Genotypic and phenotypic characterization of Pseudomonas aeruginosa PAV112: a virulent clinical strain causing severe pneumonia and lethal sepsis in a murine infection model

铜绿假单胞菌 PAV112 的基因型和表型特征:一种在小鼠感染模型中引起严重肺炎和致命性败血症的毒力强的临床菌株

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Abstract

Pseudomonas aeruginosa is an opportunistic pathogen frequently associated with hospital-acquired infections, particularly in intensive care units. This study aimed to evaluate the virulence of the clinical strain P. aeruginosa VAP112, isolated from a patient with ventilator-associated pneumonia (VAP), using a murine model of pulmonary infection. Antimicrobial susceptibility testing was performed using the VITEK(®) 2 system and disk diffusion method. Experiments were conducted to evaluate biofilm formation by VAP112, as well as the survival of Tenebrio molitor larvae and C57BL/6 mice. Animals were instilled with VAP112 via tracheal to evaluate the bacterial load in the organs, inflammatory markers, cell quantification, and histology of organs. Polymerase chain reaction (PCR) identified the presence of virulence and resistance genes, including exoU, exoT, exoS, phzI, phzM, oprI, bla(OXA− 23), and bla(OXA− 51). The strain demonstrated the ability to form biofilms and caused mortality in T. molitor larvae. In mice, tracheal instillation of VAP112 led to pneumonia with rapid progression to lethal sepsis within 48 h. This was associated with bacterial dissemination to various organs, significant increase in nitric oxide and IL-6 levels, and elevated cell counts in bone marrow and bronchoalveolar fluid. Histological analysis revealed inflammatory infiltrates, edema, and congestion in the affected organs. Taken together, these findings showed the virulence potential of P. aeruginosa VAP112 to induce severe pneumonia in animals with rapid progression to lethal sepsis. Given its great importance in the clinical context, this study underscores the urgent need for the development of novel therapeutic strategies to combat infections caused by virulent strains of P. aeruginosa. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s42770-025-01830-7.

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