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Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 118))

Abstract

Hemolysis, i.e., the lysis of erythrocytes, is a rather widespread capacity of bacteria and other microorganisms but the molecular basis of this character varies from organism to organism. Extracellular enzymes have been shown to be responsible for hemolysis by some bacteria, e.g., the phospholipases of Pseudomonas aeruginosa (Vasil et al. 1982) and Chlostridium perfringens (also called a-toxin; Smith 1979) and also the sphingiomyelinase C produced byStaphylococcus aureus (β-toxin; Freer and Arbuthnott 1983). “Nonenzymatic” proteins which disrupt the membrane of erythrocytes have been identified as the causative agents of hemolysis by, among others, Staphylococcus aureus (a-toxin; Freer and Arbuthnott 1983), Vibrio cholerae (Goldberg and Murphy 1984), Aeromonas hydrophila (Chakraborty et al. 1984), and the enterobacteria Escherichia coli (Smith and Halls 1967; Jorgensen et al. 1980; Goebel et al. 1984), Proteus mirabilis (Peerbooms et al. 1982), and Proteus morganii (Emody et al. 1983). Among other enterobacteria hemolytic strains of Serratia marcescens (Le Minor and Le Coueffic 1975) and Shigella sonnei have been described and the possibility exists that at leastShigella strains bear plasmids originating from E. coli (Stenzel 1971 b). Forming another subclass of the “Nonenzymatic” proteins are the sulfhydryl (SH)-activated hemolysins such as streptolysin Oof Streptococcus pyogenes, pneumolysin of Streptococcus pneumoniae, the θ-toxin ofClostridium perfringens, as well as cereolysin and listeriolysin of Bacillus cereus and species of Listeria (for review see Alouf 1980 and Alouf and Geoffroy 1984). These toxins are assumed to recognize cholesterol as a receptor in the erythrocyte membrane and are serologically related and oxygenlabile.

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Hacker, J., Hughes, C. (1985). Genetics of Escherichia coli Hemolysin. In: Goebel, W. (eds) Genetic Approaches to Microbial Pathogenicity. Current Topics in Microbiology and Immunology, vol 118. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70586-1_8

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