PubMed Health⌕ Search

Biomedical subjects

Usha Stiefel

Publications and source records attributed to Usha Stiefel.

12 recordsLinked to original sources
PubMed2006

Effect of carbapenem administration on establishment of intestinal colonization by vancomycin-resistant enterococci and Klebsiella pneumoniae in mice.

In a mouse model, ertapenem inhibited the anaerobic intestinal microflora and promoted overgrowth of enterococci, whereas imipenem-cilastatin had no effect on the indigenous microflora. Ertapenem, but not imipenem-cilastatin, promoted modest overgrowth of vancomycin-resistant enterococci when exposure occurred during treatment. Neither agent promoted colonization with extended-spectrum beta-lactamase-producing Klebsiella pneumoniae.

Animals↗
PubMed2006

Suppression of gastric acid production by proton pump inhibitor treatment facilitates colonization of the large intestine by vancomycin-resistant Enterococcus spp. and Klebsiella pneumoniae in clindamycin-treated mice.

Proton pump inhibitor treatment of clindamycin-treated mice elevated the gastric pH and facilitated the establishment of colonization of the large intestine by vancomycin-resistant Enterococcus spp. (75 to 80%, versus 20 to 25% for saline-treated controls) and Klebsiella pneumoniae (90%, versus 30% for saline-treated controls). These findings demonstrate a mechanism by which proton pump inhibitor therapy could contribute to the dissemination of nosocomial pathogens.

Animals↗
PubMed2006

Effect of a selective decontamination of the digestive tract regimen including parenteral cefepime on establishment of intestinal colonization with vancomycin-resistant Enterococcus spp. and Klebsiella pneumoniae in mice.

In mice, a selective decontamination of the digestive tract regimen consisting of orogastric tobramycin, polymyxin E, and amphotericin B in combination with subcutaneous cefepime inhibited gram-negative bacilli, including Klebsiella pneumoniae, and did not promote vancomycin-resistant Enterococcus spp. (VRE) colonization. However, concurrent administration of subcutaneous ampicillin-sulbactam resulted in promotion of VRE.

Animals↗
PubMed2005

Mechanisms by which anaerobic microbiota inhibit the establishment in mice of intestinal colonization by vancomycin-resistant Enterococcus.

We used a mouse model to test the hypothesis that anaerobic microbiota in the colon inhibit the establishment of vancomycin-resistant enterococci (VRE) colonization by depleting nutrients within cecal contents and limiting the association of VRE with the mucus layer. Anaerobic growth of VRE was assessed in cecal contents and cecal mucus of mice that had received treatment with subcutaneous clindamycin or saline. VRE grew to high concentrations in cecal contents of clindamycin-treated mice and in cecal mucus of both groups but not in cecal contents of saline-treated mice, unless the cecal contents were autoclaved or converted into sterile filtrates. After orogastric inoculation of VRE, clindamycin-treated mice acquired high concentrations of VRE within the mucus layer, whereas saline-treated mice did not. These results suggest that colonic microbiota inhibit VRE by producing inhibitory substances or conditions rather than by depleting nutrients. The colonic mucus layer provides a potential niche for growth of VRE.

Animals↗
PubMed2005

Effect of parenteral antibiotic administration on establishment of intestinal colonization by Candida glabrata in adult mice.

We examined the effect of antibiotic treatment on establishment of intestinal colonization by Candida glabrata in adult mice. Subcutaneous ceftriaxone, piperacillin-tazobactam, clindamycin, and metronidazole promoted increased density of stool colonization, whereas cefepime, levofloxacin, and aztreonam did not. These findings suggest that antibiotics that inhibit intestinal anaerobes promote C. glabrata colonization.

Animals↗
PubMed2005

Effects of daptomycin, linezolid, and vancomycin on establishment of intestinal colonization with vancomycin-resistant enterococci and extended-spectrum-beta-lactamase-producing Klebsiella pneumoniae in mice.

In mice, vancomycin and linezolid treatment disrupted the anaerobic intestinal microflora, based on denaturing gradient gel electrophoresis analysis, and promoted colonization by Klebsiella pneumoniae and vancomycin-resistant enterococci. However, the effects varied depending on dose and duration of treatment. Daptomycin treatment did not disrupt the anaerobic microflora or promote either pathogen.

Acetamides↗
PubMed2004

The Role of the Intestinal Tract As a Source for Transmission of Nosocomial Pathogens.

The intestinal tract provides an important source for transmission of many nosocomial pathogens, including Enterococcus species, Clostridium difficile, Candida species, Enterobacteriaceae, and other gram-negative bacilli. Recent data suggest that the intestinal tracts of hospitalized patients may also be an important reservoir of Staphylococcus aureus. Although the clinical manifestations of these pathogens are diverse, a common pathogenesis is involved in their colonization of and dissemination from the intestinal tract. Of particular importance is the role that antibiotic selective pressure plays in promotion of colonization by antibiotic-resistant pathogens. Strategies to limit the spread of these pathogens must include efforts to improve adherence to standard infection control practices and promotion of good antimicrobial stewardship. New strategies that include application of novel technologies to the problem of pathogen transmission are needed, and additional research is needed to clarify the potential utility of selective decontamination of the digestive tract.

Journal Article↗
PubMed2004

Increased susceptibility to vancomycin-resistant Enterococcus intestinal colonization persists after completion of anti-anaerobic antibiotic treatment in mice.

BACKGROUND: Antibiotic-associated disruption of the indigenous intestinal microflora may persist beyond the treatment period. Although piperacillin/tazobactam inhibits the establishment of vancomycin-resistant Enterococcus (VRE) stool colonization in mice during treatment, we hypothesized that this agent and other anti-anaerobic antibiotics would increase susceptibility to colonization during the period of recovery of the intestinal microflora. DESIGN: Mice received 10(4) colony-forming units of vancomycin-resistant E. faecium by orogastric inoculation 2, 5, or 10 days after completing 5 days of subcutaneous antibiotic treatment, or both during and 2 days after the completion of treatment. Denaturing gradient gel electrophoresis (DGGE) was performed to assess changes in the intestinal microflora. RESULTS: Anti-anaerobic antibiotics (ie, piperacillin/ tazobactam, cefoxitin, and clindamycin) caused significant disruption of the indigenous microflora (mean DGGE similarity indices < or = 27% in comparison with saline controls) and promoted the establishment of high-density colonization when VRE was inoculated 2 or 5, but not 10, days following treatment (P < .001). Piperacillin/tazobactam exhibited a biphasic effect on the establishment of colonization (ie, inhibition when exposed to VRE during treatment and promotion when exposed to VRE after discontinuation of treatment), resulting in greater overall promotion of colonization than did agents with minimal anti-anaerobic activity (ie, levofloxacin, cefepime, and aztreonam) when VRE was inoculated both during and 2 days after treatment (P < .001). CONCLUSION: Patients receiving anti-anaerobic antibiotics, including piperacillin/tazobactam, may be susceptible to the establishment of high-density VRE colonization during the period of recovery of the anaerobic microflora.

Animals↗
PubMed2004

Effect of the increasing use of piperacillin/tazobactam on the incidence of vancomycin-resistant enterococci in four academic medical centers.

BACKGROUND: The substitution of piperacillin/tazobactam, ampicillin/sulbactam, or both for third-generation cephalosporins has been associated with reduced vancomycin-resistant enterococci (VRE). However, piperacillin/tazobactam came into widespread use during a period in which the prevalence of VRE increased. We hypothesized that the increasing use of piperacillin/tazobactam and other agents with relatively enhanced anti-enterococcal activity (ie, piperacillin, ampicillin/sulbactam, and ampicillin) has been associated with increased or unchanged rates of VRE in some hospitals. DESIGN: We retrospectively evaluated the correlation between hospital antibiotic use (defined daily doses per 10,000 patient-days of care) and incidence of stool or non-stool VRE isolation. We assessed whether a high or increasing proportion of use of beta-lactam agents with relatively enhanced versus minimal (ie, third-generation cephalosporins and ticarcillin/clavulanate) anti-enterococcal activity would prevent increased VRE. SETTING: Four academic medical centers. RESULTS: With the increasing use of piperacillin/tazobactam, the use of beta-lactam agents with enhanced activity against enterococci surpassed the combined use of third-generation cephalosporins and ticarcillin/clavulanate in each hospital. In one hospital, the incidence of VRE was positively correlated with the use of piperacillin/tazobactam or beta-lactam agents with enhanced anti-enterococcal activity (P < .0001). The incidence of VRE rose steadily in another hospital despite relatively high use of beta-lactam agents with enhanced versus minimal anti-enterococcal activity. A negative correlation between VRE and piperacillin/tazobactam or beta-lactam agents with enhanced anti-enterococcal activity was observed in one hospital, but this correlation was not statistically significant. CONCLUSION: Increasing the hospital use of piperacillin/tazobactam and other beta-lactams with relatively enhanced anti-enterococcal activity may not be an effective control measure for VRE.

Academic Medical Centers↗
PubMed2004

Efficacy of oral ramoplanin for inhibition of intestinal colonization by vancomycin-resistant enterococci in mice.

Ramoplanin is a glycolipodepsipeptide antibiotic with activity against gram-positive bacteria that is in clinical trials for prevention of vancomycin-resistant Enterococcus (VRE) bloodstream infections and treatment of Clostridium difficile diarrhea. Orally administered ramoplanin suppresses VRE intestinal colonization, but recurrences after discontinuation of treatment have frequently been observed. We used a mouse model to examine the efficacy of ramoplanin for inhibition of VRE colonization and evaluated the etiology of recurrences of colonization. Eight days of treatment with ramoplanin (100 microg/ml) in drinking water suppressed VRE to undetectable levels, but 100% of mice developed recurrent colonization; a higher dose of 500 microg/ml in water was associated with recurrent colonization in 50% of mice. Two of eight (25%) mice treated with the 100-microg/ml dose of ramoplanin had low levels of VRE in their cecal tissues on day 8 despite undetectable levels in stool and cecal contents. Mice that received prior ramoplanin treatment did not develop VRE overgrowth when challenged with 10(7) CFU of oral VRE 1, 2, or 4 days later. In communal cages, rapid cross-transmission and overgrowth of VRE was observed among clindamycin-treated mice; ramoplanin treatment effectively suppressed VRE overgrowth in such communal cages. Ramoplanin treatment promoted increased density of indigenous Enterobacteriaceae and overgrowth of an exogenously administered Klebsiella pneumoniae isolate. These results demonstrate the efficacy of ramoplanin for inhibition of VRE colonization and suggest that some recurrences occur due to reexpansion of organisms that persist within the lining of the colon. Ramoplanin treatment may be associated with overgrowth of gram-negative bacilli.

Administration, Oral↗
PubMed2003

Oral administration of beta-lactamase preserves colonization resistance of piperacillin-treated mice.

We hypothesized that orally administered, recombinant class A beta-lactamase would inactivate the portion of parenteral piperacillin excreted into the intestinal tract, preserving colonization resistance of mice against nosocomial pathogens. Subcutaneous piperacillin or piperacillin plus oral beta-lactamase were administered 24 and 12 h before orogastric inoculation of piperacillin-resistant pathogens. Oral administration of beta-lactamase reduced piperacillin-associated alteration of the indigenous microflora and prevented overgrowth of pathogens.

Animals↗