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Updated: Feb 8, 2026

Isolation and Identification of Waterborne Antibiotic-Resistant Bacteria and Molecular Characterization of their Antibiotic Resistance Genes
Published on: March 3, 2023
Mobile lincosamide resistance genes in staphylococci
Andrea T Feßler1, Yang Wang2, Congming Wu2
1Institute of Microbiology and Epizootics, Centre for Infection Medicine, Department of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany.
Lincosamide resistance in staphylococci arises from enzymatic inactivation, ribosome protection, or target methylation. Genes conferring resistance can spread easily on mobile genetic elements, leading to co-selection with other antibiotics.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Lincosamide resistance in staphylococci is a growing concern.
- Three primary resistance mechanisms exist: enzymatic inactivation, ribosome protection, and target methylation.
- Several gene classes mediate these resistance mechanisms.
Purpose of the Study:
- To provide a comprehensive overview of the genetic basis of lincosamide resistance in staphylococci.
- To detail the different types of genes and proteins involved in resistance.
- To discuss the implications of gene location and dissemination.
Main Methods:
- Literature review and analysis of existing data on lincosamide resistance genes in staphylococci.
- Identification and classification of genes responsible for enzymatic inactivation (lnu), ribosome protection (vga, lsa, sal), and target methylation (cfr, erm).
- Examination of the characteristics of the encoded proteins and their resistance profiles.
Main Results:
- Two lnu genes (lnu(A), lnu(B)) encode lincosamide nucleotidyltransferases.
- ABC-F proteins, encoded by vga, lsa, and sal genes, provide ribosome protection.
- cfr and erm genes encode methylases targeting 23S rRNA, conferring resistance to multiple antibiotic classes.
Conclusions:
- Lincosamide resistance in staphylococci is multifactorial, involving diverse genetic mechanisms.
- Many resistance genes are located on mobile genetic elements, facilitating rapid spread.
- Co-location of resistance genes promotes co-selection and persistence under antibiotic pressure.
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