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 ...
Pseudomonas aeruginosa is a facultative pathogen that can cause, inter alia, acute or chronic pneumonia in predisposed individuals. The gram-negative bacterium displays considerable genomic and phenotypic diversity that is also shaped by small molecule secondary metabolites. The discrimination of virulence phenotypes is highly relevant to the diagnosis and prognosis of P. aeruginosa infections. In order to discover small molecule metabolites that distinguish different virulence phenotypes of P. aeruginosa, 35 clinical strains were cultivated under standard conditions, characterized in terms of virulence and biofilm phenotype, and their metabolomes were investigated by untargeted liquid chromatography-mass spectrometry. The data was both mined for individual candidate markers as well as used to construct statistical models to infer the virulence phenotype from metabolomics data. We found that clinical strains that differed in their virulence and biofilm phenotype also had pronounced divergence in ...
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
... 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 ... Disproved hypothesis of epidemiologist Theobald Smith Optimal virulence Super-spreader Theory of virulence - Theory by ... Ewald Verotoxin-producing Escherichia coli Virulence factor Antivirulence Wikimedia Commons has media related to Virulence. ...
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). ...
Riedmann, EM; Mylonakis, E (2010). "Virulence: A new multi-disciplinary journal". Virulence. 1 (1): 1. doi:10.4161/viru.1.1. ... Virulence is a peer-reviewed medical journal that covers microbiology and immunology specifically, microorganism pathogenicity ... "Virulence". InCites Journal Citation Reports. Retrieved 2020-12-17. Official website (Articles with short description, Short ... "Virulence". NLM Catalog. National Center for Biotechnology Information. Retrieved 2014-12-13. "Serials cited". Tropical ...
The evolution of virulence in pathogens is a balance between the costs and benefits of virulence to the pathogen. For example, ... Optimal virulence is a concept relating to the ecology of hosts and parasites. One definition of virulence is the host's ... Any movement on the virulence axis, towards higher or lower virulence, will result in lower fitness for the parasite, and thus ... Empirical Support for Optimal Virulence in a Castrating Parasite Evolution of Virulence Adaptive Dynamics of Infectious ...
Virulence is the second full-length studio album from melodic hardcore band, Only Crime. It was released on January 23, 2007 ...
Virulence-related outer membrane proteins, or outer surface proteins (Osp) in some contexts, are expressed in the outer ... The Yersinia enterocolitica Ail protein is a known virulence factor. Proteins in this family are predicted to consist of eight ... Lom is found in the bacterial outer membrane, and is homologous to virulence proteins of two other enterobacterial genera. It ... Members of this group include: PagC, required by Salmonella typhimurium for survival in macrophages and for virulence in mice ...
Virulence. 7 (5): 512-26. doi:10.1080/21505594.2016.1138201. PMC 5026795. PMID 27078171. Khurshid, Zohaib; Najeeb, Shariq; Mali ...
... virulence, and pathogenicity. The virus particle, called a virion, is pleomorphic and varies between being filamentous, ... Virulence. 8 (8): 1580-1591. doi:10.1080/21505594.2017.1365216. PMC 5810478. PMID 28812422. McCauley JW, Hongo S, Kaverin NV, ...
Virulence. 8 (8): 1580-1591. doi:10.1080/21505594.2017.1365216. PMC 5810478. PMID 28812422. "New virus gets official name, ...
Virulence. 3 (7): 583-588. doi:10.4161/viru.22330. PMC 3545935. PMID 23154286. Bolognia, Jean; Schaffer, Julie V; Cerroni, ...
Virulence. 1 (5): 367-75. doi:10.4161/viru.1.5.12796. PMID 21178472. Kourkoumpetis TK, Velmahos GC, Ziakas PD, Tampakakis E, ...
Virulence. 5: 697-702. doi:10.4161/viru.29091. PMC 4189875. PMID 25513770. (Immune system process). ...
Virulence. Taylor & Francis. 9 (1): 1344-1353. doi:10.1080/21505594.2018.1504560. ISSN 2150-5594. PMC 6177251. PMID 30146948. ...
Virulence. 6 (8): 787-801. doi:10.1080/21505594.2015.1098804. PMC 4826107. PMID 26556670. Koga Y, Tanaka S, Sakudo A, Tobiume M ...
Virulence. 5 (1): 226-235. doi:10.4161/viru.25991. ISSN 2150-5594. PMC 3916379. PMID 23973944. Coming of Phage: Celebrating the ...
Bacterial virulence factors, such as glycocalyx and various adhesins, allow colonization, immune evasion, and establishment of ... Delaloye J, Calandra T (January 2014). "Invasive candidiasis as a cause of sepsis in the critically ill patient". Virulence. 5 ... Mayr FB, Yende S, Angus DC (January 2014). "Epidemiology of severe sepsis". Virulence. 5 (1): 4-11. doi:10.4161/viru.27372. PMC ... Cross AS (January 2014). "Anti-endotoxin vaccines: back to the future". Virulence. 5 (1): 219-225. doi:10.4161/viru.25965. PMC ...
The capsule is considered a virulence factor because it enhances the ability of bacteria to cause disease (e.g. prevents ... Virulence. 10 (1): 822-831. doi:10.1080/21505594.2018.1431087. PMC 6779390. PMID 29436899. Rudolph K (1996). "Chapter 3: ...
January 2013). "Virulence factors of the Mycobacterium tuberculosis complex". Virulence. 4 (1): 3-66. doi:10.4161/viru.22329. ... It has been estimated that a third of the world population has latent tuberculosis (TB). M. tuberculosis has many virulence ... and an outermost capsule of glucans and secreted proteins for virulence. It constantly remodels these layers to survive in ...
Cheung GY, Bae JS, Otto M (December 2021). "Pathogenicity and virulence of Staphylococcus aureus". Virulence. 12 (1): 547-569. ... In fact, studies involving mutation of genes coding for protein A resulted in a lowered virulence of S. aureus as measured by ... An example of this difference is seen in the species' virulence. Only a few strains of S. aureus are associated with infections ... This such regulator has been linked to the virulence level of the bacteria. Loss of function mutations within this gene have ...
The virulence of S. pseudintermedius is an area of on going research and has many unknowns. The virulence factors carried by S ... This virulence factor induces vomiting and has been associated with food poisoning in humans. Protein A, an immunoglobulin ... Numerous virulence factors such as enzymes, toxins, and binding proteins have been associated with S. pseudintermedius strains ... Virulence. 4 (3): 255-9. doi:10.4161/viru.23526. PMC 3711984. PMID 23328490. Becker K, von Eiff C (2011-01-01). "Staphylococcus ...
It is also known that Salmonella plasmid virulence gene spvB enhances bacterial virulence by inhibiting autophagy. Infection ... and they form virulence factors and as such regulate the switch from their normal growth in the intestine into virulence. The ... "Salmonella plasmid virulence gene spvB enhances bacterial virulence by inhibiting autophagy in a zebrafish infection model". ... Fàbrega A, Vila J (April 2013). "Salmonella enterica serovar Typhimurium skills to succeed in the host: virulence and ...
Virulence. 8 (7): 1189-1202. doi:10.1080/21505594.2017.1279374. PMC 5711352. PMID 28060574. Jamet, Anne; Jousset, Agnès B; ...
Virulence. 6 (5): 476-86. doi:10.1080/21505594.2015.1020273. PMC 4601256. PMID 25751127. Sugita, T; Nishikawa, A; Shinoda, T ( ...
Casadevall, A (2012). "Amoeba provide insight into the origin of virulence in pathogenic fungi". Recent Advances on Model Hosts ... Liu TB (2012). "Molecular mechanisms of cryptococcal meningitis". Virulence. 3 (2): 173-81. doi:10.4161/viru.18685. PMC 3396696 ... "accidental virulence". In human infection, C. neoformans is spread by inhalation of aerosolized basidiospores, and can ... and this may contribute to its virulence. Infection starts in lungs, disseminates via blood to meninges and then to other parts ...
Virulence. 6 (2): 121-126. doi:10.1080/21505594.2015.1009732. PMC 4601319. PMID 25830548. Ibrahim, A. S.; Spellberg, B.; ...
Natural products may be screened for the ability to suppress bacterial virulence factors too. Virulence factors are molecules, ... Bacteriophages may harbour virulence factors or toxic genes in their genomes and, prior to use, it may be prudent to identify ... Kim HR, Shin DS, Jang HI, Eom YB (August 2020). "Anti-biofilm and anti-virulence effects of zerumbone against Acinetobacter ... Mok N, Chan SY, Liu SY, Chua SL (July 2020). "Vanillin inhibits PqsR-mediated virulence in Pseudomonas aeruginosa". Food & ...
Steverding, Dietmar (2020). "The spreading of parasites by human migratory activities". Virulence. 11 (1): 1177-1191. doi: ...
Another study by the same team of researchers revealed, for the first time, the role of YjbH in virulence and oxidative stress ... Silkworms have also been used for the identification of novel virulence factors of pathogenic microorganisms. A first large- ... Paudel, A.; Panthee, S.; Hamamoto, H.; Grunert, T.; Sekimizu, K. (2021). "YjbH regulates virulence genes expression and ... mutant library of Staphylococcus aureus USA300 strain was performed which identified 8 new genes with roles in full virulence ...
"Virulence profile". Virulence. 5: 321-5. doi:10.4161/viru.27047. PMC 3956508. PMID 24504093. (Articles with short description, ...
Chakravortty D (25 January 2018). "Virulence profile". Virulence. 5 (2): 321-5. doi:10.4161/viru.27047. PMC 3956508. PMID ... Chakravortty D (2014). "Smart Evasion Strategies by Salmonella". Virulence. 5: 321-5. doi:10.4161/viru.27047. PMC 3956508. PMID ... Virulence. 2020 Dec 26. doi: 10.1080/21505594.2020.1869441. Online ahead of print. Marathe SA, Chakravortty D, The Nobel Prize ... Role of Type III secretion system in virulence of different human and animal pathogenic bacteria. Phys Life Rev. 2021 May 26: ...
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World Health Organization. Regional Office for Africa, Health Emergencies Programme (‎World Health Organization.Regional Office for Africa, 2017-10)‎ ...
... widely employed as a model to investigate virulence mechanisms. Comparative high-throughput studies have earlier correlated its ... H37Ra is a virulence attenuated strain of ,i,Mycobacterium tuberculosis,/i, ... H37Ra is a virulence attenuated strain of Mycobacterium tuberculosis widely employed as a model to investigate virulence ... Integrated Multi-Omic Analysis of Mycobacterium tuberculosis H37Ra Redefines Virulence Attributes Front Microbiol. 2018 Jun 19; ...
... learning shows that specificity of tissue tropism and transmission biology can act as predictive risk factors for the virulence ...
Polymerase may be key to flus virulence. Model points to importance of polymerase activity in species jump. Cathy Holding( ...
US-2006134135-A1 chemical patent summary.
Virus evolution and virulence. Image Caption. There is an evolutionary trade off between virus virulence and virus transmission ... Home → Teach Evolution → Lessons and Teaching Tools → Image Library → Virus evolution and virulence ...
All the latest science news about virulence factors from ...
Learn about Streptococcus, the Streptococcus pyogenes bacterium, the diseases it causes, and its virulence factors. ... Streptococcus pyogenes virulence factors. When a S. pyogenes infection occurs, the bacteria are able to rapidly grow and avoid ... What is Streptococcus? Streptococcus pyogenes, Diseases it Causes, and its Virulence Factors. 2009-06-25. ...
Personer med emneord «Virulence» Navn. Telefon. E-post. Emneord. Simm, Roger Head of Department +47 22840337 [email protected] ... Biofilm, Antimicrobial resistance, Host-microbe interactions, Microbe-microbe interactions, Virulence, Molecular microbiology, ...
We showed that SvfA and SvfB are required for full virulence of D. dadantii and showed that svf genes are present in a variable ... Identification of new Dickeya dadantii virulence factors secreted by the type 2 secretion system. View ORCID ProfileGuy ... We showed that SvfA and SvfB are required for full virulence of D. dadantii and showed that svf genes are present in a variable ... We showed that two of them, SvfA and SvfB, are necessary for the full virulence of the bacteria. These findings show that ...
One large piece of evidence came when the long-sought co-factor for the primary virulence regulator, PrfA, was discovered to be ... Here we report that robust virulence gene expression can be recapitulated by growing bacteria in a synthetic medium (iLSM) ... Second, glutathione also functions as a post-translational regulator of the pore-forming virulence factor, Listeriolysin O (LLO ... monocytogenes interpret a combination of metabolic and redox cues as a signal to initiate robust virulence gene expression in ...
Genomic insights into multidrug-resistance, mating and virulence in Candida auris and related emerging species.. ... genomes of these emerging species to those of other Candida species identifies genes linked to drug resistance and virulence, ...
Pneumonia-Specific Escherichia coli with Distinct Phylogenetic and Virulence Profiles, France, 2012-2014 Béatrice La Combe, ... Pneumonia-Specific Escherichia coli with Distinct Phylogenetic and Virulence Profiles, France, 2012-2014. ...
food; virulence; internalin A; premature stop codon Description. The present study was designed to assess heterogeneity of ... The virulence characteristics, presence of Listeria pathogenicity island 1 (LIPI-1) as well as inlA, inlB, inlC and inlJ genes ... Genotyping and virulence factors of Listeria monocytogenes in terms of food safety. ... Genotyping and virulence factors of Listeria monocytogenes in terms of food safety ...
In Vibrio cholerae, the causative agent of the diarrheal disease cholera, quorum sensing is connected to virulence gene ... Three autoinducer molecules act in concert to control virulence gene expression in Vibrio cholerae. In: Nucleic Acids Research ... a key transcriptional activator of biofilm formation and virulence genes. In this study, we demonstrate that the recently ... reduces AphA levels at the post-transcriptional level and consequently inhibits virulence gene expression. VqmR-mediated ...
Este é o primeiro estudo a fornecer informações sobre os genótipos das cepas do H. pylori no Nordeste Argentino. Apesar da alta prevalência da infecção pelo H. pylori , a maioria dos pacientes tinha genótipos menos virulentos na cavidade oral e tecido gástrico. A combinação cagA / babA2 não foi frequente nas amostras estudadas. Não houve correlação estatística entre os genes de virulência e doenças gastroduodenais ou orais. Embora em alguns pacientes o mesmo genótipo tenha sido encontrado tanto nas amostras orais quanto gástricas, não se pode garantir que correspondam à mesma variação, pois um sequenciamento de DNA não foi realizado.. DESCRITORES: ...
The gene expression analysis was carried out for 12 genes which are related to virulence and stress in E. coli SM10, namely: ... Flavonoid-derived anisotropic silver nanoparticles inhibit growth and change the expression of virulence genes in Escherichia ... Flavonoid-derived anisotropic silver nanoparticles inhibit growth and change the expression of virulence genes in Escherichia ... on microbial growth and expressions of virulence-related genes in Escherichia coli SM10. ...
Transition from the yeast form to the hyphal form is one of the key virulence factors in C. albicans contributing to macrophage ...
... but the future study of fungal virulence requires investigators to distinguish between molecules that directly interact with ... Sophisticated molecular biological research has revealed many virulence attributes in at least four pathogenic fungi, ... The first may be essential for virulence; the second are truly virulence factors. Indeed, Retallack et al. [4] have made use ... It is therefore possible to miss virulence factors when only one model for virulence is tested. In C. albicans, disruption of ...
Other virulence elements have been reported to lesser extent (Table 2); one of which is toxic shock syndrome toxin (TSST)-1, ... Emerging virulence elements. MRSA is a well-known common pathogen in healthcare facilities and the community, and about 44% of ... One important emerging virulence factor is Panton-Valentine leucocidin (PVL) as more severe clinical sequelae have been ... The arginine catabolic mobile element and staphylococcal chromosomal cassette mec linkage: convergence of virulence and ...
... and datasets that will help in finding new regulators of virulence in the pathogen Salmonella. ... A global data-driven census of Salmonella small proteins and their potential functions in bacterial virulence ...
You searched for: Subject Switzerland Remove constraint Subject: Switzerland Subject virulence Remove constraint Subject: ... virulence Subject term Switzerland Remove constraint Subject term: Switzerland Subject term Shiga-like toxins Remove constraint ... virulence; virulent strains; Switzerland. Abstract:. ... Within 2 months, two water sources in a karst area in Switzerland were ...
... a determinant of high virulence to maize carrying Texas male sterile cytoplasm. The genetics of T-toxin production is complex ... Mutant screens indicate that all six genes are involved in T-toxin production and high virulence to maize. The nine known Tox1 ... Six New Genes Required for Production of T-Toxin, a Polyketide Determinant of High Virulence of Cochliobolus heterostrophus to ... a determinant of high virulence to maize carrying Texas male sterile cytoplasm. The genetics of T-toxin production is complex ...
Abstract Objective-To determine the comparative virulence of 5 isolates of bovine viral diarrhea virus (BVDV) type II by ... Comparative virulence of isolates of bovine viral diarrhea virus type II in experimentally inoculated six- to nine-month-old ... Objective-To determine the comparative virulence of 5 isolates of bovine viral diarrhea virus (BVDV) type II by inoculating 6- ... Objective-To determine the comparative virulence of 5 isolates of bovine viral diarrhea virus (BVDV) type II by inoculating 6- ...
These isolates yielded variable results regarding virulence genes (gtf, norB, and trx) and ability to adhere to fish gills. All ... Molecular identification, virulence property assessment, and antibiotic-sensitivity testing were performed on 10 randomly ... Molecular characterization, virulence profiling, antibiotic susceptibility, and scanning electron microscopy of Flavobacterium ...
The third project covers the exploration of the role of quorum-sensing in the virulence of P. aeruginosa LES; one of the ... The second project investigates the contribution of two pathogenicity islands, PAPI- 1 and PAPI-2 to the in vivo virulence of P ... The results showed that both pathogenicity islands contribute to virulence, but the presence of PAPI-2 is enough to maintain ... The project assessed whether over-expression of quorum-sensing products is a reliable indicator of increased virulence within a ...
... ... Moreover, PTS was shown to phosphorylate PTS regulatory domains (PRD) of a global virulence regulator, Mga, resulting in ... our studies indicate that a functional PTS is important for utilizing PTS and non-PTS sugars and influences virulence during ...
To compare the virulence of strains within the Avium-Intracellulare complex, standard inocula containing known numbers of ... The preparation of standardised inocula and their use in virulence studies are described. ... Standardisation Of Inocula for Assessing the Virulence of Strains ofAvium-Intracellulare Mycobacteria in Chickens * P. R. J. ... To compare the virulence of strains within the Avium-Intracellulare complex, standard inocula containing known numbers of ...
  • We showed that SvfA and SvfB are required for full virulence of D. dadantii and showed that svf genes are present in a variable number of copies in other Pectobacteriaceae , up to three in D. fanghzongdai . (
  • Comparing the genomes of these emerging species to those of other Candida species identifies genes linked to drug resistance and virulence, including expanded families of transporters and lipases, as well as mutations and copy number variants in ERG11. (
  • The virulence characteristics, presence of Listeria pathogenicity island 1 (LIPI-1) as well as inlA, inlB, inlC and inlJ genes of tested strains of L. monocytogenes from foods and food processing plants were comparable with human strains independently of particular serotypes. (
  • Both autoinducers share one signal transduction pathway to control the production of AphA, a key transcriptional activator of biofilm formation and virulence genes. (
  • The purpose of this study was to determine the effects of modified quercetin pentaphosphate silver nanoparticles (QPP-AgNPs) and quercetin diphosphate derived silver nanoparticles (QDP-AgNPs) on microbial growth and expressions of virulence-related genes in Escherichia coli SM10. (
  • In the case of opportunistic fungal pathogens, an understanding of host immune dysfunction is as important as an appreciation of which fungal genes may encode definable attributes of virulence. (
  • Mutant screens indicate that all six genes are involved in T-toxin production and high virulence to maize. (
  • These isolates yielded variable results regarding virulence genes (gtf, norB, and trx) and ability to adhere to fish gills. (
  • IS1562 is located in the mga regulon between the genes coding for the M protein and the C5a peptidase, both important virulence factors. (
  • Therefore, the objective of this work was to detect several virulence factors genes (fimA, papC, papG III, cnf1, hlyA and aer) and to determine the conjugative capacity in a wide collection of extended-spectrum β-lactamases-producing E. coli isolated from different sources (human, food, farms, rivers, and wastewater treatment plants). (
  • Regarding virulence genes, fimA, papC, and aer were distributed throughout all the studied environments, papG III was mostly related to clinical strains and wastewater is a route of dissemination for cnf1 and hlyA. (
  • Virulence genes expressed in Salmonella are a primary contributing factor leading to the high morbidity and mortality of salmonellosis in humans. (
  • The virulence genes of Salmonella pathogenic islands (SPIs) and Salmonella virulence plasmids (Spv) in Salmonella -positive isolates were subsequently detected. (
  • To ensure their growth and survival in both circumstances, bacteria have evolved elaborate and effective mecha-nisms for regulation of virulence genes. (
  • Virulence genes are commonly organized as regulons, and many of these share the attributes of general stress response regulons, described above. (
  • A. baumannii strains with similar genetic cluster (ERIC-Type) had the same prevalence of antibiotic resistance, antibiotic resistance genes and virulence factors. (
  • These include 2 putative virulence factors belonging to ESAT-6 like family of proteins. (
  • Upon entry to the host cell cytosol, the facultative intracellular pathogen Listeria monocytogenes coordinates the expression of numerous essential virulence factors by allosteric binding of glutathione (GSH) to the Crp-Fnr family transcriptional regulator, PrfA. (
  • The present study was designed to assess heterogeneity of virulence factors among strains of Listeria monocytogenes isolated from the food chain and humans in the Czech Republic. (
  • 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. (
  • But the rapid progress made in identifying molecular virulence factors in several fungal pathogens has also raised some caveats and paradoxes that require resolution. (
  • Effect of asiatic and ursolic acids on growth and virulence factors of" by DOROTA WOJNICZ, DOROTA TICHACZEK-GOSKA et al. (
  • Our results clearly show the influence of AA and UA on virulence factors of UPEC strains. (
  • This subdictionary is one of several MiniCOPE Dictionaries within COPE and now merges the contents of the previous Virulence Factors Dictionary and the contents of the Dictionary of Modulins . (
  • Although fbp1 mutants showed normal growth and produced normal major virulence factors, such as melanin and capsule, Fbp1 was found to be essential for fungal virulence, as fbp1 mutants were avirulent in a murine systemic-infection model. (
  • Genomic epidemiology, antimicrobial resistance and virulence factors of Enterobacter cloacae complex causing potential community-onset bloodstream infections in a tertiary care hospital of Nepal. (
  • Virulence factors encoding siderophores (24%), T6SSD (25%) and fimbriae (54%) were detected. (
  • In this study, we elucidated the MDR profiles, antibiotic resistance factors, the virulence gene complement, and hypermucoviscous phenotypes and genotypes of a set of 200 clinical K. pneumoniae isolates from two major tertiary care hospitals located in Islamabad and Rawalpindi, Pakistan. (
  • When E. coli and S. enterica envade the host, they use different virulence factors to cause infection. (
  • It is necessary to investigate the virulence-associated factors and the ability of horizontal gene transfer among bacteria for a better understanding of the pathogenicity and the mechanisms of dissemination of resistant bacteria. (
  • The pathogenicity of Salmonella is mainly determined by the specific virulence factors that it carries. (
  • These factors also confer greater virulence and play a role in infection of a host and transmission of disease, and most Salmonella enterica can cause cross-infections between humans and animals. (
  • Thermal control of virulence factors in bacteria: a hot topic. (
  • Pathogenic bacteria sense environmental cues, including the local temperature, to control the production of key virulence factors. (
  • Thermal regulation can be achieved at the level of DNA, RNA or protein and although many virulence factors are subject to thermal regulation, the exact mechanisms of control are yet to be elucidated in many instances. (
  • Understanding how virulence factors are regulated by temperature presents a significant challenge, as gene expression and protein production are often influenced by complex regulatory networks involving multiple transcription factors in bacteria. (
  • FimH (81.81%), afa/draBC (63.63%), csgA (63.63%), cnf1 (59.09%), cnf2 (54.54%) and iutA (50.00%) were the most commonly detected virulence factors. (
  • Fungal hemolysins are potential virulence factors. (
  • 5 Furthermore, there are other factors at play, such as virulence and interpretation of functional pathways for expounding multifaceted illnesses. (
  • In the case of humans, the host species has also shaped pathogen dynamics and virulence viaa multitude of factors from changes in social organization, group size, and exploitation of varied habitats and their animals and plant resources to agriculture, technology, rapid long-distance travel, medicine and global economic integration - which all continue to shape epidemics and the humanhost populations. (
  • This might be related to the emergence of non-vaccine S. pneumoniae serotypes after PCV7 introduction although it is suggested that evolutionary factors may have modified the virulence and the interactions of pneumococci. (
  • Virulence factors of Candida albicans . (
  • In this study we demonstrated the efficacy of the Arabidopsis seedling assay to study 1) the virulence factors of P. syringae pv. (
  • One of the major class of virulence factors includes effector proteins that are delivered into the host through a type III protein secretion system (TTSS) to suppress plant immune responses, and also to facilitate disease development [ 4 ]. (
  • antibiotic resistance, virulence factors and emerging strains. (
  • Considering food safety, all tested food strains should still be considered as pathogenic to humans even though some of these showed reduced virulence on the basis of genotyping results. (
  • To compare the virulence of strains within the Avium-Intracellulare complex, standard inocula containing known numbers of viable units are therefore recommended. (
  • A total of 22 A. baumanni strains were isolated from 126 animal meat samples and were genotyped by ERIC-PCR method and by PCR detection of their virulence and antimicrobial resistance determinants. (
  • That, in spite of the fact that there are no structurally variable strains of MTB, therefore all have a similar virulence capacity. (
  • The isolates were classified as phylogroups B1 (35%), B2 (33%), A (16%) and D (16%), and 14% of the strains had the eae virulence gene. (
  • Objective -To determine the comparative virulence of 5 isolates of bovine viral diarrhea virus (BVDV) type II by inoculating 6- to 9-month-old beef calves with isolates originating from the tissues of cattle affected with naturally occurring, transient, acute, nonfatal infections or naturally occurring, peracute, fatal infections. (
  • Molecular identification, virulence property assessment, and antibiotic-sensitivity testing were performed on 10 randomly selected isolates. (
  • In this work, we attempted to decipher the interplay between resistance profiles, high-risk clones, and virulence, testing a large (n = 140) collection of well-characterized P. aeruginosa isolates from different sources (bloodstream infections, nosocomial outbreaks, cystic fibrosis, and the environment) in a Caenorhabditis elegans infection model. (
  • In an earlier study performing infection experiments with human primary macrophages and aerosol-infected mice, we identified clade-specific virulence patterns of clinical isolates of MTBC. (
  • A type 2 secretion system (T2SS) named Out is necessary for bacterial virulence. (
  • Genetic determinants of antibiotic resistance and virulence were detected by PCR. (
  • Consistent with previous data, we documented a clear inverse correlation between antimicrobial resistance and virulence in the C. elegans model. (
  • Genomic insights into multidrug-resistance, mating and virulence in Candida auris and related emerging species. (
  • We showed that two of them, SvfA and SvfB, are necessary for the full virulence of the bacteria. (
  • These findings show that identification of all the proteins secreted by the Dickeya Out system is necessary for a better knowledge of the virulence of these bacteria. (
  • Here we report that robust virulence gene expression can be recapitulated by growing bacteria in a synthetic medium (iLSM) containing GSH or other chemical reducing agents. (
  • Here we highlight some recent insights into thermal regulation of virulence in pathogenic bacteria. (
  • The Fungal Biology and Pathogenicity Unit at Institut Pasteur is interested in the regulation of the yeast-to-hypha transition in C. albicans because of its role in biofilm formation and, more generally, in virulence. (
  • Sophisticated molecular biological research has revealed many virulence attributes in at least four pathogenic fungi, but the future study of fungal virulence requires investigators to distinguish between molecules that directly interact with the host, molecules that regulate these, and molecules that are always required for fungal growth and survival, independent of the host. (
  • The diversity of pathogenic potency, cellular form and route of invasion between fungal species makes it impossible to draw general conclusions about their molecular virulence attributes. (
  • Perception of the high incidence of fungal diseases, particularly those that threaten life, has led to considerable investment in research into fungal virulence, often based on cutting-edge molecular biological approaches. (
  • Although extensive studies have been conducted on signal transduction pathways important for fungal sexual reproduction and virulence, how fungal virulence is regulated during infection is still not understood. (
  • Overall, our study revealed that the F-box protein Fbp1 is essential for fungal sporulation and virulence in C. neoformans, which likely represents a conserved novel virulence control mechanism that involves the SCF E3 ubiquitin ligase-mediated proteolysis pathway. (
  • Listeria monocytogenes is a Gram-positive intracellular pathogen that is readily amenable to genetic manipulation and for which there are excellent in vitro and in vivo virulence models. (
  • We show that the human pathogen Neisseria meningitidis, the leading cause of pyogenic meningitis, can modulate gene expression via uptake of host pro-inflammatory cytokines leading to increased virulence. (
  • the rapid shift of virulence in the pathogen population, genetic uniformitity of mega-cultivars, favorability of environmental conditions, and an overlapping/ continuous crop calendar. (
  • The students are technical and methodical competent to work in infection disease research based on their understanding of the complex host-pathogen interactions during the infectious process, they have the capacity to integrate the pathogen's virulence functions and the hosts defense strategies and the principles, how both evolved during co-evolution and how these interactions shape pathogenesis and disease outcome. (
  • Repositorio consejería de sanidad de madrid: Interplay among Resistance Profiles, High-Risk Clones, and Virulence in the Caenorhabditis elegans Pseudomonas aeruginosa Infection Model. (
  • Here we examine one example, the PhoP/PhoQ system, which is essential to the virulence of Salmonella (Fig 3 - 15). (
  • Escherichia coli : mechanisms of virulence / edited by Max Sussman. (
  • Phylogenetic affiliations of UPECs and virulence-associated gene carriage have been identified. (
  • The main themes covered within this thesis are pathogenicity island characterisation in vitro and in vivo as well as investigation of in vivo virulence of P. aeruginosa. (
  • The second project investigates the contribution of two pathogenicity islands, PAPI- 1 and PAPI-2 to the in vivo virulence of P. aeruginosa PA14. (
  • The polyribosylribitol phosphate (PRP) capsule of Hib is a major virulence factor for the organism. (
  • Structurally, IncF plasmids consist of a conserved region common to all IncF plasmids which encodes conjugal transfer proteins, replication proteins and plasmid stability proteins and a 'genetic load region' or a variable region that encodes various virulence and fitness traits. (
  • The plasmid is 114,231 bp in size, belongs to the incompatibility group FIB/IIA (IncFIB/IIA), and contains a genetic load region that encodes several virulence and fitness traits such as enterotoxicity, iron acquisition and copper tolerance. (
  • However, the virulence function of a large number of potential virulence effectors encoded by the Pst DC3000 genome and their mode of action is still unknown. (
  • However, a recent sequencing study of H37Ra, has disproved several genomic differences earlier reported to be associated with virulence. (
  • A recent study that analyzed over 40 completed genomic sequences of IncF plasmids of E. coli revealed that these plasmids have evolved as virulence plasmids by acquiring novel virulence traits to their 'genetic load region' through IS-mediated site specific recombination [ 10 ]. (
  • Also, comparative genomic analysis of virulence plasmids in each pathovar of E. coli has shown that these genetic load regions encode virulence traits that are essential for and specific to their respective pathotype [ 10 ]. (
  • The fungi that cause invasive disease differ considerably in their inherent pathogenicity, even though few, if any, approach the level of virulence of the best known bacterial and viral pathogens. (
  • Use of C. elegans model to detect virulence attributes of B. pseudomallei is recommended as an alternative to tissue culture methods as this can be carried out in laboratories where a tissue culture set up is not available. (
  • The highest virulence of ST235 could be attributed to its exoU+ type III secretion system (TTSS) genotype, which was found to be linked with higher virulence in our C. elegans model. (
  • Other markers, such as motility or pigment production, were not essential for virulence in the C. elegans model but seemed to be related with the higher values of the statistical normalized data. (
  • In contrast to ST235, the ST175 high-risk clone, which is widespread in Spain and France, seems to be associated with a particularly low virulence in the C. elegans model. (
  • The fungus Cryptococcus neoformans straddles the boundary between 'true' and 'opportunistic' virulence, since it is known as a cause of community-acquired infection, even though most instances of cryptococcosis arise in an immunologically compromised host. (
  • Three pathogenicity island deletant isogenic mutants were tested for virulence in a murine acute respiratory model of infection developed for this project. (
  • The project assessed whether over-expression of quorum-sensing products is a reliable indicator of increased virulence within a murine acute respiratory model of infection. (
  • Overall, our studies indicate that a functional PTS is important for utilizing PTS and non-PTS sugars and influences virulence during GAS infection. (
  • However, mutants lacking the Us9 dileucine motif required for efficient endocytosis from the plasma membrane have wild type spread and virulence in the rat eye infection model. (
  • We identified four new Out-secreted proteins: the expansin YoaJ, the putative virulence factor VirK and two proteins of the DUF 4879 family, SvfA and SvfB. (
  • The nucleotide sequence of pRS218 showed a 41- 46% similarity to other neonatal meningitis-causing E. coli (NMEC) plasmids and remarkable nucleotide sequence similarity (up to 100%) to large virulence plasmids of E. coli associated with acute cystitis. (
  • However, a simple correlation between the virulence of the MTBC strain used and the inflammatory potential of such an isolate was not observed. (
  • These data suggest that cytosolic L. monocytogenes interpret a combination of metabolic and redox cues as a signal to initiate robust virulence gene expression in vivo. (
  • In Vibrio cholerae, the causative agent of the diarrheal disease cholera, quorum sensing is connected to virulence gene expression via the two autoinducer molecules, AI-2 and CAI-1. (
  • DPO, functioning through the transcription factor VqmA and the VqmR small RNA, reduces AphA levels at the post-transcriptional level and consequently inhibits virulence gene expression. (
  • H37Ra is a virulence attenuated strain of Mycobacterium tuberculosis widely employed as a model to investigate virulence mechanisms. (
  • This assay could also provide an excellent system for investigating the virulence mechanisms of P. syringae . (
  • Spike protein fusion peptide and feline coronavirus virulence. (
  • Vaccinia virus protein C6 is a virulence factor. (
  • But if scientists can figure out how to inhibit the protein in the human body, we could effectively eliminate the virulence of Brucella regardless of whether or not a particular strain is drug resistant. (
  • They do not appear to realise that better sanitation did reduce the spread of polio but increased its virulence through less exposure to the organism (kind of an ironic twist). (
  • IMSEAR at SEARO: Detection of virulence attributes of Burkholderia pseudomallei. (
  • Balaji V, Jesudason MV, Sridharan G, Subramanian K. Detection of virulence attributes of Burkholderia pseudomallei. (
  • One large piece of evidence came when the long-sought co-factor for the primary virulence regulator, PrfA, was discovered to be the antioxidant tripeptide, glutathione. (
  • Second, glutathione also functions as a post-translational regulator of the pore-forming virulence factor, Listeriolysin O (LLO), by reversibly binding via an S-glutathionylation reaction and preventing membrane association of the LLO monomers. (
  • Moreover, PTS was shown to phosphorylate PTS regulatory domains (PRD) of a global virulence regulator, Mga, resulting in alteration of its regulon in both M1T1 and M4 background, suggesting the ability of GAS to alter expression of Mga regulon in response to carbohydrate availability. (
  • Whole-genome sequencing can also predict phenotypic characteristics, such as virulence, serotype, and antimicrobial resistance. (
  • There's also genetic variation within dengue virus types, with some variants showing higher levels of virulence. (
  • Pst DC3000 also produces non-proteinaceous virulence effectors, including coronatine (COR), which are crucial for pathogenesis. (
  • Moreover, the previously described G154R AmpR mutation, prevalent in ST175, was found to contribute to the reduced virulence, although it was not the only factor involved. (
  • Following the Yr9 virulence epidemics , susceptible cultivars were extensively replaced with CIMMYT-derived germplasm such as Kauz, Atilla, Opata, Nacozari, Bucbuc and Crow. (
  • After 100 ic passages in mice, the prototype lost most ip virulence (1). (