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March 1989

Analysis of Amikacin-Resistant Pseudomonas aeruginosa Developing in Patients Receiving Amikacin

Author Affiliations

From the Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine (Drs Maloney, Rimland, and Stephens and Mss Terry and Whitney), and Veterans Administration Medical Center (Drs Maloney, Rimland, and Stephens and Ms Whitney), Atlanta.

Arch Intern Med. 1989;149(3):630-634. doi:10.1001/archinte.1989.00390030100019

• During a 36-month period, 28 patients treated for infections due to amikacin-susceptible Pseudomonas aeruginosa subsequently developed infections or colonization with amikacin-resistant P aeruginosa at the same site. Eleven amikacin-susceptible/-resistant pairs of isolates were analyzed for aminoglycoside-inactivating enzymes, plasmid profiles, cellular proteins, outer membrane proteins (OMPs), lipopolysaccharide (LPS) profiles, and amikacin uptake. While clearly distinct from isolates of other patients, sensitive and resistant isolates from the same patients were indistinguishable in plasmid profile, LPS profiles, and OMPs. These results suggest that the resistant P aeruginosa isolates were derived from the sensitive isolates. None of the resistant isolates produced enzymes known to inactivate amikacin. In nine of 11 resistant isolates tested, transport of amikacin into P aeruginosa was reduced. A major mechanism of in vivo development of amikacin resistance in P aeruginosa is alteration in permeability to amikacin, but the aquisition of plasmids or changes in OMPs or LPS profile may not account for this phenomenon.

(Arch Intern Med 1989;149:630-634)

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