الفهرس 
Review of the LiteratureOnly 14 pages are availabe for public view
 |  | from | 32 |  |  |
| | | from | 32 | | |
Abstract
According to the CDC, Pseudomonas aeruginosa is the fifth most common pathogen among hospital microorganisms which causes 10% of all hospital aquired infections. P. aeruginosa is an opportunistic pathogen that causes severe infections in immunocompromised patients including cancer patients, cystic fibrosis patients, patients with human immunodeficiency virus infections and patients with severe burn wounds.
P. aeruginosavirulence depends on a large number of virulence factors both cell-associated; pili, flagella, lipopolysaccharide, etc and extracellular virulence factors; exotoxin A,exoenzyme S, elastase, biofilm, etc.
One of the reasons that P. aeruginosa is a successful opportunistic pathogen is its ability to form biofilm causing chronic infections and high level of drug resistance.
Biofilms are not unstructured, homogeneous deposits of cells and accumulated slime, but complex communities of surface-associated cells enclosed in a polymer matrix containing open water channels. It has been involved in almost every human infection and is particularly resistant to many antibiotics and can persist despite sustained host defences. Biofilm causes considerable problems in medical and industrial settings, because bacteria in biofilms can resist antibiotic treatment, host immune responses, and biocide treatment.
The biofilm matrix contributes to the overall architecture and the resistance phenotype of biofilms.This matrix is a mixture of polysaccharides, extracellular DNA (eDNA), and proteins, whichfunction a glue holding the microbial cells together.
Three polysaccharides matrix (Psl, Pel and alginate) have been identifiedin P. aeruginosamatrix.
Quorum sensing (QS) system has been known for its importance in regulating the expression of numerous cellular and secreted virulence factors of P. aeruginosa, including biofilm formation.
The Las QS system was found to be essential for creation of mature, differentiated biofilms as the lasI mutant biofilm was flat and undifferentiated, in addition to being structurally altered, the mutant biofilm was functionally impaired in its ability to resist antibiotics.
This study aimed to show the ability of P. aeruginosa to produce biofilm, its antibiotic resistance and the correlation between Las R gene and biofilm formation in different P. aeruginosa clinical isolates.
In this study, thirty isolates of P. aeruginosa were obtained from burn and wound infected patients attending Ain Shams University Hospitals. Out of thirty, 18(60%) were isolated from burn wounds, 12(40%) were isolated from surgical wounds.
All P. aeruginosa strains were confirmed by standard microbiological procedures according to (Collee et al., 1996) based on colonial morphology, microscopic examination of Gram stained films and biochemical reactions of the isolated organisms.
Antibiotic sensitivity of the isolated bacteria was done using disc diffusion method, then isolated bacteria were tested for their ability to form biofilm using microtiter plate method.
Finally all samples were tested for the presence of quorum sensing LasR gene using conventional PCR technique.
It was found that:
1. P. aeruginosa strains showed a high resistance to ticarcillin /clavulonate 86.7% followed by ceftazidime 33.3%, amikacin 26.7%, levofloxacin 23.3% and Imipenem 20%.
2. All P. aeruginosa isolates were biofilm producers. Out of thirty isolates; seven isolates (23.3%) were strong biofilm producers, fourteen (46.7%) were moderate biofilm producers and nine (30%) were weak biofilm producers.
3. There is a statistically significant relationshipbetween Levofloxacin sensitivity and biofilm forming ability in these P. aeruginosa strains.
4. All P. aeruginosa isolates had Las R gene which showed the importance of Las R gene in biofilm producing ability in P. aeruginosa.