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Host resistance, population structure and the long-term persistence of bubonic plague: contributions of a modelling approach in the Malagasy focus.

Gascuel F, Choisy M, Duplantier JM, Débarre F, Brouat C - PLoS Comput. Biol. (2013)

Bottom Line: Although bubonic plague is an endemic zoonosis in many countries around the world, the factors responsible for the persistence of this highly virulent disease remain poorly known.By combining deterministic and stochastic analyses of this model, and including sensitivity analyses, we show that (i) endemicity is favoured by intermediate host population sizes, (ii) in large host populations, the presence of resistant rats is sufficient to explain long-term persistence of plague, and (iii) the metapopulation structure of susceptible host populations alone can also account for plague endemicity, thanks to both subdivision and the subsequent reduction in the size of subpopulations, and extinction-recolonization dynamics of the disease.In the light of these results, we suggest scenarios to explain the localized presence of plague in Madagascar.

View Article: PubMed Central - PubMed

Affiliation: IRD, CBGP (UMR IRD/INRA/CIRAD/MontpellierSupAgro), Montferrier-sur-Lez, France. fanny.gascuel@college-de-france.fr

ABSTRACT
Although bubonic plague is an endemic zoonosis in many countries around the world, the factors responsible for the persistence of this highly virulent disease remain poorly known. Classically, the endemic persistence of plague is suspected to be due to the coexistence of plague resistant and plague susceptible rodents in natural foci, and/or to a metapopulation structure of reservoirs. Here, we test separately the effect of each of these factors on the long-term persistence of plague. We analyse the dynamics and equilibria of a model of plague propagation, consistent with plague ecology in Madagascar, a major focus where this disease is endemic since the 1920s in central highlands. By combining deterministic and stochastic analyses of this model, and including sensitivity analyses, we show that (i) endemicity is favoured by intermediate host population sizes, (ii) in large host populations, the presence of resistant rats is sufficient to explain long-term persistence of plague, and (iii) the metapopulation structure of susceptible host populations alone can also account for plague endemicity, thanks to both subdivision and the subsequent reduction in the size of subpopulations, and extinction-recolonization dynamics of the disease. In the light of these results, we suggest scenarios to explain the localized presence of plague in Madagascar.

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Equilibrium states for a susceptible population, according to the rats' maximal birth rate, , and the transmission rate, , with (a)  rats and (b)  rats.Values for other parameters follow the ones presented in Table 1. Stable equilibrium states: (,) in black, (,) in dark grey and (,) in light grey. The dynamics for four couples of parameters are given on Supporting Figure S4.
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pcbi-1003039-g001: Equilibrium states for a susceptible population, according to the rats' maximal birth rate, , and the transmission rate, , with (a) rats and (b) rats.Values for other parameters follow the ones presented in Table 1. Stable equilibrium states: (,) in black, (,) in dark grey and (,) in light grey. The dynamics for four couples of parameters are given on Supporting Figure S4.

Mentions: Our model includes several modifications compared to the model of Keeling & Gilligan [20], [21], in order to better depict wild plague foci, and specifically that of Madagascar. In our model, (i) infectious rats do not recover, as frequently observed [4], [6], [36], (ii) free infectious fleas either find a host or quickly die from starvation, a more explicit modelling of two events that were not distinguished in [21], and (iii) the descendants of resistant rats which are resistant also have a density-dependent birth rate, while they grew exponentially in [20]. Nevertheless, the above changes do not change the main characteristics of the outputs of the model (comparison of Figures 1 and 2 with Supporting Figures S1 and S2).


Host resistance, population structure and the long-term persistence of bubonic plague: contributions of a modelling approach in the Malagasy focus.

Gascuel F, Choisy M, Duplantier JM, Débarre F, Brouat C - PLoS Comput. Biol. (2013)

Equilibrium states for a susceptible population, according to the rats' maximal birth rate, , and the transmission rate, , with (a)  rats and (b)  rats.Values for other parameters follow the ones presented in Table 1. Stable equilibrium states: (,) in black, (,) in dark grey and (,) in light grey. The dynamics for four couples of parameters are given on Supporting Figure S4.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3649974&req=5

pcbi-1003039-g001: Equilibrium states for a susceptible population, according to the rats' maximal birth rate, , and the transmission rate, , with (a) rats and (b) rats.Values for other parameters follow the ones presented in Table 1. Stable equilibrium states: (,) in black, (,) in dark grey and (,) in light grey. The dynamics for four couples of parameters are given on Supporting Figure S4.
Mentions: Our model includes several modifications compared to the model of Keeling & Gilligan [20], [21], in order to better depict wild plague foci, and specifically that of Madagascar. In our model, (i) infectious rats do not recover, as frequently observed [4], [6], [36], (ii) free infectious fleas either find a host or quickly die from starvation, a more explicit modelling of two events that were not distinguished in [21], and (iii) the descendants of resistant rats which are resistant also have a density-dependent birth rate, while they grew exponentially in [20]. Nevertheless, the above changes do not change the main characteristics of the outputs of the model (comparison of Figures 1 and 2 with Supporting Figures S1 and S2).

Bottom Line: Although bubonic plague is an endemic zoonosis in many countries around the world, the factors responsible for the persistence of this highly virulent disease remain poorly known.By combining deterministic and stochastic analyses of this model, and including sensitivity analyses, we show that (i) endemicity is favoured by intermediate host population sizes, (ii) in large host populations, the presence of resistant rats is sufficient to explain long-term persistence of plague, and (iii) the metapopulation structure of susceptible host populations alone can also account for plague endemicity, thanks to both subdivision and the subsequent reduction in the size of subpopulations, and extinction-recolonization dynamics of the disease.In the light of these results, we suggest scenarios to explain the localized presence of plague in Madagascar.

View Article: PubMed Central - PubMed

Affiliation: IRD, CBGP (UMR IRD/INRA/CIRAD/MontpellierSupAgro), Montferrier-sur-Lez, France. fanny.gascuel@college-de-france.fr

ABSTRACT
Although bubonic plague is an endemic zoonosis in many countries around the world, the factors responsible for the persistence of this highly virulent disease remain poorly known. Classically, the endemic persistence of plague is suspected to be due to the coexistence of plague resistant and plague susceptible rodents in natural foci, and/or to a metapopulation structure of reservoirs. Here, we test separately the effect of each of these factors on the long-term persistence of plague. We analyse the dynamics and equilibria of a model of plague propagation, consistent with plague ecology in Madagascar, a major focus where this disease is endemic since the 1920s in central highlands. By combining deterministic and stochastic analyses of this model, and including sensitivity analyses, we show that (i) endemicity is favoured by intermediate host population sizes, (ii) in large host populations, the presence of resistant rats is sufficient to explain long-term persistence of plague, and (iii) the metapopulation structure of susceptible host populations alone can also account for plague endemicity, thanks to both subdivision and the subsequent reduction in the size of subpopulations, and extinction-recolonization dynamics of the disease. In the light of these results, we suggest scenarios to explain the localized presence of plague in Madagascar.

Show MeSH
Related in: MedlinePlus