Study of Swarming Motility and pilB Gene among some Clinical isolates of Pseudomonas aeruginosa infections
- 1Department of Soil and Water, College of agriculture University of Sallahaddin Erbil,Kurdistan,Iran
Int. Res. J. Biological Sci., Volume 5, Issue (2), Pages 23-29, February,10 (2016)
This study was conducted to investigate the relationship between the swarming motility and pilB gene, twenty seven isolates of Pseudomonas aeruginosa were identified according to morphologicl, cultural and biochemical characteristics ,the isolates were from blood, Urine and Burn (nine isolates form each infection source). The sensitivity test of these isolates to the antibiotics was showed that all isolates were resistant of the used antibiotics except Amikacin, Tobramicin and Flucloxacillin. The ability of these isolates for swarming were tested the result showed that all isolates were able to swarming (dendritic swarming pattern). There was differences in swarming shapes among same infection and different source of infections on the semisolid surface (0.5-1)% agar plates, then these isolates were tested to evaluated the present pilB gene (type IV fimbrial biogensis protein) by PCR technique using specific primers, the result of PCR showed that this gene was moderately distribution (51.8)% in all studied isolates, since the result showed that this gene was widely disseminated in urine isolates 8/9(89)% while was 3/9(33.3)% in each of blood and burns isolates. These results clearly favored conclusion that differences swarming shapes in Pseudomonas aeruginos a from isolate to another may be the isolates have difference virolence factors for infection and it is important in all types of infections while prevalence of pilB gene perhaps related to infection site, there are no relationship between pilB gene presence and swarming motility.
- Alfred E. (2005)., Microbiological application in thelaboratory manual in general microbiology, 9th ed. MCGrow Hill company.,
- Briand Y. and Baysse C. (2009)., The pyocins ofPseudomonas aeruginosa., J. American Society forMicrobiology., 191(4), 2224-2233.
- Collee J.G., Fraser A.G., Marmion B.P. and Simmons A.(1996)., Mackie and McCartney Practical MedicalMicrobiology., 14th ed., Churchill Livingstone, NewYork, 413-423.
- Dekimpe V., Bord V. and Deziel E. (2009)., Revisitingthe quorum-sensing hierarchy in P. aeruginosa : Thetranscription regulator Rhl Rregulates Las R-specificfactors., Microbiol., 155, 712-723.
- Espinosa M. (2005)., Resident parking only:Rhamnolipids maintain fluid chnnels in biofilms., J.Bacteriol., 185, 699-700.
- Farrow M., Sund Z., Ellison M., Wade D., Coleman J.and Pesci E. (2008)., Functions independently of PqsR -Pseudomonas quinolone signal and enhances the rhl quorum-sensing system., J. Bacteriol., 190, 7043-7050.
- Asikyan M., Kus J. and Burrows L. (2008)., NovelProteins That Modulate Type IV Pilus RetractionDynamics in Pseudomonas aeruginosa., J. Bacteriol. 190,21, 7022–7034.
- Winstanley C. and Fothergill J. (2008)., The role ofquorum sensing in chronic cystic fibrosis Pseudomonasaeruginosa infections., Federation of EuropeanMicrobiological Societies. Ltd. 290, 1-9.
- Nordbring F. (1982)., Pseudomonas: Clinical problemsrelated to virulence factors and development ofresistance., Arch Intern Med., 142(11), 2010-1.
- Cruickshank R., Duguid P., Marmion P. and Swain H.eds. (1975)., Medical microbiology. 12th edition., NewYork. Churchill livingstone.
- Clinical and labratory standards institute CLSI (2009)., Performance Standards for Antimicrobial SusceptibilityTesting:., Wayne. 181, M100-S-18 EighteenthInformational Supplement.
- Tinaz G. and Ulusoy S. (2008)., Characterization of N-butnyol-L-homoserine lacton deficient clinicalisolates ofP.aeruginosa., J. Microbial pathogensis, 44, 13, 19.Microbiology.
- Mitov I.; Strateva T. and Markova B. (2010)., Prevalenceof virulence genes among bulgarian nosocomial andcystic fibrosis isolates of Pseudomonas aeruginosa., Braz.J. Microbiol., 41.
- Lister Ph.D.; Daniel J. Wolter M. and Nancy D. (2009)., Antibacterial Resistant Pseudomonas aeruginosa:Clinical Impact and Complex Regulation ofChromosomally Encoded Resistance Mechanisms., ClinMicrobiol Rev., 22(4), 582–610.
- Lambert R. (2002)., Mechanisms of antibiotic resistancein Pseudomonas aeruginosa., J of the royal society ofmedicine (section of paediatrics and child). 95(41), 22-26.
- Gad G., El Domany R., Zaki S. and Ashour H. (2007)., Characterization of Pseudomonas aeruginosa Isolatedfrom Environmental Samples in Minia Egypt:Prevalence, Antibiogram and Resistance Mechanisms, , J.Antimicrobial Chemotherapy, 5(60), 1010-1017.
- Tremblay J., Pascale A. and Richardsn X. (2007). Self -produced extracellular stimuli modulated the P.a, eruginosa swarming motility behaviour., EnvironmentalMicrobiology, 9(10), 2622-2630.
- Overhage J., Bains M., Brazas D. and Robert E. (2008)., Swarming of P. aeruginosa is acomplex adaption leadingto increased production of virulence factors and antibioticresistances., J.Bacteriol., 190(8), 2671-2679.
- Takahashi C., Nazawa T., Tanikawa T., Nakagawa Y.and Wakita J. (2007)., Sawrming of P. aeruginosa PAO1without differentiation into elongated hyperflageiiates onhard agar minimal medium., J.Bacteriology. 18(9), 3603-3612.
- Gupta R., Sannia S. and Kusum H. (2011)., Expression ofquorum sensing and virulence facters are interlinked in P., aeruginosa an in vitro approch, American J. ofBiochemical sciences, 3(2), 116-125.
- Tool A. and Kolter R. (1998)., Flagellar and twitchingmotility are necessary for Pseudomonas aeruginosbiofilm development., J. Molecular Microbiology, 30, 2,295-304.
- Bryan R., Kube D., Perez A., Davis P. and Prince A.(1998)., Overproduction of the CFTR R domain leads toincreased levels of asialoGM1 and increasedPseudomonas aeruginosa binding by epithelial cells., AmJ Respir Cell Mol Biol, 19, 269–277.
- Gupta P., Gupta R. and Harajai K. (2013)., Multiplevirulence factors regulated by quorum- sensing help inestablish coloniesation of urinary tract infections by P.aeruginosa urinary tract infections, , Indian Microbiol.,31, 29-33.
- Cornelila R., Nathalie G., Laurent M., Patrc M., Karin H.and Dieter H. (2010)., Geneticlly programmedautoinducer destructon reduces virulence gene expressionand swarming motility in P. aeruginosa., J. Microbiol,148, 923-932.
- Conrad J., Gibiansky M., Jin F., Gordon V., Motto D.,Mathewson M., Stopka W., Zelasko D., Shrout J. andWong G. (2011). F, lagella and Pili-Mediated NearSurfaceSingle-Cell Motility Mechanisms in P.aeruginosa., Biophysical Journal.100, 1608–1616.
- Nunn D., Bergman S. and Lory S. (1990)., Products ofthree accessory genes, pilB, pilC, pilD, are required forbiogenesis of P. aeruginosa pili. J. Bacterology, , 172(6),2911-2919.
- Tran V., Fleiszig M., David J. and Radke J. (2011)., Dynamic of flagellum-and pilus- mediated association ofP.aeruginosa with contact lens surfaces, , J.Environmental Microbiology, 77(11), 3644.
- Murray T. and Kazmierczak B. (2008)., Pseudomonasaeruginosa exhibits sliding motility in the absence of typelV pili and flagella., Journal of bacteriology. 190(8),2700-2708.
- Lanotte P., Watt S., Mereghetti L., Dartiguelongue N.,Rastegar Lari A., Goudeau A., Quentin R. (2004)., Genetic features of Pseudomonas aeruginosa isolatesfrom cystic fibrosis patients compared with those ofisolates from other origins, , J. Med. Microbiol., 53(1), 73-81.
- Raoof W. (2011)., Distribution of alg D, las B, pil B andnan1 genes among MDR clinical isolates of P.aeruginosa in respect to site of infection., Tikrit MedicalJournal, 17(2), 148.
- Anyan M., Amiri A., Harvey C. and Shrout J. (2014)., Type IV pili interactions promote intercellularassociation and moderate swarming of Pseudomonasaeruginosa., Proceedings of the National Academy ofPseudomonas aeruginosa. Proceedings of the NationalAcademy of Sciences, 111(50).