Role of Shiga/Vero toxins in pathogenesis.

Shiga toxin (Stx) is the primary cause of severe host responses including renal and central nervous system (CNS) disease in Shiga toxin-producing E. coli (STEC) infections. The interaction of Stx with different eukaryotic cell types is described.

Protection by a recombinant Mycobacterium bovis Bacillus Calmette-Guerin vaccine expressing Shiga toxin 2 B subunit against Shiga toxin-producing Escherichia coli in mice.

We have developed a novel vaccine against Shiga toxin (Stx)-producing Escherichia coli (STEC) infection using a recombinant Mycobacterium bovis BCG (rBCG) system. Two intraperitoneal vaccinations with rBCG expressing the Stx2 B subunit (Stx2B) resulted in an increase of protective serum IgG and mucosal IgA responses to Stx2B in BALB/c mice. When orally challenged with 10(3) CFU of STEC strain B2F1 (O91: H21), the immunized mice survived statistically significantly longer than the nonvaccinated mice.

Shiga toxin pathogenesis: kidney complications and renal failure.

The kidneys are the major organs affected in diarrhea-associated hemolytic uremic syndrome (D(+)HUS). The pathophysiology of renal disease in D(+)HUS is largely the result of the interaction between bacterial virulence factors such as Shiga toxin and lipopolysaccharide and host cells in the kidney and in the blood circulation. This chapter describes in detail the current knowledge of how these bacterial toxins may lead to kidney disease and renal failure.

Escherichia coli Shiga Toxin Mechanisms of Action in Renal Disease.

Shiga toxin-producing Escherichia coli is a contaminant of food and water that in humans causes a diarrheal prodrome followed by more severe disease of the kidneys and an array of symptoms of the central nervous system. The systemic disease is a complex referred to as diarrhea-associated hemolytic uremic syndrome (D(+)HUS). D(+)HUS is characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure.

Distribution of Gb(3) Immunoreactivity in the Mouse Central Nervous System.

We have shown previously that neurons in the mouse spinal cord express Gb(3). We show in this article that distribution of anti-Gb(3)-Ab reactivity occurs in many different types of neurons of different areas of the central nervous system (CNS). The immunoreactive neurons are in olfactory bulbs, cerebral cortex, hippocampus, striatum, amygdala, thalamus, hypothalamus, cerebellum, and medulla oblongata.