Pseudomonas fulva is an aerobic, non-fermenting, Gram-negative, oxidase-variable bacterium that Iizuka and Komagata first isolated from Japanese rice paddies in 1963 [1]. In the early 21st century, Yamamoto proved by phylogenetic analysis that P. fulva belongs to the Pseudomonas putida complex [2]. P. fulva has been identified mainly in natural environments, including rice fields, soil, water, seeds, and interior tissues of plants and marine animals [3]. In addition, P. fulva is one of the four Pseudomonas species that occupy the most widespread habitat niches in human households [4]. Despite this, P. fulva rarely infects humans and is widely used in research on degrading environmental contaminants, suppressing phytopathogens, and genetic editing [5]. To date, approximately 10 cases of human infection caused by P. fulva have been reported, including ventriculitis, sepsis, bacteraemia, cystitis, skin and soft-tissue infection, and septic shock [6].

VIM enzymes are among the most clinically essential Metallo-β-lactamases. VIM-2 and VIM-1 were first identified in Pseudomonas aeruginosa in Europe in 1996 and 1997, respectively, and subsequently reported worldwide in Enterobacterales, Pseudomonas, and Acinetobacter [7]. VIM-24, a natural variant of VIM-2 with an R228L substitution and novel phenotype, was first reported in Klebsiella pneumoniae in Colombia in 2011 [8]. The blaVIM usually coexists with one or more aminoglycoside resistance genes, integrated into class I integron embedded in transposons, which can be accommodated on plasmids and spread among bacteria through mobile genetic elements (MGEs) [9].

Tigecycline is regarded as the limited choice of therapeutic drugs against infections caused by carbapenem-resistant Gram-negative bacteria. The resistance-nodulation-division efflux pump gene cluster tmexCD1-toprJ1 or the variants (tmexCD2-toprJ2, tmexCD3-toprJ3, tmexC3.2D3.3-toprJ1b, and tmexC3.2D3-toprJ1b) represent a newly discovered mechanism mediating tigecycline resistance [10]. Interestingly, most strains harbouring the tmexCD3-oprJ3 resistance gene were isolated from non-clinical samples [11].

In this study, we report the first identification of two clinical P. fulva isolates harbouring novel transferable megaplasmid co-carrying blaVIM−24 and tmexCD3-toprJ3. The emergence of transferable multidrug-resistant (MDR) megaplasmid could result in clinical strains resistant to both carbapenems and tigecycline, posing new challenges to clinical anti-infection therapies.