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Results for “pathogen virulence”

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At least 37 records · Page 2Linked to original sources
PubMed1985

Genetic mapping of lymphocytic choriomeningitis virus pathogenicity: virulence in guinea pigs is associated with the L RNA segment.

The Armstrong CA 1371 (ARM) and WE strains of lymphocytic choriomeningitis virus (LCMV) differ in the ability to produce disease in adult guinea pigs. Infection with the ARM strain is not lethal, even at high virus doses (greater than 10,000 PFU), whereas the WE strain causes 100% mortality even at low doses (less than 10 PFU). To determine the genetic basis of this virulence, intertypic reassortants were made between the ARM and WE strains of LCMV. The two reassortants with the genotypes WE/ARM (L segment of WE and S segment of ARM) and ARM/WE (L segment of ARM and S segment of WE) were tested for their pathogenicity in guinea pigs. The ARM/WE reassortant was avirulent like the ARM/ARM parental strain. Minimal viral replication was observed in organs of guinea pigs inoculated with 10(2) or 10(5) PFU of ARM/ARM or ARM/WE, and all animals survived. In contrast, the WE/ARM reassortant was highly virulent like the WE/WE parental strain and killed all of the infected animals. High levels of viral replication were observed in guinea pigs infected with the latter two strains. In contrast to these in vivo observations, both the parental strains and the ARM/WE or WE/ARM reassortants had similar growth potential in cultured guinea pig fibroblasts. Thus, the L RNA segment of LCMV WE is important for viral replication in vivo and is associated with fatal acute disease after infection of adult guinea pigs.

Animals↗
PubMed2004

Enterococcal virulence--pathogenicity island of E. Faecalis.

Enterococcal species, though most commonly regarded as members of the microbial flora of the intestinal tract, have recently emerged as human pathogens of significant concern. The rapid spread of antibiotic resistance among enterococci, which has resulted in strains now being routinely isolated that are resistant to all bactericidal regimens, has prompted considerable interest in investigating the pathogenesis of enterococcal infection, with a view toward deriving new, information-based treatment strategies. This review summarizes major findings on the pathogenesis of enterococcal infection, fits them into a model for the dual lifestyle of enterococci as commensal and pathogen, and integrates into that model a recently discovered pathogenicity island of Enterococcus faecalis.

Drug Resistance, Bacterial↗
PubMed2003

Microbial diversity and prevalence of virulent pathogens in biofilms developed in a water reclamation system.

Bacterial biofilm is a common phenomenon in both natural and engineered systems which often becomes a source of contamination and microbially influenced corrosion. It is thought that formation of biofilm in the monoculture of several bacterial species is regulated by acylhomoserine lactone (AHL) quorum-sensing signals. In this study, we investigated the microbial diversity and existence of AHL-producing and AHL-degrading bacterial species in the biofilm samples from a water reclamation system located in a tropical environment. 16S ribosomal DNA sequencing analysis indicated the presence of at least 11 bacterial species, including the frequently encountered bacterial pathogens Pseudomonas aeruginosa and Klebsiella pneumoniae, and several rare pathogens. We showed that only two groups of isolates, belonging to P. aeruginosa and Enterobacter agglomerans, produced AHL signals. We also found that three bacterial isolates, i.e., Agrobacterium tumefaciens XJ01, Bacillus cereus XJ08, and Ralstonia sp. XJ12, expressed AHL degradation enzymes. Furthermore, we showed that P. aeruginosa isolate HL43 was virulent against animal model Caenorhabditis elegans and released 2-6-fold more pyocyanin cytotoxin than P. aeruginosa strains PA01 and PA14, the two commonly used laboratory strains. These data indicate the complexity and importance of biofilm research in water reclamation.

Animals↗
PubMed1989

A competitive exclusion principle for pathogen virulence.

For a modified Anderson and May model of host parasite dynamics it is shown that infections of different levels of virulence die out asymptotically except those that optimize the basic reproductive rate of the causative parasite. The result holds under the assumption that infection with one strain of parasite precludes additional infections with other strains. Technically, the model includes an environmental carrying capacity for the host. A threshold condition is derived which decides whether or not the parasites persist in the host population.

Animals↗
PubMedDate not supplied

Infections in the diabetic patient: the role of immune dysfunction and pathogen virulence factors.

It is a common belief that certain infections occur more frequently in patients with diabetes mellitus than in nondiabetics. In some infections, poor diabetic control is strongly linked. Diabetics comprise 50%-70% of all patients who undergo nontraumatic foot or leg amputations, the overwhelming majority of which are necessitated by infection and necrosis of soft tissue and/or bone. Imputed host defense abnormalities include defective immune responses (e.g., white blood cell function, granuloma formation), peripheral neuropathies, impaired distal arterial supply, and problems in "control" of the diabetic state eventuating in catabolic metabolism. Increased bacterial translocation as a source of the causative bacteria is another potential entry site. Possible virulence factors of the invading organisms include polymicrobial synergism, glycocalyx formation, and inoculum size. Attention to the principles of preventive education, vascular evaluation, diabetes management, and adequate debridement maximize healing potential.

Communicable Diseases↗
PubMed2003

Targeted activation tagging of the Arabidopsis NBS-LRR gene, ADR1, conveys resistance to virulent pathogens.

A transgenic Arabidopsis line containing a chimeric PR-1::luciferase (LUC) reporter gene was subjected to mutagenesis with activation tags. Screening of lines via high-throughput LUC imaging identified a number of dominant Arabidopsis mutants that exhibited enhanced PR-1 gene expression. Here, we report the characterization of one of these mutants, designated activated disease resistance (adr) 1. This line showed constitutive expression of a number of key defense marker genes and accumulated salicylic acid but not ethylene or jasmonic acid. Furthermore, adr1 plants exhibited resistance against the biotrophic pathogens Peronospora parasitica and Erysiphe cichoracearum but not the necrotrophic fungus Botrytis cinerea. Analysis of a series of adr1 double mutants suggested that adr1-mediated resistance against P. parasitica was salicylic acid (SA)-dependent, while resistance against E. cichoracearum was both SA-dependent and partially NPR1-dependent. The ADR1 gene encoded a protein possessing a number of key features, including homology to subdomains of protein kinases, a nucleotide binding domain, and leucine-rich repeats. The controlled, transient expression of ADR1 conveyed striking disease resistance in the absence of yield penalty, highlighting the potential utility of this gene in crop protection.

Amino Acid Sequence↗
PubMed1998

Highly virulent pathogens--a post antibiotic era?

The spectrum of infectious diseases is changing rapidly. Emerging infectious agents present an intriguing constellation of nosocomial challenges. Antimicrobial resistance results in increased morbidity, mortality and costs of health care. Resistance to antimicrobial agents has been recorded since 1940 with penicillin resistant Escherichia coli (E coli) (Abraham and Chain 1940). A similar pencillin resistance was reported in 1944 in Staphylococus aureus (S. aureus) (Kirby 1944) Even before the widespread global use of penicillin, resistance had already been detected in both gram-positive and gram-negative organisms. The 1990s herald the era of multiple drug resistance. To grasp further the enormity and complexity of our modern antimicrobial resistance problem, one only needs to think about how many--how fast--and in how many settings (hospitals, clinics, outpatients nursing and long term facilities, etc), these pathogens have developed antimicrobial resistance: Multiple drug-resistant Mycobacterium tuberculosis, penicillin-resistant Streptococcus pneumonia, fluconzole-resistant Candida, methicillin-resistant S. aureus (MRSA), vancomycin-resistant Enterococci (VRE) and now S. aureus with reduced susceptibility to vancomycin. Given the dramatic increase in the incidence of multiple drug-resistant organisms--and now--the mounting evidence of resistance transfer from one organism to another, we will certainly witness a combined growth of nosocomial pathogens, for which there are no antibiotic solutions. Appropriate infection control measures for such resistant strains depend, in part, on the mechanisms of genetic information exchanged among micro-organisms. Clearly we need to strengthen the basic tenets of infection prevention and control; hygiene, engineering and microbial barriers, to prevent transinfection. We need to control horizontal nosocomial transmission of organisms. Contaminated environmental surfaces are a reservoir for resistant organisms such as MRSA (Boyce et al 1997) and VRE (Karanfil et al 1992). Stringent infection control policies need to be developed and implemented. A comprehensively applied infection control programme will reduce the dissemination of resistant strains. Each patient care setting must examine its current practices and review the outcome efficacy. A consensus development conference to develop centres for disease control (CDC) formal guidelines against vancomycin intermediate-level resistant staphylococcus aureus (VISA) and vancomycin-resistant staphylococcus aureus (VRSA) may take a year or more to convene. This paper will examine the basic considerations currently offered by the CDC which may be valuable starting points for the enhancement of current infection control practices. Perspectives of the Society for Healthcare Epidemiology of America (SHEA) will also be included.

Anti-Bacterial Agents↗
PubMed1999

Pathogen virulence genes--implications for vaccines and drug therapy.

The emergence and spread of bacteria resistant to antimicrobial drugs is a major public health problem with a growing number of infections becoming virtually untreatable. There is a need to develop interventions both to prevent and to treat diseases caused by multi-resistant microbes. We review some recently developed methods (including whole genome nucleotide sequencing projects) to study bacterial pathogenesis, and discuss how knowledge gained from understanding the molecular mechanisms of disease can be applied to combat the threat of infectious diseases.

Animals↗
PubMedDate not supplied

Infections from biomaterials and implants: a race for the surface.

Microorganisms in nature and disease are dependent on substratum attachment for optimal growth and development. Similarly, implanted biomaterials tend to potentiate bacteria on their surfaces so that normally friendly special or opportunistic organisms become virulent pathogens. Virulence is also enhanced because both bacteria and biomaterials interfere with host defense mechanisms. Infections centered on biomaterials are most difficult to eliminate and usually require removal of the device. The consequences of device failure are catastrophic and costly. It is the specific nature of the biomaterial surface, which is indirectly a reflection of bulk features, that causes and directs the changes in bacterial behavior which result in virulence. Features of organisms and materials and interactions responsible for these phenomena are reviewed.

Bacterial Adhesion↗
PubMed2006

Pathogenicity islands: a molecular toolbox for bacterial virulence.

Pathogenicity islands (PAIs) are distinct genetic elements on the chromosomes of a large number of bacterial pathogens. PAIs encode various virulence factors and are normally absent from non-pathogenic strains of the same or closely related species. PAIs are considered to be a subclass of genomic islands that are acquired by horizontal gene transfer via transduction, conjugation and transformation, and provide 'quantum leaps' in microbial evolution. Data based on numerous sequenced bacterial genomes demonstrate that PAIs are present in a wide range of both gram-positive and gram-negative bacterial pathogens of humans, animals and plants. Recent research focused on PAIs has not only led to the identification of many novel virulence factors used by these species during infection of their respective hosts, but also dramatically changed our way of thinking about the evolution of bacterial virulence.

Bacteria↗
PubMed2003

Evolution of virulence in a plant host-pathogen metapopulation.

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 of Melampsora lini in resistant Linum marginale populations 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.

Basidiomycota↗
PubMed2005

Expression profiling of virulence and pathogenicity genes of Xanthomonas axonopodis pv. citri.

DNA macroarrays of 279 genes of Xanthomonas axonopodis pv. citri potentially associated with pathogenicity and virulence were used to compare the transcriptional alterations of this bacterium in response to two synthetic media. Data analysis indicated that 31 genes were up-regulated by synthetic medium XVM2, while only 7 genes were repressed. The results suggest that XVM2 could be used as an in vitro system to identify candidate genes involved in pathogenesis of X. axonopodis pv. citri.

Base Sequence↗