Migration paths saturations in meta-epidemic systems

In this paper we consider a simple two-patch model in which a population affected by a disease can freely move. We assume that the capacity of the interconnected paths is limited, and thereby influencing the migration rates. Possible habitat disruptions due to human activities or natural events are accounted for. The demographic assumptions prevent the ecosystem to be wiped out, and the disease remains endemic in both populated patches at a stable equilibrium, but possibly also with an oscillatory behavior in the case of unidirectional migrations. Interestingly, if infected cannot migrate, it is possible that one patch becomes disease-free. This fact could be exploited to keep disease-free at least part of the population

Separate seasons of infection and reproduction can lead to multi-year population cycles

International audienceMany host-pathogen systems are characterized by a temporal order of disease transmission and host reproduction. For example, this can be due to pathogens infecting certain life cycle stages of insect hosts; transmission occurring during the aggregation of migratory birds; or plant diseases spreading between planting seasons. We develop a simple discrete-time epidemic model with density-dependent transmission and disease affecting host fecundity and survival. The model shows sustained multi-annual cycles in host population abundance and disease prevalence, both in the presence and absence of density dependence in host reproduction, for large horizontal transmissibility, imperfect vertical transmission, high virulence, and high reproductive capability. The multi-annual cycles emerge as invariant curves in a Neimark-Sacker bifurcation. They are caused by a carry-over effect, because the reproductive fitness of an individual can be reduced by virulent effects due to infection in an earlier season. As the infection process is density-dependent but shows an effect only in a later season, this produces delayed density dependence typical for second-order oscillations. The temporal separation between the infection and reproduction season is crucial in driving the cycles; if these processes occur simultaneously as in differential equation models, there are no sustained oscillations. Our model highlights the destabilizing effects of inter-seasonal feedbacks and is one of the simplest epidemic models that can generate population cycles