Product Effect

C5a peptidase Inhibits recruitment of phagocytes by destroying complement component C5a

Hyaluronic acid capsule Inhibits phagocytosis

M protein Interferes with phagocytosis by causing inactivation of complement component C3b, an opsonin

Protein F Responsible for attachment to host cells

Protein G Binds to Fc portion of antibodies, thereby interfering with opsonization

Streptococcal pyrogenic exotoxins (SPEs) Superantigens responsible for scarlet fever, toxic shock, “flesh-eating” fasciitis

Streptolysins O and S Lyse leukocytes and erythrocytes

Tissue-degrading enzymes Enhance spread of bacteria by breaking down DNA, proteins, blood clots, tissue, hyaluronic acid

table 21.31 Streptococcus pyogenes enters by inhalation (nose), or by ingestion (mouth). 2 Pharyngitis, fever, enlarged lymph nodes; sometimes tonsillitis, abscess; scarlet fever with strains that produce erythrogenic toxin. Symptoms go away. 3 S. pyogenes exits by nose and mouth. Late complications appear: 4 Glomerulonephritis 5 Rheumatic fever 6 Neurological abnormalities Complications subside. 7 Damaged heart valves leak, heart failure develops.

Signs and symptoms Sore, red throat, with pus and tiny hemorrhages, enlargement and tenderness of lymph nodes in the neck; less frequently, abscess formation involving tonsils; occasionally, rheumatic fever and glomerulonephritis as sequelaeIncubation period 2 to 5 days

Causative agent Streptococcus pyogenes, Lancefield group A b-hemolytic streptococci

Pathogenesis Virulence associated with hyaluronic acid capsule and M protein, both of which inhibit phagocytosis; protein G binds Fc segment of IgG; protein F allows bacteria to attach to mucous membranes; multiple enzymes damage tissues

Epidemiology Direct contact and droplet infection; ingestion of contaminated food.

Treatment and prevention Treatment: Appropriate antibiotic.

Prevention: Avoiding crowds; adequate ventilation; daily penicillin to prevent recurrent infection in those with a history of rheumatic heart disease.