JAC Advance Access originally published online on December 5, 2007
Journal of Antimicrobial Chemotherapy 2008 61(2):464-465; doi:10.1093/jac/dkm466
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Letters to the Editor |
Comment on: Acinetobacter spp. and time–kill studies
Division of Laboratory Medicine, Changi General Hospital, 2 Simei Street 3, Singapore 529889, Singapore
* Corresponding author. Tel: +65-68504934; Fax: +65-64269507; E-mail: thean_yen_tan{at}cgh.com.sg
Keywords: killing kinetics , antimicrobial interactions , synergism , Acinetobacter baumannii
We are in agreement with Dr Lopardo1 on various issues that affect antibiotic synergy testing, and in particular, on some of the intrinsic limitations of time–kill methodology. We also agree that the MIC is not a static parameter, and that one of the limitations of our study2 (as mentioned in the Discussion section) was that we were unable to measure antibiotic concentrations within the testing medium. It is worth noting that MIC endpoints are read after 18 h of incubation, while the combination testing was performed over 24 h. It is also a point of interest that at least two other studies3,4 using similar time–killing assays against Acinetobacter baumannii have demonstrated bacterial regrowth at concentrations of 1x MIC of colistin. It remains to be determined if this is a true phenomenon or a limitation of the testing methodology. With regard to the points raised regarding bacterial counts, we would like to point out that a turbidity equivalent to that of a 0.5 McFarland standard (barely detectable turbidity) equates to a bacterial count of 1.5 x 108 cfu/mL, and Acinetobacter species will achieve substantially higher turbidity levels in Mueller–Hinton broth over a 24 h growth period. Finally, in our study, synergy was defined as a
2 log10 decrease in cfu/mL for the antibiotic combination compared with its more active constituent. We were unable to ascribe the presence of synergy to one isolate in our study because the difference between the colony count in the combined antibiotic testing (
20 cfu/mL) and the most active single antibiotic tested (colistin;1200 cfu/mL) did not fulfil the study definition.
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T. Y. T. has received funding from Wyeth Pharmaceuticals for unrelated research studies. L. S. Y. N.: none to declare.
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1 Lopardo HA. Acinetobacter spp. and time–kill studies. J Antimicrob Chemother (2007) 61:464.
2
Tan TY, Ng LSY, Tan E, et al. In vitro effect of minocycline and colistin combinations on imipenem-resistant Acinetobacter baumannii clinical isolates. J Antimicrob Chemother (2007) 60:421–3.
3
Owen RJ, Li J, Nation RL, et al. In vitro pharmacodynamics of colistin against Acinetobacter baumannii clinical isolates. J Antimicrob Chemother (2007) 59:473–7.
4 Giamarellos-Bourboulis EJ, Xirouchaki E, Giamarellou H. Interactions of colistin and rifampin on multidrug-resistant Acinetobacter baumannii. Diagn Microbiol Infect Dis (2001) 40:117–20.[CrossRef][Web of Science][Medline]
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