Step 1: Identify the molecular target.
Elongation factor 2 (EF-2) is required for the translocation step of protein synthesis on the ribosome. Inhibiting EF-2 halts host-cell protein synthesis and kills the cell.
Step 2: Recall the toxin mechanism.
Diphtheria toxin (from Corynebacterium diphtheriae) is an A-B exotoxin. Its A subunit catalyses ADP-ribosylation of the unique amino acid diphthamide on EF-2, inactivating it. Pseudomonas aeruginosa exotoxin A works by the identical mechanism, but diphtheria toxin is the classic answer.
Step 3: Eliminate the distractors.
Cholera toxin and the heat-labile toxin of E. coli ADP-ribosylate the Gs alpha subunit, locking adenylate cyclase ON and raising cAMP (watery diarrhoea) - they do not touch EF-2. Tetanospasmin is a protease that cleaves synaptobrevin, blocking inhibitory neurotransmitter release - again not EF-2.
Key fact: Diphtheria toxin inhibits EF-2 by ADP-ribosylating diphthamide, arresting host protein synthesis.