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Stochasticity and heterogeneity in host-vector models.

ABSTRACT: Demographic stochasticity and heterogeneity in transmission of infection can affect the dynamics of host-vector disease systems in important ways. We discuss the use of analytic techniques to assess the impact of demographic stochasticity in both well-mixed and heterogeneous settings. Disease invasion probabilities can be calculated using branching process methodology. We review the use of this theory for host-vector infections and examine its use in the face of heterogeneous transmission. Situations in which there is a marked asymmetry in transmission between host and vector are seen to be of particular interest. For endemic infections, stochasticity leads to variation in prevalence about the endemic level. If these fluctuations are large enough, disease extinction can occur via endemic fade-out. We develop moment equations that quantify the impact of stochasticity, providing insight into the likelihood of stochastic extinction. We frame our discussion in terms of the simple Ross malaria model, but discuss extensions to more realistic host-vector models.

SUBMITTER: Lloyd AL

PROVIDER: S-EPMC2394551 | biostudies-other | 2007 Oct

REPOSITORIES: biostudies-other

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Stochasticity and heterogeneity in host-vector models.

Lloyd Alun L AL Zhang Ji J Root A Morgan AM

Journal of the Royal Society, Interface 20071001 16

Demographic stochasticity and heterogeneity in transmission of infection can affect the dynamics of host-vector disease systems in important ways. We discuss the use of analytic techniques to assess the impact of demographic stochasticity in both well-mixed and heterogeneous settings. Disease invasion probabilities can be calculated using branching process methodology. We review the use of this theory for host-vector infections and examine its use in the face of heterogeneous transmission. Situa ...[more]

PMID: 17580290

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Project description:BackgroundIdentifying hosts of blood-feeding insect vectors is crucial in understanding their role in disease transmission. Rhodesian human African trypanosomiasis (rHAT), also known as acute sleeping sickness is caused by Trypanosoma brucei rhodesiense and transmitted by tsetse flies. The disease is commonly associated with wilderness areas of east and southern Africa. Such areas hold a diverse range of species which form communities of hosts for disease maintenance. The relative importance of different wildlife hosts remains unclear. This study quantified tsetse feeding preferences in a wilderness area of great host species richness, Serengeti National Park, Tanzania, assessing tsetse feeding and host density contemporaneously.MethodsGlossina swynnertoni and G. pallidipes were collected from six study sites. Bloodmeal sources were identified through matching Cytochrome B sequences amplified from bloodmeals from recently fed flies to published sequences. Densities of large mammal species in each site were quantified, and feeding indices calculated to assess the relative selection or avoidance of each host species by tsetse.ResultsThe host species most commonly identified in G. swynnertoni bloodmeals, warthog (94/220), buffalo (48/220) and giraffe (46/220), were found at relatively low densities (3-11/km2) and fed on up to 15 times more frequently than expected by their relative density. Wildebeest, zebra, impala and Thomson's gazelle, found at the highest densities, were never identified in bloodmeals. Commonly identified hosts for G. pallidipes were buffalo (26/46), giraffe (9/46) and elephant (5/46).ConclusionsThis study is the first to quantify tsetse host range by molecular analysis of tsetse diet with simultaneous assessment of host density in a wilderness area. Although G. swynnertoni and G. pallidipes can feed on a range of species, they are highly selective. Many host species are rarely fed on, despite being present in areas where tsetse are abundant. These feeding patterns, along with the ability of key host species to maintain and transmit T. b. rhodesiense, drive the epidemiology of rHAT in wilderness areas.

Project description:Quantifying the variation of pathogens' life history traits in multiple host systems is crucial to understand their transmission dynamics. It is particularly important for arthropod-borne viruses (arboviruses), which are prone to infecting several species of vertebrate hosts. Here, we focus on how host-pathogen interactions determine the ability of host species to transmit a virus to susceptible vectors upon a potentially infectious contact. Rift Valley fever (RVF) is a viral, vector-borne, zoonotic disease, chosen as a case study. The relative contributions of livestock species to RVFV transmission has not been previously quantified. To estimate their potential to transmit the virus over the course of their infection, we 1) fitted a within-host model to viral RNA and infectious virus measures, obtained daily from infected lambs, calves, and young goats, 2) estimated the relationship between vertebrate host infectious titers and probability to infect mosquitoes, and 3) estimated the net infectiousness of each host species over the duration of their infectious periods, taking into account different survival outcomes for lambs. Our results indicate that the efficiency of viral replication, along with the lifespan of infectious particles, could be sources of heterogeneity between hosts. Given available data on RVFV competent vectors, we found that, for similar infectious titers, infection rates in the Aedes genus were on average higher than in the Culex genus. Consequently, for Aedes-mediated infections, we estimated the net infectiousness of lambs to be 2.93 (median) and 3.65 times higher than that of calves and goats, respectively. In lambs, we estimated the overall infectiousness to be 1.93 times higher in individuals which eventually died from the infection than in those recovering. Beyond infectiousness, the relative contributions of host species to transmission depend on local ecological factors, including relative abundances and vector host-feeding preferences. Quantifying these contributions will ultimately help design efficient, targeted, surveillance and vaccination strategies.

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Stochasticity and heterogeneity in host-vector models.

Publications

Stochasticity and heterogeneity in host-vector models.

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