1991Current Opinion in Infectious DiseasesRequires access

Bacterial toxins in the pathogenesis of infections

Frank E. Berkowitz

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Abstract

Different bacterial toxins share many structural and functional properties. They may be directly toxic to tissues, they may exert their effects via endogenous mediators such as tumor necrosis factor, or they may modulate the immune response. The latter effect is accomplished by the staphylococcal and streptococcal pyrogenic exotoxins, which can act as superantigens. Several of these pyrogenic toxins play important roles in the pathogenesis of staphylococcal toxic shock syndrome and streptococcal toxic shock-like syndrome. The enterotoxins produced by the gram-negative bacilli and vibrios that cause diarrhea have a variety of mechanisms of action. These include ADP ribosylation of the stimulatory guanyl nucleotide-binding regularly protein of adenyl cyclase (cholera toxin, Escherichia coli heat-labile toxin), stimulation of guanylate cyclase (E. coli heat-stable toxin a), and inhibition of protein synthesis (Shiga toxin and the Shigalike toxins of Shigella species and enterohemorrhagic E. coli).

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What this paper is about

Different bacterial toxins share many structural and functional properties. They may be directly toxic to tissues, they may exert their effects via endogenous mediators such as tumor necrosis factor, or they may modulate the immune response. The latter effect is accomplished by the staphylococcal and streptococcal pyrogenic exotoxins, which can act as superantigens. Several of these pyrogenic toxins play important roles in the pathogenesis of staphylococcal toxic shock syndrome and streptococcal toxic shock-like syndrome. The enterotoxins produced by the gram-negative bacilli and vibrios that cause diarrhea have a variety of mechanisms of action. These include ADP ribosylation of the stimulatory guanyl nucleotide-binding regularly protein of adenyl cyclase (cholera toxin, Escherichia coli heat-labile toxin), stimulation of guanylate cyclase (E. coli heat-stable toxin a), and inhibition of protein synthesis (Shiga toxin and the Shigalike toxins of Shigella species and enterohemorrhagic E. coli).

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Available abstract

Different bacterial toxins share many structural and functional properties. They may be directly toxic to tissues, they may exert their effects via endogenous mediators such as tumor necrosis factor, or they may modulate the immune response. The latter effect is accomplished by the staphylococcal and streptococcal pyrogenic exotoxins, which can act as superantigens. Several of these pyrogenic toxins play important roles in the pathogenesis of staphylococcal toxic shock syndrome and streptococcal toxic shock-like syndrome. The enterotoxins produced by the gram-negative bacilli and vibrios that cause diarrhea have a variety of mechanisms of action. These include ADP ribosylation of the stimulatory guanyl nucleotide-binding regularly protein of adenyl cyclase (cholera toxin, Escherichia coli heat-labile toxin), stimulation of guanylate cyclase (E. coli heat-stable toxin a), and inhibition of protein synthesis (Shiga toxin and the Shigalike toxins of Shigella species and enterohemorrhagic E. coli).

Key concepts: Superantigen, Microbiology, Enterotoxin, Toxin, Cholera toxin, Toxic shock syndrome, Shigella, Pathogenesis

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