## Virulence Factors of C. diphtheriae **Key Point:** The diphtheria toxin gene is NOT chromosomally encoded in all strains — it is carried by a lysogenic bacteriophage (β-phage), and only lysogenized strains produce toxin. Non-lysogenized strains are non-toxigenic. ### Correct Statements | Feature | Details | |---------|----------| | **Toxin Structure** | A-B toxin: catalytic A subunit (inactivates EF-2) + binding B subunit | | **Mechanism of Action** | ADP-ribosylation of EF-2 → halts protein synthesis → cell death | | **Gene Location** | Carried on β-phage DNA (lysogenic conversion) | | **Iron Regulation** | DtxR (diphtheria toxin repressor) represses *tox* when Fe²⁺ is abundant | | **Low-Iron Paradox** | Iron starvation derepresses *tox* → maximum toxin production | ### Why Option 1 Is Wrong The *tox* gene is **NOT chromosomal** in all isolates. It resides on the genome of a temperate β-phage. Only lysogenized strains (those carrying integrated phage DNA) produce toxin. Non-lysogenized C. diphtheriae are avirulent, even if otherwise pathogenic. **High-Yield:** This is a classic NEET PG trap — students often confuse chromosomal vs. plasmid/phage-encoded genes. The phage-mediated toxin production is the hallmark of C. diphtheriae pathogenesis. ### Clinical Correlation **Clinical Pearl:** In the laboratory, toxin production is confirmed by the **Elek test** (immunodiffusion) or **PCR for *tox* gene**. Biotype identification (gravis, intermedius, mitis) does not predict toxigenicity — only phage lysogeny does. [cite:Jawetz & Melnick 27e Ch 18] ---
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