Role of Group A Streptococcal Infections in TS and OCD

Grant Type
Clinical
Grant Year
2005-2006
Institution Location
NY
Institution Organization Name
New York Medical College
Investigators Name
Bessen, Debra, PhD

Group A beta-hemolytic streptococci (GABHS) are bacteria that cause common infections such as strep throat. It is well-established that in genetically predisposed individuals, a strep throat infection can trigger an autoimmune attack in the form of rheumatic fever. It is postulated that in some patients, autoimmunity may be affecting the brain causing neurological symptoms similar to Tourette Syndrome (TS) and Obsessive-Compulsive Disorder (OCD). Although controversial, because not all data are supportive, there is increasing evidence that GABHS can trigger acute exacerbations of TS and OCD. Part of the problem in establishing a clear cut relationship among TS, OCD and GABHS infection is that generally these conditions are very prevalent in children. Thus, it is difficult to prove that a temporal relationship between infection and neuropsychiatric symptoms occurs significantly more frequently than would be expected by chance alone. For this study, we hypothesize that GABHS can trigger TS and OCD, but only in a highly selective manner. Not all GABHS are alike, just as not all people are alike. GABHS display tremendous variety in a family of genes that give rise to superantigens. Humans differ from one another in their immune response genes, also known as the major histocompatibility complex (MHC), which can be distinguished by HLA-typing. The superantigens of the infecting bacteria bind directly to the MHC products of the human host and modulate the immune response. However, each superantigen can bind only to certain MHC forms. Thus, we postulate that an aberrant immune response leading to TS or OCD may occur only when a particular GABHS strain infects an individual with the “matching” HLA-type. In this study, we plan to characterize the superantigen content of each GABHS strain causing infection in neuropsychiatric patients by examining the signature left behind in their antibody response. In addition the HLA profile of each patient will be characterized and scored as to whether or not the particular GABHS infection resulted in an acute exacerbation of TS or OCD symptoms. In this way, the protective and non-protective HLA-types for each GABHS superantigen will be defined. Ultimately, this effort may establish firmly whether GABHS do indeed trigger TS and OCD symptoms. Debra Bessen, Ph.D. New York Medical College, valhalla, New York Award: $74,996 Tourette Association of America Inc. – Research Grant Award 2005-2006