Investigation of antibiotic susceptibility profile and minimal inhibitor concentration changes in Pseudomonas aeruginosa isolates that exposed to subinhibitory concentrations of antibiotic
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. |
Keywords
References
- 1. Nagelhus EA, Ottersen OP. Physiological roles of aquaporin-4 in 1. Villegas MV, Hartstein AI: Acinetobacter outbreaks 1977-2000. Infect Control Hosp Epidemiol. 2003; 24(4): 284-295. DOI:10.1086/502205.
- 2. Ozer B, Inci M, Duran N, Kurtgoz S, Alagoz G, Pasa O, Kılınc C. Comparison of antibiotic resistance of Acinetobacter and Pseudomonas aerugınosa strains isolated from intensive care units with other clinics. Acta Medica Mediterranea. 2016; 32: 117.DOI: 10.19193/0393-6384_2016_1_18
- 3. Blondell-Hill E, Henry DA, Speert DP: Pseudomonas. Murray PR, Baron EJ, Jorgensen JH, Landry ML, Pfaller MA (eds). Manual of Clinical Microbiology, 9th ed., Vol 1, p.734-48, ASM Press, Washington, DC (2007).
- 4. Corbella X, Pujol M, Ayats J, Sendra M, Ardanuy C, Domínguez MA, Linares J, Ariza J, Gudiol F. Relevance of digestive tract colonization in the epidemiology of multiresistant Acinetobacter baumannii. Clin Infect Dis. 1996; 23: 329–334. DOI. 1058--4838/96/2302
- 5. Clinical and Laboratory Standards Institute. Performance standards for antimicrobial susceptibility testing. 22nd Informational Supplement, M100-S22, 2012. CLSI, Wayne, PA.
- 6. Ozturk R. Resistance development mechanisms against antimicrobial drugs and Today Resistance Status. Infections Symposium. 2002; 31: 83-100.
- 7. Livermore DM. Beta-Lactamases in laboratory and clinical resistance. Clin. Microbiol. Rev. 1995; 8(4): 557-584.
- 8. Kose S, Atalay S, Odemis I, Adar P. Antibiotic Susceptibility of Pseudomonas aeruginosa Strains Isolated from Various Clinical Specimens. Ankem. 2014; 28(3): 100-104.
Details
Primary Language
English
Subjects
Health Care Administration
Journal Section
Research Article
Publication Date
September 30, 2018
Submission Date
August 8, 2018
Acceptance Date
September 20, 2018
Published in Issue
Year 2018 Volume: 5 Number: 9