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Results for “virulence evolution”

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At least 361 records · Page 20Linked to original sources
PubMed1994

Current approaches to diagnosis and treatment of ovarian germ cell malignancies.

Ovarian germ cell malignancies are neoplasms derived from primitive germ cells of the embryonic gonad. These tumors are highly malignant, rapidly growing, and typically occur in young women. The prognosis for patients with ovarian non-dysgerminomatous germ cell malignancies was bleak before the introduction of modern combination chemotherapy. The evolution of modern chemotherapy transformed these virulent malignancies into highly curable ones. In the early 1970s, the combination of vincristine, actinomycin D, and cyclophosphamide (VAC) emerged as the first effective therapy. The efficacy of cisplatin, vinblastine, and bleomycin (PVB) was documented in treatment of men with testicular cancer and subsequently became standard treatment for women with ovarian germ cell malignancies. Bleomycin, etoposide, and cisplatin (BEP) are shown to have equal efficacy and less toxicity in the treatment of ovarian germ cell malignancies. Experience at Yale University suggested that patients with ovarian germ cell malignancies could be managed by using tumor histology to determine the type of chemotherapy, and determining treatment duration by serial assays of circulating tumor markers or by International Federation of Gynecologists and Obstetricians' staging. Preservation of reproductive function is appropriate for all patients with early stage disease and selected patients with more advanced disease.

Aftercare↗
PubMed1998

Myocardial abscess at a distant zone from the active valvular infection.

A case of an infective endocarditis with myocardial abscess due to Streptococcus anginosus at a distant location from the active valvular infection is reported. We conclude that local cardiac suppurative complications can appear in the evolution of endocarditis caused by this virulent organism.

Abscess↗
PubMed2002

Use of multiline cultivars and cultivar mixtures for disease management.

The usefulness of mixtures (multiline cultivars and cultivar mixtures) for disease management has been well demonstrated for rusts and powdery mildews of small grain crops. Such mixtures are more useful under some epidemiological conditions than under others, and experimental methodology, especially problems of scale, may be crucial in evaluating the potential efficacy of mixtures on disease. There are now examples of mixtures providing both low and high degrees of disease control for a wide range of pathosystems, including crops with large plants, and pathogens that demonstrate low host specificity, or are splash dispersed, soilborne, or insect vectored. Though most analyses of pathogen evolution in mixtures consider static costs of virulence to be the main mechanism countering selection for pathogen complexity, many other potential mechanisms need to be investigated. Agronomic and marketing considerations must be carefully evaluated when implementing mixture approaches to crop management. Practical difficulties associated with mixtures have often been overestimated, however, and mixtures will likely play an increasingly important role as we develop more sustainable agricultural systems.

Agriculture↗
PubMed1997

Speculation on possible life cycles for the clonal lineages in the genus toxoplasma.

Recent evidence suggests that the strains currently classified in the genus Toxoplasma, ie. within the species Toxoplasma gondii, may actually comprise at least two clonal lineages correlated with their virulence in mice. Here, Alan Johnson reviews these data in the context of evolution and speciation within the genus, and raises hypotheses on how the virulent lineage may undergo an asexual life cycle in nature, similar to that found for the very closely related coccidian, Neospora camnum. The putative vertical transmission life cycle of this mouse virulent lineage of T. gondii could involve passage to the foetus late in pregnancy, or transmission in milk to the neonate after birth.

Journal Article↗
PubMed2001

Fatal adenovirus type 7b infection in a child with Smith-Lemli-Opitz syndrome.

Adenovirus type 7 causes worldwide respiratory tract infections, mainly in children. Severe systemic infections can occur, especially in immunocompromised patients and in patients with underlying chronic diseases. This report describes the first case of a fatal disseminated adenovirus type 7 infection in a child with Smith-Lemli-Opitz syndrome, a rare autosomal recessive disorder due to a primary enzymatic defect in cholesterol metabolism. Nasopharyngeal secretions and autopsy specimens including liver, lung, pleural fluid, and rectum were collected for viral culture. Adenovirus serotype 7 strains were obtained from all anatomic sites, except the liver. All these clinical isolates were analyzed using restriction endonuclease digestion of the genome, identifying them as genome type 7b, a virulent type. In this case, the fatal evolution could have been accelerated by the presence of an immunodeficiency although immunodeficiency is not included in the definition of Smith-Lemli-Opitz syndrome. The frequent recurrent banal infections in Smith-Lemli-Opitz syndrome could be prevented by a cholesterol supplementation regimen. Finally, this report emphasizes the need for efficient therapy for disseminated adenovirus infections, especially for virulent genome types.

Adenovirus Infections, Human↗
PubMedDate not supplied

Biological comparison between three clones of Trypanosoma cruzi and the strain of origin (Bolivia) with reference to clonal evolution studies.

After isolating three clones of Trypanosoma cruzi (Bolivia), we first characterized them according to parasitaemia, pleomorphism and virulence, and then histopathologically. The study's interest lies on the hypothesis that clonal evolution of T. cruzi has a major impact on biologically relevant properties of this parasite. Data obtained from the studies of parasitaemia, pleomorphism and virulence showed no differences between the groups studied. As a final point, the histopathological study shows us a muscular tissue tropism both in clones and in their mother strain (Bolivia). In this paper, we conclude that Bolivia strain and clones isolated from it, pertaining to the same major clone share similar biological properties.

Animals↗
PubMed2026

Comparative genomics of ESKAPE pathogen species: Integrating pan-genome architecture, antimicrobial resistance, and virulence factor repertoires.

BACKGROUND: ESKAPE pathogens are major causes of hospital-acquired infections and are characterized by extensive antimicrobial resistance (AMR) and diverse virulence mechanisms. Although species-specific pan-genome studies have revealed substantial genomic diversity, the relationships among genome plasticity, resistance burden, and virulence remain incompletely understood across the ESKAPE complex. METHODS: We analyzed 120 high-quality genomes representing six single-species ESKAPE groups (20 genomes per species). Genome quality was assessed using CheckM2. Species-specific pan-genomes were constructed with Roary, AMR genes were identified using AMRFinderPlus, and virulence factors were detected against the VFDB database using DIAMOND. AMR genes were mapped to core and accessory genome compartments through integration of Prokka annotations and Roary outputs. Statistical associations were evaluated using Fisher's exact tests and correlation analyses, with false discovery rate correction applied within each test family. Core-genome maximum-likelihood phylogenies were reconstructed to provide an evolutionary framework. RESULTS: Pan-genome sizes ranged from 4720 to 17,272 genes, with Enterobacter and Pseudomonas possessing the largest accessory genomes. Multidrug resistance (MDR; resistance to ≥3 antimicrobial classes) was detected in 93.3% of strains. After false discovery rate correction, AMR genes remained significantly enriched in the accessory genomes of Enterobacter, Enterococcus, Klebsiella, and Staphylococcus, whereas Acinetobacter and Pseudomonas did not show significant enrichment in either genome compartment. Within-species analyses identified significant positive associations between accessory genome size and AMR class burden in Staphylococcus, Enterococcus, and Enterobacter, whereas the moderate Pearson correlation observed in Pseudomonas was not significant after FDR correction. Virulence factor repertoires varied markedly among species, with Pseudomonas exhibiting the highest burden and Enterococcus the lowest. CONCLUSIONS: ESKAPE pathogens display distinct patterns of resistance and virulence. Accessory genome expansion was associated with higher AMR burden in several species, whereas other species showed no significant association between accessory genome size and AMR burden and no significant enrichment of AMR genes in either genome compartment, highlighting the species-specific nature of AMR evolution.

Virulence Factors↗
PubMed2001

Ongoing horizontal and vertical transmission of virulence genes and papA alleles among Escherichia coli blood isolates from patients with diverse-source bacteremia.

The phylogenetic distributions of multiple putative virulence factors (VFs) and papA (P fimbrial structural subunit) alleles among 182 Escherichia coli blood isolates from patients with diverse-source bacteremia were defined. Phylogenetic correspondence among these strains, the E. coli Reference (ECOR) collection, and other collections of extraintestinal pathogenic E. coli (ExPEC) was assessed. Although among the 182 bacteremia isolates phylogenetic group B2 predominated, exhibited the greatest concentration of individual VFs, and contained the largest number of familiar virulent clones, other phylogenetic groups exhibited greater concentrations of certain VFs than did group B2 and included several additional virulent clones. Certain of the newly detected VF genes, e.g., fyuA (yersiniabactin; 76%) and focG (F1C fimbriae; 25%), were as prevalent or more prevalent than their more familiar traditional counterparts, e.g., iut (aerobactin; 57%) and sfaS (S fimbriae; 14%), thus possibly offering additional useful targets for preventive interventions. Considerable diversity of VF profiles was observed at every level within the phylogenetic tree, including even within individual lineages. This suggested that many different pathways can lead to extraintestinal virulence in E. coli and that the evolution of ExPEC, which involves extensive horizontal transmission of VFs and continuous remodeling of pathogenicity-associated islands, is a highly active, ongoing process.

Adult↗
PubMed1980

A theory of modular evolution for bacteriophages.

The modular theory of virus evolution has clear experimental support among the temperate bacteriophages of the enteric bacteria. However, there is also similar genetic and DNA heteroduplex evidence for such evolution among other families of bacteriophages: the virulent bacteriophages of the enterics comprise several families: the T-even group, the T3-T7 group (which has many members among different species of bacteria, including bacteria as widely divergent as E. coli and Caulobacter crescentus. It nicely explains the diffusion of very similar homologous bacteriophages into hosts whose own DNAs have diverged very greatly from each other in nucleotide sequence. It also accounts for the rigorous maintenance of regulatory schemes while units of function (including regions coding for proteins) diverge more rapidly. It should also be noted that the considerations that make modular evolution seem advantageous for bacteriophages apply equally well to viruses of higher organisms. Furthermore, the kinds of heteroduplex similarity observed among animal viruses are reminiscent of what is found for bacteriophages. Viruses found in widely divergent hosts show much greater similarity than would be expected; quite possibly animal viruses also evolve as a population of interchangeable modules.

Bacteriophage lambda↗
PubMed1998

Phylogenetic analysis of Escherichia coli strains causing neonatal meningitis suggests horizontal gene transfer from a predominant pool of highly virulent B2 group strains.

Phylogenetic relationships of 69 neonatal meningitis Escherichia coli strains isolated worldwide were studied. Restriction fragment length polymorphism of rrn operons (rrn RFLP) in these isolates was compared with that of the 72 strains of the ECOR reference collection. Distributions of K1 antigen, of polymerase chain reaction-detected ibe10 gene, pap, afa, sfa/foc, hly, and aer operons, and of a 14.9-kb rrn-containing HindIII fragment previously associated with neonatal meningitis were compared. Oligoclonality was observed for the meningitis strains. Factorial analysis of correspondence on the rrn RFLP data showed a frequency gradient of meningitis strains from the phylogenetic B2 group (68%) to the A group (6%), via the D and B1 groups (26%). The distribution of the virulence determinants argues for their horizontal transfer during the evolution of E. coli. Analysis of the status of some neonates further suggests that neonatal meningitis results from a balance between bacterial genes of virulence and host factors.

Bacterial Typing Techniques↗
PubMed1995

Intragenic recombination of a single plant pathogen gene provides a mechanism for the evolution of new host specificities.

Gene pthA is required for virulence of Xanthomonas citri on citrus plants and has pleiotropic pathogenicity and avirulence functions when transferred to many different xanthomonads. DNA sequencing revealed that pthA belongs to a family of Xanthomonas avirulence/pathogenicity genes characterized by nearly identical 102-bp tandem repeats in the central region. By inserting an nptI-sac cartridge into the tandemly repeated region of pthA as a selective marker, intragenic recombination among homologous repeats was observed in both Xanthomonas spp. and Escherichia coli. Intragenic recombination within pthA created new genes with novel host specificities and altered pathogenicity and/or avirulence phenotypes. Many pthA recombinants gained or lost avirulence function in pathogenicity assays on bean, citrus, and cotton cultivars. Although the ability to induce cell division (hyperplastic cankers) on citrus could be lost, this ability was not acquired on cotton or bean plants. Intragenic recombination therefore provides a genetic mechanism for the generation of multiple, different, and gratuitous avirulence genes from a single, required, host-specific pathogenicity gene.

Amino Acid Sequence↗
PubMed1996

Pathogenicity islands and the evolution of bacterial pathogens.

The term pathogenicity island has been used to refer to large chromosomal regions in pathogenic bacteria that encode virulence genes. This article reviews the recent history of this term and considers what characteristics define a pathogenicity island. It appears that pathogenicity islands can confer complex virulence phenotypes and were acquired by bacteria from unrelated organisms, leading to interesting hypotheses about how bacterial pathogens evolved. It is likely that mechanisms that generate pathogenicity islands continue to operate and may contribute to the emergence of bacterial pathogens with new virulence properties.

Bacteria↗
PubMed2002

Extraintestinal pathogenic Escherichia coli: "the other bad E coli".

Extraintestinal pathogenic Escherichia coli (ExPEC), the specialized strains of E coli that cause most extraintestinal E coli infections, represent a major but little-appreciated health threat. Although the reasons for their evolution remain mysterious, by virtue of their numerous virulence traits ExPEC clearly possess a unique ability to cause disease outside the host intestinal tract. Broader appreciation of the existence and importance of ExPEC and better understandings of their distinctive virulence mechanisms, reservoirs, and transmission pathways may lead to effective preventive interventions against the morbid and costly infections ExPEC cause.

Biological Evolution↗
PubMed1998

Complete DNA sequence and detailed analysis of the Yersinia pestis KIM5 plasmid encoding murine toxin and capsular antigen.

Yersinia pestis, the causative agent of plague, harbors at least three plasmids necessary for full virulence of the organism, two of which are species specific. One of the Y. pestis-specific plasmids, pMT1, is thought to promote deep tissue invasion, resulting in more acute onset of symptoms and death. We determined the entire nucleotide sequence of Y. pestis KIM5 pMT1 and identified potential open reading frames (ORFs) encoded by the 100,990-bp molecule. Based on codon usage for known yersinial genes, homology with known proteins in the databases, and potential ribosome binding sites, we determined that 115 of the potential ORFs which we considered could encode polypeptides in Y. pestis. Five of these ORFs were genes previously identified as being necessary for production of the classic virulence factors, murine toxin (MT), and the fraction 1 (F1) capsule antigen. The regions of pMT1 encoding MT and F1 were surrounded by remnants of multiple transposition events and bacteriophage, respectively, suggesting horizontal gene transfer of these virulence factors. We identified seven new potential virulence factors that might interact with the mammalian host or flea vector. Forty-three of the remaining 115 putative ORFs did not display any significant homology with proteins in the current databases. Furthermore, DNA sequence analysis allowed the determination of the putative replication and partitioning regions of pMT1. We identified a single 2,450-bp region within pMT1 that could function as the origin of replication, including a RepA-like protein similar to RepFIB, RepHI1B, and P1 and P7 replicons. Plasmid partitioning function was located ca. 36 kb from the putative origin of replication and was most similar to the parABS bacteriophage P1 and P7 system. Y. pestis pMT1 encoded potential genes with a high degree of similarity to a wide variety of organisms, plasmids, and bacteriophage. Accordingly, our analysis of the pMT1 DNA sequence emphasized the mosaic nature of this large bacterial virulence plasmid and provided implications as to its evolution.

Antigens, Bacterial↗
PubMed2001

Protein regions important for plasminogen activation and inactivation of alpha2-antiplasmin in the surface protease Pla of Yersinia pestis.

The plasminogen activator, surface protease Pla, of the plague bacterium Yersinia pestis is an important virulence factor that enables the spread of Y. pestis from subcutaneous sites into circulation. Pla-expressing Y. pestis and recombinant Escherichia coli formed active plasmin in the presence of the major human plasmin inhibitor, alpha2-antiplasmin, and the bacteria were found to inactivate alpha2-antiplasmin. In contrast, only poor plasminogen activation and no cleavage of alpha2-antiplasmin was observed with recombinant bacteria expressing the homologous gene ompT from E. coli. A beta-barrel topology model for Pla and OmpT predicted 10 transmembrane beta-strands and five surface-exposed loops L1-L5. Hybrid Pla-OmpT proteins were created by substituting each of the loops between Pla and OmpT. Analysis of the hybrid molecules suggested a critical role of L3 and L4 in the substrate specificity of Pla towards plasminogen and alpha2-antiplasmin. Substitution analysis at 25 surface-located residues showed the importance of the conserved residues H101, H208, D84, D86, D206 and S99 for the proteolytic activity of Pla-expressing recombinant E. coli. The mature alpha-Pla of 292 amino acids was processed into beta-Pla by an autoprocessing cleavage at residue K262, and residues important for the self-recognition of Pla were identified. Prevention of autoprocessing of Pla, however, had no detectable effect on plasminogen activation or cleavage of alpha2-antiplasmin. Cleavage of alpha2-antiplasmin and plasminogen activation were influenced by residue R211 in L4 as well as by unidentified residues in L3. OmpT, which is not associated with invasive bacterial disease, was converted into a Pla-like protease by deleting residues D214 and P215, by substituting residue K217 for R217 in L4 of OmpT and also by substituting the entire L3 with that from Pla. This simple modification of the surface loops and the substrate specificity of OmpT exemplifies the evolution of a housekeeping protein into a virulence factor by subtle mutations at critical protein regions. We propose that inactivation of alpha2-antiplasmin by Pla of Y. pestis promotes uncontrolled proteolysis and contributes to the invasive character of plague.

Amino Acid Sequence↗
PubMed2006

Intersection of fungal fitness and virulence in Cryptococcus neoformans.

The use of insertional mutagenesis to discover genes that impact laccase activity has resulted in the identification of multiple cellular processes that affect the fitness of Cryptococcus neoformans. Fitness has been defined as the ability of an organism to propagate and evolve within a given environment. Because the human host is an evolutionary dead-end for an opportunistic pathogen, we have defined pathogenic fitness here as the capability to successfully propagate within the stressful environment of the host, causing disease by expression of virulence traits that damage the host. In this review, laccase-deficient insertional mutants will be highlighted in terms of the basic biological processes in which they are involved. The impact of laccase-associated cellular functions on fitness and virulence will be discussed, as will the mutants' potential as therapeutic targets. Vacuolar function, copper homeostasis, mitochondrial function and carbon repression are covered.

Cryptococcosis↗