Sivanmaliappan (2011) suggest that Pseudomonas aeruginosa isresponsible for causing major tissue damage in the diabetic foot ulcerpatients. The major problem of P.Aeruginosa is the high level of resistance to broad spectrum ofantibiotics. The purpose of this study was to investigate the antimicrobialresistance and sensitivity of P.Aeruginosa isolates. The currentresearch study was done from june 2006 to April 2007 in the Department ofMicrobiolpogy, Dr N.G.
P Arts and Science College, Coimbatore. They investigate270 samples of pus collected from the foot ulcer of diabetic patients. For theconfirmation purposes first of all the collected samples were gram stained andthen cultured after then the antimicrobial sensitivity to 15 differentantibiotics were done. Out of all 270 samples (14.28%) 18 strains of P. aeruginosa were investigated.
Totalof the strain shows resistance ofdifferent degree to different antibiotics. Among all the isolates 55.5% showsmultidrug resistance which were resistant from 8 to 11 antibiotics.
The P.aeruginosa isolates were sensitiveonly to ciprofloxacin, cefotaxime but 100% resistant to ampicillin,erythromycin, norfloxacin and cefoperazone by disk diffusion method.Vaziri (2011) suggested that theopportunistic pathogens Pseudomonasaeruginosa can cause mainly the nosocomial infections. For the treatment ofp.aeruginosa the Aminoglycosides arebest option.
The drug modifying enzymes is commonly inactivated byAminoglycoside. The main objective of the current study was to investigate theexistence of aminoglycosides resistance and prevelance of four main modifying enzyme genes (aac (6′)-I, aac (6′)-II, aph (3′)-VI, ant(2″)-I) in P. aeruginosa in Iran.A total of 250 P. aeruginosa isolateswereisolated from different hospital in seven cities of Iran. With the help of diskdiffusion method and E-test the antimicrobial sensitivity of all the 250isolates were determined while PCR were used for the identification of thepresence of modifying enzyme. The P.aeruginosarate of resistance was 24% toward imikacin, 38% to tobramycin while 43 % togentamicin with the help of using disk diffusing method.
To investigate that genes aac (6′)-II was mostly found in phenotypic resistant isolatesfollowed by ant (2″)-1, aac (6′)-I, aph(3′)-VI. The resistance toAminoglycoside is a main problem of P. aeruginosain Iran.
Therefore, there is considerable local surveillance of aminoglycosideresistance. Paterson (2006) showedsignificance of Gram-negative rods infections as they are the main cause ofinfection in developing countries. High death rates have been linked withinfection caused by Gram-negative bacteria. Martínez(2008) studied about the P. aeruginosahabitat as they inhabits in moist and humid envoirnment.
Its flexible nature andresistance to antibiotics make it easy it to live on a broad range of naturaland artificial setting such as surfaces in medical amenities. Life threatening P. aeruginosa infections is oftennosocomial, and all are associated with weakened host defenses. Drug resistanceresults in extended hospital stay of patients and increased in healthexpenditures. Maragakiset al. (2008) workedon modifying enzymes as they are the most general mechanism of amino glycosideresistance.
Aminoglycosides resistance mechanism includes modification ofenzymes, lack of permeability, efflux pump, bio-film formation, and methylation16s rRNA. Amino glycoside resistance genes are positioned on mobile geneticelements which could easily spread among rest of bacteria. Colistin is the onlytherapy for P. aeruginosa infections. Studies showed that among 161strains of P.
aeruginosa (54.39%) were resistant to as a minimum threeof the antimicrobial groups amongst piperacillin-tazobactam, ceftazidime,aminoglycosides, fluoroquinolones, carbapenems, and colistin. Breidensteinet al. (2008) reported high resistance tociprofloxacin associated with Fluoroquinolones genes was detected in Centre forMicrobial Diseases and Immunity Research, University of British Columbia,Canada. Drlica and Zhao (2007) revealed that among fluoroquinolones, the twomain antibiotics ciprofloxacin and levofloxacin are generally used in thetreatment of P.
aeruginosa infection. Poirel, Cattoir andNordmann. (2012) worked on the resistance tofluoroquinolones as it is mediated by the production of Qnr proteins thattargets DNA Gyrases.Spanish research evaluated that ant (2″)-Ia geneoccurred commonly among P. aeruginosa strains round about 65.0% and28.0% of tested isolates in Iranian studies.
Shahcheraghi (2008) worked on ESBL-positive isolates. These isolates showedMICs i.e 4?g/ mL for different drugs. These isolates were grown in LB broth at37°C all night later DNA was extracted by extraction kit. After extraction PCR was carried out in which specific primersand annealing temperature for amplifying the blaSHV, blaTEM, blaPER-1, andblaCTX-M1 and blaVEB-1 genes were used the results showed that K. pneumoniae containing the blaSHV,blaCTX-M and blaTEM genes and P.
aeruginosa containing the blaPER gene. Reller et al. (2009) showed significance of antimicrobialsusceptibility testing in microbiology laboratory as it is use to verifysusceptibility in order to choose empirical antimicrobial agents and toidentify resistance in individual bacterial isolates by Disk diffusion test. Khuntayaporn et al.
(2012) reportedthat drug resistance among pathogens has emerged an important problem incurrent medicine all over the world. Improper use of antibiotic induced aselective pressure on the microorganism which results in development ofantimicrobial resistance.