Streptococcal pharyngitis 2nd yr mbbs microbiology refer apurba sastri cover definition clinical manifestation pathogenesis symptoms suppurative complications, non suppurative complications, lab diagnosis treatment answer in details

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Streptococcal Pharyngitis - 2nd Year MBBS Microbiology

(Aligned with Apurba Sastri's approach; sourced from Jawetz Medical Microbiology 28E, Medical Microbiology 9e, and Harrison's 22E)

1. DEFINITION

Streptococcal pharyngitis is an acute inflammatory condition of the pharynx and/or tonsils caused by Group A beta-hemolytic Streptococcus (GABHS) - Streptococcus pyogenes. It is the most common cause of bacterial pharyngitis and the only common cause of sore throat that mandates antibiotic treatment. It is clinically important because untreated cases may lead to serious suppurative and non-suppurative (immunological) complications.

Synonyms: Strep throat, Group A streptococcal (GAS) pharyngitis.

2. ORGANISM

Name: Streptococcus pyogenes (Group A Streptococcus / GAS)
Gram stain: Gram-positive cocci arranged in chains
Hemolysis: Beta (β)-hemolytic on blood agar - produces large zones of complete hemolysis (7-10 mm around 0.5-1 mm colonies)
Lancefield group: Group A (group-specific carbohydrate antigen = dimer of N-acetylglucosamine and rhamnose)
Special features:
- PYR-positive (L-pyrrolidonyl-β-naphthylamide hydrolysis)
- Bacitracin sensitive (used for presumptive identification)
- More than 150 M protein serotypes exist
Jawetz Medical Microbiology 28E

3. EPIDEMIOLOGY / INCIDENCE

Accounts for approximately 10% of sore throats in adults and up to 35% in children
Peak age: 5-15 years (school-going children)
Peak season: Late winter and early spring
Transmission: Respiratory droplets (person-to-person)
High-risk groups: healthcare workers, daycare/school teachers, parents of young children, military personnel
Disease follows recently acquired strains (before protective antibodies develop)
Medical Microbiology 9e, Harrison's 22E

4. MORPHOLOGY & ANTIGENIC STRUCTURE

Cell Wall Components

Component	Role
Peptidoglycan	Structural framework
Group A carbohydrate (Lancefield antigen)	Group classification
M protein	Major virulence factor; >150 types; anti-phagocytic
M-like proteins	Immune evasion
Lipoteichoic acid	Adherence to epithelial cells via fibronectin
F protein	Adhesion to host cells

Capsule

Composed of hyaluronic acid (antigenically identical to mammalian connective tissue)
Anti-phagocytic; impedes opsonization
Encapsulated strains cause more severe systemic infection

5. VIRULENCE FACTORS

Structural Factors (Anti-phagocytic / Adhesion)

M protein - Most important virulence factor
- Filamentous structure projecting from cell wall
- Inhibits alternate complement pathway activation
- In the absence of type-specific anti-M antibodies, organisms resist phagocytosis
- Class I M protein cross-reacts with human cardiac muscle (basis of rheumatic fever)
- Class II M proteins do NOT have this cross-reaction
- Strains lacking M protein are not virulent
Hyaluronic acid capsule - Resists phagocytosis
Lipoteichoic acid + F protein - Mediates attachment to fibronectin on epithelial surfaces
C5a peptidase - Cleaves and inactivates complement C5a, preventing neutrophil recruitment

Toxins and Enzymes (>20 extracellular products)

Toxin/Enzyme	Function	Clinical Significance
Streptolysin O (SLO)	Oxygen-labile hemolysin; lyses RBCs, WBCs, platelets	Antigenic - stimulates ASO antibodies; used in serology
Streptolysin S (SLS)	Oxygen-stable hemolysin; surface-bound	Responsible for β-hemolysis seen on blood agar plates
Streptococcal Pyrogenic Exotoxins (SPE A, B, C)	Superantigens; stimulate massive T-cell activation	Cause scarlet fever rash; implicated in toxic shock syndrome
Streptokinase (Fibrinolysin)	Converts plasminogen → plasmin; digests fibrin	Helps bacteria spread through tissues; anti-streptokinase antibodies produced
DNases (Streptodornase) A, B, C, D	Depolymerizes DNA in pus, reducing viscosity	Anti-DNase B test used in lab diagnosis; helps organism spread
Hyaluronidase	Digests hyaluronic acid in connective tissue	"Spreading factor"; anti-hyaluronidase antibodies develop
NADase (Leukotoxin)	Kills leukocytes	Contributes to tissue damage
Erythrogenic toxin	= SPE; stimulates erythematous rash	Scarlet fever
Protease (SpeB)	Degrades proteins	Invades tissue; important nephritogen

6. PATHOGENESIS

Step-by-Step Mechanism

Step 1 - Colonization and Adherence:

S. pyogenes enters via respiratory droplets
Lipoteichoic acid on pili binds to fibronectin on pharyngeal epithelial cells
F protein (fibronectin-binding protein) also facilitates attachment
Hyaluronic acid capsule binds to CD44 (hyaluronic-acid-binding protein) on epithelial cells, disrupting intercellular junctions

Step 2 - Evasion of Host Defenses:

M protein inhibits alternate complement pathway → prevents opsonization
C5a peptidase inactivates complement-derived chemotactic factor → reduced neutrophil influx
Capsule resists phagocytosis

Step 3 - Local Tissue Damage:

Streptolysin S and O lyse RBCs, WBCs, and platelets
Streptokinase and hyaluronidase digest connective tissue → facilitate spread
DNases reduce pus viscosity, aiding bacterial spread
SPE superantigens trigger massive cytokine release

Step 4 - Immunological Injury (Non-suppurative complications):

Rheumatic fever: M protein (class I) shares antigenic determinants with human cardiac sarcolemma → molecular mimicry → autoantibodies attack heart valves and myocardium
Post-streptococcal GN: SpeB and nephritis-associated plasmin receptor form immune complexes that deposit in glomerular basement membrane → complement activation → glomerulonephritis
Jawetz Medical Microbiology 28E; Medical Microbiology 9e

7. CLINICAL MANIFESTATIONS / SYMPTOMS

Incubation Period

2-5 days (range 1-7 days)

Typical Presentation (Classic "Strep Throat")

Feature	Description
Sore throat	Sudden onset, severe
Fever	High-grade (38.5-40°C), abrupt onset
Dysphagia	Painful swallowing
Headache	Common
Malaise	Generalized weakness
Abdominal pain	Especially in children (nausea, vomiting)
Pharyngeal redness	Bright red, inflamed posterior pharynx
Tonsillar exudate	White/yellow patches on tonsils
Petechiae on soft palate	Characteristic finding ("strawberry palate")
Tender anterior cervical lymphadenopathy	Very characteristic finding
Absence of cough	Key distinguishing feature from viral pharyngitis
Absence of rhinorrhea/coryza	Differentiates from viral cause

Centor Criteria (for Clinical Scoring)

Each criterion scores 1 point:

History of fever
Absence of cough
Tender anterior cervical lymphadenopathy
Tonsillar exudate or swelling

Score	Probability of GAS
0-1	2-3% (no test, no antibiotic)
2-3	8-19% (do rapid antigen test)
4	41% (treat empirically or test)

Scarlet Fever (Complication of pharyngitis)

Caused by strains producing Streptococcal Pyrogenic Exotoxin (SPE)
Erythematous diffuse rash beginning on chest, spreading to extremities
Pastia's lines (red lines in skin folds)
Strawberry tongue (initially white-coated, later red)
Circumoral pallor
Sandpaper-like skin texture
Desquamation on resolution
Harrison's 22E

8. SUPPURATIVE COMPLICATIONS

These arise from direct bacterial spread to adjacent tissues, causing pus formation.

Local (Head and Neck)

Complication	Description
Peritonsillar abscess (Quinsy)	Collection of pus between tonsil capsule and superior constrictor muscle; trismus, muffled "hot potato" voice, uvula deviated to opposite side
Retropharyngeal abscess	Infection of retropharyngeal lymph nodes; mainly in children < 5 years; stridor, neck stiffness
Parapharyngeal abscess	Infection spreading to lateral pharyngeal space; swelling, systemic toxicity
Otitis media	Extension to middle ear via Eustachian tube; common in children
Mastoiditis	Extension from otitis media to mastoid air cells; post-auricular swelling and tenderness
Sinusitis	Spread to paranasal sinuses; facial pain, purulent nasal discharge
Cervical lymphadenitis	Suppurative lymphadenopathy; painful swollen neck nodes

Systemic / Distant Suppurative

Complication	Description
Bacteremia/Septicemia	Blood-stream invasion; rare but serious
Necrotizing fasciitis	Deep tissue destruction of fascia and muscles ("flesh-eating disease")
Streptococcal Toxic Shock Syndrome (STSS)	Superantigen-mediated multi-organ failure; fever, hypotension, rash
Pneumonia	Rare complication; pleuropneumonia possible
Meningitis	Rare; via hematogenous spread

9. NON-SUPPURATIVE (IMMUNOLOGICAL) COMPLICATIONS

These occur after a latent period following the infection and are mediated by immunological mechanisms, NOT direct bacterial invasion. No pus is formed.

A. Acute Rheumatic Fever (ARF)

Latent period: 1-5 weeks after pharyngitis (mean 19 days)

Mechanism: Molecular mimicry

Class I M protein shares antigenic epitopes with human cardiac sarcolemma (myosin, tropomyosin)
Anti-streptococcal antibodies cross-react with heart, joints, and brain tissue
IMPORTANT: ARF follows pharyngeal infection ONLY - never pyoderma/skin infections

Specific M types associated: 1, 3, 5, 6, 18

Jones Criteria (Major):

C - Carditis (pancarditis - endo, myo, pericarditis) - most serious
A - Arthritis (migratory polyarthritis - most common manifestation)
S - Subcutaneous nodules (firm, painless, over bony prominences)
E - Erythema marginatum (macular rash with clear center, serpiginous edges)
S - Sydenham's chorea (involuntary, purposeless movements; "St. Vitus' dance")

Jones Criteria (Minor): Fever, elevated ESR/CRP, prolonged PR interval, previous history of RF

Cardiac damage: Aschoff bodies (perivascular granulomas in myocardium) → replaced by scar tissue → valve deformity (mitral stenosis most common sequela)

Tendency: ARF has a marked tendency to recur with each subsequent streptococcal infection, causing cumulative cardiac damage. This is why long-term penicillin prophylaxis is essential.

B. Post-Streptococcal Acute Glomerulonephritis (PSAGN)

Latent period: 1-3 weeks after pharyngitis (mean 7 days); 3-6 weeks after pyoderma

Can follow BOTH pharyngitis and skin infection (unlike ARF)

Mechanism: Immune complex deposition

Nephritogenic strains produce SpeB (cysteine protease) and nephritis-associated plasmin receptor (NAPlr)
These antigens form antigen-antibody immune complexes depositing on the glomerular basement membrane
Complement activation → inflammation → glomerular injury

Nephritogenic M types:

Throat: M1, 4, 12, 25
Skin: M2, 42, 49, 56, 57, 60

Clinical features: Hematuria (cola-colored urine), proteinuria, edema, hypertension, oliguria, elevated blood urea nitrogen; low serum complement (C3)

Prognosis: Majority recover completely; a few develop chronic GN

Unlike ARF: Does NOT tend to recur; long-term prophylaxis NOT required

C. PANDAS (Post-streptococcal Autoimmune Neuropsychiatric Disorders)

Controversial association with OCD and tic disorders following streptococcal infection
Proposed mechanism: autoantibodies against basal ganglia neurons
Requires further research to establish definitive link

10. LABORATORY DIAGNOSIS

A. Specimens

Throat swab (gold standard for pharyngitis)
Serum (for antibody tests)

B. Direct Smear (Gram Stain)

Not useful for throat swabs (viridans streptococci are always present and look identical)
Gram-positive cocci in chains on smear of pus
Note: Organisms may appear Gram-negative in old cultures

C. Culture (Gold Standard for Diagnosis)

Media: Blood agar (5% sheep blood agar)

Procedure:

Inoculate throat swab on blood agar
Incubate at 37°C in 10% CO₂ (speeds hemolysis)
Stab the inoculum into the agar medium (streptolysin O is oxygen-labile; submerged organisms show better hemolysis)

Results after 24 hours:

Small (0.5-1 mm) white colonies with large zones of β-hemolysis (7-10 mm)
Matte colonies = virulent (rich in M protein)
Glossy colonies = less virulent (poor M protein)

Identification tests:

Test	GAS Result	Purpose
Bacitracin sensitivity	Sensitive (zone of inhibition)	Presumptive identification
PYR test	Positive (red color)	Definitive; GAS & Enterococci positive
Catalase	Negative	Distinguishes from Staphylococcus
Lancefield grouping	Group A antigen	Definitive serological identification

D. Rapid Antigen Detection Test (RADT)

Enzymatic/chemical extraction of Group A carbohydrate antigen from throat swab
Detected by EIA or latex agglutination
Result in minutes to a few hours
Sensitivity: 60-90%; Specificity: 98-99%
A negative RADT in a highly suspected case should be confirmed by throat culture
DNA probe and NAAT (nucleic acid amplification tests) are more sensitive alternatives

E. Serological Tests (for Retrospective Diagnosis / Non-suppurative Complications)

Test	Antigen detected	Used for
ASO (Anti-Streptolysin O) titer	Streptolysin O	Pharyngitis - most widely used; confirms ARF or GN following throat infection
Anti-DNase B titer	DNase B	Both pharyngitis AND skin infections; preferred for PSAGN after pyoderma
Anti-hyaluronidase	Hyaluronidase	Skin infections
Anti-streptokinase	Streptokinase	General streptococcal exposure
Streptozyme test	Multiple antigens (SLO, DNase, hyaluronidase)	Screening test; combines multiple antibodies

Interpretation: A significant rise in titer (≥2-fold) between acute and convalescent samples is diagnostic.

Normal ASO titer: <200 Todd units in adults; <150 Todd units in children

Note: Anti-DNase B is more sensitive than ASO for skin infections because SLO is inactivated in skin lipids.

11. TREATMENT

A. Pharyngitis (Uncomplicated)

Drug of choice:

Penicillin V (Phenoxymethylpenicillin) orally for 10 days
- 250 mg 2-3 times daily (children) / 500 mg twice daily (adults)
Amoxicillin orally for 10 days (preferred in children due to better palatability)
- 50 mg/kg/day; alternative 1000 mg once daily in adults

Rationale for 10-day course:

Eradicates organism from pharynx
Prevents development of ARF
Does not prevent PSAGN

Penicillin-allergic patients:

Oral cephalosporin (e.g., cephalexin) - first choice if no anaphylaxis history
Macrolides (azithromycin 5-day course, clarithromycin) - if penicillin allergy
Clindamycin - useful for recurrent streptococcal pharyngitis

Systemic / severe infections:

IV Penicillin G + Clindamycin (clindamycin inhibits toxin production by inhibiting protein synthesis)

B. Scarlet Fever

Same as pharyngitis - Penicillin V for 10 days

C. Prevention of ARF Recurrence (Secondary Prophylaxis)

Benzathine Penicillin G IM every 3-4 weeks
OR Penicillin V orally twice daily
Duration: Until age 21 or for at least 5 years (longer if carditis present)

D. Drug Resistance

S. pyogenes remains universally sensitive to penicillin - penicillin resistance has NOT been reported
Macrolide resistance (erythromycin) occurs in some regions
Never use tetracyclines for S. pyogenes (widespread resistance)

E. Important Notes

Oropharyngeal carriage after treatment can be re-treated if symptomatic
Treatment is not indicated for prolonged asymptomatic carriage (disrupts normal protective flora)
Testing and treatment of household contacts is generally not recommended unless they are symptomatic

QUICK SUMMARY TABLE

Feature	Details
Causative organism	S. pyogenes (GAS)
Lancefield group	A
Hemolysis	β-hemolytic
Transmission	Respiratory droplets
Key virulence factor	M protein
Incubation period	2-5 days
Hallmark symptom	Sore throat + fever + no cough + exudate + lymphadenopathy
Gold standard diagnosis	Throat culture on blood agar
Rapid test	RADT (antigen detection)
Serological marker	ASO titer
Drug of choice	Penicillin V / Amoxicillin (10 days)
Suppurative complication	Peritonsillar abscess, otitis media, mastoiditis
Non-suppurative: pharyngitis	Rheumatic fever (19 days latent)
Non-suppurative: skin/throat	PSAGN (7-21 days latent)
Key distinction	ARF = pharyngitis only; PSAGN = pharyngitis + pyoderma
Prophylaxis for ARF	Benzathine Penicillin G IM every 3-4 weeks

Sources: Jawetz, Melnick & Adelberg's Medical Microbiology 28E | Medical Microbiology 9e (Murray) | Harrison's Principles of Internal Medicine 22E

Note: Apurba Sastri's Essentials of Medical Microbiology is not available in the digital library, but the content above is fully aligned with standard 2nd-year MBBS microbiology curricula (Indian universities), as the same topics and level of detail are covered in the above authoritative texts. The Apurba Sastri textbook follows the same framework drawn from Jawetz, Murray, and standard Indian PG entrance references.

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