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Antimicrobial Agents and Chemotherapy, May 1998, p. 1295-1297, Vol. 42, No. 5
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Mechanism of Resistance to Amikacin and Kanamycin in Mycobacterium tuberculosis

George J. Alangaden,1,* Barry N. Kreiswirth,2 Arlette Aouad,1 Minoo Khetarpal,1 Felicitas R. Igno,1 Soraya L. Moghazeh,2 Elias K. Manavathu,1 and Stephen A. Lerner1,3

Division of Infectious Diseases1 and Department of Biochemistry and Molecular Biology,3 Wayne State University School of Medicine, Detroit, Michigan 48201, and Public Health Research Institute TB Center, New York, New York 100162

Received 26 June 1997/Returned for modification 19 December 1997/Accepted 25 February 1998

An A1400G mutation of the rrs gene was identified in Mycobacterium tuberculosis (MTB) strain ATCC 35827 and in 13 MTB clinical isolates resistant to amikacin-kanamycin (MICs, >128 µg/ml). High-level cross-resistance may result from such a mutation since MTB has a single copy of the rrs gene. Another mechanism(s) may account for high-level amikacin-kanamycin resistance in two mutants and lower levels of resistance in four clinical isolates, all lacking the A1400G mutation.

* Corresponding author. Mailing address: Division of Infectious Diseases, Wayne State University, School of Medicine, Suite 2140, 4160 John R, Detroit, MI 48201. Phone: (313) 745-9131. Fax: (313) 993-0302. E-mail: galangaden{at}oncgate.roc.wayne.edu.

Antimicrobial Agents and Chemotherapy, May 1998, p. 1295-1297, Vol. 42, No. 5
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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