OBJECTIVES: A 1993 large water-borne outbreak of Salmonella typhimurium infections in Gideon, Mo, a city of 1100 with an unchlorinated community water supply, was investigated to determine the source of contamination and the effectiveness of an order to boil water. METHODS: A survey of household members in Gideon and the surrounding township produced information on diarrheal illness, water consumption, and compliance with the boil water order. RESULTS: More than 650 persons were ill; 15 were hospitalized, and 7 died. Persons consuming city water were more likely to be ill (relative risk [RR] = 9.1, 95% confidence interval [CI] = 2.9, 28.4), and the attack rate increased with increased water consumption. S. typhimurium was recovered from samples taken from a city fire hydrant and a water storage tower. Persons in 31% (30/ 98) of city households had drunk unboiled water after being informed about the boil water order, including 14 individuals who subsequently became ill. Reasons for noncompliance included "not remembering" (44%) and "disbelieving" (25%) the order. CONCLUSIONS: Communities with deteriorating water systems risk widespread illness unless water supplies are properly operated and maintained. Effective education to improve compliance during boil water orders is needed.

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Several enterohemorrhagic Escherichia coli (EHEC) strains of serotype 0157:H7 isolated from patients with hemorrhagic colitis, ischemic colitis, or hemolytic uremic syndrome were all found to be able to invade certain human epithelial cell lines in vitro. Their ability to gain entry into epithelial cells was compared with those of known invasive ShigeUla flexneri and SalmoneUla typhi strains and the noninvasive E. coli strain HB101 in invasion assays utilizing gentamicin to kill extracellular bacteria. All EHEC strains under investigation were efficiently internalized into T24 bladder and HCT-8 ileocecal cells. In striking contrast to shigellae, the same EHEC strains were not taken up into human embryonic intestinal INT407 cells or HEp-2 cells any more than the noninvasive E. coli strain HB101. The mechanism(s) of EHEC internalization was characterized by comparing the invasion efficiencies in the absence and presence of a variety of inhibitors acting on structures and processes of prokaryotic or eukaryotic cells. Also, wild-type, plasmid-containing EHEC strains were compared with their plasmid-cured isogenic derivative strains to determine if plasmid genes affect invasion ability. Plasmid-cured EHEC invaded as well as wild-type EHEC, indicating that invasion ability is chromosomally encoded. Inhibition of bacterial protein synthesis by simultaneous addition of bacteria and chloramphenicol to the monolayer blocked EHEC uptake dramatically, suggesting the presence of an invasion protein(s) with a short half-life. Studies utilizing inhibitors which act on eukaryotic cells demonstrated a strong dependence on microfilaments in the process of uptake of all EHEC strains into both T24 and HCT-8 cells. In general, depolymerization of microtubules as well as inhibition of receptor-mediated endocytosis reduced the efficiency of EHEC invasion of T24 cells, whereas interference with endosome acidification reduced EHEC entry into only HCT-8 cells. Taxol-induced stabilization of microtubules did not inhibit internalization into T24 cells or into the HCT-8 cell line. In marked contrast, the ability of S. typhi Ty2 to invade either cell line was inhibited only by depolymerization of microfilaments. In addition to the cell line specificity of EHEC invasion, not all EHEC strains displayed uniform behavior in the presence of inhibitors, suggesting the existence of variant uptake pathways in different strains. Most importantly, previous reports of the inability of EHEC to invade INT407 or HEp-2 cell lines support the currently held belief that EHEC strains are noninvasive. However, our findings demonstrate for the first time the ability of EHEC to invade selected human epithelial cell lines, a process that may be important in EHEC pathogenesis, and define some potential requirements for the invasion mechanism(s).

D iabetic ketoacidosis (DKA) is an acute metabolic complication of type 1 diabetes mellitus. This study aimed to define the DKA mortality rate in a Birmingham population and to identify risk factors for mortality and repeat admissions. An evaluation of 137 patients' notes retrieved from five hospitals in and around Birmingham, UK, identified 278 admissions over a 9-year period (2000-2009). The International Classification of Disease 10 coding system for DKA, E101, was employed to identify notes. Overall five (1.8%) patients died. Mortality was significantly associated with age, presence of comorbidity and diabetic complications. Poor control and compliance, female sex, clinic non-attendance, presence of co-morbidity and psychological problems all increased the risk of recurrent DKA admissions. Our study supports a role for improving education and glycaemic control to reduce DKA and its associated mortality. Br J Diabetes Vasc Dis 2009;9:278-282