Investigation of antibiotic susceptibility profile and minimal inhibitor concentration changes in Pseudomonas aeruginosa isolates that exposed to subinhibitory concentrations of antibiotic
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Abstract
Objective: During antibiotic use some of the bacteria in our flora can be affected by the used antibiotic in subinhibitory concentrations in addition to pathogenic microorganisms. The aim of this study to investigate in-vitro effects of subinhibitory concentrations antibiotic on antibiotic susceptibility profile of P.aeruginosa which can be found in normal flora and be a pathogenic bacteria.
Material and Method: The antibiotic effective concentrations decrease with distance from the antibiotic disc and growth-inhibition zone ends with the effect of the antibiotic falls to subinhibitory concentrations; and growth starts.We accepted this growth starting region as the area in which bacteria exposed to subinhibitory concentrations of antibiotic are located and we developed a model. We separetely exposed the standard P.aeruginosa strain to eight different antibiotics (amikacin, gentamicin, imipenem, meropenem, ceftazidime, cefepime, ciprofloxacin, colistin) for seven days in subinhibitory concentrations. P. aeruginosa strain is susceptible to these antibiotics and we monitored susceptibility and minimal inhibitor concentration changes. Moreover, we also made these procedures in 20 different clinical P.aeruginosa isolates.
Results: We observed that a resistance was developed in the standard P. aeruginosa strain starting second day of meropenem exposure, third day of ceftazidime exposure, fifth day of amikacin exposure and sixth day of gentamicin exposure. There was no resistance development after colistin, cefepime, ciprofloxacin, meropenem exposure but significant MIC value increases were detected. This resistance was not only against exposed antibiotic or antibiotic group but also against antibiotics in different antibiotic groups.
Conclusion: It was shown that especially subinhibitory concentrations using carbapenem and aminoglycoside antibiotics triggered resistance development against themselves more than other antibiotic groups. Use of colistin was not shown to cause cross resistance.
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