Route of T. gondii infection
In this patient, the T. gondii infection was probably acquired by hunting. Toxoplasma gondii is an intracellular protozoan, and cats are the definitive host. Cats become infected by ingesting cysts from the tissue
of intermediate hosts (usually rodents).2 After ingestion, encysted bradyzoites transform into tachyzoites and undergo the sexual phase of their life cycle in the
feline intestine. This phase occurs when oocysts are shed in the feces.14
People may become infected by ingesting or inhaling the oocysts in cat feces or by ingesting undercooked red meat. Most cats
become infected through hunting and will shed oocysts after initial infection for less than three weeks.9 Litter boxes should be cleaned out daily as it takes 24 hours for oocysts to sporulate and become infective. By the time
a cat shows signs of toxoplasmosis, it is no longer shedding oocysts.
Prevalence of T. gondii infection and clinical signs
It is estimated that about 30% of people and cats have been exposed to T. gondii in the United States.9 However, immunocompetent people are generally asymptomatic. Studies have shown no direct correlation between human toxoplasmosis
and cat ownership.9
Some studies have shown that as many as 74% of cats with uveitis are seropositive for T. gondii depending on the geographic area.18 Uveitis may occur in healthy cats recently exposed to T. gondii; it is unknown why some develop ocular pathology while others do not. The severity of disease is thought to be associated
with a host's ability to mount a proper cell-mediated immune response, the severity of the primary infection, and the T. gondii strain.19 Neonatal T. gondii infection can cause transient anterior uveitis and, more commonly, chorioretinitis in kittens; it is unknown what role infection
in utero plays in chronic or recurrent uveitis in adult cats.18
Clinical signs of T. gondii infection vary in cats: in one study of 100 cats, 36 had multiorgan involvement, 26 had mostly pulmonary signs, 16 had abdominal
involvement, and seven had neurologic signs.20
If T. gondii infection is present, a complete blood count may reveal nonregenerative anemia and leukocytosis. A serum chemistry profile
could reveal hypoalbuminemia, hyperglobulinemia, or elevated alanine transaminase, alkaline phosphatase, aspartate transaminase,
or creatine kinase activity.9 A fecal examination may show oocysts if the cat is actively shedding. However, serum antibody testing is necessary to confirm
The cat in this case had a high normal globulin concentration and a lymphocytosis, but it was the high IgM concentrations
against T. gondii that confirmed the diagnosis. Since IgM is not detectable nine weeks after infection, high IgM concentrations indicate recent
infection.4 A positive IgM titer or a fourfold increase in IgG titers verifies recent infection.
The cat's IgG concentrations were indicative of either exposure or infection. IgG antibodies develop about two weeks after
infection; they may remain elevated for years even in healthy animals. About 53% of healthy cats have tested positive for
IgG antibodies to Toxoplasma species.7 Thus, high IgG titers do not prove recent or active infection. Conversely, studies have shown that a positive IgM titer
was present in only 1.2% of healthy cats.21 After exposure in experimentally infected cats, a peak rise in IgG titers was reached in two to three weeks.9 Ideally, this cat's IgG titer would have been rechecked two to three weeks later to document a rise in convalescent titers.
PCR testing to detect the Toxoplasma species DNA in the aqueous humor may also have confirmed the diagnosis.2 However, the clients declined further testing.