Please use this identifier to cite or link to this item: http://gukir.inflibnet.ac.in:8080/jspui/handle/123456789/5288
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dc.contributor.authorKelmani Chandrakanth R
dc.contributor.authorRaju S
dc.contributor.authorPatil S.A.
dc.date.accessioned2020-06-12T15:06:44Z-
dc.date.available2020-06-12T15:06:44Z-
dc.date.issued2008
dc.identifier.citationCurrent Microbiology , Vol. 56 , 6 , p. 558 - 562en_US
dc.identifier.uri10.1007/s00284-008-9123-y
dc.identifier.urihttp://gukir.inflibnet.ac.in:8080/jspui/handle/123456789/5288-
dc.description.abstractAminoglycoside resistance in six clinically isolated Staphylococcus aureus was evaluated. Genotypical examination revealed that three isolates (HLGR-10, HLGR-12, and MSSA-21) have aminoglycoside-modifying enzyme (AME) coding genes and another three (GRSA-2, GRSA-4, and GRSA-6) lacked these genes in their genome. Whereas isolates HLGR-10 and HLGR-14 possessed bifunctional AME coding gene aac(6?)-aph(2?), and aph(3?)-III and showed high-level resistance to gentamycin and streptomycin, MSSA-21 possessed aph(3?)-III and exhibited low resistance to gentamycin, streptomycin, and kanamycin. The remaining three isolates (GRSA-2, GRSA-4, and GRSA-6) exhibited low resistance to all the aminoglycosides because they lack aminoglycoside-modifying enzyme coding genes in their genome. The transmission electron microscopy of the three isolates revealed changes in cell size, shape, and septa formation, supporting the view that the phenomenon of adaptive resistance is operative in these isolates. © 2008 Springer Science+Business Media, LLC.en_US
dc.titleAminoglycoside-resistance mechanisms in multidrug-resistant Staphylococcus aureus clinical isolatesen_US
dc.typeArticle
Appears in Collections:1. Journal Articles

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