Microbiology · MU Plovdiv

23. Streptococcus spp. Classification. Morphology, biology, antigenic structure. Pathogenic factors. Pathogenicity of streptococcal infections. Diseases and immunity. Microbiological diagnosis. Antimicrobial treatment. Streptococci as resident flora in the oral cavity. Streptococcus pneumoniae. Morphology, biology, biochemical production, and antigenic structure. Pathogenesis, diseases, and immunity. Microbiological diagnosis. Specific prophylaxis and therapy.

Inside: 24 sections · 16 labelled pictures · 18 tables · 43 flashcards · 12 min

Topic 23 of 41 in the MU Plovdiv syllabus for Microbiology (Dental Medicine, Year 2). The free AceMed note covers it in 24 sections, about 927 words (12 min of reading), with 43 flashcards.

In this note

  1. Group A Streptococcus (GAS) – Streptococcus pyogenes
  2. I. General Features
  3. II. Virulence Factors
  4. III. Epidemiology and Transmission
  5. IV. Clinical Diseases of S. pyogenes
  6. V. Diagnosis
  7. VI. Treatment
  8. VII. Prevention
  9. Group B, C, D & G Streptococci. Streptococcus Viridans. Genus Eneterococcus.
  10. Group B Streptococci – Streptococcus agalactiae
  11. Group C & G Streptococci
  12. Group D Streptococci (non-enterococcal) – Streptococcus bovis group
  13. Streptococcus viridans group
  14. Genus Enterococcus (Group D Enterococci)
  15. Streptococcus pneumoniae (Pneumococcus)
  16. I. General Characteristics
  17. II. Morphology and Structural Features
  18. III. Virulence Factors
  19. IV. Epidemiology
  20. V. Diseases Caused
  21. VI. Diagnosis
  22. VII. Treatment
  23. VIII. Prevention
  24. IX. Differentiation from Viridans Streptococci

I. General Features

  • Streptococcus pyogenes is a Gram-positive, non-motile, non-spore forming coccus arranged in chains or pairs under the microscope.
  • It is catalase-negative, distinguishing it from Staphylococci.
  • Grows best on blood agar, where it produces β-hemolysis — complete clearing around colonies due to lysis of red blood cells.
  • It is a facultative anaerobe, meaning it can grow with or without oxygen.
  • Classified as Group A Streptococcus based on Lancefield serotyping, which detects group-specific carbohydrate antigen in the cell wall.
  • PYR test positive — helps differentiate it from S. agalactiae.

The β-hemolysis helps in lab identification. Catalase negativity helps separate it from Staphylococcus. The Lancefield group A antigen is specific to S. pyogenes.

III. Epidemiology and Transmission

  • Humans are the only reservoir.
  • Transmitted by:
  • Respiratory droplets → pharyngitis
  • Skin contact or contaminated surfaces → skin infections
  • More common in children (ages 5–15 years).
  • Asymptomatic carriage is common, especially in the nasopharynx.

IV. Clinical Diseases of S. pyogenes

A. Suppurative (pus-forming) Infections

These involve direct bacterial invasion and local tissue destruction.

  1. Pharyngitis (Strep Throat)
  • Sudden sore throat, fever, swollen lymph nodes, tonsillar exudates.
  • Complication risk: rheumatic fever if untreated.
  1. Scarlet Fever
  • Occurs when the strain produces pyrogenic exotoxins.
  • Presents with:
  • Sandpaper-like rash
  • Strawberry tongue
  • Circumoral pallor
  • Often follows untreated pharyngitis.
  1. Impetigo (non-bullous)
  • Honey-crusted skin lesions, usually on face.
  • Spread via contact, especially in children.
  1. Erysipelas
  • Superficial skin infection with raised, red, demarcated edges.
  • Often affects face or lower limbs.
  1. Cellulitis
  • Deeper skin/subcutaneous infection. Less defined borders.
  1. Necrotizing Fasciitis
  • “Flesh-eating disease.” Rapid destruction of muscle and fascia.
  • Requires surgical debridement and IV antibiotics.
  • Caused by highly virulent strains producing SpeB exotoxin.
  1. Streptococcal Toxic Shock Syndrome (STSS)
  • Systemic illness with shock, multiorgan failure, rash.
  • Caused by superantigenic exotoxins (esp. SpeA).

B. Non-suppurative (Immune-mediated) Complications

Occur after pharyngeal infection, due to immune cross-reactivity.

  1. Acute Rheumatic Fever (ARF)
  • Autoimmune response, 2–3 weeks after pharyngitis.
  • Affects heart, joints, skin, brain.
  • JONES criteria: Joint (arthritis), O (heart), Nodules, Erythema marginatum, Sydenham chorea.
  • Due to cross-reactive antibodies against M protein and cardiac tissue.
  1. Acute Post-Streptococcal Glomerulonephritis (APSGN)
  • Occurs after pharyngitis or skin infection.
  • Immune complex deposition in glomeruli → hematuria ("cola-colored urine"), edema, hypertension.
  • Type III hypersensitivity reaction.

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