Streptococcus
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Direct answer
Catalase-negative gram-positive cocci in chains organise themselves by two parallel systems the exam expects you to carry: Lancefield cell-wall carbohydrate groups (A for Streptococcus pyogenes, B for S. agalactiae, D for the enterococci) and haemolysis on blood agar — beta (complete), alpha (partial, green) or gamma (none). Group A beta-haemolytic streptococci, bacitracin-sensitive, cause pharyngitis, impetigo, scarlet fever and then the nonsuppurative sequelae rheumatic fever and post-streptococcal glomerulonephritis; group B (CAMP test positive, hippurate hydrolysed) colonises the vagina and causes neonatal sepsis and meningitis. Streptococcus pneumoniae, an alpha-haemolytic, optochin-sensitive, bile-soluble, capsule-carrying diplococcus, causes lobar pneumonia and meningitis and is covered by both the 23-valent polysaccharide and conjugate vaccines; enterococci, bile-esculin-positive and growing in 6.5 per cent salt, bring vancomycin resistance to the ward.
What you must remember
- First divide by catalase (staphylococcus positive, streptococcus negative); then by haemolysis; then by bench tests — bacitracin for group A, optochin and bile solubility for pneumococcus, CAMP and hippurate for group B, bile esculin and salt tolerance for enterococci.
- Group A virulence: M protein (types rheumatogenic — pharyngitis strains drive rheumatic fever; nephritogenic skin strains drive glomerulonephritis), hyaluronic acid capsule, streptolysin O (immunogenic, basis of the ASO titre) and streptolysin S (oxygen-stable, surface haemolysis).
- Scarlet fever: erythrogenic (SpeA) toxin phage-encoded — rough "sandpaper" rash, circumoral pallor, Pastia lines, strawberry tongue, desquamation later.
- Rheumatic fever follows pharyngitis (not skin infection) after two to three weeks; glomerulonephritis follows either throat or skin infection and does not recur the way rheumatic fever does.
- Group B streptococcus screening at 35–37 weeks of pregnancy, with intrapartum penicillin prophylaxis, prevents early-onset neonatal sepsis.
- Pneumococcus: capsule is the key virulence factor (quellung swelling with type-specific antiserum), IgA protease aids colonisation; resistance is by penicillin-binding protein changes, treat meningitis by MIC.
- Viridans streptococci: Streptococcus mutans causes dental caries; S. sanguinis groups are the classic subacute bacterial endocarditis organisms after dental procedures.
- Enterococcus faecalis and E. faecium: treat endocarditis with synergistic penicillin or vancomycin plus gentamicin; linezolid and daptomycin cover vancomycin-resistant strains.
A sore throat walked through properly
A twelve-year-old presents with fever, tender anterior cervical nodes and tonsillar exudate without cough — a Centor-score picture favouring streptococcal pharyngitis over viral. A rapid antigen test or throat swab confirms group A. Penicillin V for ten days remains first-line everywhere including Indian practice; the duration matters, because a full course prevents rheumatic fever even though it barely shortens the sore throat. Two weeks later a migratory polyarthritis with a new murmur and a raised erythrocyte sedimentation rate would fulfil revised Jones criteria — secondary prophylaxis with monthly benzathine penicillin then begins. Had the presentation instead been impetigo with a three-week gap to periorbital oedema, tea-coloured urine and a low C3, that would be post-streptococcal glomerulonephritis: supportive care, no antibiotic prophylaxis, and essentially no recurrence risk. The pathway teaches the central doctrine — which site of infection leads to which sequela, and what prophylaxis each demands.
How the exam frames it
Bench-test matching is the commonest frame: bacitracin-sensitive beta-haemolytic colonies equal group A; optochin-sensitive alpha-haemolytic diplococci equal pneumococcus; bacitracin-resistant equal group B; catalase is the gateway separating the genera — and candidates who jump to coagulase lose the mark, because coagulase belongs to staphylococci. The second frame is sequela directionality: rheumatic fever follows pharyngitis only, glomerulonephritis follows both pharyngitis and skin infection, and only rheumatic fever warrants long-term secondary prophylaxis. The third is the pneumococcus capsule — asking which virulence factor the polysaccharide vaccine targets, or why the conjugate vaccine (part of India's universal immunisation programme) works in infants while the 23-valent does not. ASO titre questions ask what a rise means (recent infection) rather than a diagnosis of rheumatic fever by itself.
Frequently asked questions
Which bedside tests differentiate group A, group B and pneumococcus?
Group A streptococci are bacitracin-sensitive beta-haemolytic; group B are bacitracin-resistant, CAMP-positive; Streptococcus pneumoniae is alpha-haemolytic, optochin-sensitive and bile-soluble.
Why does rheumatic fever follow pharyngitis but not skin infection?
Pharyngitis strains carry rheumatogenic M proteins and the throat's immune context produces cross-reactive antibodies against cardiac tissue; skin strains with nephritogenic proteins cause glomerulonephritis instead, so the site and M type decide the sequela.
What is the role of the ASO titre?
Streptolysin O is strongly immunogenic, so a rising or significantly elevated anti-streptolysin O titre documents recent group A infection — supporting evidence in Jones criteria, never a standalone diagnosis.
How is neonatal group B streptococcal disease prevented?
Vaginorectal screening at 35–37 weeks and intrapartum intravenous penicillin for colonised women; the CAMP test or hippurate hydrolysis identifies the organism in the laboratory.
Which streptococcus causes dental caries and which causes subacute endocarditis?
Streptococcus mutans causes caries through glucan production on enamel; viridans group organisms such as S. sanguinis cause subacute bacterial endocarditis after dental procedures — the reason for prophylaxis in high-risk cardiac patients.
How is enterococcus identified and its endocarditis treated?
Bile-esculin positivity and growth in 6.5 per cent sodium chloride; endocarditis needs synergistic cell-wall agent plus aminoglycoside, with linezolid or daptomycin reserved for vancomycin-resistant strains.