Chapter 153: Streptococcal Infections¶
Chapter 153 | Part 5: Infectious Diseases
KEY CLINICAL POINTS¶
- Group A Streptococci (GAS) are the primary causative agents of pharyngitis, scarlet fever, and post-streptococcal complications (ARF/PSGN).
- Streptococcal infections are classified by Lancefield groups (A, B, C, G, D) based on cell wall carbohydrate antigens and hemolytic patterns.
- Penicillin remains the first-line treatment for GAS infections, with clindamycin added for severe cases or resistance concerns.
- Group B Streptococci (GBS) are a leading cause of neonatal sepsis and endometritis, with prophylaxis recommended for high-risk pregnancies.
- Viridans streptococci are common causes of subacute bacterial endocarditis and are part of the normal oral flora.
1. DEFINITION & OVERVIEW¶
Streptococci are gram-positive, spherical to ovoid bacteria that form chains in liquid media. They are classified by hemolytic patterns ( β , α , γ ) and Lancefield serogroups. Group A streptococci (GAS) are responsible for pharyngitis, scarlet fever, and post-infectious complications. Group B streptococci (GBS) are significant in neonatal infections. Nonenterococcal group D streptococci and viridans streptococci cause endocarditis and other infections.
Table 153-1 Classification of Streptococci¶
| LANCEFIELD GROUP | REPRESENTATIVE SPECIES | HEMOLYTIC PATTERN | TYPICAL INFECTIONS |
|---|---|---|---|
| A | S. pyogenes | b | Pharyngitis, impetigo, cellulitis, scarlet fever |
| B | S. agalactiae | b | Neonatal sepsis, meningitis, puerperal infection |
| C, G | S. dysgalactiae subsp. equisimilis | b | Cellulitis, bacteremia, endocarditis |
| D | Enterococcia: E. faecalis, E. faecium | Usually nonhemolytic | Urinary tract infection, endocarditis |
| Nonenterococci: S. gallolyticus | Usually nonhemolytic | Bacteremia, endocarditis | |
| Variable or Viridans streptococci | S. sanguis, S. mitis | a | Endocarditis, dental abscess, brain abscess |
1.1 Classification Systems¶
Lancefield grouping (A, B, C, G, D) based on cell wall carbohydrate antigens. Hemolytic patterns ( β , α , γ ) determine virulence and pathogenesis. Viridans streptococci are α -hemolytic and part of the normal oral flora.
1.2 Pathogenesis¶
GAS produce M protein (antigenic variation), pyrogenic exotoxins, and hyaluronic acid capsules. These factors contribute to immune evasion and tissue damage. GBS capsules and CAMP factor enhance virulence.
2. EPIDEMIOLOGY¶
GAS infections account for 500,000 annual deaths globally. Incidence is higher in resource-limited countries. GBS is a leading cause of neonatal sepsis and meningitis. Risk factors include poor hygiene, immunocompromise, and maternal colonization.
2.1 Demographics¶
Pharyngitis is common in children (20–40% of exudative cases). GBS infections are more prevalent in preterm infants, women with prolonged labor, and those with chorioamnionitis.
2.2 Risk Factors¶
Poor hygiene, immunocompromise, maternal GBS colonization, and underlying conditions (e.g., diabetes, malignancy) increase susceptibility to streptococcal infections.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
GAS produce M protein (immune evasion), pyrogenic exotoxins (toxic shock), and hyaluronic acid capsules (immune evasion). GBS virulence factors include capsules, CAMP factor, and adherence to host tissues. Nonenterococcal group D streptococci and virid,ans streptococci cause endocarditis and abscesses.
3.1 Molecular Mechanisms¶
M protein binds to host cells, resisting phagocytosis. Pyrogenic exotoxins trigger systemic inflammation. Capsular polysaccharides prevent phagocytosis and complement activation.
3.2 Immune Evasion¶
Streptococcal antigens (e.g., M protein, hyaluronic acid) mimic host molecules, evading immune detection. Capsules and exotoxins disrupt host defenses.
4. CLINICAL FEATURES¶
Pharyngitis presents with sore throat, fever, and exudate. Scarlet fever has a characteristic rash. Cellulitis and necrotizing fasciitis show rapid progression with systemic toxicity. GBS infections in neonates present with sepsis, meningitis, or endometritis.
4.1 Symptomatology¶
Pharyngitis: sore throat, fever, exudate. Scarlet fever: rash, strawberry tongue. Cellulitis: erythema, warmth, tenderness. Necrotizing fasciitis: severe pain, skin necrosis, systemic toxicity.
4.2 Complications¶
ARF (rheumatic fever), PSGN (post-streptococcal glomerulonephritis), septic arthritis, endocarditis, and toxic shock syndrome.
5. DIFFERENTIAL DIAGNOSIS¶
Viral pharyngitis (e.g., Epstein-Barr, CMV), bacterial infections (e.g., Staphylococcus, Streptococcus pneumoniae), and other streptococcal groups (C, G, D). Viral exanthems (e.g., measles, Kawasaki disease) must be distinguished from scarlet fever.
6. INVESTIGATIONS & DIAGNOSIS¶
Throat culture (gold standard), rapid antigen detection tests ( ≥ 95% specificity), and blood cultures for invasive infections. Imaging (e.g., ultrasound, CT) for abscesses. Serology for ARF/PSGN (ASO, anti-DNase B).
6.1 Diagnostic Tests¶
Rapid antigen detection (latex agglutination, EIA), throat culture, blood cultures, and serology (ASO, anti-DNase B).
6.2 Imaging¶
Ultrasound/CT for abscesses, MRI for endocarditis, and chest X-ray for pneumonia.
7. MANAGEMENT & TREATMENT¶
Penicillin (e.g., benzathine, penicillin V) is first-line for GAS infections. Clindamycin added for severe cases or resistance. GBS infections require ampicillin/gentamicin. Necrotizing fasciitis requires surgical debridement and broad-spectrum antibiotics.
Table 153-3 Treatment of Group A Streptococcal Infections¶
| INFECTION | TREATMENTa |
|---|---|
| Pharyngitis | Benzathine penicillin G (1.2 mU IM) or penicillin V (250 mg PO bid) × 10 days |
| Scarlet fever | Same as pharyngitis |
| Cellulitis | Penicillin G (1–2 mU IV q4h) or cephalexin (250 mg PO q6h) |
| Necrotizing fasciitis | Penicillin G (2–4 mU IV q4h) + clindamycin (600 mg IV q8h) |
7.1 Pharmacologic Therapy¶
Penicillin (250–500 mg PO bid for pharyngitis), clindamycin (600 mg IV q8h), vancomycin (1 g IV q12h) for resistant strains. GBS: ampicillin (200,000 units/kg/day) + gentamicin (1 mg/kg q8h).
7.2 Surgical Interventions¶
Debridement for necrotizing fasciitis, drainage for abscesses, and removal of prosthetic joints in septic arthritis.
8. PROGNOSIS & COMPLICATIONS¶
Mortality from necrotizing fasciitis/TSS is ≥ 30%. ARF/PSGN can lead to long-term cardiac or renal damage. GBS infections in neonates have high mortality if untreated. Complications include septic arthritis, endocarditis, and toxic shock syndrome.
8.1 Long-Term Outcomes¶
ARF: rheumatic heart disease. PSGN: chronic renal disease. Necrotizing fasciitis: limb loss or death.
8.2 Preventive Measures¶
Antibiotic prophylaxis for high-risk contacts, vaccination (experimental), and hygiene education.
9. SPECIAL CONSIDERATIONS¶
Pregnancy: GBS prophylaxis with penicillin. Pediatrics: Penicillin for pharyngitis, clindamycin for cellulitis. Elderly: Higher risk of severe infections and antibiotic resistance. Immunocompromised: Increased risk of invasive infections.
9.1 Pregnancy¶
Intrapartum GBS prophylaxis with penicillin for high-risk mothers. Avoid clindamycin if penicillin allergy is suspected.
9.2 Neonatal Infections¶
Early-onset GBS infections (within 7 days) require intravenous antibiotics. Late-onset infections (7–90 days) may require prolonged treatment.
10. KEY POINTS & CLINICAL PEARLS¶
- Use rapid antigen tests for GAS pharyngitis to avoid unnecessary antibiotics. 2. Clindamycin is recommended for severe GAS infections or resistance concerns. 3. GBS prophylaxis is critical for high-risk pregnancies to prevent neonatal sepsis. 4. Necrotizing fasciitis requires immediate surgical debridement and broad-spectrum antibiotics. 5. Viridans streptococci are common causes of endocarditis and require long-term antibiotic therapy.