Fluoroquinolone-resistant strains in cirrhotic patients with spontaneous bacterial peritonitis: microbiological and molecular aspects

Objectives This study aimed to determine the causative bacterial agents of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis and to define antibiotic-resistance patterns in addition to identifying the genetic mutations in the quinolone resistance determining regions (QRDRs). Patients and methods Twenty milliliters of ascetic fluid was obtained from 51 patients with SBP. The antibiotic-sensitivity patterns of different strains were determined by the Kirby–Bauer method. Extracted bacterial DNA was used to determine the mutations in four different genes in QRDRs ( gyrA , gyrB , parC , and parE ) by sequencing after gene amplification by PCR. Results Gram-negative bacilli were detected in 60.7% of the patients. Escherichia coli was detected in 33.3% of the patients, and Staphylococcus aureus was detected in 21.6%. Gram-negative bacilli showed the best sensitivity to meropenem (90.3%), followed by amikacin (83.9%). Gram-positive cocci were sensitive to vancomycin and oxacillin at 90 and 80%, respectively. Fluoroquinolone resistance was detected in 27% of the bacterial strains. Mutations in the gyrA and parC genes were detected in quinolone-resistant strains (64.3 and 35.7%, respectively). Several mutations were found in the gyrA gene (Ser83Leu, Ser81Phe, and Ser-84Leu). Ser80Ile and Ser79Tyr mutations were detected in the parC gene. No mutation was detected in the parE gene. Conclusion Frequent use of antibiotics as prophylaxis against SBP leads to an increase in antibiotic resistance and changes the microbial pattern of causative agents. The gyrA gene mutation was the most common mutation detected in fluoroquinolone-resistant strains.