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Pathogenic Properties (pathogenic + property)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Microbial Aetiology Of Endodontic Treatment Failure And Pathogenic Properties Of Selected Species

AUSTRALIAN ENDODONTIC JOURNAL, Issue 1 2004
Dip Endo, Dr David Figdor MDSc (Melb), FRACDS
First page of article [source]

Prevalence and diversity of insertion sequences in the genome of Bacillus thuringiensis YBT-1520 and comparison with other Bacillus cereus group members

FEMS MICROBIOLOGY LETTERS, Issue 1 2010
Ning Qiu
Abstract Members of the Bacillus cereus group are closely related bacteria that exhibit highly divergent pathogenic properties. Sequencing of Bacillus thuringiensis ssp. kurstaki strain YBT-1520 revealed an increased number of insertion sequences (ISs) compared with those of the published B. cereus group genomes. Although some of these ISs have been observed and summarized in B. thuringiensis previously, a genomic characterization of their content is required to reveal their distribution and evolution. The result shows that the larger number of transposase coding genes on YBT-1520 chromosome is mainly caused by the amplification of IS231C, IS232A and ISBth166. Some functional genes have been disrupted through the insertion of ISs, preferentially IS231C. By comparing the Southern hybridization profiles of different B. thuringiensis strains, the existence of ISBth166 was mainly found in serovar kurstaki and the recent expansion of IS231C between different kurstaki isolates was suggested. In addition to revealing the ISs profile in YBT-1520 as well as the comparison in the B. cereus group, this study will contribute to further comparative analyses of multiple B. thuringiensis strains aimed at understanding the IS-mediated genomic rearrangements among them. [source]

Biological foundation for periodontitis as a potential risk factor for atherosclerosis

JOURNAL OF PERIODONTAL RESEARCH, Issue 1 2005
Yong-Hee P. Chun
Objectives:, Links between periodontal diseases and systemic diseases have been well documented by epidemiological studies. Recently, research has shifted to elucidating the biologic mechanism for a causal relationship. One focus of interest is atherosclerosis, the underlying event of cardiovascular diseases due to its serious health impact. However, it is still not clear whether periodontopathic pathogens are truly etiologic agents or ubiquitous bystanders. This article reviews the current understanding about the molecular biological interactions between periodontal disease and atherosclerosis and the biological plausibility of periodontitis as a potential risk factor for cardiovascular disease. Materials and methods:, The current literature regarding periodontal diseases and atherosclerosis and coronary vascular disease was searched using the Medline and PubMed databases. Results:,In vitro experiments and animal models are appropriate tools to investigate the biological interactions between periodontal disease and atherosclerosis at the cell molecular level. The concepts linking both pathologies refer to inflammatory response, immune responses, and hemostasis. In particular, Porphyromonas gingivalis appears to have unique, versatile pathogenic properties. Whether or not these findings from isolated cells or animal models are applicable in humans with genetic and environmental variations is yet to be determined. Likewise, the benefit from periodontal therapy on the development of atherosclerosis is unclear. Approaches targeting inflammatory and immune responses of periodontitis and atherosclerosis simultaneously are very intriguing. Conclusion:, An emerging concept suggests that a pathogenic burden from different sources might overcome an individual threshold culminating in clinical sequela. P. gingivalis contributes directly and indirectly to atherosclerosis. [source]

Antigenic variation with a twist , the Borrelia story

MOLECULAR MICROBIOLOGY, Issue 6 2006
Steven J. Norris
Summary A common mechanism of immune evasion in pathogenic bacteria and protozoa is antigenic variation, in which genetic or epigenetic changes result in rapid, sequential shifts in a surface-exposed antigen. In this issue of Molecular Microbiology, Dai et al. provide the most complete description to date of the vlp/vsp antigenic variation system of the relapsing fever spirochaete, Borrelia hermsii. This elaborate, plasmid-encoded system involves an expression site that can acquire either variable large protein (vlp) or variable small protein (vsp) surface lipoprotein genes from 59 different archival copies. The archival vlp and vsp genes are arranged in clusters on at least five different plasmids. Gene conversion occurs through recombination events at upstream homology sequences (UHS) found in each gene copy, and at downstream homology sequences (DHS) found periodically among the vlp/vsp archival genes. Previous studies have shown that antigenic variation in relapsing fever Borrelia not only permits the evasion of host antibody responses, but can also result in changes in neurotropism and other pathogenic properties. The vlsE antigenic variation locus of Lyme disease spirochaetes, although similar in sequence to the relapsing fever vlp genes, has evolved a completely different antigenic variation mechanism involving segmental recombination from a contiguous array of vls silent cassettes. These two systems thus appear to represent divergence from a common precursor followed by functional convergence to create two distinct antigenic variation processes. [source]