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474 Chapter 19 Host-Microbe Interactions to specific receptors on cells (figure 19.12). In other words, the A subunit, usually an enzyme, is responsible for the effects the toxin has on a cell, whereas the B subunit dictates the type of cell to which the toxin is delivered. Examples of A-B toxins include:

■ Neurotoxins. Tetanus toxin, produced by Clostridium tetani, blocks the action of inhibitory neurons, allowing all muscles to contract at the same time. Botulinum toxin, produced by C. botulinum, blocks transmission of nerve signals to the muscles, causing flaccid paralysis.

■ Enterotoxins. The enterotoxins produced by Vibrio cholerae and certain strains of E. coli cause severe watery diarrhea. They do this by chemically modifying a regulatory protein in intestinal cells, inducing those cells to continuously secrete electrolytes and water.

■ Cytotoxins. Diphtheria toxin, produced by Corynebacterium diphtheriae, inhibits protein synthesis in eukaryotic cells, leading to their destruction. The toxin is an enzyme that inactivates an elongation factor of eukaryotic cells by chemically modifying it; recall that elongation factors are involved in the translocation of the ribosome during protein synthesis. Shiga toxin, produced by Shigella dysenteriae and certain strains of E. coli, including O157:H7, damages eukaryotic ribosomes, halting protein synthesis. ■ elongation factors, p. 178

The structure of A-B toxins offers novel approaches for the development of vaccines and therapies. For example, a fusion protein that contains dipththeria toxin is now being used to treat cutaneous T-cell lymphoma. By fusing the toxin to the cytokine IL-12, the toxin is delivered to T cells, including cancerous ones. The B subunit of cholera toxin has been used to develop an orally administered vaccine against cholera. Antibodies that bind the B subunit should prevent cholera toxin from binding to intestinal cells, thus protecting the vaccine recipient. Researchers are now experimenting with attaching other compounds to B subunits, allowing those compounds to be delivered specifically to the cell type targeted by the B subunit.

Membrane-Damaging Toxins

Membrane-damaging toxins disrupt plasma membranes, causing the cell to lyse. Because they damage a variety of different cell types, they are cytotoxins. Many of these also lyse red blood cells, causing hemolysis that can be observed when the organisms are grown on blood agar; thus, many of these toxins are also referred to as hemolysins. They are also called cytolysins. ■ hemolysis, p. 94 ■ blood agar, p. 92

Some membrane-damaging toxins insert themselves into membranes, forming pores that allow fluids to enter. An example of a pore-forming toxin is streptolysin O, the compound responsible for the characteristic b-hemolysis of Streptococcus pyogenes grown anaerobically on blood agar (see figure 4.6). Recall that this membrane-damaging toxin enables S. pyogenes to avoid phagocytosis.

Phospholipases are a group of membrane-damaging toxins that enzymatically remove the polar head group of the phos-pholipids in the plasma membrane, destabilizing its integrity.

A-B exotoxin

B chain attaches to receptor

Binding site

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