T. gondii antibodies implicated in mania

By Lucy Piper, Senior medwireNews Reporter

Infection with Toxoplasma gondii may confer an increased risk for mania, say researchers.

They found that immunoglobulin (Ig)M antibodies to the protozoan were significantly elevated in individuals hospitalized with mania, but not in mentally healthy individuals or individuals with other psychiatric diagnoses, such as bipolar depression and recent-onset and multi-episode psychosis.

“The finding of T. gondii antibodies in adults can be the result of either infection occurring around the time of birth or infection acquired later in life,” say lead researcher Faith Dickerson (Sheppard Pratt Health System, Baltimore, Maryland, USA) and colleagues.

Although the biological mechanisms underlying the association between T. gondii infection and mania are “not known with certainty,” the team suggests they “may be related to the replication of T. gondii within the central nervous system and subsequent effect on behavior.”

At the time of hospitalization, the 57 individuals with mania were 2.33 times more likely to have levels of IgM antibody to T. gondii above the 90th percentile of those in 314 mentally healthy individuals. The difference remained significant after controlling for demographic factors known to be associated with the infection, including age, race, gender, and socioeconomic status.

Mania patients continued to have an increased risk for elevated IgM T. gondii antibodies during their hospital stay but, by the 6-month follow-up, they were no longer at an increased risk.

“It is possible that these individuals had undergone infection with or reaction to T. gondii around the time of their hospitalization with mania,” says the team. “This is consistent with the fact that the levels decreased over time.”

The researchers note in Bipolar Disorders that the inflammatory response of mania patients to T. gondii appeared to be specific to this infection, as IgG and IgM antibodies to cytomegalovirus were not elevated in these patients, despite this viral agent also being capable of infecting the central nervous system.

The inflammatory response was also specific to IgM T. gondii antibodies, with IgG antibodies not found to be elevated. This may be related to the timing of infection, suggest Dickerson et al. “IgM class antibodies generally arise earlier in the course of infection than IgG class antibodies,” they explain.

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