Distribution and expression of T3SS virulence genes in Pseudomonas aeruginosa and its correlation with drug resistance / 临床检验杂志

ABSTRACT

Objective@#To investigate the distribution and expression of T3SS virulence genes in clinically isolated Pseudomonas aeruginosa (P. aeruginosa) strains and its correlation with drug resistance. @*Methods@#A total of 68 P. aeruginosa isolates were collected from the First Affiliated Hospital of Wenzhou Medical University in 2015. The antimicrobial susceptibility was detected by the agar dilution method. The distribution of virulence genes such as exoU, exoS, exoT and exoY from different isolates was detected by PCR. The expression levels of transcriptional regulator genes (ptrA and exsA) and effector-related genes (exoT and exoS) in some isolates were determined by real-time fluorescence quantitative PCR, and the Pearson correlation analysis was used to analyze the results. @*Results@#The detection rates of exoT and exoY in 68 P. aeruginosa isolates were higher, accounting for 79.4% and 75.0%, respectively. The detection rate of exoT in wound-sourced isolates was significantly higher than that in sputum (97.0% vs 61.8%, P＜0.01). In addition, the genotype of exoU - /exoS + was the most common, accounting for 51.5% (35/68). The resistance rates of sputum-sourced isolates to imipenem and meropenem were significantly higher than that of wound-sourced isolates (47.1% vs 8.8%, 47.1% vs 14.7%, P＜0.01). The resistance rates of isolates carrying exoU gene to carbapenems, aminoglycosides and fluoroquinolones were higher than those of isolates carrying exoS, exoT or exoY genes. Pearson correlation analysis showed that the expression level of ptrA gene was negatively correlated with those of exoT, exoS and exsA genes (P＜0.05). @*Conclusion@#The P. aeruginosa isolates from our hospital carrying T3SS virulence genes exoT and exoY are common, and the virulence genes are related to the drug resistance of P. aeruginosa. In addition, ptrA may be a potential negative regulatory gene for the expression of T3SS virulence genes.