Determination of diagnostic x-ray beam quality.

Half-value layer (HVL) checks at certain KVp settings were carried out on diagnostic x-ray machines in the Radiology Department of the University of Ilorin Teaching Hospital. A simple penetrameter technique which is based on the transmission of a hardened x-ray beam through an aluminium step wedge and reference discs simultaneously was used. The different degrees of beam attenuation were displayed on a radiographic film while a densitometer was used to measure the corresponding optical density values. Results were obtained from a calibration plot of HVL versus optical density. A comparison of results with literature values for same settings of KVp and filtration showed a very good agreement. The technique which is simple and reliable, is recommended for use in some developing countries where economic constraints would not permit the importation of essential test tools for radiodiagnostic quality assurance measurements.

Synergy with cefsulodin or piperacillin and three aminoglycosides or aztreonam against aminoglycoside resistant strains of Pseudomonas aeruginosa.

Fifty-one strains of Pseudomonas aeruginosa, with resistance to one or more amino-glycosides, were tested for synergy with cefsulodin or piperacillin plus amikacin, tobramycin, gentamicin or aztreonam by the agar dilution technique. Cefsulodin plus any one of the three aminoglycosides regardless of the degree of resistance to the aminoglycoside was synergistic against P. aeruginosa for two thirds of the isolates. In contrast, synergy rates with piperacillin were much less uniform. The highest rate of synergy with piperacillin (90.0%) was observed with gentamicin for the gentamicin resistant strains. The lowest rate of synergy was observed with piperacillin plus amikacin (32.2%) for isolates with moderate resistance to amikacin. Synergy for strains with moderate resistance to amikacin was observed more commonly with cefsulodin than with piperacillin. Synergy for strains with a known mechanism of resistance to amikacin was more common with cefsulodin regardless of the mechanism of resistance. Cefsulodin or piperacillin in combination with aztreonam was rarely synergistic (less than 12%).

Azlocillin and mezlocillin concentration in human prostatic tissue.

The concentrations of azlocillin and mezlocillin in human prostatic tissue obtained by transurethral resection or enucleation were measured after two 2.0-gram doses of either drug. The average plasma concentration of azlocillin and mezlocillin at time of tissue sampling was 64.9 and 36.3 micrograms/ml, respectively, and tissue concentration at the time of sampling was 22.9 micrograms/g for azlocillin and 9.4 micrograms/g for mezlocillin. The plasma/tissue concentration ratio for mezlocillin was 0.25 and for azlocillin 0.35. Concentrations of mezlocillin in tissue obtained by transurethral resection were similar to those obtained by enucleation. Azlocillin and mezlocillin in appropriate doses achieve a concentration in human prostatic tissue above the inhibitory concentration for common bacterial pathogens.

In-vitro antimicrobial activity of enoxacin in combination with eight other antibiotics against Pseudomonas aeruginosa, Enterobacteriaceae and Staphylococcus aureus.

Susceptibilities of 28 strains of Pseudomonas aeruginosa, 32 strains of Enterobacteriaceae and 24 strains of Staphylococcus aureus were tested against combinations of enoxacin with either cefsulodin, piperacillin, or amikacin, enoxacin with either aztreonam, latamoxef or amikacin, and enoxacin with either oxacillin, clindamycin or vancomycin, respectively. Synergy was detected by the agar dilution technique and was defined as a four-fold decrease in the inhibitory concentration of both drugs (sigma FIC less than or equal to 0.5). Against Ps. aeruginosa, synergy occurred in 28.5% of the strains for enoxacin plus cefsulodin, 17.6% for enoxacin plus piperacillin, and 3.7% for enoxacin plus amikacin. Against the Enterobacteriaceae, synergy was detected with enoxacin plus aztreonam, latamoxef or amikacin in 9.3%, 3.1% and 0% of strains, respectively. Against Staph. aureus, no synergy was demonstrable with enoxacin plus oxacillin, clindamycin or vancomycin. No antagonism was detected for any combination tested. Selected strains demonstrating synergy by the agar dilution method for enoxacin plus cefsulodin or piperacillin failed to show synergy in kinetic studies.

Comparative antimicrobial activity of enoxacin, ciprofloxacin, amifloxacin, norfloxacin and ofloxacin against 177 bacterial isolates.

The in-vitro antimicrobial activity of five new quinolones, enoxacin (CI-919, AT-2266), ciprofloxacin (Bay o 9867), amifloxacin (WIN 49375) norfloxacin (MK 0366), and ofloxacin (ORF 18489), was compared against 104 strains of Enterobacteriaceae, 51 Pseudomonas species, 7 Acinetobacter calcoaceticus var. anitratus, and 15 enterococci. In general the quinolones tested were active against most bacterial strains. Ciprofloxacin was the most active with MIC90 for all genera tested ranging from 0.03 to 4.0 mg/l. The range of MIC90 for enoxacin and amifloxacin was 0.06 to 16.0 mg/l, for ofloxacin 0.25 to 8.0 mg/l, and for norfloxacin 0.06 to 32.0 mg/l. All strains of P. aeruginosa tested were resistant to amikacin (MIC greater than or equal to 16 mg/l); those resistant by virtue of inactivating enzyme production were less susceptible to ciprofloxacin, ofloxacin, and norfloxacin than those strains exhibiting decreased uptake of amikacin. Susceptibility to enoxacin and amifloxacin was not affected by the mechanism of aminoglycoside resistance. Of 65 strains tested with four quinolones using log and lag phase bacterial growth, the MICs in log phase growth were one to two dilutions higher for 42% of strains tested with amifloxacin, 33% of those tested with norfloxacin, and 23% for those tested with enoxacin and ciprofloxacin.

Comparative in vitro activities of enoxacin (CI-919, AT-2266) and eleven antipseudomonal agents against aminoglycoside-susceptible and -resistant Pseudomonas aeruginosa strains.

The in vitro activity of enoxacin (CI 919, AT 2266), a new oral quinolone carboxylic acid compound, was compared with those of gentamicin, tobramycin, amikacin, azlocillin, piperacillin, aztreonam, moxalactam, imipenem, cefsulodin, ceftazidime, and cefoperazone against 101 aminoglycoside-susceptible and 105 aminoglycoside-resistant Pseudomonas aeruginosa strains. Among these 206 P. aeruginosa isolates were 25 strains with known mechanisms of resistance to amikacin. The activity of enoxacin was similar to that of tobramycin against aminoglycoside-susceptible strains, with MICs of 1.0 to 2.0 micrograms/ml and 0.5 to 1.0 microgram/ml, respectively, for 90% of the strains. Enoxacin was the most active agent in this in vitro study against aminoglycoside-resistant P. aeruginosa strains, with MICs of 2.0 to 4.0 micrograms/ml for 90% of the strains. Strains with enzymatic resistance to amikacin were more resistant to beta-lactams (except enoxacin and imipenem) than were strains with decreased permeability.