Q.79 Which of the statements about Corynebacterium diphtheriae biology is NOT CORRECT?
(A) All strains of C. diphtheriae are producers of diphtheria toxin
(B) Diphtheria toxin production can be minimized by high concentration of iron in the medium
(C) Diphtheria toxin inhibits protein synthesis
(D) Diphtheria toxin is an A-B toxin secreted as a polypeptide of 62 kDa
Not all strains of Corynebacterium diphtheriae produce diphtheria toxin—only those lysogenized by a tox+ bacteriophage like β-phage. Thus, (A) is NOT CORRECT, while options (B), (C), and (D) accurately describe toxin regulation, mechanism, and structure.
Option Breakdown
Corynebacterium diphtheriae causes diphtheria via an AB toxin encoded by the tox gene on a temperate phage, not the bacterial chromosome.
| Option | Statement | Correct? | Explanation |
|---|---|---|---|
| (A) | All strains produce toxin | FALSE | Only tox+ phage lysogens produce toxin (~10-20% of clinical isolates). Non-lysogenic or tox- phage strains are non-toxigenic. |
| (B) | High iron minimizes toxin | TRUE | DtxR repressor (Fe2+ activated) binds tox promoter at high iron, suppressing expression. Low iron → maximal toxin. |
| (C) | Inhibits protein synthesis | TRUE | A-fragment ADP-ribosylates eEF-2 (diphthamide residue), halting elongation. |
| (D) | 62 kDa A-B toxin polypeptide | TRUE | Single 535 aa chain (58-62 kDa); nicked into A (~21 kDa) + B (~40 kDa) subunits linked by disulfide. |
Mechanism Summary
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Phage β lysogenizes C. diphtheriae → integrates tox gene.
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Low iron → DtxR inactive → tox transcribed → secreted 62 kDa pro-toxin.
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Host cell entry: B binds HB-EGF receptor → endocytosis → A translocates to cytosol.
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Toxicity: A inactivates eEF-2 → translation arrest → cell death.
Corynebacterium diphtheriae biology questions test diphtheria toxin regulation and mechanism—crucial for CSIR NET Life Sciences, GATE Biotechnology, and microbiology grad students. This guide debunks “all strains produce toxin” (false!) while confirming iron repression, protein synthesis inhibition, and 62 kDa A-B structure.
Diphtheria Pathogenesis Core
Corynebacterium diphtheriae (Gram+, club-shaped) colonizes throat → forms pseudomembrane. Toxigenic strains (tox+ phage lysogens) secrete diphtheria toxin causing myocarditis, neuritis. Non-toxigenic strains exist and cause mild/asymptomatic infections.
Keywords: Corynebacterium diphtheriae biology, diphtheria toxin production, tox gene regulation, A-B toxin mechanism.
Iron Regulation (DtxR Pathway)
High Fe2+ → DtxR(Fe) binds tox promoter → ↓ transcription
Low Fe2+ → DtxR apo-form → toxin MAX production
Elek test confirms toxigenicity. Vaccine: formalin-inactivated toxoid.
Toxin Structure & Action
62 kDa polypeptide → Protease nicking → A(21kDa)|S-S|B(40kDa)
↓ Endocytosis, pH drop
A enters cytosol → NAD+ → ADP-ribosyl-eEF-2 → NO translation
Exam Traps
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“All strains toxigenic”: Confuses clinical isolates with lab strains.
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Iron effect reversed: High iron ↑ toxin (false—it’s ↓).
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Molecular weight: 62 kDa is pre-nicked single chain.
Clinical Correlates
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DTaP vaccine: Toxoid + pertussis/acell. tetanus.
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Schick test: Historical toxin sensitivity assay.
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Emerging: C. ulcerans/pseudotuberculosis also toxigenic.
Related Searches: diphtheria toxin structure function, DtxR iron regulation, tox phage lysogeny, CSIR NET Corynebacterium MCQs.
This Corynebacterium diphtheriae biology resource equips biotechnology/molecular biology students for entrance exams and infectious disease research. Master toxin misconceptions for success!
