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Published on: January 13, 2017
Is mad cow disease caused by a bacteria?
1Med-America Research, 148-14A 11th Avenue, Whitestpme, NY 11357, USA. medamerica1@cs.com
Abstract:
Transmissible spongioform enchephalopathies (TSE's), include bovine spongiform encephalopathy (also called BSE or "mad cow disease"), Creutzfeldt-Jakob disease (CJD) in humans, and scrapie in sheep. They remain a mystery, their cause hotly debated. But between 1994 and 1996, 12 people in England came down with CJD, the human form of mad cow, and all had eaten beef from suspect cows. Current mad cow diagnosis lies solely in the detection of late appearing "prions", an acronym for hypothesized, gene-less, misfolded proteins, somehow claimed to cause the disease. Yet laboratory preparations of prions contain other things, which could include unidentified bacteria or viruses. Furthermore, the rigors of prion purification alone, might, in and of themselves, have killed the causative virus or bacteria. Therefore, even if samples appear to infect animals, it is impossible to prove that prions are causative. Manuelidis found viral-like particles, which even when separated from prions, were responsible for spongiform STE's. Subsequently, Lasmezas's study showed that 55% of mice injected with cattle BSE, and who came down with disease, had no detectable prions. Still, incredibly, prions, are held as existing TSE dogma and Heino Dringer, who did pioneer work on their nature, candidly predicts "it will turn out that the prion concept is wrong." Many animals that die of spongiform TSE's never show evidence of misfolded proteins, and Dr. Frank Bastian, of Tulane, an authority, thinks the disorder is caused by the bacterial DNA he found in this group of diseases. Recently, Roels and Walravens isolated Mycobacterium bovis it from the brain of a cow with the clinical and histopathological signs of mad cow. Moreover, epidemiologic maps of the origins and peak incidence of BSE in the UK, suggestively match those of England's areas of highest bovine tuberculosis, the Southwest, where Britain's mad cow epidemic began. The neurotoxic potential for cow tuberculosis was shown in pre-1960 England, where one quarter of all tuberculous meningitis victims suffered from Mycobacterium bovis infection. And Harley's study showed pathology identical to "mad cow" from systemic M. bovis in cattle, causing a tuberculous spongiform encephalitis. In addition to M. bovis, Mycobacterium avium subspecies paratuberculosis (fowl tuberculosis) causes Johne's disease, a problem known and neglected in cattle and sheep for almost a century, and rapidly emerging as the disease of the new millennium. Not only has M. paratuberculosis been found in human Crohn's disease, but both Crohn's and Johne's both cross-react with the antigens of cattle paratuberculosis. Furthermore, central neurologic manifestations of Crohn's disease are not unknown. There is no known disease which better fits into what is occurring in Mad Cow and the spongiform enchephalopathies than bovine tuberculosis and its blood-brain barrier penetrating, virus-like, cell-wall-deficient forms. It is for these reasons that future research needs to be aimed in this direction.
Insights
Transmissible spongiform encephalopathies (TSEs) may not be caused by prions. Research suggests bovine tuberculosis and related mycobacteria could be the actual cause of mad cow disease and similar conditions.
Area of Science:
- Veterinary Neurology
- Infectious Diseases
- Microbiology
Background:
- Transmissible spongiform encephalopathies (TSEs), including Bovine Spongiform Encephalopathy (BSE), Creutzfeldt-Jakob disease (CJD), and scrapie, remain poorly understood.
- The current diagnostic paradigm for TSEs relies on detecting late-appearing prions, hypothesized infectious proteins.
- Recent studies challenge the prion hypothesis, revealing inconsistencies and alternative findings in TSE research.
Purpose of the Study:
- To investigate alternative causative agents for Transmissible Spongiform Encephalopathies (TSEs), questioning the established prion theory.
- To explore the potential role of bacterial infections, specifically mycobacteria, in the etiology of diseases like Bovine Spongiform Encephalopathy (BSE).
- To re-evaluate diagnostic and etiological frameworks for TSEs based on emerging evidence.
Main Methods:
- Review of existing studies on TSEs, including prion purification and experimental infections.
- Analysis of research identifying viral-like particles and bacterial DNA in TSE-affected animals.
- Epidemiological correlation between BSE incidence and bovine tuberculosis prevalence in the UK.
- Histopathological examination of affected animal brains, including isolation of Mycobacterium bovis.
- Comparative analysis of TSE pathology with known effects of mycobacterial infections.
Main Results:
- Studies show that prion purification processes may eliminate causative agents, and some BSE-infected mice lacked detectable prions.
- Viral-like particles, separate from prions, have been implicated in causing spongiform encephalopathies.
- Mycobacterium bovis has been isolated from the brains of cattle exhibiting signs of BSE.
- Epidemiological data suggests a correlation between the geographic distribution of BSE and bovine tuberculosis.
- Pathological findings in cattle with systemic M. bovis infection mimic TSEs, including a tuberculous spongiform encephalitis.
- Mycobacterium avium subspecies paratuberculosis (MAP) is linked to Johne's disease in cattle and sheep and shares antigens with human Crohn's disease, which can have neurological manifestations.
Conclusions:
- The prion hypothesis for TSEs is increasingly challenged by evidence suggesting alternative infectious agents.
- Mycobacterial infections, particularly bovine tuberculosis and its variants, present a compelling alternative etiology for BSE and related spongiform diseases.
- Future research should focus on mycobacteria and their potential role in TSEs, including their cell-wall-deficient forms, to better understand and diagnose these conditions.
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