal infection may extend into the testis

Gonococcalepididymitis

Local extensioninto testis

Suppurativeorchitis

This represents a route from lower genitourinary infection to testicular inflammation.

Slide 35 · Possible consequences of gonococcal epididymitis

Neglectedgonococcal infection

Epididymalabscess

Tissuedestruction

Fibrousscarring

The listed sequence is an illustrated severe pathway, not the inevitable course of every case.

Slide 36 · Suppurative and granulomatous patterns differ

Nonspecific bacterial epididymitis

Idiopathic granulomatous orchitis

Neutrophil-rich acute response.

Initial interstitial inflammation.

Abscess / suppurative necrosis can occur.

Rare inflammatory testicular disorder.

Granulomas restricted to spermatic tubules.

May resemble testicular neoplasm clinically.

Slide 37 · Granulomatous orchitis may simulate a tumor

Idiopathic granulomatous orchitis may present as a moderately tender mass of sudden onset.

Fever sometimes accompanies the presentation.

An insidious painless testicular mass also occurs.

This tumor-like presentation makes histologic distinction important.

Slide 38 · Granulomatous orchitis: Tubule-centered lesions

Granulomatous reaction confined to spermatic tubules

Schematic · not microscopy

Slide 39 · Granulomatous orchitis: Proposed etiologies

Trauma

One postulated mechanism, not a proven universal cause.

Infection

A proposed possible trigger in this idiopathic disorder.

Extravasated sperm

Proposed inflammatory stimulus from sperm outside its usual compartment.

Autoimmunity

Another proposed explanation; The name does not establish pathogenesis.

Robbins explicitly presents these as hypotheses, not demonstrated causes.

Slide 40 · Idiopathic granulomatous orchitis versus tuberculosis

Idiopathic granulomatous orchitis

Genital tuberculosis

Granulomas restricted to spermatic tubules.

May clinically resemble a tumor.

No caseous necrosis specified as defining feature.

Often begins in epididymis.

May spread to testis.

Typically shows caseating granulomatous inflammation.

Slide 41 · Tuberculosis commonly begins in the epididymis

Tuberculousinfection

Epididymis

Possibletesticular spread

Granulomatousinflammation

Unlike nonspecific acute bacterial disease, its characteristic response is caseating granulomas.

Slide 42 · Caseating granulomas favor tuberculous infection

A classic caseating granulomatous reaction in genital tuberculosis.

Genital infection almost invariably begins in epididymis before testicular spread.

Tuberculosis is an important differential for idiopathic granulomatous orchitis.

Distribution and caseous necrosis distinguish it from tubule-restricted idiopathic disease.

Slide 43 · Mumps orchitis mainly concerns postpubertal males

Mumps is described as a systemic viral disease often affecting school-aged children.

Testicular involvement is extremely uncommon at school age.

Orchitis in 20%–30% of postpubertal males with mumps.

The age contrast differs from the bacterial epididymitis pathogen patterns.

Slide 44 · Timing of mumps-associated orchitis

Parotid glandswelling

Approximatelyone week

Acute interstitialorchitis

The testicular phase often follows the systemic parotid presentation.

Slide 45 · Inflammatory cells help distinguish mumps

Pattern

Predominant cells

Distribution

Acute bacterial epididymitis

Neutrophils

Interstitial initially; may extend into tubules

Mumps orchitis

Lymphocytes and plasma cells

Acute interstitial orchitis

Slide 46 · Bilateral mumps orchitis may reduce fertility

Mumps-associated orchitis usually develops after parotid gland swelling.

The testicular inflammation is lymphoplasmacytic rather than neutrophil-dominant.

Bilateral testicular involvement may reduce fertility.

This effect is separate from the fibrosis-associated sterility described in bacterial infection.

Slide 47 · Syphilis often starts in the testis

Acquired orcongenital syphilis

Testis first

Possibleepididymal disease

This direction contrasts with epididymis-first gonorrhea and tuberculosis.

Slide 48 · Syphilis: Obliterative endarteritis and perivascular infiltrate

Concentric vascular-wall injury and perivascular lymphoplasmacytic cells

Schematic · not histology

Slide 49 · Gumma: The second syphilitic reaction pattern

Syphilis can cause granulomatous inflammation known as a gumma.

Gumma as an alternative to the vascular-centered reaction.

These patterns are not the neutrophilic abscess described in nonspecific bacterial epididymitis.

Syphilitic pathology therefore requires a separate morphologic category.

Slide 50 · Two morphologic patterns in syphilis

Pattern

Hallmark

Distinguishing point

Obliterative endarteritis

Vascular lesion with perivascular lymphocytes and plasma cells

Prominent vessel-centered process

Gumma

Granulomatous inflammation

Granulomatous rather than acute suppurative reaction

Slide 51 · Inflammatory patterns by selected cause

Etiology

First common site

Principal morphology

Nonspecific bacterial

Epididymis

Congestion, edema, neutrophils; possible abscess

Mumps

Testis

Acute interstitial lymphocytes and plasma cells

Tuberculosis

Epididymis

Caseating granulomas

Syphilis

Testis

Endarteritis / plasma cells or gumma

Slide 52 · Anatomic origin is a differential clue

Epididymis-first patterns

Testis-first patterns

Nonspecific bacterial epididymitis

Mumps orchitis

Gonorrhea

Syphilis

Genital tuberculosis

Some idiopathic granulomatous lesions are primarily testicular

Slide 53 · Other rare disorders listed in the source

Infectious

Leprosy; Toxoplasmosis; Fungi; Viruses; Parasites; Brucellosis.

Inflammatory / systemic

Sarcoidosis; Crohn disease; Malakoplakia.

These are listed as rare causes; The source does not provide detailed individual criteria.

Slide 54 · Abscess versus granulomatous lesion

Abscess / suppuration

Granulomatous lesion

Predominantly neutrophilic inflammatory process.

Can destroy epididymal tubules.

Described in severe gonococcal disease.

Granulomas are the organizing feature.

Tuberculosis can show caseation.

Idiopathic orchitis can be tubule restricted.

Slide 55 · Neutrophils versus lymphoplasmacytic inflammation

Bacterial epididymitis

Mumps orchitis

Neutrophils are prominent.

Congestion and edema accompany cells.

Suppurative necrosis may occur.

Lymphocytes and plasma cells.

Acute interstitial testicular pattern.

Often follows parotid swelling.

Slide 56 · Torsion belongs in the acute scrotal differential

Testicular torsion is a vascular lesion, not an infectious orchitis.

Twisting of the spermatic cord compromises testicular venous drainage.

If untreated, testicular infarction frequently follows.

Torsion as a true urologic emergency.

Slide 57 · Torsion: Venous outflow interruption

Spermatic cordtwisting

Venous drainageobstruction

Vascularengorgement

Hemorrhagicinfarction

Thick-walled arteries may remain patent while venous outflow is impeded.

Slide 58 · Torsion and infection cause different tissue injury

Finding

Acute bacterial inflammation

Torsion

Primary mechanism

Infection with inflammatory response

Mechanical interruption of venous drainage

Major acute lesion

Neutrophilic inflammation / suppuration

Engorgement and hemorrhagic infarction

Principal hazard

Scarring / possible sterility

Rapid testicular infarction

Source urgency

Source does not prescribe a timing threshold

Urologic emergency

Slide 59 · Recognizing torsion changes urgency

“Adult” torsion typically presents in adolescence with sudden testicular pain.

The bell-clapper abnormality increases mobility and predisposes to twisting.

Manual untwisting within approximately six hours may spare orchiectomy.

The stated interval is from textbook context, not a guarantee of testicular salvage.

Slide 60 · Case: Epididymitis in a child

Clinical-pathologic scenario

A boy has documented epididymal infection and a known congenital genitourinary abnormality.

Which pathogen class best fits the Robbins age pattern?

Gram-negative rods are the characteristic reported group.

Slide 61 · Case: Infection in a young sexually active adult

Clinical-pathologic scenario

A 27-year-old sexually active man develops a documented epididymal infection.

Which two organisms are emphasized by the textbook for this setting?

Chlamydia trachomatis and Neisseria gonorrhoeae.

Slide 62 · Case: Epididymitis in later adulthood

Clinical-pathologic scenario

An older man develops epididymitis in association with a urinary tract infection.

Which pathogen examples does Robbins highlight?

Escherichia coli and Pseudomonas.

Slide 63 · Case: Severe suppurative damage

Clinical-pathologic scenario

A resected epididymis shows abscess formation, broad tissue loss and subsequent scarring.

What major long-term function can be affected?

Fertility may be impaired; Leydig-cell-mediated androgen synthesis may remain relatively unaffected.

Slide 64 · Case: Tumor-like testicular inflammatory mass

Clinical-pathologic scenario

A middle-aged patient has a testicular mass; Microscopy shows granulomas limited to spermatic tubules.

Which non-neoplastic diagnosis is most consistent?

Idiopathic granulomatous (autoimmune) orchitis; Distinguish tuberculosis.

Slide 65 · Case: Orchitis after parotid swelling

Clinical-pathologic scenario

A postpubertal male develops orchitis about one week after parotid enlargement.

What inflammatory cell pattern is expected?

An interstitial lymphocytic and plasma-cell infiltrate is characteristic of mumps orchitis.

Slide 66 · Case: Sudden testicular pain in an adolescent

Clinical-pathologic scenario

An adolescent has sudden testicular pain, with a spermatic-cord vascular event suspected.

What pathologic process must be urgently excluded?

Torsion: Impaired venous drainage can produce hemorrhagic testicular infarction.

Slide 67 · A structured pathology reading strategy

Locate primarysite

Classify infiltrateor necrosis

Check spread andassociated lesion

Anticipateconsequences

Integrate distribution, inflammatory phenotype, and potential functional sequelae.

Slide 68 · Three high-yield cause–morphology links

Bacterial disease

Epididymis-first; Neutrophils, edema and congestion; Possible abscess.

Selected nonbacterial infections

Mumps: Lymphoplasmacytic orchitis. Tuberculosis: Caseating granulomas.

Postinflammatory sequelae

Fibrous scarring may produce sterility while Leydig cells are usually preserved.

Slide 69 · Concise differential of the testis and epididymis

Disease

Morphologic clue

Functional or clinical implication

Nonspecific epididymitis

Interstitial → tubular neutrophilic injury

Fibrosis may impair fertility

Idiopathic granulomatous orchitis

Spermatic-tubule granulomas

Can mimic a testicular tumor

Mumps orchitis

Lymphoplasmacytic interstitial reaction

Bilateral disease may reduce fertility

Tuberculosis

Caseating granulomas; epididymis first

Can extend to testis

Torsion

Hemorrhagic infarction

Urgent, potentially organ-threatening

Slide 70 · Key conclusions

Epididymitis is more common than primary orchitis; Ascending or lymphatic spread is typical.

Probable organisms vary with age and context.

Bacterial injury evolves from interstitial neutrophils toward possible abscess and suppurative necrosis.

Scarring may impair fertility, while Leydig-cell function is commonly relatively preserved.

Granulomatous, viral and vascular lesions have distinct morphologic and clinical patterns.

Slide 71 · Source and scope

Primary textbook

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th edition (2026). Chapter 21, “The Lower Urinary Tract and Male Genital System,” pp. 880–881.

Sections used

Nonspecific Epididymitis and Orchitis; Inflammation and Infections; Granulomatous (Autoimmune) Orchitis; Infections; Torsion.

Illustrations are original editable schematics; they do not substitute for original H&E or gross photographs.