Fitting host-parasitoid models with CV² > 1 using hierarchical generalized linear models

The powerful general Pacala-Hassell host-parasitoid model for a patchy environment, which allows host density–dependent heterogeneity (HDD) to be distinguished from between-patch, host density–independent heterogeneity (HDI), is reformulated within the class of the generalized linear model (GLM) family. This improves accessibility through the provision of general software within well–known statistical systems, and allows a rich variety of models to be formulated. Covariates such as age class, host density and abiotic factors may be included easily. For the case where there is no HDI, the formulation is a simple GLM. When there is HDI in addition to HDD, the formulation is a hierarchical generalized linear model. Two forms of HDI model are considered, both with between-patch variability: one has binomial variation within patches and one has extra-binomial, overdispersed variation within patches. Examples are given demonstrating parameter estimation with standard errors, and hypothesis testing. For one example given, the extra-binomial component of the HDI heterogeneity in parasitism is itself shown to be strongly density dependent.

Multiple attractors of host-parasitoid models with integrated pest management strategies: eradication, persistence and outbreak

Host-parasitoid models including integrated pest management (IPM) interventions with impulsive effects at both fixed and unfixed times were analyzed with regard to host-eradication, host-parasitoid persistence and host-outbreak solutions. The host-eradication periodic solution with fixed moments is globally stable if the host's intrinsic growth rate is less than the summation of the mean host-killing rate and the mean parasitization rate during the impulsive period. Solutions for all three categories can coexist, with switch-like transitions among their attractors showing that varying dosages and frequencies of insecticide applications and the numbers of parasitoids released are crucial. Periodic solutions also exist for models with unfixed moments for which the maximum amplitude of the host is less than the economic threshold. The dosages and frequencies of IPM interventions for these solutions are much reduced in comparison with the pest-eradication periodic solution. Our results, which are robust to inclusion of stochastic effects and with a wide range of parameter values, confirm that IPM is more effective than any single control tactic.

Induction of apoptosis in host cells: a survival mechanism for Leishmania parasites?

Leishmania parasites invade host macrophages, causing infections that are either limited to skin or spread to internal organs. In this study, 3 species causing cutaneous leishmaniasis, L. major, L. aethiopica and L. tropica, were tested for their ability to interfere with apoptosis in host macrophages in 2 different lines of human monocyte-derived macrophages (cell lines THP-1 and U937) and the results confirmed in peripheral blood mononuclear cells (PBMC). All 3 species induced early apoptosis 48 h after infection (expression of phosphatidyl serine on the outer membrane). There were significant increases in the percentage of apoptotic cells both for U937 and PBMC following infection with each of the 3 species. Early apoptotic events were confirmed by mitochondrial membrane permeabilization detection and caspase activation 48 and 72 h after infection. Moreover, the percentage of infected THP-1 and U937 macrophages increased significantly (up to 100%) following treatment with an apoptosis inducer. Since phosphatidyl serine externalization on apoptosing cells acts as a signal for engulfment by macrophages, induction of apoptosis in the parasitized cells could actively participate in spreading the infection. In summary, parasite-containing apoptotic bodies with intact membranes could be released and phagocytosed by uninfected macrophages.