Understanding both the mechanistic basis of virulence and the evolutionary processes under which it can arise, is fundamental if we are to increase our knowledge of disease causing bacteria in an era of ever increasing antibiotic resistance. To date, there has been a substantial effort to understand virulence evolution both theoretically and experimentally. However, comparatively little experimental work has focussed on the evolution of virulence in opportunistic pathogens, and how virulence varies across multiple host organisms. In this thesis, the opportunist Pseudomonas aeruginosa was used to study virulence and its evolution in hosts. The virulence levels of different strains of P. aeruginosa, both laboratory and clinical, were tested in the nematode Caenorhabditis elegans. It was found that virulence of P. aeruginosa was lower in clinical strains isolated from chronic infections, and laboratory strains initially isolated from chronic infections, while a strain isolated from an acute ...
The pathogenesis of Bacillus anthracis depends on several virulence factors, including the anthrax toxin. Loss of the alternative sigma factor σI results in a coordinate decrease in expression of all three toxin subunits. Our observations suggest that loss of σI alters the activity of the master virulence regulator AtxA, but atxA transcription is unaffected by loss of σI. σI-containing RNA polymerase does not appear to directly transcribe either atxA or the toxin gene pagA. As in Bacillus subtilis, loss of σI in B. anthracis results in increased sensitivity to heat shock and transcription of sigI, encoding σI, is induced by elevated temperature. Encoded immediately downstream of and part of a bicistronic message with sigI is an anti-sigma factor, RsgI, which controls σI activity. Loss of RsgI has no direct effect on virulence gene expression. sigI appears to be expressed from both the σI and σA promoters, and transcription from the σA promoter is likely more significant to virulence regulation
Aim 1: Characterize the effect of spaceflight analogue culture on microbial pathogenesis related stress responses and in vitro host-pathogen interactions. Analysis will include microbial stress responses as well as colonization and viability following pathogen challenge of three-dimensional (3-D) tissue co-culture models containing immune cells.. Aim 2: Characterize the effect of spaceflight analogue culture on the virulence potential of pathogenic microorganisms. Changes in virulence will be assessed using a mouse model of infection. To reduce and refine the use of animals for virulence studies, the selection of microorganisms for Aim 2 will be based on a combination of microbial responses from Aim 1 and previously reported spaceflight and spaceflight analogue experimental data of similar microorganisms.. Aim 3: Profile the synergistic relationship between spaceflight analogue-altered bacterial virulence characteristics and spaceflight analogue-altered immune cell function. Alterations in ...
Virulence gene expression in V. cholerae is regulated by a complex cascade of transcriptional activators. Here we show that in addition to the known regulatory factors, the cyclic nucleotide second messenger c-diGMP negatively regulates transcription of the toxT and ctxA genes under conditions that stimulate virulence factor expression. Specifically, the putative phosphodiesterase activity of the VieA EAL domain is required for maximal expression of ctxA and toxT during growth under a minimal medium plus amino acids condition. The ability of VieA to control the c-diGMP concentration is also critical during infection, since the vieA(E170A) EAL domain point mutant was attenuated 10-fold in the infant mouse model of cholera. This represents the first demonstration with any organism that the c-diGMP second messenger regulates expression of virulence factors.. Our results implicate c-diGMP as a signal that represses expression of virulence factors and suggest possible mechanisms of transcriptional ...
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Seagrass wasting disease, caused by the opportunistic marine pathogen Labyrinthula zosterae, has the potential to devastate important eelgrass habitats worldwide, yet little is known about the host-pathogen interaction and how the disease will be impacted by climate change. L. zosterae is part of a diverse taxon of opportunistic invertebrate and plant pathogens, which directly threaten fisheries and critical fisheries habitat. An area of particular concern is the role of virulence, the degree of host damage caused by a pathogen, often the product of its growth rate. Recent data suggests that temperature increases the virulence of Labyrinthulas, providing a mechanism for climate sensitivity. In this study we investigate the effect of L. zosterae strain, pathogen dosage, and temperature on the pathogen virulence. We tested L. zosterae virulence in Zostera marina by inoculating plant tissue with strains collected from a range of eelgrass populations. The 11 strains tested displayed qualitatively different
Outer membrane vesicles (OMVs) are nanoscale proteoliposomes secreted from the cell envelope of all Gram-negative bacteria. Originally considered as an artifact of the cell wall, OMVs are now recognized as a general secretion system, which serves to improve the fitness of bacteria and facilitate bacterial interactions in polymicrobial communities as well as interactions between the microbe and the host. In general, OMVs are released in increased amounts from pathogenic bacteria and have been found to harbor much of the contents of the parental bacterium. They mainly encompass components of the outer membrane and the periplasm including various virulence factors such as toxins, adhesins, and immunomodulatory molecules. Numerous studies have clearly shown that the delivery of toxins and other virulence factors via OMVs essentially influences their interactions with host cells. Here, we review the OMV-mediated intracellular deployment of toxins and other virulence factors with a special focus on intestinal
Aspergillus fumigatus is considered a common causative agent of human fungal infections. A restricted number of virulence factors have been described, and none of them lead to a differentiation in the virulence level among different strains. Variations in the virulence phenotype depending on the isolate origin, measured as survival percentage in animal infection models, have been previously reported. In this study, we analyzed the whole-genome sequence of A. fumigatus isolates from clinical and environmental origins to determine their virulence genetic content. The sample included four isolates sequenced at the University Medical Center Groningen (UMCG), three clinical (two of them isolated from the same patient) and the experimental strain B5233, and the draft genomes of one reference strain, two environmental and two clinical isolates obtained from a public database. The fungal genomes were screened for the presence of virulence-related genes (VRGs) using an in-house database of 244 genes related to
The emergence of novel pathogens poses a major public health threat causing widespread epidemics in susceptible populations. The Escherichia coli O104:H4 strain implicated in a 2011 outbreak in northern Germany caused the highest frequency of hemolytic uremic syndrome (HUS) and death ever recorded in a single E. coli outbreak. Therefore, it has been suggested that this strain is more virulent than other pathogenic E. coli (e.g., E. coli O157:H7). The E. coli O104:H4 outbreak strain possesses multiple virulence factors from both Shiga toxin (Stx)-producing E. coli (STEC) and enteroaggregative E. coli (EAEC), though the mechanism of pathogenesis is not known. Here, we demonstrate that E. coli O104:H4 produces a stable biofilm in vitro and that in vivo virulence gene expression is highest when E. coli O104:H4 overexpresses genes required for aggregation and exopolysaccharide production, a characteristic of bacterial cells residing within an established biofilm. Interrupting exopolysaccharide production and
The emergence of novel pathogens poses a major public health threat causing widespread epidemics in susceptible populations. The Escherichia coli O104:H4 strain implicated in a 2011 outbreak in northern Germany caused the highest frequency of hemolytic uremic syndrome (HUS) and death ever recorded in a single E. coli outbreak. Therefore, it has been suggested that this strain is more virulent than other pathogenic E. coli (e.g., E. coli O157:H7). The E. coli O104:H4 outbreak strain possesses multiple virulence factors from both Shiga toxin (Stx)-producing E. coli (STEC) and enteroaggregative E. coli (EAEC), though the mechanism of pathogenesis is not known. Here, we demonstrate that E. coli O104:H4 produces a stable biofilm in vitro and that in vivo virulence gene expression is highest when E. coli O104:H4 overexpresses genes required for aggregation and exopolysaccharide production, a characteristic of bacterial cells residing within an established biofilm. Interrupting exopolysaccharide production and
In vitro passages to accumulate mutations in non-essential genes for identifying in vivo virulence factorsAbstractInfertility due to tubal fibrosis/hydrosalpinx is a significant social and healthcare burden of sexuallytransmitted infection with Chlamydia trachomatis (CT). However, the pathogenic mechanisms remainunknown.
The commercial success of any vaccine is dependent on the therapeutic index, i.e., the ratio of the efficacy of the therapy to the toxicity, and the principal safety concern of modified live vaccines is reversion to virulence. Here we examined the safety of a dam mutant Salmonella vaccine by screening within infected mice for derivatives that have an increased capacity to cause disease relative to the virulence-attenuated parental dam mutant strain. Mutants that were productive for the infective process following the intraperitoneal but not the oral route of infection were isolated. The molecular basis of intraperitoneal virulence reversion correlated with deficiencies in methyl-directed mismatch repair that may suppress defects in the production of systemically related virulence functions.. Elucidation of the molecular mechanisms underlying microbial virulence provides key insights into the requisite parameters that dictate the elicitation of effective innate and adaptive immune responses. ...
Purpose. This study investigates the virulence and antimicrobial resistance in association with common clonal complexes (CCs) of enteroaggregative Escherichia coli (EAEC) isolated from Bangladesh. The aim was to determine whether specific CCs were more likely to be associated with putative virulence genes and/or antimicrobial resistance. Methodology. The presence of 15 virulence genes (by PCR) and susceptibility to 18 antibiotics were determined for 151 EAEC isolated from cases and controls during an intestinal infectious disease study carried out between 2007-2011 in the rural setting of Mirzapur, Bangladesh (Kotloff KL, Blackwelder WC, Nasrin D, Nataro JP, Farag TH et al. Clin Infect Dis 2012;55:S232-S245). These data were then analysed in the context of previously determined serotypes and clonal complexes defined by multi-locus sequence typing. Results. Overall there was no association between the presence of virulence or antimicrobial resistance genes in isolates of EAEC from cases versus controls.
Single polymerase chain reactions and sequencing. Nine of the most prevalent genes were successfully amplified using single PCR and produced the predicted sized bands during electrophoresis. To further confirm the identity of the amplicons, the bands obtained through electrophoresis were purified, concentrated and sent for sequencing. The sequences obtained (data not shown) were analysed using BLASTn and BLASTx and the amplicons were confirmed to be part of the genes of interest (data not shown).. Discussion. In this study, 45 E. coli isolates were obtained from chickens with confirmed cases of colibacillosis and screened for 12 virulence genes commonly associated with pathogenicity in APEC. Some of the virulence factors investigated have only been discovered recently. Ninety-three percent of the E. coli isolates in this study had at least one virulence gene, suggesting that the isolates used could have been APEC.. The iutA gene had the highest prevalence at 80% (Table 2). This gene has been ...
The regulatory effect of fermentable sugars on virulence genes ofL. monocytogenes has recently attracted considerable interest (2, 3, 32, 34, 35). This issue has been investigated in only four laboratory strains, at least two of which (L028 and NCTC 7973) have anomalous patterns of virulence gene expression and even regulatory mutations in prfA (41, 42). To unambiguously determine the normal pattern of this type of carbon source regulation in L. monocytogenes, we assessed the effect of a selection of carbohydrates on the expression of the PrfA-dependent gene plcB by using a panel of well-characterized wild-type strains. Our results confirmed that the repressibility of PrfA-dependent virulence genes is a general characteristic of wild-type L. monocytogenes upon growth on any fermentable sugar.. Among the strains tested, we identified a phenotypic variant of strain EGD in which virulence gene expression was still repressed by the three natural β-glucosides (cellobiose, salicin, and arbutin) but ...
The opportunistic bacterium Proteus mirabilis secretes a metalloprotease, ZapA, considered to be one of its virulence factors due to its IgA-degrading activity. However, the substrate specificity of this enzyme has not yet been fully characterized. In the present study we used fluorescent peptides derived from bioactive peptides and the oxidized ß-chain of insulin to determine the enzyme specificity. The bradykinin- and dynorphin-derived peptides were cleaved at the single bonds Phe-Ser and Phe-Leu, with catalytic efficiencies of 291 and 13 mM/s, respectively. Besides confirming already published cleavage sites, a novel cleavage site was determined for the ß-chain of insulin (Val-Asn). Both the natural and the recombinant enzyme displayed the same broad specificity, demonstrated by the presence of hydrophobic, hydrophilic, charged and uncharged amino acid residues at the scissile bonds. Native IgA, however, was resistant to hydrolysis by ZapA ...
Citation. Linz B, Ivanov YV, Preston A, Brinkac L, Parkhill J, Kim M, Harris SR, Goodfield LL, Fry NK, Gorringe AR, Nicholson TL, Register KB, Losada L, Harvill ET. Acquisition and Loss of Virulence-associated Factors During Genome Evolution and Speciation in Three Clades of Bordetella Species.. BMC Genomics. 2016 Sep 30; 17: 767.. External Citation. Abstract. The genus Bordetella consists of nine species that include important respiratory pathogens such as the classical species B. bronchiseptica, B. pertussis and B. parapertussis and six more distantly related and less extensively studied species. Here we analyze sequence diversity and gene content of 128 genome sequences from all nine species with focus on the evolution of virulence-associated factors.. ...
EN] Staphylococcus aureus is a versatile pathogen able to cause disease in both humans and animals. In rabbits, this bacterium infects animals of different ages, producing several purulent lesions. The ability of S. aureus to cause disease depends on a combination of virulence factors. The aim of this study was therefore to investigate the distribution of bacterial virulence determinants in 69 S. aureus isolates from rabbits. Some virulence factors (7 adhesins, 1 toxin and 1 protease) were positive in all rabbit S. aureus isolates analysed, while others (1 adhesin and 10 toxins) were always negative. The remaining virulence factors were more variable among isolates. An association between genotype and the different profiles of virulence factors was observed, but not with the type of lesion (P,0.05). One strain of each genotype was further analysed by multilocus sequence typing, generating ST121, ST96 and ST2951, determining a greater number of enterotoxins in ST121 isolates compared to ST96 and ...
Many opportunistic pathogens upregulate the production of virulence factors according to their density within hosts (Williams et al. 2000). The diffusible molecules capable of relaying information about density can have diverse functions. However, microbiologists commonly assert that density-dependent increases in virulence arise because of positive feedback effects on the success in combating host immunity (de Kievit & Iglewski 2000; Williams et al. 2000), what ecologists refer to as an Allee (1931) effect. Excessive virulence at low density is hypothesized to elicit an immune response in which bacteria are unable to survive, while coordinated virulence at high density is adaptive.. Evolutionary biology theory suggests a different interpretation of this phenotypic plasticity. Increasingly, microbial virulence factors have been found to be shared social traits (public goods), imposing metabolic costs on individual cells but benefiting groups of pathogens (West & Buckling 2003). If this ...
The virulence and fitness in vivo of the major human pathogen Staphylococcus aureus are associated with a cell-to-cell signaling mechanism known as quorum sensing (QS). QS coordinates the production of virulence factors via the production and sensing of autoinducing peptide (AIP) signal molecules by the agr locus. Here we show, in a wax moth larva virulence model, that (i) QS in S. aureus is a cooperative social trait that provides a benefit to the local population of cells, (ii) agr mutants, which do not pro- duce or respond to QS signal, are able to exploit the benefits provided by the QS of others (cheat), allowing them to increase in frequency when in mixed populations with cooperators, (iii) these social interactions between cells determine virulence, with the host mortality rate being negatively correlated to the percentage of agr mutants (cheats) in a population, and (iv) a higher within-host relatedness (lower strain diversity) selects for QS and hence higher virulence. Our results ...
The virulence mechanisms that allow pathogens to colonize the intestine remain unclear. Here, we show that germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with attaching and effacing bacteria. Early in infection, virulence genes were expressed and required for pathogen growth in conventionally raised mice but not germ-free mice. Virulence gene expression was down-regulated during the late phase of infection, which led to relocation of the pathogen to the intestinal lumen where it was outcompeted by commensals. The ability of commensals to outcompete C. rodentium was determined, at least in part, by the capacity of the pathogen and commensals to grow on structurally similar carbohydrates. Thus, pathogen colonization is controlled by bacterial virulence and through competition with metabolically related commensals. ...
We have determined the entire DNA sequence of pLVPK, which is a 219-kb virulence plasmid harbored in a bacteremic isolate of Klebsiella pneumoniae. A total of 251 open reading frames (ORFs) were annotated, of which 37% have homologous genes of known function, 31% match the hypothetical genes in the …
Eukaryotic parasites are a leading cause of morbidity and mortality worldwide, yet little is known about the genetic basis of their virulence. Here, we present a forward genetic screen to study pathogenesis in the protozoan parasite Toxoplasma gondii. By using modified signature-tagged mutagenesis, the growth of 6,300 T. gondii insertional mutants was compared in cell culture and murine infection to identify genes required specifically in vivo. One of the 39 avirulent mutants is disrupted in a divergent ortholog of the regulator of chromosome condensation 1 (RCC1), which is critical for nuclear trafficking in model systems. Although this RCC1 mutant grows similar to wild type in standard tissue culture conditions, it is growth-impaired under nutrient limitation. Genetic complementation of mutant parasites with the T. gondii RCC1 gene fully restores both virulence in mice and growth under low-nutrient conditions. Further analysis shows that there is a significant defect in nuclear trafficking in ...
In gram-positive bacteria, CodY is an important regulator of genes whose expression changes upon nutrient limitation and acts as a repressor of virulence gene expression in some pathogenic species. Here, we report the role of CodY in Bacillus anthracis, the etiologic agent of anthrax. Disruption of codY completely abolished virulence in a toxinogenic, noncapsulated strain, indicating that the activity of CodY is required for full virulence of B. anthracis. Global transcriptome analysis of a codY mutant and the parental strain revealed extensive differences. These differences could reflect direct control for some genes, as suggested by the presence of CodY binding sequences in their promoter regions, or indirect effects via the CodY-dependent control of other regulatory proteins or metabolic rearrangements in the codY mutant strain. The differences included reduced expression of the anthrax toxin genes in the mutant strain, which was confirmed by lacZ reporter fusions and immunoblotting. The accumulation
Carbon catabolite protein A (CcpA) is known to function as a major regulator of gene expression in different gram-positive organisms. Deletion of the ccpA homologue (saCOL1786) in Staphylococcus aureus was found to affect growth, glucose metabolization, and transcription of selected virulence determinants. In liquid culture, deletion of CcpA decreased the growth rate and yield; however, the effect was only transient during the exponential-growth phase as long as glucose was present in the medium. Depletion of glucose and production of lactate was delayed, while the level of excretion of acetate was less affected and was even higher in the mutant culture. On solid medium, in contrast, growth of the ΔccpA mutant resulted in smaller colonies containing a lower number of CFU per colony. Deletion of CcpA had an effect on the expression of important virulence factors of S. aureus by down-regulating RNAIII, the effector molecule of the agr locus, and altering the transcription patterns of hla, ...
TY - JOUR. T1 - Virulence and competitive ability in genetically diverse malaria infections. AU - De Roode, Jacobus C.. AU - Pansini, Riccardo. AU - Cheesman, Sandra J.. AU - Helinski, Michelle E.H.. AU - Huijben, Silvie. AU - Wargo, Andrew R.. AU - Bell, Andrew S.. AU - Chan, Brian H.K.. AU - Walliker, David. AU - Read, Andrew F.. N1 - Copyright: Copyright 2011 Elsevier B.V., All rights reserved.. PY - 2005/5/24. Y1 - 2005/5/24. N2 - Explaining parasite virulence is a great challenge for evolutionary biology. Intuitively, parasites that depend on their hosts for their survival should be benign to their hosts, yet many parasites cause harm. One explanation for this is that within-host competition favors virulence, with more virulent strains having a competitive advantage in genetically diverse infections. This idea, which is well supported in theory, remains untested empirically. Here we provide evidence that within-host competition does indeed select for high parasite virulence. We examine the ...
Ver más] There is scarce data about the importance of phylogroups and virulence factors (VF) in bloodstream infections (BSI) caused by extended-spectrum b-lactamase-producing Escherichia coli (ESBLEC). A prospective multicenter Spanish cohort including 191 cases of BSI due to ESBLEC was studied. Phylogroups and 25 VF genes were investigated by PCR. ESBLEC were classified into clusters according to their virulence profiles. The association of phylogropus, VF, and clusters with epidemiological features were studied using multivariate analysis. Overall, 57.6%, 26.7%, and 15.7% of isolates belonged to A/B1, D and B2 phylogroups, respectively. By multivariate analysis (adjusted OR [95% CI]), virulence cluster C2 was independently associated with urinary tract source (5.05 [0.96-25.48]); cluster C4 with sources other than urinary of biliary tract (2.89 [1.05- 7.93]), and cluster C5 with BSI in non-predisposed patients (2.80 [0.99-7.93]). Isolates producing CTX-M-9 group ESBLs and from phylogroup D ...
Shigella flexneri is a pathogenic bacterium that is the causative agent of shigellosis, an illness characterized by severe dysentery. Shigella carries many of its virulence genes on a large virulence plasmid and consequently this plasmid is the focus of research in the Wing lab. My research focuses on the transcriptional regulation of a newly identified gene called ospZ. This genes protein product is secreted outside the bacterial cell and assists in polymorphonuclear leukocyte migration, a function that is believed to enhance the virulence of Shigella. Many genes encoded by the Shigella virulence plasmid are regulated by the transcription factor VirB, which is also encoded by the virulence plasmid. VirB regulates the expression of IcsP, a gene 1.6 kilobase pairs upstream of ospZ on the divergent strand. To determine the role VirB plays in the regulation of ospZ, reporter plasmids will be constructed in which the ospZ promoter region is fused to lacZ (a gene that encodes the enzyme betagalactosidase)
General Information: Isolated from a soil sample from Nepal. Causative agent of plague. 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. It is the causative agent of plague (bubonic and pulmonary) a devastating disease which has killed millions worldwide. The organism can be transmitted from rats to humans through the bite of an infected flea or from human-to-human through the air during widespread infection. Yersinia pestis is an extremely pathogenic organism that requires very few numbers in order to cause disease, and is often lethal if left untreated. The organism is enteroinvasive, and can survive and propagate in macrophages prior to spreading systemically ...
According to evolutionary medicine, virulence increases with horizontal transmission (between non-relatives) and decreases with vertical transmission (from parent to child).[1] Paul W. Ewald has explored the relationship between virulence and mode of transmission. He came to the conclusion that virulence tends to remain especially high in waterborne and vector-borne infections, such as cholera and Dengue. Cholera is spread through sewage and Dengue through mosquitos. In the case of respiratory infections, the pathogen depends on an ambulatory host to survive. It must spare the host long enough to find a new host. Water- or vector-borne transmission circumvents the need for a mobile host. Ewald is convinced that the crowding of trench warfare provided an easy route to transmission that explains the virulence of the 1918 influenza pandemic. In crowded conditions the time to find a new host is minimal. Other epidemiologists have expanded on the idea of a tradeoff between costs and benefits of ...
Listeria monocytogenes is a common bacterium that causes human infections, like miscarriage and septicemia. Listeria uses specific virulence factors to produce proteins that will assist in invasion, replication, and escape. By manipulation of the virulence factors through knockout mutants, this study observed their role and importance in the infection and proliferation life cycle. JEG-3 cells, a human placental line, were infected with wild type Listeria or knockout mutants of individual virulence factors, Internalin A&B, Listeriolysin O, and ActA. Through Colony Forming Unit Assay, it was possible to analyze the number of colonies representing the number of Listeria bacteria after definitive time points. Each virulence factor did play a significant role in the growth and infection of Listeria in the JEG-3 cells as fewer colonies were found in the knockout mutant plates than the wild type. Each virulence factor affected a distinct portion of the invasion, replication, and escape cycle. The omission of a
TY - JOUR. T1 - Virulence profile. T2 - Carol Munro. AU - Munro, Carol. PY - 2016/8/17. Y1 - 2016/8/17. UR - http://www.scopus.com/inward/record.url?scp=84974686190&partnerID=8YFLogxK. U2 - 10.1080/21505594.2016.1190251. DO - 10.1080/21505594.2016.1190251. M3 - Comment/debate. AN - SCOPUS:84974686190. VL - 7. SP - 729. EP - 731. JO - Virulence. JF - Virulence. SN - 2150-5594. IS - 6. ER - ...
Bordetella pertussis, the human pathogen of whooping cough, when grown at 22 degrees C is nonvirulent and unable to bind eukaryotic cells. In response to a temperature shift to 37 degrees C, the bacterium acquires the ability to bind eukaryotic cells in a time-dependent fashion. By studying in vitro the temperature-induced transition, from the nonvirulent to the virulent state, we found that binding to CHO cells is mediated by the Arg-Gly-Asp-containing domain of filamentous hemagglutinin (FHA), a protein with multiple binding specificities. This protein is synthesized as a 367-kDa polypeptide within 10 min after temperature shift, but requires 2 hr before it is detected on the bacterial cell surface and starts to bind CHO cells. Mutations affecting the cell surface export of FHA abolish bacterial adhesion to CHO cells, while mutations in the outer membrane protein pertactin strongly reduce binding. This suggests that multiple chaperon proteins are required for a correct function of FHA. ...
The putative vesicle transport protein Vac1p of the human pathogenic yeast Candida albicans plays an important role in virulence. To determine the cellular functions of Vac1p, a null mutant was generated by sequential disruption of both alleles. The vac1 null mutant strain showed defective endosomal vesicle transport, demonstrating a role of Vac1p in protein transport to the vacuole. Vac1p also contributes to resistance to metal ions, as the null mutant strain was hypersensitive to Cu(2+), Zn(2+) and Ni(2+). In addition, the loss of Vac1p affected several virulence factors of C. albicans. In particular, the vac1 null mutant strain showed defective hyphal growth, even when hyphal formation was induced via different pathways. Furthermore, Vac1p affects chlamydospore formation, adherence to human vaginal epithelial cells, and the secretion of aspartyl proteinases (Saps). Avirulence in a mouse model of systemic infection of the vac1 null mutant strongly suggests that Vac1p of C. albicans is ...
The aim of this study was to identify virulence genes and antimicrobial resistance of Escherichia coli isolated from bovine clinical mastitis in dairy herds in Iran. Sampling was done from 86 inflamed quarters of dairy cows in 8 commercial farms of Alborz province, Iran in summer 2015. Shiga toxin-producing E. coli (STEC) virulence genes were detected by multiplex PCR and multi-drug resistance profiles were confirmed using disk diffusion method. Among 60 E. coli isolated from examined samples, 13 (21.6%) of them were STEC. The results of PCR assay showed that eaeA gene was carried by 4 (30.8%) of STEC isolates. Although stx1 in combination with eaeA gene was detected from 7 (53.8%) of STEC isolates, stx1 and stx2 genes were detected from only 1 (7.7%) of the examined samples. The result of the disk diffusion method showed that all E. coli isolates were resistant to penicillin, tylosin, oxytetracycline, erythromycin, ampicillin, streptomycin and neomycin. However all isolates were susceptible to
BIZARRIA JR, RODOLFO... Lack of fungal cultivar fidelity and low virulence of Escovopsis trichodermoides. Fungal Ecology 45 n. p. JUN 2020. Journal article.
Virologica Sinica publishes peer-reviewed original research articles and reviews concerning the latest developments in all branches of virology, including the research on the viruses of animals, plants and microbes. The journal welcomes studies on viruses as well as on viral infections and diseases. The journal will feature articles on new virus discovery, molecular characterization of viruses, viral pathogenesis and host immunity, vaccine development, antiviral agents and therapies.;中国病毒学杂志官方网站
Tuberculosis (TB) is a persistent lung infection that has plagued mankind for centuries and ranks as one of the most serious threats to world health today. The 2-3 million deaths attributed yearly to the disease, as well as the emergence of strains resistant to all of the available chemotherapeutic agents, urgently call for the development of new therapies to treat TB. Furthermore, the threat of drug-resistant TB as a bioterrorism agent has led to its listing as a NIAID Category C Priority Pathogen for biodefense research. The primary objective of the proposed research is to understand the mechanisms by which this pathogen manipulates its human host to evade killing by the immune system. We showed previously that M. tuberculosis utilizes the ESX-1 protein secretion system to export virulence factors that disarm host macrophages. We found that EspR is a key regulator of ESX-1 that is required for secretion and virulence in mice. EspR activates transcription of an operon that includes three ESX-1 ...
TY - JOUR. T1 - Candida albicans mutant construction and characterization of selected virulence determinants. AU - Motaung, T. E.. AU - Albertyn, J.. AU - Pohl, C. H.. AU - Köhler, Gerwald. PY - 2015/1/1. Y1 - 2015/1/1. N2 - Candida albicans is a diploid, polymorphic yeast, associated with humans, where it mostly causes no harm. However, under certain conditions it can cause infections ranging from superficial to life threatening. This ability to become pathogenic is often linked to the immune status of the host as well as the expression of certain virulence factors by the yeast. Due to the importance of C. albicans as a pathogen, determination of the molecular mechanisms that allow this yeast to cause disease is important. These studies rely on the ability of researchers to create deletion mutants of specific genes in order to study their function. This article provides a critical review of the important techniques used to create deletion mutants in C. albicans and highlights how these ...
Description: Our laboratory studies two bacterial pathogens, Vibrio cholerae, the causative agent of cholera and Yersinia pestis, the causative agent of plague. Regarding V. cholerae our laboratory studies two transcription factors, ToxR and TcpP, that regulate virulence gene transcription and environmental conditions that affect virulence gene expression levels. Our goal is to determine the nature of environmental sensing by V. cholerae as it induces virulence gene expression in hopes of interfering with that pathway with customized therapeutics. Our studies with Y. pestis focus on the ability of this organism to introduce toxic Yop proteins into targeted host cells. In addition to contributing to cell adhesion and Yop delivery, the Y. pestis surface protein Ail confers resistance to human serum, an activity required for virulence. Current work is focused on the mechanism of Ail - mediated serum - resistance with the goal of designing therapeutics interfering with this activity ...
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TY - JOUR. T1 - Evaluation of Staphylococcus aureus virulence factors using a silkworm model. AU - Miyazaki, Shinya. AU - Matsumoto, Yasuhiko. AU - Sekimizu, Kazuhisa. AU - Kaito, Chikara. PY - 2012/1/1. Y1 - 2012/1/1. N2 - Previous studies have indicated that the silkworm model is useful for identifying virulence genes of Staphylococcus aureus, a human pathogenic bacterium. Here we examined the scope of S. aureus virulence factors that can be evaluated using the silkworm model. Gene-disrupted mutants of the agr locus, arlS gene and saeS gene, which regulate the expression of cell surface adhesins and hemolysins, exhibited attenuated virulence in silkworms. Mutants of the hla gene encoding α-hemolysin, the hlb gene encoding β-hemolysin, and the psmα and psmβ operons encoding cytolysins, however, showed virulence in silkworms indistinguishable from that of the parent strain. Thus, these S. aureus cytolysins are not required for virulence in silkworms. In contrast, the gene-disrupted mutants ...
TY - JOUR. T1 - Discovery of Salmonella virulence factors translocated via outer membrane vesicles to murine macrophages. AU - Yoon, Hyunjin. AU - Ansong, Charles. AU - Adkins, Joshua N.. AU - Heffron, Fred. PY - 2011/6. Y1 - 2011/6. N2 - Salmonella enterica serovar Typhimurium, an intracellular pathogen and leading cause of food-borne illness, encodes a plethora of virulence effectors. Salmonella virulence factors are translocated into host cells and manipulate host cellular activities, providing a more hospitable environment for bacterial proliferation. In this study, we report a new set of virulence factors that is translocated into the host cytoplasm via bacterial outer membrane vesicles (OMV). PagK (or PagK1), PagJ, and STM2585A (or PagK2) are small proteins composed of ~70 amino acids and have high sequence homology to each other (,85% identity). Salmonella lacking all three homologues was attenuated for virulence in a mouse infection model, suggesting at least partial functional ...
|i|Enterococcus|/i|, a Gram-positive facultative anaerobic cocci belonging to the lactic acid bacteria of the phylum Firmicutes, is known to be able to resist a wide range of hostile conditions such as different pH levels, high concentration of NaCl (6.5%), and the extended temperatures between 5°C and 65°C. Despite being the third most common nosocomial pathogen, our understanding on its virulence factors is still poorly understood. The current study was aimed to determine the prevalence of different virulence genes in |i|Enterococcus faecalis|/i| and |i|Enterococcus faecium|/i|. For this purpose, 79 clinical isolates of Malaysian enterococci were evaluated for the presence of virulence genes. |i|pilB, fms8, efaAfm|/i|, and |i|sgrA|/i| genes are prevalent in all clinical isolates. In conclusion, the pathogenicity of |i|E. faecalis|/i| and |i|E. faecium|/i| could be associated with different virulence factors and these genes are widely distributed among the enterococcal species.
TY - JOUR. T1 - Distinctive expansion of potential virulence genes in the genome of the oomycete fish pathogen Saprolegnia parasitica. AU - Jiang, Rays H Y. AU - de Bruijn, Irene. AU - Haas, Brian J. AU - Belmonte, Rodrigo. AU - Löbach, Lars. AU - Christie, James. AU - van den Ackerveken, Guido. AU - Bottin, Arnaud. AU - Bulone, Vincent. AU - Díaz-Moreno, Sara M. AU - Dumas, Bernard. AU - Fan, Lin. AU - Gaulin, Elodie. AU - Govers, Francine. AU - Grenville-Briggs, Laura J. AU - Horner, Neil R. AU - Levin, Joshua Z. AU - Mammella, Marco. AU - Meijer, Harold J G. AU - Morris, Paul. AU - Nusbaum, Chad. AU - Oome, Stan. AU - Phillips, Andrew J. AU - van Rooyen, David. AU - Rzeszutek, Elzbieta. AU - Saraiva, Marcia. AU - Secombes, Chris J. AU - Seidl, Michael F. AU - Snel, Berend. AU - Stassen, Joost H M. AU - Sykes, Sean. AU - Tripathy, Sucheta. AU - van den Berg, Herbert. AU - Vega-Arreguin, Julio C. AU - Wawra, Stephan. AU - Young, Sarah K. AU - Zeng, Qiandong. AU - Dieguez-Uribeondo, ...
Vibrio cholerae is the causative bacteria of the diarrheal disease cholera, but it also persists in aquatic environments, where it displays an expression profile that is distinct from that during infection. Upon entry into the host, a tightly regulated circuit coordinates the induction of two major virulence factors: cholera toxin and a toxin-coregulated pilus (TCP). It has been shown that a set of bile salts, including taurocholate, serve as host signals to activate V. cholerae virulence through inducing the activity of the transmembrane virulence regulator TcpP. In this study, we investigated the role of calcium, an abundant mental ion in the gut, in the regulation of virulence. We show that whereas Ca2+ alone does not affect virulence, Ca2+ enhances bile salt-dependent virulence activation for V. cholerae. The induction of TCP by murine intestinal contents is counteracted when Ca2+ is depleted by the high-affinity calcium chelator EGTA, suggesting that the calcium present in the gut is a ...
Our studies define the elements of a signal transduction cascade that controls the production of virulence factors and pathogenicity ofC. neoformans. The Pka1 catalytic subunit of PKA regulates mating, melanin and capsule production, and virulence. The Pkr1 regulatory subunit of PKA is also a critical component, and mutants lacking Pkr1 overproduced capsule and were hypervirulent by several measures in two different animal models. pkr1 mutant cells also produced dramatically enlarged capsules during infection, and both the larger capsule size and the increased release of immunosuppressive capsular polysaccharides likely contribute to enhanced virulence.. Epistasis analysis further supports the conclusion that the Gα protein Gpa1 is an upstream controlling element for this signaling pathway and that the Ste12α transcription factor may represent one of several downstream targets of PKA that regulate differentiation and virulence. One interesting finding is that mutants with defects in an ...
The objective was to study potential bacterial virulence factors in S. aureus endocarditis. S. aureus strains isolated from patients with well-classified episodes of infective endocarditis (IE) (n=26) were compared with control S. aureus strains from consecutive patients with skin infections (n=30). The potential virulence factors studied were Staphylococcal enterotoxin A-D (SEA, SEB, SEC, SED) and toxic shock syndrome toxin-1 (TSST-1) production and binding capacity to the extracellular matrix proteins: fibronectin, collagen type I, collagen type II and bone sialoprotein (BSP). None of the potential virulence factors studied was more prevalent among the IE strains. BSP binding was more often found in the control group with skin infections. Endocarditis patients with previous damage of the heart valves were more often infected by strains not producing any enterotoxin. No correlation was found between the potential bacterial virulence factors studied and IE. Concerning the toxins known to act as ...
TY - JOUR. T1 - Virulence and arsenic resistance in Yersiniae. AU - Neyt, C. AU - Iriarte, M. AU - Thi, V H. AU - Cornelis, G R. PY - 1997. Y1 - 1997. N2 - The genus Yersinia contains three pathogenic species: Yersinia pestis, Y. pseudotuberculosis, and Y. enterocolitica. Only a few biotypes and serotypes of Y. enterocolitica are pathogenic, and these form two distinct groups: some are of low virulence, and they are encountered worldwide; others, mainly encountered in North America, are markedly more virulent. All pathogenic yersiniae possess a 70-kb virulence plasmid called pYV which encodes secreted antihost proteins called Yops as well as a type III secretion machinery that is required for Yop secretion. Genes encoding Yop synthesis and secretion are tightly clustered in three quadrants of the pYV plasmid. We show here that in the low-virulence strains of Y. enterocolitica, the fourth quadrant of the plasmid contains a new class II transposon, Tn2502. This transposon encodes a defective ...
Adaptation of Listeria monocytogenes in a simulated cheese medium: effects on virulence using the Galleria mellonella infection ...
Enteroaggregative Escherichia coli (EAEC) is associated with diarrhoea among travellers to developing countries. EAEC virulence properties predisposing to illness are not clear. Sixty-four EAEC strains identified by a HEp-2 cell assay and isolated from faecal samples from US and European travellers to developing countries were studied for the prevalence of 11 putative virulence genes by PCR: 49 EAEC strains from adults with acute diarrhoea and 15 EAEC strains from adults without diarrhoea. E. coli strains from the stools of healthy travellers to the same region were used as controls. EAEC carrying aggR, aap, astA and set1A were identified individually more often in the stools of subjects with diarrhoea compared with those without diarrhoea (P|0.05). EAEC isolates with two or three of these genes were associated with diarrhoea compared with EAEC isolates without the presence of these genes (P|0.05). Subjects with diarrhoea who shed EAEC isolates positive for these genes were more likely than subjects
Listeria (L.) monocytogenes strains show a high diversity regarding stress tolerance and virulence potential. Genome studies have mainly focused on specific sequence types (STs) predominantly associated with either food or human listeriosis. This study focused on the prevalent ST155, showing equal distribution among clinical and food isolates. We evaluated the virulence potential of 20 ST155 strains and performed comparative genomic analysis of 130 ST155 strains isolated from food, food processing environments and human listeriosis cases in different countries and years. The in vitro virulence assays using human intestinal epithelial Caco2 and hepatocytic HEPG2 cells showed an impaired virulence phenotype for six of the 20 selected ST155 strains. Genome analysis revealed no distinct clustering of strains from the same source category (food, food processing environment, and clinical isolates). All strains harbored an intact inlA and inlB locus, except four strains, which had an internal deletion in the
Avian colibacillosis is caused by a group of pathogens designated avian pathogenic Escherichia coli (APEC). Despite being known for over a century, avian colibacillosis remains one of the major endemic diseases afflicting the poultry industry worldwide. Autologous bacterins provide limited serotype-specific protection, yet multiple serogroups are associated with disease, especially O1, O2 and O78 among many others. Experimental infection models have facilitated the identification of some key APEC virulence genes and have allowed testing of vaccine candidates. Well-recognized virulence factors include Type 1 (F1) and P (Pap/Prs) fimbriae for colonization, IbeA for invasion, iron acquisition systems, TraT and Iss for serum survival, K and O antigens for anti-phagocytic activity, and a temperature-sensitive haemagglutinin of imprecise function. Intriguingly, these factors do not occur universally among APEC, suggesting the presence of multiple alternative mechanisms mediating pathogenicity. The ...
To assess the relationship between melanin production by Cryptococcus neoformans and virulence on a molecular basis, we asked: (a) is CNLAC1, the laccase structural gene of C. neoformans, expressed in vivo?; (b) can mouse virulence be restored to cnlac1 (Mel-) mutants by complementation with CNLAC1?; and (c) will targeted gene deletion of CNLAC1 decrease virulence for mice? Melanin is produced when cryptococcal laccase catalyzes the oxidation of certain aromatic compounds, including L-dopa, to quinones, which then polymerize to melanin. To assess CNLAC1 transcription, RNA was extracted from C. neoformans in cerebrospinal fluid of infected rabbits. Reverse transcriptase-polymerase chain reaction detected CNLAC1 transcript, indicating that laccase may be produced in the infected host. To assess the effect of CNLAC1 deletion on virulence, a Mel- mutant (10S) was obtained by disruption of the 5 end of the gene. After multiple backcrosses with a parental strain to remove unintended genetic defects ...
PAN Czytelnia Czasopism, Modulation of virulence genes by the two-component system PhoP-PhoQ in avian pathogenic Escherichia coli - Polish Journal of Veterinary Sciences
TY - JOUR. T1 - Virulence dynamics and phenotypic diversity of Puccinia coronata f.sp. avenae in Canada from 1974 to 1990. AU - Chong, J.. AU - Kolmer, J. A.. PY - 1993/1/1. Y1 - 1993/1/1. N2 - In the eastern region, frequency of virulence to Pc39 increased after the release of a cultivar with this resistance gene. Virulence to Pc38 and Pc39 increased in the prairie region after cultivars with these two genes were released. Frequencies of virulence to Pc35 and Pc56 fluctuated between 9-53% in the eastern region, even though these genes are not known to be present in oat cultivars grown there. In the prairie region, the frequencies of virulence to Pc35 and Pc40 fluctuate dbetween 21-60% from 1974-1990, and virulence to Pc46 increased from 7% in 1974 to 72% in 1985, even though these genes have not been used in commercial oat cultivars. The prairie population generally had higher levels of phenotypic diversity than did the eastern population in almost all years examined. -from Authors. AB - In the ...
View more ,Ascochyta blight of lentil (Lens culinaris ssp. culinaris) is caused by Ascochyta lentis. The disease causes severe damage to all aerial parts of the plant and may lead to total crop loss during extremely severe epidemics. To identify qualitative differences in resistance within Australian lentil crops, variation in virulence was examined among 17 isolates of A. lentis on six differential lentil genotypes (ILL7537, ILL5588 (cv. Northfield), ILL6002, ILL5722 (cv. Digger), ILL481 (cv. Indianhead) and CIPA203 (cv. Nipper)). Six distinct virulence patterns were identified, with Pathotype I (AL4) being highly virulent, causing disease on all genotypes except ILL7537 and pathotype VI (Kewell) exhibiting low virulence on all genotypes. Histopathology studies were carried out to further understand interaction differences between isolate-host combinations and add to the knowledge of possible resistance mechanisms underlying lentils defence to the pathogen. The infection process was compared ...
Virulence is often under selection during host-parasite coevolution. In order to increase fitness, parasites are predicted to circumvent and overcome host immunity. A particular challenge for pathogens are external immune systems, chemical defence systems comprised of potent antimicrobial compounds released by prospective hosts into the environment. We carried out an evolution experiment, allowing for coevolution to occur, with the entomopathogenic fungus, Beauveria bassiana, and the red flour beetle, Tribolium castaneum, which has a well-documented external immune system with strong inhibitory effects against B. bassiana. After just seven transfers of experimental evolution we saw a significant increase in parasite induced host mortality, a proxy for virulence, in all B. bassiana lines. This apparent virulence increase was mainly the result of the B. bassiana lines evolving resistance to the beetles external immune defences, not due to increased production of toxins or other harmful ...
Staphylococcus (S.) aureus and Pseudomonas (Ps.) aeruginosa are two of the most frequently opportunistic pathogens isolated in nosocomial infections, responsible for severe infections in immunocompromised hosts. The frequent emergence of antibiotic-resistant S. aureus and Ps. aeruginosa strains has determined the development of new strategies in order to elucidate the different mechanisms used by these bacteria at different stages of the infectious process, providing the scientists with new procedures for preventing, or at least improving, the control of S. aureus and Ps. aeruginosa infections. The purpose of this study was to characterize the molecular markers of virulence in S. aureus and Ps. aeruginosa strains isolated from different clinical specimens. We used multiplex and uniplex PCR assays to detect the genes encoding different cell-wall associated and extracellular virulence factors, in order to evaluate potential associations between the presence of putative virulence genes and the outcome of
Staphylococcus (S.) aureus and Pseudomonas (Ps.) aeruginosa are two of the most frequently opportunistic pathogens isolated in nosocomial infections, responsible for severe infections in immunocompromised hosts. The frequent emergence of antibiotic-resistant S. aureus and Ps. aeruginosa strains has determined the development of new strategies in order to elucidate the different mechanisms used by these bacteria at different stages of the infectious process, providing the scientists with new procedures for preventing, or at least improving, the control of S. aureus and Ps. aeruginosa infections. The purpose of this study was to characterize the molecular markers of virulence in S. aureus and Ps. aeruginosa strains isolated from different clinical specimens. We used multiplex and uniplex PCR assays to detect the genes encoding different cell-wall associated and extracellular virulence factors, in order to evaluate potential associations between the presence of putative virulence genes and the outcome of
Bacterial pathogens regulate virulence factor expression at both the level of transcription initiation and mRNA processing/turnover. Within Staphylococcus aureus, virulence factor transcript synthesis is regulated by a number of two-component regulatory systems, the DNA binding protein SarA, and the SarA family of homologues. However, little is known about the factors that modulate mRNA stability or influence transcript degradation within the organism. As our entree to characterizing these processes, S. aureus GeneChips were used to simultaneously determine the mRNA half-lives of all transcripts produced during log-phase growth. It was found that the majority of log-phase transcripts (90%) have a short half-life (|5 min), whereas others are more stable, suggesting that cis- and/or trans-acting factors influence S. aureus mRNA stability. In support of this, it was found that two virulence factor transcripts, cna and spa, were stabilized in a sarA-dependent manner. These results were validated by
p,Bacteria have evolved a wide range of sensing systems to appropriately respond to environmental signals. Here we demonstrate that the opportunistic pathogen Pseudomonas aeruginosa detects contact with surfaces on short timescales using the mechanical activity of its type IV pili, a major surface adhesin. This signal transduction mechanism requires attachment of type IV pili to a solid surface, followed by pilus retraction and signal transduction through the Chp chemosensory system, a chemotaxis-like sensory system that regulates cAMP production and transcription of hundreds of genes, including key virulence factors. Like other chemotaxis pathways, pili-mediated surface sensing results in a transient response amplified by a positive feedback that increases type IV pili activity, thereby promoting long-term surface attachment that can stimulate additional virulence and biofilm-inducing pathways. The methyl-accepting chemotaxis protein-like chemosensor PilJ directly interacts with the major pilin ...
TY - JOUR. T1 - Multiple fimbrial adhesins are required for full virulence of Salmonella typhimurium in mice. AU - Van Der Velden, Adrianus W M. AU - Baumler, Andreas J. AU - Tsolis, Renee M. AU - Heffron, Fred. PY - 1998/6. Y1 - 1998/6. N2 - Adhesion is an important initial step during bacterial colonization of the intestinal mucosa. However, mutations in the Salmonella typhimurium fimbrial operons lpf, pef, fim only moderately alter mouse virulence. The respective adhesins may thus play only a minor role during infection or S. typhimurium may encode alternative virulence factors that can functionally compensate for their loss. To address this question, we constructed mutations in all four known fimbrial operons of S. typhimurium: fim, lpf, pef, and agf. A mutation in the agfB gene resulted in a threefold increase in the oral 50% lethal dose (LD50) of S. typhimurium for mice. In contrast, an S. typhimurium strain carrying mutations in all four fimbrial operons (quadruple mutant) had a 26-fold ...
Virulence factors for hemolytic uremic syndrome, Denmark. Ethelberg S, Olsen KEP, Scheutz F, Jensen C, Schiellerup P, Engberg J, Petersen AM, Olesen B, Gerner-Smidt P, Mølbak K. Emerging Infectious Diseases 2004;10(5):842-847.. ABSTRACT:. Shiga-toxin producing Escherichia coli (STEC) strains are identified by the Shiga toxins (Stx); two classes, Stx1 and Stx2, are recognized. STEC strains also frequently harbor other virulence factors responsible for causing damage. Only a few epidemiologic studies have addressed the relative importance of virulence factors for serious clinical disease. This paper examines the risk factors for hemolytic uremic syndrome (HUS) and bloody diarrhea among a series of microbiologic and patient-related characteristics. From 1997 to 3002, 343 cases with STEC infections registered in Denmark, and for which complete data were available, were included in this study. HUS developed in 6% of patients and 36.4% had bloody diarrhea. The isolates comprised 74 serotypes and 49 ...
The isolation and sequence comparison of avirulent and neurovirulent strains of polio virus, alpha virus, herpes virus, immunodeficiency virus, and other viruses have identified genetic changes that are required to cause disease in the nervous system. The molecular mechanisms by which these genetic changes result in neurovirulence are unknown. An avirulent laboratory strain of the Alphavirus Sindbis kills most cultured cell lines not by lethal parasitism, but by inducing apoptosis or programmed cell death. Transfection of cultured cells with the human bcl-2 oncogene can block Sindbis virus-induced apoptosis, resulting in a persistent viral infection resembling that observed in brains of immunodeficient mice. We investigated the possibility that neurovirulent strains of Sindbis virus could overcome the protective effects of bcl-2--a potential mechanism to explain the ability of these strains to cause fatal disease. Strains of Sindbis virus that were lethal for 2- to 4-week-old mice induced ...
Smallpox, the only human infectious disease to have been eradicated, remains a threat as a potential agent of bioterrorism. Mortality rates during natural outbreaks of smallpox varied widely, a feature partially attributed to strain-specific virulence of the etiological agent, the orthopoxvirus variola virus (VARV) [1]. An understanding of the genetic determinants of virulence of VARV is critical for predicting the potential of different strains for causing severe epidemics.. We analyzed the genome-wide single nucleotide polymorphisms (SNPs) of a collection of 35 temporally, geographically and epidemiologically diverse VARV isolates housed at the US Centers for Disease Control and Preventions secure repository (previously described in [2]) for associations with VARV virulence. We investigated the only known metric of innate virulence of these isolates, their case fatality rates (CFRs), which range from ,1-30% [2]. Previously, outbreaks of smallpox have been classified as major when they ...
Brucellosis is a zoonotic bacterial disease caused by Brucella spp. The virulence of these bacteria is dependent on their ability to invade and replicate within host cells. In a previous study, a putative gene bab_RS27735 encoding an amino acid ABC transporter substrate-binding protein homologous to AapJ protein was found to be involved in Brucella abortus virulence. In this study, we successfully constructed a bab_RS27735 deletion mutant, Δ27735. Compared with the wild-type strain, the lipopolysaccharide pattern of the mutant was not changed, but the growth ability was slightly defected in the exponential phase. In tolerance tests, sensitivity of the Δ27735 mutant to oxidative stress, bactericidal peptides or low pH was not different from that of the wild-type strain. Cell infection assay showed that the mutant was reduced survival within macrophages but could efficiently escape lysosome degradation. The results of a virulence test showed that the Δ27735 mutant was attenuated in a mouse model at the
Studies have shown that radiation from radiotherapy increases the yeast colonization of patients. However it is not clear, if such radiation alters the yeast itself. The aim of the present study was therefore to report the direct impact of gamma radiation on Candida tropicalis. C. tropicalis was obtained from a patient with a carcinoma, a suspension of this yeast containing 2.0 × 103 colony forming units per milliliter was prepared. It was submitted to gamma radiation dosage similar to that used in the treatment of head and neck cancer. After a cumulative dose of 7200 cGy some virulence attributes of C. tropicalis, including macro and micromorphological characteristics, adhesion and biofilm abilities, murine experimental infection and phagocytosis resistance were evaluated on irradiated and non-irradiated yeasts. After irradiation the colony morphology of the yeast was altered from a ring format to a smooth appearance in most colonies. Scanning
|span||i|Talaromyces marneffei|/i| infection causes talaromycosis (previously known as penicilliosis), a very important opportunistic systematic mycosis in immunocompromised patients. Different virulence mechanisms in |i|T. marneffei|/i| have been proposed and investigated. In the sera of patients with ta|/span| …
Listeria monocytogenes can cause a life-threatening illness when the foodborne pathogen spreads beyond the intestinal tract to distant organs. Many aspects of the intestinal phase of L. monocytogenes pathogenesis remain unknown. Here, we present a foodborne infection model using C57BL/6 mice that have been pretreated with streptomycin. In this model, as few as 100 L. monocytogenes CFU were required to cause self-limiting enterocolitis, and systemic dissemination followed previously reported routes. Using this model, we report that listeriolysin O (LLO) and actin assembly-inducing protein (ActA), two critical virulence determinants, were necessary for intestinal pathology and systemic spread but were dispensable for intestinal growth. Sequence tag-based analysis of microbial populations (STAMP) was used to investigate the within-host population dynamics of wild-type and LLO-deficient strains. The wild-type bacterial population experienced severe bottlenecks over the course of infection, and by 5 ...
General Information: Causative agent of plague. 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. It is the causative agent of plague (bubonic and pulmonary) a devastating disease which has killed millions worldwide. The organism can be transmitted from rats to humans through the bite of an infected flea or from human-to-human through the air during widespread infection. Yersinia pestis is an extremely pathogenic organism that requires very few numbers in order to cause disease, and is often lethal if left untreated. The organism is enteroinvasive, and can survive and propagate in macrophages prior to spreading systemically throughout the host. Yersinia pestis consists of ...
Phytopathology 89:176-181...Phytopathology 89:176-181...Identification of Molecular Genetic Markers in Pyrenophora teres f. teres Associated with Low Virulence on Harbin Barley...John J. Weiland , Brian J. Steffenson , Richard D. Cartwright , and Robert K. Webster...
TY - JOUR. T1 - Activation of CpxRA in Haemophilus ducreyi primarily inhibits the expression of Its targets, including major virulence determinants. AU - Gangaiah, Dharanesh. AU - Zhang, Xinjun. AU - Fortney, Kate R.. AU - Baker, Beth. AU - Liu, Yunlong. AU - Munson, Robert S.. AU - Spinola, Stanley. PY - 2013/8. Y1 - 2013/8. N2 - Haemophilus ducreyi causes chancroid, a genital ulcer disease that facilitates the transmission of human immunodeficiency virus type 1. In humans, H. ducreyi is surrounded by phagocytes and must adapt to a hostile environment to survive. To sense and respond to environmental cues, bacteria frequently use two-component signal transduction (2CST) systems. The only obvious 2CST system in H. ducreyi is CpxRA; CpxR is a response regulator, and CpxA is a sensor kinase. Previous studies by Hansen and coworkers showed that CpxR directly represses the expression of dsrA, the lspB-lspA2 operon, and the flp operon, which are required for virulence in humans. They further showed ...
This study determined E. coli resistance to commonly used antibiotics together with their virulence properties in Ile-Ife, Nigeria. A total of 137 E. coli isolates from cases of urinary tract infection were tested for their sensitivity to commonly used antibiotics and possession of virulence factors using standard methods. Their ability to transfer resistance was also determined. The isolates demonstrated a high and widespread resistance (51.1 % to 94.3 %) to all the antibiotics used except Nitrofurantoin (7.3 %). A total of 50 (36.5 %) of the isolates were resistant to 10 of the eleven antibiotics employed. Sixty three per cent (63 %) of the 107 trimethoprim resistant E. coli transferred their resistances while amoxicillin, gentamycin, augmentin, tetracycline and erythromycin were cotransferred with trimethoprim. Fifty one (37.2 %) of these multi-resistant isolates possessed one or more virulent factors. The study concluded that urinary tract infection due to E. coli in Ile-Ife may be difficult ...
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BACKGROUND: Salmonella Enteritidis (SE) infection in poultry is one of the most important concerns in poultry. Virulence and pathogenicity of the SE isolates from Iran have not been well studied so far. OBJECTIVES: In the present study, three Salmonella Enteritidis (SE) isolates were compared with a standard SE strain (PT21) for virulence in one-day-old layer chicks. All of the isolates were supposed to be virulent because of carrying a large-sized virulence plasmid. METHODS: Fifty day-old layer chicks (LSL strain) were divided into five groups of 10 chicks and raised in separate cages until 14 days of age. All three SE isolates were cultured in brain-heart infusion (BHI) broth to reach a concentration of approximately 1010 CFU/ml. The challenged groups included three groups inoculated with three SE isolates (A20, S32, S34) and one group inoculated with SE PT21 as positive control. One group was raised as negative control without receiving any bacteria. Any mortality or morbidity observed in any group