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fab 1 2012- dr. olivier.docx

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McGill University
Microbiology and Immun (Sci)
MIMM 413

stWednesday February 1 2012 Microbial Evasion Strategy Capture and engulfment within the cell The phagosome creates small molecules that will migrate and render the mature phagosome more adapted to kill pathogens that are usually entrapped Some pathogens are able to escape howeverEvade from phagosomes T gondii infects both nonphagocytic and phagocytic cells Once inside in the phagosome if cells are activated with gamma IFN or other cytokines the parasite is killed If the cells are not activated the parasites are inside and can block fusion with the lysosome therefore there is no phagolysosome With T cruzi it will grow in the cytoplasm therefore evading molecules that makes its survival impossibleLeighmania Can survive inside the phagosome During the initial stage as the promastigote enters it will be surrounded by the phagosome At that point LPG molecule at the surface of the cell reduces the interaction between the phagosome and the lysosome therefore phagolysisome formation is retarded Therefore the parasite can turn into the amastigote and survive very easily inside the phagosome until it leaves the macrophage to invade other cellsOne way that the parasite is able to survive acidic pH remember at this point the pH of the phagosome is down to 4555 is by turning on a pump that regulates its own internal pHToxoplasma gondii infection You can see live parasites inside the cell and also dead parasites destroyed in the macrophage inside the phagosome can be seen Avoidance of Humoral and Cellular Immune Responses by Parasites Parasites find different ways to avoid the immune system here we have 4 examples T brucei is extracellular and swims freely in the blood At that body Ab would be important to control infection with this parasite Therefore the means of evasion is antigenic variationPlasmodium is in RBC a way to protect itself from the extracellular milieu Ab attack when they do escape and they are opsonised and internalized by macrophages to kill them Cellmediated immunity may play a role but it is not clear For T cruzi this lives in the macrophage permitting it to avoid Ab but Ab still has some action on it But it is mainly the cell mediated immunity that is important especially during the chronic phase to avoid the spreading of the parasites to other cells With Leishmania this is fully intracellular so Ab has very limited action not important at all Cell mediated immunity cytokines gamma IFN etc permit T cells to secrete cytokines
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