Diphtheria toxin production by Corynebacterium diphtheriae requires infection by a bacteriophage carrying the tox gene. The mechanism by which diphtheria toxin kills mammalian cells is:

• A Activation of adenylyl cyclase, increasing cAMP and causing chloride secretion
• B Cleavage of the 23S rRNA, preventing peptidyl transfer
• C Pore formation in the plasma membrane, causing osmotic lysis
• D ADP-ribosylation of EF-2 (elongation factor 2), halting protein synthesis ✓

Explanation

Diphtheria toxin (an A-B toxin) enters cells via receptor-mediated endocytosis; the A subunit (catalytic domain) ADP-ribosylates a modified histidine residue (diphthamide) on EF-2 (elongation factor 2), irreversibly blocking translocation of peptidyl-tRNA during protein synthesis. One toxin molecule can inactivate all EF-2 in a cell, leading to cell death. This mechanism is shared by Pseudomonas exotoxin A. Cholera toxin activates adenylyl cyclase. Shiga toxin cleaves 28S rRNA (not 23S). Staphylococcal alpha-toxin forms pores.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.