Bacterial traits that contribute to disease are termed virulence factors and there is much interest in therapeutic approaches that disrupt such traits. What remains less clear is whether a virulence factor identified as such in a particular context is also important in infections involving different host and pathogen types. Here, we address this question using a meta-analytic approach. We statistically analyzed the infection outcomes of 76 experiments associated with one well-studied virulence factor - pyoverdine, an iron-scavenging compound secreted by the opportunistic pathogen Pseudomonas aeruginosa. We found that this factor is consistently involved with virulence across different infection contexts. However, the magnitude of the effect of pyoverdine on virulence varied considerably. Moreover, its effect on virulence was relatively minor in many cases, suggesting that pyoverdine is not indispensable in infections. Our works supports theoretical models from ecology predicting that disease severity
Streptococcus pneumoniae is an important human pathogen in all age groups worldwide that causes a variety of diseases, ranging from life threatening septicaemia and meningitis to less severe sinusitis and otitis media. The factors that determine the virulence of S. pneumoniae are very complex but a key aspect of the organisms disease causing potential is the ability of the bacteria to regulate virulence factor expression and activity. In this study two main approaches were taken to investigate virulence gene expression in S. pneumoniae. Firstly, the feasibility of Recombinase based In vivo Expression Technology, RIVET, for use in S. pneumoniae to study gene expression in vitro, and then in vivo was assessed. However, the system was found to be unsuitable for use in this study. Secondly, the requirement for and the role of virulence gene regulators identified by Signature Tagged Mutagenesis were investigated. The requirement for different virulence gene regulators varied according to the murine ...
© 2018 Macmillan Publishers Ltd., part of Springer Nature. Plasmids have a major role in the development of disease caused by enteric bacterial pathogens. Virulence plasmids are usually large (|40 kb) low copy elements and encode genes that promote host-pathogen interactions. Although virulence plasmids provide advantages to bacteria in specific conditions, they often impose fitness costs on their host. In this Review, we discuss virulence plasmids in Enterobacteriaceae that are important causes of diarrhoea in humans, Shigella spp., Salmonella spp., Yersinia spp and pathovars of Escherichia coli. We contrast these plasmids with those that are routinely used in the laboratory and outline the mechanisms by which virulence plasmids are maintained in bacterial populations. We highlight examples of virulence plasmids that encode multiple mechanisms for their maintenance (for example, toxin-antitoxin and partitioning systems) and speculate on how these might contribute to their propagation and success.
Bacteria can monitor their population density through the perception of molecules secreted by other local bacteria. This phenomenon leads to changes in bacterial behavior and changes in gene expression, and is termed quorum sensing. Quorum sensing in Vibrio cholerae, a major pathogenic bacterium in humans, is known to exist, but the gene targets of the sensing pathway are unknown. Zhu et al. found that a two-component signal module that includes the intracellular response regulator LuxO regulates virulence genes in V. cholerae. Vibrio mutants that lacked functional LuxO produced greatly decreased amounts of virulence-associated gene products, suggesting that LuxO was important for the expression of the virulence genes. The expression of HapR, which negatively regulated the expression of virulence genes, was decreased in a LuxO-dependent manner, suggesting one mechanism by which LuxO may increase virulence gene expression indirectly. HapR was expressed in luxO mutants, but not in wild-type ...
TY - JOUR. T1 - Revealing mechanisms underlying variation in malaria virulence. T2 - Effective propagation and host control of uninfected red blood cell supply. AU - Metcalf, C. J.E.. AU - Long, G. H.. AU - Mideo, N.. AU - Forester, J. D.. AU - Bjørnstad, O. N.. AU - Graham, A. L.. PY - 2012/11/7. Y1 - 2012/11/7. N2 - Malaria parasite clones with the highest transmission rates to mosquitoes also tend to induce the most severe fitness consequences (or virulence) in mammals. This is in accord with expectations from the virulence-transmission trade-off hypothesis. However, the mechanisms underlying how different clones cause virulence are not well understood. Here, using data from eight murine malaria clones, we apply recently developed statistical methods to infer differences in clone characteristics, including induction of differing host-mediated changes in red blood cell (RBC) supply. Our results indicate that the within-host mechanisms underlying similar levels of virulence are variable and ...
Pathogenic Yersinia cause a manifold of diseases in humans ranging from mild gastroenteritis (Y. pseudotuberculosis and Y. enterocolitica) to pneumonic and bubonic plague (Y. pestis), while all three have a common virulence strategy that relies on a well-studied type III secretion system and its effector proteins to colonize the host and evade immune responses. However, the role of other protein secretion and/or translocation systems in virulence of Yersinia species is not well known. In this thesis, we sought to investigate the contribution of twin-arginine translocation (Tat) pathway and its secreted substrates to the physiology and virulence of Y. pseudotuberculosis. Tat pathway uniquely exports folded proteins including virulence factors across the cytoplasmic membranes of bacteria. The proteins exported by Tat pathway contain a highly conserved twin-arginine motif in the N-terminal signal peptide. We found that the loss of Tat pathway causes a drastic change of the transcriptome of Y. ...
The harm that pathogens cause to hosts during infection, termed virulence, varies across species from negligible to a high likelihood of rapid death. Classic theory for the evolution of virulence is based on a trade-off between pathogen growth, transmission and host survival, which predicts that higher within-host growth causes increased transmission and higher virulence. However, using data from 61 human pathogens, we found the opposite correlation to the expected positive correlation between pathogen growth rate and virulence. We found that (i) slower growing pathogens are significantly more virulent than faster growing pathogens, (ii) inhaled pathogens and pathogens that infect via skin wounds are significantly more virulent than pathogens that are ingested, but (iii) there is no correlation between symptoms of infection that aid transmission (such as diarrhoea and coughing) and virulence. Overall, our results emphasize how virulence can be influenced by mechanistic life-history details, ...
The relative amount of transmission in I2 (ϕ) also has a large effect on ESS virulence (figure 1b). As the amount of transmission in I2 increases, the ESS virulence decreases, and the rate of decrease depends on the level of mortality that occurs in the I1 class. As the level of transmission in I2 and the disease mortality rate in the I1 class (ρ) approach zero, the ESS virulence goes to infinity (figure 1b). These results can be understood by realizing that for any fixed level of virulence (α), decreases in the transmission parameter ϕ reduce the fitness benefit of reaching the second class (I2), while increases in ρ both decrease the probability of reaching the second class and decreases the infectious period in the first class. Therefore, as both parameters reach zero, there is no benefit in reaching the second class and no cost to virulence in the first class. Thus, ESS virulence is very high and virulence will have a greater tendency to increase after introduction.. The effect of the ...
Looking for Virulence? Find out information about Virulence. The ability of a microorganism to cause disease. Virulence and pathogenicity are often used interchangeably, but virulence may also be used to indicate the... Explanation of Virulence
Classical microparasite evolution theory predicts a trade-off between virulence and transmission [1-3]. This trade-off balances virulence and within-host reproduction so that transmission is maximized over the lifetime of infection. Microparasites expressing intermediate levels of virulence are favoured under those conditions, as seen in several empirical examples of viruses with high transmission success (e.g. infections of myxoma virus in rabbits, HIV in humans, and cauliflower mosaic virus in Brassica rapa) [4-6]. However, not all studies found evidence for evolution towards intermediate virulence, but instead suggested evolution towards high or low virulence [7, 8].. Host population density is a key factor in determining whether low or high virulence will be optimal [9-11]. This mechanism can be understood in the framework of a trade-off between a microparasites competitive ability and its persistence. When transmission rates are lower at low host densities, a strain that can maintain a ...
Bacterial pathogens deliver multiple effector proteins into host cells to facilitate bacterial growth. HopQ1 is an effector from Pseudomonas syringae pv. tomato DC3000 that is conserved across multiple bacterial pathogens which infect plants. HopQ1s central region possesses some homology to nucleoside hydrolases, but possesses an alternative aspartate motif not found in characterized enzymes. A structural model was generated for HopQ1 based on the E. coli RihB nucleoside hydrolase and the role of HopQ1s potential catalytic residues for promoting bacterial virulence and recognition in Nicotiana tabacum was investigated. Transgenic Arabidopsis plants expressing HopQ1 exhibit enhanced disease susceptibility to DC3000. HopQ1 can also promote bacterial virulence on tomato when naturally delivered from DC3000. HopQ1s nucleoside hydrolase-like domain alone is sufficient to promote bacterial virulence, and putative catalytic residues are required for virulence promotion during bacterial infection of tomato
Vaccines rarely provide full protection from disease. Nevertheless, partially effective (imperfect) vaccines may be used to protect both individuals and whole populations.We studied the potential impact of different types of imperfect vaccines on the evolution of pathogen virulence (induced host mortality) and the consequences for public health. Here we show that vaccines designed to reduce pathogen growth rate and/or toxicity diminish selection against virulent pathogens. The subsequent evolution leads to higher levels of intrinsic virulence and hence to more severe disease in unvaccinated individuals. This evolution can erode any population-wide benefits such that overall mortality rates are unaffected, or even increase, with the level of vaccination coverage. In contrast, infection-blocking vaccines induce no such effects, and can even select for lower virulence. These findings have policy implications for the development and use of vaccines that are not expected to provide full immunity, ...
Author Summary The AIDS epidemic claims more lives per year than any other infectious disease, even though its cause, the Human Immunodeficiency Virus (HIV), is the youngest of all major human pathogens. The recent origin and great evolutionary potential of the virus raise the possibility that the virus might still be adapting to humans. Of primary interest is whether the virulence of the virus, i.e. its ability to cause disease, has been changing over time. Unfortunately, previous results have yielded conflicting results. We investigated time trends of virulence in the Italian HIV epidemic and found increasing virulence. The use of an established methodology allowed, for the first time, direct comparison with results obtained in other epidemics. The comparisons revealed that genuine differences exist in the trends of HIV virulence between different epidemics. Thus, there is no single time trend of HIV virulence worldwide. Our results are consistent with the hypothesis of increasing HIV virulence;
Define virulence. virulence synonyms, virulence pronunciation, virulence translation, English dictionary definition of virulence. adj. 1. a. Characterized by, causing, or promoting the rapid onset of severe illness. Used of a disease or toxin. b. Capable of causing disease by...
High-virulence strain caused earlier and greater damage than low-virulence strain and also can attack lymphatic system and bone marrow.
a Pathotypes were attributed to E. coli samples based on their sets of virulence genes or markers, as follows: for EAEC, capU, shf, virK, and aggregative adherence fimbria-encoding genes; for ETEC, heat-stable and heat-labile toxin-encoding genes and F4 and F18 fimbria-encoding genes; for atypical EPEC, espA, espB, tir, eae and variants, and absence of bfpA; for UPEC, P pilus-encoding genes, hlyA, S fimbria-encoding genes, chuA, fepC, cnf1, irp1, irp2, fyuA, iroN, and usp; for MNEC, ibeA, neuA, and neuC; and for incomplete ExPEC, kpsM, iutA, iucD, traT, malX, irp1, irp2, fyuA, chuA, fepC, iss, and kfiB. Isolates which did not possess any virulence genes or had a few scattered virulence-related genes were considered nonpathogenic. ...
Staphylococcus aureus is a major human pathogen with well-characterized bacteriophage contributions to its virulence potential. Recently, we identified plasmidial and episomal prophages in S. aureus strains using an extra-chromosomal DNA (exDNA) isolation and sequencing approach, uncovering the plasmidial phage ϕBU01, which was found to encode important virulence determinants. Here, we expanded our extra-chromosomal sequencing of S. aureus, selecting 15 diverse clinical isolates with known chromosomal sequences for exDNA isolation and next-generation sequencing. We uncovered the presence of additional episomal prophages in 5 of 15 samples, but did not identify any plasmidial prophages. exDNA isolation was found to enrich for circular prophage elements, and qPCR characterization of the strains revealed that such prophage enrichment is detectable only in exDNA samples and would likely be missed in whole-genome DNA preparations (e.g., detection of episomal prophages did not correlate with higher ...
ABSTRACT: Candida albicans is a classical example of causative agent for opportunistic fungal infection. Normally, it colonizes skin, gastrointestinal tract, genital, and mucosal membranes, but in certain condition it may responsible for diseases. This phenomenon was mainly associated with immunological status of the host. However, there were fndings that showed the possibility of putative virulence factors work on the transition of commensally to pathogenic role of the yeast. In this review, some virulence factors were discussed. Indeed, there were factors that may be considered as putative virulence factors of C. albicans. ...
The evolutionary dynamics of pathogens are critically important for disease outcomes, prevalence and emergence. In this talk I will discuss some specific ecological conditions that promote the long-term maintenance of virulence polymorphisms in a pathogen population. Recent theory predicts that evolution towards increased virulence can be reversed if less virulent social cheats exploit virulent cooperator pathogens. However, there is little evidence that social exploitation operates within natural pathogen populations. I will demonstrate that for the bacterium Pseudomonas syringae, major virulence polymorphisms are maintained at unexpectedly high frequencies in the host Arabidopsis thaliana. Experiments reveal that the fitness costs of decreased virulence are eliminated in mixed infections, whereas less virulent strains have a fitness advantage in non-host environments. These results suggest that niche differentiation contributes to the maintenance of virulence polymorphisms, and that both ...
In a wild plant-pathogen system, host resistance and pathogen virulence varied markedly among local populations. Broadly virulent pathogens occurred more frequently in highly resistant host populations, whereas avirulent pathogens dominated susceptible populations. Experimental inoculations indicated a negative trade-off between spore production and virulence. The nonrandom spatial distribution of pathogens, maintained through time despite high pathogen mobility, implies that selection favors virulent strains ofMelampsora lini in resistant Linum marginalepopulations and avirulent strains in susceptible populations. These results are consistent with gene-for-gene models of host-pathogen coevolution that require trade-offs to prevent pathogen virulence increasing until host resistance becomes selectively neutral. ...
For the simultaneous and rapid identification and differentiation of diarrheagenic E. coli strains belonging to the seven major pathotypes (EPEC, ATEC, [LEE positive and LEE negative] STEC, ETEC, EIEC, and EAEC), we set up a single-step MPCR. The design and development of the MPCR were monitored with nine reference strains. All of the reference strains exhibited the expected gene pattern, as confirmed by DNA sequencing, and no cross-priming by the MPCR primer pairs was observed. Furthermore, all PCR amplicons showed comparable band intensities and are of sufficiently different sizes to be unequivocally resolved by standard agarose gel electrophoresis.. The specificity of the MPCR was validated with a subset of reference strains and further evaluated with 246 clinical E. coli isolates derived from patients from different geographic regions. Classification of all detected pathogens by the MPCR was confirmed by comparative PCR analysis performed independently and by a phenotypic analysis that ...
A team from the Institut National de la Recherche Scientifique (INRS) has made a scientific breakthrough regarding the virulence strategy employed by the Leishmania parasite to infect cells of the immune system. This microorganism is responsible for Leishmaniasis, a chronic parasitic disease that affects more than 12 million people worldwide.
I am an undergraduate student at McGill University, looking for data for a term paper. The hypothesis of the paper is that virulence and rate of infection would necessarily be highly correlated as virulence increases. The logic behind this is that if the pathogen were to kill off the host before transmission could take place, the species would quickly kill itself off in the process. As such, selection favours a higher rate of transmission in more virulent pathogens. I would like to limit my paper to bacteria which infect humans. If anyone can send me either data or references to this sort of information, it would be greatly appreciated. Please note that I would need both types of data for the information to be useful. Ideally I would like to measure virulence in time from infection to death of host and transmission in time from infection of first host to infection of second host. If this format isnt possible, please send the information anyway. Thank you very much, Jamie Bacher bnyb at ...
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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.
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Figure 2. As if microbes were puppeteers and we humans were the puppets, microbes can control what we eat by a number of marked mechanisms. Adapted from Alcock et al 2014.. People who have desires of chocolate have different microbial metabolites in urine from people indifferent to chocolate, despite having the same diet.. Dysphoria, id est, human discomfort until we eat food which improve microbial welfare, may be due to the expression of bacterial virulence genes and perception of pain by the host. This is because the production of toxins is often triggered by a low concentration of nutrients limiting growth. The detection of sugars and other nutrients regulates virulence and growth of various microbes. These directly injure the intestinal epithelium when nutrients are absent. According to this hypothesis, it has been shown that bacterial virulence proteins activate pain receptors. It has been shown that fasting in mice increases the perception of pain by a mechanism of vagal ...
There are several testing options now available, aligned with the Karmali approach, which include detection of both Shiga Toxin genes (stx1, stx2) and the eae virulence marker. An additional virulence marker for the Enteroaggregative family (aggC) has been included in a separate E. coli O104 assay in case the EFSA opinion is followed. Assurance GDS incorporates a proprietary PickPen® IMS sample preparation procedure, which captures and isolates STEC belonging to the target serogroups (O26, O45, O103, O111, O121, O145 and E. coli O157:H7), prior to detection of the gene targets. As a result, target gene detection is performed on a subset of organisms belonging only to the serogroups of concern, drastically reducing the amount of false positive results typically found with STEC testing.. ...
Virulence genes of pathogenic bacteria, which code for toxins, adhesins, invasins or other virulence factors, may be located on transmissible genetic elements such as transposons, plasmids or bacteriophages. In addition, such genes may be part of particular regions on the bacterial chromosomes, term …
Results from the CASCADE project strongly suggest that HIV has increased in virulence and transmissibility, at least in Europe, since the virus came to light at the end of the 1970s. This research was published in the Lancet HIV in November 2014. HIV is a virus with high genetic diversity. As the HIV virus reproduces, slight variations in the genetic structure of the virus begin to occur. Over time, this means that there will be several subtypes of HIV, and each subtype may be more or less able to cause illness. The term used to describe a virus ability to cause illness is virulence. If someone is infected with a more virulent form of HIV they will become ill more quickly. Additionally, more virulent forms of HIV may increase the risk of the virus being transmitted (passed on) to others. The CASCADE collaboration is a network of researchers from 14 countries, sharing data from 29 different groups of HIV-positive individuals. Through pooling data, the CASCADE researchers are able to answer ...
Pathogenic bacteria must contend with immune systems that actively restrict the availability of nutrients and cofactors, and create a hostile growth environment. To deal with these hostile environments, pathogenic bacteria have evolved or acquired virulence determinants that aid in the acquisition of nutrients. This connection between pathogenesis and nutrition may explain why regulators of metabolism in nonpathogenic bacteria are used by pathogenic bacteria to regulate both metabolism and virulence. Such coordinated regulation is presumably advantageous because it conserves carbon and energy by aligning synthesis of virulence determinants with the nutritional environment. In Gram-positive bacterial pathogens, at least three metabolite-responsive global regulators, CcpA, CodY, and Rex, have been shown to coordinate the expression of metabolism and virulence genes. In this chapter, we discuss how environmental challenges alter metabolism, the regulators that respond to this altered metabolism, and how
strains display variability in their capsular polysaccharide cell morphology karyotype and virulence but the BAPTA relationship between these variables is poorly understood. BAPTA xylose residue content linked at the 4 to 0 position. The relative virulence of the colony types was WR > PH > SM as measured by CFU in rat lungs after intratracheal […]. ...
Expression profile of virulence associated MAP genes under various stress conditions.Virulence associated MAP gene definitions were obtained by phylogenomics co
Our laboratory studies the roles of sensory transduction in bacterial-host interactions. Genes and operons that encode virulence factors are often subject to coordinate regulation in response to environmental signals, and bacterial virulence factors frequently target host cell signaling pathways. Specific areas of interest include: a) biochemical analysis of signal transduction pathways in pathogenic bacteria, b) genetic organization of bacterial virulence regulons, and c) in vivo and in vitro studies of mechanisms of pathogenesis. We are also investigating mechanisms involved in the induction of cytotoxic T cell responses by Listeria monocytogenes (LM). In the course of these studies, we have developed a new class of live Listeria-based vaccines with activity against heterologous pathogens and tumors. In a third project, we have discovered a new class of retroelements, called diversity generating retroelements, which are capable of generating vast amounts diversity in proteins involved in ...