709
Table 31.2.
Representative Toxins of Common Foodborne Pathogens, and Their
Actions in the Pathogenesis of the Bacteria
Organism
Toxin Name
Toxin Type
Size of Toxin
Effect/Mode of Action of Toxin
C. jejuni
Cytolethal
Unknown—
30, 29, and
Effects are not fully elucidated, but the toxin
distending
unrelated to
21 kDa
seems to stop host cells in the G2 phase of
toxins, CDTA,
other toxins
division (Eyigor et al. 1999, Whitehouse
CDTB and CDTC
et al. 1998).
C. perfringens
C. perfringens
Enterotoxin
35 kDa
Type A diarrhea—the enterotoxin binds to a
enterotoxin
protein receptor in the intestine, forms pores, and results in altered membrane permeability and diarrhea (Granum andBrynstad 1999).
Perfringolysin
Thiol Activated
53 kDa
Type C human necrotic enteritis—PLO,
O (PLO)
Cytolysin
-toxin and
-toxin are all produced
during vegetative growth of the organism.The PLO is normally cleaved by trypsin inthe intestine, preventing disease. PLO forms cation selective pores in endothelial cells (Brynstad and Granum 2002, Nagahama et al. 2003).
-toxin
Phospholipase
43 kDa
-toxin is the most important of the toxins mediating gas gangrene. It and PLO are involved in inhibiting the migration of inflammatory cells to the sites of infection. The phospholipase increases the ability of endothelial cells to adhere to inflammatory cells (Rossjohn et al. 1999).
-toxin
Haemolysin
42 kDa
-toxin specifically lyses cells expressing the
ganglioside GM2 (Alouf and Jolivet-Reynaud 1981, Jolivet-Reynaud et al.1993).
(Continues)