Streptococcus Pneumoniae / Pneumococcus / Diplococcus

Key Characteristics

• Encapsulated: S. pneumoniae has a polysaccharide capsule that is its primary virulence factor - it inhibits phagocytosis by blocking opsonization.
• Diploccocus: The cocci appear in pairs (diplo = two), giving it the name Diplococcus. The cells are elongated and flame/lancet shaped.
• Lancet/Flame shaped: Under microscopy, the paired cocci look like the tip of a lancet (surgical blade) or a candle flame - a classic identifier.
• IgA protease producing: It secretes an enzyme that cleaves secretory IgA, allowing it to colonize the respiratory mucosa and evade local mucosal immunity.

Diseases Caused

Meningitis caused by S. pneumoniae occurs at ALL ages except neonates. In neonates, Group B Streptococcus (GBS) is the dominant cause, not pneumococcus. A handwritten annotation in the notes adds "Thumbs Sign" - this refers to the radiological sign seen in epiglottitis on lateral neck X-ray, where the swollen epiglottis looks like a thumb.

Risk Factors

• Splenectomy (asplenia): The spleen is critical for clearing encapsulated bacteria via opsonization. Without a spleen, patients are at very high risk for overwhelming post-splenectomy infection (OPSI) from S. pneumoniae.
• Influenza: Prior viral respiratory infection damages mucociliary clearance, allowing bacterial superinfection.
• Alcoholism: Impairs neutrophil function, cough reflex, and mucociliary transport, increasing lung infection risk.

Diagnosis

• Draughtsman / Carrom coin colony: On blood agar, pneumococcal colonies have a central depression with a raised rim - resembling a draughtsman piece or carrom coin. This happens due to autolysin (amidase) activity which causes the center of the colony to collapse over time.
• Quellung's reaction (positive): Also called the capsular swelling reaction. When pneumococcal antiserum is added to the organism, the capsule appears to swell and become more visible under microscopy. This is a classic test for capsule identification and serotyping. It is positive for S. pneumoniae.
• Latex agglutination particle test (positive): A rapid antigen test that detects the pneumococcal polysaccharide capsular antigen in CSF or urine. Useful for quick diagnosis of meningitis.

Prevention (Vaccines)

• Polysaccharide vaccines (PPV 23) do NOT produce immunological memory (T-cell independent response) - they work in adults with mature immune systems.
• Conjugate vaccines (PCV 13) link polysaccharide to a protein carrier, generating a T-cell dependent response with memory - necessary for children under 2 whose immune systems cannot respond to plain polysaccharides.

Treatment

• Drug of Choice (DOC): Penicillin G - this is the classic first-line antibiotic for pneumococcal infections. For resistant strains, vancomycin + ceftriaxone is used.

Summary Mnemonics

• "MOPS" - Meningitis, Otitis media, Pneumonia, Sinusitis - the classic pneumococcal diseases.
• Lancet/Flame shape + IgA protease + Quellung positive + Draughtsman colony = S. pneumoniae on any exam.
• PPV 23 for adults (23 > 2 years), PCV 13 for children (conjugate for kids).

Streptococcus Viridans & Streptococcus Pyogenes (GAS) - Complete Explanation

PART 1: Streptococcus Viridans

Basic Characteristics

Diseases

1. Dental caries (most common): The species Streptococcus mutans produces biofilm (dental plaque), ferments sugars to lactic acid, and demineralizes enamel - the primary cause of tooth decay.
2. Infective Endocarditis (IE): Streptococcus sanguinis (sanguis) is the most common cause of late-onset prosthetic valve endocarditis (PVE). It enters the bloodstream after dental procedures and seeds previously damaged or prosthetic heart valves.
   • A handwritten annotation notes: "Sub Acute Bacterial - SABE (Subacute Bacterial Endocarditis) → Endocarditis"
   • Dx of IE: 3 sets of blood cultures (1 aerobic + 1 anaerobic each) - taken before starting antibiotics. This is per the Duke criteria protocol.
   • Rx: Penicillin G + aminoglycosides (gentamicin) - the synergistic combination for streptococcal endocarditis.

Classification Sidebar (Lancefield & Griffith)

• Lancefield groups A-G: Streptococci are grouped by their carbohydrate antigen (C antigen) in the cell wall. This is called the Lancefield grouping system. Group A = S. pyogenes, Group B = S. agalactiae, Group D = Enterococcus, etc.
• Griffith types: Streptococci are further typed by their M protein (a surface protein). GAS alone has >100 M-protein types. M protein is the key virulence factor.
• Annotation reads "Jordan City / Good Morning / Molecular Mimicry" - pointing toward how M protein mimics host tissue (molecular mimicry), which is the mechanism behind Rheumatic Fever (autoimmune cross-reactivity between streptococcal M protein and cardiac tissue).

PART 2: Streptococcus Pyogenes (GAS - Group A Streptococcus)

Basic Characteristics

• Beta-hemolytic: Causes complete (clear) hemolysis on blood agar - due to Streptolysin S.
• Bacitracin sensitive: A hallmark lab test - GAS is inhibited by bacitracin. Group B Strep (GBS) is resistant.
• PYR positive: L-pyrrolidonyl arylamidase (PYR) reaction is positive. This is another identifying test.

Virulence Factors (The Core of GAS Pathogenesis)

1. Hyaluronidase

• Breaks down hyaluronic acid in connective tissue (the "spreading factor")
• Allows the bacteria to invade deeper tissues

2. M Protein

• Anti-phagocytic surface protein - inhibits complement deposition and opsonization

• 100 types (Griffith typing)

• Molecular mimicry with cardiac myosin → triggers Rheumatic Fever

3. DNase / Streptodornase (DNAase)

• Depolymerizes extracellular DNA in pus, making the exudate less viscous
• The anti-DNase B test (titre > 300 units/ml) is the marker used to confirm PSGN (post-streptococcal glomerulonephritis), especially when it follows skin infection (because ASO may not rise after skin infections)
• Handwritten note: "This itself is responsible for Rheumatic Fever"

4. Streptolysin O (SLO) - "So" (annotated in notes)

• Immunogenic (stimulates antibody production - ASO)
• O2 labile (inactivated by oxygen - this is why it doesn't cause hemolysis on surface of agar plates)
• Cardiotoxic: directly toxic to the myocardium - relevant in Rheumatic carditis
• ASO (Anti-Streptolysin O) titre > 200 units/ml = evidence of prior pharyngeal GAS infection → used to diagnose Rheumatic Fever

5. Streptolysin S (SLS)

• Non-immunogenic (does NOT generate antibodies)
• O2 stable (not inactivated by oxygen)
• Responsible for beta-hemolysis on blood agar (surface hemolysis)

6. Streptokinase (Fibrinolysin)

• Converts plasminogen → plasmin
• Dissolves blood clots, helping the bacteria spread
• Annotation: "Strawberry tongue, Sandpaper rash" - classic signs of Scarlet Fever

7. SPE / Erythrogenic / Dick Toxin (Scarlett - annotated)

• Also called Streptococcal Pyrogenic Exotoxin (SPE)
• A Superantigen: activates large numbers of T cells non-specifically → massive cytokine release
• Causes: Scarlet Fever (strawberry tongue, sandpaper/Pastia's rash, facial flushing with circumoral pallor), Scarlatina, Streptococcal Toxic Shock Syndrome (TSS)

Diseases Caused by GAS

Suppurative (Pus-forming) Infections:

1. Pharyngitis (Strep sore throat) - the most common suppurative disease
2. Impetigo - honey-crusted skin lesions
3. Cellulitis - skin and soft tissue infection
4. Erysipelas - superficial skin infection with sharp raised borders, bright red
5. Necrotizing Fasciitis - the "flesh-eating" disease, rapidly spreading destruction of fascia

Non-Suppurative (Post-Streptococcal / Immune) Complications:

• Haematuria - C/F (clinical feature)
• Proteinuria - lab feature
• Cola-coloured urine - classic presentation
• Nephritic syndrome (not nephrotic)

Diagnosis

• Blood agar: Beta-hemolysis (clear/complete)
• Selective media: Crystal violet blood agar (inhibits gram-negative organisms)
• Transport media: Pike's Media - used for throat swabs when delay in processing is expected; contains antibiotics to prevent overgrowth of normal flora

Treatment

Quick Summary Comparison