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PubMed1996

In vitro activities of azithromycin, clarithromycin, erythromycin, and tetracycline against 13 strains of Chlamydia pneumoniae.

Thirteen strains of Chlamydia pneumoniae were evaluated for their in vitro susceptibilities to azithromycin, clarithromycin, erythromycin, and tetracycline. The MIC ranges were 0.125 to 0.5 micrograms/ml for azithromycin, 0.031 to 1.0 micrograms/ml for clarithromycin, 0.125 to 1.0 micrograms/ml for erythromycin, and 0.25 to 1.0 micrograms/ml for tetracycline. The ranges for the minimal lethal concentrations were 0.125 to 0.5 micrograms/ml for azithromycin, 0.031 to 1.0 micrograms/ml for clarithromycin, 0.125 to 1.0 micrograms/ml for erythromycin, and 0.25 to 1.0 micrograms/ml for tetracycline. Clarithromycin and azithromycin were the most active antibiotics against C. pneumoniae in vitro.

Anti-Bacterial Agents↗
PubMed1996

The erythromycin resistance gene from the Bacteroides conjugal transposon Tcr Emr 7853 is nearly identical to ermG from Bacillus sphaericus.

Tcr Emr 7853, from Bacteroides thetaiotaomicron 7853, is a large chromosomal conjugative transposon which encodes resistance to both tetracycline (Tcr) and erythromycin (Emr). The erythromycin resistance gene of Tcr Emr 7853 did not cross-hybridize with ermF, the Emr gene found on previously studied Bacteroides regular and conjugative transposons. We have cloned and sequenced the erythromycin resistance gene from Tcr Emr 7853. The DNA sequence of this gene was 99.6% identical to that of ermG from Bacillus sphaericus.

Bacillus↗
PubMed1996

MIC and time-kill study of antipneumococcal activities of RPR 106972 (a new oral streptogramin), RP 59500 (quinupristin-dalfopristin), pyostacine (RP 7293), penicillin G, cefotaxime, erythromycin, and clarithromycin against 10 penicillin-susceptible and -resistant pneumococci.

Broth MICs and time-kill studies were used to test the activity of RP 59500 (quinupristin-dalfopristin), RPR 106972, pyostacine (RP 7293), erythromycin, clarithromycin, and cefotaxime for four penicillin-susceptible (MICs of 0.008 to 0.03 microgram/ml), two penicillin-intermediate (MIC of 0.25 microgram/ml), and four penicillin-resistant (MIC of 2.0 to 4.0 micrograms/ml) strains of pneumococci: 6 of 10 strains were resistant to macrolides (MICs of > or = 0.5 microgram/ml). MICs of RP 59500 (0.5 to 1.0 microgram/ml), RPR 106972 (0.125 to 0.25 microgram/ml), and pyostacine (0.125 to 0.25 microgram/ml) did not alter with the strain's penicillin or macrolide susceptibility status. Three penicillin-susceptible strains and one penicillin-intermediate strain were susceptible to macrolides (MICs of < or = 0.25 microgram/ml); the macrolide MICs for the remaining strains were > or = 4.0 micrograms/ml. Cefotaxime MICs rose with those of penicillin G, but all strains were inhibited at MICs of < or = 2.0 micrograms/ml. RP 59500 was bactericidal for all strains after 24 h at 2 x MIC and yielded 90% killing of all strains at 6 h at 2 x MIC; at 8 x MIC, RP 59500 showed 90% killing of six strains within 10 min (approximately 0.2 h). In comparison, RPR 106972 was bactericidal for 9 of 10 strains at 2 x MIC after 24 h and yielded 90% killing of all strains at 2 x MIC after 6 h; 90% killing of six strains was found at 8 x MIC at 0.2 h. Results for pyostacine were similar to those of RPR 106972. Erythromycin and clarithromycin were bactericidal for three of four macrolide-susceptible strains after 24 h at 4 x MIC. Clarithromycin yielded 90% killing of three strains at 8 x MIC after 12 h. Cefotaxime was bactericidal for all strains after 24 h at 4 x MIC, yielding 90% killing of all strains after 6 h at 4 x MIC. All three streptogramins yielded rapid killing of penicillin- and erythromycin-susceptible and -resistant pneumococci and were the only compounds which killed significant numbers of strains at 0.2 h.

Anti-Bacterial Agents↗
PubMed1997

Variation in erythromycin and clindamycin susceptibilities of Streptococcus pneumoniae by four test methods.

Susceptibilities of 124 strains of Streptococcus pneumoniae to erythromycin and clindamycin were determined by the National Committee for the Clinical Laboratory Standards (NCCLS) broth microdilution method, with incubation for 20 to 24 h in ambient air and with modifications of this method by incubation for up to 48 h in air and CO2. Strains were also tested by agar dilution, E-test, and disk diffusion; good correlation was obtained with these methods, with clear separation into bimodal populations of susceptible and resistant stains. The broth microdilution method, however, using incubation in air for 24 h (NCCLS method), misclassified 4 of 92 erythromycin-resistant strains (1 as susceptible and 3 as intermediate) and 25 of 58 clindamycin-resistant strains (all as susceptible). With the exception of one strain with clindamycin, susceptible and resistant strains were correctly classified by the microdilution method with incubation in CO2 for 24 h or in ambient air for 48 h. Disk diffusion, agar dilution, and E-test methods with incubation in 5% CO2 are therefore reliable methods for susceptibility testing of pneumococci against these agents. However, the NCCLS microdilution method, which specifies incubation for 20 to 24 h in ambient air, produced significant very major errors (43%) clindamycin. Modification of the microdilution method by incubation in 5% CO2 or by extension of incubation time in ambient air to 48 h corrected these errors. Disk diffusion, however, was shown to be a simple, convenient, and reliable method for susceptibility testing of pneumococci to erythromycin and clindamycin and is suggested as the method of choice for these agents.

Anti-Bacterial Agents↗
PubMed1997

mefE is necessary for the erythromycin-resistant M phenotype in Streptococcus pneumoniae.

Recently, it was shown that a significant number of erythromycin-resistant Streptococcus pneumoniae and Streptococcus pyogenes strains contain a determinant that mediates resistance via a putative efflux pump. The gene encoding the erythromycin-resistant determinant was cloned and sequenced from three strains of S. pneumoniae bearing the M phenotype (macrolide resistant but clindamycin and streptogramin B susceptible). The DNA sequences of mefE were nearly identical, with only 2-nucleotide differences between genes from any two strains. When the mefE sequences were compared to the mefA sequence from S. pyogenes, the two genes were found to be closely related (90% identity). Strains of S. pneumoniae were constructed to confirm that mefE is necessary to confer erythromycin resistance and to explore the substrate specificity of the pump; no substrates other than 14- and 15-membered macrolides were identified.

Anti-Bacterial Agents↗
PubMed1998

A novel erythromycin resistance methylase gene (ermTR) in Streptococcus pyogenes.

Erythromycin resistance among streptococci is commonly due to target site modification by an rRNA-methylating enzyme, which results in coresistance to macrolide, lincosamide, and streptogramin B antibiotics (MLSB resistance). Genes belonging to the ermAM (ermB) gene class are the only erythromycin resistance methylase (erm) genes in Streptococcus pyogenes with MLSB resistance that have been sequenced so far. We identified a novel erm gene, designated ermTR, from an erythromycin-resistant clinical strain of S. pyogenes (strain A200) with an inducible type of MLSB resistance. The nucleotide sequence of ermTR is 82.5% identical to ermA, previously found, for example, in Staphylococcus aureus and coagulase-negative staphylococci. Our finding provides the first sequence of an erm gene other than ermAM that mediates MLSB resistance in S. pyogenes.

Amino Acid Sequence↗
PubMed1998

Different erythromycin resistance mechanisms in group C and group G streptococci.

Different mechanisms of erythromycin resistance predominate in group C and G streptococcus (GCS and GGS, respectively) isolates collected from 1992 to 1995 in Finland. Of the 21 erythromycin-resistant GCS and 32 erythromycin-resistant GGS isolates, 95% had the mefA or mefE drug efflux gene and 94% had the ermTR methylase gene, respectively.

Anti-Bacterial Agents↗
PubMed2002

Erythromycin-resistant pharyngeal isolates of Streptococcus pyogenes recovered in Italy.

Three classes of macrolide resistance phenotypes and three different erythromycin resistance determinants were found among 127 erythromycin-resistant group A streptococcal (GAS) isolates recovered from 355 (35.8%) pediatric pharyngitis patients in Rome, Italy. According to emm and sof sequence typing results, erythromycin-resistant isolates comprised 11 different clonal types. Remarkably, 126 of the 127 macrolide-resistant isolates were serum opacity factor (sof) gene positive. These data suggest a strong association between macrolide resistance and the presence of sof among GAS isolates recovered from Italian pediatric pharyngitis patients.

Child↗
PubMed2003

Erythromycin and clindamycin resistance and telithromycin susceptibility in Streptococcus agalactiae.

The rates of resistance to erythromycin and clindamycin among Streptococcus agalactiae strains isolated in our hospital increased from 4.2 and 0.8% in 1993 to 17.4 and 12.1%, respectively, in 2001. Erythromycin resistance was mainly due to the presence of an Erm(B) methylase, while the M phenotype was detected in 3.8% of the strains. Telithromycin was very active against erythromycin-resistant strains, irrespective of their mechanisms of macrolide resistance.

Anti-Bacterial Agents↗
PubMed2003

Presence of the tet(O) gene in erythromycin- and tetracycline-resistant strains of Streptococcus pyogenes and linkage with either the mef(A) or the erm(A) gene.

Sixty-three recent Italian clinical isolates of Streptococcus pyogenes resistant to both erythromycin (MICs >or=1 microg/ml) and tetracycline (MICs >or= 8 microg/ml) were genotyped for macrolide and tetracycline resistance genes. We found 19 isolates carrying the mef(A) and the tet(O) genes; 25 isolates carrying the erm(A) and tet(O) genes; and 2 isolates carrying the erm(A), tet(M), and tet(O) genes. The resistance of all erm(A)-containing isolates was inducible, but the isolates could be divided into two groups on the basis of erythromycin MICs of either >128 or 1 to 4 microg/ml. The remaining 17 isolates included 15 isolates carrying the erm(B) gene and 2 isolates carrying both the erm(B) and the mef(A) genes, with all 17 carrying the tet(M) gene. Of these, 12 carried Tn916-Tn1545-like conjugative transposons. Conjugal transfer experiments demonstrated that the tet(O) gene moved with and without the erm(A) gene and with the mef(A) gene. These studies, together with the results of pulsed-field gel electrophoresis experiments and hybridization assays with DNA probes specific for the tet(O), erm(A), and mef(A) genes, suggested a linkage of tet(O) with either erm(A) or mef(A) in erythromycin- and tetracycline-resistant S. pyogenes isolates. By amplification and sequencing experiments, we detected the tet(O) gene ca. 5.5 kb upstream from the mef(A) gene. This is the first report demonstrating the presence of the tet(O) gene in S. pyogenes and showing that it may be linked with another gene and can be moved by conjugation from one chromosome to another.

Anti-Bacterial Agents↗
PubMed2004

Activities of two novel macrolides, GW 773546 and GW 708408, compared with those of telithromycin, erythromycin, azithromycin, and clarithromycin against Haemophilus influenzae.

The MIC at which 50% of strains are inhibited (MIC(50)) and the MIC(90) of GW 773546, a novel macrolide, were 1.0 and 2.0 microg/ml, respectively, for 223 beta-lactamase-positive, beta-lactamase-negative, and beta-lactamase-negative ampicillin-resistant Haemophilus influenzae strains. The MIC(50)s and MIC(90)s of GW 708408, a second novel macrolide, and telithromycin, an established ketolide, were 2.0 and 4.0 microg/ml, respectively, while the MIC(50) and MIC(90) of azithromycin were 1.0 and 2.0 microg/ml, respectively. The MIC(50) and MIC(90) of erythromycin were 4.0 and 8.0 microg/ml, respectively; and those of clarithromycin were 4.0 and 16.0 microg/ml, respectively. All compounds except telithromycin were bactericidal (99.9% killing) against nine strains at two times the MIC after 24 h. Telithromycin was bactericidal against eight of the nine strains. In addition, both novel macrolides and telithromycin at two times the MIC showed 99% killing of all nine strains after 12 h and 90% killing of all strains after 6 h. After 24 h, all drugs were bactericidal against four to seven strains when they were tested at the MIC. Ten of 11 strains tested by multistep selection analysis yielded resistant clones after 14 to 43 passages with erythromycin. Azithromycin gave resistant clones of all strains after 20 to 50 passages, and clarithromycin gave resistant clones of 9 of 11 strains after 14 to 41 passages. By comparison, GW 708408 gave resistant clones of 9 of 11 strains after 14 to 44 passages, and GW 773546 gave resistant clones of 10 of 11 strains after 14 to 45 passages. Telithromycin gave resistant clones of 7 of 11 strains after 18 to 45 passages. Mutations mostly in the L22 and L4 ribosomal proteins and 23S rRNA were detected in resistant strains selected with all compounds, with alterations in the L22 protein predominating. Single-step resistance selection studies at the MIC yielded spontaneous resistant mutants at frequencies of 1.5 x 10(-9) to 2.2 x 10(-6) with GW 773546, 1.5 x 10(-9) to 6.0 x 10(-4) with GW 708408, and 7.1 x 10(-9) to 3.8 x 10(-4) with telithromycin, whereas the frequencies were 1.3 x 10(-9) to 6.0 x 10(-4) with erythromycin and azithromycin and 2.0 x 10(-9) to 2.0 x 10(-3) with clarithromycin. Alterations in the L22 protein (which were predominant) and the L4 protein were present in mutants selected by the single-step selection process. The postantibiotic effects of GW 773546, GW 708408, and telithromycin for seven H. influenzae strains were 6.6 h (range, 5.2 to 8.8 h), 4.7 h (range, 2.6 to 6.9 h), and 6.4 h (range, 3.8 to 9.7 h), respectively. The results of in vitro studies obtained with both novel macrolides were similar to those obtained with telithromycin and better than those obtained with older macrolides.

Anti-Bacterial Agents↗
PubMed2005

Macrolide efflux in Streptococcus pneumoniae is mediated by a dual efflux pump (mel and mef) and is erythromycin inducible.

Macrolide resistance in Streptococcus pneumoniae due to efflux has emerged as an important worldwide clinical problem over the past decade. Efflux is mediated by the genes of the genetic element mega (macrolide efflux genetic assembly) and related elements, such as Tn1207.1. These elements contain two adjacent genes, mef (mefE or mefA) and the closely related mel gene (msrA homolog), encoding a proton motive force pump and a putative ATP-binding cassette transporter homolog, and are transcribed as an operon (M. Del Grosso et al., J. Clin. Microbiol. 40:774-778, 2004; K. Gay and D. S. Stephens, J. Infect. Dis. 184:56-65, 2001; and M. Santagati et al., Antimicrob. Agents Chemother. 44:2585-2587, 2000). Previous studies have shown that Mef is required for macrolide resistance in S. pneumoniae; however, the contribution of Mel has not been fully determined. Independent deletions were constructed in mefE and mel in the serotype 14 macrolide-resistant strains GA16638 (erythromycin [Em] MIC, 8 to 16 microg/ml) and GA17719 (Em MIC, 2 to 4 microg/ml), which contain allelic variations in the mega element. The MICs to erythromycin were significantly reduced for the independent deletion mutants of both mefE and mel compared to those of the parent strains and further reduced threefold to fourfold to Em MICs of <0.15 microg/ml with mefE mel double mutants. Using quantitative reverse transcription-PCR, the expression of mefE in the mel deletion mutants was increased more than 10-fold. However, in the mefE deletion mutants, the expression of mel did not differ significantly from the parent strains. The expression of both mefE and mel was inducible by erythromycin. These data indicate a requirement for both Mef and Mel in the novel efflux-mediated macrolide resistance system in S. pneumoniae and other gram-positive bacteria and that the system is inducible by macrolides.

Bacterial Proteins↗
PubMed1976

Rosamicin: in vitro activity against anaerobes and comparison with erythromycin.

The in vitro activity of rosamicin was determined against 231 strains of anaerobic bacteria and compared with the activity of erythromycin against the same strains. Rosamicin and erythromycin had similar activity against strains of Peptostreptococcus and gram-positive nonsporeforming bacilli. Rosamicin was somewhat more active against strains of Peptococcus, Clostridium, and gram-negative anaerobes. All strains of Bacteroides fragilis tested were inhibited by 4 mug of rosamicin or less per ml, whereas only 76% of them were inhibited by this concentration of erythromycin. Rosamicin was distinctly more active against Fusobacterium nucleatum. Because of its in vitro activity, further investigation of the pharmacology of this drug is warranted.

Anaerobiosis↗
PubMed1969

Therapy of staphylococcal infections in monkeys. IV. Further comparison of triacetyloleandomycin and erythromycins.

Intravenous inoculation of a penicillin-resistant, phage type 80/81 staphylococcus caused lethal infection in 8 of 15 untreated monkeys. Daily intragastric administration of 50 mg/kg of triacetyloleandomycin, erythromycin estolate, and erythromycin ethylsuccinate was followed by mortalities of 0 of 16, 3 of 16, and 3 of 10, respectively. At dose levels of 25 and 12.5 mg/kg, none of 7 and 4 of 7 receiving triacetyloleandomycin and erythromycin estolate, respectively, died, as compared to 3 of 4 deaths in controls. In vitro sensitivity data and serum antibacterial levels would suggest that triacetyloleandomycin would be the least effective therapeutically. However, this prediction was not fulfilled in these studies of experimental infections in monkeys wherein triacetyloleandomycin was a very effective antimicrobial agent.

Animals↗
PubMed1971

Therapy of staphylococcal infections in monkeys. VI. Comparison of clindamycin, erythromycin, and methicillin.

Intravenous inoculation of a penicillin-resistant, phage type 80/81 staphylococcus caused lethal infection in six of eight untreated monkeys. Daily intragastric administration of clindamycin hydrochloride and erythromycin stearate and intramuscular inoculation of clindamycin-2-phosphate and methicillin, all at a dose level of 50 mg/kg, was followed by mortalities of one of eight, one of eight, none of eight, and one of eight monkeys, respectively. Duration of obvious acute illness in surviving monkeys and time required for complete recovery were not significantly different in the four therapy groups with the exception that duration of acute illness in monkeys treated with clindamycin-2-phosphate (mean, 4.1 days) was significantly shorter than in monkeys given erythromycin stearate (mean, 7.1 days). In vitro sensitivity data and serum antibacterial levels would suggest that methicillin would be the least effective therapeutically, followed by erythromycin stearate and the two clindamycin preparations in that order. However, this prediction was not fulfilled in these studies in experimentally infected monkeys.

Administration, Oral↗
PubMed1972

Effects of chloramphenicol isomers and erythromycin on enzyme and lipid synthesis induced by oxygen in wild-type and petite yeast.

The synthesis of mitochondrial enzymes induced by exposure of anaerobically grown, lipid-depleted Saccharomyces cerevisiae to oxygen is inhibited by d(-)-threo-chloramphenicol and erythromycin. The concentration of these antibiotics required to cause 50% inhibition of this synthesis is less than 1 mm; this is also approximately the concentration required to inhibit by the same amount mitochondrial protein synthesis in situ. The synthesis of unsaturated fatty acids, ergosterol, and phospholipid induced by aeration is inhibited by d(-)-threo-chloramphenicol at high concentrations (12 mm) but is unaffected by erythromycin. l(+)-threo-Chloramphenicol affects neither enzyme nor lipid synthesis and is without effect on mitochondrial protein synthesis in situ. All three compounds inhibit the oxidative activity of isolated mitochondria; the chloramphenicol isomers also inhibit phosphorylation. In a euflavine-derived petite mutant, lacking mitochondrial protein synthesis and respiration, aeration results in the normal development of lipid in the cells, but no synthesis of mitochondrial enzymes. d(-)-threo-Chloramphenicol does not inhibit lipid synthesis in these cells. Thus inhibition of mitochondrial protein synthesis with erythromycin or genetic deletion of mitochondrial protein synthesis results in loss of the capacity to synthesize enzymes during aeration. d(-)-threo-Chloramphenicol, as well as inhibiting induced enzyme formation, inhibits lipid synthesis induced by oxygen. It is unlikely that the latter effect of chloramphenicol is due to inhibition of energy production and transformation, to direct effects on lipid synthesis, or to an inhibition of mitochondrial protein synthesis. It is, however, an effect not shared with the l isomer.

Anaerobiosis↗
PubMed1973

Mutation to erythromycin dependence in Escherichia coli K-12.

A nitrosoguanidine-induced mutant of Escherichia coli K-12 strain JC12 was absolutely dependent on erythromycin or related macrolide antibiotics for growth. The only other drugs which permitted growth (lincomycin and chloramphenicol) are, like the macrolides, inhibitors of the 50S ribosome. The order of relative effectiveness of these drugs was macrolides > lincomycin > chloramphenicol. Rates of growth with all drugs were concentration dependent. Erythromycin starvation was followed by normal rates of increase in cell mass and macromolecular synthesis for approximately one mass-doubling time, after which macromolecular synthesis abruptly ceased and cell lysis and death occurred. The dependent mutant gave rise spontaneously to revertants to independence with very high frequency (10(-4)). The gene (mac) for macrolide dependence is located near minute 25 on the E. coli chromosome; it does not result in increased resistance to these drugs. A separate gene for erythromycin resistance (eryA) is located in the cluster of ribosomal structural genes near spc, close to minute 63. Dependence on macrolides was most clearly evident in strains carrying mutations at both eryA and mac.

Anti-Bacterial Agents↗
PubMed1980

Molecular cloning of an erythromycin resistance determinant in streptococci.

The erythromycin resistance determinant of plasmid pDB102, a derivative of plasmid pSM19035, was cloned into the single HindIII site of the 3.6-megadalton cryptic Streptococcus mutans plasmid pVA318 and introduced into Streptococcus sanguis strain Challis by transformation. Plasmid pDB201, which was isolated from one of the transformants, consisted of the vector plasmid and the 1.15-megadalton HindIII fragment D of pSM19035. HindIII fragment D contained within it one of the two unique "spacer" sequences of pSM19035. Electron micrographs of self-annealed molecules of the recombinant plasmid revealed classical stem-loop structures, and the resistance determinant of pSM19035 appeared as a transposon-like structure. No differences were observed in either the type or the level of erythromycin resistance by pSM19035 or pDB201. The availability of a cloned erythromycin resistance determinant should be useful for future comparative studies of macrolide, lincosamide, and streptogramin B resistance plasmids in streptococci.

Cloning, Molecular↗