Welkom bij het Lymeforum

Malaria en Toxoplasmose behoren tot de groep van Apicomplexa. Deze groep, die geheel bestaat uit parasiet organismen, delen een gemeenschappelijke eiwit genaamd AMA1.(....)
Isabelle Tardieux aan het Institut Cochin, en Markus Meissner aan de Universiteit van Glasgow, hebben net aangetoond dat Plasmodium falciparum en Toxoplasma gondii kunnen overleven en zich vermenigvuldigen in de geïnfecteerde cellen helemaal zonder de actie van AMA1. Deze ontdekking zal een belangrijke impact hebben op de zoektocht naar een behandeling voor malaria en toxoplasmose

Gebrek enzymen voor sterol synthese, de intracellulaire protozoan Toxoplasma gondii scavenges cholesterol uit gastheercellen om te vermenigvuldigen

T. gondii survival mechanisms[edit]

Once the parasite T. gondii infects a normal host cell, it resists damage caused by the host’s immune system, as well as changing the host's immune processes.

One way is by an anti-apoptotic mechanism, allowing the infected host cells to persist and replicate. One method of apoptosis resistance is by disrupting pro-apoptosis effector proteins, such as Bax and Bak.[22] In order to disrupt these proteins, T. gondii causes conformational changes to the proteins.[22] These conformational changes result in the inability of the proteins to be transported to various cellular compartments and initiate apoptosis events. T. gondii does not, however, cause downregulation of the pro-apoptosis effector proteins.[22]

T. gondii also has the ability to initiate autophagy of the host’s cells.[23] This leads to a decrease in healthy, uninfected cells, and consequently less host cells to attack the infected cells. Research by Wang et al finds that infected cells lead to higher levels of autophagosomes in normal and infected cells.[23] Their research reveals that T. gondii causes host cell autophagy using a calcium-dependent pathway.[23] Another study suggests that the parasite can directly affect calcium being released from calcium stores, which are important for the signalling processes of cells.[22]

The mechanisms above are very important ways in which T. gondii is able to persist in a host causing many serious problems for the host. Some limiting factors for the plasmid is that its effects on the host cells seem to thrive in a weak immune system and be dosage dependant, so a large number of T. gondii must be present per host cell to have a more severe effect.[24] The effect on the host also relies on the host having a weakened immune system. Immunocompetent individuals do not normally show severe symptoms or any at all, while fatality or severe complications can result in immunocompromised individuals.[24]

Als ik zoek op Toxoplasmose kom ik dus kattenpoep tegen

(.....) Transmission by bloodsucking arthropods ( arthropods zijn teken) has been postulated bij several investigators,
and a few experimental attempts have been made to test various arthropods as vectors. References to the
pertinent literature are included in the bibliographies of Weyer (1951), Pickarski (1950), Blanc, Bruneau, and Chabaud (1950)
and Jacobs (1953).
This article summarizes the results of an extensive series of experiments which
were made to test a number of arthropods (17 species) as possible vectors of Toxoplasma gondii (.....)