Microbiology
High-yield MBBS Microbiology question bank — bacteriology, immunology, virology, mycology and parasitology, with laboratory diagnosis, at Ananthanarayan & Paniker / Jawetz depth.
12chapters144questions82High-Yield
Definition
Staphylococcus aureus is a Gram-positive coccus in grape-like clusters, coagulase-positive, and a major pyogenic pathogen.
Morphology & Culture
- Gram-positive cocci in clusters, non-motile, non-sporing
- Grows on blood agar — golden-yellow β-haemolytic colonies
- Mannitol salt agar — ferments mannitol
- Catalase-positive, coagulase-positive
Virulence Factors
- Coagulase — fibrin coat, resists phagocytosis
- Toxins — haemolysins, leucocidin, enterotoxin, exfoliative toxin, TSST-1
- Protein A — binds Fc of IgG
- Enzymes — hyaluronidase, lipase, staphylokinase
Diseases
- Skin — boils, abscess, carbuncle, impetigo
- Deep — osteomyelitis, pneumonia, endocarditis, septicaemia
- Toxin-mediated — food poisoning, toxic shock, scalded skin syndrome
Coagulase walls off the organism, allowing abscess formation. Test Result Catalase Positive Coagulase Positive Mannitol Fermented Applied
- MRSA treated with vancomycin
- Nasal carriage is the main reservoir
🔑KEY POINTS TO REMEMBER- S. aureus: Gram-positive cocci in clusters, catalase- and coagulase-positive.
- Coagulase is the key virulence factor; toxins cause TSS, food poisoning, SSSS.
- Causes abscesses, osteomyelitis, endocarditis; MRSA needs vancomycin.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Streptococcus pyogenes is a β-haemolytic, Lancefield Group A streptococcus causing pyogenic and post-infectious diseases.
Morphology & Identification
- Gram-positive cocci in chains
- β-haemolytic on blood agar
- Catalase-negative
- Bacitracin-sensitive, PYR-positive
Virulence Factors
- M protein — chief virulence factor (antiphagocytic)
- Streptolysin O and S — haemolysins
- Streptokinase, hyaluronidase, DNase
- Erythrogenic toxin — scarlet fever
Diseases
- Suppurative — pharyngitis, impetigo, erysipelas, cellulitis, necrotising fasciitis
- Toxin-mediated — scarlet fever, streptococcal toxic shock
- Non-suppurative sequelae — rheumatic fever, acute glomerulonephritis
Acute infection may be followed weeks later by immune-mediated sequelae. Test Result Haemolysis β (complete) Catalase Negative Bacitracin Sensitive Applied
- Penicillin remains fully effective (no resistance)
- Treating pharyngitis prevents rheumatic fever
🔑KEY POINTS TO REMEMBER- S. pyogenes: Group A, β-haemolytic, catalase-negative, bacitracin-sensitive.
- M protein is the chief virulence factor.
- Sequelae: rheumatic fever and acute glomerulonephritis.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Streptococcus pneumoniae is a capsulated, lancet-shaped Gram-positive diplococcus and the commonest cause of bacterial pneumonia.
Morphology & Identification
- Lancet-shaped diplococci with a polysaccharide capsule
- α-haemolytic on blood agar (draughtsman colonies)
- Optochin-sensitive, bile-soluble
- Capsule shown by Quellung reaction
Virulence & Diseases
- Capsule — antiphagocytic, main virulence factor (>90 serotypes)
- Pneumolysin, IgA protease
- Diseases: lobar pneumonia, meningitis, otitis media, sinusitis, septicaemia
The capsule lets the organism survive and invade the lung. Feature Pneumococcus Viridans Haemolysis α α Optochin Sensitive Resistant Bile Soluble Insoluble Applied
- Pneumococcal polysaccharide and conjugate vaccines
- Splenectomised patients are at high risk (encapsulated organism)
🔑KEY POINTS TO REMEMBER- Pneumococcus: lancet-shaped capsulated diplococci, α-haemolytic.
- Optochin-sensitive and bile-soluble (unlike viridans streptococci).
- Capsule is the main virulence factor; vaccines are capsule-based.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Streptococci are Gram-positive cocci in chains, classified by haemolysis, Lancefield grouping and biochemical reactions.
By Haemolysis (on blood agar)
- β-haemolytic — complete clearing (S. pyogenes, S. agalactiae)
- α-haemolytic — partial, green (pneumococcus, viridans)
- γ (non-haemolytic) — enterococci
Lancefield Grouping (carbohydrate antigen)
- Group A — S. pyogenes
- Group B — S. agalactiae (neonatal sepsis, meningitis)
- Group D — enterococci, S. bovis
Other Streptococci
- Viridans group — normal oral flora → subacute bacterial endocarditis, dental caries
- S. agalactiae — screened for in pregnancy
Haemolysis and Lancefield antigens together identify the species. Organism Haemolysis Group S. pyogenes β A S. agalactiae β B Viridans α None Applied
- Viridans streptococci cause endocarditis after dental procedures
- Group B screening prevents neonatal sepsis
🔑KEY POINTS TO REMEMBER- Classified by haemolysis (α, β, γ) and Lancefield group.
- Group A = S. pyogenes; Group B = S. agalactiae (neonatal sepsis).
- Viridans streptococci cause subacute endocarditis.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Resistance in staphylococci is a major clinical problem, most importantly methicillin-resistant S. aureus (MRSA).
Mechanisms
- β-lactamase (penicillinase) — destroys penicillin (plasmid-mediated)
- Altered PBP2a (mecA gene) → methicillin resistance (MRSA)
- Efflux pumps, altered target sites
- Vancomycin resistance (VRSA) — altered cell-wall precursors
Clinical Types & Treatment
- HA-MRSA — hospital-acquired, multidrug-resistant
- CA-MRSA — community-acquired, skin infections
- Treatment: vancomycin, linezolid, daptomycin, teicoplanin
- Detection: cefoxitin disc diffusion, mecA PCR
The mecA gene alters the penicillin target, defeating all β-lactams. Resistance Mechanism Drug Penicillin β-lactamase Cloxacillin Methicillin mecA / PBP2a Vancomycin Applied
- Hand hygiene and isolation limit hospital spread
- Screening and decolonisation of carriers
🔑KEY POINTS TO REMEMBER- Resistance mechanisms: β-lactamase and mecA-encoded PBP2a (MRSA).
- MRSA is resistant to all β-lactams — treat with vancomycin or linezolid.
- Detected by cefoxitin disc or mecA PCR.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
The coagulase test detects the enzyme coagulase and distinguishes S. aureus (positive) from other staphylococci (negative).
Types
- Slide test — detects bound coagulase (clumping factor); rapid screening
- Tube test — detects free coagulase; confirmatory
- Positive result: visible clot within 1–4 hours
Principle
- Coagulase converts fibrinogen → fibrin
- Plasma clots → positive
- Fibrin coat protects the organism from phagocytosis
Clotting of plasma confirms the organism produces coagulase. Test Detects Slide Bound coagulase Tube Free coagulase Applied
- Negative slide test must be confirmed by tube test
- Coagulase is a marker of pathogenicity
🔑KEY POINTS TO REMEMBER- Coagulase test separates S. aureus (positive) from other staphylococci.
- Slide test = bound coagulase; tube test = free coagulase (confirmatory).
- Coagulase clots plasma and resists phagocytosis.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Coagulase-negative staphylococci (CoNS) are skin commensals that act as opportunistic pathogens, chiefly on implanted devices.
Important Species
- S. epidermidis — prosthetic and catheter infections
- S. saprophyticus — urinary tract infection in young women
- Distinguished by novobiocin sensitivity (epidermidis sensitive, saprophyticus resistant)
Pathogenesis & Significance
- Biofilm (slime) production on plastic surfaces
- Infects prosthetic valves, joints, shunts, IV catheters
- Frequently a blood-culture contaminant — interpret carefully
- Often multidrug-resistant
Biofilm on plastic surfaces shields the organism from drugs and defences. Species Infection Novobiocin S. epidermidis Prosthetic devices Sensitive S. saprophyticus UTI Resistant Applied
- Device removal often required for cure
- Repeat cultures help distinguish infection from contamination
🔑KEY POINTS TO REMEMBER- CoNS are skin commensals and opportunistic pathogens.
- S. epidermidis → device infections (biofilm); S. saprophyticus → UTI.
- Common blood-culture contaminant; often multidrug-resistant.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Staphylococcal food poisoning is an acute toxin-mediated illness caused by ingestion of preformed staphylococcal enterotoxin.
Features
- Caused by preformed heat-stable enterotoxin (types A–E)
- Very short incubation — 2–6 hours
- Severe vomiting, nausea, abdominal cramps; diarrhoea variable
- No fever; recovery within 24 hours
- Toxin acts as a superantigen on the vomiting centre
Source & Prevention
- Foods: custard, cream, milk products, cooked meat
- Source — food handler with skin lesion or nasal carriage
- Toxin survives boiling (heat-stable)
- Prevention: refrigeration, food-handler hygiene
Because the toxin is preformed, symptoms begin remarkably quickly. Feature Detail Incubation 2–6 hours Main symptom Vomiting Fever Absent Applied
- Reheating food does not destroy the toxin
- Treatment is supportive (fluids); antibiotics not needed
🔑KEY POINTS TO REMEMBER- Caused by preformed heat-stable enterotoxin.
- Very short incubation (2–6 h) with vomiting and no fever.
- Reheating does not help; treatment is supportive.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Post-streptococcal sequelae are non-suppurative, immunologically mediated complications following Streptococcus pyogenes infection.
Rheumatic Fever
- Follows throat infection (pharyngitis)
- Latent period 2–3 weeks
- Mechanism: molecular mimicry (M protein resembles cardiac tissue)
- Features: carditis, migratory polyarthritis, chorea, subcutaneous nodules, erythema marginatum
Acute Glomerulonephritis
- Follows throat or skin infection
- Latent period 1–3 weeks
- Mechanism: immune complex deposition in glomeruli
- Features: haematuria, oedema, hypertension, oliguria
Two different immune mechanisms follow the same organism. Feature Rheumatic fever Glomerulonephritis Preceding site Throat only Throat or skin Mechanism Molecular mimicry Immune complex Recurrence Common Rare Applied
- Penicillin prophylaxis prevents recurrent rheumatic fever
- ASO titre supports recent streptococcal infection
🔑KEY POINTS TO REMEMBER- Rheumatic fever follows throat infection (molecular mimicry, recurs).
- Glomerulonephritis follows throat or skin infection (immune complexes).
- Penicillin prophylaxis prevents rheumatic recurrence.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
The antistreptolysin O (ASO) titre measures antibodies against streptolysin O, indicating recent S. pyogenes infection.
Principle
- Streptolysin O is an oxygen-labile, antigenic haemolysin
- Infection → anti-streptolysin O antibodies
- Test: neutralisation of streptolysin O haemolytic activity
- Titre >200 Todd units is significant
Uses & Limitations
- Supports diagnosis of rheumatic fever (a minor criterion of evidence)
- Post-streptococcal glomerulonephritis (after pharyngitis)
- Rises 1–3 weeks after infection, peaks then falls
- Poor in skin infections — use anti-DNase B instead
A rising titre indicates recent streptococcal infection rather than current. Feature Detail Significant titre >200 Todd units Peak 3–5 weeks Skin infection Poor response Applied
- Rising titre on paired sera is more useful than a single value
- Anti-DNase B better after pyoderma
🔑KEY POINTS TO REMEMBER- ASO titre detects antibodies to streptolysin O.
- Titre >200 Todd units suggests recent infection.
- Poor response after skin infection — use anti-DNase B.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
The Quellung reaction is capsular swelling seen when capsulated bacteria are mixed with type-specific antiserum, used to identify pneumococci.
Principle & Method
- Type-specific antibody binds the capsular polysaccharide
- Capsule becomes refractile and appears swollen under microscopy
- Performed with methylene blue and specific antiserum
- ‘Quellung’ is German for swelling
Organisms Showing It
- S. pneumoniae (classic)
- Klebsiella pneumoniae
- Haemophilus influenzae, Neisseria meningitidis
Antibody binding makes the capsule visibly swell under the microscope. Feature Detail Reaction Capsular swelling Main organism S. pneumoniae Purpose Serotyping Applied
- Rapid identification directly from sputum or CSF
- Serotyping guides vaccine composition
🔑KEY POINTS TO REMEMBER- Quellung = capsular swelling with type-specific antiserum.
- Classic for S. pneumoniae; also Klebsiella, Haemophilus, meningococcus.
- Used for rapid identification and serotyping.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Enterococci are Gram-positive cocci of the normal intestinal flora (Lancefield Group D) that cause opportunistic infections.
Features & Identification
- E. faecalis (commonest) and E. faecium
- Grow in 6.5% NaCl and 40% bile, at pH 9.6
- Bile-esculin positive; usually γ (non-haemolytic)
- Hardy — survive harsh conditions
Infections & Resistance
- Urinary tract infection, biliary sepsis, intra-abdominal infection
- Endocarditis, neonatal sepsis
- Intrinsically resistant to cephalosporins
- VRE (vancomycin-resistant enterococci) — major hospital problem
Normally harmless gut flora become pathogens when they reach sterile sites. Test Result 6.5% NaCl Growth Bile-esculin Positive Cephalosporins Resistant Applied
- VRE treated with linezolid or daptomycin
- Endocarditis needs penicillin + aminoglycoside synergy
🔑KEY POINTS TO REMEMBER- Enterococci: Group D gut commensals, grow in 6.5% NaCl and bile.
- Cause UTI, biliary sepsis and endocarditis.
- Intrinsically cephalosporin-resistant; VRE is a hospital concern.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).