Streptococcus

Streptococcus

Subjects: Microbiology · Systems: Pathology, Microbiology · Tags: Microbiology

Streptococci — high-yield deep dive

Quick overview

• Gram-positive cocci, usually appearing in chains (or pairs for some species).
• Catalase negative (key to separate from Staphylococci).
• Facultative anaerobes.
• Classified by hemolysis on blood agar (alpha, beta, gamma) and by Lancefield grouping (group-specific cell wall carbohydrates, e.g., Group A = S. pyogenes, Group B = S. agalactiae).
• Important clinical species: S. pyogenes (GAS), S. agalactiae (GBS), S. pneumoniae, viridans group streptococci, Enterococcus (formerly group D).

Classification / quick map

• Beta-hemolytic (complete hemolysis)

  • Group A: Streptococcus pyogenes — bacitracin sensitive, PYR +
  • Group B: Streptococcus agalactiae — CAMP test +, hippurate +
  • Groups C/G: S. dysgalactiae, S. anginosus group (can cause pharyngitis, abscesses)

• Alpha-hemolytic (partial/green)

  • S. pneumoniae — optochin sensitive, bile soluble, lancet-shaped diplococci
  • Viridans streptococci (S. mutans, S. sanguinis, S. mitis) — optochin resistant, normal oral flora

• Gamma / non-hemolytic or variable

  • Enterococcus faecalis / faecium — bile esculin +, growth in 6.5% NaCl, PYR +

Lab ID shortcuts (memorize)

• Catalase negative → streptococci.
• Bacitracin (A) disk sensitive = S. pyogenes (GAS).
• PYR test positive = GAS and Enterococcus.
• CAMP test positive = GBS (S. agalactiae) — arrowhead augmentation of hemolysis next to S. aureus streak.
• Optochin sensitive & bile soluble = S. pneumoniae.
• Bile esculin + and growth in 6.5% NaCl = Enterococcus.
• Hippurate hydrolysis + = S. agalactiae.

1) Streptococcus pyogenes (Group A) — the big one

Micro/virulence

• Beta-hemolytic; bacitracin sensitive; PYR +.

• Key virulence factors:

  • M protein: antiphagocytic; many emm types; major determinant for rheumatic fever molecular mimicry.
  • Hyaluronic acid capsule: anti-phagocytic (mimics host).
  • Streptolysin O & S: hemolysins (S is oxygen stable; O is oxygen labile and antigenic → ASO antibodies).
  • Streptokinase (fibrinolysin) — helps spread.
  • DNases, hyaluronidase, C5a peptidase (disrupts neutrophil recruitment).
  • Pyrogenic exotoxins (SpeA, SpeB, SpeC, etc.) — superantigens → scarlet fever rash, streptococcal toxic shock.

Diseases / clinical syndromes

• Suppurative (direct infection): pharyngitis (strep throat), impetigo, cellulitis, erysipelas, necrotizing fasciitis (Type II), bacteremia, puerperal sepsis.

• Toxin-mediated: scarlet fever (pharyngitis + sandpaper rash + Pastia lines) and streptococcal toxic shock syndrome (STSS).

• Post-infectious immune sequelae:

  • Acute rheumatic fever (ARF) — follows untreated/undertreated pharyngitis (not skin infections).
  • Poststreptococcal glomerulonephritis (PSGN) — nephritic syndrome; follows pharyngitis or skin infection (impetigo) (immune complex deposition).

Pathogenesis notes

• Adhesion (lipoteichoic acid, M protein), tissue invasion (enzymes), immune evasion (M protein, capsule) → local damage + systemic toxin effects (superantigen cytokine storm in STSS).
• ARF: molecular mimicry between M protein and cardiac myosin / other components → autoimmune attack on heart (Aschoff bodies) — Jones criteria for diagnosis (see below).
• PSGN: immune complex deposition in glomeruli → hypocomplementemia (low C3 often temporary).

Diagnosis

• Clinical + rapid antigen detection test (RADT) for GAS (specific high, sensitivity moderate). Negative RADT with high suspicion → throat culture on blood agar (gold standard).
• Serology for recent infection: ASO titers (peak weeks after infection; useful for ARF) and anti-DNase B (useful after skin infections where ASO may be normal).

Treatment

• First-line: Penicillin (oral phenoxymethylpenicillin or IM benzathine penicillin for prophylaxis). Amoxicillin also used.
• Penicillin allergy: macrolides (erythromycin/azithro), but macrolide resistance exists (know local rates).
• Severe invasive disease (necrotizing fasciitis, STSS): IV penicillin plus clindamycin (clindamycin inhibits protein synthesis → reduces toxin production; also works in stationary phase). Early surgical debridement for nec fasc. Consider IVIG in streptococcal toxic shock in refractory cases (neutralizes superantigens) — used as adjunct in severe disease.

Exam pearls (GAS)

• Rheumatic fever follows pharyngitis but not skin infections. PSGN can follow either.
• ASO rises after GAS pharyngitis; anti-DNase B helpful after impetigo.
• M protein = major virulence factor + molecular mimicry → rheumatic heart disease.

2) Streptococcus agalactiae (Group B)

Micro/virulence

• Beta-hemolytic (sometimes weak), CAMP test +, hippurate hydrolysis +. Colonizes female genital tract and rectum.

Clinical importance

• Neonatal disease: early onset sepsis/pneumonia (first 24–48 hours, acquired intrapartum) and late onset meningitis (weeks after birth).
• In adults: UTIs, skin/soft tissue infections, bacteremia—esp. in diabetics, elderly.

Prevention & treatment

• Pregnancy screening at ~35–37 weeks (rectovaginal swab). Intrapartum antibiotic prophylaxis (IV penicillin G or ampicillin) for colonized women or those with risk factors (e.g., prolonged rupture of membranes, intrapartum fever, previous infant with GBS disease).
• Penicillin is first-line. For severe penicillin allergy, use clindamycin only if isolate susceptible; otherwise, vancomycin (local policies apply).

3) Streptococcus pneumoniae

Micro/virulence

• Alpha-hemolytic, optochin sensitive, bile soluble, lancet-shaped diplococci. Polysaccharide capsule is major virulence factor (antiphagocytic). Pneumolysin (pore forming), IgA protease.

Clinical syndromes

• Community-acquired pneumonia (classically lobar consolidation), otitis media, sinusitis, meningitis, bacteremia. Risk increased in asplenic patients, sickle cell, elderly, alcoholics.

Diagnosis

• Gram stain (gram + diplococci), culture, urine antigen test (for pneumococcal antigen) in adults with pneumonia, bile solubility test or optochin disk.

Treatment & resistance

• Historically penicillin; resistance through altered penicillin-binding proteins (PBP) is common — empiric therapy for severe disease (e.g., meningitis) often includes ceftriaxone/cefotaxime + vancomycin until susceptibilities known.
• For non-severe pneumonia, choose therapy based on local resistance patterns. Vaccines: conjugate vaccines (PCV13/15/20 etc.) and polysaccharide (PPSV23) — memorize indications per adult/child schedule (important clinically/exam).

4) Viridans group streptococci

• Normal oral flora; alpha-hemolytic, optochin resistant.
• Important for dental caries (S. mutans) and subacute bacterial endocarditis (especially after dental procedures in patients with preexisting valve damage).
• Treatment: penicillin (often with gentamicin for synergy in endocarditis depending on the case).

5) Enterococcus (E. faecalis, E. faecium)

Micro/clinical

• Gram-positive cocci, bile esculin +, grow in 6.5% NaCl, PYR +. Normal GI flora. Causes UTIs, biliary sepsis, and subacute endocarditis.

Resistance & treatment challenges

• Intrinsically less susceptible to many antibiotics (cephalosporins ineffective). Endocarditis often needs ampicillin + gentamicin (synergy).
• Vancomycin-resistant Enterococcus (VRE) — genes vanA/vanB → D-Ala→D-Lac change — serious nosocomial problem. Options: linezolid, daptomycin, tigecycline, newer agents exist (know institutionally available choices).

Mechanisms of antibiotic resistance (concise)

• S. pneumoniae: altered PBPs → reduced penicillin susceptibility.
• Macrolide resistance (GAS & pneumococcus): erm (methylase → target modification; can cause inducible clindamycin resistance) or mef (efflux pump). Use D-test to detect inducible clindamycin resistance.
• Enterococcus: vanA/vanB change D-Ala-D-Ala to D-Ala-D-Lac → vancomycin resistance.

Immunologic sequelae: ARF vs PSGN (high-yield exam points)

• Rheumatic fever (ARF)

  • Follows GAS pharyngitis, ~2–3 weeks after infection.
  • Jones major criteria — JONES: Joints (migratory arthritis), O (carditis), Nodules subcutis (subcutaneous nodules), Erythema marginatum, Sydenham chorea.
  • Requires evidence of preceding GAS infection (positive throat culture, RADT, or elevated ASO/anti-DNase B). Chronic consequence = rheumatic heart disease (valvular scarring, MR → MS).

• Poststreptococcal glomerulonephritis (PSGN)

  • Immune complex deposition in glomeruli → nephritic syndrome: hematuria (cola urine), oliguria, hypertension, edema.
  • May follow pharyngitis OR skin infection (impetigo). Complement C3 often low (transient).

Clinical & lab troubleshooting pearls

• Negative RADT but high clinical suspicion for GAS pharyngitis → do throat culture (RADT sensitivity not perfect).
• ASO useful for evidence of recent GAS exposure in suspected ARF. Anti-DNase B may be more helpful after skin infections.
• Severe invasive GAS infections → penicillin + clindamycin (clinda suppresses toxin production). In necrotizing fasciitis, early surgical debridement is lifesaving.
• CAMP test = essential to identify GBS (neonatal implications).
• Optochin distinguishes S. pneumoniae (sensitive) from viridans (resistant).

High-yield mnemonics & memory aids

• JONES for major criteria of rheumatic fever (see above).
• PYR test positive = Pyrrolidonyl arylamidase → GAS and P (Enterococcus) — both PYR+.
• CAMP = Confirms Agalactiae Making arrowhead (think “CAMP arrowhead”).

Quick practice questions (with brief answers)

1. Q: A child has sore throat and fever. RADT negative. What next? A: If high clinical suspicion (Centor criteria etc.), perform a throat culture (RADT sensitivity imperfect). Treat based on culture / clinical context.

2. Q: A neonate presents with respiratory distress within 24 hours of birth; maternal rectovaginal swab was unknown. Organism suspected? Prevention? A: GBS (S. agalactiae) early-onset sepsis. Prevention: screen at 35–37 weeks and give intrapartum IV penicillin to colonized mothers.

3. Q: Patient with rapidly progressive soft-tissue infection, severe pain out of proportion, systemic toxicity. Gram stain shows gram + cocci in chains. Next steps? A: Suspect necrotizing fasciitis due to GAS → urgent surgical debridement + IV broad-spectrum antibiotics including high-dose penicillin and clindamycin; supportive ICU care.

Two-day focused checklist (if you want a cram plan now)

• Day 1 AM: Read taxonomy + lab ID tests; memorize bacitracin/PYR/CAMP/optochin/bile esculin/6.5% NaCl rules.
• Day 1 PM: GAS deep dive — virulence, diseases, complications (ARF, PSGN), labs (ASO/anti-DNase B), treatment pearls (penicillin, clindamycin for toxins). Do 10 rapid cases.
• Day 2 AM: GBS, S. pneumoniae, viridans, Enterococcus — clinical syndromes, prevention (GBS screening; pneumococcal vaccines), resistance.
• Day 2 PM: Practice 15–20 mixed clinical vignettes with an emphasis on lab tests and management choices.

Disclaimer: For education only. Not medical advice; always follow your institution's guidance.