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PubMed2006

Pathocycles: Ustilago maydis as a model to study the relationships between cell cycle and virulence in pathogenic fungi.

Activation of virulence in pathogenic fungi often involves differentiation processes that need the reset of the cell cycle and induction of a new morphogenetic program. Therefore, the fungal capability to modify its cell cycle constitutes an important determinant in carrying out a successful infection. The dimorphic fungus Ustilago maydis is the causative agent of corn smut disease and has lately become a highly attractive model in addressing fundamental questions about development in pathogenic fungi. The different morphological and genetic changes of U. maydis cells during the pathogenic process advocate an accurate control of the cell cycle in these transitions. This is why this model pathogen deserves attention as a powerful tool in analyzing the relationships between cell cycle, morphogenesis, and pathogenicity. The aim of this review is to summarize recent advances in the unveiling of cell cycle regulation in U. maydis. We also discuss the connection between cell cycle and virulence and how cell cycle control is an important downstream target in the fungus-plant interaction.

Cell Cycle↗
PubMed2002

Constitutive expression of hrap gene in transgenic tobacco plant enhances resistance against virulent bacterial pathogens by induction of a hypersensitive response.

Hypersensitive response-assisting protein (HRAP) has been previously reported as an amphipathic plant protein isolated from sweet pepper that intensifies the harpin(Pss)-mediated hypersensitive response (HR). The hrap gene has no appreciable similarity to any other known sequences, and its activity can be rapidly induced by incompatible pathogen infection. To assess the function of the hrap gene in plant disease resistance, the CaMV 35S promoter was used to express sweet pepper hrap in transgenic tobacco. Compared with wild-type tobacco, transgenic tobacco plants exhibit more sensitivity to harpin(Pss) and show resistance to virulent pathogens (Pseudomonas syringae pv. tabaci and Erwinia carotovora subsp. carotovora). This disease resistance of transgenic tobacco does not originate from a constitutive HR, because endogenous level of salicylic acid and hsr203J mRNA showed similarities in transgenic and wildtype tobacco under noninfected conditions. However, following a virulent pathogen infection in hrap transgenic tobacco, hsr203J was rapidly induced and a micro-HR necrosis was visualized by trypan blue staining in the infiltration area. Consequently, we suggest that the disease resistance of transgenic plants may result from the induction of a HR by a virulent pathogen infection.

Base Sequence↗
PubMed2005

Large-scale screen highlights the importance of capsule for virulence in the zoonotic pathogen Streptococcus iniae.

Zoonotic pathogens have the unique ability to cross the species barrier, causing disease in both humans and specific animal hosts. Streptococcus iniae is a zoonotic pathogen of both fish and humans, and the clinical presentations of S. iniae infections in fish and humans are very similar to those caused by various human-specific streptococcal pathogens. Virulence mechanisms required for infection by this pathogen of either host have yet to be determined. Using the previously reported zebrafish infectious disease model, we performed a large-scale screening to determine genes required for systemic infection. Screening 1,128 signature-tagged transposon mutants through the zebrafish model allowed identification of 41 potential mutants that were unable to survive within the host environment. Greater than 50% of the mutants that could be identified through homology searches were highly homologous to genes found in other human-specific streptococcal pathogens, while 32% were found to have no homology to any sequences found in the databases, suggesting as yet unknown gram-positive bacterial virulence factors. A large percentage of the insertions were found to be located in several putative capsule synthesis genes, an important virulence component for other systemic pathogens. Density gradient assays demonstrated that several of these putative capsule mutants have dissimilar buoyant densities, suggesting different levels of capsule synthesis. Putative capsule mutants were also less resistant to phagocytosis in whole-blood assays than wild-type S. iniae. Our initial large-scale characterization of S. iniae virulence highlights the importance of the capsule for successful infection.

Animals↗
PubMed2003

Expressed sequence tag analysis of the human pathogen Paracoccidioides brasiliensis yeast phase: identification of putative homologues of Candida albicans virulence and pathogenicity genes.

Paracoccidioides brasiliensis, a thermodimorphic fungus, is the causative agent of the prevalent systemic mycosis in Latin America, paracoccidioidomycosis. We present here a survey of expressed genes in the yeast pathogenic phase of P. brasiliensis. We obtained 13,490 expressed sequence tags from both 5' and 3' ends. Clustering analysis yielded the partial sequences of 4,692 expressed genes that were functionally classified by similarity to known genes. We have identified several Candida albicans virulence and pathogenicity homologues in P. brasiliensis. Furthermore, we have analyzed the expression of some of these genes during the dimorphic yeast-mycelium-yeast transition by real-time quantitative reverse transcription-PCR. Clustering analysis of the mycelium-yeast transition revealed three groups: (i) RBT, hydrophobin, and isocitrate lyase; (ii) malate dehydrogenase, contigs Pb1067 and Pb1145, GPI, and alternative oxidase; and (iii) ubiquitin, delta-9-desaturase, HSP70, HSP82, and HSP104. The first two groups displayed high mRNA expression in the mycelial phase, whereas the third group showed higher mRNA expression in the yeast phase. Our results suggest the possible conservation of pathogenicity and virulence mechanisms among fungi, expand considerably gene identification in P. brasiliensis, and provide a broader basis for further progress in understanding its biological peculiarities.

Base Sequence↗
PubMed1988

Pathogenicity and virulence: another view.

The concepts of pathogenicity and virulence have governed our perception of microbial harmfulness since the time of Pasteur and Koch. These concepts resulted in the recognition and identification of numerous etiological agents and provided natural and synthetic agents effective in therapy and prevention of diseases. However, Koch's postulates--the premier product of this view--place the onus of harmfulness solely on the microbial world. Our recent experiences with polymicrobic and nosocomial infections, legionellosis, and acquired immunodeficiency syndrome point to the host as the major determinant of disease. The principles of parasitism, enunciated by Theobold Smith, approximate more accurately the disturbances of the host-parasite equilibrium we designate as infection. Many complex attributes of microbial anatomy and physiology have been obscured by our dependency on the pure-culture technique. For example, bacterial attachment organelles and the production of exopolysaccharides enable microorganisms to interact with mammalian glycocalyces and specific receptors. In addition, selection, through the use of therapeutic agents, aids in the progression of environmental organisms to members of the intimate human biosphere, with the potential to complicate the recovery of patients. These factors emphasize further the pivotal significance of host reactions in infections. Parasitism, in its negative aspects, explains the emergence of "new" infections that involve harm to more than host organs and cells: we may encounter subtler infections that reveal parasitic and host cell nucleic acid interactions in a form of genomic parasitism.

Animals↗
PubMed2004

Pathogenicity and virulence.

Invertebrate pathologists have multiple definitions for the terms pathogenicity and virulence, and these definitions vary across disciplines that focus on host-pathogen interactions. We surveyed various literatures, including plant pathology, invertebrate pathology, evolutionary biology, and medicine, and found most define pathogenicity as the broader term, which incorporates virulence. Virulence is seen as the severity of disease manifestation that can only be measured in infected individuals. These definitions readily apply to both lethal and non-lethal diseases. Invertebrate pathologists commonly use dose-response bioassays to estimate LD(50) or LC(50) (dose or concentration needed to kill 50% of hosts exposed). These bioassays measure pathogenicity if the bioassay includes a transmission component, and measure virulence if the bioassay is measured in infected individuals only. Another common bioassay estimate is LT(50) (median time to death of infected hosts), which is a measure of virulence as long as survivors are not included in its calculation.

Animals↗
PubMed1986

Phospholipase activity and virulence of pathogenic leptospirae.

Results of investigation of phospholipase activity and virulence of pathogenic leptospirae on a solid nutrient medium using the method of agar layers with 1% of L-lecithin in the medium of the second layer are presented. It has been demonstrated that only one zone of translucent medium is formed around the colonies of pathological leptospirae, which is obviously due to the release of phospholipase A. The examined virulent strains of pathogenic leptospirae were found to exhibit greater phospholipase activity (width of the translucent zones being 5.0 +/- 0.34 mm) than the avirulent strains (width of the zones being 1.5 +/- 0.11 mm).

Agar↗
PubMed2000

Parallel evolution of virulence in pathogenic Escherichia coli.

The mechanisms underlying the evolution and emergence of new bacterial pathogens are not well understood. To elucidate the evolution of pathogenic Escherichia coli strains, here we sequenced seven housekeeping genes to build a phylogenetic tree and trace the history of the acquisition of virulence genes. Compatibility analysis indicates that more than 70% of the informative sites agree with a single phylogeny, suggesting that recombination has not completely obscured the remnants of ancestral chromosomes. On the basis of the rate of synonymous substitution for E. coli and Salmonella enterica (4.7 x 10(-9) per site per year), the radiation of clones began about 9 million years ago and the highly virulent pathogen responsible for epidemics of food poisoning, E. coli O157:H7, separated from a common ancestor of E. coli K-12 as long as 4.5 million years ago. Phylogenetic analysis reveals that old lineages of E. coli have acquired the same virulence factors in parallel, including a pathogenicity island involved in intestinal adhesion, a plasmid-borne haemolysin, and phage-encoded Shiga toxins. Such parallel evolution indicates that natural selection has favoured an ordered acquisition of genes and the progressive build-up of molecular mechanisms that increase virulence.

DNA, Bacterial↗
PubMed1994

Short-sighted evolution and the virulence of pathogenic microorganisms.

For some microorganisms, virulence may be an inadvertent consequence of mutation and selection in the parasite population, occurring within a host during the course of an infection. This type of virulence is short-sighted, in that it engenders no advantage to the pathogen beyond the afflicted host. Bacterial meningitis, poliomyelitis and AIDS are three candidates for this model of the evolution of virulence.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Staphylococcus aureus: a well-armed pathogen.

Staphylococcus aureus is a virulent pathogen that is currently the most common cause of infections in hospitalized patients. S. aureus infection can involve any organ system. The success of S. aureus as a pathogen and its ability to cause such a wide range of infections are the result of its extensive virulence factors. The increase in the resistance of this virulent pathogen to antibacterial agents, coupled with its increasing prevalence as a nosocomial pathogen, is of major concern. The core resistance phenotype that seems to be most associated with the persistence of S. aureus in the hospital is methicillin resistance. Methicillin resistance in nosocomial S. aureus isolates has been increasing dramatically in United States hospitals and is also associated with resistance to other useful antistaphylococcal compounds. Possible ways to decrease the incidence of nosocomial S. aureus infections include instituting more effective infection control, decreasing nasal colonization, developing vaccines, and developing new or improved antimicrobials.

Cross Infection↗
PubMed2004

Definitions of pathogenicity and virulence in invertebrate pathology.

Accurate definition and usage of terminology are critical to effective communication in science. In a recently published article, the clarity and consistency of the terms pathogenicity and virulence as used in invertebrate pathology were called into question, and a revision of these terms was proposed. Our objective was to examine definitions of pathogenicity and virulence and their use in invertebrate pathology, and respond to this article. Although usage of the terms pathogenicity and virulence varies, we found considerable consistency in the published definitions of these terms in the invertebrate pathology literature throughout the history of the discipline, as well as among related disciplines such as medicine and microbiology. We did not find the established definitions to be lacking in clarity or utility. Therefore, we recommend that the definition and use of these terms adhere to precedence. Specifically, pathogenicity is the quality or state of being pathogenic, the potential ability to produce disease, whereas virulence is the disease producing power of an organism, the degree of pathogenicity within a group or species. Pathogenicity is a qualitative term, an "all-or-none" concept, whereas virulence is a term that quantifies pathogenicity.

Animals↗
PubMed1996

Is the ability of urinary tract pathogens to accumulate glycine betaine a factor in the virulence of pathogenic strains?

The regulation of intracellular concentrations of organic solutes, including glycine betaine, is an important adaptive response to osmotic stress for Escherichia coli. The clinical significance of glycine betaine to uropathogens is not clear. Clinical isolates of E. coli, Klebsiella pneumoniae, Enterobacter species, Pseudomonas aeruginosa, Proteus mirabilis, Staphylococcus aureus, S. saprophyticus, and Enterococcus faecalis accumulated glycine betaine from hyperosmotic media. The addition of glycine betaine to hyperosmotic minimal medium accelerated the growth rates of all species tested except P. mirabilis. However, when clinical strains of E. coli were transferred from urine with low osmolality to hyperosmotic urine, there was no slowing of the growth rate. There was no difference in growth rates of E. coli isolates from acute pyelonephritis, cystitis, and asymptomatic bacteriuria nor from fecal isolates. The ability to accumulate osmolytes, although it may be a factor in the adaptation to hypertonic environments, was not related to virulence.

Adolescent↗
PubMed2002

Listeria monocytogenes virulence and pathogenicity, a food safety perspective.

Several virulence factors of Listeria monocytogenes have been identified and extensively characterized at the molecular and cell biologic levels, including the hemolysin (listeriolysin O), two distinct phospholipases, a protein (ActA), several internalins, and others. Their study has yielded an impressive amount of information on the mechanisms employed by this facultative intracellular pathogen to interact with mammalian host cells, escape the host cell's killing mechanisms, and spread from one infected cell to others. In addition, several molecular subtyping tools have been developed to facilitate the detection of different strain types and lineages of the pathogen, including those implicated in common-source outbreaks of the disease. Despite these spectacular gains in knowledge, the virulence of L. monocytogenes as a foodborne pathogen remains poorly understood. The available pathogenesis and subtyping data generally fail to provide adequate insight about the virulence of field isolates and the likelihood that a given strain will cause illness. Possible mechanisms for the apparent prevalence of three serotypes (1/2a, 1/2b, and 4b) in human foodborne illness remain unidentified. The propensity of certain strain lineages (epidemic clones) to be implicated in common-source outbreaks and the prevalence of serotype 4b among epidemic-associated stains also remain poorly understood. This review first discusses current progress in understanding the general features of virulence and pathogenesis of L. monocytogenes. Emphasis is then placed on areas of special relevance to the organism's involvement in human foodborne illness, including (i) the relative prevalence of different serotypes and serotype-specific features and genetic markers; (ii) the ability of the organism to respond to environmental stresses of relevance to the food industry (cold, salt, iron depletion, and acid); (iii) the specific features of the major known epidemic-associated lineages; and (iv) the possible reservoirs of the organism in animals and the environment and the pronounced impact of environmental contamination in the food processing facilities. Finally, a discussion is provided on the perceived areas of special need for future research of relevance to food safety, including (i) theoretical modeling studies of niche complexity and contamination in the food processing facilities; (ii) strain databases for comprehensive molecular typing; and (iii) contributions from genomic and proteomic tools, including DNA microarrays for genotyping and expression signatures. Virulence-related genomic and proteomic signatures are expected to emerge from analysis of the genomes at the global level, with the support of adequate epidemiologic data and access to relevant strains.

Consumer Product Safety↗
PubMed2002

Paradigm shifts in vaccine development: lessons learned about antigenicity, pathogenicity and virulence of Brucellae.

As part of a program to support the USDA Animal Plant Health Inspection Service Bovine Brucellosis Eradication Program, the Brucellosis Research Unit of the National Animal Disease Center (NADC) sought to develop a bovine brucellosis vaccine that would allow vaccinated animals to be distinguished from virulent field infected animals. In order to meet that goal, several avenues of research were undertaken to construct and test candidate vaccines, including Brucella abortus RB51. In early vaccine development studies, a subunit preparation obtained by extracting B. abortus with salts was studied as a candidate subunit vaccine. Later, molecular biological techniques were used both to clone genes encoding products found in the salt extract (BCSP31 and Cu-Zn SOD) and genes encoding proteins of B. abortus that were antigenic (HtrA) or possibly essential (two-component systems) for full virulence of B. abortus. In vitro systems using mammalian cells lines such as HeLa and macrophage-related were used along with the mouse model and host animal models. Results obtained at NADC and in other Brucellosis research laboratories, using survival in mammalian cell lines and the mouse model to access pathogenicity and virulence of genetically engineered strains, do not necessarily identify loci that are essential for full virulence or pathogenicity in the natural host, the bovine. Studies at NADC and other brucellosis laboratories showed that antigenicity was not a predictor of the effectiveness of a protein as a subunit vaccine.

Animals↗
PubMed2006

AtPTR3, a wound-induced peptide transporter needed for defence against virulent bacterial pathogens in Arabidopsis.

Mutation in the wound-induced peptide transporter gene AtPTR3 (At5g46050) of Arabidopsis thaliana has been shown to affect germination on media containing a high salt concentration. The heterologous expression in yeast was utilized to verify that the AtPTR3 protein transports di-and tripeptides. The T-DNA insert in the Atptr3-1 mutant in the Arabidopsis ecotype C24 revealed two T-DNA copies, the whole vector sequence, and the gus marker gene inserted in the second intron of the AtPTR3 gene. An almost identical insertion site was found in the Atptr3-2 mutant of the Col-0 ecotype. The AtPTR3 expression was shown to be regulated by several signalling compounds, most clearly by salicylic acid (SA), but also methyl jasmonate (MeJA) and abscisic acid. Real-time PCR experiments suggested that the wound-induction of the AtPTR3 gene was abolished in the SA and JA signalling mutants. The Atptr3 mutant plants had increased susceptibility to virulent pathogenic bacteria Erwinia carotovora subsp. carotovora and Pseudomonas syringae pv. tomato, and produced more reactive oxygen species when grown on media containing paraquat or rose bengal. Public microarray data suggest that the AtPTR3 expression was induced by Pseudomonas elicitors and by avirulent P. syringae pathovars and type III secretion mutants. This was verified experimentally for the hrpA mutant with real-time PCR. These results suggest that AtPTR3 is one of the defence-related genes whose expression is reduced by virulent bacterium by type III dependent fashion. Our results suggest that AtPTR3 protects the plant against biotic and abiotic stresses.

Arabidopsis↗
PubMed1994

Pathogenicity and virulence of coagulase negative staphylococci in relation to adherence, hydrophobicity, and toxin production in vitro.

AIMS: To study the pathogenicity and virulence characteristics of Staphylococcus epidermidis, Staphylococcus haemolyticus, and Staphylococcus sapro-phyticus. METHODS: BALB/c mice were challenged intraperitoneally with graded doses of three strains belonging to each species. LD50s were measured for each strain. Haemolysin (alpha- and delta-) and enzyme (DNAase, lipase, and esterase) production in vitro were measured qualitatively and quantitatively. Adhesion to plastic was measured and related to cell surface hydrophobicity among the strains. RESULTS: S saprophyticus proved the most virulent (LD50 = 2.7-2.9 x 10(7) cfu/g body weight) while S epidermidis was the least virulent (LD50 = 6-8 x 10(7) cfu/g body weight). An enlarged spleen was the most common macroscopic pathological feature. Kidney, liver, and more rarely peritoneal abscesses were also seen in the infected animals. No direct correlation was found between adherence in vitro, cell surface hydrophobicity, or toxin/enzyme biosynthesis and virulence in mice. CONCLUSION: The results show that coagulase negative staphylococci are pathogenic in BALB/c mice. It is clear that these bacteria can cause invasive disease. However, the in vitro characteristics of coagulase negative staphylococci are not related to the pathogenicity of the organisms in mice.

Animals↗