The pathogenesis of<unk>  is not well understood or documented like other diseases of this nature. Even though<unk>  is a disease that results in neurological defects, its pathogenesis occurs in areas that reside outside of the nervous system. There was a strong deposition of PrPSc initially located in the ileal Peyer's patches of the small intestine. The lymphatic system has been identified in the pathogenesis of scrapie. It has not, however, been determined to be an essential part of the pathogenesis of<unk> . The Ileal Peyer's patches have been the only organ from this system that has been found to play a major role in the pathogenesis. Infectivity of the Ileal Peyer's patches has been observed as early as 4 months after inoculation. PrPSc accumulation was found to occur mostly in tangible body macrophages of the Ileal Peyer's patches. Tangible body macrophages involved in PrPSc clearance are thought to play a role in PrPSc accumulation in the Peyer's patches. Accumulation of PrPSc was also found in follicular dendritic cells; however, it was of a lesser degree. Six months after inoculation, there was no infectivity in any tissues, only that of the ileum. This led researchers to believe that the disease agent replicates here. In naturally confirmed cases, there have been no reports of infectivity in the Ileal Peyer's patches. Generally, in clinical experiments, high doses of the disease are administered. In natural cases, it was hypothesized that low doses of the agent were present, and therefore, infectivity could not be observed.
Bovine spongiform encephalopathy
Variant Creutzfeldt–Jakob disease
Creutzfeldt–Jakob disease
Powassan encephalitis
Saint Louis encephalitis
Eastern equine encephalitis
Japanese encephalitis
Viliuisk encephalomyelitis