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Background Providencia species are concerning due to their intrinsic resistance to colistin and tigecycline, complicating the treatment of multidrug-resistant (MDR) infections. Methods In the current study, two MDR isolates, DFU6 and DFU52 T , were recovered from infected diabetic foot ulcers in Egypt in 2024. Following their initial identification as Providencia stuartii using VITEK® 2 and MALDI-TOF-MS, the isolates were subjected to whole-genome sequencing via DNBseq. Results While the 16S rRNA gene showed 100% similarity to that of Providencia vermicola , phylogenomic analysis against the type strains in the TYGS database, including P. vermicola DSM 17385 T confirmed that these isolates represent a distinct species within the genus, further supported by overall genome-relatedness indices (ORGIs). This discrepancy prompted us to revise the taxonomy of all published genomes of P. vermicola strains ( n  = 59) which revealed misidentification of at least 56 strains that are unrelated to the type strain of this species. DFU6 and DFU52 T carried novel sequence types (ST29 and ST41, submitted to PubMLST) and harbored multiple resistance genes. Both strains contained the qnrD1 gene on a small, non-mobilizable plasmid. DFU52 T possessed a conjugative plasmid encoding bla CMY−6 , bla NDM−1 , rmtC , aac(6’)-Ib10 , sul1 , aph(3’)-Ia , and qacEΔ1 . DFU6 carried an IS Ecp 1-associated bla CTX−M−14 , along with aadA , dfrA1 , lnuF in a class 2 integron, and armA , msrE , and mphE on a resistance plasmid. Both isolates also featured a pathogenicity island (PAI) integrated into the pheV gene with fimbriae-encoding genes. Conclusion Following our reassessment of the taxonomic classification of all P. vermicola strains with published genomes, we propose reclassifying certain strains, including DFU6 and DFU52 T , into distinct species for which we propose the name Providencia pseudovermicola sp. nov. We recommend DFU52 T (= CCASU-2024-72) as the type strain for the novel species. We also shed light on the public health threat of this novel species as a human pathogen that harbours carbapenem and aminoglycoside resistance genes on mobile genetic elements.

Bioprospection for potential microbial biocontrol agents associated with three major insect pests of economic relevance for olive cultivation in the Mediterranean area, namely the olive fly, Bactrocera oleae, the olive moth, Prays oleae, and the olive psyllid, Euphyllura olivina, led to the isolation of several strains of readily cultivable Gram-negative, rod-shaped bacteria from Tunisian olive orchards. Determination of 16S ribosomal RNA encoding sequences identified the bacteria as members of the taxonomic genus Providencia (Enterobacterales; Morganellaceae). A more detailed molecular taxonomic analysis based on a previously established set of protein-encoding marker genes together with DNA-DNA hybridization and metabolic profiling studies led to the conclusion that the new isolates should be organized in a new species within this genus. With reference to their original insect association, the designation \"Providencia entomophila\" is proposed here for this hypothetical new taxon.

Desalination plants are of great interest as an alternative to supply drinking water to hundreds of locations in the Brazilian semi-arid region and it is a social technology to cope with drought. However, desalination waste can contaminate groundwater and cause serious environmental impacts. The objective of this work was, therefore, to evaluate the quality of water and the perception of users regarding the socio-environmental aspects of the use of desalination equipment installed at eight locations in the municipality of Pentecoste, Ceara. The towns of Mulungu, Muquenzinho, Irapua, Macacos, Barra do Leme, Capivara, Lagoa da Porta, and Providencia were visited. In each location, three samples were taken of desalinated well water, and desalination wastes were collected in plastic bottles, and their chemical composition was analyzed. The values of ECw of the waste ranged from 4.2 to 7.6 dS m super( -1), representing risks to the environment per established standards worldwide. The locality of Muquenzinho has the highest values of pH, ECw, Na and Ca at different water sources. Most of the desalination waste generated is used for animal feed and the vast majority of the population, regardless of location, is not aware whether the use of waste water may be harmful to human health or to the environment.

Providencia genus is known to harbor certain opportunistic pathogens capable of causing human infections. Here, we report two strains of multidrug-resistant bacteria initially identified as Providencia rettgeri by mass spectrometry, but genome analysis revealed their ANI (79.84–84.20%) and dDDH (21.1–25.6%) values to fall below the accepted species threshold for known Providencia species. We therefore propose that these isolates be recognized as a novel species, Providencia xianensis sp. nov. Alarmingly, both strains, isolated from locations far apart, exhibited resistance to last-resort antibiotics, indicating their possible wide distribution, underscoring the urgency for immediate attention and enhanced surveillance for this emerging multidrug-resistant pathogen.

Animals coexist in commensal, pathogenic or mutualistic relationships with complex communities of diverse organisms, including microorganisms 1 . Some bacteria produce bioactive neurotransmitters that have previously been proposed to modulate nervous system activity and behaviours of their hosts 2 , 3 . However, the mechanistic basis of this microbiota–brain signalling and its physiological relevance are largely unknown. Here we show that in Caenorhabditis elegans , the neuromodulator tyramine produced by commensal Providencia bacteria, which colonize the gut, bypasses the requirement for host tyramine biosynthesis and manipulates a host sensory decision. Bacterially produced tyramine is probably converted to octopamine by the host tyramine β-hydroxylase enzyme. Octopamine, in turn, targets the OCTR-1 octopamine receptor on ASH nociceptive neurons to modulate an aversive olfactory response. We identify the genes that are required for tyramine biosynthesis in Providencia , and show that these genes are necessary for the modulation of host behaviour. We further find that C. elegans colonized by Providencia preferentially select these bacteria in food choice assays, and that this selection bias requires bacterially produced tyramine and host octopamine signalling. Our results demonstrate that a neurotransmitter produced by gut bacteria mimics the functions of the cognate host molecule to override host control of a sensory decision, and thereby promotes fitness of both the host and the microorganism. A neuromodulator produced by commensal Providencia bacteria that colonize the gut of Caenorhabditis elegans mimics the functions of the cognate host molecule to manipulate a sensory decision of the host.

The precise mechanism of virulence of Providencia rustigianii is unclear, although some strains produce cytolethal distending toxin as a putative virulence factor. We have detected the presence of a type III secretion system (T3SS) for the first time on a plasmid in a P. rustigianii strain. Plasmid-mediated T3SS seems to be directly involved in virulence of P. rustigianii and may serve as a means of horizontal transfer of T3SS genes. Our results may have implication in understanding the mechanism of emergence of new pathogenic strains of P. rustigianii .

The complex aminoglycoside resistance mechanisms observed within the genus present formidable clinical challenges to the effective management of the infectious diseases caused by these species. In-depth research into the mechanisms of bacterial resistance to antimicrobials must be conducted to strengthen the response capabilities of healthcare facilities for infection prevention and control. Bacteria from wastewater from an animal farm were isolated by plate streaking. The minimum inhibitory concentrations (MICs) of the antimicrobials were determined using the standard agar dilution method. The function of the novel resistance gene was elucidated using molecular cloning technology. ANT(9)-Ie was heterologously expressed, and its kinetic parameters were determined. The biological characteristics of the genome were systematically analyzed through whole-genome sequencing and a comparative genomic analysis, and a phylogenetic analysis of the genetic background for resistance gene-related sequences was performed. In P17, a novel resistance gene, designated , conferring resistance against spectinomycin was identified. A comparative analysis revealed that among all the functionally characterized resistance proteins, ANT(9)-Ie had the highest amino acid (aa) sequence similarity to ANT(9)-Id (58.67%). Compared with the control strain DH5α (DH5α), the recombinant strain harboring (pMD19- /DH5α) showed a 64-fold increase in the MIC of spectinomycin. The results of the kinetic analysis of ANT(9)-Ie were generally consistent with the MIC for the cloned , with a high spectinomycin catalytic efficiency [ / , (8.22 ± 1.24) × 10 M ·s ). No new features were observed in the domains or motifs of the protein. The homologous genes were found only in strains and exhibited a relatively conserved genetic environment. The strains whose genomes were available in the NCBI database were isolated from different sources, most of which were from human clinical specimens. In this study, a novel spectinomycin resistance gene, , was identified, and its biological features were characterized. The identification of this novel resistance gene from might aid in the effective clinical treatment of infections caused by bacteria carrying this resistance gene in the future and paves the way for further research into the complexity of resistance mechanisms within microbial populations.

A 60-year-old male with recurrent bacteremia associated with necrotizing pancreatitis was followed over 17 months, during which six clinical isolates of were obtained. The index isolate (R1) was susceptible to aztreonam-avibactam (MIC 4 mg/L), but resistance (MIC >64 mg/L) emerged with isolate B1, collected one month later, and persisted in subsequent isolates. To investigate the genomic and phenotypic evolution of six clinical isolates, focusing on mechanisms underlying the emergence of aztreonam-avibactam resistance. Whole-genome sequencing was performed to determine species identity, phylogenetic relationships, and resistance determinants. Average nucleotide identity (ANI) and in silico DNA-DNA hybridization (DDH) were used to confirm species classification. Comparative genomic analysis with R1 as a reference identified mutations associated with resistance. Structural modelling assessed the functional impact of key mutations. All isolates were sequence type ST44. Phylogenomic analysis revealed the isolates were more closely related to than , supported by ANI (97%) and DDH (76%). All isolates harboured , correlating with carbapenem resistance. Resistant isolates displayed a glycine insertion at position 420 in PBP3 (p.Gly420dup), which structural modelling indicated disrupted aztreonam-avibactam binding. A Gly151Asp substitution in OmpC was also identified, potentially affecting drug permeability. No mutations were observed in other porins (OmpA, OmpD, or OmpW). This study identifies a glycine insertion in PBP3 as a novel mechanism driving aztreonam-avibactam resistance in , supported by structural modelling and additional mutations in OmpC. This study provides evidence of a novel resistance mechanism to aztreonam-avibactam in , driven by a glycine insertion in PBP3 and supported by alterations in OmpC.

(Pr) and (Ps) are clinically relevant opportunistic pathogens. They are resistant to several antibiotics including carbapenems. The immune response against these pathogens has never been investigated. Here, we aimed to evaluate whether neutrophils (PMN), key players against bacterial infections, were able to recognize and eliminate these bacteria. We measured PMN functions after challenge with selected clinical isolates of Pr and Ps, and used ATCC (Eco), which fully activates PMN, for comparison. Bacterial survival was evaluated after exposure of PMN to bacteria for 1 or 3 h and colony formation units (CFU) were determined. While PMN were able to partially contain Ps growth at 1 h, at 3 h both Pr and Ps were able to escape PMN-mediated killing compared to Eco, which was efficiently killed. Reactive oxygen species (ROS) generation was not induced by Pr or poorly induced by Ps, compared to Eco, but phagocytosis of Pr, Ps, and Eco was similar. Although Pr and Ps induced the release of double-stranded (d.s.) DNA early at 30 min (vital neutrophils extracellular traps or NETs), the release of late-induced NETs (3 h, suicidal NETs) was not observed, consistent with the absence of PMN death observed with Pr or Ps. In addition, Pr and Ps decreased suicidal NETs when Eco or PMA were used as inducers. This decrease was abolished by fixed bacteria, and was dependent on the release of a DNase activity. Twenty-four h after i.p. inoculation of mice with Pr, Ps or Eco, all bacteria induced migration of PMN to the peritoneum, but no PMN activation or NETs was observed in Pr or Ps-treated mice. When the distribution of bacteria in different organs was measured by CFU determination, Pr and Ps disseminated to the spleen and lungs, whereas Eco was exclusively present in the peritoneum. The isolates used in this study of Pr and Ps are poor inducers of bactericidal PMN responses and display immune evasion strategies to subvert PMN-mediated killing. These evasion mechanisms, acting on degrading vital NETs and/or blocking the formation of suicidal NETs, would favor bacterial dissemination.

species are emerging opportunistic pathogens associated with multidrug-resistant infections, yet their molecular defense mechanisms against phage or mobile genetic elements remain poorly characterized. We present a comprehensive pan-genomic analysis of antiviral defense systems across 73 complete genomes (or chromosomes) of (n = 31) and (n = 42), using DefenseFinder and CRISPRCasFinder. We further expanded analysis of contig/scaffold assemblies to confirm conservation of core defense profiles across assembly types. BacMGEnet was employed to derive spacer-MGE interaction networks. Phylogenetic reconstruction and gene gain and loss modeling were performed to assess evolutionary patterns. To validate functionality, we experimentally tested the anti-phage activity of Gabija and Septu in heterologous assays, including point mutation analysis of conserved residues. We reveal a diverse and complex defense repertoire dominated by restriction-modification systems and CRISPR-Cas Class 1 Type I-F, with significant contributions from toxin-antitoxin, GAPS2, PsyrTA, and Mokosh systems. Notably, defense genes are non-randomly distributed, often clustering into genomic islands suggestive of horizontal acquisition. Expanded analysis confirms conservation of core defense profiles across assembly types, supporting the utility of lower-quality data when complete genomes are scarce. Comparative analysis uncovers species-specific differences, with harboring a higher abundance of non-CRISPR systems. BacMGEnet-derived spacer-MGE interaction networks further highlight species-specific dynamics, dense, hub-driven networks in versus sparser networks in . Correlation analysis indicates potential associations between specific defense systems and virulence or antibiotic resistance genes. Phylogenetic reconstruction and gene gain and loss modeling further highlight dynamic evolutionary patterns. Both Gabija and Septu systems conferred robust, phage-specific protection; point mutations in conserved residues (GajA E465K and PtuB H53K) abolished defense. Our findings unveil a multi-layered, modular immune architecture in Providencia, providing crucial insights into its genome plasticity, phage resistance, and adaptation in clinical environments. This work establishes a foundation for understanding the role of defense systems in the evolution and pathogenicity of the genus.