Modelling Within-Host Spatiotemporal Dynamics Of Invasive Bacterial Disease
April 8, 2008
Global patterns and mechanistic determinants of bacterial spread in mammalian organisms are difficult to obtain through numerical and topographical mapping of a single bacterial population.
Appreciation of the true pathogenetic events during infections needs to be based on the understanding of the fine interactions that control the infection dynamics of individual subpopulations in the same host. In this week’s PLoS Biology, Andrew Grant and colleagues show how they have used multiple strains of genetically identical bacteria, called wild-type isogenic tagged strains (WITS), in simultaneous infections in the same animal to gather insights into the patterns of spread of individual subpopulations of bacteria in the tissues and interactions between bacteria and phagocytes.
Combining numerical fluctuation in the WITS populations with mathematical modeling and statistical analysis, they have gathered data on the relative occurrence of bacterial growth and death in different phases of the disease process. Their analyses support a model in which shortly after infection concomitant death and rapid bacterial replication lead to the establishment of independent bacterial sub-populations in different organs. Later, decreased microbial mortality leads to an exponential increase in the number of bacteria that spread locally, with subsequent mixing of bacteria between organs.
This work illustrates the importance of unraveling heterogeneous traits of infections to reconstruct and understand the true nature of the global disease process.
Modelling within-host spatiotemporal dynamics of invasive bacterial disease
Grant AJ, Restif O, McKinley TJ, Sheppard M, Maskell DJ, et al. (2008)
PLoS Biol 6(4):e74. doi:10.1371/journal.pbio.0060074
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PLoS Biology
