Step 1: Recall the basic biology of Toxoplasma gondii infection.
Toxoplasma gondii is an intracellular protozoan parasite. Infection in an immunocompetent host is usually mild or completely silent, and the parasite then persists as dormant tissue cysts for life, kept in check by the immune system.
Step 2: Check the claim that adult infections are mainly symptomatic.
In reality, the large majority of adult toxoplasma infections, roughly 80 to 90%, are asymptomatic or produce only mild, flu-like symptoms that often go unnoticed. Only a minority develop clear symptoms like lymphadenopathy or fever. So the statement "adult infections are mainly symptomatic" is NOT true, it is the reverse of what actually happens.
Step 3: Check the IgG and congenital infection claim.
Maternal IgG crosses the placenta, so a newborn will show positive IgG regardless of true infection at birth. But if that IgG persists beyond the time maternal antibody should have cleared (typically beyond about 12 months), it points to the infant's own ongoing antibody production, which supports a diagnosis of congenital infection. In that sense, tracking IgG over time is a genuine and accepted part of diagnosing congenital toxoplasmosis.
Step 4: Check the transmission and encephalitis claims.
Congenital toxoplasmosis passes from mother to fetus, so the transmission chain of the most clinically important form of the disease runs person to person rather than directly involving an animal reservoir at that step. Toxoplasma encephalitis is seen most often in immunocompromised patients such as those with AIDS, from reactivation of a dormant infection, but rare cases have also been reported in immunocompetent people, so this statement is accepted as true.
Step 5: Final conclusion.
The statement that fails is the one about symptoms, since most adult toxoplasma infections are actually silent, not symptomatic.
\[ \boxed{\text{Adult infections are mainly symptomatic (this is false)}} \]