Microbiology
High-yield MBBS Microbiology question bank — bacteriology, immunology, virology, mycology and parasitology, with laboratory diagnosis, at Ananthanarayan & Paniker / Jawetz depth.
12chapters144questions82High-Yield
Definition
Neisseria are Gram-negative, kidney-shaped diplococci; the two pathogens are N. meningitidis and N. gonorrhoeae.
Common Features
- Gram-negative diplococci, oxidase-positive, catalase-positive
- Fastidious — need chocolate agar, 5–10% CO₂
- Selective medium: Thayer-Martin
- Delicate — killed by drying and cold (transport promptly)
N. meningitidis
- Capsulated; ferments glucose and maltose
- Spread by droplets; nasopharyngeal carriage
- Causes meningitis, meningococcaemia, Waterhouse-Friderichsen syndrome
- Vaccine available (capsular)
N. gonorrhoeae
- Non-capsulated; ferments glucose only
- Sexually transmitted; pili aid attachment
- Urethritis, cervicitis, ophthalmia neonatorum, PID
Two species share morphology but differ in transmission and disease. Feature Meningococcus Gonococcus Capsule Present Absent Maltose Fermented Not fermented Vaccine Available None Applied
- Ceftriaxone is first-line for both
- Rifampicin prophylaxis for meningococcal contacts
🔑KEY POINTS TO REMEMBER- Neisseria: Gram-negative oxidase-positive diplococci on chocolate agar.
- Meningococcus is capsulated and ferments glucose + maltose.
- Gonococcus ferments glucose only; causes ophthalmia neonatorum.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Enteric fever is a systemic infection caused by Salmonella typhi (and paratyphi), transmitted by the faeco-oral route.
Pathogenesis
- Ingestion → invades intestinal mucosa (Peyer’s patches)
- Multiplies in mesenteric nodes → bacteraemia
- Spreads to liver, spleen, gall bladder, bone marrow
- Incubation 7–14 days
Clinical Course
- Week 1 — step-ladder fever, headache; blood culture positive
- Week 2 — rose spots, splenomegaly; Widal positive
- Week 3 — complications: intestinal perforation, haemorrhage
- Week 4 — stool and urine culture positive
Weekly progression determines which specimen is most likely positive. Week Best specimen 1st Blood culture 2nd Widal (serology) 3rd–4th Stool, urine Applied
- Treatment: ceftriaxone, azithromycin (resistance to older drugs)
- Chronic carriers harbour organisms in the gall bladder
🔑KEY POINTS TO REMEMBER- Enteric fever from S. typhi, faeco-oral spread.
- Blood culture positive in week 1; Widal in week 2; stool/urine later.
- Complications: intestinal perforation and haemorrhage in week 3.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Enterobacteriaceae are Gram-negative bacilli of the gut flora; E. coli is the commonest member and a major pathogen.
Family Characteristics
- Gram-negative bacilli, oxidase-negative
- Ferment glucose; reduce nitrate to nitrite
- Grow on MacConkey agar (lactose fermenters pink)
- Members: E. coli, Klebsiella, Proteus, Salmonella, Shigella
E. coli
- Normal gut commensal; lactose fermenter, indole-positive
- Commonest cause of urinary tract infection
- Also neonatal meningitis, septicaemia, wound infection
- Diarrhoeagenic strains: ETEC, EPEC, EHEC, EIEC, EAEC
Klebsiella
- Capsulated, non-motile, mucoid colonies
- Pneumonia (red-currant jelly sputum), UTI, hospital infection
Commensal organisms cause disease when they reach the wrong site. Organism Feature E. coli Lactose+, motile, indole+ Klebsiella Capsulated, non-motile Proteus Swarming, urease+ Applied
- ESBL-producing strains are a major resistance problem
- Klebsiella pneumonia is typical of alcoholics and diabetics
🔑KEY POINTS TO REMEMBER- Enterobacteriaceae: Gram-negative bacilli, oxidase-negative, ferment glucose.
- E. coli is the commonest cause of urinary tract infection.
- Klebsiella is capsulated, non-motile, causes lobar pneumonia.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Vibrio cholerae is a comma-shaped Gram-negative bacillus causing cholera, an acute severe watery diarrhoea.
Morphology & Culture
- Curved (comma-shaped) Gram-negative bacilli
- Darting motility (single polar flagellum)
- Oxidase-positive; grows in alkaline conditions
- Media: TCBS (yellow colonies), alkaline peptone water (enrichment)
- Serogroups O1 (classical, El Tor) and O139
Pathogenesis & Features
- Cholera toxin → ↑ cAMP → massive chloride and water secretion
- Rice-water stools, no fever, no blood
- Severe dehydration, hypovolaemic shock, metabolic acidosis
- Non-invasive (mucosa remains intact)
The toxin drives secretion without invading the mucosa. Feature Detail Medium TCBS (yellow) Stool Rice-water Toxin effect ↑ cAMP Applied
- ORS is the mainstay; doxycycline shortens illness
- Safe water and sanitation prevent epidemics
🔑KEY POINTS TO REMEMBER- V. cholerae: comma-shaped, darting motility, oxidase-positive, grows on TCBS.
- Cholera toxin ↑ cAMP → rice-water stools without fever or blood.
- Rehydration (ORS/IV) is the mainstay of treatment.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Pseudomonas aeruginosa is an aerobic Gram-negative bacillus and an important opportunistic and hospital-acquired pathogen.
Characteristics
- Gram-negative bacillus, motile, strict aerobe
- Oxidase-positive, non-lactose fermenter
- Pigments: pyocyanin (blue-green), pyoverdin (fluorescent)
- Sweet, grape-like odour; grows on simple media, survives in water
Infections
- Burns and wound infection (blue-green pus)
- Ventilator-associated pneumonia; cystic fibrosis colonisation
- Urinary tract infection (catheters), otitis externa
- Septicaemia — ecthyma gangrenosum
Its survival in moist environments makes it a classic hospital pathogen. Test Result Oxidase Positive Lactose Not fermented Pigment Pyocyanin Applied
- Intrinsically resistant to many antibiotics
- Treat with antipseudomonal β-lactams (piperacillin-tazobactam, ceftazidime) ± aminoglycoside
🔑KEY POINTS TO REMEMBER- P. aeruginosa: aerobic Gram-negative bacillus, oxidase-positive, pyocyanin pigment.
- Opportunistic — burns, ventilators, catheters, cystic fibrosis.
- Multidrug-resistant; needs antipseudomonal agents.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
The Widal test is a tube agglutination test that detects antibodies against Salmonella antigens in enteric fever.
Principle & Antigens
- Patient serum + standard Salmonella antigen suspensions
- O antigen (somatic) — rises early, falls quickly
- H antigen (flagellar) — rises later, persists longer
- Significant titre: O ≥ 1:160, H ≥ 1:160 (varies with endemicity)
Limitations
- Positive only from the second week
- False positives — previous infection, vaccination, endemic area, malaria
- False negatives — early illness, prior antibiotics
- Paired sera showing a rising titre are most reliable
Agglutination titres reflect the antibody response, not the organism itself. Antigen Appears Persists O (somatic) Early Short H (flagellar) Later Long Applied
- Blood culture is far more specific (positive in week 1)
- Interpret carefully in endemic areas
🔑KEY POINTS TO REMEMBER- Widal detects O and H antibodies from the second week.
- O rises early and falls; H rises later and persists.
- Paired rising titres are needed; blood culture is more reliable.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Bacillary dysentery is an acute invasive colitis caused by Shigella, producing blood and mucus in the stool.
Organism & Species
- Gram-negative bacilli, non-motile, non-lactose fermenting
- S. dysenteriae (most severe, Shiga toxin), S. flexneri, S. boydii, S. sonnei (mildest)
- Very low infective dose (10–100 organisms) → easy person-to-person spread
Pathogenesis & Features
- Invades colonic mucosa → ulceration and inflammation
- Shiga toxin (S. dysenteriae) → cytotoxic, can cause HUS
- Fever, cramps, tenesmus, frequent small stools with blood and mucus
- Rarely invades the bloodstream
Mucosal invasion, not toxin secretion alone, causes the bloody stools. Feature Shigella Cholera Stool Blood, mucus Rice-water Fever Present Absent Mechanism Invasive Toxin Applied
- Fluid replacement plus ciprofloxacin/ceftriaxone
- Avoid antimotility drugs (prolong illness)
🔑KEY POINTS TO REMEMBER- Shigella: non-motile Gram-negative bacilli, very low infective dose.
- Invasive colitis → fever, tenesmus, blood and mucus in stool.
- S. dysenteriae produces Shiga toxin (risk of HUS).
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Diarrhoeagenic E. coli are pathogenic strains causing distinct types of diarrhoea by different mechanisms.
Main Types
- ETEC — enterotoxigenic: heat-labile and heat-stable toxins; travellers’ diarrhoea
- EPEC — enteropathogenic: attaching-effacing lesions; infantile diarrhoea
- EHEC (O157:H7) — Shiga-like verotoxin; bloody diarrhoea, haemolytic uraemic syndrome
- EIEC — enteroinvasive: dysentery-like illness
- EAEC — enteroaggregative: persistent diarrhoea
Different strains cause diarrhoea by toxin, adherence or invasion. Type Illness ETEC Travellers’ diarrhoea EHEC Bloody diarrhoea, HUS EPEC Infantile diarrhoea Applied
- Avoid antibiotics in EHEC — may precipitate HUS
- EHEC linked to undercooked beef; sorbitol-negative on MacConkey
🔑KEY POINTS TO REMEMBER- ETEC (travellers’), EPEC (infantile), EHEC (bloody/HUS), EIEC (dysentery), EAEC (persistent).
- EHEC O157:H7 produces verotoxin.
- Antibiotics are avoided in EHEC because of HUS risk.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Proteus is a Gram-negative bacillus of the Enterobacteriaceae, characterised by swarming motility and strong urease production.
Characteristics
- Highly motile → swarming growth on blood agar
- Urease-positive (splits urea to ammonia)
- Non-lactose fermenter; fishy odour
- Species: P. mirabilis (commoner), P. vulgaris
Clinical Significance
- Urinary tract infection, especially with catheters
- Urease → alkaline urine → struvite (staghorn) stones
- Wound and burn infection, septicaemia
- Weil-Felix reaction uses Proteus OX antigens (rickettsial diagnosis)
Urease-driven alkalinisation of urine precipitates struvite stones. Feature Detail Motility Swarming Urease Positive Complication Staghorn calculi Applied
- Suspect Proteus with alkaline urine and stones
- Swarming can obscure other colonies on culture plates
🔑KEY POINTS TO REMEMBER- Proteus shows swarming motility and is strongly urease-positive.
- Causes UTI with alkaline urine and struvite (staghorn) stones.
- OX antigens used in the Weil-Felix reaction.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Haemophilus influenzae is a small, fastidious Gram-negative coccobacillus requiring X and V factors for growth.
Growth Requirements
- Needs factor X (haemin) and factor V (NAD)
- Grows on chocolate agar, not on plain blood agar
- Satellitism around S. aureus colonies on blood agar
- Capsulated (type b) and non-capsulated strains
Diseases
- Type b (Hib) — meningitis, epiglottitis, septic arthritis in children
- Non-capsulated — otitis media, sinusitis, exacerbations of COPD
- Prevented by the Hib conjugate vaccine
Its fastidious growth needs explain the special culture requirements. Feature Detail Factors X (haemin) + V (NAD) Medium Chocolate agar Vaccine Hib conjugate Applied
- Hib vaccine has dramatically reduced childhood meningitis
- Ceftriaxone for invasive disease; rifampicin prophylaxis for contacts
🔑KEY POINTS TO REMEMBER- H. influenzae needs factors X and V → grows on chocolate agar.
- Shows satellitism around S. aureus.
- Type b causes meningitis and epiglottitis — prevented by Hib vaccine.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Cholera toxin is the enterotoxin of V. cholerae responsible for the massive watery diarrhoea of cholera.
Structure & Mechanism
- A-B subunit toxin: 5 B subunits + 1 A subunit
- B subunits bind GM1 ganglioside on enterocytes
- A subunit enters and ADP-ribosylates the Gs protein
- Adenylyl cyclase permanently activated → ↑ cAMP
- ↑ Chloride secretion, ↓ sodium absorption → massive water loss
Locked-on adenylyl cyclase drives litres of fluid into the gut lumen. Subunit Role B (5) Binds GM1 receptor A (1) ↑ cAMP (ADP-ribosylation) Applied
- Mucosa is not damaged — absorption of glucose-sodium remains intact
- This is why ORS works in cholera
🔑KEY POINTS TO REMEMBER- Cholera toxin is an A-B toxin; B binds GM1, A raises cAMP.
- ↑ cAMP → chloride and water secretion → rice-water stools.
- Mucosa stays intact, so oral rehydration is effective.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).Definition
Non-typhoidal salmonellae (e.g. S. typhimurium, S. enteritidis) cause acute gastroenteritis — salmonella food poisoning.
Features
- Source: poultry, eggs, milk, meat (animal reservoir)
- Large infective dose required
- Incubation 12–48 hours
- Fever, vomiting, abdominal pain, diarrhoea (may be bloody)
- Invasive gastroenteritis — self-limiting in 3–7 days
Complications & Management
- Bacteraemia in infants, elderly, immunocompromised, sickle-cell disease
- Osteomyelitis (sickle-cell disease)
- Treatment: fluids only for uncomplicated cases
- Antibiotics only for severe or invasive disease (they prolong carriage)
Mucosal invasion produces fever and diarrhoea unlike toxin food poisoning. Feature Salmonella Staphylococcal Incubation 12–48 h 2–6 h Fever Present Absent Mechanism Invasion Preformed toxin Applied
- Cook eggs and poultry thoroughly
- Avoid antibiotics in uncomplicated cases
🔑KEY POINTS TO REMEMBER- Non-typhoidal salmonellae come from poultry, eggs and meat.
- Incubation 12–48 h with fever and diarrhoea (invasive).
- Treat with fluids; antibiotics only for invasive disease.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Textbook of Microbiology (Baveja).