The Curse of Black Sigatoka: A Backward Bifurcation Perspective
Bernard Asamoah Afful, Luis F. Gordillo
TLDR
A new model for Black Sigatoka disease reveals a backward bifurcation, explaining why reducing R0 alone fails and suggesting new control strategies.
Key contributions
- Proposes a deterministic pathogen-host model for Black Sigatoka disease dynamics.
- Identifies a backward bifurcation where endemic disease persists even when R0 < 1, explaining control failures.
- Suggests control strategies beyond R0 reduction: limiting new susceptible leaves and deploying resistant varieties.
- Formulates a stochastic model and uses Sobol's method to analyze variability and nonlinear parameter interactions.
Why it matters
This paper provides a crucial mathematical explanation for the persistence of Black Sigatoka disease despite control efforts. By identifying a backward bifurcation, it highlights the inadequacy of solely targeting R0 and offers specific, actionable strategies for more effective disease management. The stochastic analysis further enhances understanding of disease variability.
Original Abstract
Black Sigatoka disease (BSD), also known as black leaf streak disease, is an airborne fungal infection caused by \textit{Pseudocercospora fijiensis} that severely impacts global banana and plantain production. Its persistence and resistance to eradication make it one of the most challenging plant diseases to manage. In this paper, we propose a deterministic pathogen-host model to describe BSD dynamics. Due to dual transmission pathways (ascospores and conidia) and mate limitation in sexual reproduction, the model exhibits a backward bifurcation: a stable endemic equilibrium coexists with the disease-free equilibrium for certain parameter values in which the basic reproduction number, $\mathcal{R}_0$, is less than 1. This phenomenon explains why control strategies that solely reduce $\mathcal{R}_0$ below one may fail. For the backward bifurcation regime, we perform sensitivity analysis of the endemic equilibrium using normalized forward sensitivity indices, Latin Hypercube Sampling, and Partial Rank Correlation Coefficients. Results indicate that effective control must extend beyond $\mathcal{R}_0$ reduction and prioritize (1) limiting production of new susceptible leaves during high-risk periods and (2) developing and deploying disease-resistant plant varieties. To incorporate transmission variability, we also formulate a stochastic version of the model using the Stochastic Simulation Algorithm (SSA). Extensive numerical simulations compare stochastic realizations with deterministic predictions and quantify variability in disease dynamics. To identify the principal drivers of persistence and variability, we analyze the endemic equilibrium using Sobol's variance-based sensitivity method, which highlights the role of nonlinear parameter interactions in shaping variability.
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