Background J-HR manifested mainly by fever and headache is associated with a transient rise in circulating TNF-α and other proinflammatory cytokines. Different types of headaches or AM precipitated by various diseases or medications and eventually caused by liberation of endotoxin-like substances from a lysed cell wall of the killed tachyzoites meet criteria of this reaction. The aim of this study was therefore to focus on the pathomechanisms that may be responsible for these clinical features.
Methods Literature data were selected to illustrate that latent CNS T. gondii infection/inflammation intensity and/or host defense mechanisms may be affected by change in the mechanisms mediated by an IFN-γ responsive gene family, production of various cytokines, NO, tryptophan degradation by indoleamine 2,3-dioxygenase, limiting the availability of intracellular iron to T. gondii, generation of reactive oxygen species (ROS), and finally cause headache or meningitis.
Results Examples of various triggers revealing headaches or AM that were caused, at least in part, by increases in the circulating cytokines characteristic for the J-HR include: HIV-1 infection (TNF-α, IL-1, IL-4, IL-6, IL-8, IL-10), obesity (TNF-α, IL-1β, IL-6, leptin), iron deficiency anemia (TNF-α, IL-6), ibuprofen (TNF-α, IL-1β, IL-2, IL-6, IFN-γ), (rHGH treatment (TNF-α, INF-γ, IL-1β, IL-2, IL-6, IL-12; beacuse of severe headaches Molozowski et al. even suggested that therapy with rHGH in GH deficient subjects should be started from the lowest recommended dose), cholesterol contained in debris from ruptured epidermoid cysts (TNF-α, IL-6, IL-8).
Conclusion Headaches and aseptic meningitis may be features of the J-HR in CT.