Biomedical subjects
Publications and source records attributed to J C Burnham.
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A prospective, double-blinded crossover study was carried out to test whether a brief course of antibiotic therapy could eliminate bacteria adherent to uroepithelial cells and thus prolong the interval between urinary tract infections (UTIs). Thirty-two women with frequent Gram-negative urinary tract infections were randomized to receive either co-trimoxazole or enoxacin twice a day for 10 days to treat their UTI. Their urines were collected for 30 days after the onset of their UTI and quantitatively analyzed for bacteria, antibiotics, and bacteria adherent to uroepithelial cells (UECs). A subsequent infection caused the patient to be treated with the alternative antibiotic. A third infection terminated the study. Both regimens were indistinguishable in the rate of elimination of bacteria and in their inhibition of bacterial adherence to UECs for up to five days after stopping treatment. The interval between infections was inversely correlated with the number of adherent bacteria per UEC 30 days after the onset of the first UTI. Both regimens were equally effective in preventing subsequent UTI and the effect of 10 days therapy on the inhibition of bacterial adherence to UEC's did not extend beyond five days after stopping treatment.
Bacterial adherence is reported to be antagonized by several classes of antibiotics including quinolones, beta-lactams and tetracyclines, based primarily on in-vitro studies in which bacterial cells are exposed to antimicrobials, incubated in the presence of uroepithelial cells (UECs) and assessed for adherence by light microscopy. Some problems associated with the use of this approach, include low sensitivity, high variability and, in the case of adherence of mannose-sensitive Escherichia coli interference by mannose-containing uromucoid. To avoid these problems, mannosylated agarose beads (MABs) were used as a model for UECs. Adherence of E. coli strain AAEC356, which is constitutive for type-1 fimbrial expression, was maximal with 3 x 10(4) beads/mL and 1 x 10(8) bacterial cells/mL co-incubated for 35 min at 37 degrees C. Those bacterial cultures showed 40-60% adherence to MABs but only 4-10% adherence to UECs. This study reports a novel method to detect mannose-sensitive bacterial adherence, using MABs, in order to determine the effects of quinolones, cefdinir and tetracycline on E. coli adherence. Cefdinir and the quinolones ciprofloxacin, enoxacin and PD131628 caused significant reductions in the adherence of AAEC356 to UECs at concentrations equivalent to 1/2 x MIC, while up to 1 x MIC of these antibiotics had no significant effect on adherence to MABs. A direct comparison of UEC to MAB-based techniques showed that PD131628, at concentrations equivalent to 1/16x, 1/4x, 1/2x and 1 x MIC, had no effect on bacterial adherence to MABs, while reductions of 34%, 38%, 87% and 85% respectively were seen in adherence to UECs. The anti-adherent effect mediated by quinolones may not therefore be related to the specific interaction between type-1 fimbriae and mannosylated receptors. While quinolones and cefdinir had no effect on overall bacterial adherence to MABs, there was a decrease in the ability of alpha-methyl-D-mannoside (alpha-MM) to inhibit competitively this adherence. Concurrent exposure of PD131628 or cefdinir with tetracycline prevented this, suggesting that protein synthesis is required for this effect.
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Quinolone antibiotics at sub-inhibitory concentrations have been shown to antagonize the adherence of Escherichia coli to urinary tract epithelium. This may be due either to reduced expression or to alterations to the structure of the fimbriae which mediate adherence. While E. coli cells in the stationary growth phase have previously been used to investigate quinolone-induced inhibition of adherence, the present study has demonstrated that bacteria in the logarithmic phase also produce type 1 fimbriae and that the adherence of these organisms is reduced following exposure to various quinolones. In all experiments, cells in the logarithmic phase were incubated for 3 h in the presence of ciprofloxacin, enoxacin, CI-960 or PD131628 at a concentration equivalent to 0.5 x MIC. An in-vitro adherence assay which used acid-washed uroepithelial cells and a type 1-fimbriated strain of E. coli showed reductions in adherence of 47%, 72% and 95% after exposure to enoxacin, ciprofloxacin and PD131628, respectively. The effects of ciprofloxacin, enoxacin, CI-960 and PD131628 on two phase variation controlling genes, fimB and fimE, and the main structural gene, fimA, were evaluated by quantifying beta-galactosidase production encoded by chromosomally-located fim::lacZ fusions. All four quinolones tested caused reductions in beta-galactosidase production by a fimA::lacZ fusion strain, but did not significantly affect production of this enzyme by fimB::lacZ and fimE::lacZ fusion strains; these agents also led to decreases in wild-type beta-galactosidase production. Amplification of the invertible element after exposure to enoxacin at 0.25, 0.5 or 1 x MIC revealed no changes in orientation distribution compared with the antibiotic-free control. In addition, a fluorescence assay specific for type 1 fimbriae showed only 23%, 21%, 25% and 11% reductions in the surface expression of the structural subunit after incubation in the presence of ciprofloxacin, enoxacin, CI-960 and PD131628, respectively, at 0.5 x MIC.
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The postantibiotic effect (PAE) has been classically defined as the suppression of bacterial growth that persists after limited exposure of organisms to antimicrobial agents. Morphology and haemolysin activity during the PAE of three quinolones on Escherichia coli were examined in this study. A one hour exposure to the quinolones, CI-960, enoxacin and ciprofloxacin, produced a PAE of 0.5-2.0 h. When determinated by Coulter counter, at 0.5 x MIC of enoxacin or CI-960 after 1 h exposure, 58% or 42% cells, respectively, of the treated cells were filamentous (cell length greater than 12 microns). After drug removal, the population of the filamentous cells decreased, however, after even 4 h, 12% and 2% of the cells were still filamentous after exposure to enoxacin or CI-960. Further morphological studies during the PAE showed that the first division of the filamentous cell was asymmetrical, and both bacterial cell division and septation were delayed after exposure to 0.5 MIC of CI-960. Following quinolone removal, the treated E. coli did not exhibit normal activity of haemolysin for at least 2 h. Internal haemolysin activity was adversely affected for 1 h. The results of this study suggest that any consideration of postantibiotic effects should include the residual antibiotic effects on bacterial morphology and virulence factors, in addition to the defined suppression of bacterial regrowth.
Quinolones inhibit DNA gyrase, and the major effects of this inhibition are on replication and transcription of DNA. The postantibiotic effect (PAE) refers to continued inhibition of cell division, in terms of the viable count, following transient exposure to an antibiotic. Previous work has shown that quinolone-treated cells have not fully recovered by the time the classically defined PAE has ended. We describe the PAE of the quinolones CI-960, enoxacin, and ciprofloxacin on macromolecular biosynthesis in the clinical isolate Escherichia coli J96 in an attempt to relate the PAE to the time that it actually takes for the cells to recover fully. DNA synthesis was inhibited immediately upon exposure to these quinolones at 0.5x or 0.75x the MIC. This inhibition continued for several hours following quinolone removal. The effects of these quinolones on RNA and protein synthesis varied; enoxacin treatment at 0.5x the MIC resulted in an increase of over 60% in both RNA and protein synthesis per unit of cell mass, while ciprofloxacin and CI-960 at that level had no significant effects on either RNA or protein synthesis. The effects of enoxacin and ciprofloxacin on bacterial protein profiles were also distinguishable, and these changes corresponded to their PAE on DNA synthesis. Throughout the study, all measures of the physiological status of the cells returned to normal by the time DNA synthesis per unit of cell mass did so. These results suggest that DNA synthesis per unit of cell mass provides an accurate measure of the time required for quinolone-treated cells to recover fully.
Practically no historical accounts of the evolution of peer review exist. Biomedical journals appeared in the 19th century as personal organs, following the model of more general journalism. Journal editors viewed themselves primarily as educators. The practice of editorial peer reviewing did not become general until sometime after World War II. Contrary to common assumption, editorial peer review did not grow out of or interact with grant peer review. Editorial peer review procedures did not spread in an orderly way; they were not developed from editorial boards and passed on from journal to journal. Instead, casual referring out of articles on an individual basis may have occurred at any time, beginning in the early to mid-19th century. Institutionalization of the process, however, took place mostly in the 20th century, either to handle new problems in the numbers of articles submitted or to meet the demands for expert authority and objectivity in an increasingly specialized world.