Abstract
PurposeThis theoretical study aimed to identify the decisive (and controllable) factors involved in Streptococcus mutans (Sm) infection through addressing questions about (i) the time and prevalence pattern (including the raison d’etre of the discrete period for the infection or WI) of initial Sm colonisation and (ii) the infant's selection of bacterial types and their diversity, which are not yet definitely answered by empirical works. MethodA model of Sm infection (within-host type) was developed. For questions (i): using the basic model, stochastic simulation was performed to reproduce longitudinal observations of the initial colonisation time. A symmetrical or right-skewed gamma distribution was assumed for the maximum colonisable area (Kmax) and transmission rate (mx). Additionally, 3 or 4 developmental modes of colonisable area [K(t)] were assigned based on the Kmax value. For (ii): by extending the basic model to the two-bacterial type model, intraspecific competition analysis focusing on the differences in mx (received by the infancy) and colonisation ability (θD) was performed. ResultsThe basic model simulation showed that mx and K(t) played a pivotal role in determining the individual time of initial colonisation and their variations among infants in forming its prevalence patterns (with or without WI). The competition model simulation showed that higher mx could be more advantageous in competitive colonisation than higher θD under repeated invasions. Accordingly, it played a decisive role in infant's selection of initially, persistently and transiently colonising bacterial types, and thus in their diversity. Conclusions(i) The mx is the primary and controllable (risk) factor that extensively affects various aspects of the Sm infection process. (ii) Also, the growing carrying capacity, i.e., K(t) is another important factor when considering how to effectively delay the onset of the colonisation. (iii) Thus, currently, the most feasible and effective control measure for the infection should be microbiological interventions in the primary host with concurrent oral hygiene and dietary control in the exposed child.
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