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Lecture topics
- Chancroid in the genital-ulcer framework
- The mature ulcer: Surface characteristics
- Histologic architecture: Overview
- Why a layer-by-layer description matters
- Why a negative stain is not an exclusion test
- Donovanosis: Etiologic identity
- Stains for K. Granulomatis
- Selected source locations
Slide index & full transcript (67 slides)
Text from the original slides, in presentation order. Diagrams and images remain in the viewer above.
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.