avior. Manipulative parasites commonly occupy the body cavity, muscles and central nervous systems of their hosts. Acanthocephalans in the data set differed from other taxa in that they occurred exclusively in the body cavity of invertebrates. In addition, they were more likely to alter microhabitat choice than activity. Parasites in the body cavity (across parasite types) were more likely to be associated with increased host contact with predators. Parasites can manipulate the host through energetic drain, but most parasites use more sophisticated means. For instance, parasites target four physiological systems that shape behavior in both invertebrates and vertebrates: neural, endocrine, neuromodulatory and immunomodulatory. The interconnections between these systems make it difficult to isolate specific mechanisms of host behavioral manipulation.
Parasite-induced alterations of sensorimotor pathways in gammarids: collateral damage of neuroinflammation?TOXOPLASMOSIS
Some larval helminths alter the behavior of their intermediate hosts in ways that favor the predation of infected hosts, thus enhancing trophic transmission. Gammarids (Crustacea: Amphipoda) offer unique advantages for the study of the proximate factors mediating parasite-induced behavioral changes. Indeed, amphipods infected by distantly related worms (acanthocephalans, cestodes and trematodes) encysted in different microhabitats within their hosts (hemocoel, brain) present comparable, chronic, behavioral pathologies. In order to evaluate the potential connection between behavioral disturbances and immune responses in parasitized gammarids, this Review surveys the literature bearing on sensorimotor pathway dysfunctions in infected hosts, on the involvement of the neuromodulator serotonin in altered responses to environmental stimuli, and on systemic and neural innate immunity in arthropods. Hemocyte concentration and phenoloxidase activity associated with melanotic encapsulation are depressed in acanthocephalan-manipulated gammarids. However, other components of the arsenal deployed by crustaceans against pathogens have not yet been investigated in helminth-infected gammarids. Members of the Toll family of receptors, cytokines such as tumor necrosis factors (TNFs), and the free radical nitric oxide are all implicated in neuroimmune responses in crustaceans. Across animal phyla, these molecules and their neuroinflammatory signaling pathways are touted for their dual beneficial and deleterious properties. Thus, it is argued that neuroinflammation might mediate the biochemical events upstream of the serotonergic dysfunction observed in manipulated gammarids – a parsimonious hypothesis that could explain the common behavioral pathology induced by distantly related parasites, both hemocoelian and cerebral.
The significance of cerebral toxocariasis: a model system for exploring the link between brain involvement, behaviour and the immune response
Toxocara canis is a parasitic nematode that infects canines worldwide, and as a consequence of the widespread environmental dissemination of its ova in host faeces, other abnormal hosts including mice and humans are exposed to infection. In such abnormal or paratenic hosts, the immature third-stage larvae undergo a somatic migration through the organs of the body but fail to reach maturity as adult worms in the intestine. The presence of the migrating larvae contributes to pathology that is dependent upon the intensity of infection and the location of the larvae. A phenomenon of potential public health significance in humans and of ecological significance in mice is that T. canis larvae exhibit neurotrophic behaviour, which results in a greater concentration of parasites in the brain, as infection progresses. Toxocara larval burdens vary between individual outbred mice receiving the same inocula, suggesting a role for immunity in the establishment of cerebral infection. Although the systemic immune response to T. canis has been widely reported, the immune response in the brain has received little attention. Differential 