Clinical cases of VIM-producing Pseudomonas mendocina from two burned patients

Almuzara, Marisa; Montaña, Sabrina; Carulla, Mariana; Sly, Gabriela; Fernandez, Jennifer S.; Hernandez, Marlene; Moriano, Alessandro; Traglia, Germán Matías; Bakai, Romina; Ramírez, María Soledad

doi:10.1016/j.jgar.2018.08.002

Cited by 11 publications

(11 citation statements)

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“…However, 3 out of the 19 reference genomes showed antimicrobial resistance genes, EF27, VN230, and VN231. Again, this study confirmed the premise of extensive antimicrobial resistance even in clinical and some environmental P. mendocina isolates [51][52][53], with antimicrobial susceptibility more common among the environmental isolates [54,55]. However, although P. mendocina infections have to date been easily treated with antibiotics, antibiotic pressure and the spread of mobile genetic elements could reverse this in future [55].…”

Section: Discussionsupporting

confidence: 70%

Whole Genome Analysis of Environmental Pseudomonas mendocina Strains: Virulence Mechanisms and Phylogeny

Ruiz-Roldán

Toro

Sáenz

2021

Genes

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Pseudomonas mendocina is an environmental bacterium, rarely isolated in clinical specimens, although it has been described as producing endocarditis and sepsis. Little is known about its genome. Whole genome sequencing can be used to learn about the phylogeny, evolution, or pathogenicity of these isolates. Thus, the aim of this study was to analyze the resistome, virulome, and phylogenetic relationship of two P. mendocina strains, Ps542 and Ps799, isolated from a healthy Anas platyrhynchos fecal sample and a lettuce, respectively. Among all of the small number of P.mendocina genomes available in the National Center for Biotechnology Information (NCBI) repository, both strains were placed within one of two well-defined phylogenetic clusters. Both P. mendocina strains lacked antimicrobial resistance genes, but the Ps799 genome showed a MOBP3 family relaxase. Nevertheless, this study revealed that P. mendocina possesses an important number of virulence factors, including a leukotoxin, flagella, pili, and the Type 2 and Type 6 Secretion Systems, that could be responsible for their pathogenesis. More phenotypical and in vivo studies are needed to deepen the association with human infections and the potential P. mendocina pathogenicity.

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Section: Discussionsupporting

confidence: 70%

Whole Genome Analysis of Environmental Pseudomonas mendocina Strains: Virulence Mechanisms and Phylogeny

Ruiz-Roldán

Toro

Sáenz

2021

Genes

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“…Given that macrophages are a key phagocytic cell of the innate immune system, we surmise that the proapoptotic effect we have observed helps S. maltophilia to resist being engulfed and killed and/or recognized by the immune system. Finally, it is probable that the anti-Pseudomonas effect of the VirB/D4 T4SS helps S. maltophilia to survive in a variety of niches, including perhaps the human host and the CF lung, which can be infected with P. mendocina in addition to the well-known P. aeruginosa (111,112). Based upon the range of target cells utilized in this study, we strongly suspect that the S. maltophilia T4SS can modulate the death program of a wide range of cellular targets, including killing other mammalian cells that are part of the immune system (e.g., neutrophils) or other bacteria that inhabit its niches, whether planktonic in nature or coinfecting plant, animal, or human hosts.…”

Section: Discussionmentioning

confidence: 99%

Stenotrophomonas maltophilia Encodes a VirB/VirD4 Type IV Secretion System That Modulates Apoptosis in Human Cells and Promotes Competition against Heterologous Bacteria, Including Pseudomonas aeruginosa

et al. 2019

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Stenotrophomonas maltophilia is an emerging opportunistic and nosocomial pathogen. S. maltophilia is also a risk factor for lung exacerbations in cystic fibrosis patients. S. maltophilia attaches to various mammalian cells, and we recently documented that the bacterium encodes a type II secretion system which triggers detachment-induced apoptosis in lung epithelial cells. We have now confirmed that S. maltophilia also encodes a type IVA secretion system (VirB/VirD4 [VirB/D4] T4SS) that is highly conserved among S. maltophilia strains and, looking beyond the Stenotrophomonas genus, is most similar to the T4SS of Xanthomonas. To define the role(s) of this T4SS, we constructed a mutant of strain K279a that is devoid of secretion activity due to loss of the VirB10 component. The mutant induced a higher level of apoptosis upon infection of human lung epithelial cells, indicating that a T4SS effector(s) has antiapoptotic activity. However, when we infected human macrophages, the mutant triggered a lower level of apoptosis, implying that the T4SS also elaborates a proapoptotic factor(s). Moreover, when we cocultured K279a with strains of Pseudomonas aeruginosa, the T4SS promoted the growth of S. maltophilia and reduced the numbers of heterologous bacteria, signaling that another effector(s) has antibacterial activity. In all cases, the effect of the T4SS required S. maltophilia contact with its target. Thus, S. maltophilia VirB/D4 T4SS appears to secrete multiple effectors capable of modulating death pathways. That a T4SS can have anti- and prokilling effects on different targets, including both human and bacterial cells, has, to our knowledge, not been seen before.

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“…VIM-type enzymes are among the most widespread and prevalent acquired MBLs in P. aeruginosa (Hong et al, 2015), and have occasionally been reported also in other Pseudomonas spp. of clinical interest including Pseudomonas putida, Pseudomonas mosselii, Pseudomonas monteilii, Pseudomonas stutzeri , and Pseudomonas mendocina (Yan et al, 2001; Lombardi et al, 2002; Giani et al, 2012; Ocampo-Sosa et al, 2015; Almuzara et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Identification of a Novel Plasmid Lineage Associated With the Dissemination of Metallo-β-Lactamase Genes Among Pseudomonads

et al. 2019

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Acquisition of metallo-β-lactamases (MBLs) represents one of most relevant resistance mechanisms to all β-lactams, including carbapenems, ceftolozane and available β-lactamase inhibitors, in Pseudomonas spp. VIM-type enzymes are the most common acquired MBLs in Pseudomonas aeruginosa and, to a lesser extent, in other Pseudomonas species. Little is known about the acquisition dynamics of these determinants, that are usually carried on integrons embedded into chromosomal mobile genetic elements. To date, few MBL-encoding plasmids have been described in Pseudomonas spp., and their diversity and role in the dissemination of these MBLs remains largely unknown. Here we report on the genetic features of the VIM-1-encoding plasmid pMOS94 from P. mosselii AM/94, the earliest known VIM-1-producing strain, and of related elements involved in dissemination of MBL. Results of plasmid DNA sequencing showed that pMOS94 had a modular organization, consisting of backbone modules associated with replication, transfer and antibiotic resistance. Plasmid pMOS94, although not typable according to the PBRT scheme, was classifiable either in MOB F11 or MPF T plasmid families. The resistance region included the class I integron In70, carrying bla V IM-1 , in turn embedded in a defective Tn 402 -like transposon. Comparison with pMOS94-like elements led to the identification of a defined plasmid lineage circulating in different Pseudomonas spp. of clinical and environmental origin and spreading different MBL-encoding genes, including bla IMP-63 , bla BIM , and bla V IM -type determinants. Genetic analysis revealed that this plasmid lineage likely shared a common ancestor and had evolved through the acquisition and recombination of different mobile elements, including the MBL-encoding transposons. Our findings provide new insights about the genetic diversity of MBL-encoding plasmids circulating among Pseudomonas spp., potentially useful for molecular epidemiology purposes, and revealed the existence and persistence of a successful plasmid lineage over a wide spatio-temporal interval, spanning over five different countries among two continents and over 20-years.

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Clinical cases of VIM-producing Pseudomonas mendocina from two burned patients

Cited by 11 publications

References 5 publications

Whole Genome Analysis of Environmental Pseudomonas mendocina Strains: Virulence Mechanisms and Phylogeny

Whole Genome Analysis of Environmental Pseudomonas mendocina Strains: Virulence Mechanisms and Phylogeny

Stenotrophomonas maltophilia Encodes a VirB/VirD4 Type IV Secretion System That Modulates Apoptosis in Human Cells and Promotes Competition against Heterologous Bacteria, Including Pseudomonas aeruginosa

Identification of a Novel Plasmid Lineage Associated With the Dissemination of Metallo-β-Lactamase Genes Among Pseudomonads

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