Sexually Transmitted Infections

Slide 1 · Sexually Transmitted Infections

Pathogenesis, morphology and clinicopathologic correlations

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Classify major STI pathogens by microbiologic group and clinicopathologic syndrome.

Explain local infection, asymptomatic transmission, coinfection and vertical transmission.

Link representative organisms to morphology, complications and diagnostic approaches.

Distinguish genital ulcer syndromes, inflammatory tract disease and HPV-associated lesions.

Slide 3 · An etiologic framework

Pathogen class

Representative agents

Principal pathologic pattern

Viruses

HSV; HPV; HBV; HIV

Vesicles/ulcers; Papillomas or dysplasia; Systemic infection

Bacteria

N. Gonorrhoeae; T. Pallidum; H. Ducreyi

Suppurative inflammation; Chronic vasculitis; Ulcers

Obligate intracellular bacteria

C. Trachomatis

Urethritis/cervicitis; Ascending inflammation; Lymphadenitis

Protozoa

T. Vaginalis

Vaginitis or urethritis

Slide 4 · Exposure and vulnerability

Sexual contact can transmit pathogens with very different biology.

Adolescents and young adults, men who have sex with men, and people injecting drugs as groups with increased STI burden.

Sexual practices and inequitable access to care both contribute to risk.

Epidemiologic categories guide prevention; They do not establish infection in an individual.

Slide 5 · Transmission is not restricted to one route

Intimate contact

Genital, anal and oral exposure can introduce pathogens

Local colonization or invasion

Urethra, cervix, vagina, rectum or oropharynx

Variable onward spread

Local persistence, ascending infection or systemic dissemination

Schematic

Slide 6 · Predominantly sexual versus occasional sexual spread

Predominantly sexual

C. Trachomatis and N. Gonorrhoeae are mainly spread by sexual contact.

Direct mucosal exposure is central to acquisition.

Other organisms, shared transmission routes

Shigella and Entamoeba histolytica usually spread fecal–orally.

Oral–anal sexual contact can also transmit enteric pathogens.

Slide 7 · Why asymptomatic infection matters

A person may be infectious without recognizing symptoms.

Silent infection permits continuing transmission to partners.

Absence of genital pain or discharge does not exclude mucosal infection.

Upper genital tract complications may develop after unrecognized lower tract infection.

Slide 8 · STI coinfection: Two linked mechanisms

Shared exposures

Risk factors and exposure networks overlap across STIs.

Several pathogens may be transmitted to the same person.

Coinfection cannot be excluded by finding one pathogen.

Biologic facilitation

Gonococcal and chlamydial epithelial injury alters mucosal barriers.

With HIV exposure, mucosal injury can increase acquisition risk.

Risk factors and local tissue injury are distinct mechanisms.

Slide 9 · Syndromes help localize disease

Presentation

High-yield organisms

Dominant pathologic process

Urethritis/cervicitis

N. Gonorrhoeae; C. Trachomatis

Mucosal inflammation, often suppurative

Painful genital ulcers

HSV; H. Ducreyi

Viral cytolysis or ulcerative bacterial inflammation

Painless chancre

T. Pallidum

Treponemal infection with endarteritis

Papillary anogenital lesions

Low-risk HPV

Exophytic squamous proliferation

Vaginitis

T. Vaginalis

Mucosal inflammation

Slide 10 · Anatomic entry sites predict sequelae

Urethral inflammation manifests as urethritis and may coexist with upper urinary/genital tract disease.

Cervical infection can ascend through the female reproductive tract.

Rectal and oropharyngeal exposure can produce proctitis or pharyngitis.

Blood or lymphatic spread produces disseminated or nodal disease in selected STIs.

Slide 11 · Ascending infection in the female genital tract

Endocervical mucosa

Common initial site for gonococcal infection

Fallopian tube

Ascending bacterial infection and salpingitis

Adnexa and pelvic peritoneum

Pyosalpinx, tubo-ovarian abscess or chronic scarring

Schematic

Slide 12 · A pathogen may produce multiple tissue responses

Gonococcal and chlamydial infections can cause acute mucosal inflammation.

HSV causes epithelial ballooning, vesicles, ulceration and viral cytopathic change.

Syphilis produces plasma cell–rich inflammation and small-vessel endarteritis.

HPV drives productive papillomatous lesions or oncogenic squamous alterations.

Slide 13 · Robbins Table 8.4: Virus-associated disease

Agent

Key STI manifestations

Important tissue consequence

HSV

Primary or recurrent genital herpes

Painful ulceration; Neonatal visceral/CNS disease

HBV

Sexual transmission can cause hepatitis

Hepatic inflammation

HPV

Condyloma, cervical dysplasia; Anogenital cancers

Benign warts or high-risk oncogenesis

HIV

Systemic HIV infection and AIDS

Immunodeficiency

Slide 14 · Robbins Table 8.4: Nonviral agents

Agent

Typical syndrome

Complication / distinction

N. Gonorrhoeae

Urethritis; Cervicitis; Proctitis

PID; Septic arthritis; Neonatal conjunctivitis

C. Trachomatis

Urethritis; Cervicitis; LGV

PID; Lymphadenitis; Scarring

T. Pallidum

Syphilis

Multistage systemic infection

H. Ducreyi / K. Granulomatis

Ulcerative genital disease

Painful bubo / chronic granulomatous ulcer

T. Vaginalis

Vaginitis; Urethritis

Inflammatory vaginal symptoms

Slide 15 · Partner and public-health implications

Many STIs are reportable conditions; Requirements vary by jurisdiction.

Partner testing and treatment interrupt transmission chains.

Care pathways must account for people without symptoms.

Reported surveillance rates should not be treated as fixed biological properties.

Slide 16 · Gonorrhea: Mucosal infection

Neisseria gonorrhoeae is a pathogenic gram-negative diplococcus.

Infection frequently begins in urethral, cervical, pharyngeal or anorectal mucosa.

Urethritis is a common presentation in males; Cervical infection in females may be silent.

Untreated infection may ascend or disseminate.

Slide 17 · Gonococcal attachment and invasion

Pili-mediated attachment

Pili promote binding to nonciliated epithelial cells

Opa-mediated binding

Outer-membrane Opa proteins reinforce adherence and entry

Epithelial invasion and injury

Superficial tissue invasion produces mucosal inflammation

Schematic

Slide 18 · Why gonococci can reinfect

Neisseria varies surface antigens targeted by host immune responses.

Pilin gene recombination changes the expressed pilus proteins.

Variation in Opa expression further changes bacterial surface features.

These mechanisms aid immune evasion; Immunity after exposure is incomplete.

Slide 19 · Gonorrhea: Lower tract manifestations

Male genital tract

Urethritis is a classic manifestation.

Epididymitis and prostatitis are recognized complications.

Mucopurulent inflammation may cause dysuria and discharge.

Female genital tract

Cervicitis frequently has few or no symptoms.

Endometritis/salpingitis may follow upward spread.

Long-term sequelae include infertility and ectopic pregnancy.

Slide 20 · Gonococcal suppurative morphology

Acute mucosal inflammation contains abundant neutrophils.

Exudate may show intracellular gram-negative diplococci within neutrophils.

A smear can support an impression, but identification requires appropriate microbiologic testing.

Test selection depends on clinical site and local laboratory pathways.

Slide 21 · Gonorrhea: Localized versus disseminated

Pattern

Features

Pathologic significance

Localized mucosal

Urethritis, cervicitis, proctitis, pharyngitis

Surface epithelial invasion and inflammation

Ascending genital

Salpingitis; PID

Scarring and reproductive injury

Disseminated

Septic arthritis; Hemorrhagic papules/pustules

Hematogenous spread

Neonatal

Conjunctivitis; Occasional sepsis

Potentially sight-threatening infection

Slide 22 · Disseminated gonococcal infection

Bloodstream spread is less common than local mucosal infection.

Adults may develop septic arthritis with hemorrhagic papules and pustules.

Terminal complement pathway deficiency predisposes to invasive disease.

A genital symptom history may be absent despite dissemination.

Slide 23 · Gonorrhea: Microbiologic diagnosis

Nucleic-acid amplification tests detect gonococcal nucleic acids.

Culture remains valuable, including when antimicrobial resistance is relevant.

Tissue morphology alone is insufficient for organism confirmation.

Evolving cephalosporin resistance; Specific regimens require current guidance.

Slide 24 · Case: Cervicitis followed by pelvic pain

TEACHING SCENARIO

A sexually active patient has subtle lower genital tract symptoms, followed by pelvic pain and adnexal tenderness.

Reasoning prompts

Identify the initial mucosal site.

Trace the likely route of extension.

Name a potentially permanent consequence.

Clinicopathologic resolution

Endocervical infection may ascend to the fallopian tubes. Suppurative salpingitis can heal with tubal fibrosis, causing infertility or ectopic pregnancy.

Slide 25 · Chlamydia: Obligate intracellular biology

Chlamydia trachomatis is a small obligate intracellular bacterium.

Its life cycle separates an infectious elementary body from a replicating reticulate body.

Intracellular replication occurs within an altered host-derived membrane inclusion.

This biology differs fundamentally from extracellular gonococcal growth.

Slide 26 · The chlamydial developmental cycle

Elementary body

Infectious form attaches and enters the epithelial cell

Reticulate body

Metabolically active form replicates in a protected inclusion

New elementary bodies

Converted progeny leave by lysis or extrusion

Schematic

Slide 27 · C. Trachomatis serovars and syndrome

Serovars

Predominant disease

Anatomic implication

D–K

Urogenital infection; Inclusion conjunctivitis

Mucosal epithelial infection

L1–L3

Lymphogranuloma venereum

Lymphatic and anogenital disease

A–C

Trachoma

Ocular infection; Not the genital STI serovars

Slide 28 · Urogenital chlamydia is often silent

Urethritis in males may be asymptomatic more often than gonococcal urethritis.

Cervical infection frequently produces no recognized symptoms.

Chlamydial and gonococcal syndromes substantially overlap.

Absence of symptoms does not prevent subsequent PID or transmission.

Slide 29 · Chlamydial urethritis: Microscopic pattern

The mucopurulent discharge is neutrophil-rich.

Urethral histopathology can closely resemble gonorrhea.

Chlamydial organisms are not visible in routine Gram-stained exudate.

NAATs on swabs or urine are described for genital diagnosis.

Slide 30 · Gonococcal versus chlamydial urethritis

Gonococcal

A gram-negative diplococcus.

May show intracellular diplococci in purulent exudate.

Pili/Opa proteins promote epithelial entry.

Chlamydial

Obligate intracellular developmental cycle.

Routine Gram stain does not demonstrate the organism.

Can produce indistinguishable inflammatory morphology.

Slide 31 · Extragenital chlamydial disease

Recognized manifestations include proctitis, pharyngitis and conjunctivitis.

Epididymitis and prostatitis can occur in male genital infection.

Perihepatic inflammation and PID may complicate female genital infection.

The site of exposure and spread determines the disease phenotype.

Slide 32 · Pelvic inflammatory disease: Pathology pathway

Cervicitis / lower tract infection

Gonococcus and chlamydia are established causes

Acute tubal inflammation

Neutrophilic injury of mucosal plicae and purulent exudate

Healing with adhesion and fibrosis

Tubal lumen becomes distorted or obstructed

Reproductive sequelae

Infertility or ectopic pregnancy

Schematic

Slide 33 · Acute salpingitis: What happens in the tube?

Congestion and neutrophilic infiltration damage the tubal epithelium.

Mucosal folds are denuded and may slough.

Purulent exudate fills the tubal lumen and can escape via the fimbriae.

Extension can produce salpingo-oophoritis and tubo-ovarian abscess.

Slide 34 · Pyosalpinx and tubo-ovarian abscess

Pyosalpinx is accumulation of pus within a fallopian tube.

Suppurative inflammation can extend to ovarian tissue.

Combined tubal and ovarian infection can form a tubo-ovarian abscess.

These lesions represent anatomically progressive, destructive infection.

Slide 35 · Chronic salpingitis: Scarring after infection

Even after organisms disappear, epithelial loss initiates repair.

Denuded tubal plicae adhere, forming distorted blind pockets.

Fibrosis narrows the lumen and can compromise fimbrial function.

Resulting tubal dysfunction provides the basis for infertility or ectopic gestation.

Slide 36 · Acute versus chronic salpingitis

Acute

Edematous congested mucosa.

Neutrophils and luminal pus.

Tubal epithelial injury; Possible abscess.

Chronic / healed

Adhesion and fusion of mucosal plicae.

Fibrotic distortion and luminal obstruction.

Hydrosalpinx, infertility or ectopic pregnancy.

Slide 37 · Case: Infertility following a remote STI

TEACHING SCENARIO

A patient with a history of prior symptomatic cervicitis now has difficulty conceiving; Imaging suggests damaged fallopian tubes.

Reasoning prompts

Identify the microscopic injury that started the process.

Explain why infection may be absent now.

State the structural basis of infertility.

Clinicopathologic resolution

Previous suppurative salpingitis causes epithelial destruction; Chronic adhesion/fibrosis persists after microbial clearance and impairs gamete transport.

Slide 38 · Genital ulcer patterns: First distinction

Agent

Lesion pattern

Reason this is useful

T. Pallidum

Classically firm, relatively painless chancre

Vascular / plasma cell–rich inflammation

H. Ducreyi

Soft painful ulcer, often tender buboes

Necrotizing suppurative ulceration

HSV

Painful clustered vesicles evolving to ulcers

Virus-mediated epithelial cytolysis

K. Granulomatis

Chronic soft ulcer / exuberant granulation

Granulation tissue and intracellular bacteria

Slide 39 · Syphilis: A systemic spirochetal infection

Treponema pallidum subsp. Pallidum produces chronic multistage infection.

Organisms are too slender to appreciate reliably by routine Gram stain.

Silver stains or immunofluorescence may demonstrate spirochetes in tissues.

Transplacental spread can cause congenital syphilis.

Slide 40 · Syphilis: Stages and pathology

Primary

Chancre at inoculation site; Treponemal dissemination

Secondary

Generalized mucocutaneous lesions; Lymphadenopathy

Latent

Clinical quiescence despite persistent infection

Tertiary

Aortitis, neurologic disease and/or gummas in untreated disease

Schematic

Slide 41 · The vascular hallmark of syphilis

Small-vessel proliferative endarteritis is characteristic across stages.

A conspicuous plasma cell–rich perivascular infiltrate accompanies it.

Vascular narrowing contributes to downstream ischemic tissue damage.

Host responses suppress but may not eradicate treponemes.

Slide 42 · Primary syphilis: The chancre

A firm, elevated lesion arises at the site of inoculation.

The surface may erode to a shallow, usually painless ulcer.

Treponemes are abundant and can disseminate hematogenously.

Spontaneous healing does not imply elimination of systemic infection.

Slide 43 · Secondary syphilis: Dissemination

Superficial mucocutaneous lesions may involve palms and soles.

Condylomata lata are broad-based plaques in moist anogenital areas.

Lymphadenopathy and systemic symptoms may accompany the rash.

Subsequent clinical latency may conceal persistent infection.

Slide 44 · Condyloma lata versus condyloma acuminatum

Condyloma lata

Secondary syphilis manifestation.

Broad-based moist anogenital plaques.

Caused by T. Pallidum; Systemic infection.

Condyloma acuminatum

Benign low-risk HPV wart.

Exophytic papillary squamous proliferation.

Koilocytic atypia may be present.

Slide 45 · Tertiary syphilis: Organ targets

Syndrome

Anatomic target

Pathologic outcome

Cardiovascular

Ascending aorta and aortic root

Aortitis, root dilation, insufficiency / aneurysm

Neurosyphilis

CNS

Meningovascular and/or parenchymal manifestations

Gummatous

Skin, bone, oral and upper airway tissues

Nodular granulomatous-destructive lesions

Slide 46 · Syphilitic aortitis: Mechanism and effects

Tertiary inflammatory vascular injury affects the proximal aorta.

Chronic aortitis predisposes to aortic root and arch dilatation.

Aortic regurgitation and proximal aneurysm may follow.

Pathologic manifestations can arise long after initial genital disease.

Slide 47 · Neurosyphilis: Clinical–pathologic range

Treponemes can involve the CNS relatively early in infection.

Neurosyphilis may be clinically silent despite CSF abnormalities.

Symptomatic disease can include meningovascular and other neurologic syndromes.

Nervous-system involvement changes clinical evaluation and treatment decisions.

Slide 48 · Gummas: Delayed tissue destruction

Gummas are nodular, often destructive tertiary syphilitic lesions.

They can involve bone, skin and upper aerodigestive mucosa.

Delayed immune responses are believed to contribute to the lesions.

Gummas are uncommon where effective antimicrobial treatment is accessible.

Slide 49 · Syphilis testing: Two complementary serologies

Clinical suspicion

History, examination and appropriate screening

Nontreponemal

RPR or VDRL: Reagin antibodies and quantitative titers

Treponemal

Antibodies specific to T. Pallidum

Combined interpretation

Traditional or reverse-sequence testing; Assess discordance

Schematic — parallel mechanisms

Slide 50 · Treponemal versus nontreponemal tests

Nontreponemal (RPR / VDRL)

Not specific for T. Pallidum.

Quantitative titers can help monitor treatment response.

A positive result needs appropriate confirmatory evaluation.

Treponemal

Detects organism-specific antibody.

Often remains reactive after successful treatment.

Can be used for screening or confirmation.

Slide 51 · Case: Painless ulcer and later generalized rash

TEACHING SCENARIO

An initially painless indurated genital ulcer resolves; Weeks later a generalized rash including palms develops.

Reasoning prompts

Connect the two clinical episodes.

State the common histopathologic vascular lesion.

Name appropriate assay classes.

Clinicopathologic resolution

Primary and secondary syphilis form a sequence of systemic T. Pallidum infection. Plasma cell–rich endarteritis is characteristic. Use treponemal and nontreponemal testing together.

Slide 52 · Chancroid: Ulcerative infection

Haemophilus ducreyi causes an acute ulcerative STI.

The initial papule becomes an irregular, painful, nonindurated ulcer.

An inflammatory exudate often covers the ulcer base.

Tender regional nodes may suppurate and drain as buboes.

Slide 53 · Chancroid: Layered microscopic response

The ulcer surface shows neutrophilic debris and fibrin.

Underlying granulation tissue contains necrosis and thrombosed vessels.

A dense lymphoplasmacytic infiltrate is deeper in the lesion.

Organisms may be difficult to identify among colonizing bacteria.

Slide 54 · Donovanosis: Exuberant granulation and scarring

Klebsiella granulomatis causes granuloma inguinale (donovanosis).

Chronic ulcers develop prominent soft granulation tissue.

Pseudoepitheliomatous hyperplasia can mimic malignancy.

Advanced untreated disease may produce scarring, strictures and lymphedema.

Slide 55 · Donovan bodies: A diagnostic clue

Exudate smears can show minute encapsulated coccobacilli inside macrophages.

These organisms are termed Donovan bodies.

Giemsa and some silver stains can reveal the organisms.

Regional lymph nodes are typically spared or show nonspecific reactions.

Slide 56 · Lymphogranuloma venereum: Tissue progression

C. Trachomatis serovars L1–L3

Often subtle initial genital papule

Regional lymphatic spread

Tender nodal enlargement; Granulomatous inflammation

Necrosis and chronic inflammation

Suppuration and eventual fibrosis

Late anogenital disease

Strictures and lymphatic obstruction

Schematic

Slide 57 · LGV: Characteristic nodal lesion

Lymph nodes show a mixed granulomatous and neutrophilic inflammatory response.

Irregular foci of neutrophilic necrosis can form stellate abscesses.

Healing fibrosis may obstruct local lymphatic channels.

Chronic anogenital strictures are a late complication.

Slide 58 · Three bacterial ulcer syndromes

Chancroid versus donovanosis

Chancroid: Painful soft ulcer; Suppurative tender nodes.

Donovanosis: Chronic ulcer with abundant granulation; Donovan bodies.

Both can scar when untreated.

Syphilis versus LGV

Primary syphilis: Indurated usually painless chancre.

LGV: Often minor initial papule, then pronounced nodal disease.

Syphilis produces endarteritis; LGV produces granulomatous/necrotizing lymphadenitis.

Slide 59 · HSV genital infection and latency

Both HSV-1 and HSV-2 can cause genital infection; HSV-2 predominates in classic genital herpes.

Primary infection causes epithelial vesicles and painful ulcers.

Virus reaches lumbosacral sensory ganglia and establishes latency.

Reactivation explains recurrent mucocutaneous lesions.

Slide 60 · Herpetic lesion: From infection to recurrence

Epithelial viral replication

Ballooning degeneration and intraepithelial vesicles

Vesicle rupture

Painful shallow ulcers with inflammatory response

Sensory ganglion latency

Viral persistence without continuous lesions

Reactivation

Recurring mucosal or cutaneous episodes

Schematic

Slide 61 · HSV morphology: Cytopathic signature

HSV infection may produce multinucleated epithelial cells.

Intranuclear inclusions show ground-glass alteration and chromatin margination.

Biopsied lesions often show ulceration and acute inflammation.

Cytopathic changes support the diagnosis but specific viral tests provide identification.

Slide 62 · Genital HSV: Active lesions versus latency

Active mucocutaneous phase

Vesicles or ulcers contain infectious viral particles.

Symptoms may include pain, dysuria and tender nodes.

Detection from active lesions can confirm infection.

Latent / recurrent phase

Viral genome persists in sensory ganglia.

Subclinical shedding permits some transmission without lesions.

Reactivation is more frequent with impaired immune function.

Slide 63 · Neonatal HSV: Disproportionate injury

Maternal genital HSV can transmit during passage through the birth canal.

Risk is especially concerning with active primary infection at delivery.

Neonatal HSV can disseminate to viscera and the CNS.

This contrasts with the often localized disease of older immunocompetent individuals.

Slide 64 · Case: Clustered painful genital ulcers

TEACHING SCENARIO

Painful vesicles progress to superficial ulcers. A cervical smear contains multinucleated epithelial cells with ground-glass nuclear change.

Reasoning prompts

Identify the likely pathogen family.

Explain recurrent episodes.

Name a particularly vulnerable exposed population.

Clinicopathologic resolution

Genital HSV causes epithelial cytopathic change. Sensory-ganglion latency supports recurrence. Perinatally exposed newborns risk serious systemic and CNS disease.

Slide 65 · HPV has two distinct genital pathologies

Low-risk HPV types, predominantly 6 and 11, produce genital warts.

High-risk HPV types are associated with cervical and other anogenital squamous cancers.

Genital HPV infection is often asymptomatic and may clear without lesions.

Persistence of oncogenic infection increases the risk of intraepithelial neoplasia.

Slide 66 · Low-risk versus high-risk HPV

Feature

Low-risk HPV

High-risk HPV

Common types

6, 11

16, 18 and others

Typical pathology

Condyloma acuminatum

Squamous intraepithelial lesions / carcinomas

Cell behavior

Productive papillomatous proliferation

Dysregulated cell-cycle control

Clinical framing

Warts are not precancerous lesions

Persistent infection contributes to carcinogenesis

Slide 67 · Condyloma acuminatum: Gross and microscopic

External genital or perineal lesions may be sessile or pedunculated.

Exophytic branching fibrovascular papillae are lined by acanthotic squamous epithelium.

Orderly squamous maturation is generally retained in benign warts.

Koilocytes display perinuclear halos with altered nuclei.

Slide 68 · High-risk HPV: Oncogenic mechanism

Persistent high-risk HPV

Oncogenic viral proteins are expressed

E6 activity

P53 degradation and telomerase upregulation

E7 activity

RB inhibition and E2F release

Cell-cycle deregulation

Additional changes can yield squamous neoplasia

Schematic — parallel mechanisms

Slide 69 · The transformation zone and HPV

HPV infects immature basal squamous cells after access to susceptible epithelium.

The cervical transformation zone is particularly susceptible to high-risk HPV infection.

Persistent infection can give rise to precursor squamous lesions.

HPV-related cancer development generally requires additional genetic/epigenetic alterations.

Slide 70 · HPV-associated versus HPV-independent vulvar cancer

HPV-associated

Linked to high-risk HPV, especially HPV-16.

Develops from HPV-associated squamous intraepithelial lesions.

May coexist with HPV-related lesions at other anogenital sites.

HPV-independent

Usually associated with chronic vulvar disorders.

Can arise through differentiated vulvar intraepithelial neoplasia.

Frequently involves somatic TP53 alterations.

Slide 71 · HPV prevention is a pathology intervention

Vaccination against HPV prevents infections caused by vaccine-targeted types.

Prevention reduces development of low-risk genital warts and high-risk HPV precursor lesions.

Cervical screening detects intraepithelial lesions before invasive cancer.

Vaccination and screening address different steps in carcinogenesis.

Slide 72 · Case: Exophytic papillary anogenital lesion

TEACHING SCENARIO

A papillary genital lesion has thickened squamous epithelium and scattered koilocytes but preserved maturation.

Reasoning prompts

Name the lesion.

Identify the usual viral-risk category.

Distinguish it from secondary syphilis.

Clinicopathologic resolution

Condyloma acuminatum is a benign low-risk HPV lesion (usually HPV 6/11). Condyloma lata is a manifestation of secondary syphilis, not a papillary HPV wart.

Slide 73 · Trichomoniasis: Protozoal vaginitis

Trichomonas vaginalis is a flagellated protozoan transmitted commonly through sexual contact.

Vaginal infection can cause frothy yellow discharge and vulvovaginal discomfort.

Dysuria and dyspareunia may be present; Infection may also be asymptomatic.

Cervical vascular dilatation can produce a “strawberry cervix.”

Slide 74 · Not all vaginitis is an STI

Trichomoniasis

Sexually transmitted flagellated protozoan.

Inflammatory vaginitis; Frothy discharge may occur.

Characteristic erythematous cervix in some patients.

Candidiasis and bacterial vaginosis

Candidiasis usually follows disturbance of vaginal ecology and is not classified as an STI.

Bacterial vaginosis is a polymicrobial dysbiosis with malodorous discharge.

Similar symptoms do not imply identical transmission pathways.

Slide 75 · Cervicitis: Infection versus reactive atypia

Gonococci, chlamydiae, mycoplasmas and HSV can cause clinically important cervicitis.

Cervical inflammation can produce reparative epithelial change.

Reactive atypia may complicate cytologic interpretation.

Identify the infectious process and assess for upper genital tract complications.

Slide 76 · Nongonococcal urethritis is heterogeneous

Chlamydia trachomatis is one major infectious cause.

Ureaplasma and other organisms can produce urethral symptoms.

Some cases have no organism identified and some inflammation is noninfectious.

Urethritis can warn of disease elsewhere in the genitourinary tract.

Slide 77 · Morphologic clues and their limitations

Morphologic finding

Favors

Important limitation

Intracellular diplococci in exudate

Gonorrhea

Confirm with appropriate pathogen tests

Multinucleation and nuclear inclusions

HSV

Cytopathic appearance is not site-specific

Koilocytic atypia

HPV

Does not itself grade a lesion

Plasma cell–rich endarteritis

Syphilis

Needs serologic / organism correlation

Donovan bodies in macrophages

Donovanosis

Requires correct staining and specimen context

Slide 78 · Vertical transmission: Pathogen and damage

Maternal infection

Transmission / neonatal presentation

Core implication

C. Trachomatis

Perinatal neonatal conjunctivitis

Maternal diagnosis has neonatal consequences

N. Gonorrhoeae

Neonatal conjunctivitis, potentially blindness

Prevention and prompt care are essential

HSV

Peripartum CNS or disseminated disease

Primary active genital HSV is particularly concerning

T. Pallidum

Transplacental congenital syphilis

Fetal loss and multisystem childhood disease

HIV

Prenatal or perinatal HIV infection

Antiretroviral interventions markedly reduce transmission

Slide 79 · Congenital syphilis: Early and late disease

Transplacental T. Pallidum can cause fetal loss or severe neonatal disease.

Early manifestations include snuffles, skin rash, hepatomegaly and skeletal abnormalities.

Delayed disease can include interstitial keratitis, hearing loss and characteristic dental abnormalities.

Pregnancy screening and appropriate treatment interrupt mother-to-child transmission.

Slide 80 · Perinatal prevention: Interrupting the pathway

Detect maternal infection

Recognize asymptomatic disease through appropriate screening

Treat or manage maternal infection

Pathogen-specific measures during pregnancy

Protect the newborn

Neonatal prophylaxis or management when indicated

Reduce infection and injury

Lower vertical transmission and severe neonatal outcomes

Schematic

Slide 81 · Diagnostic strategy: Syndrome is a starting point

Use the distribution of symptoms and lesions to localize disease.

Combine clinical examination with pathogen-directed assays.

Do not use histology alone to exclude simultaneous infections.

Interpret tests in the context of exposure site and disease stage.

Slide 82 · Test selection: What each detects

Method

Common use in this lecture

What it contributes

Nucleic-acid amplification

Gonorrhea; Chlamydia

Direct organism nucleic-acid detection

Culture

Selected gonococcal specimens

Organism recovery; Resistance workup

Syphilis serology

RPR/VDRL plus treponemal assay

Stage-sensitive, complementary antibody information

Lesion-based HSV assay

Genital herpes

Virus detection from symptomatic lesion

Cytology / histology

HPV lesions; HSV changes; Ulcers

Tissue effect and differential diagnosis

Slide 83 · Integrated case: Pelvic pain with negative smear

TEACHING SCENARIO

A patient has cervicitis, pelvic pain and tubal tenderness. Routine Gram stain does not reveal a definitive organism.

Reasoning prompts

Does a negative direct smear exclude chlamydial disease?

Which organ injury threatens future fertility?

What test class is relevant to the common agents?

Clinicopathologic resolution

No. Chlamydia is not visible on routine Gram stain. Ascending infection may cause suppurative salpingitis and later fibrosis. NAATs are appropriate for gonorrhea/chlamydia detection.

Slide 84 · Integrated case: Painful versus painless ulcer

TEACHING SCENARIO

Two patients present with genital ulcers: One has a painful soft ulcer and tender nodes; The other has a firm painless chancre.

Reasoning prompts

Give a leading pathogen for each pattern.

Describe one discriminating microscopic feature.

Explain why a clinical pattern alone is insufficient.

Clinicopathologic resolution

Consider H. Ducreyi for the soft painful ulcer and T. Pallidum for a firm painless chancre. Chancroid shows layered neutrophilic ulcer inflammation; Syphilis favors plasma cell–rich endarteritis. Confirm with appropriate tests.

Slide 85 · Final pathology synthesis

Dominant process

Representative infection

High-value consequence

Suppurative mucosal injury

Gonorrhea; Chlamydia

Ascending tubal scarring

Endarteritis and chronic inflammation

Syphilis

Vascular, neurologic and congenital disease

Viral epithelial cytolysis

Genital HSV

Latency, recurrence; Neonatal spread

HPV-driven squamous proliferation

Condyloma / persistent high-risk HPV

Benign wart versus premalignant lesion

Granulation and chronic ulceration

Donovanosis / chancroid

Scarring, tissue destruction

Slide 86 · Clinical reasoning: Five discriminators

Which site and route of exposure are plausible?

Is inflammation purulent, ulcerative, papillary or systemic?

Could asymptomatic or multiple infections coexist?

What permanent organ injury or neonatal risk must be prevented?

Which pathogen-directed assay can establish etiology?

Slide 87 · Further reading in Robbins

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th edition.

Infectious Diseases: sexually transmitted infections and individual microbial diseases.

Neoplasia: the molecular pathogenesis of human papillomavirus-associated tumors.

The Lower Urinary Tract and Male Genital System; The Female Genital Tract: anatomic pathology and clinical sequelae.