A case of hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli after pericardiectomy.

The majority of cases of Shiga toxin-producing Escherichia coli are self-limited; however, the infection can occasionally be complicated by more severe phenomena, such as thrombotic microangiopathy, with resultant end-organ damage to the kidneys, colon, nervous system, and various other tissues. Shiga toxin-induced hemolytic uremic syndrome (ST-HUS)-the constellation of thrombocytopenia, hemolysis, and renal failure resulting from thrombotic microangiopathy in a subset of infections producing the Shiga toxin-is classically observed in the pediatric population. Nevertheless, the diagnosis should be considered in adults with this presentation, and especially in those with colonic findings suggestive of ischemia.

beta-Lactamase induction and cell wall recycling in gram-negative bacteria.

beta-Lactams with the ability to induce beta-lactamase in gram-negative bacteria bind to essential penicillin-binding proteins (PBPs) after entering the periplasmic space. This leads to inactivation of transpeptidase activities and thereby a decrease in the number of peptide cross-links, allowing further degradation of murein by soluble lytic transglycosylases. If all DD-carboxypeptidases (PBP 4, 5, 6a and 6b) are inhibited as well, the degradation product aD-pentapeptide (N-acetylglucosaminyl-1,6-anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic-acid-D-alanyl-D- alanine) accumulates, which is the case with inducing beta-lactams such as imipenem.

A North Central Cancer Treatment Group phase II trial of topotecan in relapsed gliomas.

Current systemic treatment options for patients with relapsed gliomas are limited. The topoisomerase I inhibitor topotecan has demonstrated broad antitumor activity in both preclinical studies as well as a number of phase I and II trials in humans. Studies in primates have shown good cerebrospinal fluid levels of topotecan following systemic administration.