Epidemiology and genetics of VIM-type metallo-β-lactamases in Gram-negative bacilli

Wei-Hua Zhao1, Zhi-Qing Hu

  • 1Department of Microbiology & Immunology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan. whzhao@med.showa-u.ac.jp

Future Microbiology
|April 1, 2011
PubMed

Insights

Metallo-β-lactamases (MBLs), particularly VIM variants, are spreading rapidly among Gram-negative bacteria. These enzymes confer resistance to critical antibiotics like carbapenems, often facilitated by mobile genetic elements.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Metallo-β-lactamases (MBLs) are a significant class of enzymes conferring resistance to β-lactam antibiotics, including carbapenems.
  • VIM-type MBLs represent a common and evolving family, with numerous variants identified globally in Gram-negative bacteria.

Purpose of the Study:

  • To review the diversity and spread of VIM-type metallo-β-lactamases.
  • To discuss the genetic platforms, such as integrons and plasmids, that facilitate the dissemination of bla (VIM) genes.
  • To highlight the co-occurrence of bla (VIM) with other antibiotic resistance genes.

Main Methods:

  • Literature review of studies on metallo-β-lactamases, focusing on VIM variants.
  • Analysis of genetic structures (integrons, transposons, plasmids) associated with bla (VIM) genes.
  • Examination of bacterial species, geographic distribution, and amino acid variations of VIM variants.

Main Results:

  • 27 VIM variants have been detected in at least 23 Gram-negative bacterial species across over 40 countries.
  • Amino acid similarities among VIM variants range from 72.9% to 99.6%.
  • bla (VIM) genes are predominantly located on class 1 integrons, often within mobile genetic elements like transposons and plasmids, promoting horizontal gene transfer.

Conclusions:

  • The genetic mobility of bla (VIM) genes, facilitated by diverse integron structures and plasmids, drives their widespread dissemination.
  • The co-existence of bla (VIM) with other resistance genes exacerbates the challenge of treating Gram-negative bacterial infections.
  • Understanding these genetic mechanisms is crucial for developing strategies to combat MBL-mediated antibiotic resistance.

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