meropenem inhibits acinetobacter baumannii biofilm formation by downregulating pgaa gene expression

Introduction: acinetobacter baumannii is the cause of nosocomial infections, primarily in intensive care units. the pgaa gene plays an essential role in biofilm formation, making it a promising target for developing new strategies to tackle a. baumannii infections. this study investigated the meropenem effect on pgaa gene expression and biofilm formation in a. baumannii. methods: over five months, 50 urine samples were taken from patients receiving medical care in the intensive care unit, of which 20 a. baumannii isolates were detected. antibiotic susceptibility was determined with meropenem, imipenem, trimethoprim/sulfamethoxazole, ceftazidime, ciprofloxacin, tetracycline, amikacin, as well as gentamicin disks by the kirby-bauer method. the minimum inhibitory concentration (mic) of meropenem was determined using the microdilution method. biofilm formation was investigated through the tissue culture plate (tcp) technique and imaged using an atomic force microscope (afm). reverse transcriptase polymerase chain reaction (rt-pcr) determined the expression level of the pgaa gene. results: antibiotic susceptibility testing revealed that all a. baumannii isolates were resistant to meropenem, imipenem, ciprofloxacin, and amikacin, and 71.42% were resistant to tetracycline. the mic for meropenem could not be determined for isolates. meropenem prevented biofilm formation in more than 70% of the isolates, and afm imaging revealed thin biofilms. the rt-pcr showed that exposure to meropenem significantly decreased the pgaa expression gene in over 95% of the isolates (p < 0.0001). conclusion: meropenem inhibited biofilm formation in most a. baumannii isolates by downregulating the pgaa expression, suggesting a potential role in preventing a. baumannii infections by reducing biofilm formation