Introduction: Streptococcus pneumoniae is a major Gram-positive pathogen responsible for pneumonia, bactermia, otitis media, and meningitis leading to considerable morbidity and mortality among children and elderly individuals. The primary goals of antibiotic treatment of respiratory tract infections are clinical efficacy of treatment, pathogen eradication, and prevention of resistance development. Resistance to fluoroquinolones in S. pneumoniae arises in a stepwise fashion and results from alterations in the target binding site due to the acquisition of spontaneous mutations in the quinolone resistance-determining regions (QRDRs) of the topoisomerase IV and DNA gyrase genes. Although mutations usually occur in the QRDRs of parC and gyrA, a role for mutations in the parE subunit in low-level resistance has been reported.
Aim of the work: The aim of this study was to determine the prevalence of fluoroquinolone resistance Streptococcus pneumoniae (FQRSP) and to examine the genetic relatedness of pneumococcal isolates with parE and gyrA genes mutations in different specimens in Sohag University Hospital.
Patients and Methods: This study was prospectively conducted over a period of 24 months between October 2015 and September 2017, at Sohag university hospital. During the study period, 78 patients hospitalized for a syndrome consistent with a diagnosis of community acquired pneumonia (CAP ) included in this study with a mean age of 34.5 years (range, 2 to 67), 60% of whom were males. A CAP syndrome was defined as a newly recognized pulmonary infiltrate together with 2 of the following findings: subjective fever or documented temperature 37.4 °C, increased cough, sputum production, or shortness of breath, pleuritic chest pain, confusion, rales, leukocytosis, (according to age) (1). Patients who had taken antibiotic treatment within 3 days prior to initial visit were excluded from this study.
Results: Our study illustrate the role of mutation in the gyrA&parE genes and the effect of mutations in the both genes in fluoroquinolone resistance among S. pneumoniae isolates.
Conclusion: The present study provide an opportunity to view the predominant mutations conferring reduced susceptibility to FQs in clinical pneumococcal isolates. There is a strong relationship between these mutations and decrese susceptibility to the most fameous FQs to some extent, although this varies between strains and for each drug.