Continuing on the idea of foreign-peptides inducing autoimmune disease, and how this might relate to Morgellons/Lyme given the agrobacterium aetiology described by Drs. Citovsky and Stricker/Savely in recent papers...specifically, some very interesting information predating "Morgellons" as a known name/entity, but coinciding with the time-frame of the earliest accounts of the disease (1997/1998 per the timetable in this blog-entry ).
Bovine spongiform encephalopathy (BSE) could be an autoimmune disease produced following exposure of cattle to feedstuffs containing bacteria showing molecular mimicry between bacterial components and bovine tissue. Analysis of molecular sequence databases (Genbank and SwissProt) shows that three bacteria ( Acinetobacter calcoaceticus , Ruminococcus albus , and Agrobacter tumefaciens ) share sequences with the encephalitogenic peptide of bovine myelin, while three molecules in Escherichia coli show molecular mimicry with host-encoded prion protein. Immune responses against these bacteria at both T and B cell levels may cause neurological tissue injury resembling BSE. The role of these bacteria in BSE, if any, merits further investigation. Key words : autoimmune disease, bovine spongiform encephalopathy, Gram-negative bacteria, molecular mimicry. Environ Health Perspect 105:1172-1174 (1997) .
So let me see if I got this straight -- Stricker/Savely claims there's an agrobacterium link to Morgellons aetiology, citing Dr. Citovsky and others.
In addition to the morgellons/agrobacterium implications, the other named bacteria are now regularly in the news, e.g. http://www.acinetobacter.org -- as wounded Iraq vets are coming home and dying of this disease, supposedly acquired in hospitals. E-Coli is the subject of numerous tainted beef scares, indicating it is widely in the food supply: http://www.nytimes.com/2008/
This further leads one to ponder whether the peptides that cause "mad cow disease" are in anyway deactivated when humans eat the cooked cow-flesh. Certainly, with the "prion theory" there is concern over eating the meat, cooked or not. And if those bacterial residues in cow-feed are causing disease as severe as BSE in cows... are those same residues also found in our own plant-based foodstuffs? Are they to blame for epidemic rise in auto-immune diseases, cancers, diabetes?? (The GMO foods alarmists seem to link morgellons -- because of the agrobacterium link -- to GMO: http://worldnetdaily.com/
And finally, regarding Dr. Citovsky's morgellons studies showing the presence of agrobacterium -- were the bacteria actually microscopically identified and present in tissue samples? Or cultured? My concern is that there was actally NO LIVE AGROBACTERIUM in the lesions, but that immune-response or genetic testing for agrobacteria may have simply "read" the agrobacterial peptide sequence that is present in our foodstuffs ... these complex amino acid sequences could certainly be enough to create a "match" for the purposes of identification. The lack of agrobacterium in the controls might lead to a false conclusion that agrobacterium are involved in an infective process in Morgellons patients. Unless the bacteria could be cultured and then specifically identified, there's no "control" in the experiment for live agrobacteria versus dead or killed agrobacteria that result from the GMO process. No controls to see whether the disease is infective or autoimmune related. No Controls to see whether identifiable peptide sequences derived from agrobacterium are present in the Morgellons patients.
The issue is that the killed agrobacteria resulting from the GMO process might still contain peptide sequences that induce disease. Comments from a GMO-industry insider claim "Agrobacterium is used to generate the transgenic plants, and then it is killed with a variety of antibiotics and physical/chemical treatments (autoclaving, bleach etc)". And yet, if cooking doesn't "kill" prions, autoclaving may not "kill" peptides... nor would bleach or antibiotics necessarily...http://liquidmind.wordpress.
Commercial transgenic plants DO NOT contain Agrobacterium. Release of engineered Agrobacterium is ILLEGAL, and does not occur (I work in the business). There is no permitted release of engineered Agrobacterium, and there never will be. The Agrobacterium is used to generate the transgenic plants, and then it is killed with a variety of antibiotics and physical/chemical treatments (autoclaving, bleach etc).Jerry Ranch said this on May 31, 2008 at 12:13 pm
Far more likely, since Agrobacterium is a ubiquitous soil bacterium, people may come to harbour Agrobacterium by exposure to soil. Also, the original report that the lesions contained Agrobacterium I believe did not specify which species. The industry use Agrobacterium tumefaciens. There are many species of Agrobacterium, so what was found may not even be the same species as is used in GE. If indeed, the Agrobacterium found in lesions is engineered Agrobacterium, this would be very easy to ascertain as the genetic signature performed with DNA analysis is fairly trivial.
Since you are "in the business", I'm sure that you are familiar with the following which is taken from the website of The Institute of Science in Society:
Although various antibiotics have been used to eliminate Agrobacterium following transformation, the researchers stated that "very few authors actually test to ensure that the antibiotics succeed."
The difficulty is compounded because the bacterium can remain latent within the plant tissue. So putting transgenic plant material into culture medium without antibiotics and finding no Agrobacterium is no guarantee that the transgenic plant is free of the bacterium, as was often assumed.
In their study, they investigated the ability of antibiotics to eliminate Agrobacterium tumefaciens after transformation in three model systems: Brassica (mustard), Solanum (potato), and Rubus (raspberry). The antibiotics carbenicillin, cefataxime and ticaracillin were used respectively to eliminate the bacterium at four times the minimum bactericidal concentration, as recommended. They found that none of the antibiotic succeeded in eliminating Agrobacterium.
"Genetic engineering is inherently dangerous, because it greatly expands the scope for horizontal gene transfer and recombination, precisely the processes that create new viruses and bacteria that cause disease epidemics, and trigger cancer in cells."
- Dr. Mae-Wan Ho, Institute of Science in Society
Along the same vein -- the unrecognized role of peptides as foreign antigens stimulating autoimmune misidentification and resultant disease -- another article links peptides from sandfly bites in Iraq to Gulf-War Syndrome:
English Title: Is Gulf war syndrome an autoimmune disorder of endogenous neuropeptides, exogenous sandfly maxadilan and molecular mimicry?
Personal Authors: Staines, D. R.
Author Affiliation: Gold Coast Public Health Unit, 10-12 Young Street, Southport, Qld. 4215, Australia.
Editors: No editors
Document Title : Medical Hypotheses, 2004 (Vol. 62) (No. 5) 658-664
Gulf war syndrome (GWS) remains a contentious diagnosis with conflicting laboratory investigation and lack of a biologically plausible aetiology. This paper discusses the potential role of maxadilan, a potent sandfly vasoactive peptide, in causing autoimmune responses in susceptible individuals through possible molecular mimicry with pituitary adenylate cyclase activating polypeptide (PACAP) and the PAC1R receptor. Gulf war syndrome may share some causative pathology with Chronic Fatigue Syndrome (CFS), a disorder characterised by prolonged fatigue and debility mostly associated with post-infection sequelae although ongoing infection is unproven. Immunological aberration associated with an expanding group of vasoactive neuropeptides in the context of molecular mimicry and inappropriate immunological memory has been recently raised as possible cause of CFS. Vasoactive neuropeptides act as hormones, neurotransmitters, immune modulators and neurotrophes. They are readily catalysed to small peptide fragments. They and their binding sites are immunogenic and are known to be associated with a range of autoimmune conditions. Maxadilan, while not sharing substantial sequence homology with PACAP is a known agonist of the PACAP specific receptor (PAC1R) and therefore emulates these functions. Moreover a specific amino acid sequence peptide deletion within maxadilan converts it to a PACAP receptor antagonist raising the possibility of this substance provoking a CFS like response in humans exposed to it. This paper describes a biologically plausible mechanism for the development of a GWS-like chronic fatigue state based on loss of immunological tolerance to the vasoactive neuropeptide PACAP or its receptor following bites of the sandfly Phlebotomus papatasi and injection of the vasodilator peptide maxadilan. Exacerbation of this autoimmune response as a consequence of recent or simultaneous multiple vaccination exposures deserves further investigation. While the possible association between the relatively recently discovered vasoactive neuropeptides and chronic fatigue conditions has only recently been reported in the literature, this paper explores links for further research into GWS and CFS.
Observation: the above article might be a "dodge" to purposefully ignore the mycoplasma component of Gulf War Syndrome discovered by Dr. Nicholson... language like "conflicting laboratory investigation and lack of a biologically plausible aetiology" seems dubious given that there's plenty of evidence for a direct infective component: http://www.immed.org/illness/
Question: Is a similar autoimmune-based cascade failure also occurring in Lyme/Morgellons disease -- triggered by whatever insect is transmitting morgellons (blackfly, and mosquitos and no-see-ums, IMHO). Alternately, could peptide-therapy allow for more potent antibiotic therapy while preventing or diminishing herxheimer reactions (which are essentially autoimmune response to dead borrelia that have "decloaked" from the immune system in death)?
The morgellons case definition ( http://www.morgellons.org/
4. Musculoskeletal Effects and Pain is usually present, manifest in several ways. Pain distribution is broad, and can include joint(s), muscles, tendons and connective tissue. Both vascular and "pressure" headaches and vertebral pain are particularly common, the latter usually with premature (e.g., age 20) signs of degeneration of both discs and vertebrae.
5. Aerobic limitation is universal and significant enough to interfere with the activities of daily living. Most patients meet the Fukuda Criteria for Chronic Fatigue Syndrome as well (Fukuda, Ann. Int. Med., 1994). Cardiology data and consistently elevated heart rates suggest a persistent myocarditis creating lowered cardiac output that has been partially compensated for by Starling's Law.
6. Cognitive dysfunction, includes frontal lobe processing signs interfering with logical thinking as well as short-term memory and attention deficit. All are measurable by Standard Psychometric Test batteries.
2. Numerous neurological symptoms and clinical findings. A variety of neurological symptoms and signs have been reported. Common physical findings include abnormal Romberg, peripheral neuropathy in ALL (feet, and in some cases fingers), abnormal reflexes, verifiable, probably neuropathic pain and recurrent brain control abnormalities affecting motor function, circadian rhythm, body temperature and respiratory rate.
3. Gastrointestinal symptoms, often including dyspepsia, gastroesophageal reflux, swallowing difficulty, and changes in bowel habits (Similar to IBS or Crohn's disease)
4. Acute changes in skin texture and pigment. The skin is variously thickened and thinned, with irregular texture and hyper- OR hypo-pigmentation pattern. Overgrowth or hypergrowth phenomena are common (nevi, skin tags, microangioma, lipomas, callus formation).
5. Arthralgias. Frequently reported, although arthritis is not. Common joints are in fingers, shoulders, knees and vertebrae.
Other interesting links to peptide therapy and auto-immune disease (aka every bogus "syndrome" disease put forward by mainstream medicine).
Induction of Autoimmune Thyroiditis and Hypothyroidism by Immunization of Immunoactive T Cell Epitope of Thyroid Peroxidase
Immunization with a bacterial ATP-binding cassette transporter fragment suppresses autoimmunity and prolongs survival in MRL/lpr lupus-prone mice
Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme
Vaccination with Dendritic Cells Pulsed with Peptides of Myelin Basic Protein Promotes Functional Recovery from Spinal Cord Injury
Latent autoimmune diabetes
Autoimmune Diseases: The Invasion by the Body
Antigen-Specific Suppression of Experimental Autoimmune Encephalomyelitis by a Novel Bifunctional Peptide Inhibitor
Differential induction of IgE-mediated anaphylaxis after soluble vs. cell-bound tolerogenic peptide therapy of autoimmune encephalomyelitis
Peptide-induced T-cell tolerance to prevent autoimmune diabetes in a transgenic mouse model
Synthetic peptide for treatment of autoimmune arthritis
Treatment of demyelinating autoimmune disease with ordered peptides
Posted by Niels P. Mayer in Medicine
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