• Properties: gram (+), spherical to ovoid, <2 m m diameter, grow in pairs or chains in medium, catalase (-)
• Lancefield groups: distinguished by Lancefield (1933) based on Ag composition: A, B, C, D and G
• Hemolysis: b = clear zone surrounding colony on blood agar plate = full hemolysis
• a = green zone surrounding colony on blood agar plate = partial hemolysis
• g = no hemolysis

• Basics: Group A, b -hemolytic, fimbriae-like appendages, produce hyaluronic acid and hyaluronidase, form long chains
• Charact: facultative anaerobic, b hemolysis, sheep blood- inhibition of H. haemolyticus, killed by 30min at 60° C
• Lab ID: lancefield grouping, bacitracin test (95%), 1 hr office test- extraction of CHO- highly specific
• Ag Structure:
• M protein (more than 80 serotypes)
• Extend from cell wall as fimbriae-like projections
• N-terminus confers Ag variations
• Homology between different M proteins Ý near C-terminus
• Tandem repeats within gene Þ size variation
• Others:
• C polysaccharides: L-rhammose and N-acetyl glucosamine (2:1)
• T-protein
• M-associated protein (MAP): Ag similarity to components of myocardium
• Serum opacity factor (SOF): is useful (as well as MAP) for typing Group A strep which is not M-typable
• Extracellular Proteins
• Streptolysin O: lethal to most euk cells, causes memb damage via interaction with cholesterol and induces brisk antibody response after pharyngeal or systemic infection – less after skin infection
• Ab response useful in diagnosing recent strep infection in patients suffering from acute rheumatic fever
• Streptolysin S: non-antigenic; responsible for surface hemolysis on blood agar plates; inhibited by phospholipids
• Nucleases: 4 Ag-distinct (A,B,C,D); play role in liquifaction of abscess; antibody to Dnase B Þ diagnose strep skin infection
• Strep Pyrogenic Exotoxins (SPE): at least 3 serotypes: A,B,C (now up to J);
• member of superantigen family: stimulates immune sysem in non-specific manner resulting in severe disease
• Induces erythyma (type C acts on hypothalamus to produce fever); rash also seen in some patients
• structural genes carried by bacteriophages
• Pathogenicity
• M protein: anti-phagocytic by preventing deposition of C3b (type specific antibody neutralize this ability)
• lipoteichoic acid (cell wall): mediates adherence to buccal mucosal epithelial cells
• capsular polysaccharide: possesses anti-phagocytic capabilities
• Clinical Syndromes
• Localized infections: pharyngitis(strep throat), impetigo(skin infect), erysipelas(subcutaneous tissue infect), cellulitis
• Suppurative infections: scarlet fever, abscess formation, bacteremia, osteomyelitis, necrotizing fascitis (flesh eating, destroys tissue and blood supply so cannot administer antibiotics; treatment = amputation; muscle damage predisposes you)
• Post-infectious syndromes: acute rheumatic fever and post-strep glomerulonephritis
• Diagnosis: gram stain of purulent secretions; culture; ASLO titer for evidence of recent pharyngeal infection
• Treatment (anti-microbial therapy): penicillin (main), cephalosporin, erythomycin, clindamycin, vancomycin
• any anti-microbial with gram-positive activity will be effective
• Clindamycin (should be added regimen): penetrates euk cells (lactams like penicillin do not), inhibits protein synth (and thus toxin production), eagle effect: effective against stationary phase of growth (which ß efficacy of lactams)

• Basics: Group B; b -hemolytic; colonizes pharynx, GI, vagina; colonizes ~20% of pregnant women of which ~50% pass on to their child; Ag structure: 6 capsular serotypes
• Infections: sepsis and meningitis in neonates, puerperal infections in women, skin/peripheral infections, endocarditis
• Therapy: Group B remain susceptible to penicillin so they are therapy of choice

• Basics: diverse group, a -hemolytic, micro-aerophilic (grow well in low oxygen conc)
• Treatment: viridan infection: penicillin; viridan native valve endocarditis: 4wk IV penicillin; if combine with streptomycin = 2wk
• Species: S. sanguis (endocarditis), S. mutans (dental plaque), S. anginorius (liver, brain absess), S. mitis (infection in neutropenic patients – lowered susceptibility to penicillin), S. salivarius, S. morbillorium

Group D streptococci – Streptococcus bovis and Enterococcus