Abstract

We appreciate the compliments from Alvarenga et al about our recently published article on the topic of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).1 We, in turn, want to acknowledge their group for leadership in the investigation of a possible link between rheumatic fever (RF) and obsessive-compulsive disorder (OCD). In discussing a possible etiologic role of group A β-hemolytic streptococcus (GABHS) for OCD or tics, we think that it is critical to not mix information about the RF-related condition and PANDAS, because they may well be very different conditions. PANDAS has been specifically presented as a nonrheumatological entity, with patients having no history of RF and no evidence of the sequelae of RF such as cardiac valvular abnormalities.2 It is PANDAS that our study addressed.We are unable to fully disagree with the conclusion of Alvarenga et al that “GABHS may still have a major role in PANDAS,” because as we pointed out, our study was designed to examine the relationship between acute GABHS infection and exacerbations of PANDAS but not the onset of PANDAS. Our results strongly indicate that GABHS infection does not have a major role in exacerbations. The fact that our findings contradict one of the major constructs of the PANDAS hypothesis raises the possibility that GABHS has no etiologic role, but we did not investigate its possible role in onset. We noted that Perrin et al3 followed a large number of children presenting with sore throat in a community pediatrics practice and found no evidence that those whose cultures were positive for GABHS were more likely to develop tics or OCD over the next few months. These findings cast doubt on an etiologic role of GABHS in PANDAS onset.We agree that further research on the relationship between RF and development of OCD or tics is rational. However, it may not be relevant to the controversy surrounding the veracity of the PANDAS hypothesis.

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