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.
Proteins found in any species of bacterium.
Any of the processes by which cytoplasmic or intercellular factors influence the differential control of gene action in bacteria.
The functional hereditary units of BACTERIA.
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.
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.
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.
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.
Diseases of plants.
Deoxyribonucleic acid that makes up the genetic material of bacteria.
The interactions between a host and a pathogen, usually resulting in disease.
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.
Infections with bacteria of the species ESCHERICHIA COLI.
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.
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".
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.
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.
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.
The etiologic agent of PLAGUE in man, rats, ground squirrels, and other rodents.
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.
Proteins isolated from the outer membrane of Gram-negative bacteria.
The genetic complement of a BACTERIA as represented in its DNA.
The dose amount of poisonous or toxic substance or dose of ionizing radiation required to kill 50% of the tested population.
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 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.
A serotype of Salmonella enterica that is a frequent agent of Salmonella gastroenteritis in humans. It also causes PARATYPHOID FEVER.
A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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.
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.
A species of the fungus CRYPTOCOCCUS. Its teleomorph is Filobasidiella neoformans.
Proteins obtained from ESCHERICHIA COLI.
The relationships of groups of organisms as reflected by their genetic makeup.
The etiologic agent of CHOLERA.
Substances elaborated by bacteria that have antigenic activity.
A unicellular budding fungus which is the principal pathogenic species causing CANDIDIASIS (moniliasis).
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.
A bacterium which is one of the etiologic agents of bacillary dysentery (DYSENTERY, BACILLARY) and sometimes of infantile gastroenteritis.
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.
A human and animal pathogen causing mesenteric lymphadenitis, diarrhea, and bacteremia.
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.
A species of the genus YERSINIA, isolated from both man and animal. It is a frequent cause of bacterial gastroenteritis in children.
Infections with bacteria of the genus STREPTOCOCCUS.
Process of determining and distinguishing species of bacteria or viruses based on antigens they share.
Proteins found in any species of fungus.
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).
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.
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.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
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.
Microscopic threadlike filaments in FUNGI that are filled with a layer of protoplasm. Collectively, the hyphae make up the MYCELIUM.
Ability of a microbe to survive under given conditions. This can also be related to a colony's ability to replicate.
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.
Infections in animals with bacteria of the genus SALMONELLA.
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.
Infections with bacteria of the species YERSINIA PSEUDOTUBERCULOSIS.
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.
Proteins that are structural components of bacterial fimbriae (FIMBRIAE, BACTERIAL) or sex pili (PILI, SEX).
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.)
Infections with bacteria of the genus VIBRIO.
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.
A genus of gram-negative, facultatively anaerobic rod- to coccobacillus-shaped bacteria that occurs in a broad spectrum of habitats.
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.
Infections with bacteria of the genus YERSINIA.
Established cell cultures that have the potential to propagate indefinitely.
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.
Low-molecular-weight compounds produced by microorganisms that aid in the transport and sequestration of ferric iron. (The Encyclopedia of Molecular Biology, 1994)
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.
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.
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.
Infection with a fungus of the species CRYPTOCOCCUS NEOFORMANS.
Infections with bacteria of the genus PSEUDOMONAS.
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.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in fungi.
Infections with bacteria of the genus STAPHYLOCOCCUS.
Exotoxins produced by certain strains of streptococci, particularly those of group A (STREPTOCOCCUS PYOGENES), that cause HEMOLYSIS.
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.
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.
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 found in bacteria and in capsules thereof.
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.
Substances that reduce the growth or reproduction of BACTERIA.
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.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
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)
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
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.
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.
The etiologic agent of TULAREMIA in man and other warm-blooded animals.
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.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
Genotypic differences observed among individuals in a population.
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.
Diseases of freshwater, marine, hatchery or aquarium fish. This term includes diseases of both teleosts (true fish) and elasmobranchs (sharks, rays and skates).
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
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).
Process of generating a genetic MUTATION. It may occur spontaneously or be induced by MUTAGENS.
A species of bacteria that causes ANTHRAX in humans and animals.
Ribonucleic acid in bacteria having regulatory and catalytic roles as well as involvement in protein synthesis.
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.
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.
A genus in the family XANTHOMONADACEAE whose cells produce a yellow pigment (Gr. xanthos - yellow). It is pathogenic to plants.
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.
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.
The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).
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).
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.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
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.
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.
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)
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.
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.
A species of imperfect fungi from which the antibiotic fumigatin is obtained. Its spores may cause respiratory infection in birds and mammals.
Inflammatory responses of the epithelium of the URINARY TRACT to microbial invasions. They are often bacterial infections with associated BACTERIURIA and PYURIA.
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)
Antibiotic pigment produced by Pseudomonas aeruginosa.
Toxins produced, especially by bacterial or fungal cells, and released into the culture medium or environment.
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.
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.
A plant species of the family SOLANACEAE, native of South America, widely cultivated for their edible, fleshy, usually red fruit.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A species of STREPTOCOCCUS isolated from pigs. It is a pathogen of swine but rarely occurs in humans.
A species of Ralstonia previously classed in the genera PSEUDOMONAS and BURKHOLDERIA. It is an important plant pathogen.
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.
Agents that cause agglutination of red blood cells. They include antibodies, blood group antigens, lectins, autoimmune factors, bacterial, viral, or parasitic blood agglutinins, etc.
Infections with bacteria of the genus SALMONELLA.
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.
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.
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.
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.
Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.
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).
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.
A species of gram-positive, coccoid bacteria commonly isolated from clinical specimens and the human intestinal tract. Most strains are nonhemolytic.
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.
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.
A protein which is a subunit of RNA polymerase. It effects initiation of specific RNA chains from DNA.
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)
Structures within the nucleus of bacterial cells consisting of or containing DNA, which carry genetic information essential to the cell.
A subgenus of Salmonella containing several medically important serotypes. The habitat for the majority of strains is warm-blooded animals.
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).
Infections caused by bacteria that show up as pink (negative) when treated by the gram-staining method.
A mitosporic fungal genus in the family Clavicipitaceae. It has teleomorphs in the family Nectriaceae. Metarhizium anisopliae is used in PESTICIDES.
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 that are generated from breeding two genetically dissimilar strains of the same species.
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.
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)
Deletion of sequences of nucleic acids from the genetic material of an individual.
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.
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)
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.
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.
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.
Proteins found in any species of virus.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
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.
Infections with bacteria of the genus LISTERIA.
A species of gram-negative bacteria, in the genus ERWINIA, causing a necrotic disease of plants.
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.
A species of EDWARDSIELLA distinguished by its hydrogen sulfide production. (From Bergey's Manual of Determinative Bacteriology, 9th ed)
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.
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.
Suspensions of attenuated or killed bacteria administered for the prevention or treatment of infectious bacterial disease.
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.
A species of free-living soil amoebae in the family Acanthamoebidae. It can cause ENCEPHALITIS and KERATITIS in humans.
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 ...
© 2018 Macmillan Publishers Ltd., part of Springer Nature. Plasmids have a major role in the development of disease caused by enteric bacterial pathogens. Virulence plasmids are usually large (|40 kb) low copy elements and encode genes that promote host-pathogen interactions. Although virulence plasmids provide advantages to bacteria in specific conditions, they often impose fitness costs on their host. In this Review, we discuss virulence plasmids in Enterobacteriaceae that are important causes of diarrhoea in humans, Shigella spp., Salmonella spp., Yersinia spp and pathovars of Escherichia coli. We contrast these plasmids with those that are routinely used in the laboratory and outline the mechanisms by which virulence plasmids are maintained in bacterial populations. We highlight examples of virulence plasmids that encode multiple mechanisms for their maintenance (for example, toxin-antitoxin and partitioning systems) and speculate on how these might contribute to their propagation and success.
Bacteria can monitor their population density through the perception of molecules secreted by other local bacteria. This phenomenon leads to changes in bacterial behavior and changes in gene expression, and is termed quorum sensing. Quorum sensing in Vibrio cholerae, a major pathogenic bacterium in humans, is known to exist, but the gene targets of the sensing pathway are unknown. Zhu et al. found that a two-component signal module that includes the intracellular response regulator LuxO regulates virulence genes in V. cholerae. Vibrio mutants that lacked functional LuxO produced greatly decreased amounts of virulence-associated gene products, suggesting that LuxO was important for the expression of the virulence genes. The expression of HapR, which negatively regulated the expression of virulence genes, was decreased in a LuxO-dependent manner, suggesting one mechanism by which LuxO may increase virulence gene expression indirectly. HapR was expressed in luxO mutants, but not in wild-type ...
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 ...
Looking for Virulence? Find out information about Virulence. The ability of a microorganism to cause disease. Virulence and pathogenicity are often used interchangeably, but virulence may also be used to indicate the... Explanation of Virulence
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;
Define virulence. virulence synonyms, virulence pronunciation, virulence translation, English dictionary definition of virulence. adj. 1. a. Characterized by, causing, or promoting the rapid onset of severe illness. Used of a disease or toxin. b. Capable of causing disease by...
High-virulence strain caused earlier and greater damage than low-virulence strain and also can attack lymphatic system and bone marrow.
a Pathotypes were attributed to E. coli samples based on their sets of virulence genes or markers, as follows: for EAEC, capU, shf, virK, and aggregative adherence fimbria-encoding genes; for ETEC, heat-stable and heat-labile toxin-encoding genes and F4 and F18 fimbria-encoding genes; for atypical EPEC, espA, espB, tir, eae and variants, and absence of bfpA; for UPEC, P pilus-encoding genes, hlyA, S fimbria-encoding genes, chuA, fepC, cnf1, irp1, irp2, fyuA, iroN, and usp; for MNEC, ibeA, neuA, and neuC; and for incomplete ExPEC, kpsM, iutA, iucD, traT, malX, irp1, irp2, fyuA, chuA, fepC, iss, and kfiB. Isolates which did not possess any virulence genes or had a few scattered virulence-related genes were considered nonpathogenic. ...
Staphylococcus aureus is a major human pathogen with well-characterized bacteriophage contributions to its virulence potential. Recently, we identified plasmidial and episomal prophages in S. aureus strains using an extra-chromosomal DNA (exDNA) isolation and sequencing approach, uncovering the plasmidial phage ϕBU01, which was found to encode important virulence determinants. Here, we expanded our extra-chromosomal sequencing of S. aureus, selecting 15 diverse clinical isolates with known chromosomal sequences for exDNA isolation and next-generation sequencing. We uncovered the presence of additional episomal prophages in 5 of 15 samples, but did not identify any plasmidial prophages. exDNA isolation was found to enrich for circular prophage elements, and qPCR characterization of the strains revealed that such prophage enrichment is detectable only in exDNA samples and would likely be missed in whole-genome DNA preparations (e.g., detection of episomal prophages did not correlate with higher ...
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. ...
For the simultaneous and rapid identification and differentiation of diarrheagenic E. coli strains belonging to the seven major pathotypes (EPEC, ATEC, [LEE positive and LEE negative] STEC, ETEC, EIEC, and EAEC), we set up a single-step MPCR. The design and development of the MPCR were monitored with nine reference strains. All of the reference strains exhibited the expected gene pattern, as confirmed by DNA sequencing, and no cross-priming by the MPCR primer pairs was observed. Furthermore, all PCR amplicons showed comparable band intensities and are of sufficiently different sizes to be unequivocally resolved by standard agarose gel electrophoresis.. The specificity of the MPCR was validated with a subset of reference strains and further evaluated with 246 clinical E. coli isolates derived from patients from different geographic regions. Classification of all detected pathogens by the MPCR was confirmed by comparative PCR analysis performed independently and by a phenotypic analysis that ...
A team from the Institut National de la Recherche Scientifique (INRS) has made a scientific breakthrough regarding the virulence strategy employed by the Leishmania parasite to infect cells of the immune system. This microorganism is responsible for Leishmaniasis, a chronic parasitic disease that affects more than 12 million people worldwide.
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 ...
Covert Ops Implant of Virulence Binds on pickupImplant (Rating 90)Durability: 0/0Total Stats:+45 Mastery+41 EnduranceRequires Level 37 Covert Ops Implant of Virulence is a prototype item. Covert Ops Implant of Virulence on Jedipedia Covert Ops Implant of Virulence on SWTORData
Knowledge of toxins, virulence factors and antibiotic resistance genes is essential for bio-defense applications aimed at identifying functional signatures for characterizing emerging or engineered pathogens. Whereas genetic signatures identify a pathogen, functional signatures identify what a pathogen is capable of. To facilitate rapid identification of sequences and characterization of genes for signature discovery, we have collected all publicly available (as of this writing), organized sequences representing known toxins, virulence factors, and antibiotic resistance genes in one convenient database, which we believe will be of use to the bio-defense research community. MvirDB integrates DNA and protein sequence information from Tox-Prot, SCORPION, the PRINTS virulence factors, VFDB, TVFac, Islander, ARGO and a subset of VIDA. Entries in MvirDB are hyperlinked back to their original sources. A blast tool allows the user to blast against all DNA or protein sequences in MvirDB, and a browser ...
Tuberculosis remains the greatest cause of death worldwide due to a single pathogen. In order to identify the genes required for the pathogenicity of Mycobacterium tuberculosis, a functional genomic approach was developed. A library of signature-tagged transposon mutants of this bacterium was constructed and screened for those affected in their multiplication within the lungs of mice. From 1927 mutants tested, 16 were attenuated for their virulence. The insertions harboured by the selected mutants were mapped on the M. tuberculosis genome and most of the mutated loci appeared to be involved in lipid metabolism or transport across the membrane. Four independent mutations identified a cluster of virulence genes located on a 50 kb chromosomal region. These genes might be involved in the production of phthiocerol and phenolphthiocerol derivatives, a group of molecules restricted to eight mycobacterial species, seven of them being either strict or opportunistic pathogens. The interaction of five ...
Pathogenic bacteria often use effector molecules to increase virulence. In most cases, the mode of action of effectors remains unknown. Strains of Pseudomonas syringae pv. syringae (Pss) secrete syringolin A (SylA), a product of a mixed non-ribosomal peptide/polyketide synthetase, in planta. Here we …
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.
In 2008, SLS-like gene clusters were discovered in clinically relevant Gram-positive pathogens (including S. aureus and C. botulinum) and other nonpathogenic bacteria (7), leading to the identification of the LLS gene cluster in L. monocytogenes. SLS is a potent membrane-damaging agent and a major virulence factor contributing to GAS infection through rapid destruction of eukaryotic cells and tissue damage (6, 9-11, 15, 18-20). It has been proposed that SLS-like virulence factors from other Gram-positive pathogens also behave as potent cytotoxins (6, 14). Interestingly, functional experimental data of LLS activity on eukaryotic cells are scarce (3), despite the fact that LLS is almost exclusively detected within lineage I strains (the most frequent lineage among L. monocytogenes clinical isolates) and that it has been related to the L. monocytogenes infectious potential in epidemiological and comparative genomic studies (21, 22). In the present work, we aimed to characterize the extent to which ...
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.
In addition to providing insight into host-specific virulence factor expression, we believe this study to be the first description of quantitative determination of specific bacterial mRNA levels in feces containing commensal flora. Preparation of RNA from cholera patient stools has previously been described (20, 22); however, these analytes were described as having a rice-water appearance characteristic of Vibrio cholerae stool, and microscopically, they contained few nonvibrios. Those authors did not mention any problems with inhibition and were able to extract RNA by using Trizol reagent, a phenol-chloroform based method. This suggests that cholera patient stools are relatively pure cultures of V. cholerae that possess few inhibitors. In contrast, our specimens were rarely aqueous, contained abundant commensal E. coli and other bacterial flora, and sometimes also contained blood or plant material which can inhibit PCR. We therefore believe that our RNA extraction technique can be applied to ...
A new study from researchers in the Department of Biochemistry has shed light on machinery that causes virulence in a group of pathogenic bacteria including Shigella and Salmonella.. The work from Professor Judy Armitages lab, led by Dr Andreas Diepold, reveals intriguing features of the injectisome, an essential virulence factor that is responsible for the transmission of bacterial proteins into host cells. These proteins allow the bacteria to proliferate without being eliminated by the host immune system.. Published in PLoS Biology with collaborators from the Department of Physics in Oxford and the Biozentrum in Basel, the findings suggest the possibility of a novel target for the development of anti-virulence drugs. (1). Read more (Department of Biochemistry website). ...
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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 ...
MC 6460 Candidate Joe Pharaon , Applied Mathematics, University of Waterloo Title How does social behavior influence the evolution of pathogen virulence? Abstract From historic pandemics like the bubonic plague to the more recent outbreaks of the Zika virus, human behaviour continues to influence the course of disease spread. The severity of an emerging pathogen, known as
Scientists in Georgia and New York used MiSeq and PacBio sequencers to analyze a hypervirulent strain of methicillin-resistant Staphylococcus aureus, finding a novel evolutionary event. The project offers new findings about evolutionary strategies that have an impact on virulence. The team used BluePippin for to remove fragments smaller than 7 Kb from their libraries prior to sequencing on the PacBio instrument. Citation: ...
is certainly a respected pathogen that has been resistant to the fluoroquinolone antibiotics because of widespread prescribing increasingly. subpopulation. Distinctions in mutational procedures by virulence genotype which were noticed recommend co-evolution of level of resistance and virulence attributes favoring a far more virulent genotype in the quinolone-rich scientific environment. Introduction is certainly a gram-negative pathogen that triggers opportunistic attacks in prone hosts. It really is a leading reason behind severe pneumonia in hospitalized sufferers and is in charge of chronic lung infections in sufferers with cystic fibrosis. Its capability to trigger both chronic and acute attacks could be related to its comprehensive arsenal of virulence elements. Specifically, the sort III secretion program (TTSS) has been proven to be always a main virulence determinant in the pathogenesis of severe attacks. utilizes the TTSS to provide effector poisons (ExoS, ExoU, ExoY, and ExoT) straight ...
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 ...
Pathogenic bacteria must contend with immune systems that actively restrict the availability of nutrients and cofactors, and create a hostile growth environment. To deal with these hostile environments, pathogenic bacteria have evolved or acquired virulence determinants that aid in the acquisition of nutrients. This connection between pathogenesis and nutrition may explain why regulators of metabolism in nonpathogenic bacteria are used by pathogenic bacteria to regulate both metabolism and virulence. Such coordinated regulation is presumably advantageous because it conserves carbon and energy by aligning synthesis of virulence determinants with the nutritional environment. In Gram-positive bacterial pathogens, at least three metabolite-responsive global regulators, CcpA, CodY, and Rex, have been shown to coordinate the expression of metabolism and virulence genes. In this chapter, we discuss how environmental challenges alter metabolism, the regulators that respond to this altered metabolism, and how
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 ...
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[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/ ...
Virulence and mortality[edit]. Viral and bacterial diseases that kill victims before the illnesses spread to others tend to ...
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] ...
Survival and virulence factors[edit]. *Endures prolonged periods of nutritional deprivation. *Binds to dentin and proficiently ... Several virulence factors are thought to contribute to E. faecalis infections. A plasmid-encoded hemolysin, called the ... Five of them have been shown to be involved in stress response and virulence.[28] ... is also important for virulence in animal models of infection.[9][12] ...
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 ...
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 ...
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 ...
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 ...
Further findings show that the main virulence factor of S. aureus, the pore-forming toxin α-hemolysin (Hla), is the secreted ... As mentioned before, hemolysin is a potential virulence factor produced by microorganisms, which can put a human's health at ... But the fact that hemolysins (produced by pathogenic microorganisms during infections) are combined with other virulence ... "Iron and bacterial virulence". Indian J Med Microbiol. 24 (3): 163-4. PMID 16912433 ...
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"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 ...
"Helicobacter pylori Virulence and Genetic Geography". Science. 284 (5418): 1328-1333. Bibcode:1999Sci...284.1328C. doi:10.1126/ ... Nickel enzymes such as urease are considered virulence factors in some organisms.[88][89] Urease catalyzes the hydrolysis of ... "Urease as a Virulence Factor in Experimental Cryptococcosis". Infection and Immunity. 68 (2): 443-448. doi:10.1128/IAI.68.2. ...
Selective pressures exist however in the aquatic environment that may reduce the virulence of V. cholerae.[23] Specifically, ... Researchers have discovered a complex cascade of regulatory proteins controls expression of V. cholerae virulence determinants. ... ToxT then directly activates expression of virulence genes that produce the toxins, causing diarrhea in the infected person and ... and furthermore that this loss in culturability is associated with a loss in virulence.[23][24] ...
The relationship between virulence versus transmissibility is complex; if a disease is rapidly fatal, the host may die before ... Also, the relatively low virulence allows its victims to travel long distances, increasing the likelihood of an epidemic. ... "can lead to increases in growth and virulence".[74] More recently, in 2017, bacteria were found to be more resistant to ... and their intrinsic virulence (the severity of the disease they cause) is, in part, a necessary consequence of their need to ...
Meanwhile deletion of multiple other antimicrobial peptides has no effect on P. rettgeri virulence. Yet defence against P. ... These strains display different levels of virulence. For example Providencia sneebia is highly virulent, and infection always ... results in fly mortality.[4] Alternatively, P. rettgeri displays an intermediate virulence wherein some individuals survive ...
"Mucins Suppress Virulence Traits of Candida albicans". mBio. 5 (6). doi:10.1128/mBio.01911-14. ISSN 2150-7511 ...
Virulence-related outer membrane protein family (OmpX). *Outer membrane protein W family (OmpW) ...
Leggett HC, Buckling A, Long GH, Boots M (October 2013). "Generalism and the evolution of parasite virulence". Trends in ...
The Fundamental Virulence - 553. Frozen Cross - 554. Desperate Lights - 555. THE HERO - ...
The arginine catabolic mobile element (ACME) is a virulence factor present in many MRSA strains but not prevalent in MSSA.[52] ... Carriage of large plasmids, such as SCCmecI-III, is costly to the bacteria, resulting in a compensatory decrease in virulence ... These genetic variations within different MRSA strains possibly explain the variability in virulence and associated MRSA ... December 2007). "Identification of novel cytolytic peptides as key virulence determinants for community-associated MRSA". ...
Optimal virulence is a concept relating to the ecology of hosts and parasites. One definition of virulence is the hosts ... The evolution of virulence in pathogens is a balance between the costs and benefits of virulence to the pathogen. For example, ... Any movement on the virulence axis, towards higher or lower virulence, will result in lower fitness for the parasite, and thus ... Small worlds and the evolution of virulence: infection occurs .... *Pathogen Virulence: The Evolution of Sickness - A Review ...
Retrieved from "" ...
... 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 ...
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 ...
... has made a scientific breakthrough regarding the virulence strategy employed by the Leishmania parasite to infect cells of the ... Leishmania virulence strategy unveiled. Institut national de la recherche scientifique - INRS. Journal. PLOS Pathogens. Funder ... "Most research teams study the impacts of virulence factors, but until now no one understood how Leishmania was able transfer ... Since the parasite successfully transfers its virulence factors (GP63 and LPG molecules) to the other side of the vacuoles ...
... CGE at CU.NIH.GOV CGE at CU.NIH.GOV Thu Dec 29 15:17:49 EST 1994 *Previous message: Virulence ... When virulence increases survival/representation, it will be selected for. If this is what Ewald is saying then I believe he is ... Likewise, virulence *can* only be selected for when it has a positive effect on representation. As Derek indicates, this will ... zelmeda4 at (derek a. zelmer) writes: -If virulence increases to the point of high host mortality, the -host resource ...
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. ...
"Virulence". Biology Online. Thrall, Peter H.; Burdon, Jeremy J. (2003). "Evolution of Virulence in a Plant Host-Pathogen ... virulence is the loss of fitness induced by a parasite upon its host. Virulence can be understood in terms of proximate causes- ... and intrinsic characteristics of the bacteria called virulence factors. Many virulence factors are so-called effector proteins ... Virus virulence factors allow it to replicate, modify host defenses, and spread within the host, and they are toxic to the host ...
virulence synonyms, virulence pronunciation, virulence translation, English dictionary definition of virulence. adj. 1. a. ... virulence - extreme hostility; "the virulence of the malicious old man". virulency. hostility, ill will - a hostile (very ... virulence - extreme harmfulness (as the capacity of a microorganism to cause disease); "the virulence of the plague". virulency ... virulence. (ˈvɪrʊləns) or virulency. n. 1. the quality of being virulent. 2. (Pathology) the capacity of a microorganism for ...
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. ...
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S. aureus encodes a large number of virulence factors that aid the bacterium in survival and pathogenesis. These virulence ... Role of OB-Fold Protein YdeI in Stress Response and Virulence of Salmonella enterica Serovar Enteritidis S. Enteritidis during ... AbaM Regulates Quorum Sensing, Biofilm Formation, and Virulence in Acinetobacter baumannii Acinetobacter baumannii is a ... Understanding Acinetobacter virulence gene regulation could aid the development of novel anti-infective strategies. ...
When placed at random, the transposon may be placed next to a virulence factor or placed in the middle of a virulence factor ... Small molecules being investigated for their ability to inhibit virulence factors and virulence factor expression include ... These obtained bacterial virulence factors have two different routes used to help them survive and grow: The factors are used ... Other virulence factors include factors required for biofilm formation (e.g. sortases) and integrins (e.g. beta-1 and 3). ...
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 ...
In vivo genetic analysis of bacterial virulence.. Chiang SL1, Mekalanos JJ, Holden DW. ...
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. ...
Cisco Pinpoints Here You Have Worms Virulence. E-jihadist group claims responsibility for attack, which spread rapidly ...
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 ...
... Nat Chem Biol. 2007 Sep;3(9):541-8. doi: 10.1038/nchembio.2007.24 ... We review new approaches to targeting virulence, discuss their advantages and disadvantages, and propose that in addition to ... such as virulence factors required to cause host damage and disease. This approach has several potential advantages including ... targeting virulence, new antimicrobial development strategies should be expanded to include targeting bacterial gene functions ...
Here we investigate the impact of indole and 7HI on Pseudomonas aeruginosa PAO1 virulence and quorum sensing (QS)-regula … ... Indole and 7-hydroxyindole diminish Pseudomonas aeruginosa virulence Microb Biotechnol. 2009 Jan;2(1):75-90. doi: 10.1111/j. ... Here we investigate the impact of indole and 7HI on Pseudomonas aeruginosa PAO1 virulence and quorum sensing (QS)-regulated ... most repressed genes encode the mexGHI-opmD multidrug efflux pump and genes involved in the synthesis of QS-regulated virulence ...
Genome and virulence determinants of high virulence community-acquired MRSA. Lancet. 2002 May 25. 359(9320):1819-27. [Medline] ... Virulence. In the United States, most community-associated methicillin-resistant S aureus (CA-MRSA) infections have been caused ... Clinical practice: colonization, fomites, and virulence: rethinking the pathogenesis of community-associated methicillin- ... virulence factor. [21] PVL is a bicomponent toxin that forms pores in neutrophils; it has been associated with furunculosis and ...
  • All of these offer ultimate explanations for virulence in pathogens. (
  • At one time, some biologists argued that pathogens would tend to evolve toward ever decreasing virulence because the death of the host (or even serious disability) is ultimately harmful to the pathogen living inside. (
  • The evolution of virulence in pathogens is a balance between the costs and benefits of virulence to the pathogen. (
  • Virulence factors encoded on mobile genetic elements spread through horizontal gene transfer, and can convert harmless bacteria into dangerous pathogens. (
  • It has been found that many pathogens have converged on similar virulence factors to battle against eukaryotic host defenses. (
  • Virulence factors are factors that allow pathogens to avoid host defense mechanisms and adversely affect the host. (
  • In this book, the authors present current research in the study of the virulence mechnisms, diagnosis and management of bacterial pathogens. (
  • But while immune suppression in diabetic infections has been well reported, the investigators noted, " … to our knowledge, there have been few studies that address how hyperglycemia in diabetic infections influences the virulence potential of bacterial pathogens. (
  • Significance: By attenuating the virulence of pathogens rather than eradicating them, mucin glycans are attractive candidates for novel therapeutics. (
  • Although capsules are virulence factors for other pathogens, the role of CPS in C. jejuni disease has not been well defined beyond descriptive studies demonstrating a role in serum resistance and for diarrhea in a ferret model of disease. (
  • might lead to the discovery of completely novel antibiotic scaffolds" and suggest that "considering YbeY's high level of conservation, its essential nature in many pathogens, and its ability to sensitize pathogens by disrupting stress tolerance and virulence, a YbeY-specific antibiotic could have broad-spectrum antimicrobial activity. (
  • Serum C-reactive protein relationship in high- versus low-virulence pathogens in the diagnosis of periprosthetic joint infection. (
  • Little is known about the relationship between the virulence of pathogens in periprosthetic joint infection (PJI) and C-reactive protein (CRP) levels. (
  • The initial impetus for testing these virulence factors was analogy to other pathogens and/or identification of mutant strains with an obvious phenotype. (
  • The study of fungal regulatory networks is essential to the understanding of how these pathogens respond to host environmental signals with effective virulence-associated traits. (
  • These data show that fungal virulence-associated genes are coordinately regulated and that an analysis of such transcriptomes allows for the identification of important new genes involved in the normal growth and virulence of fungal pathogens. (
  • zelmeda4 at ('derek a. zelmer') writes: -If virulence increases to the point of high host mortality, the -host resource will be depleted, and selection will be again for -less virulent forms. (
  • Thus, if producing a virulent infection increases an organism's genetic representation in the next generation, virulence will be selected for whether or not this ultimately leads to host number depletion. (
  • Presumably virulence is being selected against in this organism, unless virulent organisms have other characteristics that increase their representation in the population. (
  • The noun virulence derives from the adjective virulent, meaning disease severity. (
  • Virulence can be understood in terms of proximate causes-those specific traits of the pathogen that help make the host ill-and ultimate causes-the evolutionary pressures that lead to virulent traits occurring in a pathogen strain. (
  • Virulence is the state of being virulent, that is, highly infectious, malignant or deadly. (
  • Virulent strains of bacteria are ones that produce "virulence factors," small molecules and proteins that convert a benign bacterium into a pathogen. (
  • Bordetella species utilize the BvgAS (Bordetella virulence gene) two-component signal transduction system to sense the environment and regulate gene expression among at least three phases: a virulent Bvg+ phase, a nonvirulent Bvg- phase, and an intermediate Bvgi phase. (
  • Collaborating with the lab of David Weiss, PhD, the researchers showed that the virulence-disabled bacteria could be used as a live attenuated vaccine in mice, protecting them against later infection by the virulent form. (
  • There are infinitely many things that do not contribute to the virulence of a pathogen. (
  • Hyphae have been observed to adhere to and invade host tissues more readily than the yeast farm, suggesting that filamentous growth may contribute to the virulence of this major human pathogen. (
  • at least two of these small RNAs contribute to the virulence of Listeria monocytogenes. (
  • produce a variety of so-called virulence factors that permit them to evade the defense mechanisms of the host and thus cause disease. (
  • The ability of bacteria to cause disease is described in terms of the number of infecting bacteria, the route of entry into the body, the effects of host defense mechanisms, and intrinsic characteristics of the bacteria called virulence factors. (
  • One example of a bacterial virulence factor acting like a eukaryotic protein is Salmonella protein SopE it acts as a GEF, turning the GTPase on to create more GTP. (
  • The development of resistance in Salmonella shows that it is a multifactorial process and the acquisition of fluoroquinolone resistance might have significant influences on the bacterial fitness and virulence. (
  • The precise role of one protein in bacteria, EF-P, remains a mystery, but this team found that it plays an essential role in the virulence of Salmonella enterica typhimurium, a common foodborne pathogen causing diarrhea, fever, and abdominal cramps, and occasionally lifetime chronic arthritis. (
  • This textbook is a resource for undergraduate, graduate, and medical students, as well as other health-oriented learners, postdoctoral scholars, basic scientists, and professors intent on expanding their knowledge of bacterial infection and virulence mechanisms. (
  • As a result, virulence mechanisms that set typhoid fever apart from human gastroenteritis remain understudied. (
  • Our analysis of S. Typhi specific virulence mechanisms will be useful, and necessary, to understand how the interplay between pathogen and the innate immune system gives rise to responses that distinguish typhoid fever from gastroenteritis. (
  • This outcome will be significant, because it will have broad relevance for understanding the molecular virulence mechanisms that distinguish typhoid fever from gastroenteritis. (
  • These results open up new avenues for understanding the control of S. aureus virulence mechanisms. (
  • Thus, ec240 dysregulated several uropathogenic Escherichia coli (UPEC) virulence factors through different mechanisms and independent of its effects on type 1 pilus biogenesis and may have potential as an antivirulence compound. (
  • 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. (
  • 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. (
  • One definition of virulence is the host's parasite-induced loss of fitness . (
  • Many virulence determinants of E. amylovora have been characterized, including the Type III secretion system (T3SS), the exopolysaccharide (EPS) amylovoran, biofilm formation, and motility. (
  • To understand the role of VAD1 in virulence, a functional genomics approach was used to identify 3 additional virulence determinants dependent on VAD1: PCK1, TUF1, and MPF3, involved in gluconeogenesis, mitochondrial protein synthesis, and cell wall integrity, respectively. (
  • The virulence factors of bacteria are typically proteins or other molecules that are synthesized by enzymes. (
  • These virulence factors allow the bacteria to enter host cells and facilitate entry into the body across epithelial tissue layers at the body surface. (
  • Many bacteria produce virulence factors that inhibit the host's immune system defenses. (
  • Many virulence factors are proteins made by bacteria that poison host cells and cause tissue damage. (
  • Bacteria like Escherichia coli O157:H7 gain the majority of their virulence from mobile genetic elements. (
  • Gram-negative bacteria secrete a variety of virulence factors at host-pathogen interface, via membrane vesicle trafficking as bacterial outer membrane vesicles for invasion, nutrition and other cell-cell communications. (
  • Another group of virulence factors possessed by bacteria are immunoglobulin (Ig) proteases. (
  • There is some controversy about whether coagulase is a virulence factor, but one way coagulase contributes to pathogenicity is that it binds prothrombin to form staphylothrombin, which then cleaves fibrinogen to form fibrin clots in which the bacteria can live and avoid phagocytosis by neutrophils. (
  • identified proline as a molecular trigger in insect extracts that stimulated the production of small molecules with virulence or antibiotic properties in two species of symbiotic bacteria, Photorhabdus luminescens TT01 and Xenorhabdus nematophila ATCC19061. (
  • Thus, these bacteria appear to know they are in an insect by sensing proline, which then regulates metabolic pathways involved in producing antibiotic and virulence factors. (
  • Virulence factors allow bacteria to evade the human immune system, to infect tissues and cells and to establish a foothold within the body. (
  • Tim Wencewicz, PhD, assistant professor of chemistry in Arts & Sciences at Washington University in St. Louis, thinks we should be looking for agents that block virulence factors rather than continuing to search for ones to kill bacteria outright. (
  • Molecules known as virulence factors are produced by bacteria, viruses, and fungi to help them to infect host cells. (
  • Now Ritwij Kulkarni of Columbia University, New York, NY, and colleagues show that cigarette smoke actually boosts virulence of Staphylococcus aureus bacteria. (
  • This may account for the growing difficulty eradicating the bacteria as well as high virulence. (
  • Tat pathway uniquely exports folded proteins including virulence factors across the cytoplasmic membranes of bacteria. (
  • Because the mechanism by which the modification occurs is unique to bacteria and this system is involved in virulence it could be a potential drug target, Ibba says. (
  • Marine pathogenic bacteria are able to form biofilms on many surfaces, such as mollusc shells, and they can wait for the appropriate opportunity to induce their virulence. (
  • 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. (
  • The hypothesis of the paper is that virulence and rate of infection would necessarily be highly correlated as virulence increases. (
  • 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. (
  • We devised a noninvasive genetic selection strategy to identify positive regulators of bacterial virulence genes during actual infection of an intact animal host. (
  • Application of this technology to the human intestinal pathogen Vibrio cholerae identified several regulators of cholera toxin and a central virulence gene regulator that are operative during infection. (
  • To extend our knowledge of virulence gene regulation during infection, we developed a noninvasive genetic selection that incorporates the use of the recombination-based in vivo expression technology (RIVET) and transposon mutagenesis to identify positive regulators of virulence genes during infection. (
  • A number of these regulators are described, some of which affect virulence gene induction only during infection. (
  • Research scientists from the IRD and INSERM (1) who are studying this trypanosome found that one of the proteins it secretes, Tc52, is a virulence factor that plays a pivotal role in the infection mechanism. (
  • Research scientists from the IRD research unit "Pathogénie des Trypanosomatidae" and co-workers from INSERM have studied the parasite s development cycle, its virulence and its involvement in the infection process, with a view to identifying possible prevention and control methods. (
  • Rather than focusing on therapeutics that target in vitro viability, much like conventional antibiotics, an alternative approach is to target functions essential for infection, such as virulence factors required to cause host damage and disease. (
  • At the same time, however, the host species is evolving resistance to the infection, which then provides an environment for increasing pathogen virulence. (
  • S. L. Reckseidler, D. DeShazer, P. A. Sokol, and D. E. Woods, "Detection of bacterial virulence genes by subtractive hybridization: Identification of capsular polysaccharide of Burkholderia pseudomallei as a major virulence determinant," Infection and Immunity , vol. 69, no. 1, pp. 34-44, 2001. (
  • Production of both toxins was required for full infection virulence. (
  • To successfully establish an infection, E. amylovora uses a complex regulatory network to sense the relevant environmental signals and coordinate the expression of early and late stage virulence factors involving two component signal transduction systems, bis-(3′-5′)-cyclic di-GMP (c-di-GMP) and quorum sensing. (
  • Most models of virulence evolution assume that transmission and virulence are constant during an infection. (
  • We find that ESS virulence decreases when expressed early in the infection or when transmission occurs late in an infection. (
  • In contrast, ESS virulence first increased and then decreased with transition rate when there was little virulence early in the infection and a rapid recovery rate. (
  • In this paper, we develop a model for understanding the evolution of virulence (disease-induced mortality) when virulence and transmission change over the course of an infection. (
  • I 2 is an infectious class with a later infection age as well as class-specific transmission and virulence rates that differ from those of I 1 . (
  • An M. tuberculosis ΔRv1422 strain is markedly attenuated for virulence in a mouse infection model, where it elicits decreased inflammation in the lungs and shows impaired bacterial persistence. (
  • Its role in virulence suggests that CuvA may be a useful target for novel inhibitors of M. tuberculosis during infection. (
  • 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. (
  • Little is known about the prevalence of different virulence factors and the ability to produce toxin among Campylobacter isolates obtained from different sources. (
  • Only 13.5% of the isolates were positive for the virulence plasmid vir B11. (
  • To address their hypothesis, the authors inoculate vaccinated or unvaccinated chickens with a series of MDV isolates that range from low to high virulence. (
  • Our study showed that several pathogenic Aeromonas species possessing virulence traits and antimicrobial resistance similar to those of Aeromonas isolates causing clinical diseases were present. (
  • Since pathogen isolates showed no differential virulence to host cultivars, there is no evidence for a gene-for-gene host-pathogen relationship. (
  • Races of isolates of Plasmopara halstedii from Spain and studies on their virulence. (
  • According to the proposal of a new system for characterization of the isolates of P. halstedii in the late 1990s, Coded Virulence Formulae (CVF) were assigned to bulk isolates and single-sporangium ( ss ) isolates obtained from them. (
  • A genome-wide association study across all VNB isolates revealed sequence differences between clinical and environmental isolates in virulence factors and stress response genes. (
  • These data highlight the complex evolutionary interplay between adaptation to natural environments and opportunistic infections, and that selection on specific pathways may predispose isolates to human virulence. (
  • To examine the genetics of host-specific virulence in C. sativus , a cross was made between isolate ND90Pr (which exhibits high virulence on barley genotype Bowman and low virulence on genotype ND 5883) and ND93-1 (which exhibits low virulence on both genotypes). (
  • Ascospore progeny segregated 48:55 for low virulence/high virulence on Bowman, indicating the presence of a single virulence gene in isolate ND90Pr. (
  • The ability of the parasite to switch its antigenic profile correlates with the parasite's high virulence. (
  • An Institut Pasteur-CNRS research team has characterized a Staphylococcus aureus gene involved in virulence, biofilm formation and resistance to certain antibiotics. (
  • This component interacts with the WalKR system to control its activity and its absence leads to a strong decrease in virulence, biofilm formation (bacterial aggregates), and resistance to certain antibiotics. (
  • We think control of biofilm formation [and of numerous other virulence factors in S. aureus ] proceeds via agr. (
  • Inhibitory effect of Murraya koenigii against Candida albicans virulence and biofilm development" Biologia , vol. 71, no. 3, 2016, pp. 256-264. (
  • Transition from the yeast form to the hyphal form is one of the key virulence factors in C. albicans contributing to macrophage evasion, tissue invasion and biofilm formation. (
  • In the present study, we used RNA-seq analysis to identify biofilm- and virulence-related genes displaying altered expression in biofilms compared to the planktonic condition. (
  • The expression of genes encoding the Type VI Secretion System and associated exported proteins are strongly induced, suggesting that V. tapetis activates this virulence factor when living in biofilm. (
  • The virulence of various strains of Helicobacter pylori tends to correlate with the level of production of urease. (
  • 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 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. (
  • It is therefore possible that other factors than virulence factors are of importance for the ability of PNSP strains to expand. (
  • 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. (
  • Detection of Seven Virulence and Toxin Genes of Campylobacter jej. (
  • A high prevalence (93.3-100%) of six virulence and toxin genes (the fla A , cad F, ceu E, cdt A, cdt B, cdt C, cdt gene cluster) was found. (
  • Specifically, we show that the recent acquisition of glcA and glcC by S. aureus is essential for full toxin production and virulence potential in hyperglycemic SSTIs," they wrote. (
  • Toxigenic Vibrio cholerae causes disease by producing the primary virulence factors cholera toxin (CT) and the toxin coregulated pilus (TCP). (
  • We have identified mucins, the major gel-forming components of mucus, and their complex sugar structures (glycans) as protective molecules that suppress microbial virulence traits including toxin secretion, bacterial communication, and surface attachment. (
  • Many virulence factors are so-called effector proteins that are injected into the host cells by specialized secretion apparati, such as the type three secretion system. (
  • A major group of virulence factors are proteins that can control the activation levels of GTPases. (
  • 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 ). (
  • Analyses of selection yielded one housekeeping gene and 7 virulence genes which showed significant evidence of positive selection at loci implicated in cell surface structures and membrane proteins, metabolism and biosynthesis, transcription, translation and cell separation, and substrate binding and transport. (
  • 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. (
  • This review will focus on the molecular dissection of virulence factors of C. albicans, including adhesion, proteinases secretion, hyphal formation, and phenotypic switching. (
  • A pathogenicity island acquired by horizontal transfer, coding for a type IV secretion system, is a major determinant of virulence. (
  • However, the role of other protein secretion and/or translocation systems in virulence of Yersinia species is not well known. (
  • 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). (
  • V ibrio cholerae, the causative agent of the epidemic disease cholera, requires the coordinated expression of multiple virulence factors. (
  • Virulence factors of Candida species. (
  • Sree V. Aroori, Tristan A. Cogan, and Tom J. Humphrey, "Effect of Noradrenaline on the Virulence Properties of Campylobacter Species," International Journal of Microbiology , vol. 2014, Article ID 279075, 10 pages, 2014. (
  • Some viral virulence factors confer ability to replicate during the defensive inflammation responses of the host such as during virus-induced fever. (
  • A virulence marker is a diagnostic tool in detecting viral factors. (
  • En su libro The Tipping Point (reseñado aquí), Malcolm Gladwell habla sobre la importancia de las personas que él llama Conectores, Expertos, y Vendedores en la propagación viral de las ideas. (
  • Our objective here is to characterize the viral evolution and viral factors determining HIV virulence, the evolution of the HIV reservoir in PBMC and the co-evolution of anti-HIV CD8 T cel. (
  • 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. (
  • The data from this study demonstrate that both virulence in the pathogen and resistance in the host are under monogenic control in this specific host genotype/fungal isolate combination. (
  • Here, we describe a protocol for the identification of pathogenicity and virulence genes through random insertional mutagenesis using the fungal wilt pathogen Verticillium dahliae as an example for the protocol. (
  • 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. (
  • Chui Yoke Chin et al, A high-frequency phenotypic switch links bacterial virulence and environmental survival in Acinetobacter baumannii, Nature Microbiology (2018). (
  • The virulence factor for diphtheria is an exotoxin named diphtheria exotoxin. (
  • Borges M, cordeiro-Da-Silva A, Sereno D & Ouaissi A. Peptide-based analysis of the amino acid sequence important to the immunoregulatory function of Trypansosma cruzi Tc52 virulence factor. (
  • Now that the complex biochemistry of this virulence factor is better understood, they plan to start looking for agents that block its synthesis or activity. (
  • Besides conferring methicillin resistance, the SCCmecIV genes also code for the arginine catabolic mobile element (ACME) and Panton-Valentine leukocidin (PVL) virulence factor. (
  • Cigarette smoke does so by enhancing S. aureus' ability to form biofilms, which are an important virulence factor, according to the study. (
  • The report concludes, "Assuming that complement is as critical to orthopoxvirus containment in humans as it is in rodents, SPICE seems to be a virulence factor for variola virus. (
  • In this study, a virulence-associated DEAD-box RNA helicase-encoding gene (VAD1) was isolated from a mutant defective in the virulence factor laccase. (
  • This review will also describe briefly the virulence factors in non-albicans Candida spp. (
  • Candida parapsilosis is a major cause of human disease, yet little is known about the pathogen's virulence. (
  • To complement the study of host-specific virulence in the pathogen, an experiment also was conducted on the genetics of specific resistance in the host. (
  • Understanding Acinetobacter virulence gene regulation could aid the development of novel anti-infective strategies. (
  • Therefore, the true nature of the in vivo regulation of these virulence factors within a host remains unclear. (
  • 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. (
  • 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. (
  • Recent advancements in the field have identified new functions of encoded transcription factors and greatly expanded our understanding of virulence gene regulation. (
  • The results presented here provide a detailed structural mechanism for virulence gene regulation in V. cholerae by the UFA components of bile and other synthetic ToxT inhibitors. (
  • 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. (
  • Preventing piliation and motility through altered regulation and assembly of these important virulence factors could aid in the development of novel therapeutics. (
  • This study increases our understanding of the regulation of these virulence factors, providing new avenues by which to target their expression. (
  • 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). (
  • The findings highlight the importance of spatial genome organization in gene regulation and the control of virulence in malaria parasites. (
  • To begin to understand the molecular basis for virulence in Cryptococcus neoformans var. (
  • 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. (
  • 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. (
  • These differences are thought to reflect the environmental adaptation of these subspecies and are associated with their differences in virulence. (
  • Tests for virulence of six T. idahoensis field dikaryons on four winter wheats that differ in resistance revealed great differences in virulence on a given wheat. (
  • Using techniques of cellular and molecular biology, and of biochemistry, they sought to identify the nature and function of T. cruzi genes which code for the factors responsible for the virulence, in particular a protein called Tc52. (
  • Virulence factors of Francisella tularensis. (
  • The mechanism causing viable Francisella tularensis to lose virulence in aerosols has been investigated. (
  • Our results suggest that while the loss of functional genes through disuse could be accelerated by negative selection, the genome decay in Francisella could also be the byproduct of adaptive evolution driven by complex interactions between host, pathogen, and thier environment, as evidenced by several of its virulence genes which are undergoing strong, positive selection. (
  • These findings led us to name this gene cuvA (carbon utilization and virulence protein A) and to suggest a model in which deletion of cuvA leads to changes in nutrient uptake and/or metabolism that affect cell wall structure, morphology, and virulence. (
  • 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. (
  • Antimicrobial Resistance and Virulence: a Successful or Deleterious Association in the Bacterial World? (
  • Distribution of Antimicrobial Resistance and Virulence Genes in Enterococcus spp. (
  • Since the parasite successfully transfers its virulence factors (GP63 and LPG molecules) to the other side of the vacuole's membrane, it was necessary to determine what other compartment of the infected host cell contained these factors. (
  • They then used the latest genetic technology to identify the molecules involved in intracellular trafficking that are needed to spread Leishmania virulence factors in the infected host cell. (
  • The team found that by decreasing the expression of two host cell molecules, sec22b and syntaxin-5, that are responsible for regulating intracellular traffic in the ER, they could block the spread of virulence factors in the infected cell and interfere with their actions. (
  • 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. (
  • the most repressed genes encode the mexGHI-opmD multidrug efflux pump and genes involved in the synthesis of QS-regulated virulence factors including pyocyanin (phz operon), 2-heptyl-3-hydroxy-4(1H)-quinolone (PQS) signal (pqs operon), pyochelin (pch operon) and pyoverdine (pvd operon). (
  • Any movement on the virulence axis, towards higher or lower virulence, will result in lower fitness for the parasite, and thus will be selected against. (
  • Thus, under natural conditions, a newly emergent, highly lethal pathogen that kills very rapidly is expected to evolve lower virulence. (
  • Our results, obtained by comparing the five malaria parasites with B. microti and T. gondii , strongly suggest that genome organization in malaria parasites has been shaped by parasite-specific gene families that affect virulence," Le Roch said. (
  • Therefore, strategies to combat certain bacterial infections by targeting these specific virulence factors and mobile genetic elements have been proposed. (
  • A research team led by UC San Francisco scientists has discovered a cellular signaling system that regulates the virulence of Cryptococcus neoformans , a fungus that has been estimated to cause nearly a million cases of meningitis worldwide per year, about 625,000 of which are fatal. (
  • S. aureus encodes a large number of virulence factors that aid the bacterium in survival and pathogenesis. (
  • Richardson is senior author of the team's published paper in Science Advances , which is titled, " Lack of nutritional immunity in diabetic skin infections promotes Staphylococcus aureus virulence . (
  • They found that in the diabetic mice, the strain of S. aureus with four glucose transporters quickly formed biofilms and activated pathways that increased virulence. (
  • The AraC/XylS-family transcriptional regulator ToxT is the master virulence activator of Vibrio cholerae , the gram-negative bacterial pathogen that causes the diarrheal disease cholera. (
  • We analyzed a subset of virulence and housekeeping genes from several F. tularensis subspecies genomes to ascertain the presence and extent of positive selection. (
  • Here we review the current knowledge of environmental adaptation by F. tularensis , its transcriptional regulators and their relationship to animal virulence. (
  • 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. (
  • Thus, there is a natural force providing pressure on the parasite to "self-limit" virulence. (
  • 2004) [2] studied the malaria parasite using a rodent and chicken model respectively and found that there was trade-off between transmission success and virulence as defined by host mortality. (
  • A team from the Institut National de la Recherche Scientifique (INRS) has made a scientific breakthrough regarding the virulence strategy employed by the Leishmania parasite to infect cells of the immune system. (
  • It's like there's a train travelling among the different intracellular compartments that the parasite boards to deliver its virulence factors inside the infected cell," says Professor Descoteaux, the study's lead author. (
  • From an ecological standpoint, virulence is the loss of fitness induced by a parasite upon its host. (
  • Inspired by studies of natural host-parasite systems, we show that disengagement can be avoided by selecting for individuals that exhibit reduced levels of "virulence", rather than maximum ability to defeat coevolutionary adversaries. (
  • Phosphatidylthreonine and Lipid-Mediated Control of Parasite Virulence. (
  • An international research team led by scientists at the University of California, Riverside, and the La Jolla Institute for Immunology has found that malaria parasite genomes are shaped by parasite-specific gene families, and that this genome organization strongly correlates with the parasite's virulence. (
  • He came to the conclusion that virulence tends to remain especially high in waterborne and vector-borne infections, such as cholera and Dengue . (
  • Mycobacterial Infections, Virulence Factors and Therapy Conference aims to bring together leading academic scientists, researchers and research scholars to exchange and share their experiences and research results on all aspects of Mycobacterial Infections, Virulence Factors and Therapy Conference. (
  • It also provides a premier interdisciplinary platform for researchers, practitioners, and educators to present and discuss the most recent innovations, trends, and concerns as well as practical challenges encountered and solutions adopted in the fields of Mycobacterial Infections, Virulence Factors and Therapy Conference. (
  • Parasites infecting long-lived primates may require escape from adaptive immune responses to establish chronic infections and ensure transmission to a susceptible host, while parasites infecting short-lived rodent hosts may benefit from more flexible expression of their virulence genes. (