Microbiology chapters
Staphylococcus and Streptococcus
The Gram-positive cocci: Staphylococcus aureus (virulence factors, toxin diseases, MRSA), coagulase-negative staphylococci, and the streptococci classified by haemolysis and Lancefield group (S. pyogenes with rheumatic fever and glomerulonephritis, S. agalactiae, S. pneumoniae, viridans streptococci, enterococci), with the tests that tell them apart.
In 30 seconds
- Staphylococci are Gram-positive cocci in clusters, catalase-positive; S. aureus is coagulase-positive (golden colonies, ferments mannitol), with protein A, and causes pyogenic infections (boils, impetigo, osteomyelitis (commonest cause), septic arthritis, acute endocarditis in drug users, pneumonia after influenza) and toxin diseases (food poisoning with heat-stable enterotoxin within hours, scalded skin syndrome (exfoliatin), toxic shock syndrome (TSST-1, superantigen)); MRSA (mecA → PBP2a) needs vancomycin; S. epidermidis infects prosthetic devices (biofilm) and S. saprophyticus causes UTIs in young women (novobiocin-resistant).
- Streptococci are in chains, catalase-negative, grouped by haemolysis and Lancefield antigens: group A S. pyogenes (β, bacitracin-sensitive, M protein, streptolysin O → ASO titre) causes pharyngitis, impetigo, cellulitis, scarlet fever, necrotising fasciitis and the non-suppurative sequelae rheumatic fever (after pharyngitis only) and post-streptococcal glomerulonephritis (after pharyngitis or skin infection); group B S. agalactiae (CAMP-positive) causes neonatal sepsis and meningitis.
- S. pneumoniae (α, lancet-shaped diplococci, optochin-sensitive, bile-soluble, capsule) is the commonest cause of community-acquired pneumonia, otitis media and adult meningitis; viridans streptococci (α, optochin-resistant) cause dental caries (S. mutans) and subacute endocarditis on damaged valves; enterococci (group D, grow in bile and 6.5% salt) cause UTIs and endocarditis and resist many antibiotics.
On this page
Gram-positive cocci: first steps
| Test | Staphylococci | Streptococci |
|---|---|---|
| Arrangement | Clusters (grape-like) | Chains or pairs |
| Catalase | Positive | Negative |
Staphylococci
Staphylococcus aureus
Lab features: Gram-positive cocci in clusters; catalase +, coagulase +; golden-yellow colonies, often β-haemolytic; ferments mannitol (mannitol salt agar: yellow); DNase +. Carried in the anterior nares of about a third of people (source of infection, hospital spread).
Virulence factors:
| Factor | Role |
|---|---|
| Coagulase | Converts fibrinogen to fibrin: walls off the infection (abscess) |
| Protein A | Binds the Fc of IgG: blocks opsonisation |
| Capsule, clumping factor, fibronectin-binding proteins | Adhesion and immune evasion |
| Hyaluronidase, lipases, staphylokinase | Spread |
| α-toxin (haemolysin) | Pore-forming; tissue damage |
| Panton-Valentine leukocidin (PVL) | Kills leucocytes; severe skin infections and necrotising pneumonia (community MRSA) |
| Enterotoxins (A–E) | Food poisoning; heat-stable; superantigens |
| Exfoliative (epidermolytic) toxins | Cleave desmoglein-1: staphylococcal scalded skin syndrome, bullous impetigo |
| TSST-1 | Superantigen: toxic shock syndrome |
| β-lactamase, PBP2a (mecA) | Antibiotic resistance |
Diseases:
Pyogenic (invasive):
- Skin: folliculitis, furuncle (boil), carbuncle (several follicles), impetigo (with S. pyogenes; bullous impetigo is staphylococcal), cellulitis, wound infections, abscesses, stye, paronychia, mastitis.
- Bone and joint: osteomyelitis (commonest cause overall; haematogenous in children, metaphysis), septic arthritis (commonest cause in adults).
- Pneumonia: after influenza; cavitating, abscesses, pneumatoceles; ventilator-associated.
- Acute infective endocarditis: destroys normal valves; tricuspid valve in IV drug users; prosthetic valves.
- Bacteraemia, septicaemia, metastatic abscesses (kidney, brain), line infections.
Toxin-mediated:
- Food poisoning: preformed enterotoxin in cream, custard, milk products, salads, meat; vomiting and abdominal cramps 1–6 hours after eating; no fever; recovery within a day; reheating does not destroy the toxin.
- Scalded skin syndrome (Ritter disease): infants and young children; widespread blistering and peeling; Nikolsky sign positive; low mortality in children.
- Toxic shock syndrome: fever, hypotension, diffuse erythematous rash followed by desquamation of palms and soles, multi-organ involvement; associated with tampons, nasal packing, surgical wounds; blood cultures usually negative.
MRSA:
- mecA gene (on the SCC*mec* element) → PBP2a with low affinity for all β-lactams (except ceftaroline).
- Hospital-acquired (multi-resistant) and community-acquired (often PVL-positive, skin infections).
- Treatment: vancomycin, teicoplanin, linezolid, daptomycin (not for pneumonia); for skin infections, doxycycline, co-trimoxazole, clindamycin.
- Control: hand hygiene, screening, isolation, nasal mupirocin decolonisation, chlorhexidine washes.
- Methicillin-sensitive S. aureus is treated with flucloxacillin (or cefazolin).
Coagulase-negative staphylococci
| Organism | Key points |
|---|---|
| S. epidermidis | Normal skin flora; forms biofilm on prosthetic heart valves, joint replacements, IV catheters, shunts, peritoneal dialysis catheters; commonest contaminant of blood cultures; often methicillin-resistant (vancomycin); novobiocin-sensitive |
| S. saprophyticus | UTI in young sexually active women (second to E. coli); novobiocin-resistant; urease + |
Streptococci
Classification
By haemolysis on blood agar:
- α (partial, green): S. pneumoniae, viridans streptococci.
- β (complete, clear): group A (S. pyogenes), group B (S. agalactiae), groups C and G.
- γ (none): enterococci (usually), S. bovis (group D, non-enterococcal).
Lancefield grouping: by cell wall C-carbohydrate antigens (A, B, C, D, ...). Pneumococci and viridans streptococci have no Lancefield group.
| Organism | Haemolysis | Key tests |
|---|---|---|
| S. pyogenes (group A) | β | Bacitracin sensitive, PYR + |
| S. agalactiae (group B) | β | Bacitracin resistant, CAMP test +, hippurate hydrolysis + |
| S. pneumoniae | α | Optochin sensitive, bile soluble, quellung + |
| Viridans group | α | Optochin resistant, bile insoluble |
| Enterococcus faecalis (group D) | γ (or α) | Grows in bile (bile esculin +) and 6.5% NaCl, PYR + |
| S. bovis (S. gallolyticus) | γ | Bile esculin +, no growth in 6.5% NaCl |
High-yield
"B-BRAS": Bacitracin: group B Resistant, group A Sensitive. "OVRPS": Optochin: Viridans Resistant, Pneumococcus Sensitive.
Streptococcus pyogenes (group A)
Virulence factors:
| Factor | Role |
|---|---|
| M protein | Main virulence factor; antiphagocytic (blocks complement); many types; antibodies give type-specific immunity; cross-reacts with heart myosin (rheumatic fever) |
| Hyaluronic acid capsule | Antiphagocytic (non-immunogenic: like human tissue) |
| Streptolysin O | Oxygen-labile haemolysin, antigenic → anti-streptolysin O (ASO) titre (evidence of recent infection, especially pharyngitis) |
| Streptolysin S | Oxygen-stable, non-antigenic; causes β-haemolysis on the agar surface |
| Streptokinase | Activates plasminogen (used as a thrombolytic) |
| Hyaluronidase, DNase B | Spread (anti-DNase B rises after skin infection) |
| Pyrogenic (erythrogenic) exotoxins | Superantigens: scarlet fever rash, streptococcal toxic shock |
Suppurative diseases:
- Pharyngitis/tonsillitis ("strep throat"): commonest bacterial cause; fever, exudate, tender anterior cervical nodes, no cough; peritonsillar abscess (quinsy).
- Scarlet fever: pharyngitis + sandpaper rash (spares the area around the mouth: circumoral pallor), strawberry tongue, Pastia lines, later desquamation.
- Skin: impetigo (honey-coloured crusts), erysipelas (well-demarcated, raised, bright red: dermis and lymphatics), cellulitis, necrotising fasciitis ("flesh-eating"; surgical emergency).
- Streptococcal toxic shock syndrome, puerperal sepsis, bacteraemia.
Non-suppurative sequelae (immune-mediated):
| Feature | Acute rheumatic fever | Post-streptococcal glomerulonephritis |
|---|---|---|
| Preceding infection | Pharyngitis only | Pharyngitis or skin (impetigo) |
| Latent period | About 2–4 weeks | About 1–2 weeks (throat) or 3–6 weeks (skin) |
| Mechanism | Molecular mimicry (type II): antibodies to M protein cross-react with heart, joints, brain | Immune complexes (type III) in glomeruli; low complement (C3) |
| Features | Jones criteria: carditis (pancarditis; mitral valve), migratory polyarthritis, Sydenham chorea, erythema marginatum, subcutaneous nodules; fever, raised ESR/CRP, prolonged PR; Aschoff bodies | Nephritic syndrome: haematuria (cola-coloured urine), oedema (periorbital), hypertension, oliguria |
| Prevention | Treating pharyngitis with penicillin prevents it; secondary prophylaxis with benzathine penicillin every 3–4 weeks for years | Antibiotics do not reliably prevent it |
| Outcome | Chronic rheumatic heart disease (mitral stenosis): still common in Pakistan | Usually full recovery in children |
Laboratory: throat swab culture on blood agar (β-haemolytic, bacitracin-sensitive), rapid antigen tests; ASO (raised after pharyngitis), anti-DNase B (raised after skin and throat infection).
Treatment: penicillin (no resistance has emerged); amoxicillin; macrolide in penicillin allergy; surgery plus clindamycin and penicillin for necrotising fasciitis.
Streptococcus agalactiae (group B)
- Colonises the vagina and gut of many women.
- Neonatal sepsis, pneumonia and meningitis (the leading cause in many countries): early-onset (first week, from the birth canal) and late-onset.
- Risk factors: prolonged rupture of membranes, preterm labour, maternal fever, previous affected baby.
- Prevention: intrapartum penicillin for colonised or high-risk mothers.
- Also infects pregnant women (UTI, chorioamnionitis), diabetics and the elderly.
Streptococcus pneumoniae (pneumococcus)
- Lancet-shaped Gram-positive diplococci, α-haemolytic; "draughtsman" colonies (central dip from autolysis); optochin-sensitive, bile-soluble; polysaccharide capsule (more than 90 serotypes; quellung reaction); IgA protease, pneumolysin.
- Diseases (MOPS): Meningitis (commonest in adults), Otitis media (commonest bacterial cause in children), Pneumonia (commonest cause of community-acquired and lobar pneumonia: rusty sputum), Sinusitis; also bacteraemia, peritonitis.
- Risk: asplenia and sickle cell disease, alcoholism, extremes of age, HIV, after influenza.
- Vaccines: pneumococcal conjugate vaccine (PCV10/PCV13) in infants (Pakistan EPI at 6, 10 and 14 weeks); polysaccharide vaccine (PPSV23) for older adults and at-risk groups.
- Treatment: penicillin or amoxicillin; ceftriaxone (± vancomycin) in meningitis because of reduced penicillin sensitivity (altered PBPs).
Viridans streptococci
- α-haemolytic, optochin-resistant; normal mouth flora.
- S. mutans: makes dextrans from sucrose → dental plaque and caries.
- Subacute infective endocarditis on previously damaged valves (rheumatic, congenital) after dental procedures; Osler nodes, splinter haemorrhages, Roth spots.
- S. anginosus (milleri) group: abscesses (brain, liver).
Enterococci (E. faecalis, E. faecium)
- Group D, γ-haemolytic; very hardy: grow in 6.5% NaCl and 40% bile, at 10–45 °C.
- Normal gut flora; UTIs (especially catheters), biliary infections, subacute endocarditis (often after GI or GU procedures), wound infections.
- Intrinsically resistant to cephalosporins; treat with ampicillin + gentamicin (synergy) in endocarditis; VRE (E. faecium) needs linezolid or daptomycin.
- S. bovis (S. gallolyticus) bacteraemia or endocarditis suggests colorectal cancer: do a colonoscopy.
Exam focus
Expect: catalase and coagulase tests, S. aureus virulence factors (protein A, coagulase, toxins), staphylococcal food poisoning, scalded skin and toxic shock syndromes, commonest cause of osteomyelitis, MRSA mechanism and treatment, S. epidermidis and prosthetic devices, S. saprophyticus and novobiocin, haemolysis and Lancefield groups, bacitracin and optochin tests, M protein and ASO, scarlet fever, rheumatic fever vs post-streptococcal glomerulonephritis, group B neonatal sepsis and CAMP test, pneumococcus (capsule, diseases, vaccine), viridans and subacute endocarditis, enterococci and S. bovis with colon cancer.
Quick revision
- Staph: clusters, catalase +. Strep: chains, catalase −.
- S. aureus: coagulase +, protein A; osteomyelitis, boils, acute endocarditis; food poisoning (heat-stable toxin, 1–6 h), scalded skin, TSS.
- MRSA: mecA → PBP2a; vancomycin.
- S. epidermidis: prosthetic devices. S. saprophyticus: UTI, novobiocin-resistant.
- Group A: bacitracin-sensitive, M protein, ASO; rheumatic fever (throat only) and PSGN (throat or skin).
- Group B: neonatal sepsis; CAMP +.
- Pneumococcus: optochin-sensitive, bile-soluble, capsule; pneumonia, otitis, meningitis.
- Viridans: caries, subacute endocarditis. Enterococcus: 6.5% NaCl; UTI, endocarditis.
Written by The House Job from standard microbiology references (Levinson's Review of Medical Microbiology and Immunology).
FAQ
Which test separates staphylococci from streptococci?
The catalase test: staphylococci are catalase-positive, streptococci catalase-negative.
How do rheumatic fever and post-streptococcal glomerulonephritis differ in the preceding infection?
Rheumatic fever follows only streptococcal pharyngitis; glomerulonephritis can follow either pharyngitis or skin infection.
How is Streptococcus pneumoniae distinguished from viridans streptococci?
Pneumococci are optochin-sensitive and bile-soluble; viridans streptococci are optochin-resistant and bile-insoluble.
Which organism commonly infects prosthetic valves and catheters?
Staphylococcus epidermidis, which forms biofilms on plastic and metal surfaces.