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PubMed1985

Evidence that the clindamycin-erythromycin resistance gene of Bacteroides plasmid pBF4 is on a transposable element.

We constructed a shuttle vector, pE5-2, which can replicate in both Bacteroides spp. and Escherichia coli. pE5-2 contains a cryptic Bacteroides plasmid (pB8-51), a 3.8-kilobase (kb) EcoRI-D fragment from the 41-kb Bacteroides fragilis plasmid pBF4, and RSF1010, an IncQ E. coli plasmid. pE5-2 was mobilized by R751, an IncP E. coli plasmid, between E. coli strains with a frequency of 5 X 10(-2) to 3.8 X 10(-1) transconjugants per recipient. R751 also mobilized pE5-2 from E. coli donors to Bacteroides uniformis 0061RT and Bacteroides thetaiotaomicron 5482 with a frequency of 0.9 X 10(-6) to 2.5 X 10(-6). The Bacteroides transconjugants contained only pE5-2 and were resistant to clindamycin and erythromycin. Thus, the gene for clindamycin and erythromycin resistance must be located within the Eco RI-D fragment of BF4. A second recombinant plasmid, pSS-2, which contained 33 kb of pBF4 (including the EcoRI-D fragment and contiguous regions) could also be mobilized by R751 between E. coli strains. In some transconjugants, a 5.5-kb (+/- 0.3 kb) segment of the pBF4 portion of pSS2 was inserted into one of several sites on R751. In some other transconjugants this same 5.5-kb segment was integrated into the E. coli chromosome. This segment could transfer a second time onto R751. Transfer was RecA independent. The transferred segment included the entire EcoRI-D fragment, and thus the clindamycin-erythromycin resistance determinant, from pBF4.

Bacteroides↗
PubMed1990

Erythromycin induces expression of the chloramphenicol acetyltransferase gene cat-86.

The plasmid gene cat-86 specifies chloramphenicol-inducible chloramphenicol acetyltransferase in Bacillus subtilis. This gene, like the erythromycin-inducible erm genes, is regulated by translational attenuation. Here we show that cat-86 is also inducibly regulated by erythromycin. cat-86 does not confer resistance to erythromycin.

Bacillus subtilis↗
PubMed1994

Inhibition of erythromycin synthesis by disruption of malonyl-coenzyme A decarboxylase gene eryM in Saccharopolyspora erythraea.

Malonyl-coenzyme A (malonyl-CoA) decarboxylase is widely distributed in prokaryotes and eukaryotes. However, the biological function of this enzyme has not been established in any organism. To elucidate the structure and function of this enzyme, the malonyl-CoA decarboxylase gene from Saccharopolyspora erythraea (formerly Streptomyces erythreaus) was cloned and sequenced. This gene would encode a polypeptide of 417 amino acids. The deduced amino acid sequence matched the experimentally determined amino acid sequences of 25 N-terminal residues each of the enzyme and of an internal peptide obtained by proteolysis of the purified enzyme. This decarboxylase showed homology with aminoglycoside N6'-acetyltransferases of Pseudomonas aeruginosa, Serratia marcescens, and Klebsiella pneumoniae. Northern (RNA) blot analysis revealed a single transcript. The transcription initiation site was 220 bp upstream of the start codon. When expressed in Escherichia coli, the S. erythraea malonyl-CoA decarboxylase gene yielded a protein that cross-reacted with antiserum prepared against S. erythraea malonyl-CoA decarboxylase and catalyzed decarboxylation of [3-14C]malonyl-CoA to acetyl-CoA and 14CO2. The S. erythraea malonyl-CoA decarboxylase gene was disrupted by homologous recombination using an integrating vector pWHM3. The gene-disrupted transformant did not produce immunologically cross-reacting 45-kDa decarboxylase, lacked malonyl-CoA decarboxylase activity, and could not produce erythromycin. Exogenous propionate restored the ability to produce erythromycin. These results strongly suggest that the decarboxylase provides propionyl-CoA for erythromycin synthesis probably via decarboxylation of methylmalonyl-CoA derived from succinyl-CoA, and therefore the malonyl-CoA decarboxylase gene is designated eryM. The gene disrupted mutants also did not produce pigments.

Base Sequence↗
PubMed2002

Vancomycin tolerance induced by erythromycin but not by loss of vncRS, vex3, or pep27 function in Streptococcus pneumoniae.

Vancomycin-tolerant Streptococcus pneumoniae is a growing problem among drug-resistant human pathogens. Some vancomycin-tolerant pneumococci have been reported to carry mutations in loci encoding a two-component regulatory system designated VncRS or in a proximal ABC transporter, Vex. A model was advanced proposing that the tolerance phenotype resulted from the inability of a vncS mutant to respond to the Vex-transported Pep27 "death peptide" signal and dephosphorylate VncR, thereby preventing relief of repression of autolytic and other cell death functions in response to antibiotics. To explore this hypothesis, we constructed mutations in vncS, vncR, vex3, and pep27 in S. pneumoniae strain R6 and two additional genetic backgrounds. The lytic responses of the isogenic DeltavncS, Deltavex3, DeltavncR, and Deltapep27 mutants, but not a DeltalytA strain, to vancomycin were indistinguishable from that of the parent strain. DeltavncS strains also failed to exhibit tolerance to vancomycin at various doses in multiple media and showed wild-type sensitivity to other classes of autolysis-inducing antibiotics. In contrast, addition of subinhibitory levels of the antibiotic erythromycin led to tolerance to vancomycin during late, but not early, exponential-phase growth in a DeltavncS strain, in the parent strain R6, and in two other strains bearing erythromycin resistance markers, namely, a DeltavncR strain and an unrelated DeltacomD strain that is defective in competence-quorum sensing. Thus, this tolerance effect resulted from changes in cell growth or other erythromycin-dependent phenomena and not inactivation of vncS per se. Consistent with these results, and in contrast to a previous report, we found that a synthetic form of Pep27 did not elicit lytic or nonlytic killing of pneumococci. Finally, microarray transcriptional analysis and beta-galactosidase reporter assays revealed VncS-dependent regulation of the vex123 gene cluster but did not support a role for VncRS in the regulation of autolytic or other putative cell death loci. Based on these findings, we propose that vancomycin tolerance in S. pneumoniae does not result from loss of vncS function alone.

ATP-Binding Cassette Transporters↗
PubMed1984

Disk diffusion antimicrobial susceptibility testing of members of the family Legionellaceae including erythromycin-resistant variants of Legionella micdadei.

Disk diffusion antimicrobial susceptibility testing of members of the family Legionellaceae was accomplished on buffered charcoal yeast extract agar by allowing the bacteria to grow for 6 h before placement of the disks, followed by an additional 42-h incubation period before the inhibitory zones were measured. This system was standardized by comparing the zone sizes with the MICs for 20 antimicrobial agents of nine bacterial strains in five Legionella species and of 19 laboratory-derived, erythromycin-resistant variants of Legionella micdadei. A high, linear correlation between zone size and MIC was found for erythromycin, trimethoprim, penicillin, ampicillin, carbenicillin, cephalothin, cefamandole, cefoxitin, moxalactam, chloramphenicol, vancomycin, and clindamycin. Disk susceptibility testing could be employed to screen Legionella isolates for resistance to any of these antimicrobial agents, of which only erythromycin is known to be efficacious in the treatment of legionellosis. With selected antibiotics, disk susceptibility patterns also appeared to accurately identify to the species level the legionellae. The range of the MICs of the legionellae for rifampin and the aminoglycosides was too small to determine whether the correlation of zone size with MIC was linear. However, laboratory-derived, high-level rifampin-resistant variants of L. micdadei demonstrated no inhibition zone around the rifampin disk, indicating that disk susceptibility testing would likely identify a rifampin-resistant clinical isolate. Of the antimicrobial agents tested, the only agents for which disk susceptibility testing was definitely not possible on buffered charcoal yeast extract agar were oxacillin, the tetracyclines, and the sulfonamides.

Aminoglycosides↗
PubMed2001

Dissemination of clonally unrelated erythromycin- and glycopeptide-resistant Enterococcus faecium isolates in a tertiary Greek hospital.

Between September 1999 to February 2001, 25 glycopeptide-resistant Enterococcus faecium (GRE) isolates were recovered from a Greek hospital. The isolates exhibited 13 distinct chromosomal macrorestriction types by pulsed-field gel electrophoresis, and all were erythromycin and vancomycin resistant, carrying the genes vanA and ermB. Vancomycin resistance, always linked with erythromycin resistance, was transferable from 17 isolates. The dissemination of erythromycin-resistant GRE strains may, at least in part, reflect the extensive use of macrolides in husbandry in Greece.

Anti-Bacterial Agents↗
PubMed2002

Erythromycin-resistant group A streptococcal isolates recovered in Sofia, Bulgaria, from 1995 to 2001.

The frequency of erythromycin resistance within group A streptococci in Sofia, Bulgaria, from 1995 to 2001 was 2.1% (26 isolates). Of this, 57.7% was macrolide-lincosamide-streptogramin (MLS) inducible, 7.7% was MLS constitutive, and 34.6% had the M phenotype. Eleven different emm sequence types were found among 25 erythromycin-resistant isolates tested. Nineteen of 26 erythromycin-resistant isolates were additionally resistant to tetracycline and/or chloramphenicol.

Bulgaria↗
PubMed2002

Pharmacoepidemiological analysis of provincial differences between consumption of macrolides and rates of erythromycin resistance among Streptococcus pyogenes isolates in Spain.

The M phenotype is by far the most common mechanism of erythromycin resistance among Streptococcus pyogenes isolates in Spain. A geographic analysis of the relationship between within-country differences in the prevalence of M-type resistance to erythromycin in S. pyogenes and the level of consumption of 14- and 15-membered macrolides within different provinces was carried out. From 1998 to 1999, a nationwide multicenter surveillance study yielded 2,039 consecutive pharyngeal isolates of S. pyogenes. Data on antibiotic consumption for the same period were gathered from IMS Health, and the corresponding daily defined doses per 1,000 inhabitants per day were calculated according to the Anatomic Therapeutic Classification index. Macrolide use was subdivided into dosages given three times a day (TID), twice a day (BID), or once a day (OD). Spearman nonparametric correlation coefficients (R) were calculated, and variables proving to be significantly associated (P < 0.1) were introduced into a linear regression model. The total consumption of macrolides presented a significant correlation with the prevalence of resistance (R = 0.527; P = 0.032). Neither TID nor BID macrolide consumption showed significant correlations. Only OD consumption had a significance below 0.1. These data are consistent with the hypothesis that only the total consumption of macrolides influences the local rates of M-type erythromycin resistance in S. pyogenes, and subgroups of macrolides seem to have an additive rather than a selective effect by contributing to increasing the final amount of macrolides used. Local variations in total consumption were associated only with BID consumption (R = 0.849; P = 0.004). The simple linear regression with total macrolide consumption showed a considerable determination coefficient (R(2) = 0.678; P = 0.006). The model explains up to 68% of the measured variation and is clearly better as a predictor of the prevalence of resistance than the mere mean is. By solving the regression equation, the resultant value of 2.2 defined doses per 1,000 inhabitants per day fits with the existence of a critical threshold of selective pressure.

Anti-Bacterial Agents↗
PubMed2002

Molecular epidemiology of erythromycin resistance in Streptococcus pneumoniae isolates from blood and noninvasive sites.

Erythromycin-resistant isolates of Streptococcus pneumoniae from blood cultures and noninvasive sites were studied over a 3-year period. The prevalence of erythromycin resistance was 11.9% (19 of 160) in blood culture isolates but 4.2% (60 of 1,435) in noninvasive-site isolates. Sixty-two of the 79 resistant isolates were available for study. The M phenotype was responsible for 76% (47 of 62) of resistance, largely due to a serotype 14 clone, characterized by multilocus sequence typing as ST9, which accounted for 79% (37 of 47) of M phenotype resistance. The ST9 clone was 4.8 times more common in blood than in noninvasive sites. All M phenotype isolates were PCR positive for mef(A), but sequencing revealed that the ST9 clone possessed the mef(A) sequence commonly associated with Streptococcus pyogenes. All M phenotype isolates with this mef(A) sequence also had sequences consistent with the presence of the Tn1207.1 genetic element inserted in the celB gene. In contrast, isolates with the mef(E) sequence normally associated with S. pneumoniae contained sequences consistent with the presence of the mega insertion element. All MLS(B) isolates carried erm(B), and two isolates carried both erm(B) and mef(E). Fourteen of the 15 MLS(B) isolates were tetracycline resistant and contained tet(M). However, six M phenotype isolates of serotypes 19 (two isolates) and 23 (four isolates) were also tetracycline resistant and contained tet(M). MICs for isolates with the mef(A) sequence were significantly higher than MICs for isolates with the mef(E) sequence (P < 0.001). Thus, the ST9 clone of S. pneumoniae is a significant cause of invasive pneumococcal disease in northeast Scotland and is the single most important contributor to M phenotype erythromycin resistance.

Anti-Bacterial Agents↗
PubMed2003

emm Gene distribution among erythromycin-resistant and -susceptible Italian isolates of Streptococcus pyogenes.

The phenotypes and genetic determinants for macrolide resistance were determined for 167 erythromycin-resistant Streptococcus pyogenes strains. A cMLS phenotype was shown in 18% of the erythromycin-resistant strains, while inducible resistance was apparent in 31% and the M phenotype was apparent in 50%. The emm gene type of this set of resistant isolates and that of 48 erythromycin-sensitive isolates were determined. emm2 and emm48 were recorded only in the resistant strains of the M phenotype, while approximately all of the strains harboring the emm22 gene had the cMLS phenotype. More than 80% of the emm89-positive strains had the iMLS phenotype, and the same portion of emm4 strains presented the M phenotype. emm3 is recorded only among sensitive strains. The distribution of frequencies of the genetic determinant for the virulence factor M protein was significantly different both among organisms of different types of resistance and between resistant and sensitive populations of S. pyogenes under study.

Bacterial Proteins↗
PubMed2003

Genotypic identification of erythromycin-resistant campylobacter isolates as helicobacter species and analysis of resistance mechanism.

The correct identification of Campylobacter species remains cumbersome, especially when conventional biochemical tests and antimicrobial susceptibility patterns are used for a phenotypical identification. Correct identification is important for epidemiological purposes and for studying changes in antimicrobial resistance patterns. Six erythromycin-resistant campylobacter strains were investigated by 16S ribosomal DNA (rDNA) sequencing, 23S rDNA sequencing, and restriction fragment length polymorphism analysis of a putative heme-copper oxidase domain described as being specific for thermophilic Campylobacter species. Three erythromycin-resistant isolates from feces of human immunodeficiency virus (HIV)-seropositive patients with diarrhea and one blood isolate of from HIV-seropositive patient with cellulitis were identified by 16S rDNA analysis as Helicobacter cinaedi, whereas 23S rDNA sequencing suggested Wolinella succinogenes. The 16S rDNA sequence data of fecal isolates of two patients with travelers diarrhea revealed Helicobacter pullorum and were also in contrast with 23S rDNA sequencing. Of 4 H. cinaedi isolates, 1 contained the putative heme-copper oxidase gene thought to be specific for thermophilic species. The six erythromycin-resistant Helicobacter species had a similar point mutation A2143G in 23S rDNA resembling the macrolides resistance in Helicobacter pylori. We conclude that 16S rDNA sequencing should be preferred to 23S rDNA analysis and that macrolide-resistant campylobacter strains should be investigated by this approach for a correct identification.

Anti-Bacterial Agents↗
PubMed2004

Genetic diversity of cell-invasive erythromycin-resistant and -susceptible group A streptococci determined by analysis of the RD2 region of the prtF1 gene.

The RD2 region of the internalization-associated gene prtF1, which encodes the fibronectin-binding repeat domain type 2 of protein F1, plays a crucial role in the entry of group A streptococci (GAS) into epithelial cells. A molecular study of the variability of the RD2 region was carried out with 77 independent Italian GAS, 66 erythromycin resistant (ER) and 11 erythromycin susceptible (ES), which had previously been investigated for the association between erythromycin resistance and ability to enter human respiratory cells. The amplicons obtained from PCR analysis of the RD2 region were consistent with a number of RD2 repeats ranging from one to five, more frequently four (n = 30), three (n = 27), and one (n = 18). A new method to type cell-invasive GAS (RD2 typing) was developed by combining PCR analysis of the RD2 region and restriction analysis of PCR products with endonucleases HaeIII, DdeI, and HinfI. Overall, 10 RD2 types (a to j) were distinguished (all detected among the 66 ER isolates, four detected among the 11 ES isolates). Comparison and correlation of RD2 typing data with the genotype and phenotype of macrolide resistance and with data from PCR M typing and SmaI macrorestriction analysis allowed us to identify 41 different clones (31 among the 66 ER isolates and 10 among the 11 ES isolates). Three major clones accounted for 40% of the isolates (47% of ER strains). Some ES isolates appeared to be related to ER isolates with identical combinations of RD2 type and emm type. While simultaneous use of different typing methods is essential for a thorough investigation of GAS epidemiology, RD2 typing may be especially helpful in typing cell-invasive GAS.

Adhesins, Bacterial↗
PubMed2004

Serotypes and genotypes of erythromycin-resistant group B streptococci in Korea.

Among 78 erythromycin-resistant group B streptococcus (GBS) isolates from Korea, ermB was detected in 58 (74.4%), mefA was detected in 14 (17.9%), and ermTR was detected in 6 (7.7%). The most prevalent serotypes of erythromycin-resistant GBS were V (detected in 34 isolates [43.6%]) and III (detected in 33 isolates [42.3%]). All serotype V erythromycin-resistant GBS harbored the ermB gene.

Bacterial Proteins↗
PubMed2005

Erythromycin-resistant group a streptococcal isolates collected between 2000 and 2005 in Oahu, Hawaii, and their emm types.

We examined erythromycin and clindamycin susceptibilities with Etest methodology among 546 group A streptococcal isolates collected in Hawaii between February 2000 and November 2004. Erythromycin resistance was low (3.1%). No isolate was clindamycin resistant. The prevalence of erythromycin resistance in group A streptococci remains low in Hawaii.

Drug Resistance, Bacterial↗
PubMed1986

Erythromycin versus tetracycline for treatment of Mediterranean spotted fever.

Eighty one children aged between 1 and 13 years participated in a randomised comparative trial of tetracycline hydrochloride and erythromycin stearate for treatment of Mediterranean spotted fever. Both therapeutic regimens proved effective, but in patients treated with tetracycline both clinical symptoms and fever disappeared significantly more quickly. Likewise, when those patients who began treatment within the first 72 hours of illness are considered the febrile period had a significantly shorter duration in the group treated with tetracycline. One patient was switched to tetracycline because there was no improvement of clinical manifestations, with persistence of fever, myalgias, and prostration, after receiving eight days of treatment with erythromycin. These results suggest that tetracyclines are superior to erythromycin in the treatment of Mediterranean spotted fever.

Adolescent↗
PubMed1977

Lack of evidence for mutation to erythromycin resistance in clinical strains of Staphylococcus aureus.

The properties of 100 erythromycin resistant strains of Staphylococcus aureus obtained from clinical material have been compared with the properties of mutants selected in vitro for resistance to erythromycin. The properties, including inducibility of the resistance and cross-resistance to spiramycin and lincomycin, of the two groups of isolates were always different. The risk that staphylococci will mutate to erythromycin resistance during therapy with this antibiotic is remote.

Drug Resistance, Microbial↗
PubMed1990

Sulphaphenazole, streptomycin and sulphaphenazole combination, trimethoprim, and erythromycin in the treatment of chancroid.

One hundred and thirty six patients with chancroid were treated with four different treatment regimens; (A) Sulphaphenazole 1 g 12 hourly by mouth x 10 days (B) Inj streptomycin 1 g intramuscularly daily with sulphaphenazole 1 g 12 hourly orally x 10 days; (C) trimethoprim 200 mg 12 hourly by mouth x 7-10 days, and (D) erythromycin 500 mg 6 hourly orally x 7-10 days. Cure rates of 9% with sulphaphenazole alone, 48% with streptomycin and sulphaphenazole combination, 93% with trimethoprim and 100% with erythromycin were obtained. Sulphaphenazole alone or in combination with streptomycin were thus inferior in the treatment of chancroid. There is need for modification of treatment regimens recommended for chancroid in the textbooks of dermatology and venereology. Trimethoprim can be recommended as first line of treatment for chancroid in developing countries like India where resistance to trimethoprim is uncommon and erythromycin is suggested as a second line of therapy because by that time syphilis can be easily ruled out.

Administration, Oral↗