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Last Revised June, 1998

Ed Gherman

Spiroplasma & Transmissible Spongiform Encephalopathies

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 Papau, 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 disrespected and often abused because they were thought to steal the men's strength and resolve in battle as well as their vital semen. 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 new born 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. (1)

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 positivly 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 distroy 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 inflamation so antibodies failed to leave a calling card. Some completely new agent was essential.

Another tenacious TSE researcher is Dr. Frank O. Bastian, MD, a professor of pathology and director of neuropathology at the University of South Alabama, Mobile. He has published numerous research articles relating to the etiology of Creutzfeldt-Jakob Disease and also edited a book entitled Creutzfeldt-Jakob Disease and Other Transmissible Spongiform Encephalopathies.(2)

In 1976, 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 spiroplasmas (spiroplasmas were only discovered in 1976). In 1981, a team in New York reported finding a fibril protein in scrapie-infected brain tissue. This scrapie-associated fibril (SAF) protein was 4 nm in diameter and 200 nm long. In 1983, the team 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 spiroplasmas.

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 spiroplasmas and CJD.

Dr. Bastian has postulated that Spiroplasma bacteria causes CJD and other TSE. His twenty years of research indicates a role for Spiroplasma. The evidence includes the following: spiroplasma-like inclusions were seen in brain biopsies from patients with CJD (Arch Pathol Lab Med. 1979;103:665-669); spiroplasma internal fibril proteins are identical morphologically to those seen in TSE's; the spiroplasma proteins show immunological cross reactivity with the TSE proteins (J Clin Biol. 1987;25:2430-2431); and spiroplasma, when inoculated into rodents, produces a similar neuropathology (Amer J Pathol. 1984;114:496-514). Spiroplasmas are present in the hemolymph of almost all insects; there probably are several million strains. They can also cause diseases in plants but are usually associated with a vector. For example, a leaf hopper carries a spiroplasma that infects orange trees Spiroplasmas are similar to mycoplasmas. They do not have a cell wall (cell wall deficient) and have among the smallest genomes of any living organism. Mycoplasma are the smallest and perhaps the oldest life form. These bacteria, one cause of "walking pneumonia", 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. A common phenomenon among the mycoplasmas is that the organisms 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. The spiralin protein on the surface of spiroplasmas shows a migration pattern on gel electrophoresis with a molecular weight of 27,000 Da to 30,000 Da, similar to that of the prion protein. This biochemical similarity is compatible with spiroplasma etiology.

Bastian was able to show that spiroplasmas were neurotropic. When inoculated peripherally into suckling rats, they 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. Spiroplasmas are also within the size range of the agent that transmits CJD and other transmissible Spongiform encephalopathies. Spiroplasmas will pass through a 50 nm-pore filter. The transmissible agent's size has been determined to be 42 nm.

The obvious way to look for an agent directly is by electron microscopy, but this method may not be appropriate for spiroplasmas. Spiroplasmas are similar to mycoplasmas, and it is a well-known phenomenon that mycoplasmas are able to blend with cell membranes. What happens, possibly, is that spiroplasmas essentially fuse with host-cell organelle membranes, thereby blending with the background, so you would not see it unless you had a marker to label it. Developing such a marker has been difficult because spiroplasmas are very fastidious (difficult to cultivate)organisms. .

Bastian also inoculated suckling rats with spiroplasmas, and examined their brain tissues by electron microscopy early in the infection process; he documented the organisms in the tissues. They appeared as membrane-bound forms, except for the one instance where he observed the spiral form. Later in infection, when he knew that the tissues were infectious by broth culture, he couldn't find any evidence of spiroplasmas by looking at the tissues extensively with electron microscopy. 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. Some researchers believe prions are the cause of CJD and related illnesses because they have found prions in brain tissue from people with CJD and sheep with scrapie but not in normal brain tissue. Bastian states that a shortcoming in the prion theory is that CJD and scrapie can be transmitted without prions.

Brain material from which the prion has been removed with antibodies can still infect animals. Moreover, the prion has been found in unrelated disease processes, such as Kawsaski syndrome and inclusion body myositis. Prion researchers have jumped to conclusions and have not considered any other possibility. It is quite possible that spiroplasmas may be inducing the formation of the prion protein to protect itself from the immune system. The immune system is very important in the pathogenesis of CJD. The agent replicates in the spleen and lymph nodes and occasionally causes an immunologic reaction. Auto-antibodies are characteristically seen in the late stages of experimental and naturally occurring disease. The gene for the host protein is located on the chromosome in the region of the major histocompatibility complex (MHC) in the mouse. "Occasionally, you see elevation of immuno globulins; there are morphological alterations of the leukocytes; there is leukopenia," Bastian explains, "and auto antibodies are characteristically seen in the late stages of both experimental and naturally occurring infection. There is partial MHC restriction in both human and animal disease."

"The immune reaction seen in these Spongiform diseases can be explained by super antigen activity, Bastian says. He notes that, normally, an antigen is presented to the cell surface in the MHC and interacts with the T-cell receptor—the antigen lying in a groove in the T-cell-MHC sets in motion the standard reaction. A super antigen, on the other hand, binds outside the groove of the T-cell and interacts with the MHC. This results in some immunoglobulin production, but only transiently. The major effect is clonal deletion of T cells, resulting in a state of immune tolerance. Autoantibodies can also form. In Spongiform diseases, PrP presumably acts as a super antigen. It is noteworthy that inclusion body myositis, a condition in which prions are seen, is an established super antigen disease."

Dr. Bastian also notes that investigators have reported transmitting a TSE to mice from hay mites gathered from farms in Iceland where scrapie is endemic (Lancet. 1996;347:1114). He is virtually certain that these hay mites contain spiroplasma, noting that the investigators have not so far found PrP 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? (3) 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 disease (Spiroplasma) 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.



(1) 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 Sambia. 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  back to text

(2) JAMA August 14, 1996 DC Capital Conference spring 1996 A dissenting view on the cause of Mad Cow Disease Bastian regards the prion theory as a red herring. The cause of Transmissible Spongiform Encephalopathies (TSEs), he says, is a conventional microorganism -- a mollicute or, more specifically, a spiroplasma. "The infection-related protein is produced by the host in response to the infection,".  back to text

[Infectious Disease News Homepage] (June 1996) Spiroplasma may cause Creutzfeldt-Jakob Disease - An interview with a leading expert in infectious diseases, Frank O. Bastian, MD. In 1992, Bastian arranged an international symposium on bovine Spongiform Encephalopathy.

I used information, quotes, and descriptions from the above article and interview to weave together Dr Bastian's ideas, knowledge and words, with my own research. I edited and rearranged both words and sequence for coherence sake. I did the best I could to convey this important message.

I've had three phone conversations with Dr Bastian. He was cooperative and helpful at first and sent me much useful information which I have included. But he cut a scheduled interview short when I began to suggest that biowarfare research might help to spread the TSE agent, inadvertently. I called one more time and he refused to talk. He has refused to answer a long letter I wrote. I thought it both rude and arrogant, but even with that nonsense, I still believe Bastian's elegant hypothesis is far more rational than any I've studied.

(3) Common arthropods occuring on dead bodies: The Acari, or mites as they also are called, are small organisms, usually less than a mm in lenght. Mites occur under the dead body in the soil, during the later stages of decay. Many mites are transported to the body via other insects, such as flies or beetles. Other mites are soil dwelling forms which can be predators, fungus feeders or detritus feeders. Most species will be found in soil samples from seepage area under the body. Sarchophagidae Among the Sarcophagids we find the large flesh-flies with red eyes and a grey-checkered abdomen. These flies does not deposit eggs, but larvae on the corpse. They are, together with the Calliphorids, among the first insects to arrive at the corpse. The larvae are predators on blowfly larvae, as well as carrion feeders. Many Sarcophagids are feeding on snails and earthworms.

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