addition to diphtheria and tetanus toxoids, making it difficult to determine which vaccine, if any, could have been the precipitating event. These publications did not contribute to the weight of mechanistic evidence.
Described below is one publication reporting clinical, diagnostic, or experimental evidence that contributed to the weight of mechanistic evidence.
Lopez-Pison and colleagues (2004) described a 14-year-old girl diagnosed with ADEM 7 to 20 days after receiving a tetanus toxoid vaccine. Eight years prior the patient developed neurological symptoms 15 days after receiving a diphtheria toxoid, tetanus toxoid, whole cell pertussis vaccine, and an oral polio vaccine.
Weight of Mechanistic Evidence
The publication described above did not present clinical evidence sufficient for the committee to conclude the tetanus toxoid vaccine may be a contributing cause of ADEM. The symptoms described in the publications referenced above are consistent with those leading to a diagnosis of ADEM, but the only evidence that could be attributed to the vaccine was recurrence of symptoms upon vaccine rechallenge. Autoantibodies, T cells, and molecular mimicry may contribute to the symptoms of ADEM; however, the publications did not provide evidence linking these mechanisms to diphtheria toxoid–, tetanus toxoid–, or acellular pertussis–containing vaccine.
The committee assesses the mechanistic evidence regarding an association between tetanus toxoid vaccine and ADEM as weak based on one case.
The committee assesses the mechanistic evidence regarding an association between diphtheria toxoid or acellular pertussis vaccine and ADEM as lacking.
Conclusion 10.7: The evidence is inadequate to accept or reject a causal relationship between diphtheria toxoid–, tetanus toxoid–, or acellular pertussis–containing vaccine and ADEM.
No studies were identified in the literature for the committee to evaluate the risk of transverse myelitis after the administration of vaccines con-