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BACKGROUND. Drugs and vaccines that can interrupt the transmission of Plasmodium falciparum will be important for malaria control and elimination. However, models for early clinical evaluation of candidate transmission-blocking interventions are currently unavailable. Here, we describe a new model for evaluating malaria transmission from humans to Anopheles mosquitoes using controlled human malaria infection (CHMI). METHODS. Seventeen healthy malaria-naive volunteers underwent CHMI by intravenous inoculation of P. falciparum-infected erythrocytes to initiate blood-stage infection. Seven to eight days after inoculation, participants received piperaquine (480 mg) to attenuate asexual parasite replication while allowing gametocytes to develop and mature. Primary end points were development of gametocytemia, the transmissibility of gametocytes from humans to mosquitoes, and the safety and tolerability of the CHMI transmission model. To investigate in vivo gametocytocidal drug activity in this model, participants were either given an experimental antimalarial, artefenomel (500 mg), or a known gametocytocidal drug, primaquine (15 mg), or remained untreated during the period of gametocyte carriage. RESULTS. Male and female gametocytes were detected in all participants, and transmission to mosquitoes was achieved from 8 of 11 (73%) participants evaluated. Compared with results in untreated controls (n = 7), primaquine (15 mg, n = 5) significantly reduced gametocyte burden (P = 0.01), while artefenomel (500 mg, n = 4) had no effect. Adverse events (AEs) were mostly mild or moderate. Three AEs were assessed as severe--fatigue, elevated alanine aminotransferase, and elevated aspartate aminotransferase--and were attributed to malaria infection. Transaminase elevations were transient, asymptomatic, and resolved without intervention. CONCLUSION. We report the safe and reproducible induction of P. falciparum gametocytes in healthy malaria-naive volunteers at densities infectious to mosquitoes, thereby demonstrating the potential for evaluating transmission- blocking interventions in this model. TRIAL REGISTRATION. ClinicalTrials.gov NCT02431637 and NCT02431650. FUNDING. Bill & Melinda Gates Foundation., Introduction Considerable reductions in the global burden of malaria have been achieved in recent years, and this has led to a renewed focus on achieving malaria elimination and eventual eradication [...]

It is well known that the model equilibrium in the Nicholson-Bailey framework for parasitoid host interactions can be stabilized if there is variation in the risk of parasitism among individual hosts. We show that the shape of the distribution of risk among hosts is crucial in determining stability. Stability for all values of the reproduction rate R of the host requires the distribution to be skewed, with a modal risk of zero. As a consequence, a distribution of risk with nonzero mode but otherwise sufficiently high variability will not stabilize the host parasitoid equilibrium for certain values of R. We also develop a new, simple, and general criterion for stability, according to which the host-parasitoid equilibrium is stable if and only if the adult host equilibrium density increases as host reproductive rate R increases. This reinforces previous results that skewed risk of the type needed for stability reduces parasitoid efficiency and hence the parasitoid's ability to suppress the host. Finally, we identify appropriate measures that can be made in the field to relate skew in risk of parasitism to stability. Key words: biological control; distribution of risk; host-parasitoid models; host suppression; population dynamics.

Colorado potato beetle (CPB) is a devastating herbivorous pest of solanaceous plants. Despite the economic impact, little is known about the molecular interaction of CPB with these plants. Using an 11 421 expressed sequence tag (EST) potato microarray, we identified 320 genes differentially expressed in potato leaves in response to CPB herbivory. Amongst these were genes putatively encoding proteinase inhibitors along with enzymes of terpenoid, alkaloid, and phenylpropanoid biosynthetic pathways, suggesting the defensive chemistries that constitute potato's defense against CPB herbivory. Several genes, such as those encoding proteinase inhibitors, represent mechanisms implicated in other plantherbivory interactions, and could correspond with general defensive chemistry strategies. In other cases, products of the differentially expressed genes may represent taxa-specific defensive chemistry. For example, the presumed alkaloid products of a putative tropinone reductase I are specific to a subset of the Solanaceae. Two herbivory-induced genes, not specific to potato, are implicated in the synthesis of volatiles known to attract CPB predators. Comparison of continuous herbivore attack versus recovery from CPB attack indicates that fewer genes involved in defensive chemistry are induced after continuous feeding than after feeding and recovery, suggesting the plant's ability to mount a full defense response is enhanced under light versus heavy attack. Key words: Colorado potato beetle, herbivore, infestation, plant-insect interaction, potato. La bete a patate du Colorado (CPB) constitue une peste herbivore devastatrice chez les Solenaceae. En depit de ses impacts economiques, on connait peu de choses sur les interactions moleculaires entre le CPB et ces plantes. En utilisant un microarray 11421 EST de la pomme de terre, les auteurs ont identifie 320 genes a expression differentielle dans des feuilles de pommes de terre, en reaction a l'herbivorie par le CPB. Parmi ceux-ci, on retrouve des genes putatifs codant pour des inhibiteurs de proteinases ainsi que des enzymes des sentiers biosynthetiques de terpenoides, d'alcaloides et de phenylpropanoides, signalant la chimie defensive constituant la defense de la pomme de terre contre l'herbivorie par le CPB. Plusieurs genes, comme ceux codant des inhibiteurs de proteines, representent des mecanismes impliques dans d'autres reactions plante-herbivore, et pourraient correspondre a des strategies generales de defenses chimiques. Dans d'autres cas, les produits de l'expression genetique differentielle peuvent representer une chimie defensive specifique au taxon. Par exemple, les produits alcaloides presumes d'une reductase I de la tropinone sont specifiques a un sousensemble de Solenaceae. Deux genes induits par l'herbivorie, non specifiques a la pomme de terre, sont impliques dans la synthese de substances volatiles, reconnues pour attirer les predateurs des CPB. La comparaison d'une attaque continue vs le retablissement d'une attaque par le CPB indique que moins de genes impliques dans la chimie defensive sont induits apres une attaque soutenue qu'apres une attaque avec retablissement, ce qui suggere que la capacite de la plante a mettre en branle une reaction de defense complete est intensifiee apres une attaque courte vs une attaque prolongee. Mots-cles : bete a patate du Colorado, herbivore, infestation, interaction plante-insecte, pomme de terre. [Traduit par la Redaction], Introduction Plants respond to feeding insects through a complex interaction involving the recognition of signals induced by mechanical wounding, as well as the detection of specific elicitors produced in either [...]

Numerous loci in host organisms are involved in parasite recognition, such as major histocompatibility complex (MHC) genes in vertebrates or genes involved in gene-for-gene (GFG) relationships in plants. Diversity is commonly observed at such loci and at corresponding loci encoding antigenic molecules in parasites. Multilocus theoretical models of host-parasite coevolution predict that polymorphism is more likely than in single-locus interactions because recurrent coevolutionary cycles are sustained by indirect frequency-dependent selection as rare genotypes have a selective advantage. These cycles are stabilized by direct frequency-dependent selection, resulting from repeated reinfection of the same host by a parasite, a feature of most diseases. Here, it is shown that for realistically small costs of resistance and virulence, polycyclic disease and high autoinfection rates, stable polymorphism of all possible genotypes is obtained in parasite populations. Two types of epistatic interactions between loci tend to increase the parameter space in which stable polymorphism can occur with all possible host and parasite genotypes. In the parasite, the marginal cost of each additional virulence allele should increase, while in the host, the marginal cost of each additional resistance allele should decrease. It is therefore predicted that GFG polymorphism will be stable (and hence detectable) when there is partial complementation of avirulence genes in the parasite and of resistance genes in the host.

The production of antimicrobial compounds known as colicins has been shown to be an important mediator of competitive interactions among Escherichia coli genotypes. There is some understanding of the forces responsible for determining the frequency of colicin production in E. coli populations; however, this understanding cannot explain all of the observed variation. A survey of colicin production in E. coli isolated from native Australian mammals revealed that the frequency of colicin production in strains isolated from carnivores was significantly lower than the frequency of production in strains recovered from herbivores or omnivores. The intestine of Australian carnivores is tube-like and gut turnover rates are rapid compared with the turnover rates of the intestinal tracts of herbivores and omnivores, all of which possess a hindgut fermentation chamber. A mathematical model was developed in order to determine if variation in gut turnover rates could determine if a host was more likely to harbour a colicin-producing strain or a non-producer. The model predicted that a colicin producer was more likely to dominate in the gut of a host with lower gut turnover rates, and a non-producer to dominate in hosts with rapid gut turnover rates.

Models of the evolution of virulence have typically focused on increased mortality, one of two negative effects that parasites can inflict on their host. Those that consider the other effect, fecundity reduction, can predict that parasites should completely sterilize their hosts. Although this prediction seems extreme, sterilization features prominently in a fascinating strategy, parasitic castration. Such castration can be accompanied by gigantism (unusually large growth of infected hosts), long infectious periods, and fecundity compensation (where, before heavy parasite burdens ensue, newly infected hosts reproduce earlier/more than they would if not infected). Using a model of dynamic energy budgets (DEB), we show how these results readily emerge, assuming that parasites consume energy reserves of the host. The simple, but mechanistic, DEB model follows energy flow though hosts and parasites, starting with ingestion, and continuing with storage of assimilated energy, and use of those reserves for growth and reproduction, as allocated by the host according to the 'K-rule'. Using this model, we compare and contrast two strategies for parasites. 'Consumers' only steal energy from their hosts, thereby indirectly altering allocation of energy to growth and reproduction, reducing fecundity, and enhancing mortality. 'Castrators' steal energy but also directly modify the scheme by which hosts allocate reserve energy, shunting resources from reproduction to growth. Not surprisingly, the model predicts that this strategy should promote gigantism, but it also forecasts longer infectious periods and fecundity compensation. Thus, commonly observed characteristics of parasitic castration readily emerge from a mechanistic model of energy flow using a minimal number of assumptions. Finally, the DEB model for both 'consumers' and 'castrators' highlight that variation in resources supplied to hosts promotes variation in virulence in a given host-parasite system, holding all else equal. Such predictions highlight the potential importance of resource ecology for virulence in disease systems.

Byline: Azmy S. Ackleh (1), Linda J.S. Allen (2) Keywords: Competitive exclusion; SIR epidemic model Abstract: We study an SIR epidemic model with a variable host population size. We prove that if the model parameters satisfy certain inequalities then competition between n pathogens for a single host leads to exclusion of all pathogens except the one with the largest basic reproduction number. It is shown that a knowledge of the basic reproduction numbers is necessary but not sufficient for determining competitive exclusion. Numerical results illustrate that these inequalities are sufficient but not necessary for competitive exclusion to occur. In addition, an example is given which shows that if such inequalities are not satisfied then coexistence may occur. Author Affiliation: (1) Department of Mathematics, University of Louisiana at Lafayette, Lafayette, LA, 70504-1010, USA (2) Department of Mathematics and Statistics, Texas Tech University, Lubbock, TX, 79409-1042, USA Article History: Received Date: 10/12/2001 Online Date: 15/05/2003

Byline: Tzy-Wei Hwang (1), Yang Kuang (2) Abstract: aExperimental studies have shown that parasites can reduce host density and even drive host population to extinction. Conventional mathematical models for parasite-host interactions, while can address the host density reduction scenario, fail to explain such deterministic extinction phenomena. In order to understand the parasite induced host extinction, Ebert et al. (2000) formulated a plausible but ad hoc epidemiological microparasite model and its stochastic variation. The deterministic model, resembles a simple SI type model, predicts the existence of a globally attractive positive steady state. Their simulation of the stochastic model indicates that extinction of host is a likely outcome in some parameter regions. A careful examination of their ad hoc model suggests an alternative and plausible model assumption. With this modification, we show that the revised parasite-host model can exhibit the observed parasite induced host extinction. This finding strengthens and complements that of Ebert et al. (2000), since all continuous models are likely break down when all population densities are small. This extinction dynamics resembles that of ratio-dependent predator-prey models. We report here a complete global study of the revised parasite-host model. Biological implications and limitations of our findings are also presented. Author Affiliation: (1) Department of Mathematics, Kaohsiung Normal University, 802, Kaohsiung, Taiwan, R.O.C. Research supported by National Council of Science, Republic of China., TW (2) Department of Mathematics, Arizona state University, Tempe, AZ 85287-1804, U.S.A. e-mail: kuang@asu.edu, US Article note: Received: 30 October 2001 / Revised version: 11 February 2002 / Published online: 17 October 2002 Work is partially supported by NSF grant DMS-0077790 Mathematics Subject Classification (2000): 34C25, 34C35, 92D25. Keywords or phrases: Microparasite model -- Ratio-dependent predator-prey model -- Host extinction -- Global stability -- Biological control

An overview is presented on the element-host relationship in host genome evolution. The author argues that terms such as 'junk DNA' do not accurately reflect that relationship, and that transposable-element modeling better reflects the range of relationships on a continuum from mutualism to extreme parasitism.

The physiological and molecular aspects of viral cytopathogenesis, a by-product of host antiviral response and its countering by virus devised mechanisms, are discussed. Several models are proposed to explain the latter by incorporating transcription, RNA processing and transport, and translation as revealed by picornaviruses, influenza viruses, and rhabdoviruses

Byline: Julian Herbert (1), Valerie Isham (1) Keywords: Key words:aEpidemic model; Helminths; Parasite-induced mortality; Macroparasites; Moment closure approximations; Multivariate negative binomial distribution; AMS classification: 62P10 Abstract: aWe contribute to the discussion of causes and effects of aggregation (overdispersion) of macroparasite counts, focussing particularly upon the effects of clumped infections and parasite-induced host mortality. The simple nonlinear stochastic model for the evolution of the parasite load of a single host, investigated in Isham (1995), is extended to allow three parasite stages (larval, mature and offspring), and to allow durations of these stages to be non-exponentially distributed. As in the earlier work, exact algebraic results are possible, providing insight into the aggregation mechanisms, as long as the only source of interaction between host and parasites is an excess host mortality linearly related to the parasite load. Results are obtained on the distribution of parasite lad and on host survival. In particular, although parasite-induced host mortality is usually thought of as a process that reduces parasite aggregation (Anderson and Gordon 1982), it is shown that, for this model, parasite-induced host mortality cannot cause the index of dispersion to fall below unity. Host heterogeneity and disease control are also discussed. An approximation based on moment assumptions appropriate to a specially-constructed multivariate negative binomial distribution is proposed. This approximation, which is applicable to other processes, and an alternative based on the multivariate normal distribution are compared with exact results. Author Affiliation: (1) Department of Statistical Science, University College London, Gower Street, London WC1E 6BT, UK, GB Article note: Received: 17 December 1998 / Revised version: 2 June 1999

Resistance to parasitoids by Drosophila and its evolutionary ecology are discussed in this review article. Future work in integration of genetic, ecological, and physiological approaches to the coevolution of virulence and resistance in the system is considered. The most important natural enemies of Drosophila in field populations are parasitoid wasps, Hymenoptera species, that attack pupae or larvae. Drosophila parasitoids have numerous advantages as model organisms in behavioral and behavioral ecological studies and in those of host-parasite physiology. The parasitoids can for the most part be cultured very easily and have short generation times. Genetics of Drosophila parasitoids are still not well understood and that is a drawback. Few visual or molecular markers are available.

The Anderson and May (1980, 1981) model of insect-pathogen population cycles was extended by more closely describing the natural history of the system. This framework aims to determine if the introduction of host density dependences has an impact on the probability of limit cycle population dynamics. Density-dependent self-regulation was modeled by adding an instantaneous per capita risk of mortality that is proportional to the host population density. Findings and implications are discussed.

Byline: M. Gatto (1), G. A. De Leo (1) Keywords: Key words:aHost-parasite dynamics; Density dependence; Parasite community; Interspecific competition Abstract: aWe analyze the dynamics of a community of macroparasite species that share the same host. Our work extends an earlier framework for a host species that would grow exponentially in the absence of parasitism, to one where an uninfected host population is regulated by factors other than parasites. The model consists of one differential equation for each parasite species and a single density-dependent nonlinear equation for the host. We assume that each parasite species has a negative binomial distribution within the host and there is zero covariance between the species (exploitation competition). New threshold conditions on model parameters for the coexistence and competitive exclusion of parasite species are derived via invadibility and stability analysis of corresponding equilibria. The main finding is that the community of parasite species coexisting at the stable equilibrium is obtained by ranking the species according t! o th e minimum host density H .sup.* above which a parasite species can grow when rare: the lower H .sup.*, the higher the competitive ability. We also show that ranking according to the basic reproduction number Q .sub.0 does not in general coincide with ranking according to H .sup.*. The second result is that the type of interaction between host and parasites is crucial in determining the competitive success of a parasite species, because frequency-dependent transmission of free-living stages enhances the invading ability of a parasite species while density-dependent transmission makes a parasite very sensitive to other competing species. Finally, we show that density dependence in the host population entails a simplification of the portrait of possible outcomes with respect to previous studies, because all the cases resulting in the exponential growth of host and parasite populations are eliminated.. Author Affiliation: (1) Dipartimento di Elettronica e Informazione, Politecnico di Milano, Via Ponzio 34/5, I-20733 Milano, Italy. e-mail: gatto@elet.polimi.it, IT Article note: Received: 24 June 1996 / Revised version: 28 April 1998

Population dynamics lies at the core of ecological and evolutionary theory. It shapes the structure of communities and generates evolutionary processes, determining persistence and stability, invasion and extinction. The importance [...]

The relationship between the oviposition strategy of a parasitoid whose offspring is susceptible to attack by a hyperparasitoid and hyperparasitoid behavior was investigated. The study used a host-parasitoid-hyperparasitoid model comprised of the cabbage aphid Brevicoryne brassicae, its parasite wasp Diaeretiella rapae and the D. rapae hyperparasitoid Alloxysta victrix. The results showed that the optimal number of parasitoid eggs infecting the aphid hosts decreases with a decrease in host colony size and with a decrease in the travel time between aphid colonies. It also decreases with an increase in frequency of hyperparasitoid visits.

The relationships between calcium, adhesion and germination during the infection sequence mediated by Pythium spp. were investigated in vitro. The results showed that newly-formed zoospore cysts of P. aphanidermatum could adhere and geriminate on glass slides in the presence of calcium. Both processes could be suppressed by a calcium chelator. Based on the results, a model to explain infection of host plants is presented, which provides a central role for calcium in adhesion and germination.

The model-derived prediction that parasitoid/prey aggregation regardless of host/prey density does not destabilize host/prey populations, whereas aggregation on host/prey with high density destabilizes host/prey populations, was examined. It was suggested that the prediction be treated with caution because it is unclear which concept of aggregation was referred to - behavioral or statistical. Fruthermore, the model predictions were not robust when its underlying assumptions, which seem unrealistic, are relaxed.

Three continuous-time models of host-parasitoid interactions in which hosts and parasitoids have overlapping generations are presented. Two models follow birth, death and dispersal within patches, such that the population dynamics can be explained in terms of asynchrony in the fluctuations of the populations in each patch. The third model considers instantaneous distributions of hosts and parasitoids among patches, and population dynamics can be explained in terms of the variability in the chance that a host will be parasitized. Spatial heterogeneity and parasitoid aggregation affect population dynamics differently in each model.

Host-host-pathogen dynamics and the role of pathogens in community structure were studied using a model in which two host populations are subject to self-regulation and share the same directly transmitted pathogen. The model assumes that the hosts exhibit continuous population growth, self-regulation or intraspecific competition and settling at carrying capacity in the absence of disease. Several outcomes of the competitive interactions between the two hosts in combination with the regulatory effects of the pathogen are discussed.

Persistence, avoidance of extinction, is at the root of the most fundamental questions of ecology. All populations are threatened endogenously, by dint of the capacity for exponential growth, which can deplete resources or cause the accumulation of natural enemies. Weather is the most common exogenous threat. It is highly variable and often uncoupled from density. However, because most species are broken into subunits with some degree of linkage by dispersal, sub-populations are not autonomous. In this Special Feature, John Reeve elaborates on his discovery of the wealth of useful theory to be found in combinations of 'equilibrium' and 'spreading of risk' models of parasitoid/host interactions. These models represent concern with endogenous and exogenous threats of extinction, respectively. They have long remained fairly isolated from one another in distinct clades of theory, which treated the two classes of threats as separate phenomena. Even stronly stable interactions of parasitoid and host cannot so damp fluctuations caused by environmental variability as to completely eliminate random extinctions (Morrison and Barbosa 1987). Thus, even by extreme examples of internal equilibrium, there is much to be gained from a perspective that includes spreading of risk. Alan Hastings traces the history of theories of spatial heterogeneity in population models and comments on some of the more promising contemporary experimental work in this area. Andrew Taylor, acknowledging the potential of the catholic theoretical perspectives that include risk spreading, emphasizes the dreadful state of evidence in population dynamics. It is a field that has been long on speculation and short on hard data. We do not have much critical evidence about the bases of persistence for more than a few systems, and even our textbook examples are founded as much in imagination as in hard fact. Well-designed experimentation concerning persistence is long overdue.

The ability of cuckoo Cuculus canorus hosts to discriminate against parasitic eggs but not parasitic nestlings was explained in such a way as to make it compatible with the behavior adaptation as predicted by evolutionary theory. A model was developed which shows that while learning to recognize eggs is adaptive, learning to recognize nestlings is maladaptive. This is because in a host-parasite system wherein only the parasite nestling remains in the nest, learning to recognize the parasite nestling as the parents' own exceeds the benefit of correct learning.

Interactions between victims and enemies--between prey and predator, plant and herbivore, host and parasite, even between host and pathogen--are a central feature of all ecological communities. Even in the earliest [...]

Research is presented indicating that parasites may impact trophic cascades by influencing predator avoidance behavior in rodents. Studies showed that rodents infected with parasites which use predators as final hosts were more active and less cautious than uninfected rodents, suggesting that parasites may have an affect on rodent brain function.