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Chapter 57 : Enterotoxic Clostridia: Clostridium perfringens Type A and Clostridium difficile

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Enterotoxic Clostridia: Clostridium perfringens Type A and Clostridium difficile, Page 1 of 2

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Abstract:

This chapter discusses two enterotoxin-producing clostridia that rank among the most important enteric pathogens of humans, and enterotoxin-positive type A strains of . The major lethal toxins (LTs) are not the only biomedically important toxins; some isolates, mostly belonging to type A, express enterotoxin (CPE). Recognized outbreaks of type A food poisoning are usually very large, averaging about 100 cases. type A food poisoning is acquired by ingestion of a food item containing vegetative cells of a CPE-positive type A strain. isolates associated with non-food-borne human gastrointestinal (GI) disease consistently carry a plasmid-borne gene, which distinguishes them from food poisoning isolates carrying a chromosomal gene. is an opportunistic pathogen that causes nosocomial diarrhea and colitis after the normal GI flora has been altered, most typically by antibiotics. -mediated disease develops from the production of two toxins, toxin A and toxin B, which in some papers are referred to as the enterotoxin and cytotoxin, respectively. Toxin production occurs during the stationary phase, under conditions that limit the growth of the organism. Certain basic precautions should be taken to help control outbreaks of disease. In most instances, the incidence of disease can be reduced simply by educating health care workers about the disease and how it is spread.

Citation: McClane B, Lyerly D, Wilkins T. 2006. Enterotoxic Clostridia: Clostridium perfringens Type A and Clostridium difficile, p 703-714. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch57

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FIGURE 1

Model for the mechanism of action of CPE. (A) CPE binds to receptors, forming a small complex. At 37°C, the small complex interacts with other proteins to form an ∼155-kDa large complex. The ∼155-kDa complex is a pore that allows Ca influx. With high CPE doses, massive Ca influx occurs that triggers oncosis; with low CPE doses, there is a more moderate Ca influx that triggers apoptosis. Activation of either cell death pathway causes morphologic damage that exposes receptors on the basolateral surface of the intoxicated cell and adjacent cells to still-unbound CPE. This allows additional formation of the ∼155-kDa large complex and also permits bound CPE to interact with occludin to form an ∼200-kDa complex. Formation of those two large CPE complexes triggers internalization of tight junction proteins, which damages the tight junction and leads to paracellular permeability alterations that contribute to CPE-induced diarrhea.

Citation: McClane B, Lyerly D, Wilkins T. 2006. Enterotoxic Clostridia: Clostridium perfringens Type A and Clostridium difficile, p 703-714. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch57
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Image of FIGURE 2
FIGURE 2

(A) PaLoc carrying the and genes of . The DNA region comprising the PaLoc is approximately 19.6 kb. (B) Structural features conserved between toxins A and B.

Citation: McClane B, Lyerly D, Wilkins T. 2006. Enterotoxic Clostridia: Clostridium perfringens Type A and Clostridium difficile, p 703-714. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch57
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Tables

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TABLE 1

Toxin typing of

Citation: McClane B, Lyerly D, Wilkins T. 2006. Enterotoxic Clostridia: Clostridium perfringens Type A and Clostridium difficile, p 703-714. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch57

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