Prevalence of OXA carbapenemases genes in multidrug resistant Acinetobacter and Pseudomonas spp

Abstract

Summary Pseudomonas aeruginosa (P. aeruginosa) and Acinetobacter baumannii (A. baumannii) are both characterized by innate resistance mechanisms against multiple antimicrobials. Furthermore, these pathogens may easily acquire new resistances by different mobile elements, thus making extremely challenging the choice of appropriate antibiotic therapy. In this study, 70 clinical isolates provided from ICU El-Demardash hospital. All bacterial isolates identified by the standard microbiological methods including cultural morphology, microscopic examination and biochemical tests and vitek II cards. these indicated that 25 P. aeruginosa and 25 as A. baumanniii. According to patients’ gender Among P. aeruginosa, 18 (72%) were males and 7 (28%) were females while in A. baumannii17 (72%) were females and 8 (28%) were males According to age, the isolates were divided into3 groups: 1 - 14 year, 14 - 30and > 45 years. The high percentage of isolates was found in > 45 and1-14 years were 48 and 52% in P. aeruginosa and A. baumanni, respectively. the highest number of P. aeruginosa isolates were recovered from wound (52%) followed by blood (16%). Lower percentages were detected in urine, sputum, CSF and plural fluid samples, 12, 12, 4 and 4%, respectively. blood isolates had the highest percentage in A. baumanni were 52% followed by 32 %, 12% and 4% were sputum, CSF and wound, respectively. Antibiotic sensitivity and minimum inhibitory concentration (MIC) for 18 different antibiotics (Ticarcillin, Ticarcillin /Clavulanic acid, Piperacillin, Piperacillin-Tazobactam, Ceftazidime, Cefepime, Meropenem, Amikacin, Gentamicin, Aztreonam, Imipenem, Meropenem, Tobramycin, Ciprofloxacin, Plefloxacin, Minocyclin, Rifampcin, Trimethothoprim/Sulfamethoxazole and colistin) were carried out against all both isolates using VITEK 2 and disck diffusion method. All isolates were resistant to all these tested antibiotics except they were sensitive to Colistin. By using PCR, different OXA genes were detected. In P. aeruginosa OXA group I and group II were detected in 44 and 52%, respectively. These 2 groups were coexisted in 8 isolates. While group III, OXA51, OXA23, OXA24 and OXA58 were totally absent. While for A. baumanni, all isolates were found to have OXA51 (100%), however for OXA23, OXA24 and OXA58 were detected in 88, 60 and 60%, respectively. Where (OXA51, OXA23 and OXA24), (OXA51, OXA23and OXA58), (OXA51 and OXA23) and (OXA51and OXA58), were coexisted in 5, 3, 4 and 1 isolates, respectively. Both P. aeruginosa and A. baumannii clinical isolates were able to form biofilm with different extents. Only 44% of P. aeruginosa showed strong biofilm formation, while moderate and weak biofilm formation were detected in 28 and 12% of the isolates, respectively. No biofilm formation was detected in16% of P. aeruginosa isolates. In A. baumannii 76 and 24% were weak and moderate forming biofilm, respectively. All isolates were sensitive to colistin at ≥ 0.5mg according to Vitek 2, the MIC results using the Microtiter plate confirmed that a total 7 isolates (3 P. aeruginosa and 4 A. baumannii) were resistant to colistin at ≤ 4 mg, respectively.