Ultrastructure and DNA fragmentation analysis of arterioles in swine infected with Shiga toxin-producing Escherichia coli

Shiga toxins (Stx) produced by E. coli are potent cytotoxins that affect th e vascular system. In humans, systemic toxemia causes renal glomerular dama ge manifested as hemolytic uremic syndrome. In swine, Stx-producing E, coli (STEC) cause edema disease that is characterized microscopically by segmen tal arteriolar smooth muscle cell (SMC) lesions. Our objectives were to cha racterize ultrastructurally and by TUNEL the type of death (apoptosis or ne crosis) that occurs in SMCs during edema disease. Increased DNA fragmentati on consistent with apoptosis was detected by TUNEL in arterioles of challen ged pigs 14-15 days post inoculation. Ultrastructurally 3 grades of SMC les ions were distinguished: 1) Partial loss of SMCs, intercellular space fille d with granular cellular debris admired with membrane bound vacuoles; 2) Co mplete loss of SMCs; only granular cellular debris and clear vacuoles remai ned within basement membrane: 3) Inflammation of media: SMCs replaced by a rim of cellular debris located in the periphery of vessel wall. The most co mmon lesion detected was grade 1 (9 ilea and il brains). We did not And apo ptotic nuclear changes in SMCs or apoptotic inclusion bodies within residen t cells. Our study indicates, that (1) Stx produced during edema disease do es not cause SMC apoptosis 14-15 dpi, (2) SMCs undergo an array of changes from degeneration to necrosis.