The toxins ricin and abrin are potent inhibitors of protein synthesis. Apoptosis has been shown to be induced in some cells by cycloheximide and actinomycin D whereas the process is prevented in other cells by the same agents, both inhibitors of protein synthesis. We were interested to find whether ricin and abrin caused any apoptotic changes in rapidly dividing tissues where we believed that these toxins concentrate. Rats were injected intramuscularly with toxin and killed at time intervals, tissues being removed and examined by light and electron microscopy. Apoptotic-like bodies were abundant in para-aortic lymph nodes, Peyer's patches and ideal crypts of ricin or abrin intoxicated rats. Abrin was found to cause markedly more pronounced changes in these tissues, when compared with a similar dose of ricin. Prior to this, these toxins have been reported as causing necrosis in animal tissues.

No abstract

A case of infection with Corynebacterium ulcerans (C. ulcerans), resulted in the sudden death of a previously healthy 73-year-old woman. Death from Corynebacteriwm diphtheriae (C. diphtheriae) infection is well-documented. Fatalities following infection with C. ulcerans are unreported: this would appear to be the Erst documented death due to such infection.

Within the gut, intramuscular ricin poisoning results in major pathological changes. Immunocytochemistry and electron microscopy illustrate that these changes appear confined to the small intestine, the stomach and large intestine remaining virtually unaffected. These changes include apoptosis crypt and mucosal epithelial cells, hydropic change in enterocytes, infiltration of large numbers of plasma cells into the lamina propria, subsequent apoptosis of many of the plasma cells, and the appearance within the lamina propria of highly active macrophages. Of these changes, greatest significance is attached to the infiltration and apoptosis of large numbers of plasma cells. This is not a common pathological feature within the gastro-intestinal tract, and may prove to be specifically diagnostic for ricin or a group of toxins having structurally similar characteristics. In this study, the toxin was administered by intramuscular injection and not orally; considering this mode of administration, damage to the small intestine was far more severe than might perhaps be expected. The intensity of cellular infiltration within the lamina propria is especially interesting, as it appears to be more analogous to a local immune response triggered by an oral toxin rather than one administered by an intramuscular route.