The resistance of pseudomonas aeruginosa strains to fluoroquinolone group of antibiotics.

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.

The effect of CagA status on response to Helicobacter pylori eradication therapy in Western Turkey

If cytotoxin-associated gene A (CagA) status affects the response rates of therapy, then it may be possible to predict Helicobacter pylori eradication rates. We aimed to evaluate the response to eradication treatment of H. pylori infection in CagA-positive and CagA-negative patients. A total of 184 patients (93 males, 91 females, mean age 42.6 ± 12.8 years) with H. pylori-positive chronic gastritis were studied. Subjects underwent a gastroscopy and biopsy specimens were taken from the gastric antrum, body, and fundus. Before the eradication therapy was given all patients were tested for CagA, TNF-alpha and gastrin levels. They were then prescribed lansoprazole (30 mg bid), clarithromycin (500 mg bid), and amoxicillin (1.0 mg bid) for one week. On the 8th week a second endoscopy was performed and further biopsy specimens were obtained from the same sites as in the initial endoscopy. One hundred and twenty-seven patients (69.1 percent) were found to be CagA positive and 57 patients (30.9 percent) were CagA negative. The total eradication rate was 82.6 percent. In the CagA-positive group this rate was 87.4 percent, and in the CagA-negative group it was 71.9 percent (P = 0.019). TNF-alpha levels were higher in the CagA-positive than in the CagA-negative group (P = 0.001). However, gastrin levels were not different between groups (P = 0.421). Our findings revealed that CagA-negative status might be a risk factor for failure of H. pylori triple therapies. The CagA pathogenicity island gives a growth advantage to H. pylori strains and has been associated with an increase in the inflammatory response at the gastric mucosal level. These properties could make CagA-positive H. pylori strains more susceptible to antibiotics