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Year : 2004  |  Volume : 22  |  Issue : 2  |  Page : 112--114

The resistance of pseudomonas aeruginosa strains to fluoroquinolone group of antibiotics

U Algun, A Arisoy, T Gunduz, B Ozbakkaloglu 
 Department of Microbiology, Celal Bayar University, Manisa, India

Correspondence Address:
T Gunduz
Department of Microbiology, Celal Bayar University, Manisa


Fluoroquinolones are antibiotics that are very effective against many gram negative microorganisms, including P. aeruginosa. However, resistance to these antibiotics has been reported in recent years as well. In this study, the sensivity of 136 P. aeruginosa strains, isolated from various clinical materials, to fluoroquinolones has been investigated. The lowest resistance rate was in ciprofloxacin with 12.5%. The resistance rates of the others were as follows: norfloxacin 14.7%, levofloxacin 16.9%, ofloxacin 19.9% and pefloxacin 28.7%. The 88.2% of the resistant strains to all fluoroquinolones were originated from intensive care unit.

How to cite this article:
Algun U, Arisoy A, Gunduz T, Ozbakkaloglu B. The resistance of pseudomonas aeruginosa strains to fluoroquinolone group of antibiotics.Indian J Med Microbiol 2004;22:112-114

How to cite this URL:
Algun U, Arisoy A, Gunduz T, Ozbakkaloglu B. The resistance of pseudomonas aeruginosa strains to fluoroquinolone group of antibiotics. Indian J Med Microbiol [serial online] 2004 [cited 2020 Sep 22 ];22:112-114
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P. aeruginosa, is one of the most important microorganisms which causes problems clinically as a result of its high resistance to antimicrobial agents. Though rare in the normal flora of humans, it is isolated frequently from patients with burns, cystic fibrosis and neutropenia.[1] Nalidixic acid, the first quinolone used in the treatment of urinary system infections, has a narrow influence spectrum with high resistance rate. After 1980s, it has been discovered that adding fluorine atom and piperacine ring to its structure caused the influence spectrum to widen. However, resistance to these antimicrobial agents has been reported as well.[2] In the present study, the resistance status of P. aeruginosa strains, isolated from various clinical materials, to fluoroquinolones was investigated.

 Materials and Methods

A total of 136 clinical samples [ear swabs (40), endotracheal aspirates (12), blood (22), abscess (14), urine (10), vessel catheter (8), sputum (6) and wound (4)] from in and out-patients were cultured in 5% blood agar and EMB (eosine methylene blue) agar and after 18-24 hours of incubation at 37C, blue-green pigmented big colonies with typical aromatic odour and positive oxidase test were suspected as P. aeruginosa. API ID 32 GN (BioMerieux-France) kit was used for identification. One sample was studied from each patient. The sensivity of 136 P. aeruginosa strains to ciprofloxacin (CIP, 5mg), ofloxacin (OFX, 5mg), levofloxacin (LEV, 5mg), norfloxacin (NOR, 10mg) and pefloxacin (PEF, 5mg) was investigated by Kirby-Bauer disc diffusion method according to NCCLS (National Commitee for Clinical and Laboratory Standards) criteria.[3] The statistical analysis was performed by chi-square test and Fischer's t test.


Eighty-eight (64.7%) of the patients from whom isolates were obtained were males and 48 (35.3%) were females. Eighty-three (61%) of the isolates were obtained from in-patients while 53 (39%) were from out-patients. Most of the materials (47.2%) were from intensive care unit (ICU). The resistance status of P.aeruginosa strains to fluoroquinolones are shown in the [table]. The strains isolated from in-patients were significantly more resistant to all fluoroquinolones when compared with out-patient materials. P.aeruginosa strains isolated from ICU were more resistant to all fluoroquinolones in comparison with other clinics (p=in vitro.[4] Their effect against gram negative bacilli, including P. aeruginosa, is one of their most important features. The main mechanism in the development of resistance to fluoroquinolones is the decrease in binding of the target quinolones to enzymes because of changes in DNA gyrase enzyme and / or the topoisomerase enzyme (s). The nucleotide and amino acid sequence of gyrA, gyrB, parC and parE genes needed for the synthesis of DNA topoisomerase are very similar to those of DNA gyrase enzyme. Mutations occur in gyrA and parC genes. This kind of resistance seen with P. aeruginosa, E. coli and H. Influenzae, is usually against all quinolones. Resistance due to mutations of gyr B is less common and may not be against all quinolones.[2] The second mechanism is the decrease in the amount of quinolones entering the cells because of the defective function of porine channels.[5] The third mechanism is the various efflux systems, localized in the membranes of many bacteria, including P. aeruginosa, which pump the drug out of the bacteria.[4],[5]

In various studies investigating the resistance of P. aeruginosa to ciprofloxacin, the proportion was reported to be 0% to 89%. In a study from Spain, ciprofloxacin resistance, evaluated in 1014 P.aeruginosa strains obtained from 136 different hospitals, was found to be 23%,[6] whereas in France the proportion evaluated in 738 P.aeruginosa strains from 15 education hospitals was 40%.[7] In the present study, overall ciprofloxacin resistance was 12.5%, while it was 23.4% in the ICU, 1.9% in other clinics and 2.8% in out-patient department.

Levofloxacin has some added advantages such as its effectiveness against gram positive bacteria, its ability to concentrate more in the urine and its use of daily single dose. Yamane et al[8] reported that the activity of levofloxacin was generally two-fold greater than ofloxacin and was equal to or slightly less potent than ciprofloxacin. Levofloxacin resistance was reported in 36% of strains isolated from nosocomial infections.[9] We found the overall levofloxacin resistance to be 16.9%, but it was higher (29.7%) in ICU. Ofloxacin resistance has been reported to be 31% and 62.5% in different studies.[4],[10] In this study, the overall ofloxacin resistance was 19% while it was 32.8% in ICU. Pefloxacin seems to have highest resistance rate (28.7%) which was higher in ICU (42.2%). It has been reported to be as high as 74% in P.aeruginosa strains isolated from urine.[11]

More resistant strains in the ICU and increasing morbidity and mortality with a high multi-resistance among bacteria seem to be an important problem. Because of the increasing fluoroquinolone resistance in many hospitals, empirical usage is either abandoned or restricted in order to take the developing resistance rates under control.[12] In a study where the resistance rates of various antimicrobials against P.aeruginosa isolates were compared, the resistance of ofloxacin was 55% in 1996, whereas it declined to 49% in 2000.[13]

We found lower resistance rates when compared with similiar studies. The explanation of this may be that our hospital is new and relatively smaller with fewer patient beds and that it is easier to implement antibiotic policy within the hospital. However, the fact that most of the resistant strains were isolated from the ICU and that 15 of 17 strains resistant to all fluoroquinolones were isolated from the ICU is worrisome for the future. Development and application of antimicrobial usage policies with the aid of Hospital Infection Control Committee will decrease the apperance and spread of nosocomial infection epidemics.


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