Analysis of Amikacin-Resistant Pseudomonas aeruginosa Developing in Patients Receiving Amikacin
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• During a 36-month period, 28 patients treated for infections due to amikacin-susceptiblePseudomonas aeruginosasubsequently 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 Paeruginosaisolates 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 Paeruginosawas reduced. A major mechanism of in vivo development of amikacin resistance in Paeruginosais 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 Med1989;149:630-634)Keywords:
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This study in 12 cancer treatment centres across the United States was designed to evaluate the potential for increased resistance to amikacin with unrestricted use. An initial 3-month baseline period during which the use of amikacin was restricted and that of tobramycin and gentamicin unrestricted was followed by a period of at least 12 months when amikacin was the primary aminoglycoside. Resistance of Gram-negative bacilli to these aminoglycosides from hospitalized patients was monitored and compared for the two periods. Amikacin usage increased from a mean of 20·1 to a mean of 83·9% of aminoglycoside patient-days. A reduction in the use of tobramycin and gentamicin were observed with means of 66·1 and 10%, and 13·9 and 6·1%, respectively for the two periods. Resistance to amikacin was 0·85% at baseline and 1·3% at end-point which was not clinically significant (P = 0·614). Baseline resistance was 6·5 and 7·6%, while final resistance was 2·6 and 4·8%, respectively for tobramycin (P = 0·001) and gentamicin (P = 0·052).
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Apalcillin, at concentrations of 75, 150, 300, and 600 micrograms/ml, was combined in vitro with amikacin, gentamicin, netilmicin, or tobramycin. Incubation at 37 degrees C resulted in an apalcillin concentration-dependent and time-dependent decrease of aminoglycoside activity of up to 60%. Amikacin was the most stable and tobramycin was the least stable aminoglycoside under the conditions tested.
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A total of 319 clinical isolates known to be resistant to one or more aminoglycoside antibiotics were tested for their susceptibility to 10 aminoglycosides. The percentages of isolates found by an agar dilution method to be susceptible were: amikacin, 83.7%; tobramycin, 41.4%; butirosin A, 33.2%; dideoxykanamycin B, 32.6%; gentamicin C, 27.3%; lividomycin A, 17.6%; neomycin B, 10.7%; paromomycin, 10.3%; kanamycin A, 10.0%; and ribostamycin, 7.2%. The effectiveness of the antibiotics was related to their degree of resistance to bacterial enzymes; e.g., of the nine enzymes known to inactivate antibiotics containing 2-deoxystreptamine, amikacin was affected by one enzyme, tobramycin by five, and gentamicin and kanamycin by six. Examination of cell-free extracts from the 52 strains resistant to amikacin revealed that only four contained the amikacin-inactivating enzyme aminoglycoside-6'-acetyltransferase, a finding indicating that this mechanism of resistance is rare. Other experiments suggest that most amikacin-resistant strains, which are almost invariably resistant to all aminoglycosides, lack the ability to accumulate effectively either amikacin or presumably the other antibiotics intracellularly.
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Amikacin (Amikin - Mead Johnson) is an injectable aminoglycoside antibiotic. Unlike gentamicin (Cidomycin, Genticin) and tobramycin 1 (Nebcin), which are unmodified fermentation products, amikacin is a semi-synthetic derivative of kanamycin A.
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A sensitive and selective colorimetric biosensor for determination of gentamicin, amikacin and tobramycin was proposed with the unmodified gold nanoparticles (GNPs) as the sensing element. Gentamicin, amikacin and tobramycin can rapidly induce the aggregation of gold nanoparticles and is accompanied by a color change from red to blue. The concentration of gentamicin, amikacin and tobramycin can be determined by using UV-Vis spectrometer. The experimental parameters were optimized with regard to pH, incubation time and the concentration of the GNPs. Under optimal experimental conditions, the linear range of the colorimetric sensor for gentamicin/amikacin/tobramycin were 2.67–33.93 ng mL -1 , 13.33–66.67 ng mL -1 and 20–180 ng mL -1 , respectively. The corresponding limit of detection (3σ) was 0.354 ng mL -1 , 0.999 ng mL -1 and 0.579 ng mL -1 , respectively. This assay was simple and used to detect aminoglycoside antibiotics in milk and medicine products.
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