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In-Vivo Acquisition of Two Different Types of Aminoglycoside Resistance by a Single Strain of Klebsiella pneumoniae Causing Severe Infection

BARBARA E. MURRAY, M.D.; and ROBERT C. MOELLERING Jr., M.D.
[+] Article and Author Information

Grant support: in part by the Daland Fund, American Philosophical Society, Philadelphia, Pennsylvania.

This work was presented at the 20th Interscience Conference of Antimicrobial Agents and Chemotherapy, New Orleans, Louisiana, 1980.

▸Requests for reprints should be addressed to Barbara E. Murray, M. D.; P.O. Box 20708, University of Texas Medical School; Houston, TX 77030.


Boston, Massachusetts


© 1982 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1982;96(2):176-180. doi:10.7326/0003-4819-96-2-176
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Multiple isolates of Klebsiella pneumoniae obtained from a patient were of the same biotype and capsular type and had three common plasmids. Initially, three isolates (from blood) were susceptible to aminoglycosides. Three other isolates, obtained after gentamicin treatment was begun, were susceptible to amikacin but resistant to gentamicin and tobramycin, produced 2″aminoglycoside adenylyltransferase, and had acquired an R-factor. A later isolate, obtained after amikacin therapy was begun, was susceptible to gentamicin and tobramycin, resistant to amikacin, was a small-colony variant, produced no aminoglycoside-modifying enzymes, and no longer contained the R-factor. In-vitro protein synthesis by ribosomes from this isolate was inhibited by amikacin whereas uptake of amikacin was markedly less than with previous isolates. Thus, this case illustrates the apparent in-vivo acquisition of plasmid-mediated resistance to gentamicin and tobramycin followed by loss of the plasmid and development of amikacin resistance due to decreased aminoglycoside uptake.

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