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Parasites need a host body and the haematophagous insect triatomine (descriptions "assassin bug", "cone-nose bug", and "kissing bug") is the major vector in accord with a mechanism of infection. The triatomine likes the nests of vertebrate animals for shelter, where it bites and sucks blood for food.
When an intracellular parasite goes to enter a host cell, it is particular about the type of host cell. This is because most intracellular parasites are able to infect only a few different cell types. [21] Viruses use a number of host receptors to gain entry to the cell, usually by causing endocytosis. [7]
During the initial weeks of infection, parasite replication is brought under control by the production of antibodies and activation of the host's inflammatory response, particularly cells that target intracellular pathogens such as NK cells and macrophages, driven by inflammation-signaling molecules like TNF-α and IFN-γ. [2]
Parasite life cycles involving only one host are called "direct"; those with a definitive host (where the parasite reproduces sexually) and at least one intermediate host are called "indirect". [12] [13] An endoparasite lives inside the host's body; an ectoparasite lives outside, on the host's surface. [14]
Dividing T. gondii parasites. Toxoplasma gondii (/ ˈ t ɒ k s ə ˌ p l æ z m ə ˈ ɡ ɒ n d i. aɪ,-iː /) is a species of parasitic alveolate that causes toxoplasmosis. [3] Found worldwide, T. gondii is capable of infecting virtually all warm-blooded animals, [4]: 1 but felids are the only known definitive hosts in which the parasite may undergo sexual reproduction.
E. histolytica induces tissue damage by three main events: direct host cell death, inflammation, and parasite invasion. Once the trophozoites are excysted in the terminal ileum region, they colonize the large bowel, remaining on the surface of the mucus layer and feeding on bacteria and food particles.
This parasite is multi-cellular, and capable of movement. They have numerous rear mucosal projections, which assumedly assist propulsion through the thin layer of skin on the inside of the human host's mouth. They also have an excretory system possessing lateral canals. This parasite eats epithelial cells.
In their Parasite Immunology article on worms and viral infections, Kamal et al. explain why some parasitic worms aggravate the immune response. [13] Because parasitic worms often induce Th2 cells and lead to suppressed Th1 cells, problems arise when Th1 cells are needed. [13] Such cases occur with viral diseases. [13]
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