Upper Airways Inflammatory Lesions

Slide 1 · Upper Airways

Inflammatory Lesions

Pharyngitis • Tonsillitis • Poststreptococcal pathology

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Distinguish viral from bacterial patterns of pharyngeal inflammation.

Explain tonsillar enlargement, crypt exudates, and pseudomembranes.

Connect group A streptococcal pharyngitis to systemic sequelae.

Apply morphology and etiology to differential diagnosis.

Slide 3 · Nasopharyngeal inflammation: The scope

Microbial exposure

Pharyngeal mucosal response

Tonsillar and nodal reaction

Local or systemic consequences

The same infection can produce mucosal, tonsillar and regional lymph-node findings.

Slide 4 · The connected mucosal–lymphoid unit

Pharyngeal mucosa

Inflammatory erythema and edema

Palatine tonsils

Reactive lymphoid enlargement

Regional nodes

Reactive enlargement

Schematic — three sites can respond to the same respiratory infection.

Slide 5 · Pharyngitis: Mucosal involvement

Inflammation affects pharyngeal mucosa during respiratory infection.

The visible tissue response includes erythema and edema.

Adjacent lymphoid tissue commonly responds with enlargement.

Slide 6 · Tonsillitis: Lymphoid-tissue involvement

Tonsils enlarge during a reactive inflammatory response.

Bacterial infection may add crypt-centered exudation.

Pharyngeal mucosal findings and tonsillar findings often coexist.

Slide 7 · Two major infectious patterns

Viral pattern

Bacterial pattern

Most frequent context

Primary infection or superinfection

Diffuse erythema and edema

Exudate may be prominent

Reactive tonsils and nodes

Crypt-centered suppuration possible

Viral pattern

Bacterial pattern

Slide 8 · Primary and secondary bacterial infection

Viral upper respiratory infection

Inflamed pharyngeal mucosa

Superimposed bacterial infection

Exudative response

Secondary infection is one possible route; Bacteria can also initiate illness directly.

Slide 9 · Viruses dominate the etiologic list

Rhinoviruses, echoviruses, and adenoviruses are emphasized as common agents.

Influenza strains and respiratory syncytial virus account for additional cases.

The shared histologic outcome is a host mucosal inflammatory reaction.

Slide 10 · Viral agents: Named etiologic groups

Highlighted as common

Also implicated

Rhinoviruses

Influenza viruses

Echoviruses

Respiratory syncytial virus

Adenoviruses

Multiple strains and presentations

Highlighted as common

Also implicated

Slide 11 · Viral disease: Why the pharynx is red

Viral infection

Local host inflammatory response

Vascular congestion

Mucosal erythema

Visible redness represents a vascular component of the inflammatory response.

Slide 12 · Viral disease: Why mucosa swells

Local inflammation

Altered vascular permeability

Interstitial fluid accumulation

Mucosal edema

Edema is extracellular fluid accumulation within the inflamed mucosa.

Slide 13 · Erythema and edema are linked findings

Erythema

Edema

Dominant visible change: redness

Dominant visible change: swelling

Reflects vascular congestion

Reflects fluid in interstitium

Distributed over mucosa

Contributes to tissue fullness

Erythema

Edema

Slide 14 · Reactive enlargement of the tonsils

Antigenic stimulation

Reactive lymphoid response

Increased tonsillar volume

Visible tonsillar enlargement

Enlargement reflects an immune response rather than proof of a specific pathogen.

Slide 15 · Regional lymphadenopathy in pharyngitis

Pharyngeal antigen exposure

Drainage to regional nodes

Reactive lymphoid response

Enlarged nearby lymph nodes

Cervical node enlargement can accompany both viral and bacterial pharyngeal disease.

Slide 16 · Viral pattern: Integrated morphology

Original native schematic of an inflamed mucosal surface

Surface epithelium

Vascular congestion

Edematous stroma

Slide 17 · Morphology is a response, not a viral test

Several viruses can produce similar mucosal erythema and edema.

Reactive enlargement does not by itself identify the pathogen.

Etiologic classification requires more than gross morphology.

Slide 18 · Anatomy of the visible response

Pharyngeal mucosa

Inflammatory erythema and edema

Palatine tonsils

Reactive lymphoid enlargement

Regional nodes

Reactive enlargement

Schematic — three sites can respond to the same respiratory infection.

Slide 19 · Bacterial pharyngitis: Two routes

Primary bacterial disease

Secondary bacterial process

Bacteria initiate inflammation

Follows a viral infection

May cause tonsillitis directly

Superimposed inflammatory change

Exudate may develop

May accentuate exudation

Primary bacterial disease

Secondary bacterial process

Slide 20 · β-Hemolytic streptococci predominate

The upper-airway source identifies β-hemolytic streptococci as the most frequent bacterial pathogens.

Group A Streptococcus pyogenes is a key cause of streptococcal pharyngitis.

Late cardiac and renal sequelae make this infection consequential.

Slide 21 · Other bacterial causes remain possible

Staphylococcus aureus is named as another potential pathogen.

Other bacterial species can also infect the pharynx or tonsils.

An exudative surface alone does not establish bacterial species.

Slide 22 · Streptococcus pyogenes: Organism context

Group A β-hemolytic streptococcus; Gram-positive cocci in pairs or chains.

M protein protects against phagocytosis; A capsule also contributes to immune evasion.

The organism causes both local suppurative disease and postinfectious immune syndromes.

Slide 23 · Streptococcal immune evasion

Capsule and surface M protein

Reduced efficient phagocytosis

Persistence during local infection

Host neutrophilic response

Immune-evasion factors make streptococcal persistence biologically plausible.

Slide 24 · C5a peptidase: Another virulence factor

Streptococcal C5a peptidase

Degradation of C5a

Reduced complement-mediated chemotaxis

Altered early leukocyte recruitment

Degradation of C5a affects recruitment signals and should not be confused with bacterial invasion.

Slide 25 · Streptococcal infection can be suppurative

Diffuse neutrophilic inflammation in streptococcal infection.

Pharyngeal lesions can feature punctate abscesses of tonsillar crypts.

Cervical lymphadenopathy may accompany the local process.

Slide 26 · The tonsillar crypt is a key locus

Schematic — crypt lumen and underlying reactive lymphoid tissue

Crypt exudate

Reactive lymphoid tissue

Slide 27 · Why tonsillar exudate becomes visible

Bacterial inflammatory stimulus

Neutrophilic recruitment

Exudate in tonsillar crypts

Surface puncta or coating

Puncta on the tonsil reflect exudate reaching the crypt openings.

Slide 28 · Exudate may coat multiple surfaces

Inflammatory material may be found on nasopharyngeal mucosa.

Enlarged nasopalatine and palatine tonsils may also be covered.

A visible coating should be interpreted within its anatomic distribution.

Slide 29 · Follicular tonsillitis: Recognizable pattern

The tonsils are enlarged by reactive lymphoid hyperplasia.

Exudate emerging from crypts creates discrete surface dots.

The term describes the visible architecture of a tonsillar reaction.

Slide 30 · Tonsillar enlargement and crypt exudate

Schematic — crypt lumen and underlying reactive lymphoid tissue

Crypt exudate

Reactive lymphoid tissue

Slide 31 · Reactive follicles are not surface exudate

Tonsillar follicular response

Crypt exudate

Reactive lymphoid hyperplasia

Inflammatory material in crypt lumen

Contributes to enlargement

Appears as punctate surface dots

Within lymphoid tissue

May accompany bacterial disease

Tonsillar follicular response

Crypt exudate

Slide 32 · The term “follicular tonsillitis”

The clinical designation refers to a dotted, exudative tonsillar appearance.

Underlying lymphoid hyperplasia contributes to organ enlargement.

Crypt-centered surface changes should not be mistaken for lymphoid follicles themselves.

Slide 33 · Pseudomembranes: A pattern, not a diagnosis

“exudative membranes (pseudomembranes)” for some bacterial pharyngitides.

A membrane-like coating can have different causes and mechanisms.

Diphtheria warrants particular distinction when a tough membrane is present.

Slide 34 · Membranous inflammation: Two examples

Nonspecific bacterial exudation

Diphtheria

Coating may form on tonsils or mucosa

Toxin-induced epithelial necrosis

Source does not assign a specific toxin

Tough fibrinosuppurative membrane

Etiology remains to be determined

May cause local bleeding and systemic toxicity

Nonspecific bacterial exudation

Diphtheria

Slide 35 · Diphtheria as an important mimic

Corynebacterium diphtheriae can infect the pharynx and adjacent airway.

A dense fibrinosuppurative exudate overlies damaged epithelium.

Its characteristic tough membrane is a higher-risk pattern than ordinary exudation.

Slide 36 · Diphtheritic membrane: Pathogenesis

C. Diphtheriae colonization

Exotoxin-mediated epithelial injury

Fibrinosuppurative exudate

Tough adherent pseudomembrane

The membrane is the product of tissue necrosis plus fibrinosuppurative exudation.

Slide 37 · Why diphtheria cannot be treated as ordinary exudate

Sloughing of its vascularized underlying bed can cause bleeding.

Upper-airway obstruction or asphyxiation may follow.

Systemically distributed toxin can injure the heart and peripheral nerves.

Slide 38 · Infectious mononucleosis: Exudative mimic

Acute pharyngitis and tonsillitis with a gray-white exudative coating.

Associated findings include cervical lymph-node enlargement and palatal petechiae.

The overlap reinforces that exudate is not etiologically specific.

Slide 39 · Exudative pharyngitis: Pattern differential

Streptococcal pharyngitis

Infectious mononucleosis

Diphtheria

Crypt abscesses / tonsillar exudate

Gray-white tonsillar coating

Tough, dirty pseudomembrane

Cervical nodes may enlarge

Cervical lymphadenopathy

Toxin-mediated mucosal necrosis

Postinfectious sequelae matter

Palatal petechiae described

Risk of obstruction/systemic toxicity

Streptococcal pharyngitis

Infectious mononucleosis

Diphtheria

Slide 40 · The diagnostic question is etiologic

Clinical and mucosal pattern

Consider viral and bacterial causes

Use organism-directed tests when indicated

Interpret systemic implications

Gross features are insufficient to name the cause in many cases.

Slide 41 · Streptococcal laboratory confirmation

The infectious-disease chapter names throat culture as a diagnostic method.

Rapid streptococcal antigen testing is also described for pharyngitis.

Neither reactive tonsillar enlargement nor exudation alone identifies S. Pyogenes.

Slide 42 · What pathology can and cannot establish

Morphology supports

Morphology alone cannot establish

Inflammation is present

Exact virus or bacterial species

Crypt-centered suppuration

Risk of later immune sequelae

Reactive lymphoid enlargement

Need for organism-specific confirmation

Morphology supports

Morphology alone cannot establish

Slide 43 · Airway compromise is a local complication

Severe pharyngeal infection can produce marked swelling.

Peritonsillar or retropharyngeal abscess formation may further narrow the airway.

The anatomic extent of inflammation matters beyond the initiating pathogen.

Slide 44 · Local complication pathway

Severe pharyngeal infection

Peritonsillar or retropharyngeal abscess

Additional tissue swelling

Possible airway encroachment

Airway risk rises with the combination of inflammatory swelling and abscess location.

Slide 45 · Recurrent tonsillitis and enlargement

Whether repeated acute tonsillitis causes chronic tonsillar enlargement remains debated.

Chronic tonsillar size cannot automatically be attributed to recurrence.

Surgical excision may benefit selected patients despite this uncertainty.

Slide 46 · Inflammatory enlargement versus causation

Observed finding

Causal claim requiring caution

The tonsil is enlarged

Repeated infections necessarily drive chronic hypertrophy

Reactive lymphoid hyperplasia may be present

Robbins explicitly identifies uncertainty

The enlargement is clinically relevant

Do not present causation as established

Observed finding

Causal claim requiring caution

Slide 47 · Why streptococcal sore throat matters

Group A streptococcal pharyngitis

Host immune response after infection

Possible cardiac consequences

Possible glomerular consequences

The local infection can be followed by organ injury after the organism has cleared.

Slide 48 · Two pathways beyond the infected pharynx

Rheumatic fever

Poststreptococcal GN

Immune cross-reactivity to host proteins

Antistreptococcal immune complexes

Often begins weeks after pharyngitis

Can follow pharyngeal or skin infection

Can produce carditis and later valve scarring

Glomerular inflammation follows

Rheumatic fever

Poststreptococcal GN

Slide 49 · Acute rheumatic fever is postinfectious

Robbins characterizes it as an immunologically mediated multisystem inflammatory disease.

It classically follows group A streptococcal pharyngitis after a delay of weeks.

The cardiac lesions are immune-mediated rather than bacterial colonization.

Slide 50 · Rheumatic fever: Molecular mimicry

Group A streptococcal M protein

Cross-reactive antibodies and CD4+ T cells

Recognition of cardiac antigens

Inflammatory cardiac injury

This pathway involves immune recognition of host cardiac antigens.

Slide 51 · Rheumatic carditis: Tissue mechanism

Antibody binding can activate complement and recruit Fc receptor–bearing leukocytes.

Stimulated T cells release cytokines that activate macrophages.

These combined processes produce cardiac inflammation in the absence of organisms.

Slide 52 · Aschoff bodies: The cardiac lesion

Focal myocardial inflammatory lesions contain T lymphocytes and activated macrophages.

Anitschkow cells show elongated, ribbon-like nuclear chromatin.

The lesion links a preceding throat infection to an immune-mediated cardiac process.

Slide 53 · Healing may produce chronic valve disease

Acute rheumatic inflammation

Resolution with healing and scarring

Fibrous valve deformity

Chronic rheumatic heart disease

Fibrotic healing, not ongoing infection in the valve, explains deformity.

Slide 54 · Poststreptococcal GN is immune-complex mediated

Streptococcal antigens and antibodies form pathogenic immune complexes.

Complement activation and leukocyte recruitment damage glomeruli.

The disease is a late inflammatory complication, not direct bacterial invasion of glomeruli.

Slide 55 · Glomerulonephritis: The latent interval

Streptococcal pharyngeal infection

Antigen-specific antibody response

Formation/deposition of immune complexes

Acute glomerular inflammation

Delayed onset supports time required for antigen–antibody responses.

Slide 56 · Poststreptococcal GN: Diagnostic mechanism

A latency of approximately 1–4 weeks after infection.

Serum complement may be reduced by complement consumption.

Granular glomerular immune deposits support an immune-complex process.

Slide 57 · Immune aftermath: Comparison

Rheumatic fever

Poststreptococcal GN

M-protein cross-reactivity

Microbial antigen–antibody complexes

Targets cardiac tissues

Targets renal glomeruli

May heal with fibrotic valve damage

Inflammation with complement consumption

Rheumatic fever

Poststreptococcal GN

Slide 58 · Case 1: Diffusely inflamed pharynx

A patient with an acute upper respiratory illness has pharyngeal erythema, edema, and enlarged regional lymph nodes.

Which broad infectious pattern is common?

What can gross morphology identify—and what cannot it identify?

Discussion prompts; Suggested interpretation is in the presenter notes.

Slide 59 · Case 2: Punctate tonsillar exudates

The tonsils are enlarged and show scattered pale dots emerging at the crypt openings.

Name the tonsillar morphology.

Explain separately the cause of enlargement and of the surface dots.

Discussion prompts; Suggested interpretation is in the presenter notes.

Slide 60 · Case 3: Sore throat followed by carditis

Several weeks after a streptococcal throat infection, a patient develops inflammatory cardiac disease.

Which delayed complication is relevant?

What makes the cardiac injury immunologic rather than locally bacterial?

Discussion prompts; Suggested interpretation is in the presenter notes.

Slide 61 · Case 4: Nephritis after infection

A child develops acute glomerular inflammation in the weeks following a pharyngeal streptococcal infection.

Identify the postinfectious process.

What immune deposits and complement findings support its pathogenesis?

Discussion prompts; Suggested interpretation is in the presenter notes.

Slide 62 · Synthesis: Local lesion → systemic meaning

Mucosal erythema and edema

Reactive and exudative tonsillar changes

Identify important pathogens

Recognize local and immune complications

Observe the lesion, identify the etiology when necessary, and separate local from delayed complications.

Slide 63 · Ten high-yield discriminators

Viral pharyngitis is common; Erythema, edema, and reactive lymphadenopathy predominate.

Bacterial tonsillitis may cause crypt-centered exudate and pseudomembranes.

Follicular tonsillitis combines lymphoid hyperplasia with punctate crypt exudate.

Streptococcal infection can precede rheumatic fever or glomerulonephritis.

Slide 64 · Primary textbook and correlated chapters

Robbins, Cotran & Kumar: Pathologic Basis of Disease, 11th ed. (2026).

Chapter 16, Head and Neck: Nasopharynx; Inflammatory Lesions, p. 673.

Chapter 8, Infectious Diseases: streptococci and diphtheria.

Chapter 12, Heart: rheumatic fever; Chapter 20, Kidney: postinfectious GN.