This work allowed the first characterization of the three members of the chloride channel CLC family in T.brucei. The TbCLCs are expressed in the two proliferative stages of the parasite and two of their members appear non-essential. The three TbCLCs act as chloride transporters in X.laevis oocytes and some of their biophysical properties were determined. Furthermore, TbCLC-b appeared to be involved in lysis by the human innate immunity protein apoL-1<p>A novel function of T.brucei adenylate cyclases was discovered in their ability to suppress expression of the innate immunity protein TNF-α. The suppression of the innate response occurs before the first peak of parasitemia and reduces the host ability to control the parasite.<p> / Doctorat en Sciences / info:eu-repo/semantics/nonPublished

<p><br></p> <p>Thrips, Thysanoptera, represent an ancient (~407 m.y.a.) order of ~6000 tiny insects from 9 families. Despite the small size of the order, thrips have a diversity of life histories, diets, and survival strategies. Thrips represent a challenge to fieldworkers and axonomists alike due to the morphological similarity between species and the lack of homologies between families. Recent </p> <p>molecular evidence has reopened debate over the phylogenetic relationships of the families of Thysanoptera.</p> <p>In this thesis we use genomic approaches to elucidate and clarify the early nodes in order to answer evolutionary questions about the Thysanoptera, their mitochondrion symbiotes, and their </p> <p>coevolutionary interactions with a group of economically important viruses; tospoviruses. Our results support previous ordinal hypotheses and show families in both sub-orders radiating </p> <p>around the emergence of the angiosperms ~120 m.y.a. We show that all thrips lineages likely have highly rearranged mitochondrial genomes, even on an intraspecies level, and that this rearrangement phenomena occurs very quickly in evolutionary time. We provide comment on the caution that must be taken with mitochondrial loci in any phylogenetic analysis with this new </p> <p>evidence and argue for the impact of among-site-rate-heterogeneity to be further investigated within thrips hylogenetics. We show that much more data is needed before thrips and tospovirus relationships can be fully elucidated but that two dueling hypotheses are emergent from our studies: either 5 very new separate vector/virus relationships, or one very old relationship that has been lost by the vast amount of thrips. We call for targeted taxa selection and show how new genomic methods can target certain taxa based upon the identification of </p> <p>assembled proteins from illumine shotgun read data.</p>

Artenübergreifende Interaktionen helfen uns, Krankheitsmechanismen zu verstehen und Targets für Therapien zu finden. Die Koexpression von Genen, gemessen an der mRNA-Häufigkeit, kann Interaktionen zwischen Wirt und Pathogen aufzeigen. Die RNA-Sequenzierung von Wirt und Pathogen wird als "duale RNA-Sequenzierung" bezeichnet. Malaria ist eine der am besten untersuchten parasitären Krankheiten, so dass eine Fülle von RNA-seq-Datensätzen öffentlich zugänglich ist. Die Autoren führen entweder duale RNA-seq durch, um den Wirt und den Parasiten gleichzeitig zu untersuchen, oder sie erhalten kontaminierende Sequenzierungs-Reads aus dem Nicht-Zielorganismus. Ich habe eine Meta-Analyse durchgeführt, bei diese beiden Arten von RNA-seq-Studien verwendet wurden, um über korrelierte Genexpression auf Wirt-Parasit-Interaktionen zu schließen. Ich habe Studien mit Homo sapiens, Mus musculus und Macaca mulatta als Wirte und ihre Plasmodium-Parasiten einbezogen. Ich benutzte orthologe Einzelkopien von Genen, um ein Repertoire von Interaktionen bei Malaria und in diesen Modellsystemen zu erstellen. Ich verknüpfte die Daten von 63 Plasmodium-Phasen-spezifischen Studien und reduzierte die Zahl der Interaktionen von potenziell 56 Millionen auf eine kleinere, relevantere Menge. Die Zentralität in den Netzwerken der Blutphasen konnte die Essentialität der Plasmodium-Gene erklären. Das aus den verketteten Daten sagte die Genessenzialität besser vor als die einzelnen Studien - ein Vorteil der Meta-Analyse. Neutrophile und Monozyten Immunmarkergene waren überrepräsentiert, was auf eine Fülle von phagozytären und respiratorischen Reaktionen hindeutet. Die Analyse der Leberphase ergab Wirts- und Parasitenprozesse in frühen und späten Entwicklungsphasen. Ich fand bekannte Wirt-Parasit-Interaktionen, die für beide Phasen gleich sind, sowie bisher unbekannte Interaktionen. Dieses Prinzip lässt sich auch auf andere Krankheiten anwenden, um Mechanismen und therapeutische Ziele zu verstehen. / Cross-species interactions help us understand disease mechanisms and find targets for therapy. Gene co-expression, measured by mRNA abundance, can identify host-pathogen interactions. The RNA-sequencing of host and pathogen is termed “dual RNA-sequencing”. Malaria is one of the most studied eukayotic parasitic diseases, making an abundance of RNA-seq data sets publicly available. Authors either perform dual RNA-seq to study the host and parasite simultaneously or acquire contaminant sequencing reads from the non-target organism. I performed a meta-analysis using these two kinds of RNA-seq studies to infer host-parasite interactions using correlated gene expression. I included studies of Homo sapiens, Mus musculus and Macaca mulatta as hosts and their corresponding Plasmodium parasites. I used single-copy orthologous genes to generate a repertoire of interactions in human malaria and in these model systems. I found 63 malaria RNA-seq studies. I concatenated sequencing runs from Plasmodium stage-specific studies and reduced the number of interactions from a potential 56 million to a smaller, more relevant set. Centrality in the blood stage networks was able to explain Plasmodium gene essentiality. The network from the concatenated data predicted gene essentiality better than the individual studies, indicating a benefit of the meta-analysis. Immune marker genes for neutrophils and monocytes were over-represented, suggesting an abundance of phagocytic and respiratory burst-related responses. The liver stage analysis revealed linked host and parasite processes at early stages until late developmental stages. I found linked host and parasite processes that are common to the two stages, e.g. parasite cell gliding and invasion and host response to hypoxia and immune response. I showed that existing data can be explored for new information. This principle can be applied to other diseases to understand mechanisms and therapeutic targets.

Le parasitisme est de plus en plus considéré comme un facteur écologique pouvant créer des variations dans le comportement des individus. Toutefois, la direction de causalité entre le comportement et le parasitisme reste incertaine. Les infections expérimentales sont le plus souvent réalisées en laboratoire, limitant les inférences écologiques. À l’aide d’une infection expérimentale semi-naturelle, nous avons infecté avec succès des crapets-soleils (Lepomis gibbosus) dans un lac où ils ont été exposés à une variété de vers parasites (trématodes, cestodes), permettant d’examiner les effets de la co-infection naturelle chez les hôtes. Nous avons mesuré la témérité, l’exploration et l’activité avant et après l’infection expérimentale. En utilisant une approche bayésienne, nous avons trouvé que les traits de comportement initiaux exercent une forte influence sur la susceptibilité à l’infection : les poissons les plus téméraires et/ou les moins actifs au départ ont acquis une plus grande densité de points noirs (c.-à-d. points noirs visibles sous la peau, les nageoires et dans les muscles du poisson) et de cestodes lors de l’infection. Par ailleurs, nous avons montré que la condition corporelle est réduite par la densité de cestodes, suggérant la débilitation de l’hôte. La condition corporelle était corrélée positivement avec la distance parcourue, quel que soit le statut d’infection individuel. Nous avons également trouvé une relation négative entre la distance parcourue après l’infection et la densité de trématodes, suggérant que l’infection causant la maladie des points noirs diminue le niveau d’activité des hôtes. La témérité et l'exploration n'étaient pas affectées par la densité parasitaire ou la condition corporelle. Nous suggérons que la diminution de l’activité est causée par une réponse adaptative de l’hôte, visant à rediriger son énergie pour combattre l’infection. Sachant que les points noirs ont un cycle de vie complexe et que le crapet-soleil est un hôte intermédiaire, ce changement dans le comportement de l’hôte pourrait aider le parasite à compléter sa transmission aux oiseaux-hôtes piscivores en augmentant la prédation sur les poissons infectés. Bien que nous ne puissions confirmer la direction de causalité, nos résultats montrent qu’il existe un lien étroit entre le comportement et le parasitisme. Nous suggérons que deux mécanismes peuvent simultanément agir : le comportement initial des individus influence le risque d’infection, et l’infection peut créer de la variation au niveau de la plasticité comportementale des individus. / Parasitism is increasingly seen as an ecological factor that can create variations in individual behaviour. However, the direction of causality between behaviour and parasitism remains uncertain. Experimental infections are most often conducted in laboratories, limiting ecological inferences. Using a semi-natural experimental infection, we successfully infected pumpkinseed sunfish (Lepomis gibbosus) in a lake where they were exposed to various parasitic worms (trematodes, cestodes), allowing us to examine the effects of natural co-infection in hosts. We measured boldness, exploration, and activity before and after the experimental infection. Using a Bayesian approach, we found that initial behavioural traits strongly influence infection susceptibility: initially bolder and/or less active fish acquired a higher density of black spots (i.e., visible black spots under the skin, fins, and in the fish's muscles) and cestodes during the infection. Additionally, we found that body condition was reduced by cestode density, suggesting host debilitation. Body condition was positively correlated with distance swam, regardless of individual infection status. We also found a negative relationship between distance swam after infection and trematode density, suggesting that infection causing black spot disease decreases host activity levels. Boldness and exploration were not affected by parasite density or body condition. We suggest that a decrease in activity is caused by an adaptive host response to redirect its energy to combat the infection. However, since trematode parasites have a complex life cycle and pumpkinseed sunfish are intermediate hosts, decreases in activity levels following infection may make infected fish more susceptible to predation by piscivorous birds, which is needed for trematodes to complete their life cycles. While we cannot confirm the direction of causality, our results show a close link between behaviour and parasitism. We propose that two mechanisms may simultaneously operate: the initial behaviour of individuals influences their risk of infection, and infection can create variation in behavioural plasticity of individuals.

<p dir="ltr">In this dissertation, I explore how human actions (climate change, road salt, land use change, species invasions) interact with and influence morphology, disease, and population dynamics in freshwater organisms (amphibians and aquatic crustaceans). First, I examined how the incidence and timing of disease epidemics in native species (<i>Daphnia dentifera</i>) caused by a generalist parasite (<i>Metschnikowia bicuspidata</i>) influenced the success and impact of an invasive species (<i>Daphnia lumholtzi</i>) in freshwater zooplankton (Chapter 1). In the following chapter, I explored how host-parasite interactions are affected by the interactive effects of multiple environmental stressors, focusing on American bullfrog tadpoles (<i>Lithobates catesbeianus</i>), two of their common parasites (<i>Batrachochytrium dendrobatidis</i> (<i>Bd</i>) and trematode parasites in the family Echinostomatidae), and two common stressors (fluctuating temperatures and sublethal road salt pollution; Chapter 2). Finally, I investigated how the combination of climate (temperature and precipitation) and land use (developed and/or forested area) change have influenced the body size of a common toad (Fowler’s toad, <i>Anaxyrus fowleri</i>) from 1930 – 2020 utilizing museum specimens (Chapter 3). Together, this research establishes how emerging and persistent anthropogenic environmental stressors will interact to affect morphology, disease, and population dynamics in vulnerable freshwater organisms.</p>

This thesis examines the parasite dynamics and the mechanisms affecting parasite load and transmission focalising on the role played by host and habitat heterogeneities. This study is based on the gastrointestinal nematode Heligmosomoides polygyrus and the small mammal yellow necked mouse and uses data gathered from experimental field manipulations of parasites intensities and data gathered from trapping monitoring. Initially the parasite community of yellow-necked mouse (Apodemus flavicollis) was explored in North-Eastern Italian Alps with the aim to describe the major patterns and identify the factors affecting parasite community structure. Despite the observed spatial variability it has been found that differences within the host population such age and secondly sex and breeding conditions, were the major factors acting on parasite occurrence and intensity. Habitat differences had a less apparent effect on parasite community structure. The consequences of H. polygyrus infection on other parasite species infections have been analysed, in specific the infestation of the tick Ixodes ricinus in populations of A. flavicollis. H. polygyrus load and tick infestation were monitored as well as were carried out field manipulations of H. polygyrus intensity and were monitored changes in tick infestation. It has been found that H. polygyrus load was negatively related to I. ricinus infestations. Host factors mediated the H. polygyrus-I. ricinus interaction such that young and non-breeding mice exhibited higher I. ricinus to H. polygyrus intensity respect breeding adults. The role of host sex on parasite abundance was then investigated carrying out a field experiment where the H. polygyrus intensity were manipulated in relation to mice gender. In specific, H. polygyrus was removed alternately from either sexes and the parasite load was analysed in the untreated sex. It was found that males mice were responsible to drive parasite transmission in the host population and this was observed in absence of sex-bias in parasite infection, suggesting that this pattern was not a mere consequence of quantitative differences in parasite loads between sexes. To disentangle the possible mechanism causing this sex bias in parasite transmission mathematical simulations based on parameters obtained for the field experiment were used. Two non mutually exclusive hypotheses causing sex bias in parasite transmission were tested: a- males immune response is less efficient and this causes the development of more successful parasite infective stages or b-males behaviours allow them to be more efficient is spreading in more exposed areas parasite infective stages. Multi-host models were developed and simulations were compared with field results. While it was not disentangled the most dominant mechanism causing sex bias in parasite transmission this study underlined the importance of host sexes in affecting parasite dynamics and host-parasite interaction. In conclusion this thesis highlighted the importance of considering host and environmental differences when investigating host parasite interactions. This finding could be extremely important when planning measured of disease control or to avoid disease outbreak. Controlling target group of individuals host could avoid economical losses and a more effective measure of intervention.

Made available in DSpace on 2015-07-22T20:50:11Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-01-30. Added 1 bitstream(s) on 2015-08-11T03:26:36Z : No. of bitstreams: 1 Publico-Tese%20Paloma%20Korehiza%20Maza%20versao%20final.pdf: 1568579 bytes, checksum: 8a94eab5c79046acd8162d9a949d2c36 (MD5) / Muitos patógenos são capazes de manipular a sinalização de células do hospedeiro para facilitar sua infecção. Nesta tese, demonstramos que o fungo Paracoccidioides brasiliensis promove um aumento na ativação de ERK1/2 e SFKs em células epiteliais A549 (de pulmão humano), de aproximadamente 6 e 7 vezes, respectivamente, em relação aos níveis basais. Utilizando PP2, inibidor da atividade de SFKs, e PD98059, inibidor da ativação da via ERK1/2, verificamos que a ativação de ERK1/2 é parcialmente dependente de SFKs ativadas e que provavelmente outras quinases também estão envolvidas neste evento. Além da modulação da sinalização de células do hospedeiro, diversos estudos têm demonstrado que patógenos seqüestram domínios presentes nas membranas da célula hospedeira denominados “membrane rafts”, os quais são enriquecidos em esfingolipídeos e colesterol e estão envolvidos em diversos eventos celulares, incluindo a sinalização celular. Por diferentes metodologias, como a desorganização de “membrane rafts” por drogas que extraem (metil-β- ciclodextrina, MβCD) ou que se ligam (nistatina) ao colesterol, e a localização do gangliosídeo GM1, um marcador de “membrane rafts”, utilizando a subunidade B da toxina da cólera (CTB), mostramos o envolvimento destes domínios de membranas de células epiteliais na adesão de P. brasiliensis. A partir do isolamento de membranas resistentes a detergente (DRMs) de células epiteliais após incubação com o fungo, mostramos a ativação e o deslocamento de SFKs para as frações que contêm os “membrane rafts”. Além disso, verificamos que a depleção do colesterol com MβCD inibe completamente a ativação de SFKs, corroborando a importância dos domínios de membranas para a ativação destas quinases. Os resultados apresentados nesta tese demonstram, pela primeira vez, que fungos patogênicos modulam a organização e a atividade de “membrane rafts” de células hospedeiras para o estabelecimento da infecção. / Many pathogens are able to manipulate host cell signaling in order to facilitate infection. In this thesis, we demonstrated that the fungus Paracoccidioides brasiliensis promotes an increase of ERK12 and SFK activation in A549 epithelial cells (human lung cells), by approximately 6- and 7-fold over basal levels, respectively. By using PP2, inhibitor for SFK activity, and PD98059, inhibitor for ERK1/2 activation, we verified that ERK1/2 activation is partially dependent of activated SFKs and probably other kinases are involved in this event. Besides modulation of host cell signaling, several studies have been demonstrated that pathogens hijack domains that are present in host cell membranes called membrane rafts, which are cholesterol- and sphingolipidenriched domains, that are involved in several cell events, including cell signaling. By using several approaches, such as membrane rafts disruption with cholesterolextractor (methyl-β-cyclodextrin, MβCD) or –binding (nystatin) drugs, and the localization of ganglioside GM1, a membrane raft marker, by using cholera toxin subunit B (CTB), we showed the involvement of these epithelial cell membrane domains in P. brasiliensis adhesion. By isolating detergent-resistant membrane (DRM) from epithelial cells after incubation with this fungus, we showed the activation and the dislodgment of SFKs to fractions which contain membrane rafts. Moreover, we verified that cholesteroldepletion with MβCD completely inhibits SFK activation, corroborating the importance of membrane domains in activation of these kinases.The results presented in this thesis demonstrate for the first time that pathogenic fungi may modulate the organization and activity of host cell membrane rafts for infection establishment. / TEDE / BV UNIFESP: Teses e dissertações

Les interactions intimes et répétées entre hôtes et parasites peuvent engendrer la spécialisation d’un parasite à son hôte, grâce à des adaptations comportementales, morphologiques et/ou génétiques, combinées avec un flux de gènes limité. C’est un processus clef car il participe à l’évolution de la biodiversité parasitaire et peut ainsi permettre de mieux comprendre l’émergence d’organismes pathogènes. Encore peu étudié, une spécialisation d’hôtes a néanmoins été démontré lors de précédentes études chez deux espèces de tiques nidicoles : chez Ixodes uriae une tique dure, parasite des oiseaux marins coloniaux en zone arctique, et dans un complexe de tiques molles Ornithodoros capensis sensu lato, parasitant aussi de nombreuses espèces d’oiseaux marins, mais cette fois-ci en zones tempérées et tropicales. Ces deux espèces sont vectrices d’une grande diversité d’agents pathogènes incluant des virus, des bactéries et des protozoaires. Cependant, les facteurs impliqués dans le phénomène de spécialisation d’hôte restent inconnus. Dans ce cadre, le but de ma thèse était donc de déterminer 1) si l’évolution des divergences en fonction des hôtes est toujours accompagnée par les mêmes changements phénotypiques et 2) si ces changements pourraient permettre d’identifier les facteurs de sélection sous-jacents. Dans ce contexte, des campagnes d’échantillonnage de tiques ont été menées durant la période de reproduction des hôtes oiseaux dans les différentes zones de leur répartition et nous avons réalisé des analyses morphométriques, basées sur l’utilisation de landmarks et de contours sur chaque individu tique et des analyses phylogénétiques et génétiques des populations sur les mêmes individus. L’ensemble de ces résultats suggère la présence de convergences morphologiques au sein de ces systèmes et souligne un rôle de la sélection dans ce processus de divergence. En effet, les caractéristiques écologiques des hôtes mais aussi le micro-habitat exercent des pressions sélectives importantes dans ces deux systèmes pouvant être à l’origine de la divergence observée entre les populations. De plus, les caractéristiques biologiques de chaque espèce de tiques, telle que la capacité de dispersion, entrent également en jeu et peuvent fortement modifier l’épidémiologie des agents infectieux dont elles sont vectrices.Mots clés : Argasidae, écologie de la transmission, évolution convergente, interactions hôte-parasite, Ixodidae, oiseaux marins. / Intimate and repeated interactions between hosts and parasites can lead to parasite specialization to a given host via behavioral, morphological and/or genetic adaptations that act in combination with restricted gene flow. Specialization is a key process leading to the generation of parasite biodiversity and can help us understand the emergence of pathogenic organisms. Although little studied, host specialization has already been demonstrated to occur in previous studies of two nidicolous tick species: Ixodes uriae a hard tick parasitizing colonial seabirds in polar regions, and soft ticks of the complex Ornithodoros capensis sensu lato, that also exploit colonial seabirds, but this time in temperate and tropical zones. Both of these species act as vector to a wide variety of pathogenic organisms, including viruses, bacteria and protozoa. However, the factors involved in host specialization remain unknown. In this context, the aim of my thesis was to determine 1) whether the evolution of host specialization is always accompanied by the same phenotypic changes and 2) whether these changes could help to identify the selective factors that influence this phenomenon. In this context, tick collections were conducted during the breeding period of the host birds in different areas of their distribution and morphometric analyses, based on landmark and contour methods, were performed on each individual tick. Phylogenetic and population genetic analyses were also carried out using the same individuals. Overall, the results demonstrate that morphological convergence occurs within these systems, highlighting the role of selection in the divergence process. Indeed, the ecological characteristics of the hosts, but also their micro-habitat, may exert significant selective pressures on ticks and may cause the observed divergence among populations. Likewise, the biological characteristics of each tick species, particularly in relation to dispersal capacity, may also come into play and will greatly modify the epidemiology of associated infectious agents.Keywords: Argasidae, convergent evolution, host-parasite interactions, Ixodidae, transmission ecology, seabirds.

<p>Two species of <i>Neisseria</i>, <i>N. meningitidis</i> and <i>N. gonorrhoeae</i>, are obligate human pathogens that cause meningitis and gonorrhea, respectively. Although generally asymptomatic, <i>N. meningitidis</i> can cause invasive meningococcal disease with high mortality rate. Due to emerging antibiotic resistance strains of <i>N. gonorrhoeae</i>, the Centers for Disease Control and Prevention (CDC) have designated it as an urgent threat to public health. Therefore, immediate interventions are required for fight against these Neisserial pathogens. Iron is an essential nutrient for all bacteria, including <i>Neisseria</i>. However, free iron is scarce in human, therefore, <i>Neisseria</i> have evolved to acquire iron from host proteins. These iron acquisition systems are immunogenic and important for infection and are promising therapeutic targets.</p> <p> In the host, lactoferrin sequesters free iron and limits iron availability to pathogens. However, <i>Neisseria</i> have evolved machinery to hijack iron directly from lactoferrin itself. Lactoferrin binding proteins, LbpA and LbpB, are outer membrane proteins that together orchestrate the acquisition of iron from lactoferrin. Additionally, LbpB serves an additional role in providing protection against host cationic antimicrobial peptides and innate immune response. Despite studies aimed at deciphering the roles of LbpA and LbpB, the molecular mechanisms underpinning iron acquisition and immune protection remain unknown. Here, we investigated the role of the lactoferrin binding proteins in iron acquisition and protection against cationic antimicrobial peptides. We obtained three-dimensional structures of <i>Neisseria</i> LbpA and LbpB in complex with lactoferrin using cryo-electron microscopy and X-ray crystallography. These structures show that both LbpA and LbpB bind to C-lobe of lactoferrin, albeit at distinct sites. Structural analyses show that while lactoferrin maintains its iron-bound closed conformation in the LbpB-lactoferrin complex, it undergoes a large conformational change from an iron-bound closed to an iron-free open conformation upon binding to LbpA. This observation suggest that LbpA alone can trigger the extraction of iron from lactoferrin. Our studies also provide an explanation for LbpB’s preference towards holo-lactoferrin over apo-lactoferrin and LbpA’s inability to distinguish between holo- and apo-lactoferrin. Furthermore, using mutagenesis and binding studies, we show that anionic loops in the C-lobe of LbpB contribute to binding the cationic antimicrobial peptide lactoferricin. Solution scattering studies of the LbpB-lactoferricin complex showed that LbpB undergoes a small conformational change upon peptide binding.</p> Together, our studies provide structural insights into the role of the lactoferrin binding proteins in iron acquisition and evasion of the host immune defenses. Moreover, this work lays the foundation for structure-based design of therapeutics against <i>Neisseria</i> targeting the lactoferrin binding proteins.

Pathogens and parasites are increasingly recognized as important components within host populations, communities, and ecosystems. Parasite contributions to ecosystem function most likely manifest as density-mediated impacts of parasites on their hosts, the direct contributions of parasite biomass to a system, and via parasite-induced changes in host behavior and physiology (trait-mediated impacts). Here, a framework was constructed that can be used to conceptualize parasite contributions to ecosystem function (Chapter 1). Then the influence of parasite attack on host movement was explored to further evince the mechanistic underpinnings of trait-mediated parasite impacts (Chapter 2). Additionally, mesocosms were created across a gradient of parasitism to examine how these mechanisms are likely to unfold at larger biological scales (Chapter 3). Lastly, a series of differential equations was created to model host-parasite-ecosystem interactions and generate theoretical predictions about how and when parasites are likely to influence ecosystem processes (Chapter 4). Parasites have many characteristics of ecosystem engineers, but their role has historically been ignored. These studies begin to explore the role that parasitism may have as one of the drivers of ecosystem processes.