<p>  </p> <p>Predators and parasites are critical, interconnected members of the community and have the potential to influence host populations. Predators, in particular, can have direct and indirect impacts on disease dynamics. By removing hosts and their parasites, predators alter both host and parasite populations and ultimately shape disease transmission. Our ability to accurately predict disease dynamics requires understanding the ecological effects of predation on prey and host densities and its role in the coevolution of host resistance and parasite virulence. While the impact of predators on disease dynamics has received considerable attention, research has focused on selective predation on infected prey. There is, however, substantial evidence that some predators avoid infected prey, preferentially attacking uninfected individuals. Such different strategies of prey selectivity by predators modulate host-parasite interactions, changing the fitness payoffs both for hosts and their parasites. I use empirical results and theoretical predictions as a framework to discuss the mechanisms by which predation for infected versus uninfected individuals can affect disease dynamics. First, by integrating hypotheses from behavioral ecology and disease ecology, I outlined novel perspectives that complement the prevailing view of selective predation of infected individuals (Chapter 1). Then, exploring short-term ecological outcomes and long-term host-parasite coevolution, I investigated patterns of <em>Daphnia dentifera</em> host population densities and host susceptibility over several generations under different types of predation pressure, including selective predation on infected and uninfected individuals (Chapter 2). Finally, building on the results of this research, I developed a high school project-based lesson plan that facilitates the instruction of the nature of science, implementing on-going ecological research in activities to improve student learning based on a constructivist approach to learning (Chapter 3). Together this research highlights the differential ecological and evolutionary outcomes of host-parasite interactions under varying community contexts.</p>

This thesis explores the evolution of avian influenza A viruses (IAV), as well as host-pathogen interactions between these viruses and their main reservoir host, the Mallard (Anas platyrhynchos). IAV is a genetically diverse, multi-host virus and wild birds, particularly dabbling ducks, are the natural reservoir. At our study site, up to 30% of migratory Mallards are infected with IAV during an autumn season, and host a large number of virus subtypes. IAV diversity is driven by two main mechanisms: mutation, driving genetic drift; and reassortment following co-infection, resulting in genetic shift.   Reassortment is pervasive within an autumn season, both across multiple subtypes and within a single subtype. It is a key genetic feature in long-term maintenance of common subtypes, as it allows for independent lineage turn-over, generating novel genetic constellations. I hypothesize that the decoupling of successful constellations and generation of novel annual constellations enables viruses to escape herd immunity; these genetic changes must confer antigenic change for the process to be favourable. Indeed, in an experiment utilizing vaccines, circulating viruses escaped homosubtypic immunity, resulting in the proliferation of infections with the same subtype as the vaccine. While the host plays an important role in shaping IAV evolutionary genetics, one must consider that Mallards are infected with a multitude of other microorganisms. Here, Mallards were infected with IAV, gamma coronaviruses, and avian paramyxovirus type 1 simultaneously, and we found a putative synergistic interaction between IAV and gamma coronaviruses.   Mallards occupy the interface between humans, poultry, and wild birds, and are the reservoir of IAV diversity. New incursions of highly pathogenic H5 viruses to both Europe and North America reaffirms the role of wild birds, particularly waterfowl, in diffusion of viruses spatially. Using European low pathogenic viruses and Mallard model, this thesis contributes to aspects of epidemiology, ecology, and evolutionary dynamics of waterfowl viruses, particularly IAV

Lernaeocera branchialis (Linnaeus, 1767) is a parasitic copepod possessing a complex dual-host lifecycle. The “definitive” gadoid hosts, including Gadus morhua (Atlantic cod), Melanogrammus aeglefinus (haddock) and Merlangius merlangus (whiting), are infected by the fertilised female, which penetrates the host’s ventral aorta or bulbus arteriosus whilst undertaking extensive metamorphosis and a haematophagous lifestyle. The pathogenic effects of this activity upon the host have been well documented and mortality may occur, especially when multiple parasites are present. These negative impacts on cod, particularly juveniles, by L. branchialis have the potential to adversely affect cod aquaculture in the future, and already vulnerable wild cod stocks. This PhD project therefore, investigated the immune response of wild haddock and cultured-cod post-infection by L. branchialis, and the possible mechanisms by which the parasite modulates/evades the host’s immune response. The systemic immune response of both wild haddock and cultured-cod post-infection by L. branchialis depended on the maturation stage of the parasite, and in the former host species, upon the infection intensity. Wild haddock harbouring fully metamorphosed females showed an increase in circulating thrombocytes and a decrease in serum protein levels however; if multiple mature L. branchialis were present the haddock possessed reduced circulating monocytes, and increased circulating thrombocytes and serum anti-trypsin activity. Infection by L. branchialis was also associated with a suppressive effect on haddock serum spontaneous haemolytic activity. These responses were thought to be due to the host trying to counteract the increased damage caused by the massive increase in size and the feeding of the mature parasite, which is more pronounced when multiple parasites are present, resulting in the increase in some parameters and the ‘consumption’ of others. However, the effect of parasite-derived secretions and other pathogens due to observations on wild fish could not be discounted. The laboratory-infection of cultured-cod from two different sources was also performed in order to study the immune response over time. The two groups of cod showed differences in their immune response to L. branchialis. The first group showed suppressed respiratory burst activity of phagocytes, as the parasite reached the early penella sub-stage, whilst no suppression in phagocyte respiratory burst activity was found in the second group. The parasite was found to migrate along the afferent branchial artery of the cod where a thrombus formed and was present throughout its migration into the ventral aorta. At 14 d post-infection, leukocytes expressing Interleukin 8 mRNA were observed within the free-flowing blood at the periphery of the organising thrombus within the lumen of the ventral aorta. This was speculated to aid the recruitment and activation of leukocytes to the site, and the maturation and neovascularisation of granulation tissue. The infection of the second group subsided with the death of the parasite, and none of the parasites metamorphosed past the early penella sub-stage. The live parasites infecting the first group of cod did not possess IgM or complement component C3 binding on their cuticle, however, both IgM and C3 binding occurred on the dead parasites in the second infection trial. This may highlight the importance of these opsonins and the cytotoxic effect of phagocytes in the elimination of L. branchialis by some cod. However, the first infection was terminated as the parasite reached the early penella sub-stage due to a loss of stock cod prior to the study, so the long-term success of the infection can not be concluded. Therefore, the immune response to infection needs to be determined over the entire metamorphosis of L. branchialis to determine whether the infection was successful or not, and preferably in populations with varying susceptibility to L. branchialis. This will not be possible without further studies into the resistance of different stocks of cultured-cod. Many arthropod parasites, such as ticks and salmon lice, have been previously documented to produce pharmacologically active secretions, aiding host invasion and parasite feeding, preventing the host immune response from working effectively against the parasite, all aimed at improving survival of the parasite. Therefore, the effects of the secretory/excretory products (SEPs) produced during the initial infective stage and by the mature, fully metamorphosed female on the immune response of cultured-cod in vitro, and the location of exocrine glands associated with the oral region of the parasite were investigated. The SEPs from the infective stage of the parasite were found not to affect the intracellular hydrogen peroxide (H2O2) production of phagocytes. The practical difficulties in collecting large quantities of the SEPs from the infective stage meant that their effects could not be tested on the other host immune parameters studied. The SEPs from fully metamorphosed female L. branchialis, however, had a number of suppressive effects on the host immune response in vitro including: 1) suppression of the intracellular production of cytotoxic H2O2 during the respiratory burst of phagocytic leukocytes post-PMA stimulation, 2) suppression of the production of macrophage activating factor by leukocytes with a priming effect on naïve phagocyte function, and 3) suppression of the chemo-attraction ‘power’ of zymosan activated cod serum, i.e. anaphylatoxin activity, on head kidney-derived leukocytes. These effects were dose-dependent, and highlight the capacity of L. branchialis to suppress its host’s innate immune response at the local feeding area. Further work is required to establish the mechanisms by which the parasite-derived SEPs suppress these host immune parameters, and to identify which molecules produced by the parasite are responsible. The correlation between these in vitro results, and systemic immune parameters measured from laboratory-infected Atlantic cod and wild infected haddock are discussed. Host immuno-modulation by other arthropod parasites is mediated by pharmacologically active secretions produced by exocrine glands. Therefore, the exocrine glands of the infective and fully metamorphosed female L. branchialis were also investigated in order to identify those that might be responsible for the secretion of host-modifying products. Adult female exocrine glands were mapped using diaminobenzidine (DAB), most commonly known to stain peroxidases and catalases. These compounds are known to be involved in the neutralisation of harmful free radicals which are released during the respiratory burst and tissue damage. Such products may therefore be important protective secretory components at the site of feeding / infection. Exocrine glands were located in the infective stage associated with the oral region, one pair termed the anterior gland complex (AGC), and the other pair extending either side of the oral cone termed the circum-oral glands (CG). These were further investigated using light microscopy and transmission electron microcopy. The AGC and CGs possessed multi-component secretions and they possessed secretory vesicles, abundant and highly active rough endoplasmic reticulum and Golgi apparatus suggesting that protein is an important component of the secretory products. These glands were also observed in the fully metamorphosed females where they had increased in size within the cephalothorax post-metamorphosis. It is hoped that the identification of these glandular structures, which are thought to secrete within the local vicinity of the oral cone, will aid future studies regarding the identification and secretion kinetics of parasite-derived molecules during the infection and feeding process.

The arctic is currently experiencing some of the greatest rates of warming. Newly emerging diseases in the arctic are of particular interest due to the implications these may have at southern latitudes if temperatures continue to rise around the globe. It is important to document changes in pathogen populations, such as alterations in range, virulence, prevalence, and abundance, and the effect these may have on their host populations. Parasites influence the reproductive success of their hosts in some cases. Studies on impacts of ectoparasites on avian reproductive success have generally been focused on species with altricial young. I studied the abundance of an apparently newly emerging nest-parasite and the effects of this parasite on Rosss (<i>Chen rossii</i>) and lesser snow goose (<i>Chen caerulescens caerulescens</i>) reproductive success in the Karrak Lake goose colony, Nunavut, Canada from 2001 to 2004. <p>The nest parasite, identified as the flea <i>Ceratophyllus vagabundus vagabundus</i>, was associated with goose eggs covered with spots of blood. The proportion of goose egg-shells covered by blood was positively correlated with flea abundance in the nest. This relationship allowed the use egg blood-coverage as an index of flea abundance for remaining analyses. Flea abundance in goose nests was associated with variables associated with the host and the hosts habitat. I used general linear models in conjunction with Akaikes information criterion (AIC) to determine which factors were most important in influencing flea abundance in goose nests. The most parsimonious model to explain the relationship between egg blood coverage and flea abundance in goose nests included goose clutch size, age of nest bowl (new vs. old), history of nesting by geese on a specific plot within the colony, habitat within 0.5m of nest, and year. The best predictor of flea abundance was the age of the nest bowl, with nest bowls re-used by geese containing more fleas than new bowls. This relationship was expected as fleas over-wintered in goose nests at the Karrak Lake colony.<p> Logistic regression and AIC were used to determine whether egg blood-coverage was an important variable influencing nest success. All top five models included blood-coverage. Goose nest success was negatively influenced by fleas in most years. There was a threshold of egg blood-coverage at which nest success was affected, and this threshold varied, with >20% blood indicating a significant decline in nest success in two years, and >5% blood-coverage indicating a decrease in nest success in one year. To my knowledge, this is the first study that has examined the parasites of avian nests in an arctic ecosystem and was also the first to investigate the effect of nest parasites on birds with precocial young. More research is needed to determine what factors limit this flea population and whether fleas may become a regulating factor for geese in the Karrak Lake colony.

The arctic is currently experiencing some of the greatest rates of warming. Newly emerging diseases in the arctic are of particular interest due to the implications these may have at southern latitudes if temperatures continue to rise around the globe. It is important to document changes in pathogen populations, such as alterations in range, virulence, prevalence, and abundance, and the effect these may have on their host populations. Parasites influence the reproductive success of their hosts in some cases. Studies on impacts of ectoparasites on avian reproductive success have generally been focused on species with altricial young. I studied the abundance of an apparently newly emerging nest-parasite and the effects of this parasite on Rosss (<i>Chen rossii</i>) and lesser snow goose (<i>Chen caerulescens caerulescens</i>) reproductive success in the Karrak Lake goose colony, Nunavut, Canada from 2001 to 2004. <p>The nest parasite, identified as the flea <i>Ceratophyllus vagabundus vagabundus</i>, was associated with goose eggs covered with spots of blood. The proportion of goose egg-shells covered by blood was positively correlated with flea abundance in the nest. This relationship allowed the use egg blood-coverage as an index of flea abundance for remaining analyses. Flea abundance in goose nests was associated with variables associated with the host and the hosts habitat. I used general linear models in conjunction with Akaikes information criterion (AIC) to determine which factors were most important in influencing flea abundance in goose nests. The most parsimonious model to explain the relationship between egg blood coverage and flea abundance in goose nests included goose clutch size, age of nest bowl (new vs. old), history of nesting by geese on a specific plot within the colony, habitat within 0.5m of nest, and year. The best predictor of flea abundance was the age of the nest bowl, with nest bowls re-used by geese containing more fleas than new bowls. This relationship was expected as fleas over-wintered in goose nests at the Karrak Lake colony.<p> Logistic regression and AIC were used to determine whether egg blood-coverage was an important variable influencing nest success. All top five models included blood-coverage. Goose nest success was negatively influenced by fleas in most years. There was a threshold of egg blood-coverage at which nest success was affected, and this threshold varied, with >20% blood indicating a significant decline in nest success in two years, and >5% blood-coverage indicating a decrease in nest success in one year. To my knowledge, this is the first study that has examined the parasites of avian nests in an arctic ecosystem and was also the first to investigate the effect of nest parasites on birds with precocial young. More research is needed to determine what factors limit this flea population and whether fleas may become a regulating factor for geese in the Karrak Lake colony.

Protozoa of the Leishmania genus are transmitted between mammalian hosts by the sandfly and cause the neglected tropical disease leishmaniasis. Upon injection into the mammalian host by the sandfly promastigote-form parasites are phagocytosed by macrophages, where they differentiate into amastigotes. Although many virulence factors are known to modulate macrophage signalling pathways to favour infection, the delivery mechanisms are largely unknown. During differentiation to amastigotes the promastigote flagellum shortens dramatically and the fate of the excess flagellar membrane is unknown. Here we investigate the possibility that during Leishmania mexicana differentiation, shedding of the flagellar membrane is a source of extracellular vesicles (EVs) which provide a virulence factor delivery mechanism. The kinetics and structural mechanisms of EV release from promastigotes were investigated by live cell imaging and by measuring the concentration of shed EVs. Isolated EVs from a differentiating parasite culture or a control promastigote parasite culture were analysed by fluorescence and electron microscopy and mass spectrometry. To study the biological effects of EVs, macrophages were exposed to isolated EVs or live promastigotes and cytokine secretion was quantified by ELISA. An LPG1 null mutant was used to assess the contribution of virulence factor lipophosphoglycan (LPG) to the observed effects. Known protein virulence factors and LPG are present in L. mexicana EV fractions as well as known flagellar proteins. We show that there is a link between L. mexicana flagellar shortening and EV release, which is a recently discovered phenomenon in Chlamydomonas and mammalian cell research. We find that isolated EVs and live promastigotes induce changes in secreted cytokine levels from human and murine macrophages, including a substantial and previously unreported suppression of CXCL10, a chemokine which plays a protective role in Leishmania infection. LPG contributes to the effects observed on cytokine production, and EVs may be an important delivery mechanism for LPG.

Les filaires sont des nématodes parasites transmis à des vertébrés par des arthropodes hématophages. Les espèces filariennes qui s'installent dans les cavités cœlomiques, les vaisseaux lymphatiques ou des tissus conjonctifs ont leurs stades infestants (ou L3) qui migrent via le système lymphatique après leur inoculation dans la peau. En utilisant le modèle murin avec la filaire Litomosoides sigmodontis dont les adultes résident dans la cavité pleurale, deux phases d'interaction des filaires avec les poumons des souris BALB/c sont décrites 1) lors de la migration des L3 de la peau à la cavité pleurale ; 2) pendant la phase patente de l’infection quand les adultes pondent des microfilaires dans la cavité pleurale. Dans la 1ère phase les L3 rejoignent le système sanguin pulmonaire puis traversent les poumons pour entrer dans la cavité pleurale. Ce passage induit une pathologie aigue transitoire: tout d'abord des hémorragies consécutives à la rupture des capillaires pulmonaires, accompagnées d'une augmentation du nombre de neutrophiles pulmonaires et de la libération transitoire d'IL-1β et des alarmines IL-33 et S100A9 dans la cavité pleurale. Le S100A9 semble faciliter la survie des filaires, soit par un effet anti-inflammatoire soit en facilitant la migration des L3. Les neutrophiles peuvent libérer des NETS en réponse aux L3. Dans les jours suivant l'infection, une réponse régulatrice se met en place dans les poumons, avec le recrutement de macrophages et d'éosinophiles, la production d'IL-4, de CCL2 et d'IL9, ainsi que la baisse d'expression de molécules inflammatoires. La formation des granulomes est également observée dans le tissu pulmonaire. Le passage des L3 induit aussi une inflammation des vaisseaux sanguins pulmonaires chez les souris C57BL/6 seulement. Lors de la phase patente de l'infection, 40% des souris ne développent pas de microfilarémie sanguine. La comparaison des réponses des souris microfilarienne et amicrofilarienne montre une exacerbation de l'inflammation pleurale induite par les microfilaires. De plus, les souris microfilarémiques développent une pathologie pulmonaire dépendant des microfilaires consistant en la fibrose de la plèvre viscérale, une accumulation périvasculaire de macrophages et une inflammation bronchoalvéolaire (production de mucus et éosinophilie). Le contrôle des filaires (adultes et microfilaires), mais aussi la mise en place de la pathologie sont dépendantes de l'IL-5 et de l'IL-4R. / Filariae are parasitic nematodes transmited to vertebrates by haematophagous arthropods. The filarial species that settle in the coelomic cavities, the lymphatic vessels or the connective tissues have their infectious stages (or L3) which migrate via the lymphatic system after their inoculation into the skin. Using the murine model with the filaria Litomosoides sigmodontis, whose adults reside in the pleural cavity, two phases of interaction between filariae and the lung of BALB/c mice are described 1) during the L3 migration from the skin to the pleural cavity ; 2) during the patent phase of infection, when adults realease microfilariae in the pleural cavity. During the 1st phase L3 join the pulmonary blood system and then cross through the lungs to enter the pleural cavity. This passage induces a transient acute pathology: first haemorrhages following the rupture of the pulmonary capillaries, together with an increase in the number of pulmonary neutrophils and the transient release of IL-1β and the alarmins IL-33 and S100A9 in the pleural cavity. S100A9 appears to facilitate the survival of the filariae either by an anti-inflammatory effect or by facilitating the migration of L3. Neutrophils can release NETs in response to L3. Within days following the infection, a regulatory response takes place in the lungs, with recruitment of macrophages and eosinophils, production of IL-4, CCL2 and IL-9, and downregulation of inflammatory molecules. The formation of granulomas is also observed in pulmonary tissue. The passage of L3 also induces an inflammation of pulmonary blood vessels, in C57BL/6 mice only. During the patent phase of the infection, 40% of the mice do not develop blood microfilaraemia. Comparison of responses of microfilaremic and amicrofilaremic mice shows an exacerbation of pleural inflammation induced by microfilariae. In addition, microfilaremic mice develop microfilaria-dependent pulmonary pathology consisting on fibrosis of the visceral pleura, perivascular accumulation of macrophages and bronchoalveolar inflammation (mucus production and eosinophilia). The control of the filariae (adults and microfilariae), but also the establishment of the pathology are dependent on IL-5 and IL-4R.

Orientador: Louis Bernard Klaczko / Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia / Made available in DSpace on 2018-08-22T19:31:56Z (GMT). No. of bitstreams: 1 Ventura_IuriMatteuzzo_M.pdf: 2580161 bytes, checksum: ec78d3ac3a9cb1dcb0d410ab56b4d99c (MD5) Previous issue date: 2013 / Resumo: O resumo poderá ser visualizado no texto completo da tese digital / Abstract: The abstract is available with the full electronic document / Mestrado / Genetica Animal e Evolução / Mestre em Genética e Biologia Molecular

La spécialisation des parasites vis-à-vis de leur(s) hôte(s) et la formation de races d'hôtes sont des processus évolutifs clés dans le maintien et l'émergence de la diversité au sein des populations de parasites. Notre objectif était d'étudier ces processus chez Ixodes uriae, une tique d'oiseaux marins présentant une vaste distribution géographique et une large diversité d'hôtes, afin de mieux comprendre le rôle relatif des contraintes liées à l'hôte et aux facteurs géographiques dans l'évolution et la diversification de ce parasite. Cette question a été abordée à travers différentes approches réunissant des analyses de génétique des populations et de phylogéographie, des analyses morphologiques et une approche expérimentale sur le terrain. Les résultats obtenus montrent que le facteur spatial joue un rôle important dans la diversification d'I. uriae puisque quatre grands groupes géographiques génétiquement isolés ont été identifiés. L'évolution de races d'hôtes est également un processus récurrent de l'évolution d'I. uriae, même si la divergence entre races est plus ou moins marquée d'une région à l'autre. L'évolution des races semble impliquer une préférence d'hôte chez la tique ainsi que des contraintes adaptatives liées à l'hôte, de type mécanique ou physiologique (e.g., bec des oiseaux, digestion du sang, réponse immunitaire). L'ensemble des résultats est cohérent avec la notion d'évolution en mosaïque géographique qui prédit que les interactions entre espèces peuvent évoluer de manière différente dans un contexte spatial hétérogène ; ce qui souligne l'importance des caractéristiques écologiques des hôtes dans la diversification de la tique I. uriae. D'après nos résultats et ceux de différents collègues, la spécialisation d'hôte pourrait s'avérer être un processus commun chez les tiques et donc avoir de profondes implications épidémiologiques et évolutives pour les pathogènes qu'elles transmettent. / Host specialization and host-race formation may be key processes in maintaining and generating diversity within parasite populations. The objective of this thesis was to analyze these processes in the seabird tick Ixodes uriae, a common and widely distributed ectoparasite that exploits a great diversity of seabird host species, to better understand the relative role of host-related constraints and geographic factors in its evolution and diversification. I addressed this question using different approaches, including population genetic and phylogeographic analyses, morphometry and field experimentation. Results show that the spatial factor is a key component in shaping the diversity of I. uriae, as four geographical genetically isolated groups exist within the global distribution of this parasite. The formation of host races is also a general process in the evolution of I. uriae, but has evolved to different degrees in different geographical regions. Host preference in the tick, along with mechanical or physiological host-related constraints (e.g., beak morphology, blood digestion, immune response) are likely involved in the evolution of I. uriae host races. Overall, results fall in line with the geographic mosaic theory of evolution that predicts that the outcome of species interactions can vary across geographic landscapes, highlighting the role played by ecological characteristics of the host in the diversification of I. uriae. Given results to date, host specialization may be a common process in tick systems and thus may have strong epidemiological and evolutionary implications for the pathogens that they transmit.

Co-evolution between parasites and their hosts result in extremely well-orchestrated and intimate relationships that are characterized by remarkable adaptations in the attack response of the parasite and the defense response of the host. To fully understand host-parasite interactions, these adaptations must be considered in the context of the ecological constraints in which they evolved. As a serious pest to salmon mariculture, Lepeophtheirus salmonis has been extensively studied; however, there are still several areas that require further research. Of utmost importance, and the topic of this thesis, is molecular basis for resistance to sea lice. The following chapters investigate this phenomena under the umbrella of ecological immunology using combined modern technologies of transcriptomics, proteomics and functional immunology with a focus on the primary interaction site. In the first chapter, I describe the key players involved in this host-parasite relationship with a focus on the primary interaction site, the louse-salmon interface, where there are responses by the louse (attack) and the salmon host (defense). Previous research indicated that an early aggressive inflammatory response at the louse-skin interface contributes to resistance in coho salmon; however, there are no data characterizing a site-specific response in resistant (pink and coho) and susceptible (Atlantic, chum) species. Accordingly in Chapter 2, I define site-specific cutaneous responses in Atlantic, pink and chum salmon to establish genetic biomarkers of resistance. Chapter 3 focuses on identification of cellular effectors using histochemical localization of biomarkers to characterize cellular populations activated at the louse-attachment site, while broadening the gene targets. Our notion of pink salmon as a resistant species is challenged by the common observation of migrating pink salmon supporting large populations of L. salmonis in the field. Thus the purpose of chapter 4 was to investigate potential mechanisms to explain variations in susceptibility as a function of life history. Host-parasite relationships are a product of both host and parasite responses; therefore, in chapters 5 and 6, I shift focus to the level of the parasite. In chapter 5 I present the first documented large-scale transcriptomic profiling of L. salmonis during feeding on both resistant (coho) and susceptible (Atlantic, sockeye) salmon. This was followed (chapter 6) by describing the proteomic profile of L. salmonis secretions after feeding on Atlantic salmon. In the seventh and final chapter, I present my conclusions on the molecular mechanisms for resistance to sea lice and discuss potential applications of this information for future louse control strategies. / Graduate