The way in which<unk> s induce<unk> al changes in hosts has been compared to the way a neurobiologist would effect a similar change in a lab. A scientist may stimulate a certain pathway in order to produce a specific<unk> , such as increased appetite or lowered anxiety;<unk> s also produce specific<unk> al changes in their hosts, but rather than stimulate specific neurological pathways, they appear to target broader areas of the central nervous system. While the proximate mechanisms underlying this broad targeting have not been fully characterized, two mechanisms used by<unk> s to alter<unk>  in vertebrate hosts have been identified: infection of the central nervous system and altered neurochemical communication. Infection of the central nervous system Some<unk> s alter host<unk>  by infecting neurons in the host's central nervous system. The host's central nervous system responds to the<unk>  as it would to any other infection. The hallmarks of such response include local inflammation and the release of chemicals such as cytokines. The immune response itself is responsible for induced<unk> al changes in many cases of<unk> c infection.<unk> s that are known to induce<unk> al changes through central nervous system inflammation in their hosts include Toxoplasma gondii in rats, Trypanosoma cruzi in mice and Plasmodium mexicanum in the Mexican lizard. Toxoplasma gondii induces<unk> ral changes in rats by infecting central nervous system neurons. While some<unk> s exploit their hosts' typical immune responses, others seem to alter the immune response itself. For example, the typical immune response in rodents is characterized by heightened anxiety. Infection with Toxoplasma gondii inhibits this response, increasing the risk of predation by T. gondiis subsequent hosts. Research suggests that the inhibited anxiety-response could be the result of immunological damage to the limbic system. Altered neurochemical communication<unk> s that induce<unk> al changes in their hosts often exploit the regulation of social<unk>  in the brain. Social<unk>  is regulated by neurotransmitters, such as dopamine and serotonin, in the emotional centers of the brain – primarily the amygdala and the hypothalamus, and although<unk> s may be capable of stimulating specific neurochemical pathways to induce<unk> al changes, evidence suggests that they alter neurochemical communication through broad rather than specific targeting. For example, Toxoplasma gondii attaches to the hypothalamus rather than target a specific cellular pathway; this broad targeting leads to a widespread increase in host dopamine levels, which may in turn account for the loss of aversion to cat odor. In some cases, T. gondii is believed to cause increases in dopamine levels by secreting another compound, L-Dopa, which may trigger a rise in dopamine levels, though concrete evidence for this mechanism has not yet been demonstrated. This rise in dopamine levels induces a loss of aversion to cat odor in the rats, increasing the risk of predation by cats, T. gondiis definitive host. The mechanistic details underlying the increase in dopamine levels and the way it affects the rat's<unk> al change remain elusive. The emerald cockroach wasp alters<unk>  through the injection of venom directly into the host's brain, causing hypokinesia. This is achieved by a reduction in dopamine and octopamine activity, which affects the transmission of interneurons involved in the escape response; so while the host's brain circuitry responsible for movement control is still functional – and indeed it will slog along when pulled by the wasp – the nervous system is in a depressed state. Put differently: the wasp's toxin affects not the host's ability to move, but its motivation to do so. The original function of such secretions may have been to suppress the immune system of the host, as described above. The trematode Schistosoma mansoni secretes opioid peptides into the host's bloodstream, influencing both its immune response and neural function. Other sources suggest a possible origin in molecular mimicry. Other mechanisms Mermithid nematodes infect arthropods, residing in their haemocoel (circulatory cavity) and manipulating their hemolymph osmolality to trigger water-seeking<unk> . The means by which they do so are unknown.
Behavior-altering parasite
Carcinogenic parasite
Parasitic worm
Soil-transmitted helminthiasis
Food contaminant
Human parasite
Tick infestation
Clonally transmissible cancer