The antibacterial activities of sulbactam and YTR830H, both beta-lactamase inhibitors, were studied against Acinetobacter calcoaceticus, in vitro and in vivo. In-vitro susceptibility tests showed both to be very active against 80 clinical isolates of A. calcoaceticus. Against an intraperitioneal infection in mice, caused by A. calcoaceticus Ac54, the 50% effective doses of sulbactam and YTR830H were 1.62 and 16.7 mg/kg, respectively. Against A. calcoaceticus S31, a strain resistant to gentamicin, sulbactam and YTR830H were active both in vitro and in vivo.
The phenomenon that mixed infection with certain species of bacteria and Acinetobacter calcoaceticus is more virulent than single infection was analyzed experimentally.
E1040 is a new parenteral cephalosporin with a broad antibacterial spectrum and potent activity against Gram-negative bacteria including Pseudomonas aeruginosa. The in-vitro activities of E1040 against clinical isolates of Enterobacter cloacae, Ent. aerogenes, Providencia rettgeri, and Morganella morganii were superior to those of ceftazidime, cefoperazone, cefmenoxime, and cefuzonam. The activities of E1040 against Gram-positive cocci were comparable with those of ceftazidime, but it was less active than cefmenoxime, cefuzonam, and cefoperazone. Against Ps. aeruginosa, E1040 was more potent than the other compounds, with an MIC90 of 0.39 mg/l, 1/16 that of ceftazidime. The in-vitro activity of E1040 was well sustained in vivo as shown by results obtained in experimental infections in mice. In particular, E1040 was the most active drug against Ps. aeruginosa including gentamicin-resistant and beta-lactamase-overproducing strains. Morphological studies using a scanning electron microscope and a phase-contrast microscope showed that E1040 caused spheroplast and bulge formation in Ps. aeruginosa at low concentrations.
Summary. The adherence of Serratia marcescens to bladder epithelial cells of mice with alloxan-induced diabetes was studied. S . marcescens adhered more strongly to the bladder epithelial cells of diabetic mice than to those of normal mice both in vitro and in uiuo. The susceptibility of diabetic mice to urinary tract infection may be due to an increased adhesive capacity of bladder epithelial cells.
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