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Classify streptococci. Describe the virulence factors, diseases and non-suppurative sequelae of Streptococcus pyogenes.

Microbiology · 2nd Professional — Para-Clinical

Classification of Streptococci

Gram-positive cocci in chains or pairs, non-motile, non-sporing, catalase negative

Basis	Groups
By haemolysis on blood agar	Alpha — partial, greenish (S. Pneumoniae, viridans group); beta — complete, clear (S. Pyogenes, S. Agalactiae); gamma — none (enterococci, S. Bovis)
By lancefield grouping	Based on the cell wall C carbohydrate antigen; groups A to H and K to V. Group A = S. Pyogenes; group B = S. Agalactiae (neonatal sepsis and meningitis); group D = enterococci and S. Bovis
By biochemical reactions	S. Pyogenes is bacitracin sensitive and PYR positive; S. Agalactiae is bacitracin resistant and camp test positive; pneumococcus is optochin sensitive and bile soluble
Non-groupable	Viridans streptococci (S. Mitis, S. Sanguinis, S. Mutans) — oral commensals causing subacute endocarditis and dental caries

Virulence Factors of Streptococcus Pyogenes

Factor	Action
M protein — the major virulence factor	Antiphagocytic, and the basis of type-specific immunity. Over 100 M types exist, so infection with one gives no protection against the others — which is why repeated attacks occur and why vaccine development is difficult. Certain types are rheumatogenic and others nephritogenic
Capsule (hyaluronic acid)	Antiphagocytic, and non-antigenic because it is identical to host hyaluronic acid — molecular disguise
Streptolysin O	Oxygen-labile and strongly antigenic — the basis of the antistreptolysin O (ASO) titre. Cardiotoxic
Streptolysin S	Oxygen-stable and non-antigenic; responsible for the beta-haemolysis seen on the plate
Pyrogenic (erythrogenic) exotoxins	Superantigens, phage-encoded; cause the rash of scarlet fever and streptococcal toxic shock syndrome
Spreading enzymes	Streptokinase (fibrinolysin — dissolves the fibrin barrier, so infection spreads rather than localising), hyaluronidase, DNase B, C5a peptidase
Lipoteichoic acid and F protein	Adhesion to epithelium

Diseases

Suppurative (invasive) — pharyngitis and tonsillitis (the commonest); impetigo and pyoderma; erysipelas (a sharply demarcated superficial cellulitis) and cellulitis; necrotising fasciitis; puerperal sepsis; lymphangitis; otitis media and sinusitis; and bacteraemia
Toxin-mediated — scarlet fever (a punctate erythematous rash sparing the perioral area, with a strawberry tongue and later desquamation) and streptococcal toxic shock syndrome
Non-suppurative sequelae — the immunologically mediated complications, which are the reason streptococcal sore throat is treated at all

Feature	Acute rheumatic fever	Acute post-streptococcal glomerulonephritis
Preceding infection	Throat only — never skin	Throat or skin (pyoderma)
Latent period	2 to 3 weeks	1 to 2 weeks after throat; 3 to 6 weeks after skin
M types	Rheumatogenic — 1, 3, 5, 6, 18	Nephritogenic — 12 (throat), 49 (skin)
Mechanism	Molecular mimicry — antibody to M protein cross-reacts with cardiac myosin and sarcolemma (type II)	Immune complex deposition in the glomerulus (type III)
Features	Carditis, migratory polyarthritis, chorea, erythema marginatum, subcutaneous nodules (Jones criteria)	Haematuria, oedema, hypertension, low C3
Recurrence	Yes — each attack worsens valve damage, hence lifelong prophylaxis	Rare; prophylaxis is not indicated
Prognosis	Chronic rheumatic heart disease	Usually complete recovery in children

CLINICAL PEARL

Treating a streptococcal sore throat does not shorten it much; it prevents rheumatic fever. The pharyngitis settles in a few days with or without penicillin. What antibiotic treatment achieves is eradication of the organism before the immune response that cross-reacts with heart valves develops — and it works if given within about nine days. In India, where rheumatic heart disease remains a major cause of cardiac death in the young, that is the whole justification for treating a self-limiting illness.

Laboratory Diagnosis

Throat swab — Gram stain is of little value (the throat carries many organisms); culture on blood agar shows small beta-haemolytic colonies
Identification — catalase negative; bacitracin sensitivity and PYR positive; Lancefield grouping by latex agglutination
Rapid antigen detection tests are specific but less sensitive, so a negative result in a child is confirmed by culture
Serology for the non-suppurative sequelae, where the organism has usually gone by the time the illness appears — ASO titre rises after throat infection, but poorly after skin infection because skin lipids inhibit streptolysin O; anti-DNase B is therefore the better test after pyoderma
Streptozyme detects several antibodies together

Other Medically Important Streptococci

Organism	Group	Clinical importance
S. Agalactiae	B	Colonises the vagina in up to 30% of women; the leading cause of neonatal sepsis and meningitis. Bacitracin resistant, camp test positive, hippurate hydrolysis positive. Prevented by antenatal screening and intrapartum penicillin
Viridans group (S. Mitis, sanguinis, mutans)	Non-groupable	Alpha-haemolytic oral commensals; the commonest cause of subacute bacterial endocarditis on damaged valves after dental procedures; S. Mutans causes dental caries. Optochin resistant and bile insoluble, which distinguishes them from pneumococcus
S. Bovis (S. Gallolyticus)	D	Endocarditis and bacteraemia with a strong association with colonic carcinoma — its isolation mandates colonoscopy
S. Anginosus (milleri) group	Variable	A marked tendency to form abscesses — brain, liver and lung
Peptostreptococcus	—	Anaerobic; part of polymicrobial abscesses and intra-abdominal sepsis

Treatment and Applied Aspects

Penicillin remains the drug of choice — remarkably, S. Pyogenes has never developed penicillin resistance after eighty years of use, which is almost unique among bacteria. Erythromycin or a macrolide in penicillin allergy
Secondary prophylaxis after rheumatic fever — benzathine penicillin every 3 to 4 weeks, continued for years or for life depending on carditis; this prevents recurrent attacks and progressive valve damage, and is the single most important streptococcal intervention in India
Add clindamycin in necrotising fasciitis and toxic shock — it inhibits toxin production and is unaffected by the high organism density that renders penicillin less effective
Necrotising fasciitis is a surgical emergency; pain out of proportion to the visible signs is the early clue, and survival depends on early and radical debridement rather than on antibiotics
Group B streptococcus screening in pregnancy and intrapartum penicillin prevent neonatal sepsis and meningitis
Viridans streptococci cause subacute endocarditis after dental procedures; prophylaxis is now restricted to the highest-risk cardiac lesions, and good dental hygiene matters more than antibiotic cover
Use a clinical score to decide who needs a throat swab; most sore throats are viral, and treating all of them wastes antibiotics while treating none permits rheumatic fever
Ask specifically about a sore throat weeks earlier in a child with arthritis, chorea or heart failure; the infection is often forgotten by the time the sequel appears
Isolation of S. Bovis from blood mandates colonoscopy, because of its strong association with colonic carcinoma — a microbiological result that directly triggers a surgical investigation
Erysipelas and cellulitis differ in their margins; erysipelas is sharply demarcated and raised, involving the upper dermis and lymphatics, whereas cellulitis has an indistinct edge
Penicillin sensitivity in S. Pyogenes has never been lost, so routine sensitivity testing is unnecessary for penicillin, though macrolide resistance does occur and matters in allergic patients
Rheumatic fever is diagnosed by the JONES criteria with evidence of preceding streptococcal infection; the microbiology supports a clinical diagnosis rather than making one
Anti-DNase B is the better serological test after skin infection, since skin lipids inhibit streptolysin O and the ASO titre may not rise at all

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