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Post by skyship on Dec 14, 2011 19:13:36 GMT -5
What is the EIS?.......CDC seems to recruit folks from there.
CDC worker molesting dogs and children? What a Ploy, she is back to work........
Seems they are above the laws of humanity.
As is the EIS.......
Lymes and Plague being worked on in the 50's.......
More coming out in a minute.
skyship
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Post by skyship on Dec 14, 2011 19:19:14 GMT -5
Isolation of Rickettsia parkeri and identification of a novel spotted fever group Melanie Reber Frequent Contributor (1K+ posts) Member # 3707 posted 03-19-2010 Isolation of Rickettsia parkeri and identification of a novel spotted fever group Rickettsia sp. from Gulf Coast ticks (Amblyomma maculatum) in the United States. Until recently, Amblyomma maculatum, (the Gulf Coast tick), has garnered little attention relative to other species of human-biting ticks in the United States. A. maculatum is now recognized as the principal vector of Rickettsia parkeri, a pathogenic spotted fever group rickettsia (SFGR) that causes an eschar-associated illness in humans that resembles Rocky Mountain spotted fever. A novel SFGR, distinct from other recognized Rickettsia spp., has also been detected recently in A. maculatum specimens collected from several regions of the southeastern United States. In this study, 198 questing adult Gulf Coast ticks were collected from 4 locations in Florida and Mississippi; 28% were infected with R. parkeri and 3% with a novel SFGR. Seventeen isolates of R. parkeri were cultivated in Vero E6 cells from individual specimens of A. maculatum; however, all attempts to isolate the novel SFGR were unsuccessful. Partial genetic characterization of the novel SFGR revealed identity with several recently described, incompletely characterized, and non-cultivated SFGR including Candidatus 'Rickettsia andeanae' and Rickettsia sp. 'Argentina', detected in several species of Neotropical ticks from Argentina and Peru. hese findings suggest that each of these 'novel' rickettsiae represent the same species. Our study expands considerably the number of low-passage, A. maculatum-derived isolates of R. parkeri, and characterizes a second and sympatrically distributed Rickettsia sp. found in Gulf Coast ticks. Yes, this is very interesting in that it verifies debilitating diseases other than 'Lyme' found in tick species other than the most cited culprits. TBDs are so rarely only a manifestation of Bb! The National Lyme Disease Memorial Park Project www.lymememorial.orgPosts: 6799 | From California | Registered: Mar 2003 == A. maculatum is now recognized as the principal vector of Rickettsia parkeri, a pathogenic spotted fever group rickettsia (SFGR) that causes an eschar-associated illness in humans that resembles Rocky Mountain spotted fever. A novel SFGR, distinct from other recognized Rickettsia spp., has also been detected recently in A. maculatum specimens collected from several regions of the southeastern United States. In this study, 198 questing adult Gulf Coast ticks were collected from 4 locations in Florida and Mississippi; 28% were infected with R. parkeri and 3% with a novel SFGR. www.mdjunction.com/forums/lyme-disease-support-forums/studies-research/1339239-3510-isolation-of-rickettsia-parkeri-gulf-tickLymes was used in bioweapons.................. skyship
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Post by skyship on Dec 14, 2011 19:23:51 GMT -5
There are other organisms on the UN list not generally associated, in the public mind, with biowarfare, and it could be argued that the UN was simply being extra cautious by casting a wide net. However, whether Lyme bacteria were present in Iraq at that time or not, they certainly are today, and US Army manuals warn soldiers to protect themselves from the disease [xlii] If we are to accept the traditional Steerite explanation for the rise of Lyme – that it is a natural consequence of a recent population explosion of deer due to reforestation, combined suburbanisation, bringing humans into contact with forests – then the presence of Lyme in the dusty sand dunes of Iraq seems perverse. And what of the doctors of the opposing camp, those associated with ILADS? ILADS doctors and researchers increasingly find themselves persecuted, victims of spurious charges made against them to Medical Boards, and are hounded out of their professions. At the time of writing, paediatrician Dr Charles Ray Jones, credited by thousands of parents with restoring the health of their disabled children, is under trial, accused of misconduct. A few years ago, Dr Lida Mattman, a Nobel Prize nominee who worked on an alternative culture medium for Lyme, was ordered to shut down operations by police who arrived at her lab with handcuffs. Used in first Gulf War? ?? You bet.......... made in 80s, sold to Iraq? Was in the bioweapons we created? CIA knew all about it. more coming........
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Post by skyship on Dec 14, 2011 19:29:30 GMT -5
Same tick carrying the B. moyo
Blaming Japan? America created it in a lab......Barbour...........Steere.......covered? calling it all kinds of things.
"Lyme is often complicated by the presence of co-infecting diseases in the same tick, e.g. those caused by the microbes of babesia, bartonella, mycoplasma (believed by some researchers to be the cause of Gulf War illness), ehrlichia, microfilaria and encephalitis viruses. Investigations into some of these, too, have been led by American biowar experts.
It could be argued that some of these Lyme researchers have been awarded biowar-related grants simply because they are Infectious Disease specialists, which is a natural terrain from which to recruit. After all, research budgets for biowar have ballooned massively since the anthrax attacks of 2001; there is a demand for large numbers of personnel to work on such projects.
Well, there are two things that could be said here. First, researchers who have spent much or most of their careers studying a “hard-to-catch, easily-cured” disease would not appear to be the best choice as recipients of this type of grant, unless the “easily-cured” disease had some relation to biowarfare. Second, while some infectious disease specialists began to study biowarfare organisms for the first time after 2001, this is not necessarily the case with the Steerites. Klempner, for example, was studying ways to increase the virulence of Yersinia pestis, the causative agent of plague, over 20 years ago [xxxix]; Barbour researched anthrax for the Army in the 1970’s. [xl]"..............
Skyship
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Post by skyship on Dec 14, 2011 19:33:19 GMT -5
...................
History of Lyme Disease as a Bioweapon
Lyme is a Biowarfare Issue
A BRIEF HISTORY BY ELENA COOK
Introduction The world of Lyme disease medicine is split into two camps – the US government-backed “Steere camp”, which maintains the disease is hard-to-catch, easily cured, and rarely causes chronic neurological damage, and the “ILADS camp”, which maintains the opposite. The Steere camp is intricately bound up with the American biowarfare establishment, as well as with giant insurance and other corporate interests with a stake in the issue. The ILADS doctors lack such connections, but are supported instead by tens of thousands of patients rallying behind them.
Because the Steere camp has been massively funded and promoted by federal agencies, its view has dominated Lyme medicine not just in the US, but across much of the world. The result has been suffering on a grand scale. Below is a concise history of the military aspects of this cover-up.
- - - -
Weapons of Mass Infection The development of biological weapons has never been confined to dictatorships or “rogue” regimes. During the Second World War America, Britain and Canada collaborated closely on developing offensive bioweapons, and offensive research continued as an openly acknowledged activity of the US scientific establishment during the Cold War. Only in 1972 was this work banned by international treaty. Meanwhile the Maryland-based labs at Fort Detrick, for example, had produced millions of mosquitoes, ticks and other vectors for the purpose of spreading lethal germs. The island of Gruinard, off the coast of Scotland, was only declared habitable again in 1990, nearly fifty years after the British first contaminated it during anthrax experiments. [ii]
Ticks, which vector Lyme disease, have been studied as biowarfare instruments for decades. Such well-known biowar agents as tularaemia and Q-fever are tick-borne. The Borrelia genus of bacteria, which encompasses the Borrelia burgdorferi species-group (to which Lyme disease is attributed), was studied by the infamous WW2 Japanese biowar Unit 731, who carried out horrific experiments on prisoners in Manchuria, including dissection of live human beings. [iii] Unit 731 also worked on a number of other tick-borne pathogens.
After the war, the butchers of Unit 731 were shielded from prosecution by the US authorities, who wanted their expertise for the Cold War. [iv] The US government also protected and recruited German Nazi bioweaponeers under the aegis of the top-secret Operation Paperclip. [v]
Borreliosis, or infection with microbes belonging to the borrelia genus, had been dreaded during the Second World War as a cause of the often-fatal disease relapsing fever. The new post-war era of penicillin meant that many bacterial infections could now be easily cured. However, borrelia were known for their ability to adopt different forms under conditions of stress (such as exposure to antibiotics). Shedding their outer wall, (which is the target of penicillin and related drugs), they could ward off attack and continue to exist in the body.
Lyme disease is not usually fatal, and it is sometimes argued that, with rapidly lethal agents like smallpox and plague available, an army would have no interest in it. However, what is important to understand here is that incapacitating or “non-lethal” bioweapons are a major part of biowarfare R&D[vi], and have been for decades. For example, during the Second World War, brucellosis, chronically disabling but not usually fatal, was a major preoccupation. Military strategists understand that disabling an enemy’s soldiers can sometimes cause more damage than killing them, as large amount of resources are then tied up in caring for the casualties. An efficient incapacitating weapon dispersed over a civilian population could destroy a country’s economy and infrastructure without firing a shot. People would either be too sick to work, or too busy looking after those who were.
The EIS and the “Discovery” of Lyme Modern Lyme history begins in 1975 when a mother in the town of Old Lyme, Connecticut reported the outbreak of a strange, multi-system disease. The town lies directly opposite the Plum Island biowarfare research lab where, according to former Justice official John Loftus, Nazi scientists brought to the US after WW2 may have test-dropped “poison ticks”. [vii] It should be noted that Loftus’ reputation for gathering accurate, hard-hitting information is strong – strong enough to bring down in disgrace the former Chancellor of Austria and Secretary-General of the UN Kurt Waldheim, after the latter’s wartime SS record was revealed.
While it’s not yet known if Plum Island experimented on Lyme-causing borrelia, the lab’s directors openly admitted to Michael Carroll, author of a recently-published book which is endorsed by two former State Governors, that they kept “tick colonies”. The “hard tick” Amblyomma americanum, a known carrier of Borrelia burgdorferi, was one of the subjects of the Island’s experiments. [viii]This tick is not the one most commonly associated with transmitting Borrelia burgdorferi, but it is implicated in harbouring Borrelia lonestari, believed to be the cause of a “Lyme-like illness” in the American south. [ix]
Now compare to article 2010........and Until recently, Amblyomma maculatum, (the Gulf Coast tick), has garnered little attention relative to other species of human-biting ticks in the United States.
reply post 1.
Skyship
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Post by skyship on Dec 14, 2011 19:36:28 GMT -5
Amblyomma maculatum, (the Gulf Coast tick) Why is it in IRAQ and in AMERICA? Gulf Coast Ticks (Amblyomma maculatum) and Rickettsia parkeri, United States John W. Sumner*, Lance A. Durden†, Jerome Goddard‡, Ellen Y. Stromdahl§, Kerry L. Clark¶, Will K. Reeves*, and Christopher D. Paddock Author affiliations: *Centers for Disease Control and Prevention, Atlanta, GA, USA; †Georgia Southern University, Statesboro, GA, USA; ‡Mississippi Department of Health, Jackson, Mississippi, USA; §US Army Center for Health Promotion and Preventive Medicine, Aberdeen Proving Ground, Maryland, USA; ¶University of North Florida, Jacksonville, Florida, USA; Abstract Geographic distribution of Rickettsia parkeri in its US tick vector, Amblyomma maculatum, was evaluated by PCR. R. parkeri was detected in ticks from Florida, Georgia, Kentucky, Mississippi, Oklahoma, and South Carolina, which suggests that A. maculatum may be responsible for additional cases of R. parkeri rickettsiosis throughout much of its US range. Figure Thumbnail of Adult Amblyomma maculatum (the Gulf Coast tick). A) Female; B) Male. Photographs courtesy of James Gathany, Centers for Disease Control and Prevention Figure. Adult Amblyomma maculatum (the Gulf Coast tick). A) Female; B) Male. Photographs courtesy of James Gathany, Centers for Disease Control and Prevention The Gulf Coast tick, Amblyomma maculatum (Figure), is a Nearctic and Neotropical hard tick found in coastal areas of the southern United States, with inland range extensions in Kansas, Oklahoma, and some other states. It is also found in regions of several Central and South American countries that border the Gulf of Mexico and Caribbean Sea, including Mexico, Guatemala, Belize, Nicaragua, Honduras, Costa Rica, Colombia, Venezuela, and some parts of Ecuador and Peru (1). Rickettsia parkeri, a member of the spotted fever group rickettsiae, was initially identified in Gulf Coast ticks in 1937(2). In 2004, the first confirmed human infection with R. parkeri was reported (3). Since that report, confirmed cases of R. parkeri rickettsiosis have been identified in other persons in Mississippi, Virginia, and possibly other US states (4–6). Only a few studies, each conducted >50 years ago, document the occurrence of R. parkeri in A. maculatum ticks (2,7,8). No contemporary surveys have documented the range of R. parkeri in the United States or the frequency of R. parkeri infection in wwwnc.cdc.gov/eid/article/13/5/06-1468_article.htmSkyship
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Post by skyship on Dec 14, 2011 19:41:09 GMT -5
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Post by skyship on Dec 14, 2011 19:59:13 GMT -5
Spirochete round bodies Syphilis, Lyme disease & AIDS: Resurgence of “the great imitator”? (Received August 18, 2008; Accepted August 31, 2008) Abstract We advocate investigation of spirochete cyclical symbioses (e.g., Borrelia sp., Leptospira sp., Treponema sp.) given the newly established verification of a developmental history in these gram-negative motile helical eubacteria, both in pure culture and in mammals. Symbiotic spirochetes can be compared to free-living relatives for their levels of integration (behavioral, metabolic, gene product or genetic levels). Detailed research that correlates life histories of symbiotic spirochetes to changes in the immune system of associated vertebrates is sorely needed. Genome analyses show that in necrotrophic symbioses (Borrelia and Treponema sp.) of humans and other primates, integration of the bionts occurs at the gene product and genetic level. Spirochete round bodies (also called cysts, L-forms and sphaeroplasts) can be induced by many types of unfavorable conditions (e.g., threats of starvation, desiccation, oxidation, penicillin and other antibiotics). Reversion to familiar helical, motile active swimmers by placement of pure cultures into favorable environments in some cases can be controlled. These observations are supported by a European literature, especially Russian, apparently unknown to American medicine and medical research. Keywords: Spirochete cysts, Treponema pallidum, Borrelia burgdorferi, AIDS co-factor, immune suppression, STD, spirochetoses, Spirosymplokos, fossil spirochetes, spirochete life histories, Mixotricha paradoxa, round body reversion www1.biogema.de/WEK/312-Margulis-final.pdfThe round spirochete? ? Skyship
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Post by skyship on Dec 14, 2011 20:27:39 GMT -5
L-bodies: connection of Swine flu to Lymes:.......................... Fort ORd. cast off as beginnings of Swines flu to cover for the Lymes bioweapon......agent...? HISTORY OF SWINE FLU Back in 1975 a soldier at Fort Ord CA died in a training exercise on a very hot day. A very mild virus that came to be known as swine flu virus was found in his body, though never proven to be the cause of death. Just as probable he died of overexertion, since it was a very hot day and they were on a training exercise. The virus was a member of the H1N1 virus family reportedly found in hogs, which had not previously been transmitted to humans. So nothing was known of its virulence or its ability to cause even a local outbreak, let alone a global epidemic. There was no evidence that it could be a serious disease for humans. lymesentinel.blogspot.com/2009/06/likely-truth-about-swine-flu.html================================= Fort ORD had the new form of Lymes?..............yersinia pestis? So, Plaque and Lymes............... The L-bodies...............BIONTS ...............BIONS? ?? He first became interested in the role of atypical bacterial forms after noting that a large number of patients with urinary tract infections suffer from continual relapsing illness. Using a direct phase microscope, he examined the urine specimens of several patients with urinary tract infections and found L-form bacteria in his sample. He began to investigate L-form bacteria, striving to better understand their biology and the role they play in causing disease. Over the course of the next 30 years, he was able to explain much of the mystery behind how the bacteria are able to persist in the body, and published a wide array of clinical and experimental studies on the subject. Freshly passed urine from a patient with renal Fanconi syndrome, showing large L-form granules with dense cores Freshly passed urine from a patient with renal Fanconi syndrome, showing large L-form granules with dense cores Domingue worked with a team that included pre and post doctoral students and fellows along with faculty colleagues and laboratory assistants. Together they discovered that L-form bacteria are able to form tiny dense bodies within parent cells that already lack cell walls. They noted that the forms, which they called electron dense bodies were so small that they could pass through bacterial filters that normally withheld ordinary bacteria with cell walls. Note the granules, the circle form,,,,,,,etc... immune system goes down........... bacteriality.com/2007/08/22/domingue/Skyship "
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Post by skyship on Dec 15, 2011 1:32:07 GMT -5
Molecular Alzheimers, Spriochetes, Pathologists collects images of disease tissues: This is reason why site is filled with images from the pathologist........ What he finds. ================================== Please read statement and go to images................. www.molecularalzheimer.org/files/Website_Statement_of_Purpose.pdf=================================== Spirochete is key.........did they make a synthetic one? couldn't be traced? www.molecularalzheimer.org/
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Post by skyship on Dec 15, 2011 1:41:24 GMT -5
TAking a few of the conclusions arrived at: We have got to get to the quick here. Conclusions Various types of spirochetes, including B. burgdorferi, and six periodontal pathogen spirochetes (T. socranskii, T. pectinovorum, T. denticola, T. medium, T. amylovorum and T. maltophilum) were detected in the brains of AD patients. The pathological and biological hallmarks of AD, including increased AβPP level, Aβ deposition and tau phosphorylation were induced by spirochetes in vitro. The statistical analysis showed a significant association between spirochetes and AD. The strongly significant association, the high risk factor and the analysis of data following Koch's and Hill's criteria, are indicative of a causal relationship between neurospirochetoses and AD. Spirochetes are able to escape destruction by the host immune reactions and establish chronic infection and sustained inflammation. In vivo studies with long exposure times will be necessary to efficiently study the sequence of events and the cellular mechanisms involved in spirochete induced AD-type host reactions and Aβ-plaque, "tangle" and "granulovacuolar" formation. The characterization of all types of spirochetes and co-infecting bacteria and viruses is needed, in order to develop serological tests for the early detection of infection. The pathological process is thought to begin long before the diagnosis of dementia is made therefore, an appropriate targeted treatment should start early in order to prevent dementia. Persisting spirochetal infection and their persisting toxic components can initiate and sustain chronic inflammatory processes through the activation of the innate and adaptive immune system involving various signaling pathways. In the affected brain the pathogens and their toxic components can be observed, along with host immunological responses. The response itself is characteristic of chronic inflammatory processes associated with the site of tissue damage. The outcome of infection is determined by the genetic predisposition of the patient, by the virulence and biology of the infecting agent and by various environmental factors, such as exercise, stress and nutrition. The accumulated knowledge, the various views, and hypotheses proposed to explain the pathogenesis of AD form together a comprehensive entity when observed in the light of a persisting chronic inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Similarly to syphilis, one may prevent and eradicate dementia in AD. The impact on healthcare costs and on the suffering of the patients would be substantial. www.jneuroinflammation.com/content/8/1/90
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Post by skyship on Dec 15, 2011 2:00:42 GMT -5
Images comparison of Alz and borrelia www.molecularalzheimer.org/files/Concurrent_Neocortical_papers_1_and_2.pdffrom human autopsy: DNA hybrids.............. www.molecularalzheimer.org/postergranular.html===================== spinal: www.molecularalzheimer.org/posterspinal.html======================= Prepare Lucis Trust: freemasonrywatch.org/lucistrust.html======================================== CYSTS www.molecularalzheimer.org/CYSTS_INVADING_NERVE/CYST_INVADING.jpg===================================== Alzheimers the introduction of the synthetic tracker.............. The extra secondary system taking over your DNA. Transfection "Junk" DNA - a link to the pathogenesis of Alzheimer's disease? MacDonald AB. Source St. Catherine of Siena Medical Center, Department of Pathology, Smithtown, NY 11787, USA. inmacdonald@yahoo.com Abstract A transfection product incorporates in one molecule of human DNA, an inserted segment of DNA from another species. This communication addresses the hypothesis that a novel variation of the theme of transfection, namely "junk transfection" for which no protein product and no RNA is transcribed, might offer insights into the pathogenesis of Alzheimer's disease. It is hypothesized that spirochetal DNA gains access to the intracellular compartment of nerve cells during the subclinical latency phase of neuroborreliosis and chemically combines with human DNA. A previously reported Molecular interrogation of Alzheimer's disease autopsy tissues has yielded novel DNA sequences containing the 11 q human chromosome and a short piece of the Borrelia burgdorferi Flagellin B DNA. Although the usually encountered transfection product bundles an entire nonhuman gene within it, this model proposes that shorter inserts into the human genome constitute "junk transfection" because no protein is derived from them. Junk transfections would offer an important new cognitive model for the detection of occult infections as the root causes for the Tauopathies, which are degenerative neurological disorders, including Alzheimer's disease. www.ncbi.nlm.nih.gov/pubmed/16481123--------------------------- Will try to post the articles and the images as they apply...... We have to get to core before........................The laws are all there to go into effect 2012........ Molecular interrogation of Alzheimer Autopsy Brain tissues for evidence of NonHuman (microbial) DNA of Borrelia burgdorferi by Alan MacDonald MD (copyright 2005) www.molecularalzheimer.org/molecular1.htmlSkyship
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Post by skyship on Dec 15, 2011 2:09:03 GMT -5
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Post by skyship on Dec 15, 2011 2:30:45 GMT -5
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Post by skyship on Dec 15, 2011 2:50:27 GMT -5
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Post by skyship on Dec 15, 2011 3:09:07 GMT -5
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Post by skyship on Dec 15, 2011 3:13:45 GMT -5
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Post by skyship on Dec 15, 2011 3:16:51 GMT -5
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