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PubMed1978

Combined vs. single-drug studies of susceptibilities of Mycobacterium kansasii to isoniazid, streptomycin, and ethambutol.

The effects of combined drugs were compared uith the effects of single drugs in vitro against Mycobacterium kansasii. The single drugs isoniazid 1.0 microgram/ml, streptomycin 2.0 microgram/ml, and ethambutol 5.0 microgram/ml and the combinations of 1.0 microgram/ml isoniazid and 2.0 microgram/ml streptomycin, 1.0 microgram/ml isoniazid and 5.0 ethambutal and 1.0 microgram/ml isoniazid, 2.0 microgram/ml streptomycin and 5.0 microgram/ml ethambutol were evaluated as to their effects on M. kansasii organisms from 22 patients with pulmonary mycobacterial disease. These drugs were incorporated into Middlebrook 7H11 medium. Colonial growth was then observed and assigned numerical values for statistical analysis. The results showed that isoniazid was not significantly better than ethambutol. Streptomycin, however, was significantly better than both isoniazid and ethambutol alone. The double combinations were better than the single drugs, with isoniazid--streptomycin being better than isoniazid--ethambutol. The combination isoniazid--ethambutol was not significantly better than streptomycin alone. However, the triple combination of isoniazid--streptomycin--ethambutol was markedly better than all single drugs, better than isoniazid--ethambutol, but not better than isoniazid--streptomycin. Combined-drug testing thus showed a pattern of susceptibility not demonstrated by single-drug testing.

Ethambutol↗
PubMed1976

Coupling of rates of transcription, translation, and messenger ribonucleic acid degradation in streptomycin-dependent mutants of Escherichia coli.

The growth rates of streptomycin-dependent mutants varied in proportion to the level of streptomycin supplied; growth also varied characteristically from one dependent strain to another at a given streptomycin concentration. When cells growing at different rates (over a threefold range) were treated with rifampin, direct proportionality was observed for three parameters: (i) the rates of shutoff of transcription of total ribonucleic acid (RNA) and ribosomal RNA, as measured by pulse labeling at later times; (ii) the translation time for molecules of beta-galactosidase; and (iii) the rate of chemical degradation of messenger RNA. In contrast, the rate of functional inactivation of both total and beta-galactosidase messenger RNA was about the same at all growth rates. None of the variations of growth or other parameters were observed in an otherwise isogenic streptomycin-resistant strain treated with streptomycin. Since the mutational change in strd mutants and the site of action of streptomycin are in the 30S ribosomal subunits, it is suggested that the rate of ribosome function is set by the dependent lesion (and the level of streptomycin). One possibility is that the other correlated effects are mechanistically "coupled" to ribosome function, but the apparent coupling could also be an indirect result of differential effects of streptomycin on variables such as ribosomal miscoding and nucleotide pool size. However, since the rate of functional inactivation of messenger RNA is constant even when the RNA is broken down two- to fourfold more slowly, translation yield tends to be proportional to the growth rate of the dependent strains.

Escherichia coli↗
PubMed1978

Impaired colonization of gnotobiotic and conventional rats by streptomycin-resistant strains of Streptococcus mutans.

Colonization of streptomycin-resistant mutants derived from Streptococcus mutans strain LB1, a human isolate, and strain FA-1, a rodent isolate, was studied in gnotobiotic and conventional rats. Mutants resistent to 2.0 mg of streptomycin per ml were isolated by using both stepwise (suffix "R"M) and one-step (suffix "R"1) selections. Rats were infected with mixtures of parental and streptomycin-resistant strains, and the proportions of each strain present in samples from the intestinal canal, tongue dorsum, teeth, and fissure plaque were determined. Combinations of strains investigated were LB1 and FA-1"R"M; FA-1 and LB1"R"M; LB1 and LB1"R"1; FA-1 and FA-1"R"1. In gnotobiotic rats, nonresistant strains predominated in every oral sample studied at 7 and 21 days after infection. Similarly, when conventional exgermfree rats were infected with FA-1 and FA-1"R"1, FA-1 dominated in all samples. Streptomycin-sensitive revertants were not detected in rats monoinfected with strains LB1"R"1 and FA-1"R"1 for 21 days. No antagonistic interactions were observed between the strains in in vitro experiments. Streptomycin-resistent mutants attached to hydroxyapatite treated with rat or human saliva in equal or higher numbers than did parental strains. However, parental strains appeared to grow faster in Trypticase soy broth then streptomycin-resistant mutants. These observations indicate that induction of streptomycin resistance frequently impairs the colonization properties of S. mutans strains, possibly by altering their rate of growth.

Animals↗
PubMed1975

Intrageneric transformation of neisseria gonorrhoeae and neisseria perflava to streptomycin resistance and nutritional independence.

Auxotrophic mutants of Neisseria gonorrhoeae and Neisseria perflava were transformed to prototrophy using homologous and heterologous deoxyribonucleic acid (DNA). Within either species the efficiencies of transformation for nutritional markers were found to be very similar to the values obtained for transformation to streptomycin resistance. The number of transformants in the interspecific N. perflava (donor) - - leads to N. gonorrhoeae (recipient) cross was 100-fold lower than the number obtained in the intraspecific N. gonorrhoeae - - leads to N. gonorrhoeae cross for streptomycin resistance, as well as for several nutritional markers. In the reciprocal experiment the difference in the number of transformants in the interspecific N. gonorrhoeae - - leads to N. perflava cross and the number obtained in the intraspecific N. perflava - - leads to N. perflava cross varied from 600 to 1,000-fold for the streptomycin resistance marker. Of greater interest was the finding that N. perflava auxotrophs, although transformable to prototrophy with wild-type N. perflava DNA, were not transformed to nutritional independence by gnoncoccal DNA. These same mutants were transformable to streptomycin resistance using the heterologous gonococcal DNA. When the DNAs of N. meningitidis, N. flava, and N. lactamicus were used to transform N. gonorrhoeae to prototrophy or streptomycin resistance, the transformation frequencies obtained fell along a gradient that in general reflected taxonomic relationships. On the other hand, with N. perflava as the recipient for these same DNAs, only N. flava DNA could transform auxotrophs to prototrophy, although transformation to streptomycin resistance occurred in all cases. DNA from N. perflava - - leads to N. gonorrheae streptomycin-resistant or Ade+ intergenotic transformants transformed N. gonorrhoeae cells at a 100-fold-higher efficiency than did DNA from N. perflava. Our findings suggest that (i) N. gonorrhoeae and N. perflava are more closely related than hitherto suspected and (ii) N. perflava is more selective with respect to heterologous DNA than is N. gonorrhoeae.

Amino Acids↗
PubMed1975

Rsistance to streptomycin in a producing strain of Streptomyces griseus.

Streptomyces griseus S 104 was sensitive to streptomycin during exponential growth in a medium which, in the subsequent stationary phase, supported production of the antibiotic in yields above 200 mug/ml. When antibiotic production began cultures developed a tolerance toward their lethal metabolite. This was not due to an increase in pH associated with antibiotic production, since pH effects on streptomycin sensitivity in S. griseus were in the reverse direction. However, the degree of tolerance was directly related to the amount of cell material present. Streptomycin production caused no change in the proportion of resistant variants in the population, nor did it cause the severe inhibition of protein synthesis observed in non-producing cultures exposed to the antibiotic. The lack of an effect on protein synthesis is attributed to the absence of streptomycin with in the cytoplasm since soluble extracts from mycelium harvested in the production phase were inactive when bioassayed immediately after cell disruption. However, they developed antibacterial activity rapidly when heated, and more slowly when incubated at 25 degrees C. The addition of phosphatase inhibitors during incubation prevented the appearance of antibiotic activity, and it was concluded that a small amount of streptomycin phosphate is present in the mycelium during antibiotic production. Differences in (14C) streptomycin uptake suggested that the mycelium was appreciably less permeable to the antibiotic in the production phase than during exponential growth. However, a small amount was taken up and much of it was in the soluble fraction of disrupted cells. Bioassays showed that this 14C-labeled antibiotic within the cells had been partially inactivated, suggesting that conversion of streptomycin to an inactive derivative is involved in the mechanism which protects the organism from its metabolite.

Alkaline Phosphatase↗
PubMed1979

Interference with the mannose binding and epithelial cell adherence of Escherichia coli by sublethal concentrations of streptomycin.

When Escherichia coli was grown in sublethal concentrations of streptomycin, mannose binding activity and epithelial cell adherence of the E. coli cultures at stationary phase were significantly reduced in the drug-grown organisms. In a strain whose minimal inhibitory concentrations was 30 mug/ml, the percentage of reduction in mannose binding activity was dose related over a range of concentrations between 0.5 and 10 mug/ml streptomycin. Concomitant with the drug-induced suppression of mannose binding activity, antigenic and ultrastructural alterations on the surface of the drug-grown organisms were observed by agglutination tests and electron microscopy, respectively. The streptomycin effect was reversible, required actively growing organisms, and was most apparent in the early log-phase of growth. High doses of antibiotic were ineffective when added to cultures which had acquired mannose binding activity. An isogenic derivative with high-level resistance to streptomycin was obtained as a single-step mutation from the test E. coli strain. Whereas the isogenic mutant possessed mannose binding activity and adhering ability similar to the parent strain, it was resistant to the streptomycin-induced suppression of the two activities at enormous concentrations (up to 10,000 mug/ml) of streptomycin. Taken together the results suggest that the suppression of epithelial cell adherence and mannose binding activity of E. coli grown in sublethal concentrations of streptomycin is a result of classic mechanisms of drug action upon the bacterial ribosome. The results support the possibility that antibiotics may act through mechanisms other than inhibition of growth and bacterial killing to eradicate bacteria from mucosal surfaces.

Antigens, Bacterial↗
PubMed1975

["Typical" and "atypical" damages of the organ of hearing from the administration of streptomycin].

Two areas of the damage localization in the organs of hearing after streptomycin use were found in the experiments with guinea pigs, i.e. (1) the Corti's organ of the lower part of the basal helix, the zone of perception of the maximum frequency sounds and (2) the tympanic muscles. Administration of streptomycin subcutaneously in a daily dose of 300 mg/kg for 50 days resulted in pronounced atrophic changes in the fibres of m. tensor tympani and some atony of m. stapedius. On the basis of the histological examination of the tympanic muscles after prolonged use of streptomycin and comparison of the periods of the tonus reduction in the skeletal muscles and Preier reflex after a single administration of streptomycin in maximum tolerating doses, it was concluded that streptomycin affected the state of the tympanic muscles as a myorelaxant. The atrophic changes in the tensor as a result of prolonged streptomycin use was due to chronic atony of the muscle. The decrease in the contraction capacity of the tensor must result in loosening of the drum membrane tension, impairement of the muscle activity coordination, decreased ability for elimation of the auditory ossicle fluctuation. Increased audibility limits within middle and low frequencies and noise in the ears during prolonged treatment of patients with streptomycin may be associated with chronic atony of the tympanic muscles and mainly tensor.

Animals↗
PubMed1976

The classic. Streptomycin in tuberculous bone and joint lesions with mixed infection and sinuses.

At the present time, streptomycin represents a tremendous advance in the treatment of patients with these lesions. Streptomycin undoubtedly will be improved upon and superseded by some other agent in the future, giving us better control of this disease and possibly enabling us to eradicate it. In closed lesions streptomycin, in dosages of 90 grams in a period of 90 days, has failed to arrest the tuberculous process permanently. Failure of treatment with streptomycin suggests strongly the presence of a sequestrum, a thick-walled abscess, or inadequate surgery. Healing seems to be related to the duration of administration of streptomycin and not to the total dosage. In patients having sinuses, streptomycin should be continued after healing for a period at least half as long as the healing period itself. Surgical ankylosis, or resection of non-weight-bearing joints, is apparently as necessary now as it ever has been, but is much safer and more effective. Indeed, at times surgical attack is made possible only by the use of streptomycin.

Child↗
PubMed1979

Isolation of mutants of Escherichia coli uncoupled in oxidative phosphorylation using hypersensitivity to streptomycin.

Mutants of Escherichia coli, harbouring the uncA401 or uncB402 alleles, were found to take up streptomycin more rapidly than the coupled parent strains. The increased rate of uptake results in greater sensitivity of the uncoupled strains, compared to the parent strains, to low concentrations of streptomycin. Studies with unc+ revertants showed that hypersensitivity to streptomycin is attributable to the mutation causing uncoupling. The uptake of streptomycin in an unc- strain is abolished by addition of the chemical uncoupler carbonylcyanide m-chlorophenylhydrazone. The phenotype of hypersensitivity to streptomycin can be used as a selection procedure for the isolation of uncoupled strains. In an experiment reported here, nine out of 12 strains isolated as being sensitive to streptomycin (at 2.5 micrograms/ml), were found to be unable to grow on succinate as a sole source of carbon. Five of the nine Suc- strains were found to be uncoupled in oxidative phosphorylation, and two of the five uncoupled strains lacked Mg2+-ATPase activity. The mutations causing uncoupling were cotransducible with the ilv genes.

Escherichia coli↗
PubMed1978

Streptomycin causes misreading of natural messenger by interacting with ribosomes after initiation.

The induction of misreading by streptomycin in vitro, previously observed with synthetic messengers, is now demonstrated with natural (endogenous or viral) messenger by the use of extracts of temperature sensitive mutants lacking Glu--tRNA or Val--tRNA synthetase. With chain-elongating but noninitiating ribosomes (i.e., purified polysomes) deprived of an aminoacyl--tRNA, streptomycin and other aminoglycosides, over a wide range of concentrations, stimulate incorporation. With ribosomes initiating in the presence of streptomycin stimulation is also observed but it is restricted, just like phenotypic suppression in cells, to very low streptomycin concentrattions which evidently allow some ribosomes to initiate and later encounter them in the course of chain elongation. The stimulation is accompanied by an increase in the size of the products; hence, it is evidently due to substitution of an incorrect aminoacyl--tRNA for a missing one. The test introduced here also has revealed a misreading effect of streptomycin on resistant ribosomes. In addition, significant intrinsic misreading was observed without streptomycin, indicating that under optimal conditions for in vitro protein synthesis an empty codon is frequently read by an incorrect aminoacyl--tRNA.

Anti-Bacterial Agents↗
PubMed1977

Control of streptomycin and isoniazid in malnourished children treated for tuberculosis.

In 12 malnourished children, who were treated for tuberculosis, plasma levels of streptomycin and isoniazid were followed. Streptomycin was administered i.m. in a dose of 25-50 mg/kg/24 hours. High initial plasma levels were reached (mean: 44.3 mug/ml at 30 min). Streptomycin levels were followed for 5 hours and the mean plasma level at that time was 17.0 mug/ml. From the present data a plasma half life of streptomycin of 3.5 hours has been estimated. It is advised that streptomycin should not be given in doses above 25 mg/kg/24 hours to avoid potential toxic plasma levels especially if plasma levels cannot be measured. It is also concluded from our study that renal function is not affected in malnourished children to an extent where streptomycin clearance is greatly affected. Isoniazid was given orally, 10 mg/kg/24 hours. From 30 min to 6 hours after administration, mean plasma levels of isoniazid above 0.5 mug/ml were observed. In all children measurable plasma levels were obtained. It is concluded that also children with malnutrition can absorb isoniazid after oral administration. From our data it is suggested that the majority of the children in our study were rapid inactivators of isoniazid.

Administration, Oral↗
PubMed1979

Induction of streptomycin uptake in resistant strains of Escherichia coli.

Different streptomycin-resistant strains of Escherichia coli, including an R100 plasmid-carrying strain of E. coli W3110, the ribosomally resistant mutant SM10, and the spontaneous revertant from dependence to independence d1023, exhibited poor accumulation capacity for aminoglycoside antibiotics. This was due to a failure of these mutants to induce the general polyamine transport system that is utilized by streptomycin to enter the cell. It is shown that the aminoglycoside kanamycin, which is effective on these streptomycin-resistant strains, was capable of inducing the uptake of streptomycin, thus giving rise to streptomycin accumulation up to wild-type levels. Plasmid-determined resistance, which has been speculated to be the result of a blockage of the uptake system by modified antibiotic molecules, cannot be overcome by the induction of streptomycin transport. Increase in permeability of the antibiotic does not affect the susceptibility of the bacteria. It is shown that all of the antibiotic taken up was enzymatically modified. R-plasmid-conferred resistance to aminoglycosides is therefore explained by the inactivation of the antibiotic entering the bacterial cell.

Drug Resistance, Microbial↗
PubMed1975

Streptomycin dependence in Escherichia coli: effects of antibiotic deprivation on ribosomes.

The inhibition of cell division and the ultimate loss of viability after removal of streptomycin from growing cultures of streptomycin-dependent bacteria are not the result of "unbalanced growth" or of the breakdown of ribosomes. The streptomycin-dependent strain of Escherichia coli K-12 studied continued to synthesize ribonucleic acid (RNA) and protein during streptomycin starvation. There was no evidence of a gross imbalance in the ratio of RNA to protein synthesized or of selective degradation of either protein or RNA. Using the sedimentation of subunits in sucrose as the criterion, normal ribosomes were synthesized even after 18 h of streptomycin deprivation, although the rates of appearance of mature 30S and 50S subunits decreased with time of deprivation. Once formed, these ribosomes appeared stable, as did those synthesized before the onset of starvation. Ribosomes isolated from starved dependent cells were as "functional" as ribosomes from cells grown with streptomycin in their capacity to bind aminoacyl-transfer RNA in response to polyuridylic acid or natural messenger RNA to interconvert between active and inactive transfer RNA binding states, and to synthesize proteins in cell-free systems. The effects are consistent with an impaired rate of synthesis of ribosomal components or assembly of ribosomes resulting in a continually diminishing rate of protein synthesis. The effect on cell division may be the result of a decreased rate of protein synthesis in general and the requirement for a specific protein(s) in particular.

Escherichia coli↗
PubMed1977

[3H] dihydrostreptomycin accumulation and binding to ribosomes in Rhizobium mutants with different levels of streptomycin resistance.

Rhizobium trifolii B1, a symbiotic nitrogen fixer, is sensitive to streptomycin (10 microgram/ml) and spontaneously produces spheroplast-like forms during cultivation. Streptomycin-resistant mutants selected with high doses of antibiotic (1,000 microgram/ml) showed pleiotropic changes, including loss of spheroplast formation and infectivity to plants, whereas mutants selected with low doses of streptomycin (10 to 100 microgram/ml) retained properties of parent strain B1 (I. Zelazna-Kowalska, Acta Microbiol. Pol., in press). The present studies revealed that strain B1 and its mutant with a high level of streptomycin resistance, B1 strH, accumulated the antibiotic at similar rates. Mutant B1 strL, with a low level of streptomycin resistance (up to 100 microgram/ml), accumulated the antibiotic at a lower rate. Ribosomes isolated from strains B1 and B2 strL bound [3H]dihydrostreptomycin, whereas those from strain B1 strH did not. These observations indicate that, in R. trifolii B1, mutation to a high level of streptomycin resistance affects ribosomal structure, whereas low-level resistance involves a change in membrane permeability.

Cell Membrane Permeability↗
PubMed1977

Pharmacokinetic aspects of streptomycin treatment of neonatal septicemia.

Patients with suspected neonatal septicemia were treated with ampicillin, cloxacillin, and streptomycin. The plasma concentrations of streptomycin were followed. First, the levels were determined during a full dose interval (12 h) in 11 infants. The results were used for development of a routine system for monitoring the plasma levels in all streptomycin treated newborns. This system, the "3-point check", involved blood sampling at 1, 3, and 5 h after administration during every second dose interval. The results of this routine procedure were evaluated both in a retrospective and prospective study. The "3-point check" gave a sufficient description of the total exposure to streptomycin under routine clinical conditions and continuous information to the physician in charge of the patient about the drug level. In 9 cases of 50, the report from the laboratory resulted in dose change for correction of a too low or too high plasma concentration. The dosage used, 7.5 mg streptomycin intramuscularly every 12th hour, appeared to be satisfactory in most patients. Peak values rarely exceeded 30 microgram/ml and were usually lower than 25 microgram/ml. Almost half of the children had plasma levels below 5 microgram/ml at the end of the dose interval (after 12 h). Although the correlation between pharmacokinetics and clinical outcome is difficult to establish in neonatal sepsis, we suggest that our guiding principle to avoid plasma levels above 25 microliter/ml is reasonable. In 35 out of 78 patients an otological examination of the newborns was performed within 13 months after streptomycin treatment and no signs of hearing defects were noted.

Ampicillin↗
PubMed1977

A new type of inactivation of streptomycin by E. coli.

Previously described cases of streptomycin inactivation by R-factor carrying strains of E. coli have not lead to any measurable decrease in antimicrobial potency in the bulk substrate toward the culture. In these cases each cell inactivates only a few molecules. Out of 1,800 strains of E. coli we have isolated five strains which inactivate streptomycin in large amounts giving a final concentration of the inactivation product of 0.25 mg/ml in 36 hours. Unlike all other streptomycin-resistant strains in investigated these five strains were sensitive to butyl-streptomycylamine, a streptomycin derivative acting in the same way as streptomycin. The crude inactivation product has been isolated. Inorganic phosphate is liberated by treatment with alkaline phosphatase resulting in a streptomycin-like compound without any antimicrobial activity.

Bacillus subtilis↗
PubMed1979

[Pseudomonas aeruginosa plasmids that control streptomycin resistance].

Wide distribution of streptomycin resistance determinants (83 per cent) among the resistance plasmids of the clinical strains of Ps. aeruginosa isolated in several clinics of 2 towns was found. Nine plasmids determining resistance to this antibiotic, as well as some other antibiotics, sulfanilamides, metallic ions, hydroxyanions and UV radiation were studied. The frequency of the conjugation transfer in these plasmids was different, i.e. from 10(1) to 10(6). They belonged to the following incompatibility groups: P-1, P-2, P-5 and apparently P-3. Eight out of the 9 plasmids determined the synthesis of streptomycin phosphotransferase which was evident of wide distribution of the streptomycin inactivation mechanism by phosphorylation among the strains of Ps. aeruginosa. The strains carrying the plasmids significantly differed by the content of the enzyme. However, all the enzymes could inactivate only streptomycin and dihydrostreptomycin and had approximately the same molecular weight (about 20 000). The strain carrying plasmid pBSII had no enzyme inactivating streptomycin (by phosphorylation or adenylation). The antibiotic resistance determined by this plasmid must be connected with changes in permeability of the bacterial cell wall by streptomycin.

Cell-Free System↗
PubMed1977

[Comparative study of the action of streptomycin on the variability of levorin and amphotericin B producers].

The study of the effect of streptomycin on viability of Act. levoris, strain LIA=0868 producing levorin and Act. nodosus, strain LIA-0861 producing amphotericin B showed that streptomycin had a lethal effect which increased with increasing of its concentration from I to 6 gamma/ml. While the lethal effect of streptomycin on the above cultures was comparatively the same, it had a selective effect on the levorin-producing organism and a marked inhibitory effect on the amphotericin B-producing organism. The selective effect of streptomycin was evident from inhibition of some types of the morphological mutants and variants characterized by a high level of levorin production and from selection of streptomycin-resistant variants. The inhibitory effect of streptomycin was evident from a marked increase in the number of the morphologically changed colonies and variants characterized by a low level of the antibiotic production.

Amphotericin B↗