Microbiology · MU Sofia

48. Group A streptococci (Streptococcus pyogenes)

Covers Streptococcus pyogenes, starting with its morphology, growth on blood agar, beta-haemolysis, catalase-negativity and Lancefield grouping. A table sets out the virulence factors and their roles, followed by epidemiology and transmission. The suppurative infections and the immune-mediated complications are described next, then diagnosis, treatment and prevention.

Inside: 8 sections · 7 labelled pictures · 2 tables · 15 flashcards · 4 min

Topic 48 of 113 in the MU Sofia syllabus for Microbiology (Medicine, Year 3). The free AceMed note covers it in 8 sections, about 459 words (4 min of reading), with 15 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

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. 1. Pharyngitis (Strep Throat)
  • Sudden sore throat, fever, swollen lymph nodes, tonsillar exudates.
  • Complication risk: rheumatic fever if untreated.
  1. 2. Scarlet Fever
  • Occurs when the strain produces pyrogenic exotoxins.
  • Presents with:
  • Sandpaper-like rash
  • Strawberry tongue
  • Circumoral pallor
  • Often follows untreated pharyngitis.
  1. 3. Impetigo (non-bullous)
  • Honey-crusted skin lesions, usually on face.
  • Spread via contact, especially in children.
  1. 4. Erysipelas
  • Superficial skin infection with raised, red, demarcated edges.
  • Often affects face or lower limbs.
  1. 5. Cellulitis
  • Deeper skin/subcutaneous infection. Less defined borders.
  1. 6. 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. 7. 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. 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. 2. 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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