• Clinical and Experimental Pediatrics
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• v.51 no.10
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• pp.1031-1037
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• 2008

Macrolide antimicrobial agents including erythromycin, roxithromycin, clarithromycin, and azithromycin are commonly used in the treatment of respiratory tract infections in children. Newer macrolides that have structural modifications of older drug erythromycin show improved change in the spectrum of activity, dosing, and administration. However, recent studies reported that increasing use of macrolide antibiotics is the main force driving the development of macrolide resistance in streptococci. In particular, azithromycin use is more likely to select for macrolide resistance with Streptococcus pneumoniae than is clarithromycin use, a possible reflection of its much longer half life. Recently, erythromycin resistance rates of S. pneumoniae and Streptococcus pyogenes are rapidly increasing in Korea. Two main mechanisms of acquired macrolide resistance have been described, altered binding site on the bacterial ribosome encoded by the ermB gene and active macrolide efflux pump encoded by the mef gene. Relationship between the susceptibility of S. pneumoniae and the response to macrolides has been shown in studies of acute otitis media, but less clear in cases of pneumonia. This article reviews the spectrum of activity, pharmacokinetic properties, mechanisms of action and resistance, and clinical implication of resistance on the treatment of respiratory tract infections in children.

• YAKHAK HOEJI
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• v.26 no.3
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• pp.169-174
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• 1982

Several strains of bacteria having resistance to macrolide antibiotics were isolated. EMR-1, one of them, exhibited the induced resistance to macrolide antibiotics and this microorganism was identified as a bacterium belong to Bacillus species. The subinhibitory concentration of erythromycin or oleandomycin induced strong resistance to both erythromycin and oleandomycin themselves and to other macrolide antibiotics such as leucomycin, spiramycin and josamycin. The effective concentration of inducer, erythromycin was $0.0016-0.2\mu$g/ml. The inactivating enzyme of these antibiotics was not produced by EMR-1.

• Clinical and Experimental Pediatrics
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• v.60 no.5
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• pp.151-157
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• 2017

Purpose: Macrolide resistance rate of Mycoplasma pneumoniae has rapidly increased in children. Studies on the clinical features between macrolide susceptible-M. pneumoniae (MSMP) and macrolide resistant-M. pneumoniae (MRMP) are lacking. The aim of this study was to identify the macrolide resistance rate of M. pneumoniae in Korean children with M. pneumoniae penupmonia in 2015 and compare manifestations between MSMP and MRMP. Methods: Among 122 children (0-18 years old) diagnosed with M. pneumoniae pneumonia, 95 children with the results of macrolide sensitivity test were included in this study. Clinical manifestations were acquired using retrospective medical records. Results: The macrolide resistant rate of M. pneumoniae was 87.2% (82 of 94 patients) in children with M. pneumoniae pneumonia. One patient showed a mixed type of wild type and A2063G mutation in 23S rRNA of M. pneumoniae. There were no significant differences in clinical, laboratory, and radiologic findings between the MSMP and MRMP groups at the first visit to our hospital. The time interval between initiation of macrolide and defervescence was significantly longer in the MRMP group ($4.9{\pm}3.3$ vs. $2.8{\pm}3.1days$, P=0.039). Conclusion: The macrolide resistant rate of M. pneumoniae is very high in children with M. pneumoniae pneumonia in Korea. The clinical manifestations of MRMP are similar to MSMP except for the defervescence period after administration of macrolide. Continuous monitoring of the occurrence and antimicrobial susceptibility of MRMP is required to control its spread and establish strategies for treating second-line antibiotic resistant M. pneumoniae infection.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.127.1-127.1
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• 2003

The purpose of this study is to investigate the prevalence of resistance to macrolide, lincosamide, streptogramin and ketolide antibiotics in Korea. The antibiotic susceptibility test was performed to the macrolide erythromycin, clarithromycin, azithromycin, josamycin, the lincosamide clindamycin, the streptogramin synercid and the ketolide ABT -773 against 337 clinical Staphylococcus aureus(SAU). Coagulase-negative Staphylococci (CNS) and Enterococci isolates exhibited an average percentage of 64％, 56％, and 81 ％ of resistance to erythromycin, respectively.

• YAKHAK HOEJI
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• v.41 no.4
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• pp.530-532
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• 1997

The MICs of various macrolide, lincosamide and streptogramin B antibiotics against highly erythromycin-resistant Escherichia coli 209K strain were evaluated. E. coli 209K showed high MICs against 14-membered macrolides and the relatively weaker resistance to 16-membered macrolides, lincosamides and streptogramin B. The macrolide-phosphotransferase K from E. coli 209K showed greater substrate specificity to the 14-membered macrolide antibiotics than to the 16-membered macrolide antibiotics, lincosamide and streptogramin B. Therefore, it was considered that the high resistance was due to the macrolide-phosphotransferase K.

• YAKHAK HOEJI
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• v.30 no.6
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• pp.317-322
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• 1986

To clarify resistance mechanisms of lincosamide antibiotics, it was examined whether lincosamide antibiotics was able to induce high resistance to macrolide and lincosamide antibiotics against EMR-1 strain of Bacillus species. And it was also examined whether the inducible resistance was plasmid-mediated or chromosome-mediated. This strain was identified as Bacillus licheniformis by its morphological and physiological characteristics. The subinhibitory concentrations of lincomycin and clindamycin induced high resistance in the strain to lincosamide antibiotics, but not to macrolide antibiotics. The inducible resistance was not eliminated by treating the strain with ethidium bromide, and plasmid was not identified by the alkaline lysis method of plasmid preparation. These results indicate, therefore, that the inducible resistance to macrolide and lincosamide antibiotics in the strain may be chromosome-mediated, not plasmid-mediated.

• Korean Journal of Microbiology
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• v.28 no.1
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• pp.27-34
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• 1990

Two macrolide-lincosamide-streptogramin B (MLS) antibiotic resistance genes, one expressed inducibly and the other expressed constitutively were recognized from a single Staphylococcus aureus DH1 strain. The inducible MLS resistance gene was isolated and cloned from the R-plasmid pDE1(7.4kb) and the constitutive gene was from chromosomal DNA. Base sequence of the inducible MLS resistance gene (1.2kb) was determined and found as same that of pE194. The restriction map of the cloned constitutive MLS resistance gene was compared with that of the inducible gene. Two genes have same restriction map except leader region. In the constitutive gene there is no leader region which is doing major role in inducible expression.

• Archives of Pharmacal Research
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• v.21 no.1
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• pp.76-78
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• 1998

• YAKHAK HOEJI
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• v.48 no.6
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• pp.364-368
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• 2004

The prevalence of resistance to a range of macrolides was determined for clinical isolates of common respiratory pathogens using NCCLS testing methods and interpretative criter ia.71.4% of Streptococcus pneumoniae, 62.3% of Staphylococcus aureus, 50.8% of coagulase-negative staphylococci and 4.4% of Strpetococcus pyogenes were erythromycin resistant. Also, the rates of resistance to other macrolides and clindamycin in these clinical isolates were as high as to eryth -romycin. Almost all of the macrolide-resistant isolates were positive for erm of the methylase gene, or mef of the efflux gene.

• YAKHAK HOEJI
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• v.35 no.1
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• pp.22-29
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• 1991

pMB4 is a 2.4-kilobase plasmid of Staphylococcus aureus TR-1 that confers inducible resistance to the macrolide-lincosamide-streptogramin B(MLS) antibiotics. By subcloning studies, it was found that the MLS resistance determinant was located at 1.0Kb fragment between Sau3AI and TaqI sites. DNA sequence of the MLS resistant determinant, named ermC-4 was determined, and found to be highly homologous with that of ermC. Because the leader peptide sequence of ermC-4 was identical with that of ermC, the expression of the resistance gene is thought to be controlled by posttranscriptional attenuation in S. aureus TR-1.