Investigation of antibiotic susceptibility profile and minimal inhibitor concentration changes in Pseudomonas aeruginosa isolates that exposed to subinhibitory concentrations of antibiotic

Yıl 2018, Cilt: 5 Sayı: 9, 312 - 319, 30.09.2018

Cetin Kilinc , Ridvan Guckan Umut Safiye Say Coskun

https://doi.org/10.17546/msd.452046

Öz

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.

Anahtar Kelimeler

Subinhibitory concentrations, P. aeruginosa, antibiotic susceptibility, MIC value changes

Kaynakça

• 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.
• 9. Livermore DM. Multiple mechanisms of antimicrobial resistance in Pseudomonas aeruginosa : Our worst nightmare? Clin Infect Dis. 2002; 34: 634-640. DOI:10.1086/338782
• 10. Kohler T, Hamzehpour M, Epp SF, Pechere JC. Carbapenem activities against Pseudomonas aeruginosa: Respective contributions of OprD and efflux systems. Antimicrob Agents Chemother. 1999; 43: 424-471.
• 11. Livermore DM. Of Pseudomonas, porins, pumps and carbapenems. J Antimicrob Chemother. 2001; 47: 247-250. DOI: 10.1093/jac/47.3.247
• 12. Hancock REW. ResistanceMechanism in Pseudomonas aeruginosa and other nonfermentative gram-negative bacteria. Clin Infect Dis. 1998; 27: 93-99.
• 13. Mesaros N, Nordmann P, Plésiat P, Roussel-Delvallez M, Van Eldere J, Glupczynski Y, et al. Pseudomonas aeruginosa: resistance and thera-peutic options at the turn of the new millenium. Clin Microbiol Infect 2007; 13(6): 560-578. DOI: 10.1111/j.1469-0691.2007.01681.x
• 14. Yuce A. Mechanisms of develop resistance to antimicrobial drugs. Klimik 2001; 14: 41-46.
• 15. Akalın H. Effect of Antibiotic Use in Microbiology Laboratory. Klimik 2001; 14(2): 62-65.
• 16. Gales AC, Jones RN, Turnidge J, Rennie R, Ramphal R. Characterization of Pseudomonas aeruginosa isolates: Occurrence rates, antimicrobial susceptibility patterns, and molecular typing in the global SENTRY Antimicrobial Surveillance Program, 1997-1999. Clin Infect Dis. 2001; 32: 146-155. DOI:10.1086/320186
• 17. Tanır G, Gol N. Antibiotic Resistance. Klimik. 1999; 12 (2): 47-54.
• 18. Giamarellou H. Multidrug-resistant gram-negative bacteria: how to treat and for how long. Int J Antimicrob Agents. 2010; 36: 50-54. DOI: 10.1016/j.ijantimicag.2010.11.014
• 19. Li J, Nation RL, Turnidge JD, Milne RW, Coulthard K, Rayner CR et al. Colistin: the re-emerging antibiotic for multidrug-resistant gram-negative bacterial infections. Lancet Infect Dis. 2006; 6: 589-601. DOI:10.1016/S1473-3099(06)70580-1
• 20. Bagge N, Schuster M, Hentzer M, Ciofu O, Givskov M, Greenberg EP et al. Pseudomonas aeruginosa biofilms exposed to imipenem exhibit changes in global gene expressi¬on and beta-lactamase and alginate production. Antimicrob Agents Chemother. 2004; 48(4): 1175-1187.
• 21. Hoffman LR, D’Argenio DA, MacCoss MJ, Zhang Z, Jones RA, Miller SI. Aminoglycoside antibiotics induce bacterial biofilm formation, Nature 2005;436(7054):1171-1175. DOI:10.1038/nature 03912
• 22. Stewart PS, Costerton JW. Antibiotic resistance of bacteriain biofilms. Lancet. 2001; 358: 135-138.
• 23. Flaherty JP, Weinstein RA. Nosocomial infection caused by antibiotic-resistant organisms in the intensive care unit. Infect Control Hosp Epidemiol. 1996; 17: 236-248.
• 24. Cipriani M, Giordano A, Magni A, Papa F, Filadoro F. Outer membrane alterations in Pseudomonas aeruginosa after five-day exposure to quinolones and carbapenems. Drugs Exp Clin Res. 1995; 21: 139-144.