In Vivo Survival of Teicoplanin-Resistant Staphylococcus aureus and Fitness Cost of Teicoplanin Resistance  

Oleh:

[s.n]

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Antimicrobial Agents and Chemotherapy vol. 50 no. 07 (Jul. 2006), page 2352.
Topik: Teicoplanin-Resistant; Staphylococcus

Ketersediaan

Perpustakaan FK Nomor Panggil: A21.K, A21.K.2006.03 Non-tandon: 3 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Glycopeptide resistance, in a set of in vitro step-selected teicoplanin-resistant mutants derived from susceptible Staphylococcus aureus SA113, was associated with slower growth, thickening of the bacterial cell wall, increased N-acetylglucosamine incorporation, and decreased hemolysis. Differential transcriptome analysis showed that as resistance increased, some virulence-associated genes becamedownregulated. In a mouse tissue cage infection model, an inoculum of 100000 CFU of strain SA113 rapidly produced a high-bacterial-load infection, which triggered MIP-2 release, leukocyte infiltration, and reduced leukocyte viability. In contrast, with the same inoculum of the isogenic glycopeptide-resistant derivative NM67, CFU initially decreased, resulting in the elimination of the mutant in three out of seven cages. In the four cages in which NM67 survived, it partially regained wild type characteristic, including thinning of the cell wall, reduced N-acetylglucosamine uptake, and increased hemolysis; however, the survivor also became teicoplanin hypersusceptible. The elimination of the teicoplanin-resistant mutant and selection of teicoplanin-hypersusceptible survivor in the tissue cages indicated that glycopeptide resistance imposes a fitness burden on S.aureus and is selected against in vivo, with restoration of fitness incurring the price of resistance loss.

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