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The type A toxin of C. perfringens, also known as the CPA is responsible for food poisoning. [44] Clostridium perfringens is the most common bacterial agent for gas gangrene. [45] Gas gangrene is induced by α-toxin that embeds itself into the plasma membrane of cells and disrupts normal cellular function by altering membrane structure. [8]
The C terminal domain shows similarity with non-bacterial enzymes such as pancreatic lipase, soybean lipoxygenase, and synaptotagmin I. [4] The alpha toxin is a zinc metallophospholipase, requiring zinc for activation. First, the toxin binds to a binding site on the cell surface.
Clostridium perfringens alpha toxin (α-toxin) C. perfringens alpha toxin is widely associated with gas gangrene as it is its main virulence factor whilst invading its host. Alpha-toxin causes excessive platelet aggregation which blocks blood vessels and deprives the vital organs of oxygen supply. This creates an acidic, oxygen-deficient ...
Because C. perfringens beta toxin shares homology with S. aureus pore-forming alpha toxin, it was hypothesized that beta toxin acts in a similar way. Upon investigation, it was found that C. perfringens beta toxin forms cation-selective pores in cell membranes [4] of 1.6–1.8 nm [5] and results in swelling and lysis in HL60 cells. [6]
Clostridial necrotizing enteritis (CNE) is a severe and potentially fatal type of food poisoning caused by a β-toxin of Clostridium perfringens, [1] Type C. It occurs in some developing regions, particularly in New Guinea, where it is known as pig-bel.
Clostridium perfringens is an anaerobic, gram-positive bacteria that is often found in the large and small intestines of humans and other animals. Clostridium perfringens has the ability to reproduce quickly producing toxins relating to the cause of diseases.
Well-known exotoxins include: botulinum toxin produced by Clostridium botulinum; Corynebacterium diphtheriae toxin, produced during life-threatening symptoms of diphtheria; tetanospasmin produced by Clostridium tetani. The toxic properties of most exotoxins can be inactivated by heat or chemical treatment to produce a toxoid.
For example, Botulinum is 3x10 5 more toxic than snake venom to human and its toxic dose is only 0.8x10 −8 mg. [6] A wide variety of gram-positive and gram-negative bacteria use cytolysin as their primary weapon for creating diseases, such as Enterococcus faecalis, [7] Staphylococcus and Clostridium perfringens.