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PubMed1977

Effects of erythromycin on membrane-bound chloroplast ribosomes from wild-type Chlamydomonas reinhardi and erythromycin-resistant mutants.

1. Treatment of wild-type cells of Chlamydomonas reinhardi with high concentrations of erythromycin results in increased recovery of membrane-bound chloroplast ribosomes, presumably by preventing polysomal runoff during harvesting of cells. No such membrane-retention effect is detected if erythromycin is added after harvesting of cultures, before cell breakage. 2. Growth of wild-type cells is inhibited by 10 microgram/ml erythromycin, but a concentration twice as high is required to increase recovery of membrane-bound wild-type ribosomes. On the other hand, the concentrations of erythromycin which inhibit growth of mutant ery-M1b produce a membrane-retention effect. Mutant ery-U1a is resistant to high concentrations of erythromycin and no membrane-retention effect is detectable at concentrations which produce one in wild type and ery-M1b. 3. These results can be reconciled by a two-point model of the mechanism of erythromycin action on chloroplast ribosomes in Chlamydomonas.

Chlamydomonas↗
PubMed1978

A comparison of ampicillin, erythromycin and erythromycin with sulphametopyrazine in the treatment of infective exacerbations of chronic bronchitis.

A comparative study of ampicillin (500 mg four times daily), erythromycin (500 mg four times daily) and sulphametopyrazine (1 g at start of exacerbation) followed by erythromycin (500 mg four times daily) was carried out in infective exacerbations of chronic bronchitis. Ampicillin and erythromycin were found to be equally effective, but the combination of erythromycin and sulphametopyrazine was significantly less effective. Unwanted effects were more frequent with ampicillin and with erythromycin plus sulphametopyrazine than with erythromycin alone.

Adult↗
PubMed1987

A plasmid-coded and site-directed mutation in Escherichia coli 23S RNA that confers resistance to erythromycin: implications for the mechanism of action of erythromycin.

Primer-directed mutagenesis was employed to introduce an A2058----G transition in plasmid-encoded Escherichia coli 23S RNA at a site that has been implicated, indirectly, in erythromycin binding. The mutation raises the growth tolerance of cells from 30 to 300 micrograms/ml of erythromycin, and cells grown in the presence of erythromycin contain ribosomes with high levels of mutated 23S RNA. In these cells, wild type 50S subunits 'fall off' the message and are selectively degraded, possibly as a result of an erythromycin-induced conformational change. A fast in vitro poly(U) assay revealed minimal effects of erythromycin on elongation beyond tetrapeptides. We correlated these results with the literature data and concluded that erythromycin acts immediately post-initiation and directly, or indirectly, destabilizes mRNA-bound 70S ribosomes, and prevents their recycling by causing 50S subunit degradation.

Autoradiography↗
PubMed1984

Erythromycin uptake and accumulation by human polymorphonuclear leukocytes and efficacy of erythromycin in killing ingested Legionella pneumophila.

Studies were undertaken to demonstrate the efficacy of erythromycin in killing Legionella pneumophila organisms that have been ingested by human polymorphonuclear leukocytes. With use of an electron microscope-autoradiography method in conjunction with an antibiotic-uptake assay, it was shown that [3H]-labeled erythromycin A base penetrated into the cytoplasm of human polymorphonuclear leukocytes in concentrations up to 24 times higher than the extracellular drug level. Similar studies using [14C]benzyl penicillin revealed that this antibiotic penetrated human polymorphonuclear leukocytes very poorly. Removal of erythromycin from the extracellular environment resulted in rapid leakage of radioactivity from the cells; an assay for bioactivity showed that this material was unaltered drug. Human polymorphonuclear leukocytes were permitted to ingest L. pneumophila and were then treated with erythromycin A base. The erythromycin killed the ingested legionellae, as evidenced by bacterial plate counts and morphological destruction of ingested organisms. These data clearly demonstrate the efficacy of erythromycin in killing susceptible intracellular pathogens.

Erythromycin↗
PubMed1988

Treatment of respiratory tract infections with erythromycin acistrate and two formulations of erythromycin base.

Erythromycin acistrate (EA)--a new ester of erythromycin--was compared with erythromycin base as enterocoated pellets in capsules (EB enterocapsules) and enterocoated tablets of erythromycin base (EB enterotablets) in the treatment of respiratory tract infections. The present double-blind, multicentre study, conducted in eight occupational health centres, included 474 patients; 236 treated with EA, 117 with EB enterocapsules and 121 with EB enterotablets. The diagnoses included tonsillitis, sinusitis, otitis media, bronchitis and pneumonia. The patients were examined on admission and at the end of the treatment. The dosage of EA was 400 mg tid and that of the two erythromycin base preparations 500 mg tid. The treatment was given for seven to 14 days. In the EA-group, 97% of patients were clinically cured by the end of the treatment, while the cure rates for EB enterocapsules and EB enterotablets were 95% and 94%, respectively. Gastrointestinal side effects were reported by 36% of the patients on EA, 54% on EB enterocapsules and 50% on EB enterotablets. Discontinuations due to adverse effects occurred in 8% in the EA, in 21% in the EB enterocapsule and in 12% in the EB enterotablet groups. All three preparations were thus equally effective, but EA caused statistically significantly less gastrointestinal side effects overall (P less than 0.01), especially nausea (P less than 0.01) and abdominal pain (P less than 0.05), than the two formulations containing erythromycin base. Also discontinuations due to side effects occurred statistically significantly less frequently in the EA-group.

Adolescent↗
PubMed1988

Determination of 2'-acetyl erythromycin and erythromycin in human tonsil tissue by HPLC with coulometric detection.

A simple and sensitive high-performance liquid chromatographic method was developed for the determination of 2'-acetyl erythromycin and erythromycin in human tonsil tissue. Methyl tert-butyl ether was used as the extraction solvent after alkalization of tissue homogenates. Separation was achieved on a reverse phase C-18 column. The mobile phase consisted of acetonitrile-methanol-tetrahydrofuran-sodium acetate buffer, pH 4.5. Eluted compounds were monitored by a coulometric detector in the oxidative screen mode. The quantitation limits of 2'-acetyl erythromycin and erythromycin were 0.20 and 0.30 mg/kg of tissue, respectively. The method was linear over the concentration range of 0.60-10.0 mg/kg of tissue for 2'-acetyl erythromycin and erythromycin.

Chromatography, High Pressure Liquid↗
PubMed1998

The loading domain of the erythromycin polyketide synthase is not essential for erythromycin biosynthesis in Saccharopolyspora erythraea.

6-Deoxyerythronolide B synthase (DEBS) is a large multifunctional enzyme that catalyses the biosynthesis of the erythromycin polyketide aglycone. DEBS is organized into six modules, each containing the enzymic domains required for a single condensation of carboxylic acid residues which make up the growing polyketide chain. Module 1 is preceded by loading acyltransferase (AT-L) and acyl carrier protein (ACP-L) domains, hypothesized to initiate polyketide chain growth with a propionate-derived moiety. Using recombinant DNA technology several mutant strains of Saccharopolyspora erythraea were constructed that lack the initial AT-L domain or that lack both the AT-L and ACP-L domains. These strains were still able to produce erythromycin, although at much lower levels than that produced by the wild-type strain. In addition, the AT-L domain expressed as a monofunctional enzyme was able to complement the deletion of this domain from the PKS, resulting in increased levels of erythromycin production. These findings indicate that neither the initial AT-L nor the ACP-L domains are required to initiate erythromycin biosynthesis; however, without these domains the efficiency of erythromycin biosynthesis is decreased significantly. It is proposed that in these mutants the first step in erythromycin biosynthesis is the charging of KS1 with propionate directly from propionyl-CoA.

Acyl Carrier Protein↗
PubMed1981

The bioavailability of erythromycin stearate versus enteric-coated erythromycin base when taken immediately before and after food.

1. Erythromycin plasma concentrations were determined in twenty subjects after a single dose, immediately before food, of erythromycin, 500 mg. as: (1) erythromycin stearate (Erythrocin, 500 mg, ovaloid tablets), and (2) erythromycin base (Eryc, 250 mg, capsules containing enteric-coated pellets). 2. Plasma concentrations were again determined in eighteen of the original subjects with the same dose given immediately after food. 3. Maximum Plasma Concentrations (mcg/ml) (See formula in text) 4. Erythromycin stearate was more bioavailable than erythromycin base when administered immediately before food. The preparations were bioequivalent when given immediately after food.

Biological Availability↗
PubMed1989

Erythromycin resistance in Danish Staphylococcus aureus hospital strains with emphasis on erythromycin consumption.

Erythromycin resistance was analyzed in 280,415 Danish Staphylococcus aureus strains isolated from hospitalized patients and phage-typed in the period 1967 to 1987. Multiresistant, erythromycin-resistant strains decreased during the whole period, while strains resistant only to penicillin and erythromycin increased after 1972. This increase coincided with an increase in erythromycin consumption in Denmark from 0.4 DDD/1000 persons/day in 1978 to 1.9, in 1987. Erythromycin consumption in nine large Danish hospitals was significantly associated with the level of erythromycin-resistant S. aureus at the hospitals.

Animals↗
PubMed1996

Erythromycin as a specific substrate for cytochrome P4503A isozymes and identification of a high-affinity erythromycin N-demethylase in adult female rats.

Erythromycin N-demethylation is catalyzed by cytochrome P4503A isozymes. By using [14C]methyl-labeled erythromycin, we were able to develop a N-demethylation assay that is more sensitive and specific than the colorimetric detection of formaldehyde formation. The increased sensitivity allows the use of very low substrate concentration with good sensitivity, 1 microM compared with 400 microM for the colorimetric assay. This 1 microM concentration is within pharmacological blood levels of erythromycin. Using this assay, we detected a high-affinity erythromycin N-demethylase in liver microsomes from untreated adult female rats that was previously unknown. This low KM activity could be inhibited by polyclonal anti-P4503A1 or P4503A2 antibodies to 95%, and these antibodies also detected a band in these microsomes on Western blots that had the same molecular weight (51 kDa) as cytochromes P4503A1/3A2. Monoclonal antibodies specific for P4503A1 or P4503A2, however, did not react with this band. No inhibitory effect was observed with monoclonal antibody P124, which inhibited the erythromycin N-demethylation both in liver microsomes from untreated adult males (P4503A2) and dexamethasone-pretreated adult females (P4503A1). Alternative P4503A substrates (testosterone, troleandomycin, cortisol, corticosterone, cyclosporin A, and 17 alpha-ethinylestradiol) inhibited erythromycin N-demethylation catalyzed by liver microsomes from untreated male, untreated female, and dexamethasone-pretreated female rats, whereas digitoxin and theophylline had no inhibitory effects. Put together, these data suggest that this demethylase in liver microsomes of untreated female rats is not P4503A1 or P4503A2, but P4503A related.

Animals↗
PubMed1995

Outpatient use of erythromycin: link to increased erythromycin resistance in group A streptococci.

Resistance to erythromycin in group A streptococci has become an important problem among outpatients in Finland. The prevention of such problems requires information about the relationship between antimicrobial consumption and antimicrobial resistance. Having found considerable variation among health authority areas in the proportions of group A streptococci resistant to erythromycin, we investigated the potential impact of local differences in the consumption of this agent on the development of resistance. In 1992, 10,162 group A streptococcal isolates (nearly 100% were from outpatients) collected from 206 health authority areas were tested for erythromycin resistance; 1,647 isolates (16%) were resistant. Logistic regression analysis showed that the proportion of isolates resistant to erythromycin clearly increased with increasing local erythromycin consumption by outpatients in 1991 (P = .006). This positive association indicates that a prudent policy for the treatment of outpatients is essential to maintenance of the effectiveness of antimicrobial agents.

Ambulatory Care↗
PubMed2002

Purification and characterization of an erythromycin esterase from an erythromycin-resistant Pseudomonas sp.

An erythromycin esterase (molecular mass 51200 Da) was purified from Pseudomonas sp. GD100, which was isolated from a salmon hatchery sediment sample from Washington State. The pI of the protein was 4.5-4.8. The enzyme was inhibited by 1 mM mercuric acid, and had the substrate specificity for structurally related 14-membered macrolides, which decreased in the order of oleandomycin, erythromycin A and erythromycin A enol ether. The activity for erythromycin A varied with temperature, but the effect of pH was minimal at pH 6.0-9.0. The half-life of the enzyme was estimated to be 8.9 h at 35 degrees C and 0.23 h at 55 degrees C, and the activation energy of the catalytic reaction of erythromycin A was estimated at 16.2 kJ mol(-1).

Carboxylic Ester Hydrolases↗
PubMed1981

Influence of study design in assessing food effects on absorption of erythromycin base and erythromycin stearate.

We performed a series of six single-dose and multiple-dose studies to evaluate the effect of food on the absorption of erythromycin base and erythromycin stearate. When we used a single-dose design, we found that an unprotected erythromycin base preparation was absorbed extensively if a prolonged fast preceded administration of the drug. A shorter faster period (as occurs in clinical settings) dramatically reduced the absorption of unprotected base; however, film-coated tablets seemed to be as well protected as and were absorbed more rapidly than enteric-coated tablets when they were evaluated by single-dose testing procedures. In contrast, when a commercially available film-coated preparation of erythromycin base was evaluated in multidose fashion between meals (fasting), the drug was about 25% less well absorbed than commercially available enteric-coated base tablets. Finally, when commercially available film-coated erythromycin base and stearate formulations were administered with meals, both film-coated preparations were 43 to 59% less well absorbed than the enteric-coated base formulation. Furthermore, the enteric-coated base formulation performed equally well when administered either every 6 h between meals (fasting) or four times a day (immediately after meals and at bedtime). These studies document the need for multidose bioavailability techniques when the bioavailabilities of acid-labile drugs are evaluated.

Adult↗
PubMed1985

Characterization of the effects of erythromycin estolate and erythromycin base on the excretory function of the isolated rat liver.

To investigate the mechanisms of erythromycin cholestasis, the effects of erythromycin estolate (EE) on the excretory function of the isolated perfused rat liver and on liver plasma membrane (LM) preparations were studied and compared to those of erythromycin base (EB) and lauryl sulfate (LS), added alone or in combination. EE (at 125 to 200 microM) caused dose-dependent reductions of bile and perfusate flows, bile acid (BA) excretion, and biliary BA concentration. The alterations of the excretory function were only in part due to the decreased perfusate flow. In contrast, both 200 and 300 microM concentrations of EB elicited similar choleretic responses, which were presumably related to the osmotic activity of the drug excreted in the bile. LS did not affect hepatic excretory functions. However, the simultaneous addition of EB and LS resulted in a rate of bile flow lower than that observed with EB alone. EE, but not EB, increased canalicular permeability to [14C]sucrose as measured by bile to plasma (B:P) ratio. Neither drugs altered [14C]erythritol B:P ratio. In LM preparations both Na+,K+- and Mg2+-ATPase activities were inhibited in a dose-dependent manner by EE, but not by EB. The data suggest that EE could affect bile flow by inhibiting cotransport of Na+ and BA and by altering LM permeability and support the view that the effect of erythromycins on the liver may be related to their surface activity.

Adenosine Triphosphatases↗
PubMedDate not supplied

Metabolism of propionyl erythromycin lauryl sulfate. I. Fate of the propionyl erythromycin moiety in the rat.

The absorption, excretion, and metabolism of propionyl erythromycin (PE) has been studied in the rat. The major routes of metabolism of PE are ester hydrolysis and N-demethylation. The rates of these two reactions have been examined in vivo using radiolabeled PE. The plasma half-life of the ester is 5.5 hr. The correlation of blood levels of radioactivity with 14CO2 production indicates that the ester is continually hydrolyzed after absorption. The half-life of the dimethyl-amino moiety of the desosamine sugar is estimated at 1.5 hr. This relatively short half-life compared to that of the ester is supported by the fact that at 3.5 hr after dosing there is twice as much desmethyl-PE in plasma as PE. After oral administration of either 14C-PE or 14C-erythromycin, 70% of the radioactivity is absorbed in 6 hr. The major route of excretion is via bile. Approximatley 40% of the absorbed dose is excreted in bile in the first 6 hr after dosing. Tissue levels of radioactivity after administration of 14C-erythromycin or 14C-PE indicate that PE or a metabolite accumulates in the tissue during chronic dosing, whereas erythromycin-related levels are similar after single or multiple doses.

Animals↗
PubMed1989

Reversal of drug resistance by erythromycin: erythromycin increases the accumulation of actinomycin D and doxorubicin in multidrug-resistant cells.

Development of resistance to one type of lipophilic chemotherapeutic drug often leads to resistance to other, structurally unrelated, lipophilic drugs. This suggests that non-toxic lipophilic agents may interfere with and reverse drug resistance by saturating the pathway through which multidrug-resistant (MDR) cells protect themselves against cytotoxic drugs. The lipophilic antibiotic, erythromycin, can significantly reverse the resistance of MDR WEHI 164 murine fibrosarcoma cells to the chemotherapeutic drugs, doxorubicin and actinomycin-D. The MDR cells showed an approximately 10-fold higher expression of the P-glycoprotein than the drug-sensitive parental cells from which the resistant cells were derived. The accumulation of actinomycin-D and doxorubicin was much lower in the drug-resistant cells than in the sensitive parental cells. The concentrations of erythromycin which reversed the drug resistance of the MDR cells increased the accumulation of actinomycin-D and doxorubicin in these cells to a level comparable to that observed in the sensitive parental cells. Our data suggest that erythromycin reverses drug resistance by saturating the drug-binding sites on the P-glycoprotein, thereby reducing the capacity of this protein to pump drugs out of resistant cells. Some of our MDR cells have also become more resistant to tumour necrosis factor (TNF). However, erythromycin did not reverse TNF resistance, suggesting that the mechanisms of multi-drug and TNF resistance are different. TNF did not influence drug accumulation in MDR cells.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1989

Development of erythromycin-resistance in Staphylococcus aureus as a consequence of high erythromycin consumption.

In a mixed ward for skin and venereology patients the erythromycin consumption was 6-8 fold higher than in other wards at the same hospital. Erythromycin-resistance occurred in 15.5% of the infecting Staphylococcus aureus strains isolated from this ward, compared with 3.5% in other wards of the hospital and 2.3% in Denmark as a whole. The resistant strains belonged to different phage-type patterns, but 18 out of 19 strains contained a 1.5 MDa plasmid and had an erythromycin-inducible resistance mechanism. Erythromycin resistance was frequent (approximately 10%) among Danish S. aureus strains in the years 1963 to 1969, mainly due to the spread of multiply-resistant strains of the 83A complex. During the last ten years, however, only 1-2% of the strains have been resistant, but a slow increase in resistance has taken place during the last three years among strains of all phage patterns including strains of group II, the 94, 96 complex and type 95.

Bacteriophage Typing↗
PubMed2002

Increased prevalence of erythromycin resistance in streptococci: substantial upsurge in erythromycin-resistant M phenotype in Streptococcus pyogenes (1979-1998) but not in Streptococcus pneumoniae (1985-1999) in Taiwan.

A total of 394 nonduplicate isolates of Streptococcus pyogenes collected from 1979 to 1998 and 267 nonduplicate isolates of Streptococcus pneumoniae collected from October, 1998, to May, 1999, in Taiwan were evaluated. Among the 220 erythromycin-resistant (MIC, > or =1 microg/ml) S. pyogenes isolates, 35% had an M phenotype and 65% had an ML phenotype (inducible resistance [iML], 0.5%, and constitutive resistance [cML], 64.5%). Among the 243 erythromycin-resistant S. pneumoniae isolates, the majority (65.4%) had an ML phenotype (iML, 0.4%, and cML, 65%) and 34.6% had an M phenotype. A substantial upsurge in the incidence of M-phenotype erythromycin-resistant isolates was found with time for S. pyogenes (0% in 1979-1984 and 100% in 1997-1998), and an increasing incidence of M-phenotype among erythromycin-resistant S. pneumoniae was also noted (<20% before 1994 and 45.4% in 1999). All S. pyogenes and all but four S. pneumoniae isolates exhibiting a cML or iML phenotype had harbored the ermAM gene. The presence of the mefA gene was demonstrated in all isolates of S. pyogenes and the mefE gene in all but four S. pneumoniae isolates exhibiting the M phenotype. Due to the increasing susceptibility of S. pyogenes and S. pneumoniae isolates to clindamycin, susceptibility tests of these two organisms to macrolides and clindamycin should be performed simultaneously in the clinical microbiology laboratory, particularly in areas with high rates of macrolide resistance.

Anti-Bacterial Agents↗