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Sketchy Micro streptococci mnemonic summary

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Here is the full Sketchy-style breakdown of Streptococci:

πŸ“ 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:
SystemBasisKey Groups
LancefieldCell wall carbohydrate antigenA, B, C, D, F, G...
HemolysisType of RBC lysis on blood agarΞ±, 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

GAS antigenic structure - M protein, LTA, Lancefield carbohydrate, pili, fibronectin adhesion
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)

FactorFunctionMemory Hook
M proteinAntiphagocytic - binds Factor H β†’ blocks C3b deposition; >100 serotypes; structural homology to myosin (key for ARF)"M for Major virulence"
Hyaluronic acid capsuleAntiphagocytic, resembles host tissue β†’ poor immunogen
C5a peptidaseInactivates 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)"
StreptokinaseLyses 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 FAdhesin - 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, ↓ 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?

PopulationDisease
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 womenEndometritis, UTI, wound infections, postpartum bacteremia
Immunocompromised adultsBacteremia, 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

FactorRole
Polysaccharide capsuleAntiphagocytic - most important virulence factor
PneumolysinPore-forming toxin; damages respiratory epithelium; activates complement
IgA proteaseCleaves secretory IgA in nasopharynx β†’ colonization
Surface protein adhesinsAttachment to oropharynx
Teichoic acid / peptidoglycan fragmentsStimulate 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

VaccineTargetWho
PCV13 (Prevnar 13)13-valent conjugatedAll children <2 years; immunocompromised adults
PPSV23 (Pneumovax 23)23-valent polysaccharideAdults β‰₯65, high-risk groups (asplenia, sickle cell, DM)
PCV15/PCV20Newer conjugatesAdults 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

SpeciesDisease
S. sanguis, S. mitisSubacute bacterial endocarditis (SBE) on damaged valves after dental procedures
S. mutansDental 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

FeatureS. pyogenes (A)S. agalactiae (B)S. pneumoniaeViridansEnterococcus
HemolysisΞ²Ξ²Ξ±Ξ±Variable
LancefieldABNoneNoneD
BacitracinSensitive βœ“ResistantResistantResistantResistant
OptochinResistantResistantSensitive βœ“ResistantResistant
Bile solubilityInsolubleInsolubleSoluble βœ“InsolubleInsoluble
PYR testPositive βœ“NegativeNegativeNegativePositive βœ“
CAMP testNegativePositive βœ“NegativeNegativeNegative
CapsuleHyaluronic acidPolysaccharidePolysaccharideNoneNone

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.
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