Acute and Chronic Cervicitis

Slide 1 · Acute and Chronic Cervicitis

Pathology, microbial ecology, and clinicopathologic interpretation

A clinicopathologic teaching lecture

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Identify the epithelial compartments of the cervix and transformation zone.

Explain how estrogen-dependent glycogen and lactobacilli shape the vaginal environment.

Differentiate clinically important cervicitis from incidental inflammation and vaginitis.

Connect infection, reparative atypia, testing, and upper genital tract complications.

Slide 3 · Why cervical inflammation matters

Frequently minor

Background cervical inflammation is common.

Morphologic inflammation alone does not identify an organism.

Clinical context determines significance.

Potentially consequential

Some sexually transmissible infections involve the endocervix.

Ascending infection can affect the upper genital tract.

Marked inflammation may complicate Pap interpretation.

Slide 4 · Cervix: Two epithelial compartments

Ectocervix: Mature stratified squamous mucosa, continuous with the vagina.

Endocervical canal: Mucus-secreting columnar epithelium.

The external os connects the ectocervix to the cervical canal.

Endocervical canal

Ectocervix

External os

Simplified anatomic schematic

Slide 5 · Ectocervical squamous mucosa

Several epithelial cell layers produce a protective squamous surface.

Maturation and glycogen accumulation are hormonally regulated.

A mature surface differs from the immature epithelium of the transformation zone.

Layered squamous cells

Schematic

Slide 6 · Endocervical columnar epithelium

The endocervix is lined by mucus-secreting columnar cells.

The canal is anatomically continuous with the uterine cavity.

Columnar and squamous epithelia meet at the squamocolumnar junction.

Single columnar lining

Schematic

Slide 7 · Squamocolumnar junction

The junction is an anatomic boundary between two epithelial phenotypes.

Its position varies with age and hormonal milieu.

Location matters when interpreting cervical mucosal injury and metaplasia.

Columnar

Squamous

Schematic

Slide 8 · Transformation zone and metaplasia

Squamous metaplasia

Replacement of glandular epithelium by squamous epithelium.

A common maturation/remodeling process.

Does not itself establish infection or dysplasia.

Transformation zone

Area where columnar and squamous epithelia coexist.

Contains immature/metaplastic epithelium.

Site relevant to HPV-associated precursor lesions.

Slide 9 · Menarche reshapes the cervical milieu

Ovarian estrogen increases at menarche.

Squamous epithelium matures and accumulates intracellular glycogen.

Desquamation makes glycogen available to vaginal microorganisms.

Ovarian estrogen

Squamous maturation

Glycogen-rich cells

Desquamation

Slide 10 · Glycogen is a substrate—not a pathogen

Maturing squamous cells accumulate glycogen vacuoles.

Shed cells contribute substrate to the vaginal ecological system.

Microbial metabolism helps establish the vaginal chemical environment.

Glycogen in epithelium

Shedding of cells

Microbial use of substrate

Slide 11 · Lactobacilli dominate the usual flora

Lactobacilli as major organisms in the normal vaginal community.

The microbial ecosystem includes other endogenous aerobic and anaerobic species.

The usual community contributes to resistance against overgrowth by other organisms.

Slide 12 · Lactic acid and vaginal pH

Lactobacilli generate lactic acid.

A normally acidic vaginal environment with pH below 4.5.

Acidity suppresses growth of many other organisms.

Lactobacilli

Lactic acid

Lower vaginal pH

Growth suppression

Slide 13 · Hydrogen peroxide: Textbook mechanism

Robbins also describes bacteriotoxic hydrogen peroxide (H₂O₂) production by lactobacilli under acidic conditions.

Its production falls when the environment becomes more alkaline.

This ecological mechanism is not, by itself, a diagnostic criterion for cervicitis.

Slide 14 · The mucosal ecosystem is layered

Squamous maturation supplies glycogen-containing cells.

Microbial metabolism promotes an acidic environment.

Perturbations can permit proliferation of other organisms.

Host epithelium

Microbial substrate

Acidic milieu

Ecological balance

Slide 15 · Not all cervical inflammation is disease

Common background findings

Low-grade inflammation may be present without major clinical consequence.

An inflammatory infiltrate does not establish an STI.

Do not overinterpret a single microscopic finding.

Clinically significant cervicitis

An important pathogen may be involved.

The infection may be transmissible.

Upper tract or pregnancy-related effects require consideration.

Slide 16 · Bleeding can perturb vaginal acidity

Blood temporarily alters the local acid–base environment.

A higher pH can reduce lactobacillus-associated H₂O₂ production model.

The shift may favor overgrowth by other organisms.

Bleeding

More alkaline milieu

Reduced ecological suppression

Slide 17 · Intercourse and transient pH shifts

Sexual intercourse among events that can raise local pH.

Changes in vaginal chemistry should not automatically be equated with STI.

Clinical assessment must distinguish exposure, symptoms, and causative infection.

Intercourse

Local pH perturbation

Possible ecological shift

Slide 18 · Vaginal douching disrupts the milieu

Douching is cited as a cause of altered vaginal acidity.

A perturbed ecosystem can permit proliferation of other organisms.

This provides a mechanistic explanation for some non-specific inflammatory conditions.

Douching

Ecological disturbance

Organism overgrowth

Slide 19 · Antibiotics can alter microbial balance

Antimicrobial treatment may suppress protective lactobacilli.

Vaginal pH may rise when lactobacilli are reduced.

Disrupted flora can permit other organisms to expand.

Antibiotic exposure

Lactobacilli suppressed

Higher pH

Overgrowth possible

Slide 20 · Dysbiosis is a mechanism, not a diagnosis

Ecological alteration

Changes in bacterial composition or vaginal chemistry.

May contribute to vaginitis or nonspecific cervical inflammation.

Requires assessment of symptoms and findings.

Proven cervical STI

Defined pathogen and clinical context.

Organism-specific testing often needed.

Has transmission and upper tract implications.

Slide 21 · Anatomic level defines the syndrome

Lower genital tract

Vaginitis: Primarily vaginal mucosa and discharge.

Cervicitis: Inflammatory process at the cervix.

The two processes may coexist.

Upper genital tract

Endometritis and salpingitis suggest ascending involvement.

PID has systemic/pelvic manifestations.

A different level of urgency and assessment is required.

Slide 22 · Acute versus chronic is a host-response pattern

Acute-pattern inflammation

Prominent neutrophilic response.

May accompany mucopurulent exudate.

Not specific for one pathogen.

Chronic-pattern inflammation

Lymphocytes and plasma cells predominate.

Can coexist with tissue repair.

Duration cannot be inferred precisely from one section.

Slide 23 · Potentially important infectious causes

Organism group

Pathology relevance

Clinical implication

Chlamydiae

Endocervical infection

Can ascend to endometrium/tubes

Gonococci

Acute mucosal inflammation

Potential PID

Mycoplasmas

Association with cervicitis

Species distinction matters

Herpes simplex virus

Possible cervical infection

Recognize viral disease context

Slide 24 · Chlamydia: Endocervical infection

Chlamydia trachomatis as an important cause of cervicitis.

Cervical infection can be clinically subtle.

Anatomical continuity permits spread beyond the cervix in some patients.

Slide 25 · Chlamydial infection can ascend

Ascending disease can involve endometrium and fallopian tubes.

Endometritis and salpingitis are components of upper genital tract infection.

This is why a local cervical infection may have reproductive consequences.

Endocervix

Uterine cavity

Fallopian tubes

Potential ascending route — schematic

Slide 26 · Gonorrhea may begin in the endocervix

The endocervical mucosa as a common initial site of gonococcal infection.

Gonococci can subsequently spread toward the fallopian tubes and adnexa.

The initial infection is not necessarily confined to the cervix.

Slide 27 · Gonococcal inflammation is often suppurative

Inflammatory morphology

Marked acute inflammation of infected mucosal surfaces.

Neutrophil-rich exudate can occur.

Gram-negative diplococci may be seen in neutrophils.

Diagnostic caution

Microscopy does not replace definitive organism testing.

Culture or detection of gonococcal DNA/RNA is used.

The clinical syndrome is broader than cytomorphology.

Slide 28 · Mycoplasma terminology requires precision

Robbins discussion

Lists mycoplasmas among causes of cervical inflammation.

Earlier Ch. 22 notes M. Hominis and Ureaplasma in genital infections.

This is a broad microbiologic grouping.

Clinical interpretation

M. Genitalium is evaluated selectively, especially with persistent symptoms.

Do not treat all genital mycoplasmas as equivalent.

Species-level context changes the significance.

Slide 29 · HSV is an important viral consideration

Herpes simplex virus is named among infections associated with clinically significant cervicitis.

A viral cause differs etiologically from bacterial overgrowth.

The clinical context and targeted testing determine its relevance.

Slide 30 · Trichomoniasis can involve the cervix

Trichomonas vaginalis is a sexually transmitted protozoan.

An erythematous vaginal/cervical mucosa and a “strawberry cervix” appearance.

Vulvovaginal discharge and discomfort may dominate the clinical picture.

Slide 31 · Bacterial vaginosis is not synonymous with cervicitis

Bacterial vaginosis

Altered vaginal bacterial ecology.

Thin, malodorous discharge is.

The abnormality primarily concerns the vaginal environment.

Cervicitis

Endocervical inflammation and possible mucopurulent exudate.

May arise with a transmissible pathogen.

Coinfection or overlap is possible.

Slide 32 · Candida is a useful competing diagnosis

Typical vulvovaginal candidiasis

Often pruritus, erythema, and curdlike discharge.

May follow antibiotic-associated flora disruption.

Primarily a vulvovaginal syndrome.

Clinical distinction

Symptoms alone do not localize pathology to the cervix.

Separate vaginal findings from endocervical signs.

Targeted testing is preferable to etiologic guessing.

Slide 33 · Three pathways to cervical inflammation

Ecological disturbance may contribute to inflammatory change.

A defined infectious agent can directly affect the cervical mucosa.

Host response and epithelial repair shape subsequent cytologic appearances.

Ecological disturbance / pathogen

Mucosal inflammatory response

Epithelial injury

Repair / atypia

Slide 34 · Acute inflammation: A schematic

Neutrophils are the principal illustrated inflammatory cells.

Epithelial exudation and superficial injury may accompany an active response.

Schematic illustration: Not a diagnostic photomicrograph.

Neutrophil-rich inflammatory field

SCHEMATIC — NOT HISTOLOGY

Slide 35 · Chronic inflammation: A schematic

Lymphocytes and plasma cells illustrate the chronic inflammatory pattern.

The stromal infiltrate can persist with epithelial repair.

Schematic illustration: Not a diagnostic photomicrograph.

Lymphoplasmacytic inflammatory field

SCHEMATIC — NOT HISTOLOGY

Slide 36 · Inflammatory pattern does not name the agent

What morphology may show

Intensity and cellular composition of inflammation.

Epithelial injury or reparative changes.

Changes warranting evaluation in context.

What morphology alone cannot prove

A specific transmissible organism.

Exact duration of infection.

Whether upper genital tract infection is present.

Slide 37 · Epithelial repair follows marked inflammation

Pronounced cervical inflammation can injure the epithelial surface.

Regeneration and reparative nuclear changes follow injury.

These changes can cause atypical-appearing exfoliated squamous cells.

Inflammation

Epithelial injury

Reactive regeneration

Atypical Pap appearance

Slide 38 · Reactive atypia can alter a Pap result

Robbins explicitly links marked cervicitis to reparative/reactive epithelial changes.

Atypical-appearing cells may be shed into cytologic samples.

Cytologic abnormality therefore requires interpretation rather than automatic etiologic attribution.

Slide 39 · Inflammation and neoplasia are not equivalent

Reactive epithelial atypia

May arise in the setting of marked inflammation.

Recognized in the tissue-injury and repair context.

Does not alone establish an HPV precursor lesion.

Cervical intraepithelial lesion

Belongs to the separate HPV-associated neoplastic pathway.

Requires its own cytologic/histologic assessment.

Do not dismiss significant atypia without appropriate evaluation.

Slide 40 · Pap findings do not identify a cervical pathogen

Pap cytology screens for cellular abnormalities; It is not the preferred pathogen-specific test for common bacterial STIs.

Reactive inflammation may affect cellular appearance and reporting.

Use an organism-directed test when a transmissible cause is suspected.

Slide 41 · Two major clinical signs of cervicitis

Mucopurulent exudate

Purulent or mucopurulent material in the endocervical canal.

Can be visible or observed on swabbing.

One accepted sign of cervical inflammation.

Endocervical friability

Sustained bleeding easily induced by gentle swabbing.

Supports the clinical cervicitis syndrome.

May occur with or without exudate.

Slide 42 · Mucopurulent endocervical exudate

Focus on the endocervical canal, not only vaginal secretions.

Mucopurulent material is a clinical sign, not proof of gonorrhea or chlamydia.

Laboratory testing establishes likely etiology when indicated.

Endocervical observation

Cervicitis suspected

Etiologic testing

Slide 43 · Cervical friability and induced bleeding

Gentle contact may produce readily induced endocervical bleeding.

Friability indicates local mucosal vulnerability, not a particular pathogen.

Bleeding warrants consideration of other cervical causes as well.

Gentle contact

Sustained cervical bleeding

Cervicitis / alternate cause assessment

Slide 44 · Cervicitis may have few symptoms

CDC guidance notes that cervicitis is frequently asymptomatic.

When symptoms occur, vaginal discharge or intermenstrual/postcoital bleeding may be reported.

Absence of symptoms does not exclude a clinically relevant cervical infection.

Slide 45 · Discharge does not localize the process

Vaginal source

Pruritus, vaginal irritation, characteristic discharge.

Consider yeast, trichomoniasis, and bacterial vaginosis.

Vaginal investigations may be needed.

Cervical source

Endocervical exudate or easy bleeding on examination.

Consider gonorrhea/chlamydia and other causes.

Evaluate upper tract red flags.

Slide 46 · Clinical history shapes pretest probability

Review symptoms, timing, sexual exposure, and previous infections.

Assess pregnancy status and possible pelvic/upper tract symptoms.

Risk determines whether empiric management is considered while testing is pending.

Slide 47 · NAAT is central for chlamydia and gonorrhea

When cervicitis is suspected, assess for C. Trachomatis and N. Gonorrhoeae.

Use appropriate nucleic acid amplification testing (NAAT) specimens.

Do not infer pathogen identity from a nonspecific inflammatory infiltrate.

Clinical cervicitis

CT/NG NAAT

Pathogen-directed assessment

Slide 48 · Assess overlapping vaginal infections

CDC recommends evaluation for bacterial vaginosis and trichomoniasis in cervicitis.

Wet-mount microscopy has limited sensitivity for trichomoniasis.

If symptomatic and wet mount is negative, additional testing may be needed.

Slide 49 · Cervicitis can signal upper tract disease

The cervix is continuous with the uterus and fallopian tubes.

Ascending infection may cause endometritis or salpingitis.

Pelvic pain, tenderness, or fever requires assessment beyond the cervix.

Endocervix

Uterine cavity

Fallopian tubes

Potential ascending route — schematic

Slide 50 · Pelvic inflammatory disease: Clinical context

PID as ascending infection of the upper female genital tract.

The syndrome may involve pelvic pain, adnexal tenderness, fever, and discharge.

Its significance exceeds that of isolated mild cervical inflammation.

Slide 51 · Reproductive and pregnancy relevance

Important cervical pathogens can spread beyond their initial site.

Associations with upper tract disease and pregnancy complications.

This is one reason to identify transmissible cervical infections rather than labeling all inflammation nonspecific.

Cervical infection

Possible ascending spread

Upper tract / pregnancy implications

Slide 52 · Persistent cervicitis: Consider M. Genitalium

CDC considers M. Genitalium testing in persistent or recurrent cervicitis in selected patients.

Evaluate re-exposure and adherence before assuming resistance or an unusual organism.

A persistent syndrome should prompt a structured reassessment.

Slide 53 · Not every genital mycoplasma merits testing

Potentially actionable

M. Genitalium may be considered in persistent/recurrent disease.

Clinical context and validated tests are essential.

An organism is not automatically causal because it is detectable.

Routine testing discouraged

CDC does not recommend routine testing for Ureaplasma species or M. Hominis in cervicitis.

This limits indiscriminate microbial panels.

Distinguish carriage from disease.

Slide 54 · A structured cervicitis evaluation

Localize inflammation at the cervix by examination.

Test for common treatable infections and evaluate overlapping vaginitis.

Screen for clinical features suggesting PID; Revisit other diagnoses if persistent.

Cervical exudate and/or easy bleeding

Assess STI risk, vaginal symptoms, pelvic signs

CT/NG NAAT + BV/TV evaluation

Pelvic pain / tenderness?

Assess PID

Reassess results, clinical response, alternate causes

Slide 55 · A polyp can explain cervical bleeding

Endocervical polyp

Benign exophytic lesion from the cervical canal.

May produce irregular spotting or bleeding.

Fibrous stroma with endocervical glandular covering.

Cervicitis

Inflammatory disorder, often without a mass.

May cause contact bleeding and exudate.

Infection assessment guided by examination and risk.

Slide 56 · Persistent symptoms require a wider differential

Consider reinfection, untreated co-infection, or treatment failure.

Reassess bacterial vaginosis and other local conditions.

Gynecologic assessment may be appropriate for cervical polyps, dysplasia, or other noninfectious causes.

Slide 57 · Etiology, findings, and next investigation

Question

Clue

Approach

Cervicitis?

Exudate / friability

Localize clinically

Chlamydia or gonorrhea?

Exposure / clinical suspicion

CT/NG NAAT

Vaginal co-diagnosis?

Discharge / irritation

BV / Trichomonas evaluation

Upper tract involvement?

Pelvic pain / tenderness / fever

Assess PID urgently

Slide 58 · Case 1: Friable cervix without symptoms

An asymptomatic patient has sustained endocervical bleeding after gentle swabbing. No specific organism has been identified.

What clinical finding has been demonstrated?

Does the finding establish the etiology?

Which common STIs merit testing?

Interpretation: Endocervical friability supports cervicitis. It is not organism-specific; Assess for chlamydia and gonorrhea with NAAT in context.

Slide 59 · Case 2: Elevated vaginal pH

A patient has altered vaginal pH after recent antibiotic therapy and new discharge, but no documented endocervical inflammation.

What ecological mechanism is plausible?

Can cervical infection be diagnosed from pH alone?

What competing vaginal disorders should be considered?

Interpretation: Disruption of lactobacilli may increase pH and permit overgrowth. Vaginal pH alone does not diagnose cervicitis; Assess for vaginitis/BV and cervical findings.

Slide 60 · Case 3: Atypical squamous cells with inflammation

A cervical cytology sample is reported as inflammatory, with reactive-appearing atypical squamous cells.

How can marked inflammation affect epithelium?

Does inflammation prove an STI?

Can a significant lesion be dismissed on this basis?

Interpretation: Inflammation can cause reparative/reactive changes. Cytologic atypia neither identifies infection nor eliminates the need for appropriate neoplasia assessment.

Slide 61 · Case 4: Cervicitis plus pelvic tenderness

A patient with cervical discharge also reports pelvic pain and has adnexal tenderness.

Does isolated cervicitis explain the entire presentation?

Which anatomic pathway is concerning?

What broader syndrome must be assessed?

Interpretation: Ascending infection must be considered; Assess for pelvic inflammatory disease with possible endometritis/salpingitis.

Slide 62 · The diagnostic contrasts that matter

Entity

Predominant site

Discriminating focus

Cervicitis

Cervix

Endocervical exudate / friability

Vaginitis

Vagina

Vaginal symptoms and organism assessment

PID

Upper genital tract

Pain, tenderness, systemic findings

Endocervical polyp

Endocervical canal

Exophytic lesion / spotting

Cervical SIL

Cervical epithelium

Separate neoplastic cytology/histology pathway

Slide 63 · Integrated pathology summary

An estrogen-dependent, glycogen-rich squamous mucosa supports vaginal lactobacilli and acidity.

Microbial imbalance and defined pathogens may produce cervical inflammation; Significance varies widely.

Marked inflammation can trigger epithelial repair and atypical Pap appearances.

Clinical signs, pathogen-specific tests, and upper tract assessment determine management relevance.

Slide 64 · References and source distinctions

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. (2026). Chapter 22, The Female Genital Tract; cervical anatomy and cervicitis, pp. 904–905; infections/PID, pp. 897–899.

Centers for Disease Control and Prevention. Sexually Transmitted Infections Treatment Guidelines (2021): Urethritis and Cervicitis. https://www.cdc.gov/std/treatment-guidelines/urethritis-and-cervicitis.htm

Diagrams are original native PowerPoint schematics; histologic cell drawings are illustrative, not specimen images.