dibekacin and bekanamycin

Arbekacin (1-N-((S)-4-amino-2-hydroxybutyryl)-3',4'-dideoxykanamycin B) was active against 54 strains of methicillin-resistant Staphylococcus aureus from 16 different countries, all of which were resistant to > or = 32 mg/L amikacin. MICs of arbekacin ranged from 1 to 16 mg/L, the MIC50 was 3.2 mg/L and the mode geometric mean MICs were 4 and 4.5 mg/L respectively.

Topics: Aminoglycosides; Anti-Bacterial Agents; Dibekacin; Kanamycin; Methicillin Resistance; Microbial Sensitivity Tests; Staphylococcus aureus

In spontaneously beating sinus venosus of the frog Caudiverbera caudiverbera the effects of bekanamycin and dibekacin, two aminoglycoside antibiotics, on action potentials of cardiac primary pacemaker cells were studied by intracellular recording. Bekanamycin and dibekacin induced a concentration-dependent decrease of the amplitude, overshoot and the rate of rise of the action potential. Both also flattened the slow diastolic depolarization leading to a marked decrease in beat rate. At the highest concentration used (1 x 10(-3) M), the aminoglycosides produced a complete inhibition of primary cells action potentials. It was preceded by the appearance of subthreshold oscillations of the membrane potential which were observed for a few minutes until the electrical activity of pacemaker cell ceased. During absence of impulse initiation a stable membrane potential about -40 mV was observed. Aminoglycoside effects, excepting those on SCL, were completely suppressed when external calcium was increased to 3.6 mM. The results support the conclusion that bekanamycin and dibekacin depress the electrical activity of pacemaker cells. It is suggested that this effect is induced by aminoglycosides blockade of the slow calcium current involved in both upstroke and slow diastolic depolarization and through modification of potassium outward current. Bekanamycin at a lower concentration than that needed to induce electrophysiological effects potentiated verapamil 1 x 10(-8) effects on cardiac pacemaker cells.

Topics: Action Potentials; Animals; Anura; Calcium; Dibekacin; Heart Conduction System; In Vitro Techniques; Kanamycin; Verapamil

We examined biochemically the effect of six aminoglycoside antibiotics on the activity of lysozyme, acid phosphatase, and N-acetyl-beta-D-glucosaminidase in human tears. All six antibiotics strongly inhibited lysozyme activity, the degree of inhibition depending on the dose administered. Except for bekanamycin, antibiotics had little effect on the activity of acid phosphatase or N-acetyl-beta-D-glucosaminidase. The nature of the inhibition was competitive. Other kinds of antibiotics, such as sulbenicillin or erythromycin, had no inhibitory effect on lysozyme, acid phosphatase, or N-acetyl-beta-D-glucosaminidase. These results suggested that the inhibition of lysozyme by aminoglycosides is specific and that the decreased effectiveness of a protective system against bacterial infection in the eye is highly possible when aminoglycoside antibiotics are used without prior sensitivity testing.

Topics: Acetylglucosaminidase; Acid Phosphatase; Amikacin; Aminoglycosides; Anti-Bacterial Agents; Depression, Chemical; Dibekacin; Erythromycin; Gentamicins; Hexosaminidases; Humans; Kanamycin; Muramidase; Sulbenicillin; Tears; Tobramycin

The antimicrobial activity of kanamycin, kanendomycin, gentamicin, amikacin, sisomicin, and dibekacin against 200 strains of Pseudomonas aeruginosa was compared. Dibekacin was found to be the most active against the tested organisms, whereas the other aminoglycoside antibiotics fell in the following order of diminishing antibacterial potency: amikacin, sisomicin, gentamicin, kanendomycin, and kanamycin. Seven strains showed high-level resistance to gentamicin (minimal inhibitory concentration, 400 mug/ml), and two of them were also resistant to amikacin and sisomicin (minimal inhibitory concentration, 75 mug/ml). The minimal inhibitory concentration of dibekacin for these seven strains was 0.625 mug/ml.

Topics: Dibekacin; Drug Resistance, Microbial; Gentamicins; Kanamycin; Pseudomonas aeruginosa