Toxoplasma gondii is an obligate intracellular parasite that grows and divides inside a host cell and has no extracellular lifecycle. Toxoplasma gondii‘s importance rests upon its worldwide distribution and ability to infect almost any mammalian or avian cell. Felines (where its sexual stage occurs) are Toxoplasma gondii‘s definitive host; it lacks a vector.

The sexual stage allows for the creation of diversity and possibly more virulent strains. Toxo undergoes an asexual stage in humans with 2 forms: 1) tachyzoite (which is similar to but not exactly the same as the trophozoite so don’t mix these up) 2) bradyzoite (which is a tissue cyst similar but again not the same as the cysts formed by Giardia and Entamoeba).

Toxoplasma gondii has a haploid genome, making it amenable to loss of function mutations (achievable by chemical mutagenesis). Toxoplasma gondii can also undergo homologous recombination, making possible full knockouts of certain genes. The Toxoplasma gondii genome has been sequenced, making gene identification easier.

Humans can contract this by eating under cooked meat or cat feces. Toxoplasma gondii has a worldwide distribute, with 15-30% of Americans infected and over 70% of Europeans. Many people are already infected but because they are healthy they are asymptomatic. Toxo cause a lifelong chronic infection that is never cleared. Toxoplasma gondii only causes serious problems in immunocompromised individuals and unborn children when their mother gets a primary infection. It is the leading cause of death among AIDS patients. As an apicomplexan parasite, Toxoplasma gondii is often used as a model system because it is much easier to work with than other apicomplexan parasites such as plasmodium.

Apicoplast or plastid which has some features in common with the chloroplast and like the mitochondria and chloroplast it originated from an endosymbiotic event. The important organelles to know are the micronemes, the rhoptries, and the dense granules as these all appear to be secretory organelles that originated from the golgi (not from endosymbiosis) and they are all involved in host cell invasion. Conoid is a microtubule based tip on the parasite body (don’t worry about this one too much). Another structure to keep in mind is the inner membrane complex which is also involved in host cell invasion.

Micronemes secrete adhesive proteins that anchor in the parasite plasma membrane. The adhesive proteins attach to the host plasma membrane to mediate the initial attachment of the parasite to the host cells. Micronemes secrete additional proteins which bind the parasite’s actin-myosin motor through a parasite protein called aldolase. This connection drives motility/invasion.

Rhoptry proteins form the moving junction, which is the ring that forms around the parasite cell through which the parasite squeezes into the host cell. Rhoptry proteins also act a molecular sieve to filter out host cell transmembrane proteins from the parasite vacuole to keep the vacuole from being targeted to the lysosome.

Dense granules are involved in remodeling the parasite vacuole so the parasite can live, grow and divide within it.

Microneme proteins attach to the host cell, and also to the parasite’s actin-myosin motor. Myosin is anchored in the inner membrane complex and drives host cell invasion by the parasite. Aldolase mediates the connection between microneme proteins and the actin-myosin motor. As the parasite invades the host cell, a protease cleaves microneme adhesion proteins. This releases them from the parasite plasma membrane. Microneme protein, aldolase and protease activity is collectively the glideosome.

A yellow spot means the gene is expressed equally in both infected and uninfected cells. A red spot means the gene is induced in infected cells. If the spot is green then the gene is repressed in infected cells. Typical of a general response, proinflammatory genes are upregulated. Some other changes were induced by Toxoplasma gondii infection but they were unremarkable.