Kuru, madcow, and the TSEs

An investigation of the origins of madcow disease.

by Edward Gehrman

Part One. Kuru, a few facts.

Transmissible Spongiform Encephalopathy (TSE) is identified by the plaques of mutated amyloid protein that form within the brain tissue and destroy synapses and neurotransmitter functions and take on a characteristic sponge or Swiss cheese appearance. CJD, Scrapie and Kuru are all members of this degenerative disease family, afflictions known about for over two hundred years but not studied intently until the early sixties when they were found to be transmissible.


Dr. Carleton Gajdusek was a young researcher looking for unusual diseases when he visited the Fore Peoples of Papua, New Guinea during the late 1950s. The Papuans of those years were suffering from a population density that put a strain on very limited resources. They practiced female infanticide and cannibalism and were in a constant state of warfare with their neighbors over land and pigs. Severe limitations on normal heterosexual relations were imposed; the men spent most of their time at the men's clubhouse where they prepared for war and engaged in homosexual relations with the young boys. This homosexual activity was all part of an elaborate bonding thought needed to ensure macho warriors and dependable compatriots. The warfare was brutal, often hand-to-hand; capture meant being tortured and killed. Solidarity was essential and achieved through the sharing of semen. The females of the group were often abused because they were thought to steal the men's strength and resolve in battle. The malnourishment of females and young children was part of this intense process; they supplemented their diet by eating anything that "crawled or crept". Midwives ate placentas of the newborn and women dug up the partly decomposed bodies of relatives and ate and shared with young children the flesh, brains and the accumulations of maggots and mites. This was not a religious ceremony but an attempt to fend off malnutrition.


( This information comes from several sources. It is well known to anthropologists that these conditions existed among the Fore peoples and many other New Guinea tribes like the Samba. I know it's hard to believe in these modern times but we must if we are to understand the world in which we live. My main source is “Our Kind” by Marvin Harris; Harper & Row; 1989. He took much of his information from Shirley Lindenbaum, Kuru Sorcery: Disease and Danger in the New Guinea Highlands; 1979; Mayfield )

Gajdusek observed that some of the Fore women and a few children died from symptoms indicating a neurological disorder: dementia, frenzied behavior, blindness and eventual agonizing death. He studied the tribal dynamics and soon hypothesized that the condition, known as Kuru, came from their habit of eating the brains of dead relatives. He brought some diseased brain tissue back to the USA. Gajdusek soon discovered that when he made a broth from the Kuru tissue and injected this mixture into lab animals, they too exhibited the Kuru symptoms. He then processed Kuru diseased lab animals' brains and injected the mixture into other lab animals. They also died the same excruciating deaths. This meant that the condition could be transmitted from organism to organism and was therefore, transmissible, hence Transmissible Spongiform Encephalopathy (TSE).
Gajdusek and his colleagues at the National Institute of Health were never able to isolate or positively identify the agent that causes the TSE even though they've been trying since the early sixties. Scrapie and CJD were also studied and found to be transmissible. All this was well known underground medical information; many doctors refused to autopsy CJD victims. For years the NIH conjectured that the infective culprit was a "slow virus". Nothing seemed to destroy the agent; not heat, cold, or any of the normal chemical disinfectants. Nor could they find a trace of its chemical or molecular identity. Furthermore, the virus didn't cause inflammation so antibodies failed to leave a calling card. Some completely new agent was essential.


Part Two. Dr. Frank Bastian’s research vs. “prions”

Dr. Frank O. Bastian, MD, a professor of pathology has published numerous research articles relating to the etiology of Creutzfeldt-Jakob Disease. He also edited a book entitled Creutzfeldt-Jakob Disease and Other Transmissible Spongiform Encephalopathies. In 1976, Dr. Bastian examined a brain biopsy from a patient with CJD using electron microscopy. He saw a spiral structure foreign to the tissue. It had features of the newly reported Spiroplasma (discovered in 1976). In 1981, a team in New York also reported finding a fibril protein in scrapie-infected brain tissue. In1983, they looked at various tissues of CJD and Kuru and demonstrated scrapie-associated fibrils consistently in these diseases but not in control tissues. These SAF were identical morphologically to the internal fibrils of Spiroplasma. Moreover, antibodies to SAF react with internal fibrillar proteins from Spiroplasma and digested brain material from people with CJD, suggesting that these proteins essentially are the same. This similarity solidified in Bastian's mind the link between Spiroplasma and CJD.


Spiroplasma are present in the hemolymph of almost all insects; there probably are several million strains. They can also cause diseases in plants. They do not have a cell wall (cell wall deficient) and have among the smallest genomes of any living organism and are the smallest and perhaps the oldest life form. These bacteria are thought by many to be rather fragile, but nothing could be further from the truth. They tolerate extreme fluctuations in temperature, lay dormant in the soil for generations and survive the harshest elements; only Drano-like chemicals kill them effectively outside the body. Under normal circumstances our immune system efficiently deals with this complicated, membrane enclosed piece of DNA but Spiroplasma bind host proteins that often are of identical molecular weight to their surface proteins and, therefore, are looked at by the immune system as being the same as the host.


Bastian proved that spiroplasmas were neurotropic. When inoculated peripherally into suckling rats, spiroplasma will eventually localize to the brain tissues. The organisms will produce a persistent infection and produce a spongy change in the brain tissue of these animals. The neuropathologic changes are similar to those seen in CJD. The obvious way to look for an agent directly is by electron microscopy, but this method may not be appropriate for spiroplasma since they blend with cell membranes, blending with the background, unnoticed without an identifying marker. Developing such a marker has been difficult because spiroplasma are very fastidious (difficult to cultivate) organisms. .
Dr.Bastian insists that the infection-related protein that most researchers refer to as a "prion" is produced by the host in response to the infection and is not the causative agent. Prions are thought to be self-replicating proteins. and the cause of CJD and other TSE because researchers have found prions in brain tissue from people with CJD and brain tissue from sheep with scrapie but not in normal brain tissue. Dr. Bastian states that a shortcoming in the prion theory is that CJD and scrapie can be transmitted by brain material from which the prion has been removed with antibodies. Prion researchers have jumped to conclusions and have not considered any other possibility. It is quite possible that Spiroplasma may be inducing the formation of the prion protein to protect itself from the immune system. Investigators have reported transmitting a TSE to mice from hay mites gathered from farms in Iceland where scrapie is endemic. Dr. Bastian is virtually certain that these hay mites contain Spiroplasma, noting that the investigators have not so far found Prions in the mites.


If hay mites can cause TSE, why couldn't the same be true for the maggots and mites on the Fore corpses? Could Gajdusek have overlooked the main factor connecting Kuru to the Fore women and children? Was the initial cause of Kuru the ingesting of large quantities of maggots and mites by protein famished women and children? We know that the maggots and mites contain Spiroplasma. By eating the brains of the Papuans that died from Kuru, the Spiroplasma infection was retransmitted to those remaining, in a deadly cycle. Transmissible Spongiform Encephalopathies will continue to be misunderstood unless we begin to study and understand these simple connections.

 

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Chronic wasting disease spreads west across Wyoming

CASPER, WYO.
Chronic wasting disease is spreading west. Wildlife officials find new cases each season of the deadly illness in deer and elk moving closer and closer to the state's feedgrounds.

And recent research shows it could be a bigger deal than biologists originally thought.

"CWD is a significant concern for Wyoming's wildlife — particularly for our deer populations," said Dr. Mary Wood, state wildlife veterinarian for the Wyoming Game and Fish Department. "As prevalence increases in southeastern Wyoming, we are now seeing negative impacts in some of our deer herds from CWD."

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Is MSA a prion disease?

The fundamental cause of multiple system atrophy (MSA) is a loss of oligodendroglial and neuronal cells in the brain and central nervous system. The loss of cells is gradual and progressive, leading to slowly worsening symptoms.

Degeneration is found in three parts of the nervous system: the basal ganglia, the cerebellum, and parts of the brain that regulate the autonomic nervous system. The basal ganglia are a set of nerves in the cerebrum that in part control voluntary movements. The cerebellum also controls voluntary muscle movements and contributes to balance.

However, what triggers the initial and ongoing loss of cells is unknown.

 

Read the full article HERE.

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Gut Bacteria May Affect Parkinson's Disease

The germs living inside a person's digestive system may affect symptoms of Parkinson's disease, researchers reported Thursday.

Tests done on mice showed their symptoms worsened when they were dosed with microbes taken from human Parkinson's patients but not when they got samples from healthy patients. And other tests on mice that develop Parkinson's-like symptoms showed they only developed symptoms if they had gut germs to begin with.

 

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Doom for Scandinavia's Elk?

Earlier this summer, the first cases of chronic wasting disease (CWD), a deadly deer sickness, were registered in Europe. The sickness was first occurred in two elk in Norway, near the Swedish border. Today, major Swedish authorities and competent bodies launch a campaign to investigate whether the disease already spread itself further to affect deer animals in Sweden. According to scientists, the creatures move freely across the border to Sweden, further raising the risk of infecting their Swedish cousins.

 

Read the full article HERE.

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