An outbreak of wound infection in cardiac surgery patients caused by Enterobacter cloacae arising from cardioplegia ice.

This paper describes an outbreak of postoperative sternal wound infections. A cardiac surgeon noted a cluster of serious infections leading to wound dehiscence, despite the fact that none of his colleagues had noticed a rise in infection rates. The infections were predominantly with Enterobacter cloacae, and molecular typing and serotyping showed these isolates to be indistinguishable. Observation of the surgeon's practice revealed nothing untoward, and there were no infections among his patients operated on in another hospital. There appeared to be no significant difference between the modes of operation of the different surgeons. The operating theatres were screened to exclude an environmental source, with samples cultured on CHROMagar Orientation, a selective/differential medium designed for urine samples. Further questioning revealed one difference between the practices of the different surgeons; this surgeon used semi-frozen Hartmann's solution to achieve cardioplegia. The freezer used for this was swabbed and yielded E. cloacae, indistinguishable from the clinical isolates. It is hypothesized that this organism contaminated the freezer, and that the contamination was passed on to the ice/slush solution, thus infecting the patients. There have been no more cases since the freezer was replaced, a rigorous cleaning schedule instituted, and steps taken to reduce the possibility of any further contamination.

Insulin regulation of glucose metabolism in HT29 colonic adenocarcinoma cells: activation of glycolysis without augmentation of glucose transport.

The effects of insulin on glucose transport and metabolism were examined in cultured HT29 human colonic adenocarcinoma cells. The presence of glucose transporters was verified by D-glucose displaceable [3H]cytochalasin B binding. The Kd and Bmax values from cytochalasin B binding studies were 190 +/- 30 nM and 8.4 +/- 1.4 pmol/mg protein, respectively. Glucose transport determined with 3-O-methylglucose showed saturable kinetics with a Km of 5.8 +/- 0.4 mM and a Vmax of 0.047 +/- 0.003 mumol/mg protein per min at 25 degrees C. Moreover, in HT29 cells, two classes of insulin binding sites were detected in radioligand binding experiments. Although insulin failed to stimulate glucose transport, it was found to activate glycolysis in HT29 cells. Glucose consumption increased from 0.33 +/- 0.03 mumol/mg protein per h to 0.49 +/- 0.05 mumol/mg protein per h and lactate production was augmented from 0.67 +/- 0.04 mumol/mg protein per h to 0.87 +/- 0.06 mumol/mg protein per h in response to 10(-7) to 10(-5) M insulin. Insulin also enhanced mannose metabolism. Apart from these two hexoses, HT29 cells exhibited a surprisingly narrow substrate specificity. With the possible exception of glyceraldehyde, little lactate was produced from alternative substrates, including adenosine, inosine, ribose, deoxyribose, dihydroxyacetone, galactose and fructose either with or without insulin. Despite its limited utilization by the glycolytic pathway, adenosine was readily salvaged for de novo synthesis of adenine nucleotides. These findings suggest that insulin directly influences substrate utilization through the glycolytic pathway in HT29 cells without activating the glucose transport pathway.

Serum lipids and acyl group composition of alcoholic patients.

The lipid content and acyl group composition of serum from a group of alcoholic patients at a VA Medical Center were compared to control subjects sampled either from University of Missouri personnel or from subjects who were undergoing a preemployment physical examination at the same VA Medical Center. Plasma of alcoholic patients indicated an elevated triacylglycerol level (24-35%) as compared to both control groups. In addition, the acyl groups of triacylglycerols of alcoholic patients showed a markedly lower proportion of 18:2 and a higher proportion of 18:0 and 18:1 as compared to the control groups. The level of phosphatidylcholines in the plasma of alcoholic patients was not different from controls. However, acyl group composition of phosphatidylcholines from alcoholics indicated a lower proportion of 22:6 (n-3) as compared to controls. Although the cholesteryl ester level in serum was higher in alcoholics than in controls, the difference did not reach a level of significance. There was a similar decrease in 18:2 and an increase in 18:0 in cholesteryl esters of alcoholics as compared to controls. Results indicate that alcoholics in the United States show a similar change in certain serum lipids as reported for the Swedish alcoholics. This study also shows the complexities involved in selecting appropriate control groups to be compared with alcoholic patients.