Brains and Brawn: Toxoplasma Infections of the Central Nervous System and Skeletal Muscle

Toxoplasma gondii is a widespread parasitic pathogen that infects over a third of the world's population. Following an acute infection, the parasite can persist within its mammalian host as intraneuronal or intramuscular cysts. Cysts will occasionally reactivate, and – depending on the host's immune status and site of reactivation – encephalitis or myositis can develop. Because these diseases have high levels of morbidity and can be lethal, it is important to understand how Toxoplasma traffics to these tissues, how the immune response controls parasite burden and contributes to tissue damage, and what mechanisms underlie neurological and muscular pathologies that toxoplasmosis patients present with. This review aims to summarize recent important developments addressing these critical topics. Toxoplasma gondii establishes a chronic infection state in the brain and skeletal muscle of its mammalian host. Toxoplasma crosses the blood–brain barrier as either extracellular tachyzoites that infect and replicate within brain endothelial cells or within an infected monocyte. There is limited understanding of how Toxoplasma infections of the brain and skeletal muscle and the resulting inflammation impacts the tissues’ function. Recent studies have revealed that Toxoplasma alters both excitatory and inhibitory neurotransmission in the central nervous system and that these changes lead to unbalanced synaptic activity and seizures. Regulatory T cells have a pathogenic role in Toxoplasma-infected skeletal muscle.