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DNB CET Microbiology Syllabus

The Microbiology syllabus for DNB CET in full: 4 chapters and 15 topics, every one listed below, plus 60 Microbiology flashcards with answers.

4Chapters
15Topics
60Flashcards

Microbiology syllabus: all 4 chapters

Expand any chapter to see its topics and sub-topics.

  1. General Microbiology and Immunology

     4 topics
    • Bacterial structure, growth and sterilization
    • Innate and adaptive immunity
    • Hypersensitivity reactions and immunodeficiency
    • Vaccines and immunization schedules

  2. Systemic Bacteriology

     4 topics
    • Gram-positive cocci - Staphylococcus and Streptococcus
    • Enterobacteriaceae and gram-negative bacilli
    • Mycobacteria and acid-fast organisms
    • Anaerobes and spirochetes

  3. Virology and Mycology

     4 topics
    • DNA and RNA viruses of clinical importance
    • Hepatitis viruses and HIV
    • Superficial and systemic mycoses
    • Opportunistic fungal infections

  4. Parasitology and Applied Microbiology

     3 topics
    • Protozoa - Plasmodium, Entamoeba, Leishmania
    • Helminths - cestodes, trematodes, nematodes
    • Hospital-acquired infections and antimicrobial stewardship

DNB CET Microbiology flashcards — 60 questions with answers

  1. Which structural component of the bacterial cell wall is the target of penicillin and confers shape/rigidity?

    Peptidoglycan (murein) - a polymer of N-acetylglucosamine and N-acetylmuramic acid cross-linked by peptide bridges; penicillin inhibits transpeptidase (PBP) cross-linking.

  2. What are the key differences in cell wall between Gram-positive and Gram-negative bacteria?

    Gram-positive: thick peptidoglycan layer, teichoic acid, no outer membrane (stain violet). Gram-negative: thin peptidoglycan, outer membrane with LPS (endotoxin), periplasmic space (stain pink/red).

  3. What is the active component of endotoxin (LPS) and which part is responsible for toxicity?

    Lipopolysaccharide of the Gram-negative outer membrane; Lipid A is the toxic moiety, causing fever, hypotension and DIC (septic shock).

  4. Name the four phases of the bacterial growth curve in order.

    Lag phase, Log (exponential) phase, Stationary phase, Decline (death) phase.

  5. What temperature, pressure, and time define standard autoclave sterilization?

    121 degrees C at 15 psi (15 lb/sq inch) for 15-20 minutes (moist heat / saturated steam).

  6. Which biological indicator is used to test autoclave efficiency vs hot air oven?

    Autoclave: spores of Geobacillus stearothermophilus (Bacillus stearothermophilus). Hot air oven: spores of Bacillus subtilis (atrophaeus / Clostridium tetani).

  7. What temperature and time are used for hot air oven (dry heat) sterilization?

    160 degrees C for 1-2 hours (dry heat); used for glassware, metal instruments, oils and powders.

  8. Differentiate sterilization, disinfection, and antisepsis.

    Sterilization: complete removal/killing of ALL microbes including spores. Disinfection: killing of vegetative pathogens (not necessarily spores) on inanimate objects. Antisepsis: use of chemicals on living tissue to inhibit microbes.

  9. Which cells and molecules constitute the FIRST line of innate immune defense?

    Physical/chemical barriers (skin, mucosa, lysozyme, acid pH), phagocytes (neutrophils, macrophages), NK cells, complement, and inflammatory cytokines - non-specific, no memory.

  10. What is the key distinction between innate and adaptive immunity?

    Innate: rapid, non-specific, no immunological memory (germline-encoded receptors, e.g. TLRs). Adaptive: slower, antigen-specific, has memory, mediated by T and B lymphocytes (clonal selection).

  11. Which immunoglobulin crosses the placenta and which is the first produced in a primary response?

    IgG crosses the placenta (passive immunity to fetus). IgM is the first/largest antibody produced in the primary immune response (pentamer).

  12. Which immunoglobulin is the main antibody in mucosal secretions, and which mediates type I hypersensitivity?

    IgA (secretory, dimer) is the predominant mucosal/secretory antibody. IgE mediates type I hypersensitivity and parasite defense.

  13. What are the three pathways of complement activation and the common convergence point?

    Classical (antigen-antibody), Alternative (microbial surfaces), and Lectin (MBL binding mannose) pathways; all converge at C3 activation leading to the membrane attack complex (MAC, C5b-9).

  14. Which complement components are anaphylatoxins and which is the major opsonin?

    Anaphylatoxins: C3a, C4a, C5a (C5a is also a potent chemotactic). Major opsonin: C3b.

  15. List the four types of hypersensitivity reactions (Coombs and Gell classification).

    Type I: immediate/anaphylactic (IgE). Type II: cytotoxic/antibody-mediated (IgG/IgM). Type III: immune complex-mediated. Type IV: delayed/cell-mediated (T cells).

  16. Give a classic example of each hypersensitivity type.

    Type I: anaphylaxis/asthma/atopy. Type II: hemolytic transfusion reaction, Goodpasture. Type III: SLE, serum sickness, Arthus reaction. Type IV: tuberculin/Mantoux test, contact dermatitis.

  17. Which hypersensitivity type is the only antibody-INDEPENDENT one, and which cells mediate it?

    Type IV (delayed-type); mediated by sensitized T lymphocytes (CD4 Th1 / CD8) and macrophages, not antibodies. Peaks at 48-72 hours.

  18. Differentiate DiGeorge syndrome and Bruton agammaglobulinemia.

    DiGeorge: thymic aplasia -> T-cell deficiency (22q11 deletion, hypocalcemia, cardiac defects). Bruton (X-linked) agammaglobulinemia: BTK mutation -> absent B cells and all immunoglobulins.

  19. Which immunodeficiency causes recurrent Neisseria infections, and which causes infections by catalase-positive organisms?

    Terminal complement deficiency (C5-C9/MAC) -> recurrent Neisseria. Chronic granulomatous disease (NADPH oxidase defect) -> catalase-positive organisms (S. aureus, Aspergillus, Serratia).

  20. What is the difference between active and passive immunization?

    Active: host's own immune system produces antibodies after antigen exposure (vaccine/infection) - slow onset, long-lasting, has memory. Passive: ready-made antibodies given (immunoglobulin/antitoxin) - immediate, short-lived, no memory.

Show the other 40 Microbiology flashcards

  1. Name the live attenuated vaccines in routine immunization.

    BCG, OPV (oral polio), MMR (measles, mumps, rubella), varicella, yellow fever, rotavirus, intranasal influenza, oral typhoid.

  2. At what ages are BCG, OPV-0, and Hepatitis B birth dose given per India's National Immunization Schedule?

    All given at birth (BCG, OPV-0, and Hepatitis B birth dose within 24 hours).

  3. What is the schedule for DPT/Pentavalent primary doses and boosters in the Indian UIP?

    Pentavalent (DPT+HepB+Hib): 6, 10, 14 weeks. DPT boosters at 16-24 months and 5-6 years. TT/Td at 10 and 16 years.

  4. Differentiate Staphylococcus aureus from coagulase-negative staphylococci on key tests.

    S. aureus: coagulase-positive, mannitol fermenter (golden colonies), DNase-positive. CoNS (e.g. S. epidermidis): coagulase-negative; S. saprophyticus is novobiocin-resistant (causes UTI).

  5. Which toxins of S. aureus cause toxic shock syndrome, scalded skin syndrome, and food poisoning?

    TSST-1 (superantigen) -> toxic shock. Exfoliatin/epidermolytic toxin -> scalded skin syndrome. Heat-stable enterotoxins -> food poisoning (rapid onset 2-6 h).

  6. How are streptococci classified by hemolysis on blood agar?

    Alpha (partial/green, e.g. S. pneumoniae, viridans), Beta (complete/clear, e.g. S. pyogenes, S. agalactiae), Gamma (non-hemolytic, e.g. Enterococcus).

  7. How do you distinguish S. pneumoniae from viridans streptococci, and S. pyogenes from S. agalactiae?

    Pneumoniae: optochin-sensitive, bile-soluble. Viridans: optochin-resistant, bile-insoluble. S. pyogenes (Group A): bacitracin-sensitive, PYR-positive. S. agalactiae (Group B): bacitracin-resistant, CAMP-positive, hippurate-positive.

  8. Name the non-suppurative complications of Streptococcus pyogenes infection.

    Acute rheumatic fever (follows pharyngitis) and acute post-streptococcal glomerulonephritis (follows pharyngitis or skin infection); ASO titre rises after pharyngeal infection.

  9. What biochemical features define the family Enterobacteriaceae?

    Gram-negative bacilli, facultative anaerobes, oxidase-negative, glucose fermenters, reduce nitrate to nitrite, catalase-positive.

  10. Differentiate E. coli, Klebsiella, and Proteus on classic biochemical reactions.

    E. coli: lactose fermenter, indole-positive, motile, IMViC ++--. Klebsiella: lactose fermenter, mucoid/capsulated, non-motile, IMViC --++. Proteus: non-lactose fermenter, swarming, urease-positive, H2S-positive.

  11. What is the difference between Shigella and Salmonella on motility, H2S, and lactose?

    Shigella: non-motile, H2S-negative, non-lactose fermenter (except some), no gas. Salmonella: motile, H2S-positive (most), non-lactose fermenter, produces gas.

  12. Which media are selective/differential for enteric Gram-negative bacilli?

    MacConkey agar (lactose fermenters pink), DCA, XLD, and Wilson-Blair (BBSA) for Salmonella; SS agar for Salmonella/Shigella; TCBS for Vibrio.

  13. What stain is used for Mycobacterium tuberculosis and why does it stain that way?

    Ziehl-Neelsen (acid-fast) stain - retains carbol fuchsin after acid-alcohol decolorization due to mycolic acids in the cell wall (acid-fast); appears red against blue background.

  14. What is the gold standard culture medium and approximate growth time for M. tuberculosis?

    Lowenstein-Jensen (LJ) medium (egg-based); growth takes 2-8 weeks (slow grower, generation time ~18-24 h). Liquid MGIT systems are faster (~2 weeks).

  15. Which mycobacterium causes leprosy, how is it diagnosed, and where is it cultured?

    Mycobacterium leprae; diagnosed by slit-skin smear (ZN/Fite stain showing AFB), cannot be cultured in vitro (grown in mouse footpad/armadillo); Lepromin test assesses cell-mediated immunity.

  16. Differentiate obligate anaerobes from microaerophiles and name a key obligate anaerobe genus.

    Obligate anaerobes: killed by oxygen, lack catalase/superoxide dismutase (e.g. Clostridium, Bacteroides). Microaerophiles: need low O2 (e.g. Campylobacter, Helicobacter).

  17. Match the Clostridium species to its disease and mechanism.

    C. tetani: tetanus (tetanospasmin blocks GABA/glycine release -> spastic paralysis). C. botulinum: botulism (toxin blocks acetylcholine -> flaccid paralysis). C. perfringens: gas gangrene/food poisoning (alpha toxin, lecithinase). C. difficile: pseudomembranous colitis (toxins A and B).

  18. Which spirochete causes syphilis and what serological tests are used?

    Treponema pallidum; non-treponemal tests (VDRL, RPR - screening, become negative after treatment) and treponemal tests (TPHA, FTA-ABS - confirmatory, remain positive for life). Seen by dark-ground microscopy.

  19. Name the spirochetes causing leptospirosis and Lyme disease and a diagnostic clue.

    Leptospira interrogans -> leptospirosis (Weil's disease; MAT is reference test; exposure to rodent urine/water). Borrelia burgdorferi -> Lyme disease (erythema migrans rash, tick-borne).

  20. How are viruses classified by nucleic acid and an example of each major group?

    DNA viruses: mostly double-stranded (Herpesviruses, Adenovirus, Poxvirus, Hepadnavirus); Parvovirus is ssDNA. RNA viruses: mostly single-stranded (Picornavirus, Orthomyxovirus, Retrovirus); Reovirus/Rotavirus is dsRNA.

  21. Name the eight human herpesviruses and one disease each.

    HSV-1 (oral herpes), HSV-2 (genital herpes), VZV/HHV-3 (chickenpox/shingles), EBV/HHV-4 (infectious mononucleosis), CMV/HHV-5 (congenital infection), HHV-6/7 (roseola), HHV-8 (Kaposi sarcoma).

  22. Which RNA virus causes antigenic shift/drift and what do these terms mean?

    Influenza virus (Orthomyxovirus). Antigenic drift: minor point mutations in HA/NA -> epidemics. Antigenic shift: major reassortment of genome segments -> pandemics.

  23. List the five hepatitis viruses with their genome type and route of transmission.

    HAV (RNA, feco-oral), HBV (DNA, parenteral/sexual/vertical), HCV (RNA, parenteral), HDV (RNA defective, needs HBV), HEV (RNA, feco-oral - severe in pregnancy).

  24. What does each Hepatitis B serological marker indicate?

    HBsAg: active infection (acute/chronic). Anti-HBs: immunity/recovery or vaccination. HBeAg: high infectivity/replication. Anti-HBc IgM: acute infection. HBV DNA: viral load.

  25. What is the marker of the 'window period' in acute Hepatitis B?

    Anti-HBc IgM is the only positive marker during the window period (HBsAg has disappeared and anti-HBs has not yet appeared).

  26. What type of virus is HIV, which cells does it infect, and what enzymes does it carry?

    HIV is an enveloped ssRNA retrovirus (Lentivirus); infects CD4+ T cells (via gp120 binding CD4 + CCR5/CXCR4 coreceptors); carries reverse transcriptase, integrase, and protease.

  27. Which dermatophyte genera cause superficial mycoses and what are dermatophytes called collectively?

    Trichophyton, Microsporum, and Epidermophyton; collectively called dermatophytes causing tinea (ringworm); they invade keratinized tissue (skin, hair, nails).

  28. Match each systemic dimorphic fungus to its endemic clue.

    Histoplasma capsulatum (bird/bat droppings, intracellular in macrophages), Blastomyces dermatitidis, Coccidioides immitis (spherules, desert/SW USA), Paracoccidioides. All are thermally dimorphic (mold at 25 C, yeast at 37 C).

  29. Which opportunistic fungus causes infection in neutropenic patients and shows septate acute-angle branching hyphae?

    Aspergillus (especially A. fumigatus); septate hyphae with acute-angle (45 degree, dichotomous) branching. Mucor/Rhizopus show broad aseptate ribbon-like hyphae with wide-angle (90 degree) branching.

  30. What is the diagnostic clue for Cryptococcus neoformans and Pneumocystis jirovecii in immunocompromised patients?

    Cryptococcus: India ink shows capsulated yeast in CSF; cryptococcal antigen (CrAg) positive; causes meningitis. Pneumocystis jirovecii: causes PCP pneumonia; cysts seen on silver (GMS) stain, treated with cotrimoxazole.

  31. Name the malarial Plasmodium species and which two cause relapses.

    P. falciparum (most severe, cerebral malaria), P. vivax, P. ovale, P. malariae, P. knowlesi. P. vivax and P. ovale cause relapses due to dormant hypnozoites in the liver.

  32. Differentiate the cyst and trophozoite features of Entamoeba histolytica from commensal amoebae.

    E. histolytica: mature cyst has 4 nuclei; trophozoite contains ingested RBCs (erythrophagocytosis - pathognomonic), causes amoebic dysentery and liver abscess (anchovy-sauce pus).

  33. How is Leishmania transmitted, what form is seen in tissue, and what disease does L. donovani cause?

    Transmitted by sandfly (Phlebotomus) bite; amastigote (LD bodies) form seen intracellularly in macrophages; L. donovani causes kala-azar (visceral leishmaniasis) with fever, splenomegaly, pancytopenia.

  34. Classify helminths into the three major groups with an example of each.

    Cestodes (tapeworms - Taenia, Echinococcus), Trematodes (flukes - Schistosoma, Fasciola), Nematodes (roundworms - Ascaris, hookworm, Enterobius, Wuchereria).

  35. Differentiate Taenia solium from Taenia saginata and which causes cysticercosis.

    T. solium (pork tapeworm): scolex with rostellum and hooklets, gravid segment has <13 uterine branches; causes neurocysticercosis if eggs ingested. T. saginata (beef tapeworm): no hooklets, >13 branches; no cysticercosis in humans.

  36. Which nematode causes lymphatic filariasis, how is it diagnosed, and when is the parasite found in blood?

    Wuchereria bancrofti (and Brugia malayi); diagnosed by demonstrating microfilariae in a nocturnal (night) peripheral blood smear (nocturnal periodicity); causes elephantiasis.

  37. What is the difference between exotoxins and endotoxins?

    Exotoxins: secreted proteins, highly toxic, specific action, heat-labile, antigenic (form toxoids), from Gram +/-. Endotoxins: LPS/Lipid A in Gram-negative cell wall, released on lysis, heat-stable, poorly antigenic, non-specific (fever/shock).

  38. Define hospital-acquired (nosocomial) infection and name the most common type.

    An infection acquired in a healthcare setting, not present or incubating at admission (typically appearing >48 hours after admission). Catheter-associated urinary tract infection (CAUTI) is the most common nosocomial infection.

  39. What does the acronym ESKAPE stand for in hospital-acquired multidrug-resistant pathogens?

    Enterococcus faecium, Staphylococcus aureus (MRSA), Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, Enterobacter species - leading MDR nosocomial pathogens.

  40. What are the core objectives of an antimicrobial stewardship program?

    Optimize antimicrobial use to improve patient outcomes, reduce resistance, minimize toxicity/adverse effects, and decrease costs - via the 'right drug, right dose, right duration, right route', de-escalation, and audit/feedback.

DNB CET Microbiology FAQ

What is in the DNB CET Microbiology syllabus?

DNB CET Microbiology is split into 4 chapters: General Microbiology and Immunology, Systemic Bacteriology, Virology and Mycology and Parasitology and Applied Microbiology. Together they contain 15 topics.

How many chapters are in DNB CET Microbiology?

4 chapters, containing 15 topics. The largest chapter is General Microbiology and Immunology, with 4 topics.

Are there flashcards for DNB CET Microbiology?

Yes — a 60-card Microbiology deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.