NEET-PG Microbiology Previous Year Questions (2017–2026)

Correct answer: D. Cholera activates Gs; pertussis inactivates Gi

Cholera toxin ADP-ribosylates the Gs alpha subunit, locking it in the active GTP-bound state so adenylyl cyclase runs continuously and cyclic AMP rises, driving massive intestinal chloride and water secretion. Pertussis toxin ADP-ribosylates Gi, preventing it from inhibiting adenylyl cyclase; with the brake removed, cyclic AMP again rises. So cholera activates Gs and pertussis inactivates Gi. Both raise cyclic AMP but from opposite ends of the same pathway.

Incorrect Options:

• A. Cholera activates Gq; pertussis inactivates Gs: cholera acts on Gs, not Gq; pertussis acts on Gi, not Gs.
  
  Cholera activates Gq; pertussis inactivates Gs.
• B. Cholera inactivates Gs; pertussis activates Gq: cholera turns Gs on, and pertussis targets Gi, not Gq.
  
  Cholera inactivates Gs; pertussis activates Gq.
• C. Cholera inactivates Gi; pertussis activates Gs: the targets are swapped: cholera is Gs, pertussis is Gi.
  
  Cholera inactivates Gi; pertussis activates Gs.

High-Yield Facts:

• Both toxins act by ADP-ribosylation and both raise intracellular cyclic AMP.
• Cholera toxin locks Gs on; pertussis toxin locks Gi off.
• Cholera gives voluminous rice-water diarrhoea; pertussis gives whooping cough with lymphocytosis.
• Heat-labile toxin of enterotoxigenic E. coli acts like cholera toxin on Gs.

Correct answer: B. Missing-self NK recognition.

The large granular lymphocytes are natural killer (NK) cells. NK activity is set by a balance between activating and inhibitory receptors. Inhibitory receptors (KIRs) engage self MHC class I and hold the NK cell in check. When a tumour or virus-infected cell downregulates MHC class I to evade cytotoxic T cells, it loses that inhibitory signal -- activating signals now dominate and the NK cell kills it. This is the missing-self hypothesis.

Incorrect Options:

• A. Antibody-dependent cellular cytotoxicity: ADCC needs target-bound antibody engaging CD16 -- it does not depend on loss of MHC class I.
  
  ADCC is triggered by antibody-coated targets, not by missing MHC class I.
• C. Complement-mediated lysis: Requires antibody or lectin activation forming the membrane-attack complex, again unrelated to MHC loss.
  
  Complement lysis works through the membrane-attack complex, not NK missing-self.
• D. Increased presentation on MHC class II: The cell is losing MHC I, and class II activates CD4 helper cells, not the described killing.
  
  MHC class II presents to CD4 helper T cells -- it does not explain NK killing.

High-Yield Facts:

• NK cells are the main defence against cells that hide by losing MHC class I.
• Missing-self: absent inhibitory MHC-I signal lets activating signals kill the target.
• NK cells also mediate ADCC through their CD16 (FcgammaRIII) receptor.
• Key NK cytokines: interleukin-2, interleukin-15 activate -- they secrete interferon-gamma.

Correct answer: A. Bacilli in Virchow foam cells.

In lepromatous leprosy cell-mediated immunity fails, so vast numbers of Mycobacterium leprae accumulate inside lipid-laden foamy macrophages called Virchow (lepra) cells, sometimes packed into globi. The bacillary load is very high and the lepromin test is negative.

Incorrect Options:

• B. Index = solid:broken ratio: the ratio of solid (viable) to fragmented bacilli is the morphological index. The bacteriological index grades the total load on a 0 to 6 logarithmic scale. Ziehl-Neelsen smear: solid versus fragmented bacilli define the morphological index.
• C. Lepromin positive in lepromatous: the lepromin (Mitsuda) reaction is negative in lepromatous disease (anergy) and positive in tuberculoid leprosy. Induration of a delayed hypersensitivity skin test, as read in the lepromin reaction.
• D. Lepromin is type III reaction: the lepromin response is a type IV delayed cell-mediated reaction, not an immune-complex (type III) one. Immunofluorescence band of type III immune-complex deposition, contrasted with the type IV lepromin test.

High-Yield Facts:

• Bacteriological index grades load 0 to 6 (log scale); morphological index reflects viability and treatment response.
• Lepromatous pole: T-helper-2 skew, low cell-mediated immunity, high bacilli, lepromin negative.
• Tuberculoid pole: T-helper-1 skew, strong cell-mediated immunity, few bacilli, lepromin positive.
• Virchow (lepra) cells are foamy macrophages stuffed with bacilli.