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Antimicrobial Agents and Chemotherapy, June 2008, p. 2287-2288, Vol. 52, No. 6
0066-4804/08/$08.00+0     doi:10.1128/AAC.00022-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

LETTER TO THE EDITOR

Nomenclature of Plasmid-Mediated 16S rRNA Methylases Responsible for Panaminoglycoside Resistance{triangledown}


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Production of 16S rRNA methylase has recently drawn attention as a novel aminoglycoside resistance mechanism in pathogenic gram-negative bacteria (1). It confers very-high-level resistance to all aminoglycosides that are currently available for parenteral formulation. Six distinct genes, rmtA, rmtB, rmtC, rmtD, armA, and npmA, encoding their respective enzymes have been identified in clinical and veterinary strains from various geographic areas, including East Asia, Europe, and the Americas, since 2003 (1, 10). NpmA is the only enzyme among them that methylates residue A1408, whereas the others methylate residue G1405, both within the aminoacyl site (A site) of the 16S rRNA (7, 10). All six genes are confirmed to be or are likely to locate on plasmids (3, 4, 10, 11, 12, 14). Recent findings also indicate that some of these genes are capable of crossing the barrier between glucose-fermenting and nonfermenting species. For instance, armA has been identified in both members of the family Enterobacteriaceae and in Acinetobacter baumannii (5, 13), and rmtD has been identified in Klebsiella pneumoniae and Pseudomonas aeruginosa (unpublished data). We will likely see an increasing number of reports about this resistance mechanism, including identification of genes encoding new 16S rRNA methylases.

Historically, the nomenclature of genes and enzymes for many resistance mechanisms has become complicated and nonsystematic (6). An extreme example is that of aminoglycoside acetyltransferases, where new gene names are arbitrarily assigned from one of the two coexisting nomenclature systems (9). The situation is somewhat better with β-lactamases and macrolide resistance genes, due to a registry and guidelines, respectively (http://www.lahey.org/Studies/) (8). To prevent confusion over the nomenclature of 16S rRNA methylases, we would like to propose practical rules for the nomenclature of these enzymes, which shall apply to any relevant enzymes to be identified in the future.

Currently, the highest and lowest identities of amino acid sequences among the G1405 16S rRNA methylases are 81.7% between RmtA and RmtB and 25.8% between ArmA and RmtD, respectively (2, 3). On the other hand, identities lower than 10% are observed between the G1405 16S rRNA methylases and the NpmA that methylates A1408 (10) (Table Go). Thus, we propose the following rules. A gene that has an amino acid identity greater than 95% with the closest known 16S rRNA methylase gene will be assigned a variant number starting from two in the order of the dates on which the sequences are deposited in the GenBank/EBML/DDBJ, e.g., rmtA2 and then rmtA3, analogous to the nomenclature of the qnr genes. A gene that has between 50 and 95% amino acid identity with the closest known 16S rRNA methylase gene will be assigned a new alphabet letter according to the closest existing gene name, e.g., rmtE, rmtF, armB, or armC, provided that the gene is shown to confer a consistent aminoglycoside resistance profile. A gene that has either an amino acid identity of less than 50% with the closest known 16S rRNA methylase gene or that is proven to methylate a new residue of 16S rRNA may be assigned a brand new gene name, like npmA, contingent upon demonstration of 16S rRNA methylation activity of the gene product and attributable resistant phenotype. Data regarding 16S rRNA methylase genes in pathogenic bacteria will be accumulated and provided at the following website http://www.nih.go.jp/niid/16s_database/index.html.


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  		TABLE 1. Identity of amino acid residues among the sequences of plasmid-mediated 16S rRNA methylases

 


   ACKNOWLEDGMENTS
 
Studies of plasmid-mediated 16S rRNA methylases identified among pathogenic microbes were supported by a grant (H18-Shinkou-011) from the Ministry of Health, Labor and Welfare, Japan.


   FOOTNOTES
 
{triangledown} Published ahead of print on 31 March 2008. Back


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  1. Doi, Y., and Y. Arakawa. 2007. 16S ribosomal RNA methylation: emerging resistance mechanism against aminoglycosides. Clin. Infect. Dis. 45:88-94.[CrossRef][Medline]
  2. Doi, Y., D. de Oliveira Garcia, J. Adams, and D. L. Paterson. 2007. Coproduction of novel 16S rRNA methylase RmtD and metallo-β-lactamase SPM-1 in a panresistant Pseudomonas aeruginosa isolate from Brazil. Antimicrob. Agents Chemother. 51:852-856.[Abstract/Free Full Text]
  3. Doi, Y., K. Yokoyama, K. Yamane, J. Wachino, N. Shibata, T. Yagi, K. Shibayama, H. Kato, and Y. Arakawa. 2004. Plasmid-mediated 16S rRNA methylase in Serratia marcescens conferring high-level resistance to aminoglycosides. Antimicrob. Agents Chemother. 48:491-496.[Abstract/Free Full Text]
  4. Galimand, M., P. Courvalin, and T. Lambert. 2003. Plasmid-mediated high-level resistance to aminoglycosides in Enterobacteriaceae due to 16S rRNA methylation. Antimicrob. Agents Chemother. 47:2565-2571.[Abstract/Free Full Text]
  5. Galimand, M., S. Sabtcheva, P. Courvalin, and T. Lambert. 2005. Worldwide disseminated armA aminoglycoside resistance methylase gene is borne by composite transposon Tn1548. Antimicrob. Agents Chemother. 49:2949-2953.[Abstract/Free Full Text]
  6. Hall, R., and S. Partridge. 2003. Unambiguous numbering of antibiotic resistance genes. Antimicrob. Agents Chemother. 47:3998-3999.[Free Full Text]
  7. Liou, G. F., S. Yoshizawa, P. Courvalin, and M. Galimand. 2006. Aminoglycoside resistance by ArmA-mediated ribosomal 16S methylation in human bacterial pathogens. J. Mol. Biol. 359:358-364.[CrossRef][Medline]
  8. Roberts, M. C., J. Sutcliffe, P. Courvalin, L. B. Jensen, J. Rood, and H. Seppala. 1999. Nomenclature for macrolide and macrolide-lincosamide-streptogramin B resistance determinants. Antimicrob. Agents Chemother. 43:2823-2830.[Free Full Text]
  9. Vanhoof, R., E. Hannecart-Pokorni, and J. Content. 1998. Nomenclature of genes encoding aminoglycoside-modifying enzymes. Antimicrob. Agents Chemother. 42:483.[Free Full Text]
  10. Wachino, J., K. Shibayama, H. Kurokawa, K. Kimura, K. Yamane, S. Suzuki, N. Shibata, Y. Ike, and Y. Arakawa. 2007. Novel plasmid-mediated 16S rRNA m1A1408 methyltransferase, NpmA, found in a clinically isolated Escherichia coli strain resistant to structurally diverse aminoglycosides. Antimicrob. Agents Chemother. 51:4401-4409.[Abstract/Free Full Text]
  11. Wachino, J., K. Yamane, K. Shibayama, H. Kurokawa, N. Shibata, S. Suzuki, Y. Doi, K. Kimura, Y. Ike, and Y. Arakawa. 2006. Novel plasmid-mediated 16S rRNA methylase, RmtC, found in a Proteus mirabilis isolate demonstrating extraordinary high-level resistance against various aminoglycosides. Antimicrob. Agents Chemother. 50:178-184.[Abstract/Free Full Text]
  12. Yamane, K., F. Rossi, M. G. Barberino, J. M. Adams-Haduch, Y. Doi, and D. L. Paterson. 2008. 16S ribosomal RNA methylase RmtD produced by Klebsiella pneumoniae in Brazil. J. Antimicrob. Chemother. 61:746-747.[Free Full Text]
  13. Yamane, K., J. Wachino, Y. Doi, H. Kurokawa, and Y. Arakawa. 2005. Global spread of multiple aminoglycoside resistance genes. Emerg. Infect. Dis. 11:951-953.[Medline]
  14. Yokoyama, K., Y. Doi, K. Yamane, H. Kurokawa, N. Shibata, K. Shibayama, T. Yagi, H. Kato, and Y. Arakawa. 2003. Acquisition of 16S rRNA methylase gene in Pseudomonas aeruginosa. Lancet 362:1888-1893.[CrossRef][Medline]
Yohei Doi
Division of Infectious Diseases
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Jun-ichi Wachino
Yoshichika Arakawa*
Department of Bacterial Pathogenesis and Infection Control
National Institute of Infectious Diseases
4-7-1 Gakuen
Musashi-Murayama, Tokyo 208-0011
Japan

* Phone: 81-42-561-0771, ext. 500, Fax: 81-42-561-7173, E-mail: yarakawa{at}nih.go.jp

Antimicrobial Agents and Chemotherapy, June 2008, p. 2287-2288, Vol. 52, No. 6
0066-4804/08/$08.00+0     doi:10.1128/AAC.00022-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.




This Article
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