OBJECTIVES: Methicillin-resistant Staphylococcus aureus (MRSA) infection is increasing and causing global concern. The mechanism of MRSA resistance to amikacin is poorly understood. We report on the first matched-pair study to reveal that the phenotypic cell wall thickening of MRSA is associated with adaptive resistance to amikacin. METHODS: Two MRSA strains (CY001 and CY002) were isolated from blood and synovial fluid samples, respectively, from a 12-year-old male patient with osteomyelitis. The strains were subjected to a matched-pair study, including antimicrobial agent susceptibility determination, molecular typing, morphological observation and in vitro resistance induction. RESULTS: Both strains are Panton-Valentine leucocidin-positive, multilocus sequence type 59, staphylococcal cassette chromosome mec type IV and spa type 437 MRSA with identical PFGE profiles. The drug susceptibility spectra of the two isolates are similar. However, CY001 is resistant to amikacin (CY001-AMI(R); MIC = 64 mg/L), contrary to the susceptible CY002 (CY002-AMI(S); MIC = 8 mg/L). CY001-AMI(R) may have developed adaptive resistance, because it lacks aminoglycoside-modifying enzymes and has an altered growth curve. Interestingly, CY001-AMI(R) has a thicker cell wall (36.43 ± 4.25 nm) than CY002-AMI(S) (18.15 ± 3.74 nm) in the presence of amikacin at its MIC. The thickened cell wall can also be observed in an in vitro-induced strain (CY002-AMI(R)) in the presence of amikacin at its MIC (36.78 ± 3.41 nm); this strain was obtained by gradually increasing the amount of amikacin. However, the cell wall-thickened strains cultured in the presence of amikacin are still susceptible to vancomycin. CONCLUSIONS: Cell wall thickening is associated with adaptive resistance in MRSA and alternative antibiotics can be used to treat patients when adaptive resistance to amikacin has developed.
OBJECTIVES: Methicillin-resistant Staphylococcus aureus (MRSA) infection is increasing and causing global concern. The mechanism of MRSA resistance to amikacin is poorly understood. We report on the first matched-pair study to reveal that the phenotypic cell wall thickening of MRSA is associated with adaptive resistance to amikacin. METHODS: Two MRSA strains (CY001 and CY002) were isolated from blood and synovial fluid samples, respectively, from a 12-year-old male patient with osteomyelitis. The strains were subjected to a matched-pair study, including antimicrobial agent susceptibility determination, molecular typing, morphological observation and in vitro resistance induction. RESULTS: Both strains are Panton-Valentine leucocidin-positive, multilocus sequence type 59, staphylococcal cassette chromosome mec type IV and spa type 437 MRSA with identical PFGE profiles. The drug susceptibility spectra of the two isolates are similar. However, CY001 is resistant to amikacin (CY001-AMI(R); MIC = 64 mg/L), contrary to the susceptible CY002 (CY002-AMI(S); MIC = 8 mg/L). CY001-AMI(R) may have developed adaptive resistance, because it lacks aminoglycoside-modifying enzymes and has an altered growth curve. Interestingly, CY001-AMI(R) has a thicker cell wall (36.43 ± 4.25 nm) than CY002-AMI(S) (18.15 ± 3.74 nm) in the presence of amikacin at its MIC. The thickened cell wall can also be observed in an in vitro-induced strain (CY002-AMI(R)) in the presence of amikacin at its MIC (36.78 ± 3.41 nm); this strain was obtained by gradually increasing the amount of amikacin. However, the cell wall-thickened strains cultured in the presence of amikacin are still susceptible to vancomycin. CONCLUSIONS: Cell wall thickening is associated with adaptive resistance in MRSA and alternative antibiotics can be used to treat patients when adaptive resistance to amikacin has developed.
Authors: Edward M Schwarz; Alex C McLaren; Thomas P Sculco; Barry Brause; Mathias Bostrom; Stephen L Kates; Javad Parvizi; Volker Alt; William V Arnold; Alberto Carli; Antonia F Chen; Hyonmin Choe; Débora C Coraça-Huber; Michael Cross; Michelle Ghert; Noreen Hickok; Jessica Amber Jennings; Manjari Joshi; Willem-Jan Metsemakers; Mark Ninomiya; Kohei Nishitani; Irvin Oh; Douglas Padgett; Benjamin Ricciardi; Kordo Saeed; Parham Sendi; Bryan Springer; Paul Stoodley; Joseph C Wenke Journal: J Orthop Res Date: 2020-03-02 Impact factor: 3.102
Authors: Yanmin Hu; Alexander Liu; James Vaudrey; Brigita Vaiciunaite; Christiana Moigboi; Sharla M McTavish; Angela Kearns; Anthony Coates Journal: PLoS One Date: 2015-02-18 Impact factor: 3.240
Authors: Ana Belén García; José Manuel Viñuela-Prieto; Laura López-González; Francisco Javier Candel Journal: Infect Drug Resist Date: 2017-10-17 Impact factor: 4.003
Authors: Dagmar Chudobova; Simona Dostalova; Iva Blazkova; Petr Michalek; Branislav Ruttkay-Nedecky; Matej Sklenar; Lukas Nejdl; Jiri Kudr; Jaromir Gumulec; Katerina Tmejova; Marie Konecna; Marketa Vaculovicova; David Hynek; Michal Masarik; Jindrich Kynicky; Rene Kizek; Vojtech Adam Journal: Int J Environ Res Public Health Date: 2014-03-19 Impact factor: 3.390
Authors: Luis Zea; Michael Larsen; Frederico Estante; Klaus Qvortrup; Ralf Moeller; Sílvia Dias de Oliveira; Louis Stodieck; David Klaus Journal: Front Microbiol Date: 2017-08-28 Impact factor: 5.640