The natural infection of final host (FH) and intermediate host (IH) happens per os, i.e. by feeding either an infected IH or feeding contaminated gras. The heteroxenic live cycle is based on a predator and prey, i.e. a carnivor and herbivor relation. The FH sheds the infecive stages (oocysts) by its faeces. Coprophagous insects (flies, beetles) transform the macrofaeces of the predator into microfaeces of the insects dispersing the infective stages without development on the graslands where the herbivores feed. The initial tissue contact of T. gondii with its FH and IH happens with the intestinal epithelium to be paased and followed by phagocytation by macrophages (IH) or division and gamogonia in the epithelium cells Avoiting passage of epithelium and shedding oocysts by faeces (FH). In short: intraperitoneal injection bypasses the immune apparatus of the IH and the sporozoites multiplicate in the peritoneal fluid without activation of the immune response by the primary intial tissue contact. That is a general feature of heteroxenic eukaryotic parasites particularly necessary when FH and IH have the same immune apparatus in order to distinguish the two categories of hosts (hypotheis by Peter Wenk).  

Thanks Dear professor Peter Wenk, according to the article published in 2001 with title of “Acute Toxoplasmosis Leads to Lethal Overproduction of Th1 Cytokines1” death mechanism is relate to extremely elevated levels of Th1 cytokines in the serum, including IFNγ, TNFα, IL-12, and IL-18. Extensive liver damage and lymphoid degeneration accompanied the elevated levels of cytokines produced during lethal infection and overstimulation of immune responses lead to death in experimentally infected mice intraperitoneal with RH strain.

Is it true?