Pathology Lectures

Chancroid Soft Chancre

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Slide 1 · Chancroid

(Soft Chancre)

An ulcerative bacterial sexually transmitted infection

Etiology • temporal evolution • morphology • diagnostic limitations • differential diagnosis

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Recognize

Identify the characteristic painful, nonindurated genital ulcer.

Explain

Connect the clinical lesion with its three-layer histologic architecture.

Distinguish

Contrast chancroid with syphilis, genital herpes and donovanosis.

Appraise

Explain why a suspected case can be difficult to confirm microbiologically.

Slide 3 · Chancroid in the genital-ulcer framework

Sexually transmitted infection

Acute local papule

Painful genital ulcer

Possible tender regional bubo

Core sequence; Node involvement is not universal.

Slide 4 · Etiologic identity

Causative organism: Haemophilus ducreyi.

Classified among bacterial sexually transmitted infections.

The dominant tissue lesion is an acute ulcer, rather than a chronic mass.

The clinical and histologic findings must be integrated with laboratory limitations.

Slide 5 · Four organisms in the differential

Condition

Etiologic agent

Characteristic source description

Chancroid

Haemophilus ducreyi

Acute painful soft ulcer

Primary syphilis

Treponema pallidum

Firm, typically nontender chancre

Genital herpes

HSV-1 or HSV-2

Vesicles → superficial ulcers

Donovanosis

Klebsiella granulomatis

Soft painless granulation-rich mass

Slide 6 · The meaning of “soft chancre”

Unlike a primary syphilitic chancre, the chancroid ulcer is not indurated.

The term describes the clinical consistency of the lesion.

Softness alone does not establish H. Ducreyi infection.

Assess tenderness, ulcer contour, exudate, multiplicity and regional nodes together.

Slide 7 · Typical evolution after inoculation

4–7 days

Tender erythematous papule

Several days later

Surface erosion → painful ulcer

Within 1–2 weeks

Tender regional nodes may enlarge

If untreated

Bubo may drain through skin

Intervals and subsequent events are source descriptions, not a universal course.

Slide 8 · The earliest visible lesion

A tender erythematous papule develops at the site of inoculation.

Its appearance four to seven days after inoculation.

At this stage an established crater-like ulcer is not yet required.

The lesion evolves through surface erosion over ensuing days.

Slide 9 · Usual anatomic sites described

In males

The primary lesion is usually on the penis.

External genital location supports direct local inoculation.

In females

Lesions most often in the vagina or periurethral area.

Site variation changes how readily the lesion is seen.

Slide 10 · Papule to ulcer: The local tissue sequence

Erythematous raised papule

Epidermal / mucosal surface erodes

Irregular painful ulcer

Exudate covers the base

Schematic clinical evolution — not a patient photograph.

Slide 11 · The mature ulcer: Surface characteristics

The ulcer is irregular in outline.

The lesion is painful.

The base carries shaggy yellow-gray exudate.

The absence of induration is a key contrast with the syphilitic chancre.

Slide 12 · Multiplicity is compatible with chancroid

More than one ulcer may be present.

A single lesion does not rule out chancroid.

Lesion count should be documented alongside pain, consistency and exudate.

Do not rely on multiplicity as a stand-alone diagnostic criterion.

Slide 13 · Clinical descriptors are not synonyms

Painful

Clinical symptom reported at the ulcer.

Nonindurated

Palpation finding: No characteristic firmness.

Irregular

Description of the ulcer border and configuration.

Exudative

Shaggy yellow-gray material covering the base.

Slide 14 · Chancroid versus primary syphilis

Chancroid

Painful irregular ulcer

Not indurated

May be multiple

Yellow-gray shaggy exudate

Primary syphilis

Typically nontender

Firm primary chancre

Often a single lesion

Different pathogen: T. Pallidum

Slide 15 · Tender regional lymphadenopathy

Regional nodes may enlarge and become tender.

This finding in about 50% of cases.

The reported time is within one to two weeks after primary infection.

Absence of enlarged nodes therefore does not exclude chancroid.

Slide 16 · Formation of a bubo

Genital ulcer

Tender regional node enlargement

Marked swelling (bubo)

Possible erosion and draining ulcer

Progression to cutaneous drainage is described for untreated disease.

Slide 17 · When lymphadenitis complicates the ulcer

The genital ulcer and a regional bubo are distinct anatomic lesions.

Nodes are tender as well as enlarged.

Buboes can erode overlying skin when untreated.

The late result can be a chronic draining ulcer over the node.

Slide 18 · Primary ulcer and draining bubo

Primary inoculation-site ulcer

Originates from the tender papule

Irregular, painful and exudative

Located on genital epithelium

Secondary bubo-related ulcer

Begins in an enlarged regional node

Develops after nodal erosion through skin

May become chronically draining

Slide 19 · Histologic architecture: Overview

SURFACE

Neutrophilic debris and fibrin

INTERMEDIATE

Granulation · necrosis · thrombosed vessels

DEEP

Dense lymphoplasmacytic infiltrate

Schematic cross-section — not a histologic specimen

Teaching interpretation

The ulcer has three recognizable vertically arranged inflammatory zones.

Slide 20 · Surface layer: Neutrophilic debris

SURFACE

Neutrophilic debris and fibrin

INTERMEDIATE

Granulation · necrosis · thrombosed vessels

DEEP

Dense lymphoplasmacytic infiltrate

Schematic cross-section — not a histologic specimen

Teaching interpretation

The uppermost zone contains neutrophilic debris and fibrin.

Slide 21 · Surface layer: Fibrin

SURFACE

Neutrophilic debris and fibrin

INTERMEDIATE

Granulation · necrosis · thrombosed vessels

DEEP

Dense lymphoplasmacytic infiltrate

Schematic cross-section — not a histologic specimen

Teaching interpretation

Fibrin accompanies the superficial neutrophil-rich ulcer debris.

Slide 22 · Middle layer: Granulation tissue

SURFACE

Neutrophilic debris and fibrin

INTERMEDIATE

Granulation · necrosis · thrombosed vessels

DEEP

Dense lymphoplasmacytic infiltrate

Schematic cross-section — not a histologic specimen

Teaching interpretation

A reparative-appearing granulation-tissue zone lies below the surface debris.

Slide 23 · Middle layer: Necrosis

SURFACE

Neutrophilic debris and fibrin

INTERMEDIATE

Granulation · necrosis · thrombosed vessels

DEEP

Dense lymphoplasmacytic infiltrate

Schematic cross-section — not a histologic specimen

Teaching interpretation

Foci of tissue necrosis within the granulation zone.

Slide 24 · Middle layer: Thrombosed vessels

SURFACE

Neutrophilic debris and fibrin

INTERMEDIATE

Granulation · necrosis · thrombosed vessels

DEEP

Dense lymphoplasmacytic infiltrate

Schematic cross-section — not a histologic specimen

Teaching interpretation

Thrombosed vessels are another component of the intermediate ulcer zone.

Slide 25 · Deep layer: Lymphoplasmacytic infiltrate

SURFACE

Neutrophilic debris and fibrin

INTERMEDIATE

Granulation · necrosis · thrombosed vessels

DEEP

Dense lymphoplasmacytic infiltrate

Schematic cross-section — not a histologic specimen

Teaching interpretation

A dense lymphoplasmacytic inflammatory infiltrate underlies the granulation zone.

Slide 26 · Microscopy: Top-to-bottom reading

Anatomic level

Dominant appearance

Interpretive task

Superficial

Neutrophilic debris + fibrin

Locate ulcer surface

Intermediate

Granulation, necrosis, thrombosed vessels

Describe tissue injury and response

Deeper

Dense lymphoplasmacytic infiltrate

Recognize subjacent inflammation

Slide 27 · Why a layer-by-layer description matters

Orientation

A surface-to-depth sequence prevents conflating superficial debris with deeper inflammation.

Coexistence

Acute neutrophil-rich injury and deeper mononuclear inflammation coexist.

Vascular changes

Necrosis and thrombosis belong to the granulation-tissue zone.

Slide 28 · Histology supports, but does not name, the agent

The three-zone pattern describes a tissue reaction to the ulcerative infection.

Necrosis and thrombosed vessels should not be mistaken for proof of a unique pathogen.

Organism detection is difficult even when the inflammatory pattern is present.

Clinicopathologic interpretation must account for potentially overlapping genital-ulcer causes.

Slide 29 · H. Ducreyi on tissue-based stains

Coccobacilli may occasionally be demonstrated with Gram or silver stains.

They are not reliably seen in routine lesion material.

Other bacteria often colonize the ulcer base and obscure the pathogen.

An organism-negative stain does not contradict the described ulcer morphology.

Slide 30 · Why lesion Gram staining is unreliable

Ulcerated surface

Other bacteria colonize the base

Coccobacilli become difficult to distinguish

Low-confidence direct visualization

Diagnostic limitation described in the Robbins source; No sensitivity figure is given.

Slide 31 · Culture is technically demanding

H. Ducreyi grows poorly in culture.

It requires uncommon, highly enriched culture media.

Routine culture workflows may therefore fail to demonstrate the organism.

Culture limitations contribute to uncertainty in clinical recognition.

Slide 32 · PCR availability is another constraint

PCR-based tests for H. Ducreyi are not widely available account.

Availability is distinct from analytic performance.

Robbins provides no PCR sensitivity or specificity values here.

Avoid treating absent testing as a negative molecular result.

Slide 33 · The evidence bottleneck in chancroid

Characteristic ulcer / bubo

Gram stain can miss pathogen

Special culture is difficult

PCR access is limited

Consequence: Cases may be underdiagnosed.

Slide 34 · Separate clinical evidence from organism proof

Clinical pattern

Painful, irregular, nonindurated ulcer; Possible bubo.

Histologic pattern

Surface debris → granulation + injury → deep lymphoplasmacytic infiltrate.

Microbial evidence

H. Ducreyi is difficult to demonstrate by stain and culture.

Slide 35 · Why a negative stain is not an exclusion test

Organisms are sometimes demonstrable, rather than consistently visible.

Colonizing organisms may visually obscure H. Ducreyi.

The specimen reflects the ulcer’s mixed microbial environment.

A negative result must be interpreted against the clinical presentation.

Slide 36 · Limits of the supplied diagnostic evidence

Poor culture growth and restricted PCR access.

The chapter section does not supply a formal case-definition algorithm.

It does not provide test performance characteristics or recommended drug regimens.

The lecture therefore treats diagnosis as a clinicopathologic problem, not an invented quantitative score.

Slide 37 · Geographic distribution

Sub-Saharan Africa

Identified as a region of relatively greater occurrence.

Southeast Asia

Several affected settings are described.

South America

Part of the listed geographic distribution.

Central America

Part of the listed geographic distribution.

Slide 38 · Trends should be reported with their context

Falling prevalence in Thailand and several African nations.

Chancroid is described as uncommon in the United States.

The figure of fewer than 20 U.S. Reports per year refers to “the past several years” in the source.

Do not interpret that textbook figure as a live 2026 surveillance count.

Slide 39 · Recognized burden versus underlying burden

Relatively uncommon reports

Gram and culture limitations

Restricted molecular access

Potential underdiagnosis

Qualitative relationship only; The source gives no estimate of the hidden burden.

Slide 40 · Relationship with HIV transmission

Chancroid as an important cofactor in HIV transmission.

The STI chapter notes that co-infection risks can coexist through shared exposures.

An ulcerative STI has implications beyond the visible local lesion.

The chancroid section does not quantify an HIV risk multiplier.

Slide 41 · An STI is not evaluated in isolation

Local lesion

Document ulcer morphology and regional-node findings.

Coinfection context

The STI chapter states that one STI increases the likelihood of others.

Partner/public health context

STI transmission depends on person-to-person contact; Reporting may support contact testing.

Slide 42 · Donovanosis: Why it belongs in this lecture

The project topic file explicitly groups granuloma inguinale with chancroid.

Both conditions are sexually transmitted bacterial infections with genital ulceration.

Their typical lesion morphology and nodal behavior differ.

The comparison sharpens the distinction between acute ulcer and chronic granulation-rich lesion.

Slide 43 · Donovanosis: Etiologic identity

Also called granuloma inguinale.

Caused by Klebsiella granulomatis, formerly Calymmatobacterium donovani.

Described as a chronic inflammatory sexually transmitted infection.

The organism is a minute encapsulated coccobacillus.

Slide 44 · Donovanosis lesion evolution

Papule

Raised lesion on genital squamous epithelium

Ulceration

Surface loses continuity

Granulation

Protuberant soft, painless mass

Progression

Borders become raised and indurated

A different lesion sequence from the painful chancroid ulcer.

Slide 45 · Granulation-rich morphology in donovanosis

Abundant granulation tissue creates a protuberant mass.

The typical described lesion is soft and painless.

As the lesion enlarges, its borders become raised and indurated.

This pattern is clinically distinct from the acute painful chancroid ulcer.

Slide 46 · Regional nodes discriminate the two entities

Chancroid

Tender lymphadenopathy is common enough to be a core finding.

Buboes may erode and drain when untreated.

Donovanosis

Regional lymph nodes typically are spared.

If affected, changes are generally nonspecific and reactive.

Slide 47 · Late morbidity in untreated donovanosis

Disfiguring scars may develop.

Scarring can be associated with urethral, vulvar or anal strictures.

Lymphatic obstruction may produce genital lymphedema.

Robbins refers to severe genital swelling as genital elephantiasis.

Slide 48 · Donovanosis at the ulcer edge

Marked epithelial hyperplasia may develop at the borders.

The epithelial proliferation may resemble carcinoma.

Robbins calls this pseudoepitheliomatous hyperplasia.

Interpretation requires recognizing a reactive change in the ulcer’s setting.

Slide 49 · Donovanosis: Inflammatory compartment

Neutrophils and mononuclear inflammatory cells mix at the ulcer base.

The infiltrate also extends beneath nearby epithelium.

This differs from the particularly described three-zone chancroid architecture.

Bacterial demonstration relies on examining exudate smears or biopsy material.

Slide 50 · Donovan bodies: What the pathologist seeks

Macrophage (schematic)

Conceptual vector diagram — not an observed smear

Organism localization

Giemsa-stained ulcer exudate can show encapsulated coccobacilli within macrophages; These are Donovan bodies.

Slide 51 · Stains for K. Granulomatis

Giemsa staining of exudate smears can demonstrate Donovan bodies.

Silver stains, including Warthin–Starry, may show the organisms.

Routine culture is difficult; PCR is not widely available account.

The microscopic search is therefore central to the source-described diagnostic approach.

Slide 52 · Chancroid versus donovanosis

Feature

Chancroid

Donovanosis

Agent

H. Ducreyi

K. Granulomatis

Course

Acute painful ulcer

Chronic painless granulation mass

Node response

Tender buboes may develop

Usually spared / reactive

Microscopy

Three-zone ulcer with thrombosis

Pseudoepitheliomatous edge; Donovan bodies

Sequelae

Chronic draining buboes

Scarring, strictures, lymphedema

Slide 53 · Genital herpes: A different initiating lesion

Chancroid

Tender papule → erosion → irregular painful ulcer

Bacterial agent: H. Ducreyi

Ulcer with layered inflammatory architecture

Genital herpes

Vesicles → superficial ulcerations

Usually HSV-2, also HSV-1

Viral cytopathic change may show multinucleation / inclusions

Slide 54 · Syphilis: Distinct initial and vascular features

Chancroid

Irregular, tender, nonindurated ulcer

Multiple lesions possible

Granulation zone may contain thrombosed vessels

Primary syphilis

Single firm, typically nontender chancre

Organism is T. Pallidum

Proliferative endarteritis is a characteristic pathologic process

Slide 55 · Genital ulcer comparison: Read across

Disease

Initial morphology

Histologic / laboratory clue

Chancroid

Painful nonindurated irregular ulcer

Surface debris; Granulation; Deep lymphoplasmacytic cells

Syphilis

Firm usually single nontender chancre

T. Pallidum; Proliferative endarteritis

Herpes

Vesicles progressing to superficial ulcers

Cowdry A inclusions / syncytia

Donovanosis

Soft painless granulation-rich ulcerated mass

Donovan bodies in macrophages

Slide 56 · Case 1: Painful ulcer with nodes

Clinical vignette

A patient develops a tender genital papule. Several days later there is an irregular, painful ulcer with yellow-gray exudate. One week afterward the ipsilateral regional nodes are tender and enlarged.

Which Robbins-described syndrome is most consistent, and which findings carry the greatest weight?

Assess evolution, induration, exudate and the node response.

Slide 57 · Case 1: Clinicopathologic reasoning

A chancroid pattern is supported by papule-to-painful-ulcer evolution.

The irregular, nonindurated, exudative ulcer is characteristic in the source.

Tender regional nodes support associated lymphadenitis.

Microbiologic confirmation remains difficult; Do not confuse a characteristic pattern with proven isolation.

Slide 58 · Case 2: Protuberant painless lesion

Clinical vignette

A chronic genital ulcer becomes a soft, protruding, painless granulation-rich lesion. Its edge is raised. Regional nodes are clinically unremarkable.

Which related bacterial ulcerative STI should be prioritized in the morphologic differential?

Consider which entity typically spares regional nodes.

Slide 59 · Case 2: Donovanosis interpretation

Granuloma inguinale is a strong source-supported match.

K. Granulomatis causes this chronic ulcerative infection.

Raised indurated margins and nodal sparing fit the description.

A Giemsa-stained smear may reveal Donovan bodies within macrophages.

Slide 60 · Case 3: Firm, nontender lesion

Clinical vignette

A solitary genital lesion is described as firm and nontender. It is called a “chancre,” but the examiner is uncertain whether “chancre” automatically implies chancroid.

What is the key terminology and diagnostic distinction?

The adjective “soft” matters.

Slide 61 · Case 3: Do not equate the two chancres

A firm, nontender primary chancre is characteristic of syphilis.

Chancroid more often gives a painful, nonindurated ulcer.

The organisms differ: T. Pallidum versus H. Ducreyi.

Descriptive terminology alone is not microbiologic confirmation.

Slide 62 · Case 4: Negative lesion Gram stain

Clinical vignette

A genital ulcer has the classic clinical appearance of chancroid, but the direct Gram stain does not convincingly show H. Ducreyi.

What pathology-based limitations prevent a simple exclusion?

Think about the composition of the ulcer base.

Slide 63 · Case 4: Explain the discordance

Coccobacilli may be difficult to demonstrate by Gram stain.

Bacteria colonizing the ulcer base can obscure the causative organism.

Culture requires uncommon enriched media; PCR may not be accessible.

The source explicitly notes that the disease may be underdiagnosed.

Slide 64 · Practical morphology-first synthesis

Describe ulcer: Pain • margin • induration • base

Assess nodes and temporal sequence

Use histologic pattern where sampled

Interpret pathogen tests with limitations

This is a teaching framework derived descriptions, not a formal clinical diagnostic guideline.

Slide 65 · High-yield distinctions

Chancroid

Painful, nonindurated ulcer; Regional bubo; Layered ulcer reaction.

Primary syphilis

Firm, typically nontender primary chancre.

Herpes

Genital vesicles progressing to shallow ulcers.

Donovanosis

Painless granulation-rich lesion; Nodal sparing; Donovan bodies.

Slide 66 · What the source does not establish

No validated numerical diagnostic score or stain-test sensitivity is given.

No drug-treatment schedule is presented in the extracted chancroid subsection.

No genuine chancroid micrograph is included among the accessible project assets.

Clinical examples and diagrams here are source-derived teaching constructs, not observed patients.

Slide 67 · Selected source locations

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. (2026). Chapter 8, pp. 333–334: chancroid and granuloma inguinale.

Chapter 8, pp. 321–322: herpes simplex virus; pp. 341–342: syphilis.

Chapter 8, pp. 313–314: sexually transmitted infection framework and etiologic table.

All diagrammatic lesions in this deck are original, editable schematics—not diagnostic specimens.

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