Perspective: bacterial endocarditis in the presence of arteriovenous fistulae.
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Biomedical subjects
Publications and source records attributed to D Kaye.
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The effect of early bilateral pyelonephritis on urinary concentrating ability was studied in rats injected intravenously with enterococci or Staphylococcus aureus and in rats inoculated with Escherichia coli into the medullae of both kidneys. The mean maximum urinary osmolality of normal rats was 2352 mOsm/kg of water. Inoculation of E. coli caused reversible pyelonephritis with sterilization of the kidneys within 12 wk. By 1 day after injection the mean maximum urinary osmolality had decreased to about 1100 mOsm. remained at this level for 3 wk, and then rose to normal by 12 wk. After injection of enterococci and staphylococci, the mean maximum urine osmolality decreased over 3-4 days to about 1000 and 800 mOsm respectively. In the enterococcal infection (which is chronic) the maximum urine osmolality remained about 1200 mOsm for at least 12 wk whereas in the staphylococcal infection (which is reversible) the osmolality gradually rose. Antimicrobial therapy of E. coli renal infection with colistimethate sodium and S. aureus infection with ampicillin rapidly reduced bacterial titers in the kidneys with an associated rise in maximum urinary osmolality. Therapy of enterococcal renal infection with ampicillin produced less impressive decreases in bacterial titers in the kidneys and little or no improvement in urinary concentrating ability. With antimicrobial therapy or with the self-limited infections, the rate of increase in concentrating ability was directly correlated with the rate of decrease of bacterial titers. However, there was poor correlation between histological findings in the kidneys and urinary concentrating ability. These studies demonstrate that early experimental pyelonephritis is associated with a concentrating defect that can be rapidly reversed and therefore is not related to permanent renal damage.
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Concentrations of cephalexin (an orally absorbed derivative of cephalosporin C) in serum and urine were determined in normal volunteers and patients. The in vitro antibacterial activity was also studied. All strains of group A beta-hemolytic streptococci and Diplococcus pneumoniae were inhibited by 3.1 mug/ml. Of the Staphylococcus aureus strains, 88% were inhibited by 6.3 mug/ml, and 12.5 mug/ml was inhibitory for all S. aureus, 80% of Escherichia coli, 72% of Klebsiella-Aerobacter, and 56% of Proteus mirabilis strains. About 90 to 96% of E. coli, Klebsiella Aerobacter, and P. mirabilis strains were inhibited by 25 mug of cephalexin per ml. Pseudomonas and indole-positive Proteus strains proved to be quite resistant to cephalexin. Cephalexin was well absorbed after oral administration. A peak serum concentration of cephalexin of at least 5 mug/ml was achieved in each volunteer with 250 and 500-mg doses. A mean peak serum concentration of 7.7 mug/ml was achieved with 250-mg doses; 12.3mug/ml was achieved with 500-mg doses of antibiotic. Food did not interfere with absorption. Probenecid enhanced both the peak serum concentration and the duration of antibiotic activity in the serum. Over 90% of the administered dose was excreted in the urine within 6 hr. The mean peak serum concentration of cephalexin after an oral dose of 500 mg was adequate to inhibit all group A streptococci, D. pneumoniae, and S. aureus, 85% of E. coli, and about 40 to 75% of Klebsiella-Aerobacter and P. mirabilis strains. Levels of cephalexin in urine were adequate to inhibit over 90% of E. coli, and P. mirabilis and 80 to 96% of Klebsiella-Aerobacter strains.
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