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Antibacterial and inducer activities concerning inducible macrolide resistance in Staphylococcus aureus were investigated using 32 erythromycin, oleandomycin and other macrolide antibiotic derivatives and analogues. The macrolides were classified into five groups from very high to none according to their inducer activity.
Haemophilus vaginalis is highly sensitive to oleandomycin. The MIC ranged from 0.035 to 0.15 mug/ml. The sensitivity of H. vaginalis to spectinomycin was 2.5-5.0 mug/ml. The sensitivity of H. vaginalis to spectinomycin is 3-4 times higher than that of Neisseria gonorrhoeae. A favourable effect in the treatment of vaginitis caused by H. vaginalis could thus be expected.
1000 chickens were used to investigate up to 24 weeks under high environmental temperatures the addition of different types (oxytetracycline and oleandomycin) and different levels (5 or 20 ppm) of antibiotics to the basal diet. Supplementation with 20 ppm had--with both types of antibiotics--a marked positive effect on the growth rate and various quality characteristics of the products. The effect was higher in male animals than in females.
Growth inhibitory effect of combined treatment of tetracycline (TC) and oleandomycin (OM), at a ratio of 2:1, on certain species of pathogenic bacteria including drug-resistant ones was examined. By the crossed paper strip method, synergistic effects were demonstrated against 9 of the 16 strains of Staphylococcus aureus, and all of the 5 strains of Escherichia coli studied. Antagonism was observed with none of the strains and with 2 strains of Streptococcus pyogenes and 2 strains of Streptococcus pneumoniae tested in the present experiments. The MICs determined by the agar dilution method, also gave similar results, although synergism was not conclusively demonstrated by this method. With representative strains of S. aureus, synergism was evidenced by quantitative measurement of growth inhibition. In some strains, 1.0 mug of one drug per ml of medium inhibited the induction of resistance to the second drug. Such a small dose of one drug also inhibited the development of a mutant resistant to the second drug. These inhibitory actions were thought to be one of the important factors causing the synergistic effect of TC and OM on drug resistant bacteria.
The combination effect of tetracycline (TC) and oleandomycin (OM) on acute infection of mice with four strains of Staphylococcus aureus including TC or OM resistant ones was examined by the quantitative determination of protective potencies of single and combined drugs. The grade of synergism was expressed by the synergistic ratio (SR), a ratio of experimentally determined potency of the combined drug over a hypothetical potency in which additive effect of the both drugs is assumed. With 3 out of the 4 strains of S. aureus synergism between TC and OM or triacetyloleandomycin (TAO) was demonstrated by the determination of the 50% effective dose and by statistical examination of the SR. The grade of synergistic protection by these drugs varied with the strains infected and it did not depend upon the sensitivity to antibiotics or grade of synergism in vitro. There was no synergistic enhancement of acute toxic action in the combined administration of TC and OM to mice.
The authors report a case of ischaemia of all four limbs in an adolescent following the simultaneous ingestion of triacetyl oleandomycin and ergotamine tartrate in low dosage. Two cases involving this same association of medications have appeared in the literature and attention is therefore drawn to the possible danger of use of these two drugs together.
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The resistance mechanism of Escherichia coli BM2506 to macrolides was found to be due to inactivation. Inactivated oleandomycin was identified as oleandomycin 2'-phosphate by thin-layer chromatography. A new type of macrolide-phosphorylating enzyme, macrolide 2'-phosphotransferase type II (MPH(2')II), was detected, purified 95-fold and its enzymological properties investigated. MPH(2')II was a constitutive intracellular enzyme which showed high levels of activity with both 14-member-ring and 16-member-ring macrolides. The optimum pH for the inactivation of oleandomycin was 8.2 and the optimum temperature of the reaction was 40 degrees C. Enzyme activity was lost by heat treatment at 60 degrees C for 1 min. The isoelectric point and M(r) of the enzyme were 5.3 and 48,000, respectively. Purine nucleotides, such as ITP, GTP and ATP, were effective as cofactors in the inactivation of macrolides. An inhibitory effect of iodine, EDTA, or divalent cations on MPH(2')II activity was observed.
Multi-drug resistance of Salmonella heidelberg was transmitted to normal intestinal flora (E. coli organisms were resistant to ampicillin, streptomycin, tetracycline, erythromycin, and oleandomycin. The donor strains of Salmonella heidelberg used in the experiment was a carrier of the following nine markers of resistance: ampicillin, streptomycin, chloramphenicol, kanamycin, neomycin, novobiocin, tetracycline, erythromycin, and oleandomycin. The donor strains of Salmonella heidelberg used in the experiment was a carrier of the following nine markers of resistance: ampicillin, streptomycin, chloramphenicol, kanamycin, neomycin, novobiocin, tetracycline, erythromycin, and oeandomycin, novobiocin, tetracycline, erythromycin, and oleandomycin. The resistance to drugs was transmitted with the oral administration of the donor strain at the preliminary neutralization of the action of hydrochloric acid in the stomah secretion through sodium bicarbonate (1 cm3 of a 10 per cent sol.) an hour prior to feeding the birds with Salmonella heidelberg (1 cm3 of 10(10). In other experiments carboneum tetrachloratum was injected at rates of 0.08 to 0.15 cm3 (acocrting with the body weight of birds) one day prior to infection, followed by the administration of 0.20 to 0.40 cm3 of a 2 per cent solution of omnopon. Escherichia coli organisms acquired new markers of resistance--to chloramphenicol, kanamycin, neomycin and novobiocin. The level of resistance proved equal with that to the donor strain. A total of 1.8 to 5.4 per cent of the intestinal E. coli investigated proved to be carriers of the indicated markers of resitance. Highest level in acquiring markers of multi-drug resistance (13 per cent) showed E. coli organisms isolated from the liver of birds injected additionally with C. tetrachloratum omnopon.
The factors affecting the sensitivity of nafcillin, vancomycin, oleandomycin, chloramphenicol, methacycline and novobiocin assay, using the paper disc diffusion method, were studied. Agar concentration and pour volume were found to influence the assay sensitivity of antibiotics. The type of assay medium was effective e.g. brain heart infusion agar was the best medium for nafcillin and methacycline; synthetic amino acid medium for oleandomycin; Muller Hinton agar for vancomycin and chloramphenicol; and G & R medium for novobiovicin. All additives, including inorganic ions, sugar, organic acids, complexing agents, surface active agents and blood, decreased the activities of the studied antibiotics. Higher activities of vancomycin, methacycline were observed at pH = 5, of nafcillin, chloramphenicol, and novobiocin at pH = 6, and of oleandomycin at pH = 7.
Staphylococcus aureus 8325(pEP2104), a transductant derived from S. aureus PM2104 isolated clinically in Hungary (L. Janosi, and E. Ban, Acta Microbiol. Acad. Sci. Hung., 29: 187-200, 1982), exhibited an inducible resistance to the 14-membered macrolides [erythromycin (EM) and oleandomycin (OL)] and streptogramin B (MKM-B) antibiotics, but not to the 16-membered macrolides and lincosamides. This resistance was referred to as PMS-resistance phenotype (L. Jánosi, Y. Nakajima, and H. Hashimoto, Microbiol. Immunol., 34: 723-735, 1990). In addition to EM, OL, and MKM-B, however, the strain was recently and first observed to have inducible resistance to mycinamicin, a 16-membered ring macrolide. Thereby, we propose that the reference stated just above as PMS-resistance has to be extended to such 16-membered macrolides as mycinamicin. An optimum concentration of erythromycin or oleandomycin for induction of PMS-resistance was 1.35 mu g/ml in the strain 8325(pEP2104). The concentration was about 30 times as great as that (0.05 mu g/ml) required for induction of well-known co-resistance to macrolide-lincosamide-streptogramin B antibiotics in S. aureus ISP447.
Growing cultures, as well as broken and lyophilized cells of pseudomonas 56 were found to degrade erythromycin A, and lyophilized cells inactivated erythromycins A and B. The enzyme system involved in this degradation was constitutive and the enzyme level in the cells could be increased about 8-fold when oleandomycin or erythromycin B was added to the growth medium. The ability of whole or broken cells to inactivate erythromycin A was completely lost when these preparations were boiled, and the erythromycin A-inactivating activity was localized in the cell membrane fraction. The lyophilized cells did not degrade oleandomycin, methymycin, tylosin, a mixture of leucomycins, josamycin, or maridomycin III.
Reaction of the strains of the tularemia causative agent to erythromycin (100 gamma/ml) or oleandomycin (400 gamma/ml) is one of the taxonomic tests. The study of 82 strains of the holarctic race and 63 strains of the Central Asiatic race according to this test showed that the strains of the holarctic race were divided with respect to these macrolides into sensitive (biotype I) and resistant (biotype II). The strains of the both races were isolated at the territory of the Kazakh SSR. Such a reaction of the strains of the holarctic race is a stable feature and is not connected with virulence, the isolation source and the biochemical properties of the strains. Division of the holarctic race into the biotypes (I and II) with respect to erythromycin and oleandomycin may be of definite significance in epidemiological and epizootological examination for tularemia with a purpose of determining the source of the infection, as well as in defining the borders of the infection focus area with circulation of this or that biotype of the holarctic race of the tularemia causative agent.