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The phagotrophic origin of eukaryotes and phylogenetic classification of Protozoa.

Eukaryotes and archaebacteria form the clade neomura and are sisters, as shown decisively by genes fragmented only in archaebacteria and by many sequence trees. This sisterhood refutes all theories that eukaryotes originated by merging an archaebacterium and an alpha-proteobacterium, which also fail to account for numerous features shared specifically by eukaryotes and actinobacteria. I revise the phagotrophy theory of eukaryote origins by arguing that the essentially autogenous origins of most eukaryotic cell properties (phagotrophy, endomembrane system including peroxisomes, cytoskeleton, nucleus, mitosis and sex) partially overlapped and were synergistic with the symbiogenetic origin of mitochondria from an alpha-proteobacterium. These radical innovations occurred in a derivative of the neomuran common ancestor, which itself had evolved immediately prior to the divergence of eukaryotes and archaebacteria by drastic alterations to its eubacterial ancestor, an actinobacterial posibacterium able to make sterols, by replacing murein peptidoglycan by N-linked glycoproteins and a multitude of other shared neomuran novelties. The conversion of the rigid neomuran wall into a flexible surface coat and the associated origin of phagotrophy were instrumental in the evolution of the endomembrane system, cytoskeleton, nuclear organization and division and sexual life-cycles. Cilia evolved not by symbiogenesis but by autogenous specialization of the cytoskeleton. I argue that the ancestral eukaryote was uniciliate with a single centriole (unikont) and a simple centrosomal cone of microtubules, as in the aerobic amoebozoan zooflagellate Phalansterium. I infer the root of the eukaryote tree at the divergence between opisthokonts (animals, Choanozoa, fungi) with a single posterior cilium and all other eukaryotes, designated 'anterokonts' because of the ancestral presence of an anterior cilium. Anterokonts comprise the Amoebozoa, which may be ancestrally unikont, and a vast ancestrally biciliate clade, named 'bikonts'. The apparently conflicting rRNA and protein trees can be reconciled with each other and this ultrastructural interpretation if long-branch distortions, some mechanistically explicable, are allowed for. Bikonts comprise two groups: corticoflagellates, with a younger anterior cilium, no centrosomal cone and ancestrally a semi-rigid cell cortex with a microtubular band on either side of the posterior mature centriole; and Rhizaria [a new infrakingdom comprising Cercozoa (now including Ascetosporea classis nov.), Retaria phylum nov., Heliozoa and Apusozoa phylum nov.], having a centrosomal cone or radiating microtubules and two microtubular roots and a soft surface, frequently with reticulopodia. Corticoflagellates comprise photokaryotes (Plantae and chromalveolates, both ancestrally with cortical alveoli) and Excavata (a new protozoan infrakingdom comprising Loukozoa, Discicristata and Archezoa, ancestrally with three microtubular roots). All basal eukaryotic radiations were of mitochondrial aerobes; hydrogenosomes evolved polyphyletically from mitochondria long afterwards, the persistence of their double envelope long after their genomes disappeared being a striking instance of membrane heredity. I discuss the relationship between the 13 protozoan phyla recognized here and revise higher protozoan classification by updating as subkingdoms Lankester's 1878 division of Protozoa into Corticata (Excavata, Alveolata; with prominent cortical microtubules and ancestrally localized cytostome--the Parabasalia probably secondarily internalized the cytoskeleton) and Gymnomyxa [infrakingdoms Sarcomastigota (Choanozoa, Amoebozoa) and Rhizaria; both ancestrally with a non-cortical cytoskeleton of radiating singlet microtubules and a relatively soft cell surface with diffused feeding]. As the eukaryote root almost certainly lies within Gymnomyxa, probably among the Sarcomastigota, Corticata are derived. Following the single symbiogenetic origin of chloroplasts in a corticoflagellate host with cortical alveoli, this ancestral plant radiated rapidly into glaucophytes, green plants and red algae. Secondary symbiogeneses subsequently transferred plastids laterally into different hosts, making yet more complex cell chimaeras--probably only thrice: from a red alga to the corticoflagellate ancestor of chromalveolates (Chromista plus Alveolata), from green algae to a secondarily uniciliate cercozoan to form chlorarachneans and independently to a biciliate excavate to yield photosynthetic euglenoids. Tertiary symbiogenesis involving eukaryotic algal symbionts replaced peridinin-containing plastids in two or three dinoflagellate lineages, but yielded no major novel groups. The origin and well-resolved primary bifurcation of eukaryotes probably occurred in the Cryogenian Period, about 850 million years ago, much more recently than suggested by unwarranted backward extrapolations of molecular 'clocks' or dubious interpretations as 'eukaryotic' of earlier large microbial fossils or still more ancient steranes. The origin of chloroplasts and the symbiogenetic incorporation of a red alga into a corticoflagellate to create chromalveolates may both have occurred in a big bang after the Varangerian snowball Earth melted about 580 million years ago, thereby stimulating the ensuing Cambrian explosion of animals and protists in the form of simultaneous, poorly resolved opisthokont and anterokont radiations.

Animals↗

Identification of a G protein alpha subunit from Neurospora crassa that is a member of the Gi family.

Heterotrimeric G proteins, consisting of alpha, beta, and gamma subunits, are implicated in major signal transduction pathways controlling a diversity of functions in eukaryotic organisms. In the filamentous fungus Neurospora crassa, G proteins are implicated in the regulation of several environmental responses. As a first step in studying the role of G proteins in these processes, we have cloned the genes for two alpha subunits, gna-1 and gna-2, from Neurospora. The genes are located on different chromosomes and are differentially regulated during asexual development. The encoded proteins (Gna-1 and Gna-2) are the same size as members of the Gi-alpha family (approximately 40 kDa). The Gna-1 protein sequence is 55% identical overall to members of the Gi family and contains the consensus sequences for ADP-ribosylation by pertussis toxin and incorporation of myristic acid, which are found in this group. These properties make Gna-1 the first identified microbial alpha subunit to be a member of any class. Furthermore, incubation of a N. crassa plasma membrane fraction with pertussis toxin results in ADP-ribosylation of a protein substrate which is the approximate size of Gna-1. The predicted Gna-2 protein sequence does not share a high degree of sequence identity with the Gi class. However, the coding region contains at least one intron in a position conserved in the Gi family. We propose that the Gi family of alpha subunits is ancient and during evolution may have first appeared in filamentous fungi.

Adenosine Diphosphate Ribose↗

[Neonatal bacterial infections at the CUH of Dakar].

OBJECTIVES: It's a retrospective study in order to determine the epidemiology of neonatal bacterial infection and to evaluate the efficiency of the antibiotic protocol in University Teaching Hospital in Dakar. MATERIAL AND METHODES: From January 1st 1997 to December 31st 1998 we have registered 7461 live births, samples of blood are taken from 2312 new-born baby and they received antibiotherapy (beta-lactamine + gentamycin) at the first day based on infections risk evaluated by anamnestic criterias. The treatment is seven to one days long, the antibiotic was adapted according to the antibiogram result. RESULTS: The neonatal infection diagnosis is confirmed in 246 cases, about 33 per 1000 live births or 10.6% of newborn babies having on antibiotherapy. Most current risk factors are premature rupture of membranes (85%) and neonatal suffering (87.8%). Isolated gerras are: Klebsiella pneumoniae (61.5%), Enterobacteria (11.5 Staphylococcus (8.7%), colibacille (6%), Streptococcus (5.5%), Enterococcus (4.1%) and Pseudomonas (2.7%). Most of these germs are resistant to antibiotics currently used in first intention (ampicillin, cefotaxim, gentamycin), in particularly 95% of Klebsiella. Most efficient antibiotics are amikacin, colistin, ceftriaxon and ciprofloxacine. Deaths occurs in 48 cases with 36 in early neonatal period, 79% of mortality rate related to infection by Klebsiella. CONCLUSION: First intention antibiotherapy must be always adapted to the bacterial ecology evolution and must be more selective by using major infections risk factors. We promote early infection diagnosis by using biologic markers which reference is represented by C Reactive Protein.

Anti-Bacterial Agents↗

Resource competition and social conflict in experimental populations of yeast.

Understanding the conditions that promote the maintenance of cooperation is a classic problem in evolutionary biology. The essence of this dilemma is captured by the 'tragedy of the commons': how can a group of individuals that exploit resources in a cooperative manner resist invasion by 'cheaters' who selfishly use common resources to maximize their individual reproduction at the expense of the group? Here, we investigate this conflict through experimental competitions between isogenic cheater and cooperator strains of yeast with alternative pathways of glucose metabolism, and by using mathematical models of microbial biochemistry. We show that both coexistence and competitive exclusion are possible outcomes of this conflict, depending on the spatial and temporal structure of the environment. Both of these outcomes are driven by trade-offs between the rate and efficiency of conversion of resources into offspring that are mediated by metabolic intermediates.

Biological Evolution↗

Haemophilus influenzae bla(ROB-1) mutations in hypermutagenic deltaampC Escherichia coli conferring resistance to cefotaxime and beta-lactamase inhibitors and increased susceptibility to cefaclor.

The clinical use of cefaclor has been shown to enrich Haemophilus influenzae populations harboring cefaclor-hydrolyzing ROB-1 beta-lactamase. Such a selective process may lead to the increased use of extended-spectrum cephalosporins or beta-lactams plus beta-lactamase inhibitors and, eventually, resistance to these agents, which has not previously been observed in H. influenzae. In order to establish which bla(ROB-1) mutations, if any, could confer resistance to extended-spectrum cephalosporins and/or to beta-lactamase inhibitors, a plasmid harboring bla(ROB-1) was transformed into hypermutagenic strain Escherichia coli GB20 (DeltaampC mutS::Tn10), and this construct was used in place of H. influenzae bla(ROB-1). Strain GB20 with the cloned gene was submitted to serial passages in tubes containing broth with increasing concentrations of selected beta-lactams (cefotaxime or amoxicillin-clavulanate). Different mutations in the bla(ROB-1) gene were obtained during the passages in the presence of the different concentrations of the selective agents. Mutants resistant to extended-spectrum cephalosporins harbored either the Leu169-->Ser169 or the Arg164-->Trp164 substitution or the double amino acid change Arg164-->Trp164 and Ala237-->Thr237. ROB-1 mutants that were resistant to beta-lactams plus beta-lactamase inhibitors and that harbored the Arg244-->Cys244 or the Ser130-->Gly130 replacement were also obtained. The cefaclor-hydrolyzing efficiencies of the ROB-1 variants were strongly decreased in all mutants, suggesting that if bla(ROB-1) mutants were selected by cefaclor, this drug would prevent the further evolution of this beta-lactamase toward molecular forms able to resist extended-spectrum cephalosporins or beta-lactamase inhibitors.

Amoxicillin-Potassium Clavulanate Combination↗

The putative response regulator BaeR stimulates multidrug resistance of Escherichia coli via a novel multidrug exporter system, MdtABC.

Overproduction of the response regulator BaeR confers resistance to novobiocin and bile salts in a DeltaacrAB mutant by stimulating drug exporter gene expression. The mdtABC (multidrug transporter ABC, formerly known as yegMNO) genes, which encode a resistance-nodulation-cell division (RND) drug efflux system, are responsible for resistance. The MdtABC system comprises the transmembrane MdtB/MdtC heteromultimer and MdtA membrane fusion protein. MdtAC also confers bile salt, but not novobiocin, resistance. This indicates that the evolution from an MdtC homomultimer to an MdtBC heteromultimer contributed to extend the drug resistance spectrum. A BLAST search suggested that such a heteromultimer-type RND exporter constitutes a unique family among gram-negative organisms.

Anti-Bacterial Agents↗

Genome macrorestriction analysis of diversity and variability of Pseudomonas aeruginosa strains infecting cystic fibrosis patients.

Genome macrorestriction fingerprinting with XbaI and DraI was used to analyze the relatedness of 166 Pseudomonas aeruginosa isolates collected from 31 cystic fibrosis patients over a 1- to 20-month period and to correlate their genotype with patterns of resistance to 14 antimicrobial agents. Quantitative comparison of intra- and interpatient similarities of P. aeruginosa macrorestriction patterns disclosed two discrete ranges that clearly discriminated subclonal variation (> 80% relatedness) and clonal diversity (10 to 70% relatedness). Cloning-derived mutants exhibited up to 20% divergence of genomic macrorestriction patterns during the course of chronic colonization of individual patients. Change of susceptibility to multiple antimicrobial agents developed in 50% of sequential pairs of isolates from individual patients. Only 19% of these susceptibility changes were attributable to strain substitution, while the majority (56%) of resistance changes were associated with minor genomic variations of a persistent strain. Sixty-six percent of patients harbored one strain, and 33% carried two strains. Three common strains colonized 5 (28%) of 18 patients attending a cystic fibrosis clinic, and another two strains colonized two patient pairs (31%) of 13 patients staying at a rehabilitation center, suggesting potential cross-infection in these settings. By indexing regional polymorphisms throughout the chromosome structure, macrorestriction analysis can monitor subclonal evolution of P. aeruginosa and identify isogenic resistance mutants. Quantitative macrorestriction fingerprinting enables discrimination between clonal variants and clones of distinct origins and should therefore provide a reliable tool for investigating the mode of acquisition of P. aeruginosa in cystic fibrosis patients.

Cross Infection↗

Clinical data sets of human immunodeficiency virus type 1 reverse transcriptase-resistant mutants explained by a mathematical model.

Treatment of human immunodeficiency virus type 1 (HIV-1) infection during the clinical latency phase with drugs inhibiting reverse transcriptase (RT) reduces the HIV-1 RNA load and increases the CD4+ T-cell count. Typically, however, the virus evolves mutations in the RT gene that circumvent the drugs. We develop a mathematical model for this situation. The model distinguishes quiescent from activated CD4+ T cells, incorporates the fact that only activated cells can become productively infected by HIV-1, embodies empirical estimates for the drug resistance and the mutation frequency for each of the HIV-1 drug-resistant mutants, and assumes the antiviral immune response to remain constant over the course of the experiments. We analyze clinical data on the evolution of drug-resistant mutants for the RT inhibitors lamivudine and zidovudine. The results show that the evolutionary sequence of the drug-resistant mutants in both data sets is accounted for by our model, given that lamivudine is more effective than zidovudine. Thus, current empirical estimates of the mutation frequencies and the drug resistances of the mutants suffice for explaining the data. We derive a critical treatment level below which the wild-type HIV-1 RNA load can rebound before the first drug-resistant mutant appears. Our zidovudine data confirm this to be the case. Thus, we demonstrate in the model and the data that the rebound of the HIV-1 RNA load in the case of zidovudine is due to the outgrowth of wild-type virus and the first drug-resistant mutant, whereas that in the case of lamivudine can only be due to the drug-resistant mutants. The evolution of drug resistance proceeds slower in the case of zidovudine because (i) zidovudine is not as effective as lamivudine and (ii) the first zidovudine drug-resistant mutant is competing with the rebounding wild-type virus.

Drug Resistance, Microbial↗

[Evolution of bacteria in hospital (author's transl)].

This study reports the evolution of bacterial ecology during twelve years in a general hospital : prevalence of the different species isolated and their resistance to antibiotics. It appears, in the etiology of serious infections, a great stability in the repartition of bacterial groups responsible. Likewise, the evolution of bacterial resistance during this period did not show a gradual increase. A certain balance seems to occur in function of local conditions, among which a controlled use of antibiotics is certainly an important factor.

Adult↗

The dynamical analogy between microbial growth on mixtures of substrates and population growth of competing species.

There is a similarity between the metabolic dynamics of a microbial species growing on a mixture of two substrates and the dynamics of growth of two competing populations. Specifically, the enzymes catalyzing the uptake and catabolism of substrates exhibit phenomena analogous to extinction and coexistence."Extinction" of the enzymes associated with one of the substrates results in sequential utilization of the substrates (diauxie) (Monod, 1942). "Coexistence" of the enzymes associated with the substrates results in simultaneous utilization of the substrates (Egli, 1995). Here, we formulate a simple model that shows the basis for this dynamical similarity: The equations describing the evolution of the enzyme levels are dynamical analogs of the Lotka-Volterra model for two competing species. The analogy suggests ways of capturing the experimentally observed preculture-dependent growth patterns, i.e., growth patterns that vary depending on the physiological state of the preculture.

Bacteria↗

Lipoxin A(4) analogues inhibit leukocyte recruitment to Porphyromonas gingivalis: a role for cyclooxygenase-2 and lipoxins in periodontal disease.

The potential involvement of the inducible cyclooxygenase isoform (COX-2) and the role of novel lipid mediators were investigated in the pathogenesis of periodontal disease. Crevicular fluids from localized juvenile periodontitis (LJP) patients contained prostaglandin (PG)E(2) and 5-lipoxygenase-derived products, leukotriene B(4), and the biosynthesis interaction product, lipoxin (LX)A(4). Neutrophils from peripheral blood of LJP patients, but not from asymptomatic donors, also generated LXA(4), suggesting a role for this immunomodulatory molecule in periodontal disease. To characterize host responses of interest to periodontal pathogens, Porphyromonas gingivalis was introduced within murine dorsal air pouches. In the air pouch cavity, P. gingivalis elicited leukocyte infiltration, concomitant with elevated PGE(2) levels in the cellular exudates, and upregulated COX-2 expression in infiltrated leukocytes. In addition, human neutrophils exposed to P. gingivalis also upregulated COX-2 expression. Blood borne P. gingivalis gave significant increases in the murine tissue levels of COX-2 mRNA associated with both heart and lungs, supporting a potential role for this oral pathogen in the evolution of systemic events. The administration of metabolically stable analogues of LX and of aspirin-triggered LX potently blocked neutrophil traffic into the dorsal pouch cavity and lowered PGE(2) levels within exudates. Together, these results identify PMN as an additional and potentially important source of PGE(2) in periodontal tissues. Moreover, they provide evidence for a novel protective role for LX in periodontitis, limiting further PMN recruitment and PMN-mediated tissue injury that can lead to loss of inflammatory barriers that prevent systemic tissue invasion of oral microbial pathogens.

Aggressive Periodontitis↗

Chromosomal DNA fingerprinting analysis using the insertion sequence IS6110 and the repetitive element DR as strain-specific markers for epidemiological study of tuberculosis in French Polynesia.

The polymorphism of Mycobacterium tuberculosis strains was evaluated in French Polynesia, an area with a low incidence of tuberculosis and a population which has been geographically stable during recent decades. Nonrepetitive strains isolated from 64 patients during 1991 and 1992 were subjected to DNA restriction fragment length polymorphism (RFLP) analysis, using the insertion sequence IS6110 and the repetitive element DR as probes. Thirty-eight different IS6110 RFLP types were identified. They could be clustered in 11 groups. All the members of each group are identical or differ by one to three bands. All the other strains are gathered in the miscellaneous group. In some cases, transmission of strains with identical RFLP types between patients of the same family or between patients living in the same area was identified. Strains exhibiting similar IS6110 RFLP types also exhibited identical DR RFLP patterns, confirming that strains with similar types were genetically linked. Strains belonging to two different IS6110 clusters exhibited the same DR RFLP type. These data may also indicate a common origin for these strains and evolution to new IS6110 types. The results obtained in this study suggest that not only reactivation of latent tuberculous infections but also active transmissions are still occurring in French Polynesia.

Adolescent↗

Genetic deficiencies of the complement system and association with disease--early components.

Genetic deficiency of one of the early components of the classical pathway of complement (C1q, C1r, C1s, C4 and C2) is often associated with clinical symptoms and immunochemical abnormalities common in idiopathic autoimmune diseases, such as lupus erythematosus, but also with an increased incidence of various, local and generalized infections. These observations are consistent with the current view of the complement system's role in handling immune complexes and combating microbial invasion. However, the absence of absolute correlations in these experiments of nature suggests that genetic defects of the classical pathway act only epistatically to other host factors and the primary etiologies of the associated diseases. In contrast, the strong association of properdin and factor D deficiency with serious infections caused by encapsulated Gram-negative bacteria suggests a more immediate involvement of the alternative pathway in a specific segment of immunity and its pathology. This concept is also supported by the primordial role of the alternative pathway in the evolution of the complement system and the apparent lethality of factor B deficiency. The gene structures of most of these early components have now been elucidated providing the basis for detailed analyses of the defective alleles, the determination of carrier status, and prenatal diagnosis.

Complement C1↗

Long-term antibiotics in the management of non-CF bronchiectasis--do they improve outcome?

In addition to bacteria and inflammatory cells, the sputum of patients with bronchiectasis contains mediators that damage the airway epithelium and promote inflammatory change. The deleterious effects of these mediators, such as neutrophil elastase, reduce host defences and consequently perpetuate the propensity to recurrent infection. This 'vicious cycle' of infection and inflammation in bronchiectasis suggests that long-term antibiotic therapy might be beneficial in these patients by reducing microbial load and, in doing so, inhibit inflammation in the lung allowing tissue repair to occur. Short courses of antibiotics achieve clinical improvements and also have been shown to reduce the levels of harmful mediators in the sputum. This article will cite the studies reported for long-term antibiotic treatment in bronchiectasis and overall there seems to be benefits for patients with chronic sputum purulence. The evidence that supports the postulated pathological mechanisms will also be discussed. Important issues in clinical practice such as the usefulness of antibiotic sensitivities, the evolution of resistance patterns, and drug delivery will also be discussed.

Anti-Bacterial Agents↗

Innate immunity: New approaches to understanding its clinical significance.

Immunologists view innate immunity as evolution's ancient host response to infectious agents. Unlike vertebrates, in which antibodies and T-cell subsets rely on somatic mutations, molecular participants of innate immunity are encoded in the genome. Despite its heritage, many of innate immunity's sentinel molecules, intracellular transcriptional controls, and effector molecules participate in the pathogenesis of numerous complex human diseases. Toll-like receptors (TLRs), an important starting point, contact the environment and provide specific sensing for an important component of innate immunity. TLRs, found on macrophages, dendritic cells, and endothelial cells, recognize specific microbial molecular patterns. Beginning with these sentinel molecules, the process leads through intracytoplasmic mediators of transcription control and culminates with an array of host immune responses. Effector molecules include cytokines and the complement system. Polymorphisms within TLR genes might contribute to the pathogenesis of complex diseases. Disease associations linked to single nucleotide polymorphisms are in the early stage of experimental discovery; important clinical insights are emerging. Along these lines, studies of asthma provide an excellent example of how ancient ligand-receptor interactions and TLR polymorphisms provide new understanding of a common disease. New knowledge could facilitate the development of novel therapies.

Asthma↗

Mimivirus and the emerging concept of "giant" virus.

The recently discovered Acanthamoeba polyphaga Mimivirus is the largest known DNA virus. Its particle size (750 nm), genome length (1.2 million bp) and large gene repertoire (911 protein coding genes) blur the established boundaries between viruses and parasitic cellular organisms. In addition, the analysis of its genome sequence identified many types of genes never before encountered in a virus, including aminoacyl-tRNA synthetases and other central components of the translation machinery previously thought to be the signature of cellular organisms. In this article, we examine how the finding of such a giant virus might durably influence the way we look at microbial biodiversity, and lead us to revise the classification of microbial domains and life forms. We propose to introduce the word "girus" to recognize the intermediate status of these giant DNA viruses, the genome complexity of which makes them closer to small parasitic prokaryotes than to regular viruses.

Acanthamoeba↗

Genomic characterization of blaIMP-harboring plasmids in Klebsiella spp.

UNLABELLED: The spread of carbapenem-resistant Klebsiella spp. poses a significant public health threat, partly due to the acquisition of the blaIMP genes, which encode IMP-type metallo-β-lactamases. These enzymes confer resistance to a broad spectrum of β-lactam antibiotics, including carbapenems, thereby complicating treatment options. This study aims to provide a comprehensive genomic characterization of blaIMP-harboring plasmids across different species within the genus Klebsiella, based on the genomic characteristics of the plasmid pT117-2 of Klebsiella variicola strain T117 isolated from clinical settings in China, along with all available blaIMP-harboring plasmids of Klebsiella spp. fromthe GenBank database until 26 April 2025. Among the 123 blaIMP-harboring plasmids of Klebsiella spp., nine variants were identified, with blaIMP-4 (carried by 69 plasmids) and blaIMP-1 (carried by 37 plasmids) being the most prevalent. The blaIMP-4 gene was associated with IncN type (~50 kb, conjugative) and untypeable (~300 kb, non-mobilizable) plasmids in China, whereas in Australia, it was linked to IncC (~200 kb) and IncM2 (~80 kb) type conjugative plasmids. Meanwhile, blaIMP-1 was found to be associated with IncN (~50 kb), IncM (~80 kb), and IncFII (80 ~200 kb) type conjugative plasmids mainly in Japan. Notably, our results highlight the prevalence of IncN-type conjugative plasmids, including the plasmid pT117-2 identified in this study, as key vehicles for the dissemination of blaIMP genes. This study provides critical insights into the genetic mechanisms of blaIMP-harboring plasmids persistence and spread in Klebsiella spp., advancing our understanding of their dissemination. IMPORTANCE: Carbapenem-resistant Enterobacterales (CRE) mediated by metallo-β-lactamases (MBLs) pose a major global public health threat that challenges clinical antimicrobial therapy; based on our study, blaIMP-4 in China is predominantly associated with IncN plasmids (forming the "IncN-blaIMP-4-qnrS1" axis), while blaIMP-1 in Japan links to IncN/IncM/IncFII plasmids, with these regional differences highlighting the need for geographically targeted surveillance, and notably, the high-risk ST146 Klebsiella variicola carrying blaIMP-4 on a conjugative IncN plasmid serves as an underrecognized reservoir for resistance genes, extending surveillance beyond common pathogenic Enterobacterales; limitations of this study include restricted sample size and geographic scope, and future research should validate these patterns via multi-center studies, explore plasmid evolution mechanisms, and integrate findings into routine surveillance to optimize antibiotic stewardship and infection control, thereby mitigating the global spread of MBL-mediated CRE.

Plasmids↗

An evaluation of bacterial resistance to chemo-antibiotics in a homogeneous area comprising East Veneto and South Friuli.

The experiment, now in progress, consists in the gathering and processing of data obtained from the Antibiotic Sensitivity Test done in all the hospital laboratories in the aforesaid area and within which there may well be some interchange of patients. The Antibiotic Sensitivity Tests are arrived at from the identification of all the microorganisms found in the various biological specimens by rigorously standardized methodology. The data, reported on identical modules by all the laboratories and computerized by the CED of Treviso Hospital for half-yearly evaluation, will furnish information on the evolution of bacterial resistance and the related activity of the chemo-antibiotics for each individual hospital, for hospital groups, and for all the hospitals taken together. Details of the program of this operation, of the difficulties encountered, and of the current state of the survey are discussed.

Anti-Bacterial Agents↗