Volume 6, Issue 2 And 3 (4-2018)                   JoMMID 2018, 6(2 And 3): 72-76 | Back to browse issues page

XML Print

Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Motevasel M, Haghkhah M. Antimicrobial Resistance Profiles and Virulence Genes of Pseudomonas aeruginosa Isolates Originated from Hospitalized Patients in Shiraz, Iran. JoMMID. 2018; 6 (2 and 3) :72-76
URL: http://jommid.pasteur.ac.ir/article-1-164-en.html
Department of Pathobiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
Abstract:   (1655 Views)
Introduction: Multidrug-resistant (MDR) Pseudomonas aeruginosa isolates are among the common cause of Nosocomial infections. In P. aeruginosa infections, several genes, mexA, and mexB are involved in resistance to antibiotics and pslA, pelA and brlR contribute to biofilm formation. This study aims to investigate the prevalence of these genes in P. aeruginosa isolates and to determine their relationship with biofilm formation, antibiotic resistant, pigment production, and source of infection. Methods: We collected 63 specimens out of 90 samples from patients hospitalized in a hospital affiliated to Shiraz University of Medical Sciences. The specimens belonged to 42 men and 21 women and included urine, sputum, wound, skin, blood, body fluid, and central venous blood (CVB). The samples were cultured on solid media and diagnosed according to standard phenotypic characteristics. Disk diffusion method was used to identify the clinical MDR P. aeruginosa isolates, and the genes pslA, pelA, brlR, mexA, and men were detected by PCR detected. Results: about 25.4% of the clinical isolates were MDR, i.e., resistant to three or more antibiotics. The prevalence of the genes in the clinical isolates was as follows: pslA (92.1%), pelA (68.3%), brlR (93.7%), mexA (95.2%) and mexB (50.8%). The highest and lowest prevalence of drug resistance belonged to ceftriaxone and amikacin, respectively. The highest MDR P. aeruginosa isolates originated from wound, urine and sputum specimens. Conclusion: The presence of MDR isolates correlated significantly with the patients’ gender, the origin of specimens, and bacterial pigment production.  In this study, the detected genes did not significantly correlate with the MDR features of the isolates. J Med Microbiol Infec Dis, 2018, 6 (2): 5 pages.
Full-Text [PDF 178 kb]   (330 Downloads)    
Type of Study: Original article | Subject: Anti-microbial agents, resistance and treatment protocols
Received: 2018/06/4 | Accepted: 2018/08/25 | Published: 2019/03/18

1. 1. Colvin KM, Irie Y, Tart CS, Urbano R, Whitney JC, Ryder C, et al. The pel and psl polysaccharides provide Pseudomonas aeruginosa structural redundancy within the biofilm matrix. Environ Microbiol. 2012; 14 (8): 1913-28. [DOI:10.1111/j.1462-2920.2011.02657.x]
2. Selim S, El Kholy I, Hagagy N, El Alfay S, Aziz MA. Rapid identification of Pseudomonas aeruginosa by pulsed-field gel electrophoresis. Biotechnol Biotechnol Equip 2015; 29 (1): 152-6. [DOI:10.1080/13102818.2014.981065]
3. Liao J, Sauer K. The MerR-like transcriptional regulator BrlR contributes to Pseudomonas aeruginosa biofilm tolerance. J Bacteriol. 2012; 194 (18): 4823–36. [DOI:10.1128/JB.00765-12]
4. Chambers JR, Liao J, Schurr MJ, Sauer K.BrlR from Pseudomonas aeruginosa is ac‐di‐GMP‐responsive transcription factor. Mol Microbiol. 2014; 92 (3): 471-87. [DOI:10.1111/mmi.12562]
5. Stewart PS. Mechanisms of antibiotic resistance in bacterial biofilms. Int Med Microbiol. 2002; 292 (2): 107-113. [DOI:10.1078/1438-4221-00196]
6. Stoodley P, Sauer K, Davies DG, Costerton JW. Biofilms as complex differentiated communities. Ann Rev Microbiol. 2002; 56 (1): 187-209. [DOI:10.1146/annurev.micro.56.012302.160705]
7. Mah T-FC, O'toole GA. Mechanisms of biofilm resistance to antimicrobial agents. Trends in Microbiol. 2001; 9 (1): 34-9. [DOI:10.1016/S0966-842X(00)01913-2]
8. Stewart PS, Costerton JW.Antibiotic resistance of bacteria in biofilms. The Lancet. 2001; 358 (9276): 135-8. [DOI:10.1016/S0140-6736(01)05321-1]
9. Byrd MS, Sadovskaya I, Vinogradov E, Lu H, Sprinkle AB, Richardson SH, et al. Genetic and biochemical analyses of the Pseudomonas aeruginosa psl exopolysaccharide reveal overlapping roles for polysaccharide synthesis enzymes in psland LPS production. Mol Microbiol. 2009; 73 (4): 622-38. [DOI:10.1111/j.1365-2958.2009.06795.x]
10. Friedman L, Kolter R. Genes involved in matrix formation in Pseudomonas aeruginosa PA14 biofilms. Mol Microbiol. 2004; 51 (3): 675-90. [DOI:10.1046/j.1365-2958.2003.03877.x]
11. Winn Jr W, Allen S, Janda W, Koneman E, Procop G, Schreckenberger P, Woods G. Koneman's Color Atlas and Textbook of Diagnostic Microbiology: Lippincott Williams & Wilkins; 6th editon. 2006.
12. Spilker T, Coenye T, Vandamme P, LiPuma JJ. PCR-based assay for differentiation of Pseudomonas aeruginosa from other Pseudomonas species recovered from cystic fibrosis patients. J Clin Microbiol. 2004; 42 (5): 2074-9. [DOI:10.1128/JCM.42.5.2074-2079.2004]
13. Wolfensberger A, Sax H, Weber R, Zbinden R, Kuster SP, Hombach M. Change of antibiotic susceptibility testing guidelines from CLSI to EUCAST: influence on cumulative hospital antibiograms. PLOS One. 2013; 8 (11): e79130. [DOI:10.1371/journal.pone.0079130]
14. Obritsch MD, Fish DN, MacLaren R, Jung R. National surveillance of antimicrobial resistance in Pseudomonas aeruginosa isolates obtained from intensive care unit patients from 1993 to 2002. Antimicrobial Agents and Chemoth.2004; 48 (12): 4606-10. [DOI:10.1128/AAC.48.12.4606-4610.2004]
15. Shahandashti EF, Molana Z, Asgharpour F, Mojtahedi A, Rajabnia R. Molecular detection of Integron genes and pattern of antibiotic resistance in Pseudomonas aeruginosa strains isolated from intensive care unit, Shahid Beheshti Hospital, North of Iran. Int J Mol Cell Med. 2012; 1 (4): 209-216.
16. Yayan J, Ghebremedhin B, Rasche K. Antibiotic resistance of Pseudomonas aeruginosa in pneumonia at a single university hospital center in Germany over a 10-year period. PLOS One. 2015; 10 (10): e0139836. [DOI:10.1371/journal.pone.0139836]
17. Yousefi S, Nahaei M, Farajnia S, Ghojazadeh M, Akhi M, Sharifi Y, Milani M, Ghotaslou R. Class 1 integron and imipenem resistance in clinical isolates of Pseudomonas aeruginosa: prevalence and antibiotic susceptibility. Iranian J Microbiol. 2010; 2 (3): 113-119.
18. Nikokar I, Tishayar A, Flakiyan Z, Alijani K, Rehana-Banisaeed S, Hossinpour M, Amir-Alvaei S, Araghian A. Antibiotic resistance and frequency of class 1 integrons among Pseudomonas aeruginosa, isolated from burn patients in Guilan, Iran. Iranian J Microbiol.2013; 5 (1): 36-41.
19. Burjanadze I, Kurtsikashvili G, Tsereteli D, Tsertsvadze E, Kekelidze M, Imnadze P, et al. Pseudomonas aeruginosa infection in an intensive care unit. Int J Infect Control. 2007; 3 (2).
20. Ghadaksaz A, Fooladi AAI, Hosseini HM, Amin M. The prevalence of some Pseudomonas virulence genes related to biofilm formation and alginate production among clinical isolates. J Appl Biomed. 2015; 13 (1): 61-8. [DOI:10.1016/j.jab.2014.05.002]
21. Magiorakos AP, Srinivasan A, Carey R, Carmeli Y, Falagas M, Giske C, et al. Multidrug‐resistant, extensively drug‐resistant and pandrug‐resistant bacteria: an international expert proposal for interim standard definitions for acquired resistance. Clin Microbiol Infect. 2012; 18 (3): 268-81. [DOI:10.1111/j.1469-0691.2011.03570.x]
22. Olayinka A, Onile B, Olayinka B. Prevalence of multi-drug resistant (MDR) Pseudomonas aeruginosa isolates in surgical units of Ahmadu Bello University Teaching Hospital, Zaria, Nigeria: an indication for effective control measures. Ann Afr Med, 2004, 3(1):13 -16.

Add your comments about this article : Your username or Email:

Send email to the article author

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.