Streptococcal and Enterococcal Infections

Slide 1 · Streptococcal and Enterococcal Infections

Mechanisms · Morphology · Clinicopathologic correlations

Streptococci and enterococci: distinct pathogens, overlapping lesions

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Classify clinically important streptococci and enterococci by disease setting.

Connect virulence factors with inflammatory and immune-mediated injury.

Recognize characteristic tissue reactions, complications, and diagnostic clues.

Explain enterococcal persistence and vancomycin resistance.

Slide 3 · The organisms: A clinicopathologic map

Organism

Major disease context

Dominant theme

S. pyogenes (group A)

Pharyngitis; skin disease; postinfectious syndromes

Toxin, phagocyte evasion, autoimmunity

S. agalactiae (group B)

Chorioamnionitis; neonatal sepsis/meningitis

Maternal–neonatal infection

S. pneumoniae

Pneumonia; meningitis

Capsule and pneumolysin

Viridans / S. mutans

Endocarditis; dental caries

Oral flora and plaque

Enterococcus spp.

Healthcare-associated UTI; bacteremia; endocarditis

Persistence and antibiotic resistance

Slide 4 · Gram-positive cocci: Arrangement is a clue, not a species ID

Pairs

Chains

Shared Gram-positive coccal morphology

Schematic — not an authentic clinical or histologic specimen

Streptococci and enterococci grow as cocci in pairs or chains.

Enterococci can resemble streptococci on routine morphology.

Culture and organism identification establish the etiology.

Slide 5 · Hemolysis and antigens organize the streptococci

Group

Organisms

Teaching implication

β-hemolytic; group A

S. pyogenes

Pharyngitis, scarlet fever, skin infection

β-hemolytic; group B

S. agalactiae

Maternal colonization; neonatal infection

α-hemolytic

S. pneumoniae

Encapsulated pneumonia and meningitis

α- or nonhemolytic

Viridans streptococci

Oral flora; infective endocarditis

Slide 6 · Same broad morphology, different clinical niches

Bacterial group

Source or niche

Illustrative consequence

Group A streptococci

Oropharynx and skin disease

Acute suppuration; immune sequelae

Group B streptococci

Female genital tract

Pregnancy and neonatal infection

Pneumococcus

Respiratory tract

Consolidating pneumonia; meningitis

Viridans streptococci

Oral microbiota

Endocarditis; dental plaque

Enterococci

Gut commensals

Healthcare-associated UTI and invasive infection

Slide 7 · Two mechanisms of disease must be separated

Acute bacterial infection

Host inflammatory response

Tissue injury / dysfunction

Postinfectious rheumatic fever and glomerulonephritis instead follow immune responses to prior streptococcal infection.

Slide 8 · Virulence factors linked to injury

Organism

Factor

Consequences

S. pyogenes

Capsule; M protein; C5a peptidase

Impaired phagocytosis / recruitment

S. pyogenes

Pyrogenic exotoxin

Fever and scarlet-fever rash

S. pneumoniae

Capsule; pneumolysin

Resistance to phagocytosis; cell lysis

S. mutans

Acid + glucans

Enamel demineralization; bacterial plaque

Enterococci

Capsule, biofilm, enzymes

Persistence and host tissue injury

Slide 9 · Capsules impair phagocyte clearance

Capsular barrier

Phagocyte

Encapsulation → less efficient engulfment

Schematic — not an authentic clinical or histologic specimen

Capsules are present in S. Pyogenes, S. Agalactiae, and S. Pneumoniae.

Antiphagocytic surface protection favors persistence despite host defenses.

The pneumococcal capsule is its principal virulence factor.

Slide 10 · S. Pyogenes M protein: Surface-mediated evasion

M protein at surface

Reduced phagocytosis

Bacterial survival

M-protein–directed adaptive immunity also links prior group A infection to rheumatic heart disease.

Slide 11 · C5a peptidase blunts neutrophil recruitment

Bacterial C5a peptidase

Degradation of C5a

Less chemotactic signaling

C5a is a complement-derived chemoattractant; Its degradation weakens early inflammatory recruitment.

Slide 12 · A toxin-mediated syndrome: Scarlet fever

S. Pyogenes pharyngitis

Phage-encoded pyrogenic exotoxin

Fever + characteristic rash

The rash is a toxin-associated manifestation, not simply a map of bacteria spreading through skin.

Slide 13 · Mechanism predicts phenotype

Mechanistic pattern

Characteristic example

Pathologic interpretation

Antiphagocytic surface

Capsule and M protein

Persistent viable bacteria

Toxin-related

Pyrogenic exotoxin

Fever and rash

Direct destructive infection

Necrotizing fasciitis

Rapidly progressive soft-tissue necrosis

Postinfectious immune injury

Rheumatic fever / GN

Disease after preceding infection

Slide 14 · Group A streptococcus: Disease spectrum

Oropharyngeal infection: Pharyngitis with possible suppurative extension.

Skin infection: Impetigo and erysipelas with a neutrophilic tissue reaction.

Toxin-associated disease: Scarlet fever and toxic shock syndrome.

Severe invasive phenotype: Rapidly progressive necrotizing fasciitis.

Slide 15 · Most streptococcal lesions are diffusely neutrophilic

Epidermis

Dermis

Subcutis

Diffuse interstitial neutrophils

Schematic — not an authentic clinical or histologic specimen

Typical pattern: Interstitial neutrophils and tissue edema.

Compared with destructive abscess-forming patterns, necrosis is often limited.

Virulent necrotizing fasciitis is an important exception.

Slide 16 · Erysipelas: The clinical boundary matters

Rapidly spreading erythematous swelling, often involving the face.

A sharp, well-demarcated, serpiginous edge is characteristic.

Facial disease may produce a bilateral “butterfly” distribution.

Extremity or truncal involvement is also described.

Slide 17 · Erysipelas: Superficial tissue reaction

Epidermis

Dermis

Subcutis

Inflamed upper skin

Schematic — not an authentic clinical or histologic specimen

Diffuse edema and neutrophilic inflammation involve dermis and epidermis.

Inflammation can extend into subcutaneous tissue.

Microabscesses may occur; Overt necrosis is generally minor.

Slide 18 · Erysipelas morphology from cause to appearance

Streptococcal skin infection

Dermal edema + neutrophils

Red, raised, sharply bounded swelling

The outline of erythema is a clinical clue; The tissue response explains swelling and warmth.

Slide 19 · Skin manifestations: Shared versus exceptional features

Feature

Typical streptococcal lesion

Necrotizing fasciitis

Inflammatory cells

Interstitial neutrophils

Severe invasive inflammation

Tissue destruction

Usually relatively limited

Rapidly progressive tissue necrosis

Clinical pattern

Impetigo / erysipelas

Rapidly progressive soft-tissue disease

Interpretive caution

Surface appearance may mimic staph

Do not extrapolate “minor necrosis”

Slide 20 · Impetigo and skin infection: Avoid morphology alone

Overlap between streptococcal and staphylococcal skin lesions.

Shared appearances do not establish the microbiologic species.

Use an organism-directed diagnostic approach when etiology matters.

Slide 21 · Streptococcal pharyngitis: Gross features

Edema and swelling in the oropharyngeal region.

Punctate suppurative foci in the tonsillar crypts.

Cervical lymphadenopathy may accompany the infection.

Marked swelling can threaten airway patency.

Slide 22 · Tonsillar crypt abscesses: Focal pus within inflammation

Tonsillar crypt

Punctate crypt exudate

Schematic — not an authentic clinical or histologic specimen

Punctate abscesses form in the tonsillar crypts.

Local edema and lymphoid reactivity can enlarge tonsils.

The site of the inflammatory exudate explains focal pale spots.

Slide 23 · Anatomic progression can threaten the airway

Pharyngitis / swelling

Peritonsillar or retropharyngeal abscess

Airway encroachment

Severe pharyngeal swelling is important because obstruction is a structural complication, not just pain.

Slide 24 · Scarlet fever: Clinical distribution

Occurs in association with S. Pyogenes pharyngitis.

Punctate erythematous rash favors the trunk and inner limbs.

Facial involvement with relative circumoral pallor is characteristic.

During recovery, skin may become scaly and hyperkeratotic.

Slide 25 · Scarlet fever: Localization of the rash

Trunk: Prominent punctate rash

Inner limbs: Involved

Around mouth: Relatively spared

Schematic — not an authentic clinical or histologic specimen

A generalized toxin-associated eruption is most prominent over trunk and proximal limbs.

Relative sparing around the mouth creates circumoral pallor.

Desquamation occurs as fever subsides.

Slide 26 · Erysipelas and scarlet fever are not the same rash

Feature

Erysipelas

Scarlet fever

Primary setting

Localized skin infection

Associated with GAS pharyngitis

Distribution

Sharply bounded expanding plaque

Diffuse punctate eruption

Histopathology

Edematous neutrophilic dermatitis

Rash attributed to pyrogenic exotoxin

Characteristic clue

Serpiginous edge

Circumoral pallor / later scaling

Slide 27 · Necrotizing fasciitis: The severe invasive phenotype

Some highly virulent S. Pyogenes strains cause rapidly progressive fascial infection.

Necrosis—not merely a dense neutrophilic infiltrate—defines the danger.

Clinical progression may far exceed the apparent initial surface findings.

Slide 28 · Why immune sequelae appear after infection

Group A infection

Development of specific immunity

Cross-reactivity or immune complexes

A temporal gap and a second pathogenic mechanism distinguish postinfectious disease from local suppuration.

Slide 29 · Rheumatic fever: Molecular mimicry

Group A M protein

Cross-reactive antibody / T cell

Cardiac antigen recognition

Immune-mediated injury without myocardial bacteria

Schematic — not an authentic clinical or histologic specimen

Antibodies and CD4+ T cells against streptococcal M proteins recognize cardiac antigens.

Complement and recruited immune cells produce cardiac inflammation.

Bacteria are absent from the rheumatic cardiac lesions.

Slide 30 · Rheumatic fever follows an immune-response interval

Group A infection

About 2–3 weeks

Acute rheumatic inflammatory disease

The latency is compatible with time needed to mount cross-reactive adaptive immune responses.

Slide 31 · Aschoff bodies: The signature cardiac lesion

Activated macrophages + lymphocytes

Schematic — not an authentic clinical or histologic specimen

A focal aggregate contains T lymphocytes and activated macrophages.

Anitschkow cells display a central ribbon-like (“caterpillar”) nuclear chromatin pattern.

The lesion reflects immune-mediated myocardial inflammation, not bacterial colonies.

Slide 32 · Rheumatic carditis spans three heart layers

Site

Acute inflammatory consequence

Pericardium

Pericarditis

Myocardium

Myocarditis and Aschoff bodies

Endocardium / valves

Valvulitis, fibrinoid necrosis, small verrucae

Slide 33 · Chronic rheumatic disease: Scarring reshapes valves

Acute valvulitis

Healing with fibrosis

Leaflet thickening · commissural fusion · chordal shortening

Schematic — not an authentic clinical or histologic specimen

Mitral leaflets thicken and commissures fuse.

Chordae tendineae shorten, thicken, and may fuse.

Valve deformity produces chronic dysfunction, especially mitral stenosis.

Slide 34 · Endocarditis has two different streptococcal contexts

Feature

Poststreptococcal rheumatic valvulitis

Infective endocarditis

Driver

Cross-reactive host immunity

Microbial colonization of valve

Organisms within lesion

Absent

Present in infective vegetation

Main morphologic clue

Small verrucae and later fibrosis

Friable, potentially destructive vegetation

Example

Group A postinfectious disease

Viridans streptococci / enterococci

Slide 35 · Poststreptococcal glomerulonephritis: Immune complexes

Streptococcal antigen + antibody

Glomerular immune deposits

Complement + leukocyte injury

The disease is postinfectious: Immune-mediated glomerular inflammation follows pharyngeal or skin infection.

Slide 36 · Poststreptococcal GN: Timing and setting

Typically appears 1–4 weeks after a throat or skin infection.

Occurs most frequently in childhood but may affect other age groups.

The lag is consistent with antibody production and immune-complex formation.

Slide 37 · Postinfectious GN: A glomerular morphologic triad

Glomerular capillary loops + deposits

Schematic — not an authentic clinical or histologic specimen

Light microscopy: Diffuse endocapillary proliferation and leukocyte infiltration.

Immunofluorescence: Granular IgG/C3 pattern.

Electron microscopy: Characteristic subepithelial humps.

Slide 38 · Immune injury: Distinguish rheumatic fever from GN

Feature

Rheumatic fever

Poststreptococcal GN

Major target

Heart (including valves)

Glomeruli

Dominant immune mechanism

Cross-reactive antibodies and T cells

Immune complexes

Morphology

Aschoff bodies; valvulitis

Proliferative GN; granular deposits

Persistent bacterial invasion

No

No required glomerular infection

Slide 39 · Nephritic syndrome connects pathology to symptoms

Inflamed glomerular capillary loops lead to hematuria and red-cell casts.

Glomerular injury may produce proteinuria and edema.

Fluid retention and altered renal hemodynamics contribute to hypertension.

Slide 40 · Group B streptococcus: The obstetric reservoir

S. Agalactiae is a group B streptococcus.

It colonizes the female genital tract.

During pregnancy, ascending infection may cause chorioamnionitis.

Neonatal sepsis and meningitis are major clinical consequences.

Slide 41 · Group B disease may affect mother or neonate

Female genital tract colonization

Maternal chorioamnionitis

Neonatal sepsis / meningitis

Distinct maternal and neonatal syndromes

Schematic — not an authentic clinical or histologic specimen

Female genital tract carriage is the maternal reservoir.

Maternal chorioamnionitis and neonatal invasive disease are distinct outcomes.

Neonatal sepsis and meningitis are especially important presentations.

Slide 42 · Group B streptococcus: Capsule and invasive disease

Capsular barrier

Phagocyte

Encapsulation → less efficient engulfment

Schematic — not an authentic clinical or histologic specimen

S. Agalactiae has an antiphagocytic capsule.

A vulnerable neonatal host may develop disseminated infection.

Clinical setting and identification both matter: Appearance is not enough.

Slide 43 · Group A versus group B: Clinical discrimination

Feature

S. pyogenes (A)

S. agalactiae (B)

Representative source

Pharynx / skin infections

Female genital tract carriage

Typical context

Pharyngitis, erysipelas, scarlet fever

Chorioamnionitis; neonatal sepsis

Shared virulence

Antiphagocytic capsule

Antiphagocytic capsule

Distinct late sequelae

Rheumatic fever / PSGN

Not emphasized in the source

Slide 44 · Pneumococcus: Capsule plus pneumolysin

Capsular barrier

Phagocyte

Pneumolysin → host-cell lysis

Schematic — not an authentic clinical or histologic specimen

The capsule is the principal pneumococcal virulence factor.

Pneumolysin inserts into membranes and lyses host cells.

The combination promotes persistence and tissue damage.

Slide 45 · Pneumolysin amplifies the inflammatory injury

S. Pneumoniae in lung

Membrane injury by pneumolysin

Increased parenchymal damage

The toxin is distinct from the antiphagocytic effect of the polysaccharide capsule.

Slide 46 · Pneumococcal pneumonia: An alveolar exudate

S. Pneumoniae is a major cause of community-acquired acute pneumonia.

Bacterial invasion fills alveolar spaces with inflammatory exudate.

Accumulation of alveolar exudate causes airspace consolidation.

Slide 47 · Lobar consolidation: Why the lung becomes solid

Air space

Exudate / consolidation

Air replaced by inflammatory material

Schematic — not an authentic clinical or histologic specimen

Normal alveolar spaces are air-filled.

Acute bacterial exudate replaces air with neutrophils and protein-rich fluid.

Confluent involvement produces a consolidated lung region.

Slide 48 · Pneumococcal diagnosis: Sample and inference

Test / finding

Interpretation

Limitation

Sputum Gram stain

Lancet-shaped gram-positive diplococci with neutrophils

Airway colonization can confound

Blood culture

A specific invasive-disease clue when positive

Insensitive early in some cases

Clinical / radiology

Identifies pneumonia syndrome

Alone cannot reliably define organism

Slide 49 · Host vulnerability to encapsulated pneumococci

Defective or absent splenic function increases susceptibility to encapsulated bacteria.

Extremes of age, chronic illnesses, and immunodeficiency predispose to pneumonia.

An antiphagocytic capsule explains the importance of host clearance mechanisms.

Slide 50 · Pneumococcal prevention targets the capsule

Pneumococcal vaccines include polysaccharide and conjugate formulations.

Vaccines are recommended for young children, older adults, and selected risk groups.

Capsule-directed immunity reduces vulnerability to invasive pneumococcal infection.

Slide 51 · Pneumococcus also causes meningitis

S. Pneumoniae causes meningitis in children and adults.

Clinical presentation and the site of infection define the diagnostic workup.

A single organism can cause both pulmonary and central nervous system disease.

Slide 52 · Viridans streptococci: Oral residents, valvular pathogens

The viridans group comprises α-hemolytic and nonhemolytic streptococci.

They are normal components of oral microbiota.

They are a common cause of infective endocarditis.

Slide 53 · Infective endocarditis: Vegetations differ from scarring

Attached infective vegetation

Simplified valve surface — not an anatomical cross-section

Schematic — not an authentic clinical or histologic specimen

Viridans endocarditis can produce large, friable valve vegetations.

The lesion is microbial and potentially embolic.

It is not synonymous with sterile rheumatic verrucae.

Slide 54 · Valve infection generates systemic hazards

Infected valve vegetation

Valvular dysfunction / embolization

Sepsis and organ injury

The heart-valve lesion creates both local mechanical disease and distant infectious consequences.

Slide 55 · Infective endocarditis: Clinicopathologic diagnosis

Evidence combines microbiology with valve/implant imaging and examination.

Repeated blood cultures and anatomic evidence support the diagnosis.

Embolic and immunologic phenomena provide additional clues.

Slide 56 · S. Mutans: The metabolic pathway to dental caries

Sucrose fermentation

Lactic acid production

Enamel demineralization

Acid production is a direct biochemical route from oral carbohydrate metabolism to tooth destruction.

Slide 57 · S. Mutans: Glucans stabilize dental plaque

High-molecular-weight glucans

Bacterial aggregation

Plaque retention

Glucan-mediated adherence and acid production reinforce the cariogenic niche.

Slide 58 · Two viridans-related clinical pathways

Context

S. mutans caries

Viridans endocarditis

Setting

Tooth surface; oral plaque

Heart valve

Key mechanism

Acid + glucan biofilm matrix

Valve colonization with vegetations

Main damage

Demineralization of enamel

Valve dysfunction and embolism

Slide 59 · Enterococci: Commensals with invasive potential

Enterococci normally inhabit the gut.

E. Faecalis and E. Faecium are the main clinical species.

They produce urinary, wound, intraabdominal, bloodstream, and valve infections.

Pairs or chains do not reliably separate them from streptococci.

Slide 60 · Enterococcal clinical burden: Interpret context

Setting

Clinical significance

Hospital-associated UTI

Enterococci are major nosocomial uropathogens

Bloodstream infection

Bacteremia may have serious outcomes

Infective endocarditis

A significant cause of valve infection

Immunosuppressed hosts

Increased risk, particularly after transplantation

Slide 61 · Enterococcal biofilm: Persistence on a surface

Adherent bacterial community

Surface

Schematic — not an authentic clinical or histologic specimen

An antiphagocytic capsule contributes to biofilm formation.

Adherent communities support persistent colonization.

Tissue-damaging enzymes contribute to host injury.

Slide 62 · Transplant recipients: Converging infection risks

Immunosuppression

Frequent antibiotics

Altered gut microbiota

Higher enterococcal infection risk

Schematic — not an authentic clinical or histologic specimen

Immunosuppression impairs host defense.

Frequent antimicrobial exposure selects altered microbial communities.

Changes in commensal microbiota coexist with enterococcal infection risk.

Slide 63 · Enterococcal pathogenicity is not mainly exotoxin driven

Streptococcal strategy

Enterococcal strategy

Pyrogenic exotoxin / pneumolysin

No comparable toxin repertoire in Robbins account

Capsular immune evasion

Antiphagocytic capsule and biofilm

Immune complications after group A infection

Persistence and antimicrobial resistance

Species-specific tissue injury

Tissue-damaging enzymes

Slide 64 · Intrinsic and acquired resistance coexist

Intrinsic resistance

Mobile genetic elements

Acquired resistance traits

Reduced antimicrobial options

Schematic — not an authentic clinical or histologic specimen

Enterococci have intrinsic resistance to several antibiotic classes.

Additional resistance can be transferred on mobile genetic elements.

Both mechanisms contribute to difficult-to-treat infection.

Slide 65 · VanA changes the vancomycin binding target

D-Ala—D-Ala

D-Ala—D-Lac

VanA-associated substitution

Reduced vancomycin affinity

Schematic — not an authentic clinical or histologic specimen

VanA-associated resistance alters the cell-wall peptide terminus.

D-Ala–D-Ala is replaced by D-Ala–D-Lac.

The altered terminus has reduced affinity for vancomycin.

Slide 66 · VanA mechanism: Molecular cause and consequence

Step

Cell-wall precursor

Vancomycin consequence

Usual target

D-Ala–D-Ala

High-affinity binding target

vanA-associated alteration

D-Ala–D-Lac

Reduced vancomycin binding

Phenotypic effect

Modified precursor is used

Resistance mechanism

Slide 67 · Resistance is not a species identification test

E. Faecalis and E. Faecium both require organism-level identification.

Resistance phenotype must be determined separately from Gram morphology.

Antimicrobial-resistance mechanisms are clinically consequential but do not define the inflammatory lesion.

Slide 68 · Laboratory logic: Choose samples by syndrome

Syndrome

Diagnostic direction

Key caution

Streptococcal pharyngitis

Culture or rapid group A antigen test

A clinical rash alone is insufficient

Pneumonia

Respiratory specimens; selected blood cultures

Colonization can confound sputum

Suspected endocarditis

Blood culture and cardiac imaging

Requires clinicopathologic integration

Enterococcal infection

Culture with species and susceptibility

Morphology alone is nonspecific

Slide 69 · Clinicopathologic application: Pharyngitis plus rash

Case

A school-age child develops pharyngitis and fever, followed by a fine punctate erythematous eruption and relative circumoral pallor.

Which virulence factor links the infection to the systemic rash?

Discuss before revealing the explanation in speaker notes

Slide 70 · Clinicopathologic application: Delayed renal syndrome

Case

A child has hematuria and edema several weeks after a sore throat. Kidney biopsy shows endocapillary neutrophils and granular immunodeposits.

What explains the delay and glomerular injury?

Discuss before revealing the explanation in speaker notes

Slide 71 · Clinicopathologic application: A transplant recipient

Case

An immunosuppressed stem-cell transplant recipient develops a culture-confirmed enterococcal bloodstream infection despite repeated antibiotic courses.

What two source-supported factors favor this setting?

Discuss before revealing the explanation in speaker notes

Slide 72 · Final diagnostic contrasts

Entity

Mechanism / hallmark

Important consequence

Group A streptococcus

Pyogenic + toxin + immune sequelae

Erysipelas, scarlet fever, RF, GN

Group B streptococcus

Genital colonization; capsule

Maternal / neonatal invasive disease

Pneumococcus

Capsule + pneumolysin

Pneumonia and meningitis

Viridans / S. mutans

Oral flora, glucans, acid

Endocarditis or caries

Enterococci

Biofilm + antibiotic resistance

Healthcare-associated infection

Slide 73 · Take-home synthesis

Streptococcal syndromes range from local suppuration to toxin-mediated and delayed immune injury.

Organism identity, anatomic site, and virulence mechanism jointly predict the tissue lesion.

Enterococcal disease is distinguished by gut origin, healthcare exposure, biofilm, and resistance.

A schematic teaches mechanism; Microbiologic assays and true specimens establish diagnoses.

Slide 74 · Primary reading

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

Topic section: Streptococcal and Enterococcal Infections.

Relevant discussions of rheumatic heart disease, postinfectious glomerulonephritis, pneumonia, and infective endocarditis.

Related organ-system chapters clarify cardiac, pulmonary, renal, and oral manifestations.