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author:("pohland, D")
1.  Effect of quinolones and other antimicrobial agents on cell-associated Legionella pneumophila. 
Antimicrobial Agents and Chemotherapy  1987;31(10):1529-1534.
We evaluated the in vitro susceptibility of Legionella pneumophila ATCC 33152 (serogroup I) to 13 antibiotics alone and in combination with rifampin (0.1 mg/liter) by three methods. Extracellular susceptibility was determined by MIC determinations and time kill curves in buffered yeast extract broth, while intracellular susceptibility was determined by peripheral human monocytes in RPMI 1640 culture medium. Antibiotic concentrations equal to or greater than the broth dilution MIC inhibited or killed L. pneumophila by the time kill method, except this was not the case for trimethoprim-sulfamethoxazole. Antibiotic concentrations below the broth dilution MIC did not inhibit Legionella growth. The only antibiotic-rifampin combinations which produced improved killing of L. pneumophila by the time kill method were those in which the logarithmic growth of L. pneumophila occurred during the experiment (rosoxacin, amifloxacin, cinoxacin, trimethoprim-sulfamethoxazole, clindamycin, and doxycycline). Neither direct MICs nor time kill curve assays accurately predicted intracellular L. pneumophila susceptibility. Rifampin, erythromycin, ciprofloxacin, rosoxacin, enoxacin, amifloxacin, gentamicin, clindamycin, and doxycycline all inhibited intracellular L. pneumophila growth at readily achievable concentrations in serum. Cefoxitin and thienamycin showed no inhibition of growth, although they were present extracellularly at concentrations that were 20 to 1,000 times their broth dilution MICs. Clindamycin was the only antibiotic that was able to inhibit intracellular L. pneumophila growth at an extracellular concentration below its MIC. The gentamicin (5 mg/liter)-rifampin combination was the only antibiotic-rifampin combination which demonstrated decreased cell-associated Legionella survival in this model of in vitro susceptibility.
PMCID: PMC174984  PMID: 3435101
2.  In vitro susceptibility of gram-positive cocci to paldimycin. 
Paldimycin (U-70138F) is a new antimicrobial agent with activity against gram-positive cocci. Clinical isolates of staphylococci and streptococci were tested. MICs were higher in Mueller-Hinton broth than in nutrient broth. Change in pH had minimal effect on the MICs in either broth. When inoculum size was varied, an inoculum effect was observed. The gram-positive cocci tested were generally more susceptible to paldimycin than to vancomycin.
PMCID: PMC174662  PMID: 3105438
3.  Single-dose cephalexin therapy for acute bacterial urinary tract infections and acute urethral syndrome with bladder bacteriuria. 
The efficacy of single-dose therapy with 3 g of cephalexin was evaluated in 129 women with symptoms of acute uncomplicated lower urinary tract infections. Of 91 patients with significant bacteriuria, 61 (67%) were cured of their original infection; this was similar to the 54 to 79% cure rates reported in unselected populations of women of a wide age range treated for acute uncomplicated urinary tract infections with a single dose of amoxicillin or trimethoprim-sulfamethoxazole (J. Rosenstock, L. P. Smith, M. Gurney, K. Lee, W. G. Weinberg, J. N. Longfield, W. B. Tauber, and W. W. Karney, Antimicrob. Agents Chemother. 27:652-654, 1985; N. E. Tolkoff-Rubin, M. E. Wilson, P. Zuromskis, I. Jacoby, A. R. Martin, and R. H. Rubin, Antimicrob. Agents Chemother. 25:626-629, 1984). The cure rates of (87%) for our younger patients, those less than 25 years of age, was better than that (46%) for our patients over 40 years of age (P less than 0.001). Patients with infections that were negative in an antibody-coated bacteria test were cured at a significantly higher rate than those with infections that were positive in an antibody-coated bacteria test (71 versus 19%; P = 0.003). Those patients with infections caused by cephalexin-susceptible organisms were cured at a rate similar to that for patients with infections caused by cephalexin-resistant organisms (68 versus 50%; P = 0.62). The cure rate for suburban patients was 90%, versus 45% for inner-city patients (P = 0.008). Of the 28 women with acute urethral syndrome due to low-level bacteriuria, 27 were cured.
PMCID: PMC180398  PMID: 3717940
4.  Comparison of enzyme-multiplied immunoassay technique with fluorescence polarization immunoassay for determination of gentamicin and tobramycin levels in serum. 
Journal of Clinical Microbiology  1984;20(5):866-868.
We assayed serum gentamicin and tobramycin specimens by the enzyme multiplied immunoassay technique (Syva EMIT) and the fluorescence polarization immunoassay (Abbott TDx). When interassay and intraassay control samples were evaluated, both methods gave an overall coefficient of variation of less than +/- 10%. Using patient serum samples, we obtained excellent correlation with both methods in the assay of gentamicin (correlation coefficient, 0.985) and tobramycin (correlation coefficient, 0.982).
PMCID: PMC271461  PMID: 6392321
5.  Comparison of fluorescence polarization immunoassay and bioassay of vancomycin. 
Journal of Clinical Microbiology  1984;20(2):159-161.
Human serum samples were analyzed for vancomycin concentrations by two different methods: the fluorescence polarization immunoassay and the disk plate bioassay. Each assay method offered acceptable precision. The correlation between both assay methods was excellent (correlation coefficient = 0.985). Excluding technical time, the bioassay was the least expensive method to perform but was more labor intensive than the fluorescence polarization immunoassay.
PMCID: PMC271276  PMID: 6436291
6.  In vitro susceptibilities of 393 recent clinical isolates to WIN 49375, cefotaxime, tobramycin, and piperacillin. 
The in vitro susceptibilities of 393 recent clinical isolates to WIN 49375, a new quinolone derivative, were determined and concurrently tested with cefotaxime, tobramycin, and piperacillin. In general, members of the family Enterobacteriaceae were not as susceptible to tobramycin and piperacillin as they were to WIN 49375. Methicillin-resistant and -susceptible Staphylococcus aureus were equally susceptible to WIN 49375.
PMCID: PMC185523  PMID: 6326666
7.  In vitro susceptibility patterns of methicillin-resistant and-susceptible Staphylococcus auerues strains in a population of parenteral drug abusers from 1972 to 1981. 
Since 1980, infections caused by methicillin-resistant (MR) Staphylococcus aureus have been epidemic among Detroit-area parenteral drug abusers. Because of the increasing importance of this pathogen, in vitro susceptibilities were compared for 39 isolates of MR S. aureus from 1980 to 1981, and for 56 strains of methicillin-susceptible (MS) S. aureus from 1972 to 1981, recovered from drug abusers with community-acquired infections. Agar dilution studies were performed at 35 degrees C, and minimal inhibitory concentrations were determined after incubation for 18 and 48 h. MR S. aureus exhibited cross-resistance to other beta-lactam antibiotics which frequently required 48 h for expression. MR S. aureus isolates were also resistant to tetracycline, clindamycin, tobramycin, and amikacin. All MR S. aureus isolates investigated synthesized an aminoglycoside 4'-nucleotidyltransferase. Emergence of resistance to cefotaxime, tetracycline, and clindamycin was noted among current MS S. aureus isolates. Vancomycin, fusidic acid, trimethoprim/sulfamethoxazole, and rifampin were the most active agents against MR S. aureus and were equally effective against MS S. aureus.
PMCID: PMC184668  PMID: 6552151
8.  Failure of probenecid to alter the pharmacokinetics of ceforanide. 
This investigation evaluated the effect of probenecid on ceforanide concentrations in eight healthy volunteers. Each volunteer was given 1 or 2 g of ceforanide either alone or with 1 g of probenecid. Concentrations of ceforanide in plasma, urine, and saliva were then measured. Probenecid did not alter the plasma concentrations of ceforanide, nor did it affect the urinary excretion of this agent. Ceforanide was not secreted into saliva in any detectable amount either when administered alone or with probenecid. It is not clear why probenecid has a negligible effect on ceforanide concentrations in plasma. It may be that tubular secretion plays less of a role in the excretion of ceforanide than expected, or that the physical properties of ceforanide prevent probenecid from affecting its excretion.
PMCID: PMC181737  PMID: 7342878
9.  Effect of clavulanic acid on minimal inhibitory concentrations of 16 antimicrobial agents tested against Legionella pneumophila. 
A total of 15 Legionella pneumophilia isolated were tested against 16 antimicrobial agents used singly and in combination with clavulanic acid. When combined with clavulanic acid, 4 of the 16 antimicrobial agents produced no enhanced effect. However, the minimal inhibitory concentrations of 12 of the antimicrobial agents were reduced by one-half to one-third when in combination with clavulanic acid. These reductions reflected only a one-dilution decrease, however, in the original minimal inhibitory concentrations. Thus, clavulanic acid combinations appear to be only nominally effective beta-lactamase inhibitors against L. pneumophilia.
PMCID: PMC283995  PMID: 6969575
10.  Effect of Renal Failure and Dialysis on the Serum Concentration of the Aminoglycoside Amikacin 
Serum and dialysate levels of amikacin were determined at appropriate intervals after a 300-mg intravenous dose as a continuous infusion in six patients with end-stage renal failure undergoing hemodialysis and in three patients on peritoneal dialysis. The mean serum half-life of amikacin was 3.75 h during (or after) hemodialysis and 29 h during (or after) peritoneal dialysis. Although not on hemodialysis in the same six patients, the serum half-life was 28 h. The results indicate that the maintenance dose of amikacin should be markedly decreased in patients with severe renal failure even if they are treated with peritoneal dialysis, and that serial serum antibiotic concentrations are essential to prevent cumulative toxicity of the drug.
PMCID: PMC429772  PMID: 984789

Results 1-10 (10)