Here is the full Sketchy-style breakdown of Streptococci:
π Streptococci - Sketchy Micro Style
Overview: The Classification Ladder
Streptococci are gram-positive cocci in chains, catalase-negative. The two major classification systems used clinically are:
| System | Basis | Key Groups |
|---|
| Lancefield | Cell wall carbohydrate antigen | A, B, C, D, F, G... |
| Hemolysis | Type of RBC lysis on blood agar | Ξ±, Ξ², Ξ³ |
1. Streptococcus pyogenes (Group A Strep = GAS)
Trigger words: Group A, pharyngitis, pyoderma, rheumatic fever, glomerulonephritis
Basics
- Gram-positive cocci in short to medium chains (4-10 cells)
- Ξ²-hemolytic (complete clear zone on blood agar)
- Ξ²-hemolysis caused by Streptolysin O (oxygen-labile) and Streptolysin S (oxygen-stable)
- Aerobically: only Streptolysin S is active β incubate anaerobically for best yield
- More than 100 M-protein serotypes
GAS Cell Wall Structure
M protein and lipoteichoic acid (LTA) extend from cell wall surface. LTA + Protein F bind fibronectin on host epithelial cells. Lancefield group A carbohydrate sits inside the peptidoglycan matrix.
Virulence Factors (High-Yield Table)
| Factor | Function | Memory Hook |
|---|
| M protein | Antiphagocytic - binds Factor H β blocks C3b deposition; >100 serotypes; structural homology to myosin (key for ARF) | "M for Major virulence" |
| Hyaluronic acid capsule | Antiphagocytic, resembles host tissue β poor immunogen | |
| C5a peptidase | Inactivates C5a β blocks PMN chemotaxis | |
| Streptolysin O (SLO) | Oxygen-labile, pore-forming toxin; Ξ²-hemolysis; immunogenic β ASO antibodies | "O = Oxygen-labile, Oh so immunogenic" |
| Streptolysin S (SLS) | Oxygen-stable; causes surface hemolysis; NOT immunogenic | "S = Stable in air, Silent (non-immunogenic)" |
| Streptokinase | Lyses fibrin clots - promotes spread | |
| Hyaluronidase | "Spreading factor" - breaks down connective tissue | |
| DNase (streptodornase) | Degrades DNA in pus; anti-DNase B antibody used for skin infections | |
| Pyrogenic exotoxins (SPE A, B, C) | Superantigens β massive cytokine release β scarlet fever, STSS | "Pyrogenic = fire = rash/fever" |
| Protein F | Adhesin - binds fibronectin | |
| Lipoteichoic acid (LTA) | Adhesin - binds fibronectin | |
Diseases
Suppurative (direct infection):
- Pharyngitis - #1 cause in children 5-15 yrs; sandpaper-like tonsils, exudate, tender anterior cervical nodes; no cough
- Impetigo / Pyoderma - golden-crusted skin lesions; children 2-5 yrs with poor hygiene; different M protein types than pharyngitis strains
- Scarlet fever - pharyngitis + SPE exotoxin β strawberry tongue + diffuse sandpaper rash (starts trunk, spares palms/soles) + circumoral pallor
- Erysipelas - bright red, raised, sharply demarcated skin infection (superficial dermis/lymphatics)
- Cellulitis - deeper soft tissue
- Necrotizing fasciitis - "flesh-eating bacteria"; rapidly spreading; surgical emergency
- Streptococcal Toxic Shock Syndrome (STSS) - SPE superantigens β massive cytokine storm β shock, renal failure, coagulopathy, rash; more invasive than staph TSS
Non-suppurative / Post-infectious (sequelae):
Acute Rheumatic Fever (ARF) - 2-4 weeks after pharyngitis only (not skin)
- Mechanism: Molecular mimicry - M protein homology to myosin β anti-streptococcal antibodies cross-react with cardiac tissue
- Jones Criteria (major): JONES = Joint (migratory polyarthritis), cOreA (Sydenham chorea), Nodules (subcutaneous), Erythema marginatum, heart (carditis)
- Prevention: treat pharyngitis with penicillin within 9 days
Post-streptococcal Glomerulonephritis (PSGN) - 1-4 weeks after pharyngitis OR 3-6 weeks after skin infection
- Immune complex deposition β diffuse proliferative glomerulonephritis
- Clinical: edema, hypertension, hematuria (cola-colored urine), proteinuria, β serum complement (C3)
- Usually self-limited; does NOT prevent PSGN by treating the infection
Diagnosis
- Throat culture on sheep blood agar (anaerobically for best yield)
- Rapid strep test (antigen detection) - quick but less sensitive
- Identification: Bacitracin-sensitive (GAS unique among streptococci), PYR-positive, Lancefield group A antigen
- Serology: ASO titer - confirms prior pharyngitis; Anti-DNase B - for pharyngitis OR skin infection (more sensitive for PSGN)
Treatment
- Penicillin V or amoxicillin (pharyngitis) - no resistance ever documented
- Penicillin + clindamycin (systemic/invasive disease) - clindamycin blocks toxin production
- Penicillin-allergic: oral cephalosporin or macrolide
- No vaccine
2. Streptococcus agalactiae (Group B Strep = GBS)
Trigger words: Group B, neonatal disease, screening pregnant women
Basics
- Ξ²-hemolytic, gram-positive cocci in chains
- Group-specific B carbohydrate antigen + type-specific capsular polysaccharides (types Ia, Ib, II-VIII)
- Primary virulence = antiphagocytic polysaccharide capsule
- CAMP test positive (enhances hemolysis of Staph aureus sphingomyelinase)
- Bacitracin-resistant (unlike Group A)
Who Gets It?
| Population | Disease |
|---|
| Neonates (early-onset, 0-7 days) | Acquired during birth; sepsis, pneumonia, meningitis; premature rupture of membranes is a risk factor |
| Neonates (late-onset, 1 week - 3 months) | Meningitis, bacteremia |
| Pregnant women | Endometritis, UTI, wound infections, postpartum bacteremia |
| Immunocompromised adults | Bacteremia, pneumonia, bone/joint infections (diabetics, cancer, alcoholism) |
Prevention
- Screen all pregnant women at 35-37 weeks with vaginal/rectal swab culture
- Give IV penicillin G intrapartum (β₯4 hours before delivery) if GBS positive
- No vaccine currently available
Treatment
- Penicillin G (drug of choice) Β± aminoglycoside for serious infections
- Cephalosporin or vancomycin for penicillin-allergic patients
3. Streptococcus pneumoniae (Pneumococcus)
Trigger words: Diplococci, capsule, pneumonia, meningitis, vaccine, optochin, bile-soluble
Basics
- Ξ±-hemolytic (partial/green hemolysis)
- Lancet-shaped gram-positive diplococci (pairs)
- No Lancefield group antigen
- Distinctive polysaccharide capsule (>90 serotypes) = major virulence factor
- Cell wall has C-polysaccharide (teichoic acid with phosphorylcholine) - binds CRP; activates autolytic enzyme amidase
Virulence Factors
| Factor | Role |
|---|
| Polysaccharide capsule | Antiphagocytic - most important virulence factor |
| Pneumolysin | Pore-forming toxin; damages respiratory epithelium; activates complement |
| IgA protease | Cleaves secretory IgA in nasopharynx β colonization |
| Surface protein adhesins | Attachment to oropharynx |
| Teichoic acid / peptidoglycan fragments | Stimulate local inflammation |
Epidemiology
- Nasopharynx colonizer β endogenous spread to lungs, sinuses, ears, blood, meninges
- Highest colonization in young children and their contacts
- Disease more common in cool months
- At-risk: antecedent viral URI (influenza), asplenia (sickle cell β overwhelming sepsis), elderly, immunosuppressed, alcoholics
Diseases (mnemonic: MOPS)
- Meningitis (most common bacterial in adults; #1 overall with H. flu and N. meningitidis)
- Otitis media (most common bacterial cause in children)
- Pneumonia (most common bacterial CAP in adults; lobar pneumonia, rust-colored sputum)
- Sinusitis
Diagnosis
- Gram stain: gram-positive lancet-shaped diplococci
- Culture on sheep blood agar; Ξ±-hemolysis
- Identification: Optochin-sensitive (distinguishes from viridans strep), bile-soluble (bile salts lyse the organism by activating autolytic amidase)
- Quellung reaction (capsular swelling with type-specific antibody)
- Urine antigen test (C-polysaccharide) - sensitive for meningitis CSF, less sensitive for urine
- PCR - test of choice when antibiotics already given
Treatment
- Penicillin (susceptible strains)
- Vancomycin + ceftriaxone (empirical meningitis / until sensitivities known)
- Resistance: PBP2a-mediated (especially in meningitis dosing)
Vaccines
| Vaccine | Target | Who |
|---|
| PCV13 (Prevnar 13) | 13-valent conjugated | All children <2 years; immunocompromised adults |
| PPSV23 (Pneumovax 23) | 23-valent polysaccharide | Adults β₯65, high-risk groups (asplenia, sickle cell, DM) |
| PCV15/PCV20 | Newer conjugates | Adults β₯65 (current preference over PPSV23) |
4. Viridans Streptococci
Trigger words: Oral flora, endocarditis, dental procedure, Ξ±-hemolytic
Basics
- Ξ±-hemolytic (green partial hemolysis)
- No Lancefield antigens, no capsule
- Optochin-resistant (key to distinguish from Pneumococcus), bile-insoluble
- Normal residents of oral cavity (and GI, GU tract)
- Species: S. sanguis, S. salivarius, S. mitis, S. mutans, S. intermedius
High-Yield Associations
| Species | Disease |
|---|
| S. sanguis, S. mitis | Subacute bacterial endocarditis (SBE) on damaged valves after dental procedures |
| S. mutans | Dental caries (produces glucan/dextran from sucrose β plaque) |
| S. bovis (now S. gallolyticus) | Endocarditis + colon cancer - always colonoscope if isolated! |
| S. anginosus group (S. constellatus, S. intermedius) | Abscesses (brain, liver, lung); variable hemolysis; associated with A, B, C, G Lancefield antigens |
| Granulicatella / Abiotrophia (nutritionally variant strep, NVS) | Need pyridoxal (B6) to grow; striking association with endocarditis |
Endocarditis
- Dental procedures β bacteremia β viridans strep adhere to damaged/abnormal valves (prior rheumatic fever, MVP, prosthetic valves)
- Antibiotic prophylaxis (amoxicillin 1 hour before dental procedure) in high-risk cardiac conditions
5. Enterococcus (Group D - formerly Streptococci)
Trigger words: GI flora, UTI, resistant, peritonitis, nosocomial
Basics
- Gram-positive cocci in pairs and short chains (morphologically similar to pneumococcus)
- Group D glycerol teichoic acid cell wall antigen
- Variable hemolysis (Ξ±, Ξ², or Ξ³)
- Naturally resistant to cephalosporins (important!)
- Can form biofilms
- Two clinically important species: E. faecalis (more common, less resistant) and E. faecium (more resistant)
Epidemiology
- Colonizes the GI tract of humans and animals
- Spreads when broad-spectrum antibiotics (especially cephalosporins) disrupt normal flora
- Nosocomial; survives on environmental surfaces for prolonged periods
Diseases
- UTI (catheter-associated, most common)
- Peritonitis (polymicrobial)
- Endocarditis (especially in elderly, GI/GU instrumentation)
- Bacteremia, wound infections
Treatment
- Ampicillin (E. faecalis) Β± gentamicin (synergy for endocarditis)
- Vancomycin for penicillin-resistant strains
- Linezolid or daptomycin for VRE (vancomycin-resistant enterococcus)
Quick Differentiation Table
| Feature | S. pyogenes (A) | S. agalactiae (B) | S. pneumoniae | Viridans | Enterococcus |
|---|
| Hemolysis | Ξ² | Ξ² | Ξ± | Ξ± | Variable |
| Lancefield | A | B | None | None | D |
| Bacitracin | Sensitive β | Resistant | Resistant | Resistant | Resistant |
| Optochin | Resistant | Resistant | Sensitive β | Resistant | Resistant |
| Bile solubility | Insoluble | Insoluble | Soluble β | Insoluble | Insoluble |
| PYR test | Positive β | Negative | Negative | Negative | Positive β |
| CAMP test | Negative | Positive β | Negative | Negative | Negative |
| Capsule | Hyaluronic acid | Polysaccharide | Polysaccharide | None | None |
Sketchy Mnemonics to Remember
- GAS (Group A) = "SHoP": Scarlet fever, Heart (rheumatic fever), glomerulonePHritis
- ASO titer = Confirms pharyngitis; Anti-DNase B = Confirms pharyngitis OR pyoderma
- GBS (Group B) = "Baby's Bug" - think neonatal meningitis/sepsis; screen mom at 35-37 weeks
- Pneumococcus = "MOPS" + optochin + bile soluble + diplococci
- S. bovis endocarditis = always rule out colon cancer
- Viridans = optochin-resistant Ξ±-hemolytics = oral flora endocarditis; S. mutans = dental caries
- Enterococcus = intrinsically cephalosporin-resistant; VRE treated with linezolid/daptomycin
Sources: Sherris & Ryan's Medical Microbiology 8e; Murray's Medical Microbiology 9e - comprehensive cross-referenced coverage of all streptococcal species.