How does Corynebacterium diphtheriae produce toxins?

Diphtheria toxin is an exotoxin secreted by Corynebacterium, the pathogenic bacterium that causes diphtheria. The toxin gene is encoded by a prophage called corynephage β. The toxin causes the disease in humans by gaining entry into the cell cytoplasm and inhibiting protein synthesis.

What is the mechanism of pathogenicity for diphtheria?

The pathogenesis of diphtheria is based upon two primary determinants: (1) the ability of a given strain of C diphtheriae to colonize in the nasopharyngeal cavity and/or on the skin, and (2) its ability to produce diphtheria toxin.

What is the receptor for diphtheria toxin?

Iwamoto, R. et al. Heparin-binding EGF-like growth factor, which acts as the diphtheria toxin receptor, forms a complex with membrane protein DRAP27/CD9, which up-regulates functional receptors and diphtheria toxin sensitivity.

How diphtheria inhibit protein synthesis?

Diphtheria toxin (DT) functions like other toxins by inhibiting protein synthesis either by modifying elongation factor-2 (EF2) or by acting directly on the ribosome (Siegall, 1994).

What is the mechanism of action of Corynebacterium toxin?

Diphtheria toxin is secreted from Corynebacterium diphtheriae as a single polypeptide chain containing two major domains: DT-A, which carries the active site for ADP ribosylation of EF-2, and DT-B, which promotes binding of toxin to cells and the entry of the A chain into the cytosolic compartment.

How does the diphtheria toxin exert its action?

It is concluded from the present studies that diphtheria toxin exerts a primary, reversible effect at the surface of susceptible cells where it inhibits cytochrome-linked phosphorylation concerned with transport of inorganic phosphate across the cell membrane.

What is the major virulence factor of Corynebacterium diphtheriae?

Toxins Diphtheria toxin
Toxins. Diphtheria toxin is the main virulence factor of C. diphtheriae and responsible for the life-threatening symptoms of respiratory diphtheria (Burkovski 2013b). The toxin is encoded on a temperate bacteriophage, which during lysogeny is capable of toxin production (Sangal and Hoskisson 2014).

How does pertussis toxin work?

Pertussis toxin (PT) utilizes a retrograde transport pathway through the Golgi complex and endoplasmic reticulum (ER) to gain entry to the cell cytosol. ATP binding to PT B oligomer (PTB) in the ER promotes holotoxin dissociation for further transport of the active subunit.

Which toxin inhibit protein synthesis?

Ricin, Shiga toxin, exotoxin A, and diphtheria toxin are AB-type protein toxins that act within the host cytosol and kill the host cell through pathways involving the inhibition of protein synthesis. It is thought that a single molecule of cytosolic toxin is sufficient to kill the host cell.

What does AB toxin do?

AB toxins exploit host receptors to coordinate host cell binding and delivery of A into the host cell cytosol. Members of the BoNT family have dual host receptors, often a glycolipid (ganglioside) and a protein receptor, while TeNT utilizes two gangliosides as receptors.

What is the mechanism of action of tetanus toxin?

Mechanism of Action. Tetanus toxin prevents the release of inhibitory neurotransmitters, particularly glycine, from neurons in the central nervous system, which results in uncontrolled muscular contractions.

What is the major virulence factor associated with Corynebacterium diphtheriae?

Toxin. The main virulence factor of C. diphtheriae is diphtheria toxin (DT), an exotoxin, released by the bacteria after entering the human body.

How does diphtheria pathogen form pseudomembrane?

A membrane typically develops on one or both tonsils, with extension to the tonsillar pillars, uvula, soft palate, oropharynx, and nasopharynx. C. diphtheriae multiplies on the surface of the mucous membrane, resulting in the formation of the “pseudomembrane” [7].

How does Corynebacterium diphtheriae become virulent?

For Corynebacterium diphtheriae to cause diphtheria, it must produce two virulence factors: diphtherial cord factor and diphtheria toxin. The cord factor allows the bacteria to grow in rope-like lateral aggregates to colonize in the upper respiratory tract.

How does pertussis toxin affect G protein?

Pertussis toxin is isolated from the bacteria Bordetella pertussis. It is shown to modify the function of G proteins by catalyzing the ADP-ribosylation of a cysteine residue on the carboxy terminal of α subunit of Gi and Go.

How does adenylate cyclase toxin work?

The adenylate cyclase toxin (CyaA) of Bordetella pertussis is a major virulence factor required for the early phases of lung colonization. It can invade eukaryotic cells where, upon activation by endogenous calmodulin, it catalyzes the formation of unregulated cAMP levels.

How do toxins inhibit protein synthesis?

Abstract. Ricin, Shiga toxin, exotoxin A, and diphtheria toxin are AB-type protein toxins that act within the host cytosol and kill the host cell through pathways involving the inhibition of protein synthesis. It is thought that a single molecule of cytosolic toxin is sufficient to kill the host cell.

What is the mechanism of action of cholera toxin?

Abstract. Cholera diarrhoea is due to the action of a toxin that acts on all animal cells by stimulating the enzyme adenylate cyclase, which catalyses the production oc cyclic AMP from ATP.

How do Enterotoxins work?

Enterotoxins are frequently cytotoxic and kill cells by altering the apical membrane permeability of the mucosal (epithelial) cells of the intestinal wall. They are mostly pore-forming toxins (mostly chloride pores), secreted by bacteria, that assemble to form pores in cell membranes. This causes the cells to die.