Food Biochemistry and Food Processing

(Ben Green) #1
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)
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