The hyperacute form of allergic encephalomyelitis produced in rats without the aid of pertussis vaccine.

The hyperacute form of experimental allergic encephalomyelitis (EAE), characterized by a short incubation period, severe paralysis, high mortality, and abundant polymorphonuclear leukocytes and fibrin in the lesions, was produced in rats without the use of pertussis vaccine (previously considered an essential requirement) or Freund's adjuvant. Carbonyl iron or mineral oil without mycobacteria were effective adjuvants and whole rat spinal cord was the best antigen. Hyperacute EAE was produced in this manner in some Lewis rats, most dark agouti (DA) rats and most F1 hybrids of these two strains. Clinical signs were earlier in onset and more severe in the DA strain than in the Lewis strain in all adjuvant-antigen combinations that were tested. Dark agouti rats developed clinical signs in six days, histological lesions in five days, and localized EAE lesions could be induced in four days. The data support the hypothesis that hyperacute type lesions (neutrophils and fibrin) can be caused by an exceptionally strong immune response to neural antigen, whether that response is engendered by a particular adjuvant (pertussis vaccine) or by an unusual degree of genetic susceptibility (DA rats).