Staphylococcus aureus Colonization Modulates Tic Expression and the Host Immune Response in a Girl with Tourette Syndrome.

摘要: A 9-year-old girl with Tourette syndrome and increased antibody levels against Streptococcus pyogenes was monitored longitudinally for the presence of nasopharyngeal bacteria, specific titers, autoimmunity directed brain antigens. Microbiological monitoring indicated that child an intermittent Staphylococcus aureus carrier. Clinical improvements in motor tic frequency severity were observed during S. colonization phase, temporally correlated downregulation anti-streptococcal anti-D1/D2 dopamine receptor production. After decolonization, clinical conditions reverted to poor scores previously observed, suggesting a possible role immune response bacterial clearance as trigger symptom recrudescence. These findings imply cause-effect relationship exists between improvement, well decolonization exacerbation. Understanding impact on host adaptive function autoantibodies pathogenesis may alter approaches managing autoimmune neuropsychiatric disorders.