PGIMER Entrance Microbiology Syllabus

Microbiology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Microbiology in PGIMER Entrance, not a summary of it.

1. 1

   General and Immunology

   4 topics

   • Bacterial structure, growth and genetics
   • Sterilization and disinfection methods
   • Host defense and antigen-antibody reactions
   • Vaccines and immunization schedule
2. 2

   Bacteriology

   4 topics

   • Gram-positive cocci and bacilli
   • Gram-negative enteric and respiratory pathogens
   • Mycobacteria and spirochetes
   • Anaerobes and zoonotic bacteria
3. 3

   Virology, Mycology and Parasitology

   4 topics

   • DNA and RNA viruses of medical importance
   • Hepatitis viruses and HIV
   • Systemic and opportunistic fungal infections
   • Protozoa and helminths
     • Malaria and amoebiasis
     • Intestinal and tissue helminths

Microbiology flashcards for PGIMER Entrance

24 of 57 cards from the Microbiology deck — real questions with worked answers.

1. What is the chemical composition and function of the bacterial peptidoglycan (murein) cell wall?

   A polymer of alternating N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) cross-linked by peptide chains. It provides rigidity and shape and protects against osmotic lysis. It is the target of penicillins (inhibit transpeptidase/cross-linking) and lysozyme (cleaves NAG-NAM bond).

2. Compare the cell wall of Gram-positive and Gram-negative bacteria.

   Gram-positive: thick peptidoglycan (multiple layers) with teichoic/lipoteichoic acids, no outer membrane, retains crystal violet (stains purple). Gram-negative: thin peptidoglycan, outer membrane containing LPS (endotoxin), periplasmic space; loses crystal violet and takes safranin counterstain (stains pink/red).

3. What is the structure and clinical significance of bacterial lipopolysaccharide (LPS/endotoxin)?

   Found in the outer membrane of Gram-negative bacteria. Composed of lipid A (toxic/endotoxin activity), core polysaccharide, and O-antigen (somatic antigen, basis of serotyping). Lipid A triggers fever, hypotension, DIC, and septic shock via cytokine (TNF-alpha, IL-1) release; it is heat-stable and released on cell lysis.

4. Contrast bacterial endotoxin and exotoxin.

   Endotoxin: LPS lipid A from Gram-negative cell wall, heat-stable, poorly antigenic (no toxoid), nonspecific effects (fever, shock), released on lysis. Exotoxin: secreted proteins from Gram-positive and Gram-negative bacteria, heat-labile, highly antigenic (can form toxoids/antitoxins), specific potent effects, often plasmid/phage encoded.

5. Describe the four phases of the bacterial growth curve.

   1) Lag phase: adaptation, no division. 2) Log (exponential) phase: maximal, constant division rate; most susceptible to antibiotics. 3) Stationary phase: nutrient depletion/toxin accumulation, growth = death, spore formation begins. 4) Decline (death) phase: death exceeds growth, exponential decline.

6. What is generation (doubling) time and the formula for number of bacteria after n generations?

   Generation time is the time required for a bacterial population to double. Number of cells N = N0 x 2^n, where N0 = initial number and n = number of generations. E. coli generation time is ~20 min; M. tuberculosis is ~18-24 hours.

7. Name and define the three main mechanisms of bacterial genetic transfer.

   1) Transformation: uptake of naked DNA from the environment by a competent cell. 2) Transduction: transfer of bacterial DNA by a bacteriophage (generalized or specialized). 3) Conjugation: direct cell-to-cell transfer of plasmid (e.g., F factor) DNA via a sex pilus.

8. What are bacterial spores and why are they clinically important?

   Dormant, highly resistant structures formed (mainly by Bacillus and Clostridium) under adverse conditions; contain dipicolinic acid and calcium, little water, and are metabolically inactive. They resist heat, desiccation, chemicals, and radiation. Killed only by autoclaving (121C/15 min) or sporicidal agents; basis for sterilization controls.

9. What is the difference between sterilization and disinfection?

   Sterilization: complete destruction/removal of ALL microorganisms including bacterial spores. Disinfection: destruction of vegetative pathogenic organisms on inanimate objects, but not necessarily all spores. Antisepsis is the use of chemicals (antiseptics) on living tissue.

10. What are the standard autoclave (moist heat) operating parameters for sterilization?

    121C at 15 lb/in2 (psi) pressure for 15-20 minutes (or 134C at 30 psi for ~3 min). Moist heat kills by coagulation/denaturation of proteins. It is the most common and reliable method; Bacillus stearothermophilus spores are the biological indicator.

11. Which biological indicator (spore) is used to test the efficacy of autoclaving versus hot-air oven?

    Autoclave (moist heat): Geobacillus (Bacillus) stearothermophilus. Hot-air oven (dry heat): Bacillus subtilis var. niger (globigii). Ethylene oxide gas: Bacillus subtilis var. niger. These spores confirm sterilization cycles.

12. Describe dry heat sterilization parameters (hot-air oven).

    160C for 2 hours (or 170C for 1 hour, 180C for 30 min). Dry heat kills by oxidation and denaturation. Used for glassware, powders, oils, and metal instruments that withstand high temperature; not suitable for rubber or plastics.

13. What is ethylene oxide used for and what are its limitations?

    Ethylene oxide (EtO) is a gaseous chemical (alkylating agent) used to sterilize heat-sensitive items such as plastics, catheters, endoscopes, and heart-lung machine components. It is mutagenic, carcinogenic, explosive, and requires prolonged aeration to remove toxic residue.

14. Define pasteurization and its two main methods.

    Pasteurization is mild heating to kill non-spore-forming pathogens (e.g., M. bovis, Coxiella, Brucella) in milk without sterilizing it. Holder method: 63C for 30 min. Flash/HTST method: 72C for 15-20 seconds, then rapid cooling. Phosphatase test confirms adequacy.

15. Name the three lines of host defense in immunity.

    1) Physical/chemical barriers: skin, mucous membranes, lysozyme, gastric acid, normal flora. 2) Innate (nonspecific) immunity: phagocytes (neutrophils, macrophages), NK cells, complement, inflammation. 3) Adaptive (specific) immunity: humoral (B cells/antibodies) and cell-mediated (T cells), with memory.

16. Contrast innate and adaptive immunity.

    Innate: present from birth, immediate, nonspecific, no memory, same response on re-exposure (barriers, phagocytes, complement, NK cells). Adaptive: develops after exposure, specific to antigen, slower initially, possesses memory (faster/stronger secondary response), mediated by B and T lymphocytes.

17. List the five classes of immunoglobulins and one key feature of each.

    IgG: most abundant in serum, only Ig crossing placenta, secondary response. IgM: largest (pentamer), first in primary response, best at complement fixation. IgA: secretory (dimer) in mucosa/breast milk. IgE: mediates type I hypersensitivity and antiparasitic response (binds mast cells). IgD: B-cell surface receptor.

18. Describe the three pathways of complement activation and the common end result.

    Classical pathway: activated by antigen-antibody (IgG/IgM) complexes, starts at C1. Alternative pathway: activated by microbial surfaces (LPS), antibody-independent. Lectin pathway: mannose-binding lectin binds microbial carbohydrates. All converge on C3 cleavage and form the C5-C9 Membrane Attack Complex (MAC) causing lysis; C3a/C5a are anaphylatoxins, C3b is an opsonin.

19. Classify the four types of hypersensitivity reactions (Gell and Coombs).

    Type I: immediate/anaphylactic, IgE-mediated (anaphylaxis, atopy). Type II: cytotoxic, IgG/IgM against cell-surface antigens (hemolytic anemia, transfusion reaction). Type III: immune-complex mediated (serum sickness, SLE, Arthus). Type IV: delayed, T-cell mediated (tuberculin/Mantoux test, contact dermatitis).

20. Differentiate the precipitation, agglutination, and ELISA antigen-antibody reactions.

    Precipitation: soluble antigen + antibody form a visible precipitate (e.g., VDRL, immunodiffusion). Agglutination: particulate antigen + antibody form visible clumps (e.g., Widal, blood grouping). ELISA: enzyme-labeled antibody/antigen produces a colored signal, highly sensitive (e.g., HIV screening).

21. What is the difference between active and passive immunization, with examples?

    Active immunity: host's own immune system makes antibodies after exposure to antigen/vaccine; slow onset, long-lasting, has memory (e.g., toxoids, live/killed vaccines). Passive immunity: preformed antibodies given directly; immediate but short-lived, no memory (e.g., antitoxins, immunoglobulins, maternal IgG, breast milk).

22. Classify vaccines into their main types with examples.

    Live attenuated: BCG, OPV, MMR, varicella, rotavirus. Killed/inactivated: IPV (Salk), whole-cell pertussis, rabies, hepatitis A. Toxoid: diphtheria, tetanus. Subunit/conjugate: HepB (recombinant), Hib, pneumococcal, HPV. Live vaccines generally give stronger, longer immunity but are contraindicated in pregnancy/immunocompromised.

23. List the vaccines given at birth under India's National Immunization Schedule.

    At birth: BCG (against tuberculosis), OPV-0 (oral polio zero dose), and Hepatitis B birth dose. These are given as early as possible within 24 hours (HepB) / before discharge.

24. What vaccines does the Indian National Immunization Schedule provide at 6, 10, and 14 weeks?

    At 6, 10, and 14 weeks: OPV (1,2,3), Pentavalent vaccine (DPT + Hepatitis B + Hib) doses 1,2,3, Rotavirus vaccine (1,2,3), and fIPV (fractional inactivated polio) at 6 and 14 weeks. PCV (pneumococcal conjugate) is given at 6 and 14 weeks with a booster at 9 months in the UIP.

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