Introduction and Objectives: Chronic inflammation of middle ear is defined as chronic
suppurative otitis media (CSOM). Infection can cause complications such as mastoid abscess, deafness, meningitis, and intracranial abscess. The most common bacteria isolated from CSOM are P. aeruginosa, Staphylococcus aureus, Proteus mirabilis, Klebsiella pneumonia, and Escherichia coli [7, 8]. CSOM caused by p. aeruginosa usually is treated with topical ciprofloxacin. One of the mechanisms behind fluoroquinolone resistances (FRs) in bacteria such as P. aeruginosa, is mutations in gyrA and parC genes. Materials and Methods: A 24-year-old male patient with CSOM was reported. CSOM was prolonged for ten years and physician prescribed topical ciprofloxacin drops, pus suctioning and ear pH alteration. The treatment wasn’t effective and the patient came back to the clinic with relapse of suppurative otitis media. Antibiotics resistance investigated with disc diffusion method for ten antibiotics. We investigated three fluoroquinolone resistance genes including gyrA, parC, and nfxB by polymerase chain reaction (PCR) (Table 1). Results: P. aeruginosa was isolated as the cause of CSOM and the isolate was resistant to ciprofloxacin, aztreonam, imipenem, gentamicin, doripenem, cefepime, levofloxacin, amikacin and susceptible to colistin and ceftazidime. We observed two mutations in gyrA and eight mutations in nfxB genes. parC gene had no mutation. Conclusion: CSOM is a major public health concern associated with hearing loss. Mutations in gyrA, parC, nfxB genes are the main causes of fluoroquinolone resistance (FRs) including ciprofloxacin resistance [8]. Any change in the structure of the middle ear can cause CSOM. In our study, the first mutation in the gyrA gene (threonine 83 isoleucine) was similar to the study of Xiaoyan Yang et al. in 2015 [14]. The routine and primary treatment for CSOM did not seem sufficient and tympanomastoidectomy is suggested to be the best treatment approach for these patients.