Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.Bacterial Proteins: Proteins found in any species of bacterium.Gene Expression Regulation, Bacterial: Any of the processes by which cytoplasmic or intercellular factors influence the differential control of gene action in bacteria.Genes, Bacterial: The functional hereditary units of BACTERIA.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Gene Deletion: A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus.Bacterial Adhesion: Physicochemical property of fimbriated (FIMBRIAE, BACTERIAL) and non-fimbriated bacteria of attaching to cells, tissue, and nonbiological surfaces. It is a factor in bacterial colonization and pathogenicity.Plant Diseases: Diseases of plants.DNA, Bacterial: Deoxyribonucleic acid that makes up the genetic material of bacteria.Host-Pathogen Interactions: The interactions between a host and a pathogen, usually resulting in disease.Quorum Sensing: A phenomenon where microorganisms communicate and coordinate their behavior by the accumulation of signaling molecules. A reaction occurs when a substance accumulates to a sufficient concentration. This is most commonly seen in bacteria.Escherichia coli Infections: Infections with bacteria of the species ESCHERICHIA COLI.Hemolysin Proteins: Proteins from BACTERIA and FUNGI that are soluble enough to be secreted to target ERYTHROCYTES and insert into the membrane to form beta-barrel pores. Biosynthesis may be regulated by HEMOLYSIN FACTORS.Genomic Islands: Distinct units in some bacterial, bacteriophage or plasmid GENOMES that are types of MOBILE GENETIC ELEMENTS. Encoded in them are a variety of fitness conferring genes, such as VIRULENCE FACTORS (in "pathogenicity islands or islets"), ANTIBIOTIC RESISTANCE genes, or genes required for SYMBIOSIS (in "symbiosis islands or islets"). They range in size from 10 - 500 kilobases, and their GC CONTENT and CODON usage differ from the rest of the genome. They typically contain an INTEGRASE gene, although in some cases this gene has been deleted resulting in "anchored genomic islands".Bacterial Toxins: Toxic substances formed in or elaborated by bacteria; they are usually proteins with high molecular weight and antigenicity; some are used as antibiotics and some to skin test for the presence of or susceptibility to certain diseases.Adhesins, Bacterial: Cell-surface components or appendages of bacteria that facilitate adhesion (BACTERIAL ADHESION) to other cells or to inanimate surfaces. Most fimbriae (FIMBRIAE, BACTERIAL) of gram-negative bacteria function as adhesins, but in many cases it is a minor subunit protein at the tip of the fimbriae that is the actual adhesin. In gram-positive bacteria, a protein or polysaccharide surface layer serves as the specific adhesin. What is sometimes called polymeric adhesin (BIOFILMS) is distinct from protein adhesin.Plasmids: Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.Yersinia pestis: The etiologic agent of PLAGUE in man, rats, ground squirrels, and other rodents.Mice, Inbred BALB CEscherichia coli: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.Bacterial Outer Membrane Proteins: Proteins isolated from the outer membrane of Gram-negative bacteria.Genome, Bacterial: The genetic complement of a BACTERIA as represented in its DNA.Lethal Dose 50: The dose amount of poisonous or toxic substance or dose of ionizing radiation required to kill 50% of the tested population.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Mutagenesis, Insertional: Mutagenesis where the mutation is caused by the introduction of foreign DNA sequences into a gene or extragenic sequence. This may occur spontaneously in vivo or be experimentally induced in vivo or in vitro. Proviral DNA insertions into or adjacent to a cellular proto-oncogene can interrupt GENETIC TRANSLATION of the coding sequences or interfere with recognition of regulatory elements and cause unregulated expression of the proto-oncogene resulting in tumor formation.Salmonella typhimurium: A serotype of Salmonella enterica that is a frequent agent of Salmonella gastroenteritis in humans. It also causes PARATYPHOID FEVER.Sequence Analysis, DNA: A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.Genetic Complementation Test: A test used to determine whether or not complementation (compensation in the form of dominance) will occur in a cell with a given mutant phenotype when another mutant genome, encoding the same mutant phenotype, is introduced into that cell.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Streptococcus pyogenes: A species of gram-positive, coccoid bacteria isolated from skin lesions, blood, inflammatory exudates, and the upper respiratory tract of humans. It is a group A hemolytic Streptococcus that can cause SCARLET FEVER and RHEUMATIC FEVER.Pseudomonas aeruginosa: A species of gram-negative, aerobic, rod-shaped bacteria commonly isolated from clinical specimens (wound, burn, and urinary tract infections). It is also found widely distributed in soil and water. P. aeruginosa is a major agent of nosocomial infection.Cryptococcus neoformans: A species of the fungus CRYPTOCOCCUS. Its teleomorph is Filobasidiella neoformans.Escherichia coli Proteins: Proteins obtained from ESCHERICHIA COLI.Phylogeny: The relationships of groups of organisms as reflected by their genetic makeup.Vibrio cholerae: The etiologic agent of CHOLERA.Antigens, Bacterial: Substances elaborated by bacteria that have antigenic activity.Candida albicans: A unicellular budding fungus which is the principal pathogenic species causing CANDIDIASIS (moniliasis).Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Shigella flexneri: A bacterium which is one of the etiologic agents of bacillary dysentery (DYSENTERY, BACILLARY) and sometimes of infantile gastroenteritis.Listeria monocytogenes: A species of gram-positive, rod-shaped bacteria widely distributed in nature. It has been isolated from sewage, soil, silage, and from feces of healthy animals and man. Infection with this bacterium leads to encephalitis, meningitis, endocarditis, and abortion.Yersinia pseudotuberculosis: A human and animal pathogen causing mesenteric lymphadenitis, diarrhea, and bacteremia.Staphylococcus aureus: Potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications.Yersinia enterocolitica: A species of the genus YERSINIA, isolated from both man and animal. It is a frequent cause of bacterial gastroenteritis in children.Streptococcal Infections: Infections with bacteria of the genus STREPTOCOCCUS.Serotyping: Process of determining and distinguishing species of bacteria or viruses based on antigens they share.Fungal Proteins: Proteins found in any species of fungus.Fimbriae, Bacterial: Thin, hairlike appendages, 1 to 20 microns in length and often occurring in large numbers, present on the cells of gram-negative bacteria, particularly Enterobacteriaceae and Neisseria. Unlike flagella, they do not possess motility, but being protein (pilin) in nature, they possess antigenic and hemagglutinating properties. They are of medical importance because some fimbriae mediate the attachment of bacteria to cells via adhesins (ADHESINS, BACTERIAL). Bacterial fimbriae refer to common pili, to be distinguished from the preferred use of "pili", which is confined to sex pili (PILI, SEX).Plague: An acute infectious disease caused by YERSINIA PESTIS that affects humans, wild rodents, and their ectoparasites. This condition persists due to its firm entrenchment in sylvatic rodent-flea ecosystems throughout the world. Bubonic plague is the most common form.Bacterial Capsules: An envelope of loose gel surrounding a bacterial cell which is associated with the virulence of pathogenic bacteria. Some capsules have a well-defined border, whereas others form a slime layer that trails off into the medium. Most capsules consist of relatively simple polysaccharides but there are some bacteria whose capsules are made of polypeptides.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Regulon: In eukaryotes, a genetic unit consisting of a noncontiguous group of genes under the control of a single regulator gene. In bacteria, regulons are global regulatory systems involved in the interplay of pleiotropic regulatory domains and consist of several OPERONS.Hyphae: Microscopic threadlike filaments in FUNGI that are filled with a layer of protoplasm. Collectively, the hyphae make up the MYCELIUM.Microbial Viability: Ability of a microbe to survive under given conditions. This can also be related to a colony's ability to replicate.DNA Transposable Elements: Discrete segments of DNA which can excise and reintegrate to another site in the genome. Most are inactive, i.e., have not been found to exist outside the integrated state. DNA transposable elements include bacterial IS (insertion sequence) elements, Tn elements, the maize controlling elements Ac and Ds, Drosophila P, gypsy, and pogo elements, the human Tigger elements and the Tc and mariner elements which are found throughout the animal kingdom.Salmonella Infections, Animal: Infections in animals with bacteria of the genus SALMONELLA.Operon: In bacteria, a group of metabolically related genes, with a common promoter, whose transcription into a single polycistronic MESSENGER RNA is under the control of an OPERATOR REGION.Yersinia pseudotuberculosis Infections: Infections with bacteria of the species YERSINIA PSEUDOTUBERCULOSIS.Colony Count, Microbial: Enumeration by direct count of viable, isolated bacterial, archaeal, or fungal CELLS or SPORES capable of growth on solid CULTURE MEDIA. The method is used routinely by environmental microbiologists for quantifying organisms in AIR; FOOD; and WATER; by clinicians for measuring patients' microbial load; and in antimicrobial drug testing.Fimbriae Proteins: Proteins that are structural components of bacterial fimbriae (FIMBRIAE, BACTERIAL) or sex pili (PILI, SEX).Macrophages: The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)Vibrio Infections: Infections with bacteria of the genus VIBRIO.Gene Knockout Techniques: Techniques to alter a gene sequence that result in an inactivated gene, or one in which the expression can be inactivated at a chosen time during development to study the loss of function of a gene.Yersinia: A genus of gram-negative, facultatively anaerobic rod- to coccobacillus-shaped bacteria that occurs in a broad spectrum of habitats.Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.Yersinia Infections: Infections with bacteria of the genus YERSINIA.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Species Specificity: The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.Siderophores: Low-molecular-weight compounds produced by microorganisms that aid in the transport and sequestration of ferric iron. (The Encyclopedia of Molecular Biology, 1994)Salmonella: A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria that utilizes citrate as a sole carbon source. It is pathogenic for humans, causing enteric fevers, gastroenteritis, and bacteremia. Food poisoning is the most common clinical manifestation. Organisms within this genus are separated on the basis of antigenic characteristics, sugar fermentation patterns, and bacteriophage susceptibility.Bacterial Secretion Systems: In GRAM NEGATIVE BACTERIA, multiprotein complexes that function to translocate pathogen protein effector molecules across the bacterial cell envelope, often directly into the host. These effectors are involved in producing surface structures for adhesion, bacterial motility, manipulation of host functions, modulation of host defense responses, and other functions involved in facilitating survival of the pathogen. Several of the systems have homologous components functioning similarly in GRAM POSITIVE BACTERIA.Vibrio vulnificus: A species of halophilic bacteria in the genus VIBRIO, which lives in warm SEAWATER. It can cause infections in those who eat raw contaminated seafood or have open wounds exposed to seawater.Cryptococcosis: Infection with a fungus of the species CRYPTOCOCCUS NEOFORMANS.Pseudomonas Infections: Infections with bacteria of the genus PSEUDOMONAS.Rhodococcus equi: A species of RHODOCOCCUS found in soil, herbivore dung, and in the intestinal tract of cows, horses, sheep, and pigs. It causes bronchopneumonia in foals and can be responsible for infection in humans compromised by immunosuppressive drug therapy, lymphoma, or AIDS.Gene Expression Regulation, Fungal: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in fungi.Staphylococcal Infections: Infections with bacteria of the genus STAPHYLOCOCCUS.Streptolysins: Exotoxins produced by certain strains of streptococci, particularly those of group A (STREPTOCOCCUS PYOGENES), that cause HEMOLYSIS.Vibrio: A genus of VIBRIONACEAE, made up of short, slightly curved, motile, gram-negative rods. Various species produce cholera and other gastrointestinal disorders as well as abortion in sheep and cattle.Host-Parasite Interactions: The relationship between an invertebrate and another organism (the host), one of which lives at the expense of the other. Traditionally excluded from definition of parasites are pathogenic BACTERIA; FUNGI; VIRUSES; and PLANTS; though they may live parasitically.Poultry Diseases: Diseases of birds which are raised as a source of meat or eggs for human consumption and are usually found in barnyards, hatcheries, etc. The concept is differentiated from BIRD DISEASES which is for diseases of birds not considered poultry and usually found in zoos, parks, and the wild.Polysaccharides, Bacterial: Polysaccharides found in bacteria and in capsules thereof.Cloning, Molecular: The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.Anti-Bacterial Agents: Substances that reduce the growth or reproduction of BACTERIA.4-Butyrolactone: One of the FURANS with a carbonyl thereby forming a cyclic lactone. It is an endogenous compound made from gamma-aminobutyrate and is the precursor of gamma-hydroxybutyrate. It is also used as a pharmacological agent and solvent.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Candidiasis: Infection with a fungus of the genus CANDIDA. It is usually a superficial infection of the moist areas of the body and is generally caused by CANDIDA ALBICANS. (Dorland, 27th ed)Gene Expression Profiling: The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.Pseudomonas syringae: A species of gram-negative, fluorescent, phytopathogenic bacteria in the genus PSEUDOMONAS. It is differentiated into approximately 50 pathovars with different plant pathogenicities and host specificities.Sequence Alignment: The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.Francisella tularensis: The etiologic agent of TULAREMIA in man and other warm-blooded animals.Serial Passage: Inoculation of a series of animals or in vitro tissue with an infectious bacterium or virus, as in VIRULENCE studies and the development of vaccines.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.Genetic Variation: Genotypic differences observed among individuals in a population.Cytotoxins: Substances that are toxic to cells; they may be involved in immunity or may be contained in venoms. These are distinguished from CYTOSTATIC AGENTS in degree of effect. Some of them are used as CYTOTOXIC ANTIBIOTICS. The mechanism of action of many of these are as ALKYLATING AGENTS or MITOSIS MODULATORS.Fish Diseases: Diseases of freshwater, marine, hatchery or aquarium fish. This term includes diseases of both teleosts (true fish) and elasmobranchs (sharks, rays and skates).Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Drug Resistance, Bacterial: The ability of bacteria to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).Mutagenesis: Process of generating a genetic MUTATION. It may occur spontaneously or be induced by MUTAGENS.Bacillus anthracis: A species of bacteria that causes ANTHRAX in humans and animals.RNA, Bacterial: Ribonucleic acid in bacteria having regulatory and catalytic roles as well as involvement in protein synthesis.Iron: A metallic element with atomic symbol Fe, atomic number 26, and atomic weight 55.85. It is an essential constituent of HEMOGLOBINS; CYTOCHROMES; and IRON-BINDING PROTEINS. It plays a role in cellular redox reactions and in the transport of OXYGEN.Blood Bactericidal Activity: The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST.Xanthomonas: A genus in the family XANTHOMONADACEAE whose cells produce a yellow pigment (Gr. xanthos - yellow). It is pathogenic to plants.Culture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as AGAR or GELATIN.Ascomycota: A phylum of fungi which have cross-walls or septa in the mycelium. The perfect state is characterized by the formation of a saclike cell (ascus) containing ascospores. Most pathogenic fungi with a known perfect state belong to this phylum.Phagocytosis: The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).Open Reading Frames: A sequence of successive nucleotide triplets that are read as CODONS specifying AMINO ACIDS and begin with an INITIATOR CODON and end with a stop codon (CODON, TERMINATOR).Cell Wall: The outermost layer of a cell in most PLANTS; BACTERIA; FUNGI; and ALGAE. The cell wall is usually a rigid structure that lies external to the CELL MEMBRANE, and provides a protective barrier against physical or chemical agents.Transcription, Genetic: The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.Streptococcus pneumoniae: A gram-positive organism found in the upper respiratory tract, inflammatory exudates, and various body fluids of normal and/or diseased humans and, rarely, domestic animals.Pectobacterium chrysanthemi: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria that causes vascular wilts on a wide range of plant species. It was formerly named Erwinia chrysanthemi.Multigene Family: A set of genes descended by duplication and variation from some ancestral gene. Such genes may be clustered together on the same chromosome or dispersed on different chromosomes. Examples of multigene families include those that encode the hemoglobins, immunoglobulins, histocompatibility antigens, actins, tubulins, keratins, collagens, heat shock proteins, salivary glue proteins, chorion proteins, cuticle proteins, yolk proteins, and phaseolins, as well as histones, ribosomal RNA, and transfer RNA genes. The latter three are examples of reiterated genes, where hundreds of identical genes are present in a tandem array. (King & Stanfield, A Dictionary of Genetics, 4th ed)Escherichia coli O157: A verocytotoxin-producing serogroup belonging to the O subfamily of Escherichia coli which has been shown to cause severe food-borne disease. A strain from this serogroup, serotype H7, which produces SHIGA TOXINS, has been linked to human disease outbreaks resulting from contamination of foods by E. coli O157 from bovine origin.Prophages: Genomes of temperate BACTERIOPHAGES integrated into the DNA of their bacterial host cell. The prophages can be duplicated for many cell generations until some stimulus induces its activation and virulence.Aspergillus fumigatus: A species of imperfect fungi from which the antibiotic fumigatin is obtained. Its spores may cause respiratory infection in birds and mammals.Urinary Tract Infections: Inflammatory responses of the epithelium of the URINARY TRACT to microbial invasions. They are often bacterial infections with associated BACTERIURIA and PYURIA.Flagella: A whiplike motility appendage present on the surface cells. Prokaryote flagella are composed of a protein called FLAGELLIN. Bacteria can have a single flagellum, a tuft at one pole, or multiple flagella covering the entire surface. In eukaryotes, flagella are threadlike protoplasmic extensions used to propel flagellates and sperm. Flagella have the same basic structure as CILIA but are longer in proportion to the cell bearing them and present in much smaller numbers. (From King & Stansfield, A Dictionary of Genetics, 4th ed)Pyocyanine: Antibiotic pigment produced by Pseudomonas aeruginosa.Exotoxins: Toxins produced, especially by bacterial or fungal cells, and released into the culture medium or environment.Aeromonas hydrophila: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria that may be pathogenic for frogs, fish, and mammals, including man. In humans, cellulitis and diarrhea can result from infection with this organism.Mycobacterium tuberculosis: A species of gram-positive, aerobic bacteria that produces TUBERCULOSIS in humans, other primates, CATTLE; DOGS; and some other animals which have contact with humans. Growth tends to be in serpentine, cordlike masses in which the bacilli show a parallel orientation.Lycopersicon esculentum: A plant species of the family SOLANACEAE, native of South America, widely cultivated for their edible, fleshy, usually red fruit.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Streptococcus suis: A species of STREPTOCOCCUS isolated from pigs. It is a pathogen of swine but rarely occurs in humans.Ralstonia solanacearum: A species of Ralstonia previously classed in the genera PSEUDOMONAS and BURKHOLDERIA. It is an important plant pathogen.Enterohemorrhagic Escherichia coli: Strains of ESCHERICHIA COLI that are a subgroup of SHIGA-TOXIGENIC ESCHERICHIA COLI. They cause non-bloody and bloody DIARRHEA; HEMOLYTIC UREMIC SYNDROME; and hemorrhagic COLITIS. An important member of this subgroup is ESCHERICHIA COLI O157-H7.Hemagglutinins: Agents that cause agglutination of red blood cells. They include antibodies, blood group antigens, lectins, autoimmune factors, bacterial, viral, or parasitic blood agglutinins, etc.Salmonella Infections: Infections with bacteria of the genus SALMONELLA.Porphyromonas gingivalis: A species of gram-negative, anaerobic, rod-shaped bacteria originally classified within the BACTEROIDES genus. This bacterium produces a cell-bound, oxygen-sensitive collagenase and is isolated from the human mouth.Oligonucleotide Array Sequence Analysis: Hybridization of a nucleic acid sample to a very large set of OLIGONUCLEOTIDE PROBES, which have been attached individually in columns and rows to a solid support, to determine a BASE SEQUENCE, or to detect variations in a gene sequence, GENE EXPRESSION, or for GENE MAPPING.Cholera: An acute diarrheal disease endemic in India and Southeast Asia whose causative agent is VIBRIO CHOLERAE. This condition can lead to severe dehydration in a matter of hours unless quickly treated.Diarrhea: An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.Trans-Activators: Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.Gene Transfer, Horizontal: The naturally occurring transmission of genetic information between organisms, related or unrelated, circumventing parent-to-offspring transmission. Horizontal gene transfer may occur via a variety of naturally occurring processes such as GENETIC CONJUGATION; GENETIC TRANSDUCTION; and TRANSFECTION. It may result in a change of the recipient organism's genetic composition (TRANSFORMATION, GENETIC).Chickens: Common name for the species Gallus gallus, the domestic fowl, in the family Phasianidae, order GALLIFORMES. It is descended from the red jungle fowl of SOUTHEAST ASIA.Enterococcus faecalis: A species of gram-positive, coccoid bacteria commonly isolated from clinical specimens and the human intestinal tract. Most strains are nonhemolytic.Pectobacterium carotovorum: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria that causes rotting, particularly of storage tissues, of a wide variety of plants and causes a vascular disease in CARROTS; and POTATO plants.Bacterial Typing Techniques: Procedures for identifying types and strains of bacteria. The most frequently employed typing systems are BACTERIOPHAGE TYPING and SEROTYPING as well as bacteriocin typing and biotyping.Sigma Factor: A protein which is a subunit of RNA polymerase. It effects initiation of specific RNA chains from DNA.HomoserinePlant Tumors: A localized proliferation of plant tissue forming a swelling or outgrowth, commonly with a characteristic shape and unlike any organ of the normal plant. Plant tumors or galls usually form in response to the action of a pathogen or a pest. (Holliday, P., A Dictionary of Plant Pathology, 1989, p330)Chromosomes, Bacterial: Structures within the nucleus of bacterial cells consisting of or containing DNA, which carry genetic information essential to the cell.Salmonella enterica: A subgenus of Salmonella containing several medically important serotypes. The habitat for the majority of strains is warm-blooded animals.Swine: Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).Gram-Negative Bacterial Infections: Infections caused by bacteria that show up as pink (negative) when treated by the gram-staining method.Metarhizium: A mitosporic fungal genus in the family Clavicipitaceae. It has teleomorphs in the family Nectriaceae. Metarhizium anisopliae is used in PESTICIDES.Francisella: The lone genus of bacteria in the family Francisellaceae, frequently found in natural waters. It can be parasitic in humans, other MAMMALS; BIRDS; and ARTHROPODS.Animals, Outbred Strains: Animals that are generated from breeding two genetically dissimilar strains of the same species.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.O Antigens: The lipopolysaccharide-protein somatic antigens, usually from gram-negative bacteria, important in the serological classification of enteric bacilli. The O-specific chains determine the specificity of the O antigens of a given serotype. O antigens are the immunodominant part of the lipopolysaccharide molecule in the intact bacterial cell. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)Sequence Deletion: Deletion of sequences of nucleic acids from the genetic material of an individual.Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.Chicory: A thick-rooted perennial (Cichorium intybus) native to Europe but widely grown for its young leaves used as salad greens and for its roots, dried and ground-roasted, used to flavor or adulterate coffee. (From Webster, 3d ed)Vaccines, Attenuated: Live vaccines prepared from microorganisms which have undergone physical adaptation (e.g., by radiation or temperature conditioning) or serial passage in laboratory animal hosts or infected tissue/cell cultures, in order to produce avirulent mutant strains capable of inducing protective immunity.Beauveria: A mitosporic fungal genus. Teleomorphs are found in the family Clavicipitaceae and include Cordyceps bassiana. The species Beauveria bassiana is a common pathogen of ARTHROPODS and is used in PEST CONTROL.Legionella pneumophila: A species of gram-negative, aerobic bacteria that is the causative agent of LEGIONNAIRES' DISEASE. It has been isolated from numerous environmental sites as well as from human lung tissue, respiratory secretions, and blood.Viral Proteins: Proteins found in any species of virus.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Tularemia: A plague-like disease of rodents, transmissible to man. It is caused by FRANCISELLA TULARENSIS and is characterized by fever, chills, headache, backache, and weakness.Listeriosis: Infections with bacteria of the genus LISTERIA.Erwinia amylovora: A species of gram-negative bacteria, in the genus ERWINIA, causing a necrotic disease of plants.Mice, Inbred C57BLVirus Replication: The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.Edwardsiella tarda: A species of EDWARDSIELLA distinguished by its hydrogen sulfide production. (From Bergey's Manual of Determinative Bacteriology, 9th ed)Recombination, Genetic: Production of new arrangements of DNA by various mechanisms such as assortment and segregation, CROSSING OVER; GENE CONVERSION; GENETIC TRANSFORMATION; GENETIC CONJUGATION; GENETIC TRANSDUCTION; or mixed infection of viruses.Adhesins, Escherichia coli: Thin, filamentous protein structures, including proteinaceous capsular antigens (fimbrial antigens), that mediate adhesion of E. coli to surfaces and play a role in pathogenesis. They have a high affinity for various epithelial cells.Bacterial Vaccines: Suspensions of attenuated or killed bacteria administered for the prevention or treatment of infectious bacterial disease.Aeromonas: A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria that occurs singly, in pairs, or in short chains. Its organisms are found in fresh water and sewage and are pathogenic to humans, frogs, and fish.Acanthamoeba castellanii: A species of free-living soil amoebae in the family Acanthamoebidae. It can cause ENCEPHALITIS and KERATITIS in humans.DNA Primers: Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.

Role of DnaK in in vitro and in vivo expression of virulence factors of Vibrio cholerae. (1/14670)

The dnaK gene of Vibrio cholerae was cloned, sequenced, and used to construct a dnaK insertion mutant which was then used to examine the role of DnaK in expression of the major virulence factors of this important human pathogen. The central regulator of several virulence genes of V. cholerae is ToxR, a transmembrane DNA binding protein. The V. cholerae dnaK mutant grown in standard laboratory medium exhibited phenotypes characteristic of cells deficient in ToxR activity. Using Northern blot analysis and toxR transcriptional fusions, we demonstrated a reduction in expression of the toxR gene in the dnaK mutant strain together with a concomitant increase in expression of a htpG-like heat shock gene that is located immediately upstream and is divergently transcribed from toxR. This may be due to increased heat shock induction in the dnaK mutant. In vivo, however, although expression from heat shock promoters in the dnaK mutant was similar to that observed in vitro, expression of both toxR and htpG was comparable to that by the parental strain. In both strains, in vivo expression of toxR was significantly higher than that observed in vitro, but no reciprocal decrease in htpG expression was observed. These results suggest that the modulation of toxR expression in vivo may be different from that observed in vitro.  (+info)

Alpha-toxin and gamma-toxin jointly promote Staphylococcus aureus virulence in murine septic arthritis. (2/14670)

Septic arthritis is a common and feared complication of staphylococcal infections. Staphylococcus aureus produces a number of potential virulence factors including certain adhesins and enterotoxins. In this study we have assessed the roles of cytolytic toxins in the development of septic arthritis by inoculating mice with S. aureus wild-type strain 8325-4 or isogenic mutants differing in the expression of alpha-, beta-, and gamma-toxin production patterns. Mice inoculated with either an alpha- or beta-toxin mutant showed degrees of inflammation, joint damage, and weight decrease similar to wild-type-inoculated mice. In contrast, mice inoculated with either double (alpha- and gamma-toxin-deficient)- or triple (alpha-, beta-, and gamma-toxin-deficient)-mutant S. aureus strains showed lower frequency and severity of arthritis, measured both clinically and histologically, than mice inoculated with the wild-type strain. We conclude that simultaneous production of alpha- and gamma-toxin is a virulence factor in S. aureus arthritis.  (+info)

Role of antibodies against Bordetella pertussis virulence factors in adherence of Bordetella pertussis and Bordetella parapertussis to human bronchial epithelial cells. (3/14670)

Immunization with whole-cell pertussis vaccines (WCV) containing heat-killed Bordetella pertussis cells and with acellular vaccines containing genetically or chemically detoxified pertussis toxin (PT) in combination with filamentous hemagglutinin (FHA), pertactin (Prn), or fimbriae confers protection in humans and animals against B. pertussis infection. In an earlier study we demonstrated that FHA is involved in the adherence of these bacteria to human bronchial epithelial cells. In the present study we investigated whether mouse antibodies directed against B. pertussis FHA, PTg, Prn, and fimbriae, or against two other surface molecules, lipopolysaccharide (LPS) and the 40-kDa outer membrane porin protein (OMP), that are not involved in bacterial adherence, were able to block adherence of B. pertussis and B. parapertussis to human bronchial epithelial cells. All antibodies studied inhibited the adherence of B. pertussis to these epithelial cells and were equally effective in this respect. Only antibodies against LPS and 40-kDa OMP affected the adherence of B. parapertussis to epithelial cells. We conclude that antibodies which recognize surface structures on B. pertussis or on B. parapertussis can inhibit adherence of the bacteria to bronchial epithelial cells, irrespective whether these structures play a role in adherence of the bacteria to these cells.  (+info)

Role of Bordetella pertussis virulence factors in adherence to epithelial cell lines derived from the human respiratory tract. (4/14670)

During colonization of the respiratory tract by Bordetella pertussis, virulence factors contribute to adherence of the bacterium to the respiratory tract epithelium. In the present study, we examined the roles of the virulence factors filamentous hemagglutinin (FHA), fimbriae, pertactin (Prn), and pertussis toxin (PT) in the adherence of B. pertussis to cells of the human bronchial epithelial cell line NCI-H292 and of the laryngeal epithelial cell line HEp-2. Using B. pertussis mutant strains and purified FHA, fimbriae, Prn, and PT, we demonstrated that both fimbriae and FHA are involved in the adhesion of B. pertussis to laryngeal epithelial cells, whereas only FHA is involved in the adherence to bronchial epithelial cells. For PT and Prn, no role as adhesion factor was found. However, purified PT bound to both bronchial and laryngeal cells and as such reduced the adherence of B. pertussis to these cells. These data may imply that fimbriae play a role in infection of only the laryngeal mucosa, while FHA is the major factor in colonization of the entire respiratory tract.  (+info)

Virulence of a spaP mutant of Streptococcus mutans in a gnotobiotic rat model. (5/14670)

Streptococcus mutans, the principal etiologic agent of dental caries in humans, possesses a variety of virulence traits that enable it to establish itself in the oral cavity and initiate disease. A 185-kDa cell surface-localized protein known variously as antigen I/II, antigen B, PAc, and P1 has been postulated to be a virulence factor in S. mutans. We showed previously that P1 expression is necessary for in vitro adherence of S. mutans to salivary agglutinin-coated hydroxyapatite as well as for fluid-phase aggregation. Since adherence of the organism is a necessary first step toward colonization of the tooth surface, we sought to determine what effect deletion of the gene for P1, spaP, has on the colonization and subsequent cariogenicity of this organism in vivo. Germ-free Fischer rats fed a diet containing 5% sucrose were infected with either S. mutans NG8 or an NG8-derived spaP mutant strain, PC3370, which had been constructed by allelic exchange mutagenesis. At 1-week intervals for 6 weeks after infection, total organisms recovered from mandibles were enumerated. At week 6, caries lesions also were scored. A significantly lower number of enamel and dentinal carious lesions was observed for the mutant-infected rats, although there was no difference between parent and mutant in the number of organisms recovered from teeth through 6 weeks postinfection. Coinfection of animals with both parent and mutant strains resulted in an increasing predominance of the mutant strain being recovered over time, suggesting that P1 is not a necessary prerequisite for colonization. These data do, however, suggest a role for P1 in the virulence of S. mutans, as reflected by a decrease in the cariogenicity of bacteria lacking this surface protein.  (+info)

Identification of a cytolethal distending toxin gene locus and features of a virulence-associated region in Actinobacillus actinomycetemcomitans. (6/14670)

A genetic locus for a cytolethal distending toxin (CDT) was identified in a polymorphic region of the chromosome of Actinobacillus actinomycetemcomitans, a predominant oral pathogen. The locus was comprised of three open reading frames (ORFs) that had significant amino acid sequence similarity and more than 90% sequence identity to the cdtABC genes of some pathogenic Escherichia coli strains and Haemophilus ducreyi, respectively. Sonic extracts from recombinant E. coli, containing the A. actinomycetemcomitans ORFs, caused the distension and killing of Chinese hamster ovary cells characteristic of a CDT. Monoclonal antibodies made reactive with the CdtA, CdtB, and CdtC proteins of H. ducreyi recognized the corresponding gene products from the recombinant strain. CDT-like activities were no longer expressed by the recombinant strain when an OmegaKan-2 interposon was inserted into the cdtA and cdtB genes. Expression of the CDT-like activities in A. actinomycetemcomitans was strain specific. Naturally occurring expression-negative strains had large deletions within the region of the cdt locus. The cdtABC genes were flanked by an ORF (virulence plasmid protein), a partial ORF (integrase), and DNA sequences (bacteriophage integration site) characteristic of virulence-associated regions. These results provide evidence for a functional CDT in a human oral pathogen.  (+info)

Complete nucleotide sequence of the 27-kilobase virulence related locus (vrl) of Dichelobacter nodosus: evidence for extrachromosomal origin. (7/14670)

The vrl locus is preferentially associated with virulent isolates of the ovine footrot pathogen, Dichelobacter nodosus. The complete nucleotide sequence of this 27.1-kb region has now been determined. The data reveal that the locus has a G+C content much higher than the rest of the D. nodosus chromosome and contains 22 open reading frames (ORFs) encoding products including a putative adenine-specific methylase, two potential DEAH ATP-dependent helicases, and two products with sequence similarity to a bacteriophage resistance system. These ORFs are all in the same orientation, and most are either overlapping or separated by only a few nucleotides, suggesting that they comprise an operon and are translationally coupled. Expression vector studies have led to the identification of proteins that correspond to many of these ORFs. These data, in combination with evidence of insertion of vrl into the 3' end of an ssrA gene, are consistent with the hypothesis that the vrl locus was derived from the insertion of a bacteriophage or plasmid into the D. nodosus genome.  (+info)

Expression of the plague plasminogen activator in Yersinia pseudotuberculosis and Escherichia coli. (8/14670)

Enteropathogenic yersiniae (Yersinia pseudotuberculosis and Yersinia enterocolitica) typically cause chronic disease as opposed to the closely related Yersinia pestis, the causative agent of bubonic plague. It is established that this difference reflects, in part, carriage by Y. pestis of a unique 9.6-kb pesticin or Pst plasmid (pPCP) encoding plasminogen activator (Pla) rather than distinctions between shared approximately 70-kb low-calcium-response, or Lcr, plasmids (pCD in Y. pestis and pYV in enteropathogenic yersiniae) encoding cytotoxic Yops and anti-inflammatory V antigen. Pla is known to exist as a combination of 32.6-kDa (alpha-Pla) and slightly smaller (beta-Pla) outer membrane proteins, of which at least one promotes bacterial dissemination in vivo and degradation of Yops in vitro. We show here that only alpha-Pla accumulates in Escherichia coli LE392/pPCP1 cultivated in enriched medium and that either autolysis or extraction of this isolate with 1.0 M NaCl results in release of soluble alpha and beta forms possessing biological activity. This process also converted cell-bound alpha-Pla to beta-Pla and smaller forms in Y. pestis KIM/pPCP1 and Y. pseudotuberculosis PB1/+/pPCP1 but did not promote solubilization. Pla-mediated posttranslational hydrolysis of pulse-labeled Yops in Y. pseudotuberculosis PB1/+/pPCP1 occurred more slowly than that in Y. pestis but was otherwise similar except for accumulation of stable degradation products of YadA, a pYV-mediated fibrillar adhesin not encoded in frame by pCD. Carriage of pPCP by Y. pseudotuberculosis did not significantly influence virulence in mice.  (+info)

Bacterial traits that contribute to disease are termed virulence factors and there is much interest in therapeutic approaches that disrupt such traits. What remains less clear is whether a virulence factor identified as such in a particular context is also important in infections involving different host and pathogen types. Here, we address this question using a meta-analytic approach. We statistically analyzed the infection outcomes of 76 experiments associated with one well-studied virulence factor - pyoverdine, an iron-scavenging compound secreted by the opportunistic pathogen Pseudomonas aeruginosa. We found that this factor is consistently involved with virulence across different infection contexts. However, the magnitude of the effect of pyoverdine on virulence varied considerably. Moreover, its effect on virulence was relatively minor in many cases, suggesting that pyoverdine is not indispensable in infections. Our works supports theoretical models from ecology predicting that disease severity
Streptococcus pneumoniae is an important human pathogen in all age groups worldwide that causes a variety of diseases, ranging from life threatening septicaemia and meningitis to less severe sinusitis and otitis media. The factors that determine the virulence of S. pneumoniae are very complex but a key aspect of the organisms disease causing potential is the ability of the bacteria to regulate virulence factor expression and activity. In this study two main approaches were taken to investigate virulence gene expression in S. pneumoniae. Firstly, the feasibility of Recombinase based In vivo Expression Technology, RIVET, for use in S. pneumoniae to study gene expression in vitro, and then in vivo was assessed. However, the system was found to be unsuitable for use in this study. Secondly, the requirement for and the role of virulence gene regulators identified by Signature Tagged Mutagenesis were investigated. The requirement for different virulence gene regulators varied according to the murine ...
TY - JOUR. T1 - Revealing mechanisms underlying variation in malaria virulence. T2 - Effective propagation and host control of uninfected red blood cell supply. AU - Metcalf, C. J.E.. AU - Long, G. H.. AU - Mideo, N.. AU - Forester, J. D.. AU - Bjørnstad, O. N.. AU - Graham, A. L.. PY - 2012/11/7. Y1 - 2012/11/7. N2 - Malaria parasite clones with the highest transmission rates to mosquitoes also tend to induce the most severe fitness consequences (or virulence) in mammals. This is in accord with expectations from the virulence-transmission trade-off hypothesis. However, the mechanisms underlying how different clones cause virulence are not well understood. Here, using data from eight murine malaria clones, we apply recently developed statistical methods to infer differences in clone characteristics, including induction of differing host-mediated changes in red blood cell (RBC) supply. Our results indicate that the within-host mechanisms underlying similar levels of virulence are variable and ...
Pathogenic Yersinia cause a manifold of diseases in humans ranging from mild gastroenteritis (Y. pseudotuberculosis and Y. enterocolitica) to pneumonic and bubonic plague (Y. pestis), while all three have a common virulence strategy that relies on a well-studied type III secretion system and its effector proteins to colonize the host and evade immune responses. However, the role of other protein secretion and/or translocation systems in virulence of Yersinia species is not well known. In this thesis, we sought to investigate the contribution of twin-arginine translocation (Tat) pathway and its secreted substrates to the physiology and virulence of Y. pseudotuberculosis. Tat pathway uniquely exports folded proteins including virulence factors across the cytoplasmic membranes of bacteria. The proteins exported by Tat pathway contain a highly conserved twin-arginine motif in the N-terminal signal peptide. We found that the loss of Tat pathway causes a drastic change of the transcriptome of Y. ...
The harm that pathogens cause to hosts during infection, termed virulence, varies across species from negligible to a high likelihood of rapid death. Classic theory for the evolution of virulence is based on a trade-off between pathogen growth, transmission and host survival, which predicts that higher within-host growth causes increased transmission and higher virulence. However, using data from 61 human pathogens, we found the opposite correlation to the expected positive correlation between pathogen growth rate and virulence. We found that (i) slower growing pathogens are significantly more virulent than faster growing pathogens, (ii) inhaled pathogens and pathogens that infect via skin wounds are significantly more virulent than pathogens that are ingested, but (iii) there is no correlation between symptoms of infection that aid transmission (such as diarrhoea and coughing) and virulence. Overall, our results emphasize how virulence can be influenced by mechanistic life-history details, ...
The relative amount of transmission in I2 (ϕ) also has a large effect on ESS virulence (figure 1b). As the amount of transmission in I2 increases, the ESS virulence decreases, and the rate of decrease depends on the level of mortality that occurs in the I1 class. As the level of transmission in I2 and the disease mortality rate in the I1 class (ρ) approach zero, the ESS virulence goes to infinity (figure 1b). These results can be understood by realizing that for any fixed level of virulence (α), decreases in the transmission parameter ϕ reduce the fitness benefit of reaching the second class (I2), while increases in ρ both decrease the probability of reaching the second class and decreases the infectious period in the first class. Therefore, as both parameters reach zero, there is no benefit in reaching the second class and no cost to virulence in the first class. Thus, ESS virulence is very high and virulence will have a greater tendency to increase after introduction.. The effect of the ...
Classical microparasite evolution theory predicts a trade-off between virulence and transmission [1-3]. This trade-off balances virulence and within-host reproduction so that transmission is maximized over the lifetime of infection. Microparasites expressing intermediate levels of virulence are favoured under those conditions, as seen in several empirical examples of viruses with high transmission success (e.g. infections of myxoma virus in rabbits, HIV in humans, and cauliflower mosaic virus in Brassica rapa) [4-6]. However, not all studies found evidence for evolution towards intermediate virulence, but instead suggested evolution towards high or low virulence [7, 8].. Host population density is a key factor in determining whether low or high virulence will be optimal [9-11]. This mechanism can be understood in the framework of a trade-off between a microparasites competitive ability and its persistence. When transmission rates are lower at low host densities, a strain that can maintain a ...
Bacterial pathogens deliver multiple effector proteins into host cells to facilitate bacterial growth. HopQ1 is an effector from Pseudomonas syringae pv. tomato DC3000 that is conserved across multiple bacterial pathogens which infect plants. HopQ1s central region possesses some homology to nucleoside hydrolases, but possesses an alternative aspartate motif not found in characterized enzymes. A structural model was generated for HopQ1 based on the E. coli RihB nucleoside hydrolase and the role of HopQ1s potential catalytic residues for promoting bacterial virulence and recognition in Nicotiana tabacum was investigated. Transgenic Arabidopsis plants expressing HopQ1 exhibit enhanced disease susceptibility to DC3000. HopQ1 can also promote bacterial virulence on tomato when naturally delivered from DC3000. HopQ1s nucleoside hydrolase-like domain alone is sufficient to promote bacterial virulence, and putative catalytic residues are required for virulence promotion during bacterial infection of tomato
Vaccines rarely provide full protection from disease. Nevertheless, partially effective (imperfect) vaccines may be used to protect both individuals and whole populations.We studied the potential impact of different types of imperfect vaccines on the evolution of pathogen virulence (induced host mortality) and the consequences for public health. Here we show that vaccines designed to reduce pathogen growth rate and/or toxicity diminish selection against virulent pathogens. The subsequent evolution leads to higher levels of intrinsic virulence and hence to more severe disease in unvaccinated individuals. This evolution can erode any population-wide benefits such that overall mortality rates are unaffected, or even increase, with the level of vaccination coverage. In contrast, infection-blocking vaccines induce no such effects, and can even select for lower virulence. These findings have policy implications for the development and use of vaccines that are not expected to provide full immunity, ...
Author Summary The AIDS epidemic claims more lives per year than any other infectious disease, even though its cause, the Human Immunodeficiency Virus (HIV), is the youngest of all major human pathogens. The recent origin and great evolutionary potential of the virus raise the possibility that the virus might still be adapting to humans. Of primary interest is whether the virulence of the virus, i.e. its ability to cause disease, has been changing over time. Unfortunately, previous results have yielded conflicting results. We investigated time trends of virulence in the Italian HIV epidemic and found increasing virulence. The use of an established methodology allowed, for the first time, direct comparison with results obtained in other epidemics. The comparisons revealed that genuine differences exist in the trends of HIV virulence between different epidemics. Thus, there is no single time trend of HIV virulence worldwide. Our results are consistent with the hypothesis of increasing HIV virulence;
ABSTRACT: Candida albicans is a classical example of causative agent for opportunistic fungal infection. Normally, it colonizes skin, gastrointestinal tract, genital, and mucosal membranes, but in certain condition it may responsible for diseases. This phenomenon was mainly associated with immunological status of the host. However, there were fndings that showed the possibility of putative virulence factors work on the transition of commensally to pathogenic role of the yeast. In this review, some virulence factors were discussed. Indeed, there were factors that may be considered as putative virulence factors of C. albicans. ...
The evolutionary dynamics of pathogens are critically important for disease outcomes, prevalence and emergence. In this talk I will discuss some specific ecological conditions that promote the long-term maintenance of virulence polymorphisms in a pathogen population. Recent theory predicts that evolution towards increased virulence can be reversed if less virulent social cheats exploit virulent cooperator pathogens. However, there is little evidence that social exploitation operates within natural pathogen populations. I will demonstrate that for the bacterium Pseudomonas syringae, major virulence polymorphisms are maintained at unexpectedly high frequencies in the host Arabidopsis thaliana. Experiments reveal that the fitness costs of decreased virulence are eliminated in mixed infections, whereas less virulent strains have a fitness advantage in non-host environments. These results suggest that niche differentiation contributes to the maintenance of virulence polymorphisms, and that both ...
In a wild plant-pathogen system, host resistance and pathogen virulence varied markedly among local populations. Broadly virulent pathogens occurred more frequently in highly resistant host populations, whereas avirulent pathogens dominated susceptible populations. Experimental inoculations indicated a negative trade-off between spore production and virulence. The nonrandom spatial distribution of pathogens, maintained through time despite high pathogen mobility, implies that selection favors virulent strains ofMelampsora lini in resistant Linum marginalepopulations and avirulent strains in susceptible populations. These results are consistent with gene-for-gene models of host-pathogen coevolution that require trade-offs to prevent pathogen virulence increasing until host resistance becomes selectively neutral. ...
I am an undergraduate student at McGill University, looking for data for a term paper. The hypothesis of the paper is that virulence and rate of infection would necessarily be highly correlated as virulence increases. The logic behind this is that if the pathogen were to kill off the host before transmission could take place, the species would quickly kill itself off in the process. As such, selection favours a higher rate of transmission in more virulent pathogens. I would like to limit my paper to bacteria which infect humans. If anyone can send me either data or references to this sort of information, it would be greatly appreciated. Please note that I would need both types of data for the information to be useful. Ideally I would like to measure virulence in time from infection to death of host and transmission in time from infection of first host to infection of second host. If this format isnt possible, please send the information anyway. Thank you very much, Jamie Bacher bnyb at ...
General Information: Specific virulence factors are encoded within pathogenicity islands (PAIs) that are required for the invasive phenotype associated with Yersinia infections. One key virulence plasmid contained by the three human-specific pathogens is pCD1/pYv, which encodes a type III secretion system for the delivery of virulence proteins that contribute to internalization into the host cell. This species is a food and waterborn pathogen that causes gastroenteritis (inflammation of the mucous membranes of the stomach and intestine) and is able to proliferate at temperatures as low as 4 degrees C. ...
Robet Koch formulated in 1890 the Koch´s postulates as general guidelines that should be followed to identify pathogens causing diseases. One century later, Stanley Falkow established the molecular version of Kochs postulates to guide, this time, the identification of microbial genes encoding virulence factors. A key point of the molecular postulates is to test the virulence of the microorganism with the inactivated candidate virulence gene in an appropriate animal model. However, this is not always possible. Suitable animals models are lacking for many diseases such as brucellosis, typhoid and leprosy. And the models for tuberculosis and cholera do not reflect the biology of human infections. In addition, large scale analysis of virulence are costs prohibited due to the high number of animals that should be infected to get statistically significant results. And, last but not least, there are important ethical concerns on the use of vertebrate animals models (including mice and rats) for ...
Transmission bottlenecks occur in pathogen populations when only a few individual pathogens are transmitted from one infected host to another in the initiation of a new infection. Transmission bottlenecks can dramatically affect the evolution of virulence in rapidly evolving pathogens such as RNA viruses. Characterizing pathogen diversity with the quasispecies concept, we use analytical and simulation methods to demonstrate that severe bottlenecks are likely to drive down the virulence of a pathogen because of stochastic loss of the most virulent pathotypes, through a process analogous to Mullers ratchet. We investigate in this process the roles of host population size, duration of within-host viral replication, and transmission bottleneck size. We argue that the patterns of accumulation of deleterious mutation may explain differing levels of virulence in vertically and horizontally transmitted diseases ...
Given that antibiotics are losing effectiveness faster than replacements are being found, chemist Timothy Wencewicz suggests we try a new approach. Drugs that hobble the production of virulence factors, small molecules that help bacteria to establish an infection in a host, would put much less selective pressure on bacteria and delay the evolution of resistance. In Infectious Diseases he describes recent work on a target virulence factor.
Read "A hypothesis explaining why so many pathogen virulence proteins are moonlighting proteins, Pathogens and Disease" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
Handprinted in the UK, 100%Heavy Cotton Fruit of the Loom Virulence tshirt in BlackThe printing wont fade or crack even when tumble dried so your shirt will stay as soft and silky for years to come. an Ideal gift for anyone interested in virulence Sizes are Small 35 - 37, Medium 38 - 40, Large 40 - 41, XL 44 - 46, XXL 47 - 49, XXXL 50 -52
LINK TO PAPER HERE … Hmm … did you catch that? "HIGHLY SOPHISTICATED MECHANISMS FOR REGULATING VIRULENCE FACTOR EXPRESSION IN RESPONSE TO ENVIRONMENTAL SIGNALS OR BY REVERSIBLE MUTATIONS." So … just as Eric and Dylan were no doubt affected by their environment which in turn was partly to blame for their behavior, in the same way, B. Pertussis is ALSO affected by its environment in the human body and this environment has a direct effect on VIRULENCE FACTOR EXPRESSION, i.e. whether the bacterium is dangerous to humans or not. This definitely calls for more study. (Note to self: do a full blog research article on this). This is a fascinating topic in light of the info on microbe pleomorphism (must read Wiki article on this topic HERE) and the resulting virulence (or non-virulence) discovered by Antoine Bechamp way back in Pasteurs day. To explain simply the difference between Pasteur and Bechamp, Pasteur taught that "microbes - viruses and bacteria - are bad guys" and you need to have ...
This volume brings together studies on the differences and profound similarities in the molecular mechanism of virulence between bacteria pathogenic for humans, animals and plants. Topics covered include: host cell recognition and binding, pathogen ingression and invasive mechanism, enzymes, toxins and other pathogenic factors, regulation of virulence genes and signal transduction, and pathogen of host-defence mechanisms.
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Figure 2. As if microbes were puppeteers and we humans were the puppets, microbes can control what we eat by a number of marked mechanisms. Adapted from Alcock et al 2014.. People who have "desires" of chocolate have different microbial metabolites in urine from people indifferent to chocolate, despite having the same diet.. Dysphoria, id est, human discomfort until we eat food which improve microbial "welfare", may be due to the expression of bacterial virulence genes and perception of pain by the host. This is because the production of toxins is often triggered by a low concentration of nutrients limiting growth. The detection of sugars and other nutrients regulates virulence and growth of various microbes. These directly injure the intestinal epithelium when nutrients are absent. According to this hypothesis, it has been shown that bacterial virulence proteins activate pain receptors. It has been shown that fasting in mice increases the perception of pain by a mechanism of vagal ...
There are several testing options now available, aligned with the Karmali approach, which include detection of both Shiga Toxin genes (stx1, stx2) and the eae virulence marker. An additional virulence marker for the Enteroaggregative family (aggC) has been included in a separate E. coli O104 assay in case the EFSA opinion is followed. Assurance GDS incorporates a proprietary PickPen® IMS sample preparation procedure, which captures and isolates STEC belonging to the target serogroups (O26, O45, O103, O111, O121, O145 and E. coli O157:H7), prior to detection of the gene targets. As a result, target gene detection is performed on a subset of organisms belonging only to the serogroups of concern, drastically reducing the amount of false positive results typically found with STEC testing.. ...
Virulence genes of pathogenic bacteria, which code for toxins, adhesins, invasins or other virulence factors, may be located on transmissible genetic elements such as transposons, plasmids or bacteriophages. In addition, such genes may be part of particular regions on the bacterial chromosomes, term …
Results from the CASCADE project strongly suggest that HIV has increased in virulence and transmissibility, at least in Europe, since the virus came to light at the end of the 1970s. This research was published in the Lancet HIV in November 2014. HIV is a virus with high genetic diversity. As the HIV virus reproduces, slight variations in the genetic structure of the virus begin to occur. Over time, this means that there will be several subtypes of HIV, and each subtype may be more or less able to cause illness. The term used to describe a virus ability to cause illness is virulence. If someone is infected with a more virulent form of HIV they will become ill more quickly. Additionally, more virulent forms of HIV may increase the risk of the virus being transmitted (passed on) to others. The CASCADE collaboration is a network of researchers from 14 countries, sharing data from 29 different groups of HIV-positive individuals. Through pooling data, the CASCADE researchers are able to answer ...
strains display variability in their capsular polysaccharide cell morphology karyotype and virulence but the BAPTA relationship between these variables is poorly understood. BAPTA xylose residue content linked at the 4 to 0 position. The relative virulence of the colony types was WR > PH > SM as measured by CFU in rat lungs after intratracheal […]. ...
Expression profile of virulence associated MAP genes under various stress conditions.Virulence associated MAP gene definitions were obtained by phylogenomics co
Our laboratory studies the roles of sensory transduction in bacterial-host interactions. Genes and operons that encode virulence factors are often subject to coordinate regulation in response to environmental signals, and bacterial virulence factors frequently target host cell signaling pathways. Specific areas of interest include: a) biochemical analysis of signal transduction pathways in pathogenic bacteria, b) genetic organization of bacterial virulence regulons, and c) in vivo and in vitro studies of mechanisms of pathogenesis. We are also investigating mechanisms involved in the induction of cytotoxic T cell responses by Listeria monocytogenes (LM). In the course of these studies, we have developed a new class of live Listeria-based vaccines with activity against heterologous pathogens and tumors. In a third project, we have discovered a new class of retroelements, called "diversity generating retroelements," which are capable of generating vast amounts diversity in proteins involved in ...
The type 3 secretion systems (T3SSs) are virulence mechanisms used by various Gram-negative bacteria to overcome the host immunity. They are often target-cell contact induced and activated. Activation results in targeting of virulence effector substrates into host cells. One class of secreted substrates, translocators, are required for the intracellular targeting of the second class, the virulence effectors, into host target cells. T3SSs are mainly regulated at 2 levels; a shift from environmental to host temperature results in low level induction of the system whereas target cell contact further induces and activates the system. In the Yersinia T3SS, YopN, one of the secreted substrates, is involved in the latter level of activation. Under non-inducing conditions, YopN complexes with TyeA, SycN and YscB and this complex suppresses the T3SS via an unknown mechanism. When the system is induced, the complex is believed to dissociate and YopN is secreted resulting in the activation of the system. ...
the_virulence_characteristic_of_hiv1the_virus_predominantly_responsible_for_human_aidsmight_amount_to_an_accident_of_evolution_new_evidence_reveals_a_gene_function_lost_during_the_course_of_viral_evolution_predisposed_hiv1_to_spur_the_fatal_immune_system_failures_that_are_the_hallmarks_of_aids_researchers_report_in_the_june_16_2006_cell
What gives HIV the ability to mutate?. HIV is a single standed RNA virus. DNA is much more stable than RNA as it has a stronger backbone and it is typically double stranded. But HIV mutates at a rate far higher than just being a RNA virus. Thats because it uses an enzyme called reverse transcriptase (RT) to build its RNA genome from RNA bases.. RT is meant to copy the old HIV and make a new one but it does a rubbish job. Most the time it copies it well but every now and then (3 x 10−5 per nucleotide base) it puts in a random base. That might seem like a small rate but thats HUGE if that was coding our genome we would die (if we ever even lived). And since HIVs replication rate is enormously high, theres always going to be a range of good and junk HIV (but its mostly just junk - next answer for why thats not a bad thing).. But thats not all, RT doesnt just use one old HIV to make a new one. It can use several different old HIVs to make a new one thats not only a combination of all the ...
Importantly, this effector-triggered immunity has been shown to be a powerful means of augmenting the defense response specifically to pathogens but not to harmless commensals, and makes a major contribution to how plants cope with microbial attack and restrict pathogen growth. Our previous work revealed in metazoans an innate immune pathway that specifically responds to virulence factors encoded by virulent bacteria that we referred to as AVI (Boyer et al., 2011, Diabate et al., 2015). The identification of such system with similarities to plant ETI is paradigm-shifting and indicates that animals like plants have evolved sophisticated strategies to gauge the virulent potential of microbes and respond commensurately (Stuart et al., 2013). Using the prototypal RhoGTPase targeting toxin CNF1 we proved that the animal host is able to monitor the activity of virulence factors (Boyer et al., 2011). Our initial work has been extended to SopE a Salmonella virulence factor activating RhoGTPases. SopE ...
Bacterial pathogens must adapt to available nutrients in their host, so they have linked metabolism with virulence. We want to understand the mechanisms by whic...
Escherichia coli is transformed from a commensal organism into a pathogen by acquisition of genetic elements called pathogenicity islands (PAIs). Katsowich et al. investigated how the PAI virulence genes of enteropathogenic E. coli (EPEC) respond when the bacterium attaches to a host gut cell. EPEC first sticks to the host by means of pili and then uses a PAI-encoded type 3 secretion system (T3SS) to inject multiple effectors into the host cell. But not all virulence mediators are injected. For example, CesT, a bacterial chaperone, delivers virulence effectors into the T3SS apparatus. Then, within the bacterial cytoplasm, it interacts with a gene repressor called CsrA, which reprograms bacterial gene expression to help the bacteria to adapt to epithelial cell-associated life.. Science, this issue p. 735 ...
Transformation. Fred Griffith worked with virulent S and nonvirulent R strain Pneumoccocus bacteria. He found that R strain could become virulent when it took in DNA from heat-killed S strain. Study suggested that DNA was probably the genetic material. Slide 5. ...
Study Flashcards On USMLE 2011 Bacterial Toxins/Virulence Factors at Cram.com. Quickly memorize the terms, phrases and much more. Cram.com makes it easy to get the grade you want!
I have read several text regarding this, but I still cant manage do discriminate between them. So far what Ive got is: Pathogenicity = The potential/ability of a infectious agent to cause damage. Virulence = The actual level of damage caused ...
The outer membrane (OM) of Gram-negative pathogenic bacteria represents a platform for the secretion and presentation of surface-localized virulence factors. Th...
A SARS-CoV lacking the full-length E gene (SARS-CoV-∆E) was attenuated and an effective vaccine. Here, we show that this mutant virus regained fitness after serial passages in cell culture or in vivo, resulting in the partial duplication of the membrane gene or in the insertion of a new sequence in gene 8a, respectively. The chimeric proteins generated in cell culture increased virus fitness in vitro but remained attenuated in mice. In contrast, during SARS-CoV-∆E passage in mice, the virus incorporated a mutated variant of 8a protein, resulting in reversion to a virulent phenotype. When the full-length E protein was deleted or its PDZ-binding motif (PBM) was mutated, the revertant viruses either incorporated a novel chimeric protein with a PBM or restored the sequence of the PBM on the E protein, respectively. Similarly, after passage in mice, SARS-CoV-∆E protein 8a mutated, to now encode a PBM, and also regained virulence. These data indicated that the virus requires a PBM on a ...
Virulence, relative Dirty Fighting is one of three Ranged DPS Discipline for Snipers and Gunslingers. It is one of 18 different DPS Disciplines. The two support buffs for the raid are Marked and Assailable. Its strength is DoT. ...
View Notes - FinalStudyGuide_2010BIEB128 from BIEB 128 at UCSD. make good vectors? What is virulence? What is the difference between a horizontally transmitted and a vertically transmitted disease?
In this book, we present the state of the art of S. aureus virulence mechanisms and antibiotic-resistance profiles, providing an unprecedented and comprehensive collection of up-to-date research about the evolution, dissemination, and mechanisms of different staphylococcal antimicrobial resistance patterns alongside bacterial virulence determinants and their impact in the medical field ...
Inflammation mediated by the inflammasome and the cytokine IL-1β are some of the earliest and most important alarms to infection. These pathways are responsive to the virulence factors that pathogens use to subvert immune processes, and thus are typically activated only by microbes with potential to cause severe disease. Among the most serious human infections are those caused by the pathogenic streptococci, in part because these species numerous strategies for immune evasion. Since the virulence factor armament of each pathogen is unique, the role of IL-1β and the pathways leading to its activation varies for each infection. This review summarizes the role of IL-1β during infections caused by streptococcal pathogens, with emphasis on emergent mechanisms and concepts countering paradigms determined for other organisms ...
Answer Yes, if you are spotting you need to take it easy for a few days, also if you have any type of bleeding or spotting you shouldnt have sex.
Typically, viruses that rapidly kill their host have a very short history, as they rapidly run out of places to reproduce. Im quoting John Timmer from Ars Technicas Nobel Intent, from a couple of weeks ago. I feel kind of bad about this because Im only quoting to disagree with him, and I always like Nobel Intent
The process of bacterial pathogenesis involves complex and dynamic responses from both pathogen and host. While the host can mount an array of defense mechanisms to counteract an infection, bacterial pathogens utilize a number of virulence mechanisms to help them in their quest to invade, colonize, and infect. The expression pattern of virulence factors such…
If you have a question about this talk, please contact Sue Griffin.. Host: Professor Jim Kaufman ([email protected]). Abstract not available. This talk is part of the Immunology in Pathology series.. ...
This editorial presents some of the latest evidence to support the antivirulence approach, also highlighting some of the issues that should considered.
Virulence[edit]. H5N1 has mutated into a variety of strains with differing pathogenic profiles, some pathogenic to one species ... Due to the high lethality and virulence of HPAI A(H5N1), its endemic presence, its increasingly large host reservoir, and its ... LPAI viruses have negligible virulence, but these viruses can serve as progenitors to HPAI viruses. The current strain of H5N1 ...
Virulence[edit]. Virulence (the tendency of a pathogen to cause damage to a host's fitness) evolves when that pathogen can ... Definitions: pathogenicity vs virulence; incidence vs prevalence". COLOSS.. *^ Carl Nathan (2015-10-09). "From transient ... Pathogenicity is related to virulence in meaning, but some authorities have come to distinguish it as a qualitative term, ... A bacterium may participate in opportunistic infections in immunocompromised hosts, acquire virulence factors by plasmid ...
Virulence[edit]. Lipooligosaccharide (LOS) is a component of the outer membrane of N. meningitidis. This acts as an endotoxin ... and is responsible for septic shock and hemorrhage due to the destruction of red blood cells.[13] Other virulence factors ... sticking to them with long thin extensions called pili and the surface-exposed proteins Opa and Opc and has several virulence ...
Virulence[edit]. Virulence (the tendency of a pathogen to cause damage to a host's fitness) evolves when that pathogen can ...
Virulence and mortality[edit]. Viral and bacterial diseases that kill victims before the illnesses spread to others tend to ...
Virulence[edit]. As other virulent bacteria, GBS harbors an important number of virulence factors (virulence factors are ... inflammation and virulence". Sci. Rep. 6: 29000. doi:10.1038/srep29000. PMC 4935997 . PMID 27383371.. ... The capsular polysaccharide of GBS is not only an important GBS virulence factor but it is also an excellent candidate for the ... "Understanding the regulation of Group B Streptococcal virulence factors" (PDF). Future Microbiol. 4: 201-221. doi:10.2217/ ...
Competition favoring virulence[edit]. Competition between parasites can be expected to favour faster reproducing and therefore ... Among competing parasitic insect-killing bacteria of the genera Photorhabdus and Xenorhabdus, virulence depended on the ... Ebert, Dieter; Hamilton, William D. (1996). "Sex against virulence: the coevolution of parasitic diseases". Trends in Ecology ... and their virulence was less than when the insect was infected by a single strain.[76] ...
Relationship with virulence and survival[edit]. This section does not cite any sources. Please help improve this section by ... The relationship between virulence and transmission is complex, and has important consequences for the long term evolution of a ... this cost may be overwhelmed by the short term benefit of higher infectiousness if transmission is linked to virulence, as it ...
Virulence. If This Isn't a Dream... 1985-1989. 2010. CD 113. Twilight. Monument to Time End. 2010. CD ...
Fu Manchu originally formed in 1985 as a hardcore punk band called Virulence. The line up was vocalist Ken Pucci, guitarist ...
One disease may enhance the virulence of another, as for example, herpes simplex virus co-infection exacerbates HIV infection ... the virulence of the virus causing the pandemic, the speed of global spread, the underlying features and vulnerabilities of the ... with progression to AIDS,[citation needed] periodontal bacteria may enhance the virulence of herpesvirus,[citation needed] HIV- ... "Virulence. 1 (1): 10-18. doi:10.4161/viru.1.1.9933. PMC 3080196. PMID 21178409.. ...
"Mycobacterial virulence. Virulent strains of Mycobacteria tuberculosis have faster in vivo doubling times and are better ...
On January 23, 2007, Only Crime released their second album, Virulence, on Fat Wreck Chords, followed by a Split EP with ...
Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization ...
VirulenceEdit. Virulence (the tendency of a pathogen to reduce a host's fitness) evolves when a pathogen can spread from a ... Definitions: pathogenicity vs virulence; incidence vs prevalence". COLOSS. Archived from the original on 2017-04-24. Retrieved ... Pathogenicity is related to virulence in meaning, but some authorities have come to distinguish it as a qualitative term, ... A bacterium may participate in opportunistic infections in immunocompromised hosts, acquire virulence factors by plasmid ...
The cagA gene codes for one of the major H. pylori virulence proteins. Bacterial strains with the cagA gene are associated with ... Genes involved in virulence and pathogenesisEdit. Study of the H. pylori genome is centered on attempts to understand ... nucleotide resolution by differential RNA-seq that confirmed the known acid induction of major virulence loci, such as the ...
"Candida infection and colonization among non-trauma emergency surgery patients." Virulence 1.5 (2010): 359-366. Lalla, RV; ...
Schmid-Hempel, Paul; Frank, Steven A (2017-04-07). "Pathogenesis, Virulence, and Infective Dose". PLoS Pathogens. 3 (10). doi: ...
Virulence factors are the attributes of microorganisms that enable it to colonise a particular niche in its host, overcome the ... Fives-Taylor, P. M.; Meyer, D. H.; Mintz, K. P.; Brissette, C. (June 1999). "Virulence factors of Actinobacillus ... host defences and initiate a disease process.[7] Fives Taylor et al. (2000) have categorised the virulence factors of ...
Virulence. 3 (7): 583-588. doi:10.4161/viru.22330. PMC 3545935 . PMID 23154286. "Immune Reconstitution Syndrome" at TheBody.com ...
Virulence. 1 (5): 367-75. doi:10.4161/viru.1.5.12796. PMID 21178472. Kourkoumpetis TK, Velmahos GC, Ziakas PD, Tampakakis E, ...
The relationship between virulence and transmission is complex, and has important consequences for the long term evolution of a ... Virulence. 4 (4): 295-306. doi:10.4161/viru.24041. PMC 3710332 . PMID 23552814. Wesolowski A, Metcalf CJ, Eagle N, Kombich J, ... this cost may be overwhelmed by the short term benefit of higher infectiousness if transmission is linked to virulence, as it ...
Virulence. 5: 697-702. doi:10.4161/viru.29091. PMC 4189875 . PMID 25513770. ...
Manuelidis L (2013). "Infectious particles, stress, and induced prion amyloids: a unifying perspective". Virulence. 4: 373-83. ... Manuelidis, Laura (1 July 2013). "Infectious particles, stress, and induced prion amyloids". Virulence. 4 (5): 373-383. doi: ... Virulence. 6 (2): 132-44. doi:10.4161/21505594.2014.989795. PMC 4601501 . PMID 25585171. Bastian, Frank O.; Jennings, Roger A ...
Bacterial virulence factors, such as glycocalyx and various adhesins, allow colonization, immune evasion, and establishment of ... Delaloye, J; Calandra, T (January 2014). "Invasive candidiasis as a cause of sepsis in the critically ill patient". Virulence. ... Mayr, FB; Yende, S; Angus, DC (January 2014). "Epidemiology of severe sepsis". Virulence. 5 (1): 4-11. doi:10.4161/viru.27372. ... Cross, AS (January 2014). "Anti-endotoxin vaccines: Back to the future". Virulence. 5 (1): 219-25. doi:10.4161/viru.25965. PMC ...
The purification of the Shigella flexneri virulence plasmid. The purification of the Shigella flexneri virulence plasmid. Save ... flexneri virulence plasmid is a highly stable single copy plasmid that is approximately 230kb in size. The stability of the ... flexneri virulence plasmid is a highly stable single copy plasmid that is approximately 230kb in size. The stability of the ... The projects first goal was to successfully isolate the large virulence plasmid from the chromosomal DNA using the technique ...
Serotype- and Virulence-Associated gene profile of streptococcus suis isolates from pig carcasses in Chiang Mai province, ...
Retrieved from "https://en.wiktionary.org/w/index.php?title=virulence&oldid=48323635" ...
... produce a variety of so-called virulence factors that permit them to evade the defense mechanisms of the host and thus cause ... Other articles where Virulence factor is discussed: necrotizing fasciitis: … ... Virulence factor. microbiology. Learn about this topic in these articles:. necrotizing fasciitis. * In necrotizing fasciitis. … ... produce a variety of so-called virulence factors that permit them to evade the defense mechanisms of the host and thus cause ...
Information about the open-access journal Virulence in DOAJ. DOAJ is an online directory that indexes and provides access to ... Publishers keywords: microbial pathogenicity, antimicrobial agents, host-pathogen interactions, virulence factors, infectious ...
The hypothesis of the paper is that virulence and rate of infection would necessarily be highly correlated as virulence ... pathogen virulence. Jamie BNYB000 at MUSICB.MCGILL.CA Mon Nov 20 12:24:59 EST 1995 *Previous message: Amphipathic Helices ... Ideally I would like to measure virulence in time from infection to death of host and transmission in time from infection of ...
Virulence of antibiotic-resistant Salmonella typhimurium. Johanna Björkman, Diarmaid Hughes, and Dan I. Andersson ... Drug resistance-virulence relationship in Plasmodium falciparum causing severe malaria in an area of seasonal and unstable ... Virulence of Pigmented Serratia marcescens Strain SM6 and its Nalidixic Acid-Resistant Derivative in White Outbred Mice ... Antibiotic resistance and virulence: Understanding the link and its consequences for prophylaxis and therapy ...
Virulence factor BrkB (IPR017039). Short name: Virul_fac_BrkB Family relationships *Virulence factor BrkB (IPR017039) *Inner ...
Virulence factors of Francisella tularensis.. Hood AM.. Abstract. The mechanism causing viable Francisella tularensis to lose ... virulence in aerosols has been investigated. Fully virulent organisms were found to be encapsulated and avirulent organisms ...
Virulence factors of Candida species.. Yang YL1.. Author information. 1. Department of Biological Science and Technology, ... This review will focus on the molecular dissection of virulence factors of C. albicans, including adhesion, proteinases ... This review will also describe briefly the virulence factors in non-albicans Candida spp. ...
... Mircea Radu Mihu1 and Joshua Daniel Nosanchuk2 ... the current knowledge regarding the multiple facets of the dynamic host-pathogen relationship in the context of the virulence ...
Using this approach, we detect well-known pathogenicity islands and identify new potential virulence genes in several human ... include virulence genes that appear to be absent in related strains or species present in the microbiome of healthy individuals ... can be used to detect pathogenicity regions in species where the genes involved in virulence are poorly characterized. ... Virulence factors Is the Subject Area "Virulence factors" applicable to this article? Yes. No. ...
bacterial infection host-pathogen interaction virulence factors pathology vaccines antibiotics virulence human host microbiome ... and professors intent on expanding their knowledge of bacterial infection and virulence mechanisms. ...
Cette variété est liée à un certain nombre de facteurs de virulence qui lui permettent dadhérer à la surface, denvahir ou ... Virulence de s.doré. La virulence de s.doré Est multifactorielle et due à laction combinée de plusieurs causes déterminantes ... La virulence des bactéries est encore réglée par les composantes extracellulaires et de paroi cellulaire qui sont exprimées ... Cette variété est liée à un certain nombre de facteurs de virulence qui lui permettent dadhérer à la surface, denvahir ou ...
... Mike Treder Sep 11, 2009 Ethical Technology A mistake in a factory can result in scores of ... error-what I have dubbed the democratization of virulence. ...
Thank you for your interest in spreading the word about Science.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
The roles that chemotaxis and motility play in virulence of V. cholerae are not fully understood. Richardson et al. (25) showed ... Selection for in vivo regulators of bacterial virulence. Sang Ho Lee, Susan M. Butler, and Andrew Camilli ... During infection of a host, V. cholerae induce the expression of ToxT and CT to regulate the expression of virulence factors ... This delay may be because of the inability of the nonchemotactic strains to swim toward a preferred niche optimal for virulence ...
Read AF (1994) The evolution of virulence. Trends Microbiol 2(3):73-76CrossRefPubMedGoogle Scholar ... Francisella tularensis Genome decay Natural selection TreeSAAP Virulence Electronic supplementary material. The online version ... Su J, Yang J, Zhao D, Kawula TH, Banas JA, Zhang J-R (2007) Genome-wide identification of Francisella tularensis virulence ... Eleven previously identified virulence genes were screened for positive selection along with 10 housekeeping genes. Analyses of ...
Virulence refers to the degree of pathology caused by the organism ... What are virulence factors. ?. Virulence is the degree of pathogenicity within a types of parasites. The factors of virulence ... What is virulence gene. ?. a gene in any pathogen which codes for the virulence factor like protein or polysacchride is called ... What is a virulence marker. ?. A virulence marker is a diagnostic tool in detecting viral factors. The importance of ...
Using this approach, we detect well-known pathogenicity islands and identify new potential virulence genes in several human ... include virulence genes that appear to be absent in related strains or species present in the microbiome of healthy individuals ... can be used to detect pathogenicity regions in species where the genes involved in virulence are poorly characterized. ...
Osmotic stress also contributes to the regulation of virulence factors, contributing to the detection of a new host, and L- ... identified proline as a molecular trigger in insect extracts that stimulated the production of small molecules with virulence ... Proton motive force (PMF), a consequence of metabolic activity, also contributes to the regulation of bacterial virulence, and ... suggesting that L-proline or its metabolites differentially regulate the production of virulence factors. ...
... is a virulence factor that plays a pivotal role in the infection mechanism. Combining different in-vitro and in-vivo approaches ... its virulence and its involvement in the infection process, with a view to identifying possible prevention and control methods ... cruzi genes which code for the factors responsible for the virulence, in particular a protein called Tc52. As in any parasitic ... analysis of the amino acid sequence important to the immunoregulatory function of Trypansosma cruzi Tc52 virulence factor. ...
Twitching Motility Is Essential for Virulence in Dichelobacter nodosus Xiaoyan Han, Ruth M. Kennan, John K. Davies, Leslie A. ... Effects of Oxygen on Virulence Traits of Streptococcus mutans Sang-Joon Ahn, Zezhang T. Wen, Robert A. Burne ... The HopZ Family of Pseudomonas syringae Type III Effectors Require Myristoylation for Virulence and Avirulence Functions in ... Swarming of Pseudomonas aeruginosa Is a Complex Adaptation Leading to Increased Production of Virulence Factors and Antibiotic ...
Drugs that hobble the production of virulence factors, small molecules that help bacteria to establish an infection in a host, ... In Infectious Diseases he describes recent work on a target virulence factor. ... One class of virulence factors common to many pathogens is siderophores, small molecules whose job is to seek out iron in the ... Virulence factors allow bacteria to evade the human immune system, to infect tissues and cells and to establish a foothold ...
... Published Tuesday 20 December 2016 Published Tue 20 Dec ... "Tuberculosis virulence factor identified, may be target for new drug." Medical News Today. MediLexicon, Intl., 20 Dec. 2016. ... 2016, December 20). "Tuberculosis virulence factor identified, may be target for new drug." Medical News Today. Retrieved from ...
  • In wild rabbits, the combination of host resistance and increased viral virulence resulted in typical myxomatosis presentation, but when naive rabbits were exposed to the new viral strains, bacterial infections bloomed in their immunosuppressed bodies, killing nearly all of the hosts before they developed the classic disease. (the-scientist.com)
  • The virulence of various strains of Helicobacter pylori tends to correlate with the level of production of urease. (wikipedia.org)
  • Mice usually succumb very quickly to C. neoformans infections, but the research group found that mice infected with strains carrying mutations in QSP1 lived twice as long as those infected with the normal fungus, indicating that the gene plays an important role in virulence. (ucsf.edu)
  • The researchers also studied the virulence of two strains of the pandemic H1N1 virus in a nonhuman primate model as a way to predict how the strains would affect humans. (infectioncontroltoday.com)
  • In order to better understand the mechanisms behind the rapid expansion of these strains, the virulence of 10 clinical and two transformed PNSP strains were compared with the virulence of three fully susceptible strains in a mouse model of bacteremia and a rat model of acute otitis media. (diva-portal.org)
  • It is therefore possible that other factors than virulence factors are of importance for the ability of PNSP strains to expand. (diva-portal.org)
  • The distribution of MgrA, R1rA and PPI2 varied between clinical S. pneumoniae isolates emphasizing the likelihood of a different repertoire of virulence genes and regulators amongst different serotypes and strains of this important human pathogen. (bl.uk)
  • Dominated by three clonal strains (Type I, II, and III demonstrating distinct virulence profiles), T. gondii exhibits a remarkably broad host range. (biomedsearch.com)
  • We propose that these observed differences reflect an evolutionary strategy that allows the parasite to extend its host range, as well as result in a subsequent partitioning into discrete strains that display altered virulence profiles across different hosts, different organs, and even cell types. (biomedsearch.com)
  • Regulation of these factors involves the concerted actions of three proteins, ToxR, TcpP, and ToxT, which together form the V. cholerae virulence gene regulatory cascade ( 3 - 5 ). (pnas.org)
  • Therefore, the true nature of the in vivo regulation of these virulence factors within a host remains unclear. (pnas.org)
  • Osmotic stress also contributes to the regulation of virulence factors, contributing to the detection of a new host, and L-proline enhanced the bacterial response to high osmotic medium. (sciencemag.org)
  • Proton motive force (PMF), a consequence of metabolic activity, also contributes to the regulation of bacterial virulence, and the addition of proline to the medium allowed P. luminescens to form colonies in the presence of drugs that disrupted PMF, suggesting that proline oxidation may provide an electron source for generation of PMF. (sciencemag.org)
  • Recent advancements in the field have identified new functions of encoded transcription factors and greatly expanded our understanding of virulence gene regulation. (frontiersin.org)
  • For example, σ B has been linked with regulation of virulence gene expression in S. aureus ( 6 , 12 ). (asm.org)
  • We found that the loss of Tat pathway causes a drastic change of the transcriptome of Y. pseudotuberculosis in stationary phase at environmental temperature with differential regulation of genes involved in virulence, carbon metabolism and stress responses. (diva-portal.org)
  • Preventing piliation and motility through altered regulation and assembly of these important virulence factors could aid in the development of novel therapeutics. (asm.org)
  • This study increases our understanding of the regulation of these virulence factors, providing new avenues by which to target their expression. (asm.org)
  • In order to further understand the regulation of virulence factors in F. tularensis, we have systematically determined the genomic regions associated with all of the transcription factors implicated in virulence using chromatin immunoprecipitation coupled with high-throughput DNA sequencing (ChIP-Seq). (harvard.edu)
  • Metabolic reconstruction identifies strain-specific regulation of virulence in Toxoplasma gondii. (biomedsearch.com)
  • Several current aspects related to the virulence of S. aureus and CoNS are discussed, including isolates of different origins, phenotypic and genotypic techniques for the detection of these toxins, and the gene regulation mechanism involved in the expression of these toxins. (novapublishers.com)
  • We hypothesized that the observed frequency of gene loss/pseudogenes may be an artifact of evolution in response to a changing environment, and that genes involved in virulence should be under strong positive selection. (springer.com)
  • My group is involved in identifying novel virulence factors and studying their potential as vaccine targets for the development of both live and subunit vaccines against shigellosis. (edu.au)
  • Genes expressed in the Bvg+ phase encode known virulence factors, including adhesins such as filamentous hemagglutinin (FHA) and fimbriae, as well as toxins such as the bifunctional adenylate cyclase/hemolysin (ACY). (mendeley.com)
  • V ibrio cholerae, the causative agent of the epidemic disease cholera, requires the coordinated expression of multiple virulence factors. (pnas.org)
  • A well established statistical tool known as multivariate linear regression may offer a new approach in determining contributions of multiple virulence factors to the overall virulence of pathogenic microbes say researchers from Albert Einstein College of Medicine, Bronx, New York and Westminster College, Salt Lake City, Utah. (rxpgnews.com)
  • On the basis of prior knowledge of virulence factors in C. neoformans , a number of genes have been mutated and their contribution to virulence analyzed using these model systems. (genetics.org)
  • Conclusions: Our results demonstrate that the function of the CaCla4p protein kinase is essential for virulence and morphological switching of C. albicans in a mouse model. (mendeley.com)
  • Deletion of the candidate proline transporters from P. luminescens abolished the induction of some small molecules and increased the abundance of others, suggesting that L-proline or its metabolites differentially regulate the production of virulence factors. (sciencemag.org)
  • Taken together, this thesis presents a thorough analysis of the involvement of Tat pathway in the overall physiology and virulence strategies of Y . pseudotuberculosis . (diva-portal.org)
  • We could give anti-virulence antibiotics to people with healthy immune systems, who would be able to clear infections with this assistance," he said, "and traditional antibiotics combined with antivirulence therapies to people with compromised immune systems, who really need them. (eurekalert.org)
  • Taken together, our results showed that these factors were important features for fungal virulence in humans and suggested that thermolabile components in the blood serum may induce M. circinelloides virulence. (bioportfolio.com)
  • The results of this comprehensive "transcriptomic" analysis firstly showed that when the bacterium reaches the intestine, and then the bloodstream, it radically changes the activity of its genome and successively activates various groups of virulence genes. (pasteur.fr)
  • However, when an autoinducer binds to LuxR it forms a stable complex that activates virulence genes. (phys.org)
  • Antimicrobial Resistance and Virulence: a Successful or Deleterious Association in the Bacterial World? (pnas.org)
  • We analyzed a subset of virulence and housekeeping genes from several F. tularensis subspecies genomes to ascertain the presence and extent of positive selection. (springer.com)
  • Here we review the current knowledge of environmental adaptation by F. tularensis , its transcriptional regulators and their relationship to animal virulence. (frontiersin.org)
  • Many factors required for F. tularensis virulence have been identified, yet we know relatively little regarding how these factors are regulated at the level of transcription. (harvard.edu)
  • This efficient system for targeted gene deletion holds great promise for rapidly enhancing our knowledge of the biology and virulence of this increasingly common invasive fungal pathogen. (jci.org)
  • In this study two main approaches were taken to investigate virulence gene expression in S. pneumoniae. (bl.uk)
  • Genetic disruption of TgPTS abrogates de novo synthesis of PtdThr and impairs the lytic cycle and virulence of T. gondii. (sigmaaldrich.com)