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Biomedical subjects

W E Sanders

Publications and source records attributed to W E Sanders.

At least 55 records · Page 3Linked to original sources
PubMed1990

Acute pulmonary edema associated with use of low-molecular weight dextran for prevention of microvascular thrombosis.

Low-molecular weight dextran is commonly used to prevent thrombosis after microvascular procedures; however, the potential complications of this drug are not well known. We report a case of acute pulmonary edema in a healthy person after elective microsurgery for treatment of a malignant tumor of the forearm. The mechanism of action of dextran and the pathophysiology of two potential adverse reactions to this drug are discussed. It is thought that in this patient pulmonary edema was caused by dextran toxicity.

Acute Disease↗
PubMed1990

Beta-lactamase production in members of the family Enterobacteriaceae and resistance to beta-lactam-enzyme inhibitor combinations.

Recent reports that members of the family Enterobacteriaceae that produce high levels of certain beta-lactamases are often resistant to ticarcillin-clavulanate prompted this study to assess the relationship between type and amount of enzyme produced and susceptibility to ticarcillin-clavulanate, piperacillin-tazobactam, and cefoperazone-sulbactam. Agar dilution MICs were determined by using 73 strains of Enterobacteriaceae that produced a single beta-lactamase that had been characterized and quantified and a beta-lactamase-negative control strain of Escherichia coli. For E. coli and Klebsiella pneumoniae, MICs of each combination increased as levels of TEM, SHV-1, or class IV enzymes increased. However, the percentage of strains that were resistant was highest for ticarcillin-clavulanate (32%), with only 18 and 6% resistant to piperacillin-tazobactam and cefoperazone-sulbactam, respectively. Strains producing PSE-1, regardless of level, were resistant or moderately susceptible to ticarcillin-clavulanate but were susceptible to piperacillin-tazobactam and cefoperazone-sulbactam. HMS-1 and OHIO-1 beta-lactamases were associated with resistance to ticarcillin-clavulanate and piperacillin-tazobactam, respectively. High levels of class IV enzymes in Klebsiella oxytoca were associated with resistance to all three combinations. These results indicate that the level and type of beta-lactamase produced by members of the family Enterobacteriaceae are important determinants of susceptibility to beta-lactam-inhibitor combinations, especially ticarcillin-clavulanate.

Anti-Bacterial Agents↗
PubMed1989

Meropenem: activity against resistant gram-negative bacteria and interactions with beta-lactamases.

The activity of meropenem, a new carbapenem, was determined against 82 Gram-negative bacteria in agar dilution tests. Many of these isolates were resistant to one or more beta-lactam antibiotics and the mechanisms responsible for the resistance had been characterized. The production of beta-lactamases had little influence on susceptibility to either meropenem or imipenem except in tests with Aeromonas hydrophila and Pseudomonas (Xanthomonas) maltophilia. These species produced metalloenzymes capable of hydrolyzing the carbapenems, and strains expressing high levels of these enzymes were resistant to both meropenem and imipenem. Clinical isolates of P. aeruginosa that had developed resistance to imipenem during therapy with the drug were two- to 32-fold less susceptible to meropenem than the corresponding pretreatment isolates. Alterations in outer membrane proteins were associated with this change in susceptibility to the carbapenems. Meropenem was a less potent inducer of Class I beta-lactamases than imipenem but was still a better inducer than ceftazidime or piperacillin. Overall, meropenem showed excellent activity against bacteria producing a variety of beta-lactamases, but cross-resistance between meropenem and imipenem due to enzymatic and non-enzymatic mechanisms did occur.

Carbapenems↗
PubMed1989

Functional assessment of the total artificial heart by blood-pool radionuclide angiography.

Blood-pool radionuclide angiography was used to image a patient with a Jarvik 7-(70) total artificial heart. Excellent delineation of the chambers was achieved, allowing assessment of the total artificial heart pumping function. Estimation of the left ventricular volumes, cardiac output, and filling rates by radionuclide angiography corresponded closely with those simultaneously obtained from the total artificial heart driving lines. Radionuclide angiography affords the unique possibility to assess the function of the artificial heart noninvasively.

Adult↗
PubMed1988

Evaluation of single-dose ciprofloxacin in the eradication of Neisseria meningitidis from nasopharyngeal carriers.

The ability of a single oral 750-mg dose of ciprofloxacin to eradicate Neisseria meningitidis from persistent nasopharyngeal carriers was prospectively evaluated in a placebo-controlled, randomized, double-blinded study. Cultures of specimens taken from all 23 ciprofloxacin-dosed subjects 1 day postdose were negative; cultures from 96% of these subjects were negative at 7 and 21 days postdose, including a specimen from a subject colonized with a minocycline-resistant strain. Of 22 placebo recipients, 20 (91%) remained culture positive. Single-dose ciprofloxacin appears efficacious for meningococcal prophylaxis.

Carrier State↗
PubMed1988

Heterogeneity of class I beta-lactamase expression in clinical isolates of Pseudomonas aeruginosa.

Expression of chromosomal beta-lactamase was examined in 85 clinical isolates of Pseudomonas aeruginosa. beta-Lactamase assays with and without cefoxitin induction revealed four phenotypes of enzyme expression: low basal, inducible; moderate basal, inducible; moderate basal, constitutive; and high basal, constitutive. The isoelectric points of the major beta-lactamase bands were 9.4, 9.2, and 8.4. These results indicate that there is a limited heterogeneity in expression of chromosomal beta-lactamase of P. aeruginosa.

Anti-Bacterial Agents↗
PubMed1988

Thrombotic thrombocytopenia with von Willebrand factor deficiency induced by botrocetin. An animal model.

Thrombotic thrombocytopenia with severe von Willebrand factor (vWF) depletion was induced in rats by intraperitoneal injection of botrocetin, a Bothrops factor requiring vWF for platelet aggregation. The vWF deficiency state with thrombocytopenia was produced in 12 animals by single or multiple injections of botrocetin. Single botrocetin injection (450 units/kg) reduced plasma vWF activity to less than 0.01 mu/ml for 24 hours and less than 0.2 units/ml up to 72 hours. During this period, multimeric analysis of plasma vWF:Ag revealed loss of intermediate and high molecular weight forms. A moderate reduction in vWF:Ag (Laurell) and FVIII:C was observed. Bleeding time remained prolonged during the deficiency state. Recovery of plasma vWF and platelet count occurred in 4 to 5 days. Multiple botrocetin injections (450 units/kg/injection) at 48-hour intervals produced a sustained severe vWF depletion (less than 0.2 units/ml) for 1 week. On the 8th day, vWF and platelet count had recovered to preinjection levels. Recovery was associated with the appearance of increased levels of very high molecular weight multimers of vWF:Ag in the plasma. After each botrocetin administration (single or repeat), a transient thrombocytopenia developed which was most severe at 1 to 5 hours postinjection. Another group of 10 animals was given a single botrocetin injection and specimens of lung, liver, kidney, and spleen were obtained at varying time intervals postinjection. Transmission electron micrographs of the lung and spleen 2 hours after botrocetin administration showed platelet aggregates and platelet microthrombi in the lung and spleen. The platelet thrombi in the lung had disappeared within 24 hours, and in the spleen by 48 hours. Liver sinusoids and kidney glomeruli were free of thrombi. A comparison is made of the thrombocytopenia and the ultrastructure of the platelet microthrombi induced by botrocetin with that of other agents.

Animals↗
PubMed1987

Overview of preclinical studies with ciprofloxacin.

Ciprofloxacin is a new 6-fluoro-7-piperazino-4-quinolone that is highly active against a broad array of microbial pathogens. Minimal inhibitory concentrations (MICs) of ciprofloxacin are generally below 0.5 micrograms/ml for Hemophilus, Neisseria, and Enterobacteriaceae and are 1.0 microgram/ml or less for many non-fermentative gram-negative bacteria. Most staphylococci, including strains resistant to methicillin, are inhibited by 1.0 microgram/ml or less of ciprofloxacin, whereas streptococci are somewhat less susceptible. Obligate anaerobes are generally not susceptible to ciprofloxacin at concentrations below 1.0 microgram/ml. The antimicrobial potency of ciprofloxacin is twofold to fourfold greater than that of norfloxacin and is considerably greater than that of cephalosporins and aminoglycosides in tests with most gram-negative bacteria. Factors diminishing the in vitro activity of ciprofloxacin include acidic pH, high levels of magnesium ions, and an inoculum size of 10(7) colony-forming units/ml or greater. Ciprofloxacin is bactericidal at concentrations near its MIC for most bacteria. In vivo tests with experimentally induced infections in animals confirm the potency of ciprofloxacin. Doses required to protect 50 percent of animals from death are generally less than 2.0 mg/kg for gram-negative infections and range from 0.7 to 7.0 mg/kg for staphylococcal infections. The antimicrobial spectrum and potency of ciprofloxacin demonstrated in these preclinical studies make this quinolone a promising new antimicrobial agent.

Animals↗
PubMed1987

Clinical importance of inducible beta-lactamases in gram-negative bacteria.

The clinical problems caused by inducible beta-lactamases in certain gram-negative bacteria are being recognized with increasing frequency. These problems include the rapid emergence of multiple beta-lactam resistance during therapy with many of the newer beta-lactam antibiotics. Such multiply resistant organisms are now spreading within the hospital and have become important nosocomial pathogens. This has been a particularly difficult problem for intensive care units, cystic fibrosis centers and burn units where there are clusters of patients who are highly susceptible to infections with organisms like Enterobacter spp., Serratia spp. and Pseudomonas aeruginosa, which possess inducible beta-lactamases. Only through an awareness of these problems, their cause, and restriction of the use of certain newer beta-lactam antibiotics can these problems be controlled.

Anti-Bacterial Agents↗
PubMed1987

Activity of ciprofloxacin against Mycobacteria in vitro: comparison of BACTEC and macrobroth dilution methods.

Various clinical isolates of mycobacteria were tested for susceptibility to ciprofloxacin by a standard macrobroth dilution test and the radiometric BACTEC method. Agreement between the two test systems was species dependent: Mycobacterium tuberculosis (80%), M. kansasii with M. scrofulaceum (30%), M. avium-intracellulare (20%), and 0% for the rapidly growing mycobacteria. Most mycobacterial strains other than M. tuberculosis were susceptible to the breakpoint ciprofloxacin concentration of 2 mg/l as determined by BACTEC MICs, whereas none were susceptible by macrobroth testing. Seven of nine M. tuberculosis isolates were susceptible by either method. Ciprofloxacin merits further study as a potential antimycobacterial agent.

Ciprofloxacin↗
PubMed1987

Leakage of beta-lactamase: a second mechanism for antibiotic potentiation by amdinocillin.

Discrepancies were observed between results of different beta-lactamase induction tests with amdinocillin, which appeared to be a strong inducer in whole-cell assays but a weak inducer in assays with cell-free sonic extracts. Results of a nitrocephin-disk test with constitutive beta-lactamase producers indicated that the positive results obtained in whole-cell assays were due to drug-produced leakage of enzyme from the cell and not to induction. Imipenem was also found to cause leakage of beta-lactamase from a similar number of constitutive enzyme producers, while cefoxitin was much less likely to cause leakage. A split-dose regimen was employed to treat mice infected with a strain of Enterobacter cloacae which appeared to leak enzyme on exposure to amdinocillin. Results indicated that prior treatment with amdinocillin significantly enhanced (P less than 0.025) the efficacy of azlocillin, an enzyme-labile drug, but did not affect the efficacy of cefotaxime, a relatively enzyme-stable drug. Conversely, prior treatment with amdinocillin did not potentiate the efficacy of either azlocillin or cefotaxime in the treatment of mice infected with an Escherichia coli strain that was highly susceptible to all three drugs. Thus, it appears that amdinocillin may potentiate the activity of other beta-lactam drugs not only by binding to a complementary penicillin-binding protein but also by causing leakage of beta-lactamase from the cell. This effect may be related to its ability to bind to penicillin-binding protein 2 and subsequently produce changes in outer membrane permeability.

Amdinocillin↗