Host damage from bacterial toxins

Abstract

Bacterial infection often involves toxin-mediated damage to the host. This can occur at mucosal epithelial surfaces, in subepithelial tissues (involving connective tissue, blood vessels and host defence cells), or at organ or tissue sites distant from the focus of infection. This paper deals with host damage at each of these levels and examples have been selected of toxins that have a well defined role in pathogenesis and for which evidence is less clear cut. Current views of mechanisms of host damage are presented along with summaries of mode of action at the molecular level where this is known. Certain unifying features of mechanisms of toxin action on host cells are emphasised. Modern genetic methods and gene cloning techniques should help in the assessment of the role of individual toxic factors where pathogenesis is multifactorial, and preliminary examples of this approach are mentioned. The search for new toxins continues and this is illustrated with reference to the toxins involved in the staphylococcal scalded skin syndrome and staphylococcal toxic shock syndrome. This overview is intended to convey an impression of the rapid development that has taken place in knowledge of the role of toxins in pathogenesis.

Ion modulation of membrane permeability: Effect of cations on intact cells and on cells and phospholipid bilayers treated with pore-forming agents

“…Miller, Castellot & Pardee, 1978, 1979Dunn & Holz, 1983;Wilson & Kirshner, 1983), and more recently Sendai virus and S. aureus s-toxin have been employed to bring Ca 2+ chelates (Gomperts, Baldwin & Micklem, 1983; Ahnert-Hillger, Bhakdi & Gratzl, 1985), GTP analogues (Gray et al, 1983;Barrowman, Cockroft & Gomperts, 1986) or antibiotics (Cameron et al, 1986) into metabolically competent cells to study processes such as exocytosis. Pore-forming agents therefore have a role as biological tools, in addition to their relevance to diseases of viral (Pasternak, 1987a), microbial (McCartney & Arbuthnott, 1978;Arbuthnott, 1983), animal (e.g. Prince, Gunson & Scarpa, 1985) or immune (Schreiber, 1983;Morgan et al, 1984) origin.…”