The wide range in clinical disease manifestations of oral candidiasis (pseudomembranous, erythematous, hyperplastic) is not explicable by differences in Candida virulence or host factors.
The specific pathogenic features of L. ivanovii may be caused by sequence differences in virulence genes shared with L. monocytogenes or by differences in the gene content of these 2 species (1, 6 ).
The global regulators HrpG and HrpB, and the protein expression profiles identified suggest that virulence at low temperatures can be partially explained by differences in regulation of virulence factors present in all the strains.
To assess if any IS6110 insertions in the SMI-049 genomes could account for differences in virulence by the OP6110 promoter we mapped what genes were present nearby inserted IS6110 (Table 4).
Despite the poor correlation between invasive disease and ARs that contain virulence genes, differences in virulence between different clones of the same serotype could be explained by the distribution of such ARs in some cases (evidence provided below).
Whether these infections are produced by different Apophysomyces spp., have different responses to antifungal drugs, or have differences in virulence is unknown.
The objective of the present study was to determine if genetic differences, as defined by molecular typing, directly correlate with differences in virulence in infected mice.
Epidemiological analyses of human infections in the United States suggest that A1b infections are associated with a significantly higher mortality rate as compared to infections caused by A1a, A2 and type B. To determine if genetic differences as defined by molecular typing directly correlate with differences in virulence, A1a, A1b, A2 and type B strains were compared in C57BL/6 mice.
In the current study we used an objective clinical scoring system [38] to investigate the differences in virulence induced by a collection of Sp strains that included 8 of the serotypes most frequently associated with OM, including multiple isolates of serotype 9.
In this study, we demonstrate that genetic differences (clades A1a, A1b and A2) among F. tularensis subsp. tularensis strains, as identified by PFGE and SNP typing, correlate directly with differences in virulence as assessed using C57BL/6 mice.
