Epidemiology and Molecular Genetics of Macrolide Resistance in Staphylococcus aurous.

Research Project

Project/Area Number	63044025
Research Category	Grant-in-Aid for international Scientific Research
Allocation Type	Single-year Grants
Section	Joint Research
Research Institution	Gunma University School of Medicine
Principal Investigator	HASHIMOTO Hajime Gunma University, School of Medicine, 医学部, 教授 (90008235)
Co-Investigator(Kenkyū-buntansha)	MILCH Hedda National Institute of Hygiene, Hungary, Head JA^^′NOSL La Dept. of Phage Res. NIH. Hungary, Specialist INOUE Matsuhisa Gunma University, School of Medicine, 医学部, 助教授 (10008336) JANOSI Laszlo National Institute of Hygiene, Hungary
Project Period (FY)	1988 – 1990
Project Status	Completed (Fiscal Year 1990)
Budget Amount *help	¥5,100,000 (Direct Cost: ¥5,100,000) Fiscal Year 1990: ¥1,600,000 (Direct Cost: ¥1,600,000) Fiscal Year 1989: ¥1,700,000 (Direct Cost: ¥1,700,000) Fiscal Year 1988: ¥1,800,000 (Direct Cost: ¥1,800,000)
Keywords	Staphylococcus aurous / Macrolide resistance / 14-membered macrolide / Streptogramin type B / PMS plasmid / ストレプトグラミンB
Research Abstract	Types of macrolide resistance in Staphylococcus aureus are classified into 3 groups, A, B and C. Group A strains are constitutively resistant to macrolides (M), lincosamides (L), and streptogramin Type B antibiotics (S). Group C strains are inducibly resistant to MLS. Group B strains are inducibly resistant to 14-member macrolides and S. We referred to this phenotype as PMS. During a period from 1978 to 1989, 413 PMS-resistant S. aurous strains were isolated in Hungary. They were also resistant to penicillin (99%), tetracycline (79%) and chloramphenicol (63%). Most of them (94%) belonged to the phase type 52-complex, suggesting that they are from the same origin. 43 strains were further examined, and we found that the determinant for PMS phenotype was located on one of 3 kinds of plasmid, which also encoded beta-lactamase production and cadmium ion resistance, but not arsenate resistance. Tetracycline and chloramphenicol resistances were encoded by independent plasmids whose DNA size were 4.4kb and 2.9kb respectively. The DNA size of PMS plasmids was 50kb, 23.8kb or 16.8kb. 23.8kb and 50kb plasmids also carried genes for mercury resistance. The incompatibility of the PMS-plasmids was incl as pI258, which encodes group A macrolide resistance. 23.8kb and 16.8kb DNA of PMS plasmids were examined for their fragment pattern by restriction enzymes. The DNA areas encoding beta-lactamase and replication were the same between PMS plasmids and pI258, but fragments between the 2 areas were quite different. Non-homologous 10kb area of pI258 is known as the site of group A MLS determinants, and 4kb area on PMS plasmids is the site of PMS determinants. 16.8kb PMS plasmid lacked mercury resistance genes, but other area was the same as that of 23.8kb plasmid.