Perez v. HHS, (Fed. Cl. Spec. Mstr. Dec. 8, 2015) (Hamilton-Fieldman, SM)
In this case, Petitioner’s expert was not claiming that homology between the tetanus vaccine and myelin could cause GBS through the process of molecular mimicry, rather it was argued that a tetanus vaccine can “rev up” an individual’s innate immune system, causing the expression of toll-like receptors, that may play a role in the pathogenesis of GBS. After this revving up, the immune system “smolders” for a period of days or even weeks, before the GBS manifests.
Petitioner argued that one of the infections from which she suffered, or the prior flu vaccine she received, elicited an adaptive immune response that resulted in molecular mimicry and an attack on the myelin sheaths, but that that process did not manifest as symptomatic GBS until it was triggered by the later tetanus vaccine. The gap between tetanus vaccine and onset of GBS was almost eight weeks.
The special master was not convinced that the innate immune response somehow persists and “smolders” for an eight-week time period without triggering the adaptive immune system’s molecular mimicry process, or that the adaptive immune system’s process, once triggered, “smolders,” instead of causing symptoms of GBS within a few days or at most a few weeks, as the scientific literature would suggest. Thus, prong one was not established.
Although unnecessary to consider prongs two and three, the Court essentially concluded that a gastrointestinal virus virulent enough to bring Petitioner to the emergency room, one week prior to the onset of GBS, was a more likely cause of her GBS than a tetanus vaccine eight weeks prior.