Title : A novel extreme thermoacidophilic bacterium (spiroplasma sp.) is the cause of CJD and other TSES
Abstract:
Creutzfeldt Jakob disease (CJD) is a fatal transmissible spongiform encephalopathy (TSE) similar to diseases occurring in animals. Management of these diseases has been a disaster over the past fifty years since there has been total reliance on a flawed theory regarding pathogenesis. Since the transmissible agent possessed unusual biologic properties including survival after significant radiation, boiling, autoclaving and formalin treatment, the idea of a replicating protein arose despite the irrationality of the concept. The theory would not have happened if the Archaea microbes had been known at the time since they possess similar extreme biologic properties. However the novelty of the ‘prion theory’ despite lack of supporting data caught on and the idea became dogma consuming all research funds. THE RESULT WAS ESSENTIALY NO PROGRESS OVER THE PAST FIFTY YEARS. Not a problem when only a few CJD patients died of the disease, but the problem became more apparent when the faulty science was applied to handling the outbreak of Chronic Wasting disease (CWD) in deer. Our laboratory has over this same time-period shown presence of a novel bacterium in TSE-affected tissues. The microbe was first demonstrated by electron microscopy in a CJD brain biopsy (Bastian, 1979), then by molecular means such as Polymerase Chain Reaction (PCR). More recently we have isolated the microbe from 100% of TSE-affected tissue samples. It is noteworthy that unique fibrillar proteins discovered by negative stain electron microscopy (TEM) in synaptosomal fractions from ultracentrifuged disrupted TSE tissues is a biological marker of TSE infection. These ultrastructural unique fibril proteins are referred to as scrapie associated fibrils (SAF). SAF ARE FOUND IN 100% OF TSE-AFFECTED TISSUES. The SAF fibril proteins are identical to fibril proteins seen by negative stain electron microscopy (TEM) in disrupted novel Spiroplasma sp. It is noteworthy that rabbit sera specific for SAF has immune reacted with internal Spiroplasma fibril proteins, which are part of the mechanism of locomotion for this microbe. We and others have grown this novel bacterium from 100 % of TSE-affected tissues in Brucella media of low oxygen tension and as subsurface colonies on agar plates made with that culture medium. We have shown that this novel TSE isolate possesses the identical biologic properties attributed to the transmissible agent of the TSEs. We have confirmed Koch’s postulates of causality in our animal inoculation experiments. We are proceeding to fully characterize this microbe, which we believe to be the causal agent of CJD and the other TSEs. Currently our laboratory is planning to develop accurate live diagnostic tests for the TSEs based upon detection of this novel microbe and potentially develop a cure for these now lethal conditions. An accurate live diagnostic test for CWD would be extremely important in handling the ongoing panzootic CWD infection in deer.
Audience Take Away Notes:
- Audience will better understand why we have not solved this problem.
- It is important to realize that there is no such a mechanism as replicating protein and the infection of CJD is more conventional
- Those involved in management of these diseases either medical or wild life will be more encouraged that the problem can be solved
- The misinformation of the prion theory will show others that there may be other possibilities of research on the disease
- This revelation will show a wrong approach could disable the progress in resolving an issue such as TSE
- It is interesting how to compare research showing presence of a bacterium vs an unsupported theory suggesting the presence of a replicating protein. For example, the one experiment that has been put forward to support the prion theory is that if you remove the normal prion isoform on the surface of cells, you can prevent TSE. However, Japanese researchers have showll that the surface prion normal isoform serves as a receptor for Brucella bacterium. Thus if you remove the receptor protein for a bacterium, you cannot produce the disease. Presumably Spiro plasma sp. uses the prion receptor.
- Future research based upon the bacterium will lead to resolution of the problem with development of diagnostic tests and therapies
