ArXiv TLDR

From Individual-Based Models to Macroscopic Dynamics of Antimicrobial Resistance

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2605.04117

Marco Menale, Giuseppe Toscani, Mattia Zanella

q-bio.PE

TLDR

This paper introduces a kinetic framework using Boltzmann and Fokker-Planck equations to model and quantify antimicrobial resistance spread.

Key contributions

  • Developed a kinetic framework with Boltzmann-type equations for SIRR antimicrobial resistance.
  • Quantifies how excessive antimicrobial use accelerates resistance spread.
  • Shows Boltzmann system approximates to Fokker-Planck equations in grazing collision limit.
  • Analyzes long-term population dynamics and equilibrium using the Fokker-Planck model.

Why it matters

This paper offers a novel multiscale perspective on antimicrobial resistance, bridging kinetic theory with classical epidemic models. It provides a tractable analytical tool to understand and predict long-term resistance dynamics, highlighting the critical impact of antimicrobial use.

Original Abstract

We introduce and discuss a kinetic framework describing the time evolution of the statistical distributions of a population divided into the compartments of susceptible, infectious, recovered, and resistant in the presence of a microbial infection driven by susceptible infectious interactions. Our main objective is to quantify the impact of excessive and inappropriate antimicrobial use, which accelerates the spread of resistance by enabling a fraction of infectious individuals to transition into the resistant compartment. The model consists of a system of Boltzmann type equations capturing binary interactions between susceptible and infectious individuals, complemented by linear redistribution operators that represent recovery, the development of resistance, and reinfection processes. In the grazing collision limit, we show that this Boltzmann system is well approximated by a system of coupled Fokker Planck equations. This limiting description allows for a more tractable analysis of the dynamics, including the characterization of the long-time behavior of the population densities. Our analysis highlights how interaction terms drive the system toward a stable equilibrium and quantifies the effects of inappropriate antimicrobial use on the distribution of resistant individuals. Overall, the results offer a multiscale perspective that bridges kinetic theory with classical epidemic modeling.

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