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Post by skyship on Sept 23, 2011 22:55:58 GMT -5
Please look at this and consider that where ever there is war, the diseases most prominent in those areas of war, will visit the service men and women, and they will bring it home. So, the the war goes on after all return home. If this Oncho is brougt here by servicemen, and they are ignored, for what diseases they can pick up in area they work in or are stationed at, then these need to be examined. Someone did bring this to the attention of Congress.
This is what recently happened to me. This is now in America, and most will not examine this, they are given the same diagnosis, as we are.
So, to even push this envelope for truth on this, has been covered many times, in many ways, by those who will not admit that GWS is a real filaria disease, or should I say parasite infection, and it is ignored here.
Yet, it exists. These oncho diseases could have been put in those bioweapons used in first Gulf War........ This has been forgotten.==================================== Why did Garth Nicholson not mention this? in his studies on Gulf War Syndrome, knowing that oncho as well as leishmaniasis, and chagas are and were present during GULF WAR I , early 90s.=================================== EMAIL TESTIMONY of John David Brown to THE SUB-COMMITTEE ON NATIONAL SECURITY, EMERGING THREATS, AND INTERNATIONAL RELATIONS chaired by Representative Christopher Shays COMMITTEE ON GOVERNMENT REFORM HOUSE OF REPRESENTATIVES OF THE UNITED STATES OF AMERICA SUBJECT: Examining the Department of Veterans’ Affairs’ implementation of the Persian Gulf War Veterans Act of 1998 VENUE: Room #2154 Rayburn House DATE: November 15th 2005 _________________________________________________ 01. John Brown is a British citizen who contracted onchocerciasis in Saudi Arabia. He has an American friend with similar symptoms but a different diagnosis. The American is diagnosed with Gulf War syndrome (GWS). The sole purpose of his testimony is to alert Congress to a specific shortcoming in the screening of 1991 Gulf War veterans (GWVs) in the hope that government intervention will ensure that Americans with onchocerciasis are screened for onchocerciasis and treated for onchocerciasis and not left to rot. John Brown has no other agenda. 02. Between 1983 and 1986, Brown was employed at Dhahran by the General Directorate of Military Works of the Saudi Ministry of Defence and Aviation. He had previously worked on the construction of the Al-Khobar power and desalination plant a few miles to the east on the Persian Gulf coast. 03. In autumn 1983 he fell acutely ill. The illness was never properly investigated but has been retrospectively diagnosed as probable fascioliasis contracted eating contaminated salad vegetables from the local market (refer section 13). Following concomitant infection with Onchocerca volvulus, he remains ill to this day and has been too sick to work since 1991, the year of Operation Desert Storm. 04. In 1997, and quite by chance, he presented with frank signs of onchocerciasis. On acquiring a rare suntan (he is white) he discovered that his shins were depigmented and his shoulders covered in ‘leopard skin’. Onchocerciasis is the only disease known to localise depigmentation to the shins and this presentation is unique to longstanding chronic disease. His legs looked absurd yet doctors could not diagnose the cause. One specialist could only think it must be sunburn. 05. Depigmentation cannot be seen on white skin, although his shins itched and twitched at night in bed; a condition known as restless legs or Ekbom’s syndrome. His itching and twitching resolved with onchocerciasis treatment. 06. Psychiatrists like to diagnose Ekbom’s as delusional parasitosis. The evidence herein testifies to the fact that the only delusional aspect of delusional parasitosis is that it is delusional. Concomitant with the hypopigmentation and hyperpigmentation, Brown suffered from the full range of multiple symptoms known as GWS but he never had an inflammatory rash. 07. An inflammatory rash that comes and goes is one of the multiple manifestations of his American friend’s illness. Brown provided this friend with information to take to his VA clinic supporting a request to be investigated by Mazzotti Test. This reveals onchocerciasis within a matter of hours. 08. His friend’s specialist looked up onchocerciasis in a textbook and suggested first trying treatment for another condition. As always, this treatment was ineffective. 09. Within the last few weeks the American returned to the clinic to report the failure of the treatment and again requested to be investigated for onchocerciasis by the Mazzotti test. Once again his request was ignored. 010. It looks unlikely that any GWVs will receive the diagnostics and treatment they need without intervening government directives.
============== I have been asking my doctor to check this out, as well. Two years in a row, for 3 months now, unable to go outside. She knows not what it is. This is how even filaria will not be investigated, so Morgellons is just another thing to throw into the soup of delusional parasitosis.
Oncho is not delusional, believe me.........
The itchy rash you get, face, arms, legs, and the scaling of that rash, the 3 to 4 month recovery of just the itch, itself, is horrendous. This is same time it takes what we call Morgellons lesions to heal. These lesions have the worms in them.
However, in Morgellons it has been modified for bioweapon use, most likely during Operation Desert Storm.
I think many studying GWS have covered up the fact that oncho was used in the bioweapon. It comes home to roost, folks.
So, where is G. Nicholson's report on the oncho? leishmaniasis, and chagas?
They did better in Middle East than in Africa? Come on!
We have seen all the elephantiasis in the oncho folks in Africa, from vector Black Fly, in Middle East is the Sand Fly, in America another fly. even mosquitoes can carry this, reduvid, Chagas, and those leaf hopper assassin bugs are in America, leishmaniasis, is GWS affliction as well delivered by sandfly.================= contin......... SOURCES AND QUALITY OF EVIDENCE 011. Firstly Brown draws on some five years work experience in the Eastern Province of Saudi Arabia. 012. Secondly he draws on his personal experience with specialists in infectious diseases whose knowledge of onchocerciasis he has found to be deficient. 013. Thirdly he submits medical evidence gleaned since 1997 when he realised that he had been infected with onchocerciasis for a dozen or more years. 014. The integrity of the medical evidence has secured Brown a clinical diagnosis and treatment on the grounds that he inevitably contracted onchocerciasis in Saudi Arabia. It therefore follows that some GWVs also contracted onchocerciasis in Saudi Arabia and probably elsewhere in the Gulf War theatre. 015. Unfortunately Brown has failed to persuade doctors to publish a letter or paper advocating the investigation and treatment of others with Gulf related illnesses. His view is that, in the medical profession, dog prefers not to eat dog. He senses a determined reluctance, by doctors, to stand up and be seen to be the individual that blows the whistle on the GWS debacle. Accordingly, the impetus to secure medical interventions for his sick friend and others will have to come from outside of the medical profession; from congressmen for instance. 016. All but two of the medical references cited herein are available from the National Library of Medicine, Maryland. The critical references by Chumbley and Woodruff should be available from other sources but if not, I will supply copies upon request. CONTENTS 1. Synopsis 2. Introduction to worms and flukes 3. Symptoms of the ultimate multi-symptom disease 4. Onchocerciasis immune deficiency 5. Autoimmunity 6. Doxycycline is anthelminthic 7. Recommended treatment 8. Blue skin disease and the hide-and-seek history of filariasis in Arabia9. Impediments to the detection and recognition of onchocerciasis in different ethnic groups and in new Arabian endemic regions10 . Exposure to onchocerciasis11. Variations in presentations occurring in natives of endemic zones compared to lightly infected expatriates like the GWVs 12. Problems with laboratory findings for GWVs 13. Fascioliasis 14. The French 15. Conclusion 16. References 1.0 SYNOPSIS 1.1 In 1980, heavily infected cases of onchocerciasis presenting as river blindness were reported by Chumbley[1] from the military hospital on the Gulf War, Stealth bomber base at Khamis Mushayt[2]. 1.2 In the late 1970s the zoologist, Buttiker, observed the presence of the blackfly vectors in the region and alerted Chumbley to the possibility of onchocerciasis in the area. Buttiker then published Chumbley’s report in a volume of obscure Swiss tomes on the flora and fauna of Saudi Arabia, thereby eluding inclusion in the Index Medicus, and skipping the attention of Gulf War syndrome investigators[3,4]. Navigation to Chumbley is provided by Connor and co-workers in their 1983 study of sowda in North Yemen[5] so a conscientious search of the medical literature would have inevitably led GWS researchers to Chumbley. 1.3 Additional heavily infected cases presenting as sowda were reported from Riyadh in 1991[6]. From the medical literature, therefore, it is predictable that virtually everyone at Khamis Mushayt and Riyadh are, at least to some small extent, infected[7]. Yet not a single American[3] or British[4] veteran has been screened for this disease. 1.4 Tens of thousands of Arabian expatriates, of all ethnicities, must have contracted onchocerciasis over the years, yet no expatriate case has ever been reported in the medical literature; an anomaly first noticed 40 years ago[8]. The expatriate presentations have gone unrecognised. Expatriate disease does not present as river blindness or sowda, so it is unknown how the disease presents in expatriates from America, Europe, India and South East Asia working in Arabia. 1.5 Multiple cycles of long courses of doxycycline, prescribed to GWVs for mycoplasmal infections[9], also kill endosymbiotic bacteria essential for the homeostasis of adult Onchocerca, interrupting embryogenesis and accelerating their degeneration and death[10]. That is, the antibiotic treatment regimens recommended by Garth Nicolson for mycoplasma infections also resolve onchocerciasis, albeit not very efficiently.========================================= Nichoson should know that Doxycycline only kills the wohlbachia in the oncho filaria and worm. You have a worm living in lymph nodes, the filaria travel around, the wohlbachia is released when the filaria die. But, the worm remains, often for rest of lives. In Africa, they were given Ivermectin, many on LB have used Ivermectin. What we call the hexheimer reaction, is the same as Marzotti reaction.
When the worm does die the calcium released with wolbachia creates a horrendous itch. This itch can only be alleviated by extreme hot water, and then by putting either vicks, eukalyptus, or noxema, and the itch creates wrinkles in the skin, which often turn burgundy, or purplish.
Every crease is filled with the wohlbachia.
It is being denied in America, yet it is everywhere. en.wikipedia.org/wiki/Wolbachia====================== continued............ Large numbers of American servicemen fighting in the Pacific during World War II were infested by other genera of filarial parasites with pathogeneses that were different and more acute than presentations occurring amongst the endemic population with heavier parasite loads[11]. History repeats itself. Will we never learn? 1.7 Regardless of the obscurity of Chumbley’s report from Khamis Mushayt, the evidence submitted herein testifies to the enormity of the medical negligence and incompetence that resulted in the avoidable misery and morbidity known as Gulf War syndrome. In the case of the 1991 Gulf War veterans (GWVs), it will be demonstrated herein that their multisymptom illness is caused by the parasitic filarial worm, Onchocerca volvulus, the secondary insect vectors of which are blackfly species of the genus, Simulium. The disease is called onchocerciasis and the longer the time spent in an endemic zone, the greater the build up of the parasite load, which in turn may cause more patently recognisable disease manifestations. 2.5 Consequently, the parasite loads of briefly exposed GWVs, are very much lower than those of the long term residents of Arabia, and GWVs’ minimal parasite loads will frequently be undetectable by laboratory screening, whereas the higher parasite loads and frank disease manifestations of long term residents are typically detectable and have been reported in medical journals. Protocols for determining the cut-off between positive and negative serology in natives of endemic zones compared to minimally infected GWVs should, therefore, vary to accommodate differences in parasite loads and duration of exposure but variations have not been allowed for by doctors who have little or no experience of lightly infected cases. 2.6 The GWVs’ Onchocerca parasite loads were therefore 'fixed' when they returned home from the Gulf War theatre. Indeed, since arriving home their parasite loads have gradually decreased as the worms have died off naturally. This has rendered their infection progressively more difficult to isolate while symptoms due to chronicity have been getting progressively more serious and severe. Consensus of opinion estimates the life of adult O. volvulus to be nominally 15 to 20 years so there is no time to lose investigating the GWVs for onchocerciasis. 2.7 In very lightly infected cases, few if any symptoms may be directly attributable to the parasite per se. Filarial worms are known to be immunosuppressive (refer section 4). They suppress inflammatory immune responses which accounts for the paucity of non-specific serological evidence in GWVs. Consequently, most symptoms may occur as a consequence of the affects of secondary pathogenic processes caused by opportunistic infectious agents, toxic exposures and vaccines, that have already been implicated in the GWVs’ pathology. In both South-East Asia and Africa, non-white natives of endemic regions are known to tolerate quite heavy parasite loads, but there are reports in the medical literature of Europeans falling seriously ill upon minimal exposure. gulfwarcouncil.com/email_testimony_of%20John%20Brown.htmmore........
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Post by skyship on Sept 23, 2011 23:02:46 GMT -5
Compare symptoms of Morgellons to this: Both are Multisystem. ================================= SYMPTOMS OF THE ULTIMATE MULTISYMPTOM DISEASE 3.1 Onchocerciasis is universally known by the misleading tag, ‘river blindness’. Puyuelo and Holstein[12] reported blindness from Upper Volta where there is a proverb, “Nearness to streams eats the eyes” whereas Hughes and Sarkies[13] reported that eye lesions are absent in eyes streaming with microfilariae in Lower Volta. Suffice to say that onchocerciasis may or may not cause ocular disease ranging in severity from blurred vision to blindness. Other common manifestations of onchocerciasis are less well known, but as with river blindness and GWS, the epidemiology is random. 3.2 In 1965 Woodruff provided an internal report to the WHO Expert Committee on Onchocerciasis, on the disabling non-opthalmological effects of the disease[14]. It listed the following symptoms; pruritis; erysipelas de la costa (dermatitis) – This is the nearest documented presentation to that of my American colleague; lymphoedema; atrophy of the skin (premature wrinkling); leonine facies (folds in facial skin); mal morado (violet coloured dermatitis like lichen planus) - I have met a British veteran with this presenting on his legs; hyper/hypopigmentation (leopard skin and depigmented shins) - I presented with this manifestation – the hypopigmentation cannot be seen on white skin and the hyperpigmentation is a freckle rash; lymphadenopathy (enlarged and sclerosed lymph nodes sometimes known as ‘hanging groins’); calcinosis; subcutaneous nodules; and nakalanga syndrome (retarded growth and development associated with epilepsy). 3.3 Of importance to GWVs who claim to have reproductive problems was his observation that microfilariae in the investing membranes of the testes may be associated with the serious depopulation that occurs in highly endemic regions. Interestingly Gasparini[15] observed the ‘obliteration’ of the saphenous veins and its different branches at the cural ring (groin). I have this manifestation. 3.4 Woodruff’s report contained a single case history to illustrate debility which he regarded as an affect of great importance. He wrote: “Personal experience of some 1500 patients with onchocerciasis studied in East and West Africa, Central America and in London has led to the unmistakable conclusion that the disease may be associated with significant degrees of debility and loss of energy. The importance of this symptom was first made clear by the case of a vigorous and active person much given to mountaineering whose presenting symptom was lack of energy which had caused him to forego mountaineering expeditions to which he had been greatly looking forward. His debility led to him being investigated and eventually to a definitive diagnosis of onchocerciasis being made in the absence of any other cause for his symptoms. Following treatment his vigour has been restored and he has undertaken the various climbs that he had earlier foregone.” 3.5 This is, so far as I am aware, the only reference in existence to a case of chronic fatigue syndrome (CFS) being diagnosed as onchocerciasis, that is, CFS is an onchocerciasis-like illness and since Gulf War syndrome has been described as a CFS-like illness, it too is by definition an onchocerciasis-like illness. 3.6 Woodruff's observations, like those of McCarthy[16] and Pryce[17] demonstrate the remarkable variations between lightly infected cases, who may have detectable microfilariae yet be asymptomatic, or who may have no detectable signs of disease, like the mountaineer, but who are ill and debilitated. There are no hard and fast rules as to whom or when to treat. Woodruff’s final summarising sentence also nutshells Gulf War syndrome. He wrote: “ Though many of the symptoms of onchocerciasis taken individually are not serious, in summation they may cause a state of great human misery, and almost certain economic incapacity.” 3.7 These days the mountaineer's onchocerciasis could be detected by Recombinant Antigen Panel (RAP) serology or Polymerase Chain Reaction (PCR) skin probe but doctors are not investigating cases with these assays. Today the mountaineer would be wrongly diagnosed with CFS or Gulf related multisymptom illness, as I was and as thousands of my fellow invalids have been. And like us, he might be given unhelpful and inappropriate cognitive behaviour and graded exercise therapy (CBT/GET) to help him cope with his ailment; or he might be diagnosed as hyperventilating and treated with sessions of breathing in and out of a paper bag; or he might be given some other useless and stupid treatment, but he would definitely not be diagnosed with, and treated for, onchocerciasis. In the light of such incompetence is it any surprise that Woodruff’s observation was that cases may resort to alcohol abuse. In lieu of treatment it seems to me as good a means of coping as any other. 3.8 The myriad of presentations described by Woodruff is not exhaustive. There is increasing evidence of an association between onchocerciasis and epilepsy[18], with claims that onchocerciasis control programmes in endemic areas have eliminated seizures completely[19] or reduced their incidence and severity[20]. Microfilariae have been found in cerebrospinal fluid[21] and the optic nerve[22], suggesting the potential to cause serious neurological disease. 3.9 This is particularly relevant in the light of Robert Haley’s findings of damage to basal ganglia in GWVs[23,24] and the US Department of Veterans’ Affairs’ announcement that GWVs are twice as likely to develop the neuromuscular disease, amyotrophic lateral sclerosis, as personnel not deployed in the 1991 Gulf War. There are also recent claims by GWVs that they are more likely to develop Parkinson’s disease. I submit that onchocerciasis is, variously or in part, involved in this neurological pathology. 3.10 Other observations relevant to GWVs’ illness have come from rheumatologists working in Africa. Parasitic rheumatism due to Dracunculus medinensis, the guinea worm[25,26], and to Strongyloides stercoralis[27] have been reported, but onchocerciasis may be the largest single cause of rheumatism in the tropics[28]. 3.11 In Cameroon one study indicated onchocerciasis to be the biggest cause of morbidity with 87% infected and accounting for 20% of all working days lost. Occular disease only presented in 5% of these cases and there was no permanent blindness[29]. As long ago as 1965, arthralgia was reported in 54% of cases in Tanzania[30] and in 1967 backache and musculoskeletal pain were reported in 64% of cases in Nigeria[31]. 3.12 In Nigeria, cases of musculoskeletal pain were investigated for onchocerciasis with a single skin snip from the iliac crest region. This revealed that 70% of all onchocerciasis cases were presenting with musculoskeletal pain, half of them with backache. If only the textbook symptoms of cutaneous or ocular manifestations had prompted suspicion of the disease, the diagnosis would have been missed in nearly 3/4 of the total cases presenting. The commonest presentation of onchocerciasis was found to be the middle aged farmer with backache[32,33]. Another seldom recognized, but very common symptom was found to be insomnia[34]. 3.13 In a letter[28] to the British Journal of Rheumatology in 1988, CA Pearson, a former Chief Medical Officer in Nigeria, wrote: “Overseas workers do return after many years in endemic areas, and if our index of suspicion is not high when dealing with such travellers who present with backache or other musculoskeletal pains, we might miss the opportunity of achieving a most satisfying therapeutic success. Should we not rethink our approach to third world rheumatism? Their problem may become our problem. As rheumatoid arthritis is relatively rare in the tropics would it not be helpful to tag onchocerciasis, not only with the well-established name of 'river blindness', but also with the name of 'tropical rheumatism' or 'tropical backache'? This would remind physicians and general practitioners in endemic areas, and those who serve patients who have lived temporarily in those areas, of the importance of rheumatic symptoms in this disease.” 3.14 I submit that, in respect of onchocerciasis, the Gulf War syndrome debacle has demonstrated that Pearson’s 'index of suspicion' of onchocerciasis by doctors in the USA and UK is absolute zero. Worse still, American[3] and British[4] investigators found that Gulf War syndrome was not unique to the veterans, but occurred in personnel not deployed in the 1991 Gulf War. In consequence, it is likely that there are few physicians in North America and Europe who, at some point in their career, have not missed the diagnosis with dire, and sometimes fatal, consequences for their patients. Thus we have, in all probability, the biggest goof-up in medical history. 3.15 In summary, the above reports from the medical literature indicate that onchocerciasis is an extraordinarily ‘multi’ symptom illness that may present with any combination of the following symptoms: fatigue; debility; rheumatic musculoskeletal pain; ocular disease that may cause blindness; vascular disease; lymphatic disease; many presentations of dermatitis, pruritis; neurological disease; insomnia; and disease of the reproductive organs. And when it presents with these predictable symptoms, as it has in the Gulf War veterans, the diagnosis is serially and universally missed. I find this mind-boggling. gulfwarcouncil.com/email_testimony_of%20John%20Brown.htm======================================== Are the fibers mimics of filaria? or filaria and worms, different sizes, like different sizes of amyloids. like different sizes of nanotubes.?? Oncho like, filaria like, amyloid like etc........1991 was first year to use "buckyballs" and not in war theater?
Helen Keller went blind from this, from water from the well? These are in flies which inhabit running water. Midges do this too.
Skyship
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Post by skyship on Sept 23, 2011 23:28:01 GMT -5
Some of us may have had this since we were very young. Horses get this. Cattle get this. Other animals, raccoons, possums, and other animals. Sowda same as Oncho....... seems prions related to this? Are prions really wolbachia? This well gets deeper as the lies mount, doesn't it? ============================================ Here the IDIOTS are using wolbachia to kill malaria? Swap one disease for another? wolbachia draws the flies that carry the oncho?............. ==================================== "The data suggest that if stable transinfections act in a similar manner to somatic infections, Wolbachia could potentially be used as part of a strategy to control the Anopheles mosquitoes that transmit malaria. Infection with Wolbachia bacteria has been shown to reduce pathogen levels in multiple mosquito species. Anopheles mosquitoes (the obligate vectors of human malaria) are naturally uninfected with Wolbachia, and stable artificial infections have not yet succeeded in this genus; however somatic infections can be established that can be used to assess the effect of Wolbachia infection in Anopheles. Here, we show that infection with two different Wolbachia strains (wMelPop and wAlbB) can significantly reduce levels of the human malaria parasite Plasmodium falciparum in Anopheles gambiae. After infection, Wolbachia disseminate throughout the mosquito but are notably absent from the gut and ovaries. The mosquito immune system is first induced in response to Wolbachia infection, but is then suppressed as the infection progresses. The Wolbachia strain wMelPop is highly virulent to Anopheles only after blood feeding. If stable infections can be established in Anopheles, and they act in a similar manner to somatic infections, Wolbachia could potentially be used as part of a strategy to control malaria."............ www.citeulike.org/user/AJCann/article/9355529Wolbachia is associated with ricketts......... skyship
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Post by skyship on Sept 23, 2011 23:32:52 GMT -5
Back to the GWS oncho coverup. ....."ONCHOCERCIASIS IMMUNE DEFICIENCY 4.1 There is a Th1/Th2 (Th = T-helper cell) cytokine response imbalance occurring in GWS cases described by Roberto Montero, Nancy Klimas, and Mary Ann Fletcher (University of Miami School of Medicine) in the Journal of Chronic Fatigue Syndrome[1] from which I quote, "affected individuals are biased toward a T-helper-2-type, or humoral (antibody producing) immunity-oriented cytokine expression pattern, over a Th1-type, or cellular mediated (natural killer cell and macrophage activating) immunity orientated one." 4.2 In simple English this means that while our antibody producing immunological mechanisms are over-performing, our inflammatory (think red and sore) mechanisms are suppressed and under-performing. This informative paper discusses the effectiveness of various convoluted interventions to correct this imbalance, and from which GWVs variously seemed to benefit. 4.3 Various stimuli will manipulate either humoral or cellular responses separately, in the manner described by the Miami researchers. For instance, vaccines, amongst other things, enhance humoral cytokine responses, and boozing, amongst other things, suppresses cellular cytokine responses, but very few stimuli will simultaneously do both, leaving little room for manoeuvre. 4.4 I spent many weeks conscientiously trawling the medical electronic databases, every-which-way, for any pathogens that are known to simultaneously affect cytokine responses in this manner. The only papers to be trawled up identified tissue-invasive helminths, specifically filaria and schistosomes, and that was my lot. I submit that it is significant that not one of the pathogens often hypothesised as being the aetiological basis of GWS were picked up by my search. I submit that this effectively excludes them as possible underlying aetiological agents of GWS, but not as secondary pathogens. 4.5 The immunological aberration described in the Montero/Klimas/Fletcher paper is identical to that described in a paper on onchocerciasis by Stewart and co-workers, published in 1999[36]. This paper demonstrates that Onchocerca volvulus suppresses Th1-type responses to both parasite and non-parasite antigens with a corresponding enhancement of Th2-type responses. The relevance of this finding, when applied to GWS, is that when microbe infections are concomitant with onchocerciasis, they do not necessarily provoke the all-important, telltale non-specific inflammatory responses that they would otherwise provoke. 4.6 Microbes (bacteria, viruses, mycoplasmas, fungi etc) and, by the way, cancer cells provoke an inflammatory immune response that is a product of cellular (Th1) immunity. As a physician's rule of thumb, but no more, infectious disease causes inflammation, so their attitude is that no inflammation equates to no infection. 4.7 It is the detection of components of non-specific inflammation; rheumatoid factor, antinuclear factor, extractable nuclear antigen, reactive protein and, most commonly, ESR that doctors rely on to determine whether a patient is genuinely sick, albeit on account of microbes or cancer, or whether they are mad or malingering. When these telltale haematological signs of inflammation are absent, the patient may be wrongly diagnosed as mad or malingering. 4.8 In this event, the correct finding is that the patient may indeed be mad or malingering, UNLESS they are infested with tissue-invasive helminths that are suppressing their inflammatory responses. Further investigation is then required, with exquisitely sensitive pathogen-specific tests (section 9.0 and para 12.1), for the differential diagnosis to be correctly determined. 4.9 Published research into GWS reveals that this has not been happening in the USA[3] or UK[4], possibly because the assays are not commercially available. Under these circumstances, I submit that the only legitimate means of determining such a patient's state of health is by their response to empirical treatment with anthelmintic therapy that may need to be prolonged. 4.10 An obstacle that GWVs must overcome is doctors’ assumption that tissue-invasive helminths are not causing disease in their patients. Doctors assume, through no fault of their own, but shortcomings in their training, that microbes are the only likely causes of disabling chronic infection; re-education is required.".... ....."Immunology driven by adults and embryos 4.1 1 With onchocerciasis, the suppression of cellular immunity is directly related to the microfilarial load as demonstrated by the reversal of hyporesponsiveness after chemotherapy[37-40]. This post treatment increase in cellular responsiveness is transient lasting for around six months and is only maintained with ongoing treatment, that is; continuous cycles of chemotherapy are required to clear microfilariae and maintain the correction of the immune imbalance. 4.12 The enhancement of humoral responses is thought not to be directly related to the microfilarial load, but to the age of the patient (maturation of the immune system and duration of exposure to the parasite) and inversely to the microfilarial load[36]. In lymphatic filariasis, however, it has been demonstrated that the adult female worms of Brugia malayi are the driving force of type-2 polarisation in mouse infections[41]. Whether this is also the case in onchocerciasis is unclear, because the Th1/Th2 imbalance is corrected with ivermectin (drug of choice) treatment that clears microfilariae but not macrofilariae. Thus, the question as to whether all adult worms must be killed to fully resolve the complex immune imbalance remains unanswered by research to date."................... "5.0 AUTOIMMUNITY 5.1 O nchocerca volvulus is a large pathogen with a complex cell structure that shares many antigens with human tissues and is therefore capable of causing autoimmune disease. For instance, a worm antigen is cross-reactive with a component of the retinal pigment epithelium[42] and another antigen is shared with keratin[43]. Antibodies against autoantigens of nerve fibre, ganglion cell and Muller cell have also been found in cases, which may implicate autoimmune mechanisms in the development of river blindness[44]. Auto-antibodies as well as parasite specific antibodies are reduced, however, following treatment with ivermectin so microfilariae are certainly involved in part, if not entirely. But this still does not exclude adult worms as a significant factor in the immune imbalance. 5.2 The question as to the importance of autoimmunity is complicated. Gallin and co-workers[45] demonstrated that the enhanced immune activity resulting in the Arabian hyperreactive presentation of sowda was due to the development of autoantibodies to defensin, whereas in generalised African onchocerciasis, parasite antigens are tolerated and there is no reactivity to defensins. It is therefore conceivable that there may be autoimmune variations in the Caucasian presentations of GWS between, say, blondes, brunettes and redheads. 5.3 In post HIV/AIDS times one might imagine that emphasis would be placed on immune deficiency diseases in doctors’ training but this is not the case. Duke addresses onchocerciasis immune deficiency in the Oxford Textbook of Medicine under the subheading, 'Generalized signs and symptoms'[46(p915)]. He writes, "Extreme wasting, dwarfism with delayed sexual development, epilepsy, AND A FAILURE TO REACT IMMUNOLOGICALLY TO ANTIGENIC, STIMULI (my emphasis) have all been associated with heavy O. volvulus infection." That's the lot; just nine words, the limit of our primary care doctors’ training on this serious immune deficiency. Symptomatic secondary cofactors 5.4 Researchers in the field of GWS have allowed themselves to be distracted from the underlying immunological aberration described above, by the possible affects of vaccinations and battlefield toxins to which GWVs were exposed. Of CFS Ramsey wrote: "It is not so much the aetiological agents, as the immunological state of the patient which determines the development of the disease. This was suggested to me several years ago when two friends on holiday contracted the same respiratory virus infection: one recovered uneventfully, the other (a doctor) developed ME (CFS) and has become a chronic sufferer."[47] It is therefore the case with onchocerciasis that Ramsay's 'immunological state of the patient' is temporarily corrected by treatment with ivermectin.'............. gulfwarcouncil.com/email_testimony_of%20John%20Brown.htm======================================== A NEW EARTH will require that "truth in the medical field be exposed". Real Medicine is not being practiced at all.Skyship
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Post by skyship on Sept 23, 2011 23:43:59 GMT -5
Now, Nicholson did use doxy on some patients:===== "6.0 DOXYCYCLINE IS ANTHELMINTHIC 6.1 Ivermectin is microfilaricidal but not macrofilaricidal, although repeated doses degenerate and accelerate the death of adult worms[46]. The adult worms, however, have an Achilles' heel in that they harbour essential symbiotic bacteria that are sensitive to antibiotics which, in turn, renders the parasite vulnerable to antibiotic therapy. 6.2 In 2000, Hoerauf and co-workers published a paper[48] documenting novel therapy from which I quote: "Endosymbiotic bacteria living in plasmodia or worm parasites are required for the homeostasis of their host. We show that targeting of Walbachia spp bacteria (order Rickettsiales) in Onchocerca volvulus filariae by doxycycline leads to a sterility of adult worms to an extent not seen with drugs used against onchocerciasis. Present chemotherapy, such as ivermectin (drug of first choice) is mainly targeted against mature microfilariae, and not at adult worms or early embryos, leading to a reappearance of skin microfilariae several months after treatment. There is therefore a pressing need for new antifilarial drugs that have macrofilaricidal efficacy or that show total or long-lasting suppression of embryo production, to complement microfilaricides such as ivermectin." 6.3 Hoerauf and co-researchers treated a group of Ghanaian onchocerciasis cases, presenting with nodules, with 100mg/day Vibramycin (doxycycline) for 6 weeks. Four months after the end of treatment, which was well tolerated in all cases, onchocercoma (nodules containing 1 to 6 female worms) were excised and examined for wolbachia, adult worm degeneration, and disturbance of embryogenesis. Only 5 of 90 worms were positive for bacteria showing only a few organisms. No worms had intact embryogenesis, and only 9 showed any embryos, all of which were degenerated. The researchers commented that there was a clear trend to the more frequent degeneration or death of adult worms. 6. 4 A modest course of doxycycline was thus demonstrated to cause disabling damage to the majority of adult worms. Unfortunately, the regimen of doxycycline required to kill the worms is not yet known. It is surely significant that, for around a decade, Garth Nicolson has been resolving GWS and CFS with multiple 6-week courses of doxycycline that would be predicted to eventually kill adult Onchocerca. 6.5 Following the controversy in the early 1990s over whether or not Gulf War Syndrome was a non-disease and all-in-the-mind, Garth Nicolson successfully treated sick USAF veterans in Texas with repeat 6-week courses of doxycycline. He detected DNA sequences of an invasive mycoplasma species [M. fermentans (incognitus strain)], the isolation and culture of which is beyond the capacity of most laboratories. Accordingly he wrote a letter to JAMA[49] urging physicians to treat the veterans empirically. 6.6 It is particularly significant that most of Nicolson's GWS patients were airforce personnel, some of whom would have been stationed far from combat zones at remote airbases, such as the Stealth bomber base at Khamis Mushayt. He has identified DNA sequences of 4 mycoplasma species (M. fermentans, M. pneumoniae, M. hominis, M. penetrans) in the blood of CFS, fibromyalgia[50] and rheumatoid arthritis[51] cases, but he has not cultured any, so far. His assertion is that leukocytes are infected, precluding proof by culture with today's technology. Encouragingly he reports that all of these cases have either resolved or responded, with varying degrees of success, to antibiotic therapy and particularly to doxycycline.".....gulfwarcouncil.com/email_testimony_of%20John%20Brown.htmBut, did it work?Skyship
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Post by skyship on Sept 23, 2011 23:57:26 GMT -5
Well, it depends on what you are being treated for, now doesn't it?=========================== "Nicolson nutshelled his case for treatment thus: "87 GWI patients that tested positive for mycoplasmal infections were treated with antibiotics. All patients relapsed after the first six-week cycle of therapy, but after up to six cycles of therapy 69 OF THE 87 PATIENTS RECOVERED AND RETURNED TO ACTIVE DUTY (my emphasis). The clinical responses that are seen are not due to placebo effects, because administration of some antibiotics, such as penicillins, resulted in patients becoming more, and not less, symptomatic, and they are not due to immunosuppressive effects that can occur with some of the recommended antibiotics. INTERESTINGLY, CFS, FMS AND GWS PATIENTS THAT SLOWLY RECOVER AFTER SEVERAL CYCLES OF ANTIBIOTICS ARE GENERALLY LESS ENVIRONMENTALLY SENSITIVE, SUGGESTING THAT THEIR IMMUNE SYSTEMS MAY BE RETURNING TO PRE-ILLNESS STATES (my emphasis). If such patients had illnesses that were caused by psychological or psychiatric problems, or solely by chemical exposures they should not respond to the recommended antibiotics and slowly recover. In addition, if such treatments were just reducing autoimmune responses, then patients should relapse after the treatments are discontinued."[52] 6.8 It is important to take cognizance of Nicolson's observation that cases become less environmentally sensitive as they recover, since this is consistent with the down-regulation of a predominant Th2 response, typically associated with atopy and autoimmunity. Most helminthologists concur that the life span of microfilariae in the human body is up to 2 years, although I have not seen where they get this figure from. Correspondingly, it is the case that Nicolson's Gulf War onchocerciasis patients achieve a permanent resolution of their infection after up to 24 months of therapy when their microfilarial load has been greatly or completely reduced through natural causes, that is; when the Th1/Th2 cytokine response imbalance has been corrected and full competence restored to the patient's inflammatory responses. 6.9 It is during the initial period of treatment when Nicolson's cases relapse if therapy is abandoned. This coincides with the period when the mature microfilarial load is high, that is; when the Th1/Th2 cytokine response imbalance is still intact, and inflammatory reactions remain suppressed. 6.10 Nicolson's antibiotic therapies are not microfilaricidal, but only prevent the microfilarial load from increasing. I submit that this is why Donta’s study[ ] indicated that 12 months treatment with doxycycline was of no benfit to GWVs. Onchocerciasis cases could not be expected to feel the benefit of treatment with doxycycline alone for roughly 2 years or more."...................... 7.0 RECOMMENDED TREATMENT 7.1 There is no clinical experience of combined antibiotic and anthelminthic drug therapy. Accordingly, I submit the following regimen for consideration. Six-week courses of 200mg/day doxycycline with six-weeks interval between courses. A single 12mg dose of ivermectin to be taken at the end of each course. That is, at 3 month intervals which is the recommended expatriate dose. A three weeks course of 12mg/kg/body weight diethylcarbamazine to be commenced 3 weeks after taking ivermectin (to ensure absence of microfilariae in the eyes), i.e. the completion of diethylcarbamazine course is immediately prior to commencement of successive courses of doxycycline. The treatment should be continued until the illness resolves.gulfwarcouncil.com/email_testimony_of%20John%20Brown.htmSo, a combination of treatments necessary to kill wolbachia, that is all doxy does, does not kill filaria and the macrofilaria. It is a multiple stage parasite. Wolbachia filaria macrofilaria female/male worm fly/midge/insect bite itself============== BLUE SKIN DISEASE AND THE HIDE-AND-SEEK HISTORY OF FILARIASIS IN ARABIA 8.1 A strange dermatitis of unknown aetiology was recorded by Petrie and Seal[53] in Yemen in 1939/40. They gave it the curious name of Blue Skin Disease. 8.2 This dermatitis was known to the local Yemenis as, ‘sowda’, the feminine form of the Arabic, ‘aswad’ meaning black, because of the dark colour of the affected skin. It typically occurs on a single limb, usually a leg starting low down and spreading upwards. It also appears to be self-curing within a period of 2 to 5 years which is not consistent with other reports of onchocerciasis. The native people believe the source of their dermatitis to be the local lymph nodes that enlarge, become solid and rubbery without adhesions so they can be moved about. 8.3 Petrie and Seal reported that: “An outstanding feature is the enlargement of the groin glands. Arab sufferers usually insist that these glands are the main seat of the disease and come asking that this, ‘umm’ (Arabic for mother or origin) be removed. The Bedouin treatment for the condition is to bite these glands through the skin so that they are broken into small masses.” 8.4 The aetiology remained a mystery until Alan Woodruff (Professor of Clinical Tropical Medicine at the London Hospital for Tropical Diseases) visited Aden in 1955 and suggested it might be onchocerciasis. At that time onchocerciasis had not been reported outside of Africa, Central America and South America. Attempts were made to isolate microfilariae from skin snips but were unsuccessful. 8.5 In Fawdry’s article of 1957 confirming the involvement of onchocerciasis in blue skin disease[54] he recounted previously dismissing this possibility since text books that he had consulted misinformed him that subcutaneous tumours were the presenting feature of onchocerciasis. These were not what patients in the Yemen complained of. 8.6 This indicates the importance of physicians recognising the presentations of helminthiases and being trained to have a high ‘index of suspicion’ of these diseases. Fawdry recollected seeing ‘insignificant’ single lumps resembling fibromata in one or two previous cases, and in due course a typical case of sowda arrived at his hospital asking for lumps in his groins to be removed. He was found to have a half inch diameter subcutaneous tumour on the inner aspect of the mid-thigh that caused him no discomfort. Fawdry excised this tumour and found a bundle of filarial worms inside. Buckly at the London Hospital for Tropical Diseases identified these as Onchocerca volvulus and the patient’s reaction to chemotherapy: swelling, increased itching and eruptions in the affected limb only, confirmed the filarial origin of the disease. Fawdry was, however, unable to follow up the case and could not comment on whether this chemotherapy resolved it. 8.7 Fawdry also reported the excision of the inguinal and femoral glands of a patient who insisted on the removal of their ‘umm’ despite Fawdry’s assurances that this was unnecessary. This patient developed a solid oedema of the thigh but retained an unswollen but still itching lower leg. No comment was made as to whether this surgery was ultimately successful on follow up. 8.8 Sowda was unlike any of the many other presentations of onchocerciasis known at that time, so to recognise it as onchocerciasis in a region from which the disease had not previously been reported evidences Woodruff’s genius. It is therefore puzzling that he did not mention it in his WHO Report of 1965 (section 3) despite reporting extensively on pruritis and dermatitis. The evidence suggests that, by 1965, Woodruff was undecided whether secondary agents like environmental toxic agents or opportunistic infectious agents were determining the multiple symptoms and presentations of onchocerciasis. This followed three publications in 1964 by Giuseppe Gasparini[8,15,55], Senior Surgeon and Director of Dermatological Services of the Republic Hospital of Tiaz (Italian Technical Assistance to Yemen). 8.9 In his medical survey of the Tiaz-Mokha region, Gasparini identified schistosomiasis and malaria as the main health problems followed by treponematosis (endemic syphilis) and sowda. He was suspicious that sowda could not be straight forward onchocerciasis per se. In all three publications he reports that over a period of 5 years he had treated patients with suramin and hetrazan without resolving the condition. Gasparini’s experience was that the only efficacious treatment was the removal of the inguinal and femural lymph nodes. He reported pruritis subsiding 2 or 3 days after the operation and the gradual recovery of the leg. But there is no question that Fawdry demonstrated the involvement of filaria and unlike Gasparini, had not been able to resolve the disease by the removal of lymph glands from the groin but it is not known if Fawdry’s case (para 8.7) would have gone on to recover eventually. 8.10 In 1964, Gasparini also told a conference that he frequently encountered cases of sowda complicated by other infections. He reported that the dark lesions of sowda are often mixed with papillomata and skin gummata or bone involvement typical of endemic syphilis. Indeed, he found that papules on the legs dried and fell off with antibacterial treatment indicating that they were not onchocercomas but secondary bacterial manifestations. 8.11 Both Gasparini and Fawdry reported seeing elephantiasis of the Bancroftian type, sometimes concomitant with onchocerciasis but to this day it remains unclear if this is a manifestation of onchocerciasis or whether the region is also endemic for lymphatic filariasis. There has since been a report of hydrocele and mild elephantiasis of the legs in Africans with onchocerciasis[56] and reports of American and British expatriates returning from Africa with the unilateral swelling of an upper limb[57,58]. Accordingly, it is certainly possible that cases of suspected lymphatic filariasis in Arabia were cases of atypical onchocerciasis. 8.12 Of great relevance to GWS is that Gasparini reasoned that all ethnic groups in Arabia, including expatriates, would be equally exposed to onchocerciasis. If sowda was a straightforward form of onchocerciasis, therefore, it would be predicted to occur in all ethnic groups. Sowda, however, is not found in the non-Arab community and there is no record in the medical literature of it occurring except in Arabs and Liberians. In the 1960s the possibility of different presentations of onchocerciasis being modulated by different host reactions in genetically different ethnic groups was not considered. Since then, many studies have confirmed that onchocerciasis is indeed involved in the manifestation of sowda, but the role of secondary agents in this presentation remains unknown. 8.13 It appears that Gasparini’s unease about the origins of sowda was the spark that inspired Woodruff’s 1968 article on helminths being vehicles and synergists for microbial infections[59] which, I submit, lies at the heart of GWS. For instance, I submit that the involvement of mycoplasmas in GWS, identified by Garth Nicolson, is a consequence of helminthiasis. 8.14 Seventeen years before Operation Desert Storm, doctors in Arabia were concerned that infected migrant workers could establish new foci of lymphatic filariasis as happened in Sri Lanka. In 1974 Sebai and co-workers[60] reported 10 cases of Saudi nationals with disease manifestations of lymphatic filariasis without microfilaraemia, thought to have been acquired in the south-west of the country. Microfilariae were not found, however, during subsequent night blood surveys. 8.15 This is consistent with a report from Kuwait in 1988 of 4 cases of bancroftian filariasis[61], 2 of which presented without nocturnal microfilareamia. Presentations were atypical without the classic symptoms and signs of tropical pulmonary eosinophilia, and the diagnosis was through the uncommon cytological identification of microfilariae in pleural fluid. 8.16 Sebai speculated that the risk of filariasis spreading throughout Arabia was high due to favourable conditions created by rapid urbanisation and the large influx of expatriate workers from the endemic regions of South-East Asia[62]. 8.17 Bearing in mind that Sebai’s original 10 suspected Saudi cases were from the same region from which Chumbley[1] was to report river blindness a few years later, it is quite possible that the reason for microfilariae not being found in their nocturnal blood was because these cases had onchocerciasis and not lymphatic filariasis. 8.18 In 1986, however, Holmes[63] optimistically considered it unlikely that filariasis would be transmitted by mosquitoes in Dubai, but 10 years later Omar[64] was so concerned about Saudi Arabia becoming a new self-sustaining lymphatic filariasis endemic region that he recommended mandatory screening of expatriate workers in their country of origin prior to employment. 8.19 Culex pipiens is the predominant mosquito in the temperate mountains of South-West Saudi Arabia, and is a known vector of Bancroftian filariasis in the Eastern Mediterranean and Egypt. But in the low-lying towns of Saudi Arabia and in the Emirates, Culex quinquefasciatus is predominant. This mosquito species is the principal vector of Bancroftian filariasis in India[65,66] and is also a known vector in the Caribbean, hence my opinion that Holmes’ prediction was optimistic. 8.20 The Arabian Peninsula nestles between the filariasis endemic zones of Africa and South-East Asia, which together account for two thirds of the world’s filariasis. It has been a melting-pot of civilisation for 5 millennia, so it is not clear why Sebai and Omar ignored the immediate threat on their doorstep of importing filariasis from Yemen, or from Africa across the Red Sea. 8.21 Historically, trade with the ancient Kingdom of Sheba (2150 BC to 427 BC), and wars have brought an assortment of peoples to Arabia; Ethiopians, Egyptians, Greeks, Romans, Persians, Turks, Jews and Indians. More recently, pilgrims performing the hadj and expatriate workers from all corners of the world have arrived to swell the Arabian populace. 8.22 Jeddah is Arabia’s gateway to Africa being the principal port on the Red Sea. It is the main trading port with Egypt, Sudan, Eritrea/Ethiopia, Djibouti and Somalia, all of which are endemic for various filariases. These places, together with Yemen, provided the peninsula with expatriate workers prior to mass-recruitment from South-East Asia, so the threat of importing filariasis from adjacent regions was ever-present. Indeed, minimal levels of transmission have probably been occurring in the wetter south-west mountains of Arabia for centuries. But the dry central and eastern regions would not have supported the life-cycle of the vectors until a few decades ago. 8.23 There are no recent authoritative studies demonstrating whether or not onchocerciasis, lymphatic filariasis or Perstans filariasis (endemic in nearby North Africa) are now endemic throughout Arabia and the Gulf States, where man has recently provided ample nourishment to nurture the vectors of these diseases. In consequence, I respectfully submit that the world will feel a safer place when a worm savvy boffin provides us with the answer. 8.24 Please excuse me for leaving the last few lines of this section of my testimony to the telltale cryptic remarks borrowed from William Blake by the thoughtful Alan Woodruff and co-workers[67] who would not have been the least bit surprised by the involvement of onchocerciasis in GWS. ‘The distribution of onchocerciasis is very incompletely known and may be much more widespread than has hitherto been recognized.......The natural history of the disease is still incomplete and it may be necessary for us to alter many of our opinions concerning it. That, however, may not be a bad thing, for “The man who never alters his opinion is like standing water, and breeds reptiles of the mind.” gulfwarcouncil.com/email_testimony_of%20John%20Brown.htmWell, Blake has been right more than once: How does he describe it? The Sick Rose:
================ I believe that Tam Tam quoted him once.
Skyship
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Post by skyship on Sept 24, 2011 0:44:25 GMT -5
It does appear Canada is targeting some populations: mmmm Same treatment for scabies, used for Oncho and strongyloids? =============================== Future measures Ivermectin, a member of a family of macrolytic lactones, the avermectins, has broad spectrum activity against parasites. It binds to glutamate-gated chloride ion channels, which are present in invertebrate nerve and muscle cells, causing paralysis and the death of the parasite. It does not easily cross the blood-brain barrier in humans and has a low affinity for mammalian ligand-gated chloride channels. Ivermectin has been used for many years in veterinary medicine to control a wide variety of parasites in farm and domestic animals. Since 1987, it has been used to control onchocerciasis and strongyloidiasis. The United States Food and Drug Administration has licensed it for the treatment of these diseases, but not for the treatment of scabies. As noted above, ivermectin has not been licensed in Canada. However, since 1993, it has been successfully used in other countries to treat human scabies that is resistant to other treatment. The advantage of using ivermectin is that it is given orally as a single dose. It has been used as a public health measure to control widespread scabies in population groups. Currently, any advantage of ivermectin over standard topical therapy is questionable. One study did not find any advantage over permethrin, which acts at all stages of the parasite’s life cycle (6). Ivermectin acts only at certain stages of the life cycle of the parasite, as reported with onchocerciasis and strongyloidiasis (6-12) www.cps.ca/english/statements/ii/ii01-01.htm===================================== I am noticing a connection between scabies and oncho, here! Scabies, where do they come from? Other people? or the Environment? Scabies with wolbachia? scabies with oncho? inside simulium? ... ?mmmmmm ===================== In 1920, two dermatologists in Algiers, Montpellier and Lacroix, studying a form of scabies observed in infantrymen from West Africa, discover microfilaria of Onchocerca volvulus in the dermis. They call it "scabies of filaria" ("gale filarienne"). Ouzilleau*, Laigret* and Lefrou* report the same phenomenon in Brazzaville in 1921. The cutaneous lesions are manifestly of the allergic type, the proteins of the microfilaria sensitizing the dermic tissues. The lesions due to scratching are a gateway for the entrance of microbes which aggravate the clinical situation. Scabies of filaria due to Onchocerciasis www.asnom.org/en/442_onchocercose.html=========================================== Awwwwwwwwwww, we don't have rivers in America do we? ============================= "THE MODE OF TRANSMISSION The intervention of a mosquito having been established in the transmission of Malaria, Ouzilleau*, in 1913 in the Congo, blames a mosquito of the genus Culex for the spread of Onchocerciasis. A few years later, the Belgians Rodhain and Van den Braden suspect mosquitoes of the genus Stegomyia and bugs. Roblès in Guatemala finds the culprit in another species in 1919. His observations lead him to conclude that the transmitting agent is a stinging and sucking insect which has a predilection for the temples and the neck. There is only one such insect in the region under study : the female simulium, a genus of little black flies two millimetres in length. Blacklock in 1924 in Sierra Leone confirms the conclusions arrived at by Roblès and clarifies the evolution of the microfilaria in the infected simulium : in the course of eight days, the microfilaria pass from the digestive tube into the thoracic muscles and then reach the proboscis, whence they escape at the moment of stinging. His work will be confirmed in 1946. Unlike the American simulium, that of Africa has a tendency to sting the legs. In Africa, these little flies are to be found in swarms during the day. Their stings are painful and bloody. They are capable of flying long distances, tens of kilometres. The simulium lay eggs on plants and rocks amidst troubled running waters that are strongly oxygenated. In a few days, they can colonise a whole river. The eggs are stuck together in packets by a viscous substance. Before turning into flies, the larvae live in the stream of water."............................ www.asnom.org/en/442_onchocercose.htmlSkyship
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Post by skyship on Sept 24, 2011 1:12:25 GMT -5
Now, these are used as antigens? ?? The subject matter of the invention concerns three cosmid vectors which are ...... unit from amylaceous saccharides having a degree of glucose polymerization ...... encoding antigens of onchocerca volvulus - U.S. Patent Number 5021342 ... If this is not the most insane idea. Infect people with the antigen that actually causes the damage from reaction to the antigens already on the worm that is inside the patient. ================================================= "Because neither vector control nor chemotherapy has proven successful in controlling the disease, the development of a vaccine against infection with the parasite has become a high priority (Strategic Plan for Onchocerciasis Research, Edna McConnell Clark Foundation, N.Y., N.Y., (1985)). In order to develop a vaccine, it is necessary to first identify antigens which induce immunity against the parasite. In the case of onchocerciasis, however, the identification of such antigens is complicated by the fact that much of the pathology seen during the course of the disease may be caused by the induction of the immune response of the host to certain antigens of the parasite (C. D. MacKenzie, J. F. Williams, B. M. Sisley, M. W. Steward and J. O'Day, "Variations in Host Responses and the Pathogenesis in Human Onchocerciasis", Rev. Info Dis., 7: 802-808, (1985)). Because of this concern, it is necessary to delineate as fully as possible which parasite antigens are involved in inducing potentially beneficial, as opposed to harmful aspects of the host immune response."........................ www.patentstorm.us/patents/5021342/fulltext.html======================================= the host immune response, is what can kill the pateint. Skyship
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Post by skyship on Sept 24, 2011 1:16:20 GMT -5
Okay, back to the EMAIL from our friend, John Brown=============== IMPEDIMENTS TO THE DETECTION AND RECOGNITION OF ONCHOCERCIASIS IN DIFFERENT ETHNIC GROUPS AND IN NEW ARABIAN ENDEMIC REGIONS. 9.1 Onchocerciasis is routinely discovered to be endemic in regions where it was thought not to present a health threat. A recent example was reported by Maia-Herzog and co-workers[68] who recently identified a new endemic region, 2000 km away from the only previously known focus in Brazil. Their study employed state of the art investigative techniques that are not commercially available; namely, recombinant antigen panel (RAP) ELISA, and polymerase chain reaction (PCR) skin probe. 9.2 Maia-Herzog’s investigation was prompted by the case of a sixteen years old girl who had never been outside of the region, and who was confirmed with onchocerciasis in 1986. Since the case was autochthonous, skin biopsies from 2000 local individuals were investigated by the traditional parasitological method but none were found to be infected. 9.3 In 1999, the investigation by Maia-Herzog’s team identified very lightly infected cases from three towns in the region by both RAP/ELISA and PCR methods. The researchers considered that the route for the introduction of the parasite into the region was through the immigration of large numbers of garimpeiros (gold miners) from Brazil’s Amazonia focus between 1970 and 1980. This prompted questions regarding the geographical extent and location of unknown endemic zones in Brazil; questions that could only be answered by sampling large numbers of people throughout the whole country. In parallel, it is legitimate to hypothesise that, along side the known endemic regions, unidentified endemic zones also exist in Arabia because large numbers of the native Arab and expatriate populations have not been investigated for the disease. The GWVs are a case in point; don’t look, don’t find.Blackflies at Dhahran, Saudi Arabia, 1983 9.4 When I arrived at Dhahran in January 1983, the installation of irrigation pipes for the landscaping around the new houses where I lived [refer attached photo] was almost complete. This landscaping was an experimental model for the landscaping on an adjacent military base the size of a large village that was then under construction. Any health problems associated with the experimental landscaping, therefore, would have been replicated many times over on the military base by the start of the Gulf War in 1991. 9.5 During the summer months the midday temperature reached 55 deg C (130 deg F). There is little, if any, shade in a sandy desert. Insects and reptiles cannot survive for more than a few seconds during daylight hours in such extreme conditions, so I never saw any of these. Prior to installing the landscaping I could sit in my garden of sand and not see a single insect all day. 9.6 Medical tracts on onchocerciasis, such as that found in the Oxford Textbook of Medicine, advise that blackflies (Simulium species) require fast flowing rivers and streams for breeding. They crawl down overhanging vegetation and lay their eggs up to 100mm below the water surface. Most importantly, the flies mate at sites of white water; waterfalls, rapids, weirs, fords, hydro-electric facilities and the like. They are attracted by the spume. Ordinarily, their diet is exclusively cellulose but, like mosquitoes, the female requires a blood meal to achieve ovulation. Hence the historical link between white water and biting flies. Blackflies’ behaviour becomes aggressive in proximity to a spray of water. This is partly how onchocerciasis acquired the tag, ‘river blindness’. 9.7 Dhahran is as dry as a bone and as flat as a pancake so there are no fast flowing watercourses or sites of white water in the entire Gulf region. There is barely a single day of rain in a year. I estimate that the nearest river or stream to Dhahran would be in Iraq or Oman, between 600km and 800km away. It is clearly the case that going back several decades, blackflies could not have survived or existed in Eastern Arabia adjacent to the Persian Gulf. 9.8 Over recent decades, however, rapid urbanisation and the provision of abundant water supplies have literally changed the colour of the Arabian landscape. From an aeroplane one sees how desert settlements are delineated by their emerald green landscaping. 9. 9 I was able to sit in my sandy garden and enjoy a barbeque free from flies for my first few months at Dhahran while the irrigation piping was installed around my house. However, within a few days of opening the irrigation valves and planting shrubs to provide shade, swarms of blackflies homed in on the sprinklers like a biblical plague. Heaven knows where they came from. Wherever there was a sprinkler there was a cloud of buzzing blackflies. 9.10 I only considered where the flies laid their eggs after leaving Arabia so this remains unknown to me. There were 2 evaporation ponds from sewage treatment plants quite nearby with well established reed beds. There was also an ozone (not chlorine) treated swimming pool approximately a kilometre away. I guess the evaporation ponds would have been the more likely egg depositories, but I cannot be sure. 9.11 Either way, man’s best endeavours to tame the Arabian desert have provided an alternative to fast flowing river environments for blackflies to flourish and facilitate the transmission of onchocerciasis in regions where Mother Nature alone precludes transmission. In parallel, increases in the incidence of lymphatic filariasis were reported from Pacific regions following the introduction of large irrigation projects. Once again history has repeated itself. gulfwarcouncil.com/email_testimony_of%20John%20Brown.htm======================================== HOW SOON WE FORGET "DESERT STORM"?? Many things took our eyes away from what went down in Kuwait!skyship
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Post by skyship on Sept 24, 2011 1:26:50 GMT -5
continued report to Congress............... VARIATIONS IN PRESENTATIONS OCCURRING IN NATIVES OF ENDEMIC ZONES COMPARED TO LIGHTLY INFECTED EXPATRIATES LIKE THE GWVs 11.1 A considerable difficulty in searching for onchocerciasis in GWVs is that the signs and symptoms that doctors must look for (section 3) have been published in disparate and obscure journal reports that vary according to the geographical locations and ethnic groups investigated. The point was previously made that the Arabian presentation of sowda, the black disease, has only been reported occurring in Arabians and Liberians, and certainly not in white Caucasians, and that case reports of onchocerciasis in native Arabians will not inform doctors of the different presentations expected to occur in GWVs infected with exactly the same species and strain of Onchocerca. Unfortunately and so far as I am aware, these reports have not been collated into a comprehensive diagnostic manual. Standard medical references on the subject, such as found in The Oxford Textbook of Medicine, are so incompetent that they merely serve to misinform and must be completely rewritten. 11.2 Furthermore, reported observations of presentations have been contradictory as the comparison of two studies, one of Americans and the other of Europeans illustrates. Woodruff and co-workers published an investigation of lightly infected expatriate cases as long ago as 1965[67] focussing on the insidiousness and chronicity of the pathogenesis in such cases. They looked at 76 cases with microfilariae in their skin, 72 of whom were Europeans, and compared them to 59 cases diagnosed clinically (characteristic rash, pruritis, known exposure, eosinophilia, positive filarial skin test), but in whom microfilariae could not be found. Unlike the GWVs who were only exposed for a matter of months, the mean exposure of this group was 11.6 years, mostly in various regions of Africa. 11.3 McCarthy and co-workers[16] compared a group of 20 Americans who had acquired onchocerciasis during visits to Central and West Africa with a group of 21 infected native residents of endemic areas in Africa or Central America. The Americans were Peace Corps volunteers and their mean exposure was 2 years compared to 11.6 years for Woodruff’s cases. A similarity with GWVs is that they became symptomatic between 3 months and 3 years (mean 18 months) after departing the endemic region. 11.4 McCarthy’s findings were (with Woodruff’s findings bracketed for comparison) 85% (68% Europeans) of Americans compared to 67% of natives presented with pruritis, while 60% (46% Europeans) of Americans had rashes, as do many GWVs, compared to only 29% of natives. Significantly, no Americans (34% Europeans) had any form of ocular disease, whereas 81% of the natives had ocular symptoms (river blindness) or abnormal findings. Subcutaneous nodules also occurred in 81% of natives but did not occur at all in the Americans (significantly 23% Europeans). All of the natives had microfilariae in their skin but they were present in only 45% of Americans. 11.5 Of significance to apparently healthy GWVs is that 15% (16% Europeans) of the Americans with proven infection had minimal or no symptoms or signs of disease and were evaluated only because of their exposure history. This prompted McCarthy to emphasise the need for case finding in travel companions when one member of a group is found to be infected. So far as the GWVs are concerned I, John Brown, am their infected travelling companion. It therefore inevitably follows that every GWV, whether sick or healthy, must now be screened since, according to these studies, 15-16% of healthy GWVs are asymptomatic cases at risk of developing late onset disease. The example to follow is that of Pryce and co-workers[17] who found that 9% of European cases of onchocerciasis contracted on an expedition to Cameroon were asymptomatic. Although the report does not say so, I have ascertained that this expedition was the film crew shooting the Tarzan movie, ‘Greystoke’ on location in the jungle. 11.6 Following the diagnosis of a movie maker 15 months after exposure, Pryce and co-workers sent questionnaires and an invitation to be investigated to the whole film crew. Of the 60% that responded, 22% were deemed to be laboratory positives determined by traditional diagnostic techniques, but 49% of laboratory negatives were symptomatic, indicating that some were false negatives that would have been positive if evaluated by RAP/ELISA and PCR skin probe. The negatives were to be re-evaluated to detect late onset disease. GWVs were not evaluated for early or late onset onchocerciasis, but significantly the first cases of Gulf War syndrome, as it was then known, did not surface until a few years after the war had ended, which is consistent with the shortest time taken for onchocerciasis to become symptomatic. PROBLEMS WITH LABORATORY FINDINGS FOR GWVs 12.1 Freedman and co-workers[73] investigated 500 residents of a village in the Volta River basin of Ghana. Traditional parasitological examination of skin snips, palpitation for nodules, and slit lamp ocular examination identified 10 subjects without clinical or parasitological evidence of infection, who would ordinarily be considered to be, “putatively immune.” When these 10 individuals were investigated by PCR skin probe, however, 9 were found to have O. volvulus DNA in their skin, indicating current infection with the parasite. This leaves little room to doubt that if GWVs were investigated by the same cutting-edge techniques, signs of exposure to the parasite would be detected in most symptomatic cases and some asymptomatic cases. 12.2 There is a consensus between researchers that adult O. volvulus have a nominal life of 15 years, though some have speculated that it is nearer to 20. It is therefore predictable that Onchocerca parasites would have died off in some sick GWVs whose antibody levels would be negligible, though they could still be very ill due to the consequences of chronicity. The GWVs were exposed for a short period to what could only be very low infection rates that provoke correspondingly low antibody levels. In consequence, it is important that the GWVs are investigated by the most sensitive means available, instead of the standard methods with their shortcomings that are routinely employed. Standard diagnostic procedures 12.3 Outside of research settings, laboratory diagnosis is dependent on three unsophisticated investigations. Firstly, parasitological demonstration of microfilariae in skin snips is definitive, but rarely achievable in lightly infected travellers or expatriates like the GWVs, so it is of little or no use here. 12.4 Secondly, and when microfilariae cannot be found, suspected cases may be given a provocative 50-mg dose of diethylcarbamazine. This is known as the Mazzotti test. Within 15 minutes to 24 hours, but most often within 3 hours, infected patients will develop pruritis with or without a reddening of the skin (erythema). In London, patients are hospitalised for this test since severe reactions occasionally occur. These days the test is rarely performed. This is the test that my American colleague bravely requested twice, because he has a rash, only for his requests to be ignored. Route one to getting a rudimentary handle on the involvement of onchocerciasis in Gulf related illness is to investigate a dozen or so GWVs with rashes by this method. The test is very cheap, very simple and will provide rapid results. This should be done immediately albeit 12 years too late. 12.5 Thirdly, the currently available serology consists of a crude antigenic preparation of a non-onchocercal filarial parasite; the filaria ELISA. Standardisation is poor, a positive result, at best, cannot differentiate between the 8 filarial human parasites and at worst may cross-react with other helminthiases like stronyloidiasis. Despite the lack of specificity, the sensitivity of this type of serology is almost 100%. Most native residents of filariasis endemic areas will have antibodies whether they are currently infected or not, and most will also be asymptomatic[75]. Thus, serological investigation of this type is only useful for evaluating travellers and expatriates, like the GWVs, from non-endemic regions who are presumed seronegative initially or to detect a quantitive decrease in antibody levels in response to treatment. When investigating GWVs with this assay, it is probably prudent to interpret any minimal recognition of the antigens as positive. 12.6 A standardised protocol based on units of standard deviation (SD) above the mean optical density of sero-recognition by presumed infection-free controls defines the negative cut-off value of assays for both native residents of endemic regions and travellers, expatriates and GWVs. Such protocols are derived from research of the native populations of endemic regions but have not been separately standardised for the sero-diagnosis of non-endemic visitors. Yet the recognition of antigens by sera from minimally infected but highly symptomatic travellers and expatriates must be comparable to that of minimally infected asymptomatic or infection-free native residents who may be deemed to be seronegative based on current protocol cut-offs; so most cases like the GWVs would be predicted to be falsely seronegative, according to the current filaria ELISA protocol. 12.7 As explained in section 4, studies of endemic native populations have shown that tissue invasive helminthiasis induces a skewing from Th1-type cytokine responses (inflammatory) towards Th2-type cytokine responses (antibody producing). McCarthy and co-workers[16] found that there was no difference in the production of Th1-like cytokines between American expatriate onchocerciasis cases and cases who were residents of endemic regions. But they found that the endemic native residents produced significantly more Th2-like cytokines than the Americans suggesting that they would produce a further enhanced antibody response. Clearly a separate protocol with a much lower negative cut-off value is required to more accurately identify GWVs with onchocerciasis and who may currently be deemed to be seronegative (falsely). 12.8 In summary, the results of currently available serology are far from clear-cut. They are highly susceptible to misinterpretation in briefly exposed cases like the GWVs. The Mazzotti test might be the only available means of achieving a definitive diagnosis in GWVs. 12.9 By comparison to the general filarial ELISA, the RAP/ELISA comprising of a cocktail of three O. volvulus antigens has been shown to be 100% specific by Bradley and co-workers[76] with the exception of cross-reactive infections by Brugia malayi (lymphatic filaria) which has not been reported from Arabia (YET!).gulfwarcouncil.com/email_testimony_of%20John%20Brown.htmcontinued......... Skyship
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Post by skyship on Sept 24, 2011 1:49:14 GMT -5
FASCIOLIASIS 13.1 Fascioliasis is not such a serious disease as onchocerciasis but it nevertheless incapacitates cases[77]. Its importance in GWS is that some symptoms are different to those of onchocerciasis and when symptoms overlap, the clinical picture is confusing. 13.2 Fasciola liver flukes (there are two species: F. hepatica and F. gigantica, sometimes called aegyptica) are endemic throughout the world’s sub-tropical and temperate zones. The leaf-shaped parasites infect many herbivores such as cattle, sheep, goats, rabbits and the like as well as humans. Snails are intermediate hosts essential to the parasite’s lifecycle. The flukes are ingested with infected salad vegetables on which they are encysted, and then burrow through the gut to the liver, where they mature in the bile ducts to an adult length of three to four centimetres. 13.3 The Journal of the Egyptian Society of Parasitology needs to be made compulsory reading for quartermasters, kitchen superintendents and whoever else purchases salad vegetables for allied forces serving in the Middle East. Fascioliasis is rife in Egypt where salad leaves are the vehicles of infection. Fasciola gigantica is the species[78]. The vegetables are watered from irrigation canals that are the habitats of the intermediate snail hosts. Infected goats, and to a lesser extent camels, are also watered from these watercourses and reservoirs causing a serious public health hazard[79]. Egyptian parasitologists recommend preparing salad leaves for consumption by soaking them in a solution of potassium permanganate, together with liquid soap, acetic and citric acid to clear amoeba and hookworm, for 10 minutes before rinsing under running water for a further 10 minutes[78]. I doubt that many of us wash our salads so conscientiously, and submit that it is impossible to remove 100% of Fasciola metacercariae (cysts) in mess hall kitchens. 13.4 Egypt is exporting salad vegetables and strawberries to the UK so presumably Egypt is a major supplier to the Middle East market. Iraq produces its own salad vegetables but whether or not they are irrigated via canals from the Tigris and Euphrates and whether the canals are contaminated with Fasciola I do not know. I have not seen anything published, but Iraqi medicos have had more pressing matters to deal with in recent times that could account for this paucity of information. Pathology 13.5 A lucid description of the symptoms and pathology along with a useful bibliography was provided by Facey and Marsden in 1960[77]. The pathology has 3 stages: 1. Onset — may be acute with fever or uneventful lasting 4 to 6 months. 2. Latent — malaise and vague syptoms lasting several years. 3. Obstructive — may last a lifetime without surgery. 13.6 I am unaware of any research demonstrating that fascioliasis causes an immunosuppressive syndrome in the same manner as filariasis and schistosomiasis. Nevertheless, despite the fluke not having a cycle in the chest, hyperreactivity of the airways was identified in 1997 as an allergic reaction often seen in the onset stage, which may present as chest pains or sore throat or bronchitis[80]. I submit that, in the USA and UK, lightly infected cases presenting with these symptoms may be misdiagnosed as cases of flu or miscellaneous viral infections. In this event it follows that the vague symptoms and malaise typical of the latent stage may be misdiagnosed as post-viral fatigue syndrome. This raises the question of how many cases of GWS are misdiagnosed cases of fascioliasis. There have been recent press reports of soldiers presently serving in Iraq being invalided out of active service with a flu-like illness. This illness could be fascioliasis. gulfwarcouncil.com/email_testimony_of%20John%20Brown.htm======================================= When the AMA and CDC and WHO, put this under the rug, Oh, we have irradicated ONCHO from Africa? Really?................. Then it became prevalent in the Middle East? Strange, how the destruction of Africa, then now the destruction of the Middle East, seem to follow each other?
As our troops move in, and put demon cracy into govt, with all our bases bordering the people, they are coming home with these incurable maladies called GWS, which can be traced to the environment of which nothing was familiar, or even safe to be in, nevertheless the fake war goes on there are the same bioweapons in Afghanistan as well, Yeman, adding Leishmaniasis to the soup.
I have seen people in America with this, and they are amongst us. We ignore it, and it goes away? How they suffer!========================== ==========================================
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Post by skyship on Sept 24, 2011 2:02:49 GMT -5
contin....... ..."Anomalies in geographical distribution 13.7 A comprehensive review of the literature reported that between 1970 & 1990, more than 8000 cases from 42 countries had been documented. It is thought that the actual number of human cases is much greater than this[81]. In Europe; France (8898 cases between 1950 & 1983) and Portugal (1099 cases between 1970 & 1990) would appear to be the most endemic areas. Many of the French cases were reported from the Pas de Calais (Strait of Dover) region, which is just twenty miles from Britain, where only 93 cases were reported between 1970 & 1990[5]. 13.8 Why the incidence of disease is so much greater in France than in Britain is puzzling because the population of the two countries is roughly the same. In Australia and New Zealand, both of which are world leaders in livestock production, zoonotic infection is very high yet only eight human cases were reported from Australia between 1970 & 1990, and none from New Zealand[81]. 13.9 The most puzzling statistic, however, is that only two cases have ever been reported from the USA[82,83] with a population in the region of 290 million. The whole country is endemic for F. hepatica and 33% of the rabbits on the Texas Gulf plain are infected providing a, ‘vast reservoir of infection’[84]. 13.10 Is the incidence of infection really so much higher in France than in the USA and UK or is it that American and British cases are underdiagnosed or underreported? The reported incidence of disease in the USA, UK, Australia, and New Zealand is not credible. It is thought that the higher French number of reported cases is partly due to their use of serological tests in preference to the parasitological techniques that we employ[81]. Diagnosis and treatment 13.11 In areas where the disease is rarely reported or thought to be absent, such as the USA, the diagnostic possibility of fascioliasis may not be considered by physicians who are unfamiliar with it. It was thought that only 5% of cases were diagnosed during the acute phase[85] and that many cases go unrecognised and unreported due to unfamiliarity[86]. 13.12 American physicians were surprised to come across the two chronic cases of nine and fifteen years standing, reported from the USA, leading them to speculate that the diagnosis was routinely being missed, a view held by many authors on this subject. American and British case histories indicate that our doctors do not consider the possible diagnosis of fascioliasis unless alerted by a pain in the right hypochondrium. Clearly, the suspicion of French primary care doctors is triggered by other telltale signs or symptoms but I do not know what they are and respectfully submit that American and British doctors need to apprise themselves of French practice. 13.13 From the French experience it is clear that serology offers an efficacious and economical diagnosis. ELISAs are highly sensitive and, although cross-reactions with other helminths have been reported, permit a presumptive diagnosis. This is particularly so in regions where concomitant helminth infections are unlikely to occur. 13.14 It would appear, on the face it, that English speaking countries have much to learn from the French on the diagnosis and management of this disease and, most significantly, the French claim that their military personnel that served in the 1991 Gulf War were not affected by GWS. 13.15 The earliest possible diagnosis should be aimed for, ideally before the immature flukes reach the bile ducts. Triclabendazole, a well tolerated anthelminthic, taken orally in two doses on a single day kills all flukes regardless of their stage of development[87]. 13.16 Liver flukes contracted during the 1991 Gulf War will have died by now so chemotherapy is not required. However, Robert Haley’s identification of gall bladder disease in GWVs could be a consequence of chronic obstructive fascioliasis. Hence, when gall bladder disease is detected in GWVs it would be sage to check the bile ducts for obstructions which, if the gall bladder is removed, can be surgically cleared at the same time. 13.17 Gall bladder disease is the predictable outcome of longstanding obstructive fascioliasis. Allied personnel currently serving in Iraq will certainly succumb to this in years to come if they are fed salads contaminated with Fasciola. 13.18 Accordingly, I respectfully submit that it is prudent for military caterers to stop feeding allied troops in Iraq with uncooked vegetables forthwith, unless obtained from a known, safe, uncontaminated source. 14.0 THE FRENCH 14.1 The French Foreign Legion served as ground troops in the 1991 Gulf War. Historically they were permanently stationed in Africa making them unique. There is no equivalent American or British Africa based force. Many helminthiases are endemic in Africa so the French must have evolved unique military medical procedures to control and manage these ubiquitous infections occurring in the legionnaires. That is, legionnaires with onchocerciasis and or fascioliasis, without knowing where their disease was contracted, may have received efficacious anthelminthic treatments that have spared them the misery of GWS. 14.2 I therefore submit that it will be expedient and informative for the American military to ask NATO to provide the following information: 1. How is filariasis, especially onchocerciasis, controlled, diagnosed and managed in the Foreign Legion. 2. What signs and symptoms prompt French primary care doctors to suspect fascioliasis and how do they confirm the diagnosis." gulfwarcouncil.com/email_testimony_of%20John%20Brown.htmAnyone seen the AMA? or the CDC? or the DHHS, or the NIH? ?? who do they work for? Skyship
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Post by skyship on Sept 24, 2011 2:07:27 GMT -5
A true Brit, picking up King Arthur's Sword!15.0 CONCLUSION 15.1 I submit that the evidence presented herein demonstrates that the failure to screen GWVs for onchocerciasis was negligent and incompetent in the extreme. This has resulted in the health of GWVs being permanently damaged. Whilst it is too late to turn the clock back it is not too late to stop the rot. Consequently, rigorous treatment should be commenced as soon as possible. 15.2 Furthermore, there are lessons to be learned from this debacle: 1. That many onchocerciasis endemic regions are unkown and shall remain so unless they are sought out. 2. That human onchocerciasis may be endemic wherever zoonotic onchocerciasis is endemic. 3. That minimal parasite loads cause debility, misery and morbidity. Accordingly ALL infections should be taken seriously and treated rigorously if required. 4. That onchocerciasis is not unique to those who served in the 1991 Gulf War. 15.3 I conclude my testimony with this entertaining riddle to which I do not know the answer. Given the above and given that the USA is endemic for zoonotic onchocerciasis from coast to coast, what happened to human onchocerciasis imported into the USA with slavery, bearing in mind that the origin of slaves was the onchocerciasis hyperendemic regions of West Africa? 16.0 REFERENCES 1. Chumbley LC, (1980). Onchocerciasis in Saudi Arabia, pages 412—418 in Fauna of Saudi Arabia vol. 2. Edited by Wittmer W, and Buttiker W. Pro Entomologia, c/o Natural History Museum, Basel, Switzerland; and Ciba- Geigy Ltd., Basel, Switzerland. Note: This paper eluded inclusion in the Index Medicus. The British MoD was unaware of it until I provided them with a copy in autumn 2000. They have been sitting on it ever since. 2. Sir Peter de la Billiere (1992). Chapter 9 in, Storm Command: A personal account of the Gulf War. London: Harper Collins 3. Fukuda K, Nisenbaum R, Stewart G, et al (1998). Chronic Multisymptom Illness Affecting Air Force Veterans of the Gulf War. JAMA 280(1):981—988 4. Coker WJ, Bhatt BM, Blatchley NF, and Graham JT, (1999). Clinical findings for the first 1000 Gulf War veterans in the Ministry of Defence's medical assessment programme. BMJ 318(7179):290—294 5. Connor DH, Gibson DW, Neafie RC, et al (1983). Sowda—Onchocerciasis in North Yemen: A clinicopathalogic study of 18 patients. Journal of Tropical Medicine and Hygiene. 32(1):123-37 6. Siddiqui MA, and Al-Khawajah MM, (1991). The Black Disease of Arabia, Sowda- onchocerciasis: New Findings. International Journal of Dermatology 30(2):130-33 7. Freedman DO, Unnasch TR, Merriweather A, and Awadzi K, (1994). Truly infection-free persons are rare in areas hyperendemic for African onchocerciasis. Journal of Infectious Diseases 170:1054—1055 8. Gasparini G, (1964). Problems of onchocerciasis in new suspected areas sowda and onchocerciasis (Report for the First International Congress of Tropical Dermatology, Naples, Italy. June 1964.) Archivio Italiano di Science Mediche Tropicali e Parassitologia 45:243-260 9. Nicolson GL (1998). Considerations when undergoing treatment for Gulf War illness/CFS/FMS/rheumatoid arthritis. International Journal of Medicine 1:123-128 10. Hoerauf A, Volkmann L, Hamelmann C, et al (2000). Endosymbiotic bacteria in worms as targets for a novel chemotherapy in filariasis. The Lancet 355:1242-1243 11. Wartman WB, (1947). Filariasis in American armed forces in World War II. Medicine 26:333—394 12. Puyuelo R and Holstein MM (1950). Revista da Sociedade Brasileira de Medicina Tropical. 10:397 13. Hughes MH and Sarkies JWR (1951). Annals of Tropical Medicine and Parasitology 45:73 14. Woodruff AW. (1965). Disabling non-opthalmological effects of onchocerciasis. Reference number ONCHO/WP/1.65. Geneva, 29th June - 5th July. 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Nicolson GL, Nasralla M, Haier J and Nicolson NL (1998). Diagnosis and treatment of chronic mycoplasmal infections in fibromyalgia and chronic fatigue syndromes: Relationship to gulf war illness. Biomedical Therapy 16(4):266-271 51. Haier J, Nasralla M, Franco AR, and Nicolson GL, (1999). Detection of mycoplasmal infections in blood of patients with rheumatoid arthritis. Rheumatology 38:504-509 52. Nicolson LG, Nasralla M, Haier J et al (1999). Myoplasmal infections in chronic illnesses: Fibromyalgia and chronic fatigue syndromes, Gulf War illness, HIV-Aids and rheumatoid arthritis. Medical Sentinel 4(5):172-175 & 191 53. Petrie PWR and Seal KS (1943). Blue skin disease. Page 88 in, A Medical Survey of the Western Aden Protectorate, 1939-40. Report No 66, Colonial Office, London. 54. Fawdry AL (1957). Onchocerciasis in South Arabia. Transactions of the Royal Society of Tropical Medicine and Hygiene 51(3):253-255 55. Gasparini G (1964). 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Cytologic diagnosis of bancroftian filariasis in a non-endemic area. Acta Cytologica 32(2):267-269 62). Sebai ZA (1985). Filariasis in the western part of Saudi Arabia. Health in Saudi Arabia 1:151-158 63). Holmes PR (1986). A study in population changes in the adult Culex quinquefasciatus Say (Diptera: Culicidae) during a mosquito control programme in Dubai, United Arab Emirates. Annals of Tropical Medicine and Parasitology 80:107-116 64). Omar MS (1996). A survey of bancroftian filariasis among South-East Asian expatriate workers in Saudi Arabia. Tropical Medicine and International Health 1(2):155-160 65). Rajasekariah GR, Das PK, Parab PB et al (1988). Wuchereria bancrofti larvae in naturally infected Culex quinquefasciatus. Annals of Tropical Medicine and Parasitology 82:637-639 66). Ramiah KD and Das PK (1992). Seasonality of adult Culex quinquefasciatus and transmission of bancroftian filariasis in Pondicherry, South India. Acta Tropica 50:275-283 67). Woodruff AW, Bell S, Ridley DS, and Schofield FD. (1965). Clinical, Diagnostic and theraputic aspects of onchocerciasis. Transactions of the Royal Society of Tropical Medicine and Hygiene. 521:97—108 68. Maia-Herzog M, Shelley AJ, Bradley JE, et al (1999). Discovery of a new focus of human onchocerciasis in central Brazil. Transactions of the Royal Society of Tropical Medicine and Hygiene 93:235—239 69. Cheema AH, El-Bihari S, Ashour NA, and Ali AS (1984). Onchocerciasis in camels (Camelus dromedaries) in Saudi Arabia. Journal of Helminthology 58(4):279-285 70. Nasher AK (1986). Incidence and intensity of Onchocerca fasciata Railliet and Henry 1910 in local camels in Saudi Arabia. Annales de Parasitologie Humaine et Comparee 61(1):77-80 71. Ghandour AM, al-Amoudi AA, and Banaja AA (1991). Onchocerca fasciata Railliet and Henry 1910 and its nodule development in camels in Saudi Arabia. Veterinary Parasitology 39(1-2):67-77 72. Steele L (2000). Prevalence and Patterns of Gulf War Illness in Kansas Veterans: Association of Symptoms with Characteristics of Person, Place, and Time of Military Service. American Journal of Epidemiology 152:992–1002. 73. Freedman DO, Unnasch TR, Merriweather A, and Awadzi K. (1994). Truly infection-free persons are rare in areas hyperendemic for African onchocerciasis. Journal of Infectious Diseases 170:1054-1055 74. Botto C, Gillespie AJ, Vivas-Martinez S, et al (1999). Onchocerciasis hyperendemic in the Unturán Mountains: the value of recombinant antigens in describing a new transmission area in Southern Venezuela. Transactions of the Royal Society of Tropical Medicine and Hygiene 93:25—30 75. Mackenzie CD, Williams JF, Sisley BM et al (1985). Variations in host responses and pathogenesis of human onchocerciasis. Reviews of Infectious Diseases 7:802-808 76. Bradley JE, Trenholme K, Gillespie A et al (1993). A ocktail of recombinant antigens provide a sensitive serodiagnostic test for onchocerciasis. American Journal of Tropical Medicine and Hygiene 48:198-204 77. Facey RV, and Marsden PD, (1960). Fascioliasis in man: an outbreak in Hampshire. British Medical Journal 2:619—62 78. El-Sayad MH, Allam AF, and Osman MM, (1997). Prevention of human fascioliasis: A study on the role of acids detergents and potassium permanganate in clearing salads from metacercariae. Journal of the Egyptian Society of Parasitology 27(1):163—169 79. Farag HF, Salem AI, Khalil SS, & Farahat A, (1993) . Studies on human fascioliasis in Egypt. Seasonality of transmission. Journal of the Egyptian Society of Parasitology 23(2):331—340 80. Gabbour SN, Allam AF, and Sultan MM, (1997). The pulmonary performance and airway reactivity in acute and chronic fascioliasis before and after triclabendazole treatment. Journal of the Egyptian Society of Parasitology 27(1):113—129 81. Chen MG, and Mott KE, (1990). Progress in assessment of morbidity due to Fasciola hepatica infection. Tropical Diseases Bulletin 87(4):1—38 82. Norton RA, and Monroe L, (1961). Infection by Fasciola hepatica acquired in California.Gastroenterology 41:46—48 83. Hauser SC, and Bynum TE, (1984). Abnormalities on ERCP in a case of human fascioliasis. Gastrointestinal Endoscopy 30(2):80—82 84. Olsen OW, (1948). Wild rabbits as reservoir hosts of the common liver fluke, Fasciola hepatica in southern Texas. Journal of Parasitology 34:119—123 85. Belding (1952). Textbook of Clinical Parasitology 2nEdition. Appleton-Century-Crofts. New York. 1952. page 629 86. Catchpole BN, and Snow D, (1952). Human ectopic fascioliasis. The Lancet 2:711—712 87. Apt W, Aguilera X, Vega F, et al (1995). Treatment of human chronic fascioliasis with triclabendazole: drug efficacy and serologic response. American Journal of Tropical Medicine and Hygiene 52(6):532—535 ____________________________________________________ Physicians of the Utmost Fame Were called at once, but when they came They answered, as they took their fees, 'There is no cure for this disease.' ____________________________________________________ Under penalty of perjury, I swear that the above statement is true and correct to the best of my knowledge, information and belief. John David Brown British Citizen Date of testimony: November 17th 2005 STATEMENT OF FEDERAL SUPPORT No federal or other funding received and no conflict of interest
Presented::::::::::::::::::::::::::::[/i] EMAIL TESTIMONY of John David Brown to THE SUB-COMMITTEE ON NATIONAL SECURITY, EMERGING THREATS, AND INTERNATIONAL RELATIONS chaired by Representative Christopher Shays COMMITTEE ON GOVERNMENT REFORM HOUSE OF REPRESENTATIVES OF THE UNITED STATES OF AMERICA SUBJECT: Examining the Department of Veterans’ Affairs’ implementation of the Persian Gulf War Veterans Act of 1998 VENUE: Room #2154 Rayburn House DATE: November 15th 2005 gulfwarcouncil.com/email_testimony_of%20John%20Brown.htmSkyship
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Post by skyship on Sept 24, 2011 2:50:27 GMT -5
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Post by skyship on Sept 29, 2011 23:19:46 GMT -5
Reports from Gulf Vets...... =================================== "Onchocerciasis will not be found unless it is specifically sought out, that is specifically tested for. This has not happened, even though it was identified by the US military as an endemic health threat before the deployment of forces to the Gulf region.I too have been prescribed doxycycline for onchocerciasis. In my case the dose is 200 mg/day for 6 weeks. I have been taking this dose every 6 months for two and a half years. The difference is that I also take a single dose of ivermectin towards the end of each cycle to clear any Onchocerca parasite embryos and hopefully further damage or kill the adult worms. That sounds like an Onchocerca subcutaneous fibrous nodule, not a cyst. The docs should have had it carefully investigated by a pathologist; the foreign body might have been be a dead worm. Onchocerca is a parasitic worm that produces up to 10,000 embryos per day, but there are Wolbachia bacteria inside the worms and embryos that are responsible for most of the pathology. This is why doxy is helpful. It also accelerates the death of adult worms. When an adult worm dies it becomes encysted within a fibrous nodule. Sometimes live worms in a bundle are also encysted when one of the bundle of worms die. If you have a particularly big nodule it would be worth asking for it to be excised and investigated to see what’s inside. Other guys on this board have asked to be investigated for onchocerciasis but have been ignored. Gulfvet1, who also has a rash, even presented his doc with irrefutable proof that onchocerciasis is involved in GWS but was still not investigated. I am at a loss to think of any way to get docs to look for this disease. It’s hopeless. But at least the medical literature that London docs accepted as proof of the involvement of onchocerciasis in GWS, is now in the USA. The question now is what to do with it. " www.gulfwarvets.com/cgi-bin/ultimatebb.cgi?ubb=print_topic;f=1;t=000350there is more to this story. skyship
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Post by skyship on Sept 30, 2011 2:36:51 GMT -5
Leishmaniasis(linked with trypanasoma) and oncho.............. in this case.....leishmaniasis used and infectious agent........ Settlements, security fence and emergence of leishmaniasis Preparing a presentation on leishmaniasis for a medical meeting which was held at the end of last November near Bethlehem (National Palestinian Authority), I came across this article published in Emerging Infectious Diseases : “ Ecoepidemiology of Cutaneous Leishmaniasis Outbreak, Israel” by Singer et al. (1). This interesting paper reported 161 cases of cutaneous leishmaniasis caused by Leishmania tropica which occurred in the Jerusalem district during 2004–2005. These cases occurred in Ma’ale Adumim, a town just outside Jerusalem. In fact, Ma’ale Adumim is a new Israeli settlement and a city in the West Bank, on the edge of the Judean desert and cannot be considered, according to international laws (though disputed by the Israeli government) as part of Israel as stated in the title of the paper. Moreover, the discussion evoked the role of global warming in this outbreak without emphasizing on the consequences of the construction of the security wall, the building of bypass roads and the establishment of new settlements on hyrax populations, the small mammal reservoir host for Leishmania (2). This point was mentioned by Agenda item 14 presented at the 2007 WHO health assembly (3). The picture below, shot near Bethlehem, illustrates quite well the ecological damages caused by Israeli settlements and the possible consequences on the epidemiology of leishmaniasis.
Nasereddin & Jaffe (4), as soon as 2004, pointed out the possible consequences of the security fence on the incidence of visceral leishmaniasis by this premonitory sentence: ““it is certain that this manmade barrier will change the dynamics of zoonotic infectious disease transmission in Israel and the West Bank. It may be true that diseases do not respect borders, but governmental decisions can disrupt local ecologies thus changing epidemiological patterns of diseases in both Israel and Palestine, and such changes may have important ramifications for public health”. parasito-myco.onetudie.com/t200-settlements-security-fence-and-emergence-of-leishmaniasis change the ecology, as in Kuwait etc.....as in GAZA........give the people, soldiers, etc leishmaniasis, oncho or chagas.
co factor with mycoplasmas? and brimstone?skyship
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Post by skyship on Sept 30, 2011 3:01:48 GMT -5
Morgellons like? Disfiguring disease caused by an alliance between three parasites " Her condition is known as mucocutaneous leishmaniasis, or espundia. It’s the result of a combined assault from three different parasites, separated by billions of years of evolution and united in their disfigurement of this woman’s face.The first partner is a sandfly. Through its bite, this blood-sucking insect spreads the ringleader of the infectious trio – a single-celled protozoan called Leishmania guyanensis (which gives the disease its name). Once inside the skin, Leishmania takes down our immune system from within. It gets sucked up by white blood cells but instead of being digested, it converts the cells into factories for producing more Leishmania. In doing so, it triggers an intense wave of swelling and inflammation – this is what causes the disfiguring ulcers.
But Leishmania doesn’t work alone. Annette Ives from the University of Lausanne has found that it uses a virus called LRV-1 to usurp the host’s immune system. Only 5-10% of people infected with Leishmania go on to develop disfiguring ulcers. When Ives looked at the parasites responsible for the worst symptoms, she found that they were loaded with LRV-1, or Leishmania RNA virus-1 in full.
Paradoxically, the virus actually helps the parasite by triggering the host’s immune defences. Its outer shell is made of molecules that are recognised by a host protein called TLR3. This sentinel alerts white blood cells to the presence of foreign molecules. When it detects the virus, it raises the alarm and the cells starts pumping out chemicals that trigger inflammation. This is all part of our normal response to infections. It normally helps, but in the case of Leishmania, it makes things worse because the swollen tissues provide a safe refuge for the parasite. When Ives studied infected mice, she found that those with the strongest immune responses were actually more vulnerable to infections, and suffered from the worst symptoms. If the mice lacked TLR3 entirely, they were better at resisting Leishmania and their symptoms were milder. Ives thinks that after the immune system fights off an initial Leishmania assault, the dead parasites release their viruses and create the ideal conditions for later infections. This could explain why the first espundia ulcer usually heals, only to return in force later. Ives’s discovery is promising. It means that doctors could work out which patients run the greatest risk of disfiguring lesions by searching for the LRV1 virus. It also means that the disease could be treated more effectively with a combination of drugs that target both Leishmania and its viral accomplice. This isn’t an isolated example. The slideshow below describes four other parasite alliances, all involving viruses. Reference: Ives et al. Leishmania RNA Virus Controls the Severity of Mucocutaneous Leishmaniasis Science dx.doi.org/10.1126/science.1199326blogs.discovermagazine.com/notrocketscience/2011/02/10/disfiguring-disease-caused-by-an-alliance-between-three-parasites/Virus linked to leishmaniasis: humanvirosphere.blogspot.com/2011/02/virally-infected-leishmania-cause.htmlAlso found in oysters..... skyship
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Post by skyship on Sept 30, 2011 3:14:20 GMT -5
DISSEMINATED CUTANEOUS LEISHMANIASIS DUE TO LEISHMANIA GUYANENSIS: CASE OF A PATIENT WITH 425 LESIONS Disseminated cutaneous leishmaniasis is characterized by the presence of a large (≥10) number of lesions at several anatomic sites (head, limbs, and trunk). Most of the lesions are small, papular, and appear simultaneously with or secondarily to one or several ulcerated lesions of localized cutaneous leishmaniasis. We report the first case of disseminated cutaneous leishmaniasis in French Guiana. It concerns a 24-year-old woman who tested negative for human immunodeficiency virus (HIV). The disease began with three lesions that became ulcerated. One week later, multiple papulo-nodular lesions appeared. We counted a total of 425 lesions. Leishmania were observed in the lesions. The species involved was L. guyanensis, which has never been described in a case of disseminated cutaneous leishmaniasis. The patient was rapidly cured by a single course of pentamidine. Disseminated cutaneous leishmaniasis should be distinguished from other types of leishmaniasis with multiple lesions. These include anergic diffuse cutaneous leishmaniasis, post-kala-azar leishmaniasis, and leishmaniasis associated with HIV infection. Previous SectionNext Section INTRODUCTION Certain forms of cutaneous leishmaniasis result in large numbers of lesions. This is the case for anergic diffuse cutaneous leishmaniasis, post-kala-azar cutaneous leishmaniasis, and cutaneous leishmaniasis arising in a context of immunodeficiency, such as infection with human immunodeficiency virus (HIV). Brazilian scientists have identified another form of cutaneous leishmaniasis, which was named disseminated cutaneous leishmaniasis (DCL).1–,3 This form can be differentiated from classic localized cutaneous leishmaniasis (LCL) by the large (≥10) number of lesions, the clinical type of the major elementary lesions (papular and or acneiform), and the weaker response to classic treatments. These non-ulcerated secondary lesions are thought to be formed following the dissemination of the protozoan in the lymph and blood from the initial lesions. The species involved are Leishmania braziliensis and L. amazonensis.2 In French Guiana, LCL is particularly frequent, with an annual incidence of approximately 0.2%.4 Leishmania guyanensis is responsible for most of the cases.4 We present a patient who developed a form of cutaneous leishmaniasis due to L. guyanensis that met the criteria for DCL. Previous SectionNext Section CASE REPORT A 24-year-old woman with no particular medical history was hospitalized in the Dermatology Department of the Centre Hospitalier de Cayenne in February 1997. She lived in Cayenne, but for two years, she had regularly accompanied her husband into a forested area to help him to develop a small farm, which involved cutting down trees. Upon questioning, the patient described the appearance in December 1996 of three cutaneous lesions on her right hand, left breast, and back. About a week later, a profusion of lesions appeared, covering almost her entire body. These lesions gradually increased in size, while the initial lesions became ulcerated. She consulted a general practitioner in January 1997 who prescribed oxacilline. However, she did not respond to this treatment and she was then referred to a dermatologist who admitted her to the Dermatology Department of the Centre Hospitalier de Cayenne. Clinical examination on admission showed the patient to be in good general condition without fever. She presented cutaneous lesions, most of which were papulonodular, infiltrated, and slightly squamous. Her entire body was affected, with the exception of the scalp, palms of the hands, and soles of the feet. We counted a total of 425 lesions. The largest lesions, located on her back (Figure 1⇓), on the middle finger of her right hand, and on her left breast (Figure 2⇓), were ulcerated and had scabs. Palpation revealed signs of painless, non-inflammatory lymphangitis around certain lesions, and left inguinal adenopathy. The mucous membranes, particularly those within the nose, were free of lesions. www.ajtmh.org/content/71/5/558/F1.expansion.htmlwww.ajtmh.org/content/71/5/558.fullNotice relationship to HIV......... skyship
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Post by skyship on Sept 30, 2011 3:23:09 GMT -5
According to G. Nicholson HIV needs a co factor, another virus, or parasite or something to move in past the immune system. First the HIV knocks down the immune system, anything can move in............including parasites, like leish and oncho.......
There were a large number of soldiers came back after WWII who were in MID EAST. They all had these type diseases.
This becomes hereditary......Once you have it........Never goes away until you die.
Is the replicator of Morgellons in the HIV/aids?........or is it in the INFLU ABCD package? What is its co factor?
they both can break through the cell membranes..
Does it aid the flu? or Leish or oncho? trypan kinetoplastid in the RNA vector? Only need a protein from something, heh?
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Post by skyship on Sept 30, 2011 3:25:57 GMT -5
Leishmania virus:Non enveloped, icosahedral virion composed of a single capsid protein (CP), about 33 nm in diameter. The capsid has a T=2 symmetry. GENOMEdsRNA linear genome of 5.3 kb. The genome has two large, overlapping ORFs on the positive strand respectively encoding CP and RdRp, and a small 5’-proximal potential ORF. GENE EXPRESSIONThe dsRNA genome is never completely uncoated, to prevent activation of antiviral state by the cell in response of dsRNA. The viral polymerase synthesizes a mRNA, which is translocated to the cell cytoplasm where it is translated.Translation is initiated on a unique internal ribosome entry site (IRES) element situated at the 5’-UTR.The plus-strand viral transcript directs the translation of the major CP (Gag) and the minor fusion protein CP-RdRP (Gag-Pol) via a -1 ribosomal frameshift. REPLICATIONCYTOPLASMIC 1. Virus remains intracellular. 2. Transcription of the dsRNA genome by viral polymerase occurs inside the virion, so that dsRNA is never exposed to the cytoplasm. This plus-strand transcript is used as template for translation. 3. (+)RNAs are encapsidated in virion particle, inside which they are transcribed to give RNA (-) molecules with which they become base-paired to produce dsRNA genomes. 4. Mature virions may be transmitted to new cell during cell division.DB LINKS ICTV: 00.075.0.03 Nucleotide DB: NCBI Protein DB: UniProtKB Virus DB: DPV TAXONOMY Group III: dsRNA viruses Family: TotiviridaeGenus: LeishmaniavirusSPECIES Type: Leishmania RNA virus 1-1 (LRV-1-1) Main:Leishmania RNA virus 1-2 (LRV-1-2) Leishmania RNA virus 1-3 (LRV-1-3) Leishmania RNA virus 1-4 (LRV-1-4) Leishmania RNA virus 1-5 (LRV-1-5) Leishmania RNA virus 1-6 (LRV-1-6) Leishmania RNA virus 1-7 (LRV-1-7) Leishmania RNA virus 1-8 (LRV-1-8) Leishmania RNA virus 1-9 (LRV-1-9) Leishmania RNA virus 1-10(LRV-1-10) Leishmania RNA virus 1-11(LRV-1-11) Leishmania RNA virus 1-12(LRV-1-12) Leishmania RNA virus 2-1 (LRV-2-1) REFERENCE STRAIN Leishmania RNA virus 1-1Sequence | Genome | Proteome HOST Protozoa (Leishmania sp.)CELL RECEPTOR (S) - Epidemiology GEOGRAPHY Worldwide.ASSOCIATED DISEASES - TRANSMISSION Probably during cell division.Matching UniProtKB/Swiss-Prot entries 3 entries Leishmania RNA virus 1 - 1 (isolate Leishmania guyanensis) (LRV-1-1) Select_all Deselect_all CAPSD_LRVLGMajor capsid protein ( Major coat protein)ORF1_ LRVLGPutative ORF1 proteinRDRP_ LRVLGProbable RNA-directed RNA polymerase (EC 2.7.7.48) Swiss Institute of Bioinformatics > ExPASy viralzone.expasy.org/all_by_species/648.htmlSo, now there is a virus inside the protozoan......and this is inside the trypanasoma. Now this is not Oncho. but it could the the glycoprotein from oncho was used in the cell membrane issue. skyship
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Post by skyship on Sept 30, 2011 3:39:55 GMT -5
Mar 3, 2010 – BioInfoBank Library :: Latest papers on Leishmaniavirus, ... a subtilisin-like convertase from the filarial parasite, Onchocerca volvulus. ===================================== Purification, identification, and biochemical characterization of a host-encoded cysteine protease that cleaves a leishmaniavirus gag-pol polyprotein. [My paper] Ricardo Carrion Jr, Young-Tae Ro, Jean L Patterson Department of Virology and Immunology, Southwest Foundation for Biomedical Research, San Antonio, Texas 78227-5301, USA. Leishmania RNA virus (LRV) is a double-stranded RNA virus that infects some strains of the protozoan parasite leishmania As with other totiviruses, LRV presumably expresses its polymerase by a ribosomal frameshift, resulting in a capsid-polymerase fusion protein. We have demonstrated previously that an LRV capsid-polymerase polyprotein is specifically cleaved by a Leishmania-encoded cysteine protease. This study reports the purification of this protease through a strategy involving anion-exchange chromatography and affinity chromatography. By using a Sepharose-immobilized lectin, concanavalin A, we isolated a fraction enriched with LRV polyprotein-specific protease activity. Analysis of the active fraction by sodium dodecyl sulfate-polyacrylamide gel electrophoreses and silver staining revealed a 50-kDa protein that, upon characterization by high-pressure liquid chromatography electrospray tandem mass spectrometry (electrospray ionization/MS/MS), was identified as a cysteine protease of trypanosomes. A partial amino acid sequence derived from the MS/MS data was compared with a protein database using BLAST software, revealing homology with several cysteine proteases of Leishmania and other trypanosomes. The protease exhibited remarkable temperature stability, while inhibitor studies characterized the protease as a trypsin-like cysteine protease-a novel finding for leishmania. To elucidate substrate preferences, a panel of deletion mutations and single-amino-acid mutations were engineered into a Gag-Pol fusion construct that was subsequently transcribed and translated in vitro and then used in cleavage assays. The data suggest that there are a number of cleavage sites located within a 153-amino-acid region spanning both the carboxy-terminal capsid region and the amino-terminal polymerase domain, with LRV capsid exhibiting the greatest susceptibility to proteolysis. and Cloning and biochemical characterization of blisterase, a subtilisin-like convertase from the filarial parasite, Onchocerca volvulus. [My paper] Catherine B Poole, Jingmin Jin, Larry A McReynolds Molecular Parasitology Division, New England Biolabs, Beverly, Massachusetts 01915, USA. Blisterase is a subtilisin-like proprotein convertase of nematodes. The enzyme is named after the blistered cuticle found in Caenorhabditis elegans with the bli-4 e937 mutation. The critical role of the enzyme in cuticle production makes it a potential drug target for parasitic nematodes. We have cloned and expressed blisterase from the parasitic nematode Onchocerca volvulus, a major cause of blindness in Africa. The catalytic domain of the protease exhibits 84% identity with the corresponding domain of its closest homologue, C. elegans blisterase. O. volvulus blisterase expressed in insect cells has maximal activity in 1 mm calcium at neutral pH. The protease is inhibited by EDTA, the suicide substrate decanoyl-RVKR-chloromethylketone, alpha1-antitrypsin Portland and by its own propeptide. Substrate assays with fluorescent peptides show that O. volvulus blisterase requires a P4 arginine and a basic amino acid at P1 for cleavage. The kcat of blisterase on the peptide substrate, t-butyloxycarbonyl-RVRR-4-methylcoumaryl-7-amide was determined to be 0.018 s-1. In vitro cleavage studies with the nematode polyprotein antigen demonstrated that blisterase cleaved at tetrabasic (RRKR) but not at dibasic (KR) sites. This report describes the first biochemical characterization of the nematode specific protease, blisterase. Keywords: volvulu; nematode; convertase; onchocerca; subtilisin-like; onchocerca volvulu; filarial; bly; filarial parasite; parasite onchocerca; biochemical characterization; parasite; cuticle; protease; elegan; lib.bioinfo.pl/pmid:12855702blisterase along with flippase scramblases and NANA! =========================== Blisterase (OvBli-4) is a subtilisin-like proprotein convertase (SPC) from Onchocerca volvulus, the filarial parasite that causes river blindness (1-3). Blisterase appears to be a nematode specific SPC; a homologue has not been identified in humans. The blisterase homologue in Caenorhabditis elegans has been localized to hypodermal tissue and is likely involved in processing cuticular proteins like collagen (4). The cleavage site of Onchocerca volvulus blisterase is on the carboxyl side of Arg-X-(Lys/Arg)-Arg↓. The enzyme is inhibited by EGTA and α1-Antitrypsin Portland (1,5). Note: Both Blisterase and Furin (NEB #P8077) will cleave peptide substrates with the sequence, Arg-X-(Lys/Arg)-Arg. However, the ability of either enzyme to cleave a particular protein substrate depends on its tertiary structure as well as on the amino acids immediately surrounding the cleavage site (1). Source: Isolated from Spodoptera frugiperda (Sf9) insect cells infected with recombinant baculovirus carrying truncated Onchocerca volvulus blisterase. www.neb.com/nebecomm/products/productP5204.asp========================= Skyship Lot going on with those proteins, biochemically...........
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Post by skyship on Sept 30, 2011 3:48:14 GMT -5
Of course, we knew this was coming next didn't we?BOLD sobs aren't they? ====================================== « Leishmaniasis: DNA helps ID vectors, parasite, control agent Evidence »Why we need DNA IDa) Culex pipiens, b) Culicens incidens, c) C. pipiens larvae, d) C. pipiens eggsBiting insects transmit human and animal diseases, including protozoan (e.g., malaria, leishmania, trypanosoma (sleeping sickness, Chagas disease)), filiarial (e.g., onchocerciasis, Guinea worm), and viral (e.g., yellow fever, West Nile, dengue) diseases. Control measures rely on identifying the insects, which generally requires expert training.There are 174 mosquito species and subspecies in North America (“Identification and Geographical Distribution of the Mosquitos of North America, North of Mexico,” Richard F. Darsie, Jr. and Ronald A. Ward, University Press of Florida, 2005). Many species bite humans, but only a handful are important disease vectors. It takes an expert to identify Culex pipiens (panel A), which is the major vector for West Nile virus in eastern U.S., and to distinguish this from other species, for example, Culiseta incidens (panel B), which does not transmit human disease. Even experts are challenged by larvae (C), and eggs (D), and the latter are small and easily overlooked (egg raft size shown in inset). Planning and/or applying control measures is best done before adults hatch, but the early stages are what is most difficult. The reference work cited above includes morphologic keys for identification of adult females and fourth-instar larvae. However, only an expert could make use of these (e.g. “lower mesepimeral setae absent, pale basal band on abdominal tergum II narrowed, or completely interrupted, medially). If mosquito identification is important for society, then reference DNA barcodes are what is needed, as these enable many more persons to name specimens, regardless of life stage. It does not make sense to rely on reference works for the world’s mosquitos that are incomprehensible to anyone who is not already a mosquito specialist.phe.rockefeller.edu/barcode/blog/2010/05/10/why-we-need-dna-id/Same for what the bug leaves under your skin too? And YOU?
Create the immune disfunction, tag the fly, the worm, the person, Walla............ what a neat system........ direct the em to that person, either kill them while trying to kill the worm, virus, fly, or come up with a med you can experiment with and can be dumped on area where the oncho, leish is. If it works the person animal lives, if it don't person/animal dies.
Really brainy ain't it? So, America now is the experiment, covered all those other countries, now, by population density, or movement, can control it, just like in Mid East and Africa. Genetically can select or deselect. What a system.
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Post by skyship on Sept 30, 2011 4:12:17 GMT -5
L eishmania virus totivirus;tolweb.org/57938Leishmania in Europe Splenomegaly: an(other) approach to its causes (2) TWiV 128: Virologists in the mist Massive splenomegaly The Drudge Report today linked to an AP story on the spread of cutaneous leishmaniasis, the incidence of which has quadrupled in the past few years. The parasitic skin disease comes from the female phlebotomine sand fly. There is treatment, but treatment is expensive, and of course, in Afghanistan it can be dangerous to be a caregiver. It's Read on » Study of health in Brazil hi ... by Dr. Rubens D. Medical Doctor Posted Tue 10 May 2011 10:05am maternal and child health. But the nation still faces problems – including some infectious diseases such as dengue and leishmaniasis, rising obesity and a high number of murders... leishmaniasis control is also poor, with current efforts focusing on control of the sandfly vectors and removing domestic animals that can act as reservoirsdiseases. DNDi's initial drug development efforts are aimed at chloroquine-resistant malaria, human African trypanosomiasis (sleeping sickness), visceral leishmaniasis (also called... leishmaniasis, and 200 million are at risk of contracting it. Chagas disease afflicts an estimated 18 million in Latin America and threatens about a quarter of the region's population www.wellsphere.com/articleSearch.s?searchString=leishmaniasis&articleTypeId=3&order=relevance&pageIndex=0============ People with cutaneous leishmaniasis have one or more sores on their skin. The sores can change in size and appearance over time. They may end up with a raised edge and central crater (ulcer). The sores can be painless or painful. Some people have swollen glands near the sores. People with visceral leishmaniasis usually have fever, weight loss, and an enlarged spleen and liver. They may have abnormal blood tests, low blood counts, including a low red blood cell count (anemia), low white blood cell count, and low platelet count. The complete 5284-nucleotide sequence of the double-stranded RNA genome of leishmania RNA virus 1 (LRV1) contains three open reading frames (ORFs) on the plus (+) (mRNA) strand. Similar to the RNA binding properties of synthetic and recombinant HIV-1 nucleocapsid protein (NCp7) and fragments observed in the 5'-HIV-1 RNA. ORFs may encode the major viral coat protein, overlapping ORF-3 by 71 nucleotides.
The HIV viral genome mutates at a high rate. As the worldwide rate of HIV infection increases, the need for a leishmaniasis vaccine needs to becomes more urgent. In an IFA test, HIV antigen is mixed with a fluorescent compound and then with a sample of the patient's blood, testing were positive for Leishmania. Leishmaniasis accelerates the onset and worsens the course for people infected with HIV. Leishmaniasis is a spectrum of diseases, each distinctly manifested and all with potentially devastating consequences. Treatment of leishmaniasis requires the administration of toxic and poorly tolerated drugs.In October 2002, well prior to the invasions of Iraq and Afghanistan, the US Defense Intelligence Agency's Armed Forces Medical Intelligence Center (AFMIC) warned that leishmaniasis would be a danger for troops. Insect repellant and bed nets were frequently in short supply, and commanders failed to emphasize the risk of Leishmaniasis. Almost all of the people in the United States who have leishmaniasis became infected while traveling or living in other countries. Over 90 percent of the cases of cutaneous leishmaniasis occur in parts of Afghanistan, Algeria, Iran, Iraq, Saudi Arabia, Syria, Brazil and Peru. Over 90 percent of the cases of visceral leishmaniasis occur in parts of India, Bangladesh, Nepal, Sudan, and Brazil. The World Health Organization estimates that 12 million people worldwide are infected with leishmaniasis. The WHO says that the public health impact of this disease has been grossly underestimated. During the past 10 years, endemic areas have been spreading, with 350 million people thought to be at risk of infection. Antiparasitic pentavalent antimonials, such as sodium stibogluconate (Pentostam) or meglumine antimoniate, are the mainstays of therapy.Sodium stibogluconate was the only recommended treatment in the United States and was available only through the CDC, but amphotericin B in its liposomal form has recently been approved and is now considered to be the drug of choice for visceral leishmaniasis because of its shorter course and lower toxicity. Treatment of cutaneous leishmaniasis differs according to the etiology and geographic location of the infection. For certain types where the potential for mucosal spread is low, topical paromycin can be used. For more invasive lesions sodium stibogluconate, meglumine antimonate, or pentamidine can be used. Amphotericin B deoxycholate may be first-line therapy for advanced mucosal disease. Visceral leishmaniasis, treatment with a pentavalent antimonial compound usually is effective, outside of India. Transfusions may be necessary for severe bleeding or anemia. Antibiotics are indicated to treat intercurrent infectious conditions. A major advance has been the advent of liposomal formulations of amphotericin B, in which various alternative lipids have replaced deoxycholate. These formulations, which passively target amphotericin to macrophage-rich organs, are much more costly than conventional amphotericin B. Miltefosine, a chemotherapeutic agent, is the first extremely effective oral agent for visceral leishmaniasis.gonnabebedlam.blogspot.com/2009/11/sand-flies-disease-of-destruction.html
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Post by aqt on Sept 30, 2011 13:48:11 GMT -5
sky, I am grinning ear to ear as I "watch" you connect these dots through the reading of the material you posted.
I love you my friend. You are one tenacious hound!!
aqt
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Post by skyship on Sept 30, 2011 15:02:09 GMT -5
aqt,
Thank you, but, something keeps pushing me.........that the environmental changes, due to the trumped up global warming scam, yes, global warming happens, but, it is a natural phenomenon.
What I am seeing is the un natural and inhuman manner in which man wishes to put his signature on us, the environment and every living creature. It amazes me the money that went into the making of "destruction", in the name of "manufactured geniuses".
To me, geniuses are those who really see and hear and talk about what really is going on.
This illusion is what is controlling, while people die, right in front of us, but, yet, those who cannot or refuse to see, because the "illusional norm" that is establishes is consider "normal" to them, are just as responsible as those who perpetuate this lie of delusion. We are not delusional. Those who play along to satisfy the powers of deceit, are "gutless", cold, heartless and that box they live in is so gilded, that the Luciferian illumination controls what they do. I don't feel sorry for them, anymore, because it is what they choose, so what we choose is what we will do.
It takes courage, loving kindness, and sight of the heart to see this. Most just say, they can do nothing about it. Yes, they can, but they are timid, they are so full of programmed fear, that they cannot and will not make a stand.
To know and feel the plight of those in Palestine, and those in the Mid East. They are human. Cannot we see that? By not seeing it, the pain of suffering is not there, but, yet when these people are confronted with this right in front of their faces, they cannot even connect to the fact that those suffering from this biological/chemical/geological/physics convergence for the sake of some LSD machine centered, automation transformation idea, drummed up in the pipe of someone's drug brought to them by those who know the power of drugs, they follow the "guru".
So many men/women have died horrible deaths in the Middle East, and some are probably wandering around the desert due to psychotropic machines controlling their moves. They have been mentally altered, and do not know where they are, hopefully they are still alive, the rest are suffering the most "egregious lives" due to the incorporation of experiments done by those who would never even know how to carry a "sword"! The wimps of society controlling it all. Why are we letting this happen? Those who help make the weapons, just say they are doing their jobs.
They are the ones who could stop this, yet, they turn a deaf ear, blind eye, and "go silent". The "silent generation" finally woke up and it may be too late, for they are dying, yet they hold the secrets to what "really happened" in those wars they participated in. They too brought home the "gifts of war". All in the "destructive plan", while those in the Institutions of Higher Learning and "financial gifts" from those who own the money, created "newer" "better" more devastating experiments, denovo, reductionism, incapacitating endeavors to bring about " a change". This change, adaptation, fallout from war, from dwaddling experiments rewarded by Nobel Prizes for their participation in the "destruction of those not befitting the perfect person" has left a "trail of death", like the "trail of tears". This is a "trail of stolen souls" who believe they cannot think for themselves. In fact, they are gutless.
So, when people say they can do nothing, they are lying to themselves!
God Bless Us Each and Everyone, and may The Power of the Spirit of "good and caring" and heartful love and compassion hit those folks on the heads, and wake them up!
There is another spirit, not the one that has descended upon us. We must remain vigilant! the ton of destruction covering the "light of life" has not been removed. Many have never "rolled away the stone". If you are Jewish/Cather/gypsy/and understand the "shepherd" genetically, it is in your bones, and you know it, the mixture of the tribes is in all of us. For that is where it began. If people can see that the answer is very simple, they can make the "good and right and moral" changes.
If we can but hear "The Rhythm Of The Saints" and the "Ancients", the "music of the spheres" we know their is a "higher spirit" who is fighting the other "spirit", the "spirit of darkness" which is just as powerful. The choice is up to us!
Thanks for granting us the freedom here, aqt, to post our "free spirit knowledge" on this board.
When one thinks, acts, and does what is moral, what is genuine, honest and loving, it is amazing what can happen.
Skyship
To me that is
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Post by skyship on Sept 30, 2011 15:29:45 GMT -5
What connection does a parasite have to HIV? Seems they are co factors of the HIV? So, the HIV would have a viral component related to the leishmania parasite, and that would be in the "membrane protein". the M protein in Influe ABCD, in HIV itself. What is that membrane protein? ......an exosome? non viral so passes by the immune system? ========================= HIV protein Gag, which possesses these general exosomal sorting elements, requires only these elements to bud from human cells. Others have proposed that the HIV p6 domain and the host class E vacuolar protein-sorting (VPS) machinery play direct, essential, and mechanistic roles in HIV budding. However, we show here that p6-deficient HIV can bud from cells at normal levels and that both p6-deficient HIV and exosomes can bud independently of class E VPS function. Thus, it appears that exosome biogenesis pathways mediate the budding of HIV from cells, whereas the HIV p6 domain and the class E VPS machinery promote budding indirectly. www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0050158What is this HIV GAG protein? =================== HIV-1 Gag: a Molecular Machine Driving Viral Particle Assembly and Release HIV-1 and other primate lentiviruses assemble at the plasma membrane and are released by budding from the cell surface. Apart from offering a nonlytic pathway for virus egress, this mode of assembly leads to the acquisition of a host cell-derived lipid envelope that enwraps the nascent viral capsid and protects it from the environment. HIV-1 assembly is controlled primarily by the Gag protein, one of the three gene products that are encoded by all retroviruses. Gag orchestrates assembly by recruiting all the building blocks required for the formation of a fully infectious virion, which in the case of HIV-1 include both viral and cellular components. Furthermore, Gag provides the principal driving force for virus assembly, as illustrated by the fact that HIV-1 Gag can efficiently form virus-like particles even when expressed in the absence of other viral proteins (Gheysen et al., 1989). Gag thus constitutes an autonomous molecular machine for particle assembly. The HIV-1 Gag precursor is synthesized on cytosolic ribosomes (Tritel and Resh, 2000) and becomes cotranslationally modified by the N-terminal attachment of a myristoyl group, which increases its affinity for membranes (Bryant and Ratner, 1990; Gottlinger et al., 1989). Myristoylated Gag precursor molecules associate with the inner leaflet of the plasma membrane, where they coalesce into a patch, the first stage in the assembly process that can be visualized by electron microscopy (Swanstrom and Wills, 1997). Through the continuous lateral addition of extra Gag molecules, the electron-dense patch grows into a spherical structure that increasingly protrudes from the cell surface and eventually pinches off, releasing an immature virus particle into the extracellular environment. How Gag reaches the site of virus assembly is not known. There is evidence that Gag can form oligomeric complexes in the cytoplasm, but whether these represent assembly intermediates or dead-end products remains controversial (Lee et al., 1999; Lee and Yu, 1998; Lingappa et al., 1997; Tritel and Resh, 2000). Immature HIV-1 particles are non-infectious (Gottlinger et al., 1989; Kohl et al., 1988), and it is thought that this is at least in part because the palisade-like shell of radially arranged, unprocessed Gag precursor molecules which forms the immature capsid is too stable to permit its disassembly. Figure 1. Schematic illustration of Gag-driven particle production. Gag oligomerizes underneath the plasma membrane through protein-protein and protein-RNA interactions, with the MA domain oriented towards the lipid bilayer. Eventually, a spherical Gag protein shell is formed and a membrane fusion event at the neck of the bud becomes necessary to release the assembled particle. Subsequently, the Gag polyprotein is processed by the viral protease and the cleavage products are rearranged as indicated. The location of p6 in the mature particle remains uncertain. www.hiv.lanl.gov/content/sequence/HIV/REVIEWS/GOTTLINGER2001/Gottlinger.html============================== biology.kenyon.edu/slonc/gene-web/Lentiviral/hiv_image.jpg======================= transmembrane glycoprotein TM gp 41 gp120..... Description: HIV ENV is a polyprotein precursor (gp160), which is processed by cellular proteases to give a non-covalent complex of an external glycoprotein (SU / gp120) and a transmembrane glycoprotein (TM / gp41). Localization: * Cell plasma membrane * Virion envelope Function: * Mediates virion attachment and entry * Polyprotein precursor for glycoproteins that occur on the surface of virions * Fsorm complexes with CD4 receptors within Endoplasmic Reticulum, decreases their presence on the cell surface www.bioafrica.net/proteomics/ENVprot.html=============== skyship So what would this GAG have to do with lentivirus? or SV40? or the original MS2?
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Post by skyship on Sept 30, 2011 15:30:40 GMT -5
Here shows the membrane protein working same way in Influ A virion...... "Summary The envelope glycoprotein of human immunodefi- ciency virus type 1 (HIV-1) consists of a complex of gp120 and gp41. gp120 determines viral tropism by binding to target-cell receptors, while gp41 mediates fusionbetween viraland cellularmembranes.Previous studies identified an a-helical domain within gp41 composed of a trimer of two interacting peptides. The crystal structure of this complex, composed of the peptides N36 and C34, is a six-helical bundle. Three N36 helices form an interior, parallel coiled-coil trimer, while three C34 helices pack in an oblique, antiparallel manner into highly conserved, hydrophobic grooves on the surface of this trimer. This structure shows striking similarity to the low-pH-induced conformation of influenza hemagglutinin and likely represents the core of fusion-active gp41. Avenues for the design/ discovery of small-molecule inhibitors ofHIV infection are directly suggested by this structure." www.cco.caltech.edu/~chanlab/PDFs/Chan_Cell_1997.pdf======================= FIG. 1. Targeting adenoviral vectors using sCAR bifunctional fusion proteins. (A) The sCAR targeting strategy consists of adding a protein molecule comprising sCAR genetically fused to a targeting ligand, represented by the arrow, to an adenoviral vector. Interaction of the bifunctional sCAR targeting molecule with the fiber knob blocks the normal tropism of the vector and will redirect the viral complex to an alternate receptor. (B) The interaction of the sCAR targeting molecule with the fiber knob can be improved via trimerization using a heterologous trimerization domain. The proposed interaction of the sCAR-m-ligand (sCAR-m-L) and sCAR-t-L targeting molecules with the fiber is shown schematically. jvi.asm.org/cgi/content/full/76/4/1892/F1========================== sCar-t-L the sCAR-m-L ligand (fiber knob?) going after the knob of the fiber:::::::::::::::::: ================ FIG. 1. Display of the Ad5 knob on the surface of filamentous bacteriophage. For a detailed explanation, see the text. jvi.asm.org/cgi/content/full/75/15/7107/F1Coxsackie and Adenoviruses............. CAR ===================== There is the knob, the shaft, the straw within a straw.... www.bioscience.org/2009/v1e/af/32/fulltext.asp?bframe=figures.htm&doi=yesskyship
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Post by skyship on Sept 30, 2011 16:18:38 GMT -5
Coxsackie Virus: comes full circle folks....................... Coxsackie Virus cox·sack·ie·vi·rus /kɒkˈsækiˌvaɪrəs, kʊkˈsɑki-/ Show Spelled[kok-sak-ee-vahy-ruhs, kook-sah-kee-] Show IPA noun, plural -rus·es. any of a group of viruses closely related to the virus of poliomyelitis, causing certain diseases of humans, as herpangia and epidemic pleurodynia. Origin: cox·sack·ie·vi·rus Origin: 1945–50; after Coxsackie, N.Y., where the first known case appeared neumonoultramicroscopicsilicovolcanoconiosis. Does it mean: So is supercalifragilisticexpialidocious. Does it mean: (used as a nonsense word by children to express approval or to represent the longest word in English.) a white, crystalline, water-insoluble, powerful high explosive, C3H6N6O6, used chiefly in bombs and shells. the estimation of something as valueless (encountered mainly as an example of one of the longest words in the English language). an obscure term ostensibly referring to a lung disease caused by silica dust, sometimes cited as one of the longest words in the English language. (used as a nonsense word by children to express approval or to represent the longest word in English.) a white, crystalline, water-insoluble solid, C14H9Cl5, usually derived from chloral by reaction with chlorobenzene in the presence of fuming sulfuric acid: used as an insecticide and as a scabicide and pediculicide: agricultural use prohibited in the U.S. Link To coxsackievirus Explore the Visual Thesaurus » Related Words for : coxsackievirus Coxsackie virus View more related words » Merriam-Webster Medical Dictionary cox·sack·ie·vi·rus definition Pronunciation: /(ˈ)käk-ˌsak-ē-ˈvī-rəs/ Function: n : any of numerous serotypes of three picornaviruses of the genus Enterovirus (species Human enterovirus A, Human enterovirus B, and Human enterovirus C ) associated with human diseases (as meningitis or herpangina) see EPIDEMIC PLEURODYNIA Merriam-Webster's Medical Dictionary, © 2007 Merriam-Webster, Inc. Cite This Source American Heritage coxsackievirus or Coxsackie virus n. Any of various Enteroviruses that are associated with a variety of illnesses including herpangina, epidemic pleurodynia, and a disease resembling poliomyelitis but without paralysis. dictionary.reference.com/browse/coxsackievirus========================= EPIDEMIC PLEURODYNIA this gets deeper and deeper.............. Skyship
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Post by skyship on Sept 30, 2011 16:55:18 GMT -5
I keep coming back to origin of polio...........could it be leishamania virus itself? The Coxsackie viruses subsequently were found to cause a variety of infections, including epidemic pleurodynia (Bornholm disease), and were subdivided into groups A and B based on their pathology in newborn mice. (Coxsackie A virus causes paralysis and death of the mice, with extensive skeletal muscle necrosis; Coxsackie B causes less severe infection in the mice, but with damage to more organ systems, such as heart, brain, liver, pancreas, and skeletal muscles.) Would this not be the core of Musc dystrophy? I think so, but coxsackie is not its real name, Coxsackie in a prision, in Coxsackie, NY? What is it really? Hand, Foot and Mouth DISEASE................... www.health.state.ny.us/diseases/communicable/hand_foot_mouth/docs/fact_sheet.pdfskyship IT LOOKS to me that it is the cause of Muscular dystrophy..........why dynein is important.
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Post by skyship on Sept 30, 2011 17:18:50 GMT -5
An Elf sent me this which needs to be examined in relationship to the GWS.
Blood changes.
============================ Study finds chronic abnormal brain blood flow in Gulf War veteransOAK BROOK, Ill. – Blood flow abnormalities found in the brains of veterans with Gulf War illness have persisted 20 years after the war, and in some cases have gotten worse, according to a new study published online in the journal Radiology. "We confirmed that abnormal blood flow continued or worsened over the 11-year span since first being diagnosed, which indicates that the damage is ongoing and lasts long term," said principal investigator Robert W. Haley, M.D., chief of epidemiology in the Departments of Internal Medicine and Clinical Sciences at the University of Texas (UT) Southwestern Medical Center in Dallas. "We also identified a special MRI procedure that better diagnoses and distinguishes between the three main types of Gulf War illness." Gulf War illness is a poorly understood chronic condition associated with exposure to neurotoxic chemicals and nerve gas. It affects an estimated 25 percent of the 700,000 military personnel deployed to the 1991 Persian Gulf War, according to the U.S. Department of Veterans Affairs' scientific advisory committee. There are three main syndromes associated with Gulf War illness, producing a variety of symptoms, including fatigue, neuropathic pain, memory and concentration deficits, balance disturbances and depression.The hippocampus is the part of the brain responsible for forming long-term memories and helping with spatial navigation. Many Gulf War illness neurological symptoms, such as memory loss, confusion, irritability and disorders in motion control suggest impairment of the hippocampus. In 1998, Dr. Haley's research team published a study using single photon emission computed tomography (SPECT) to assess hippocampal blood flow in veterans with Gulf War Syndrome. For the current study, the researchers used a novel technique called arterial spin labeled (ASL) MRI to assess hippocampal regional cerebral blood flow (rCBF) in 13 control participants and 35 patients with Gulf War syndromes 1 (impaired cognition), 2 (confusion-ataxia) and 3 (central neuropathic pain). Each patient received intravenous infusions of saline in an initial session, and physostigmine in a second session 48 hours later. Physostigmine is a short-acting cholinesterase inhibitor, used to test the functional integrity of the cholinergic system, a neurotransmitter system involved in the regulation of memory and learning. "ASL scanning after giving this medication is particularly well suited to diagnosing Gulf War illness, because it picks up brain abnormalities too subtle for regular MRI to detect," said co-author Richard W. Briggs, Ph.D., professor of radiology at UT Southwestern. "This allows us to make the diagnosis in a single two-hour session without the need for exposure to ionizing radiation." The findings replicated the results of the initial SPECT study of largely the same group of veterans. The results showed that abnormal hippocampal blood flow persisted and may have progressed 11 years after initial testing and nearly 20 years after the Gulf War, suggesting chronic alteration of hippocampal blood flow.Physostigmine significantly decreased rCBF in control participants and veterans with syndrome 1, but significantly increased rCBF in the right hippocampus of veterans with syndrome 2 in the original study. The abnormal increase in rCBF was now found to have progressed to the left hippocampus with syndrome 2 and to both hippocampi of the veterans with syndrome 3.
"Having an objective diagnostic test allows researchers to identify ill veterans for future clinical trials to test possible treatments," Dr. Haley said. "It is also critical for ongoing genomic studies to see why some people are affected by chemical exposures, and why others are not." ### "Hippocampal Dysfunction in Gulf War Veterans: Investigation with ASL Perfusion MR Imaging and Physostigmine Challenge." Collaborating with Drs. Haley and Briggs on this paper were Xiufeng Li, Ph.D., Jeffrey S. Spence, Ph.D., David M. Buhner, M.D., M.S., John Hart Jr., M.D., C. Munro Cullum, Ph.D., Melanie M. Biggs, Ph.D., Andrea L. Hester, Ph.D., Timothy N. Odegard, Ph.D., and Patrick S. Carmack, Ph.D. The study was funded by a federal research contract administered by the Department of Veterans Affairs Medical Center, Dallas, Texas, and grants from the U.S. Army Medical Research and Materiel Command and the National Institutes of Health. Radiology is edited by Herbert Y. Kressel, M.D., Harvard Medical School, Boston, Mass., and owned and published by the Radiological Society of North America, Inc. (http://radiology.rsna.org/) RSNA is an association of more than 46,000 radiologists, radiation oncologists, medical physicists and related scientists committed to excellence in patient care through education and research. The Society is based in Oak Brook, Ill. (RSNA.org) For patient-friendly information on magnetic resonance imaging (MRI), visit RadiologyInfo.org. www.eurekalert.org/pub_releases/2011-09/rson-sfc090611.phprCBF: More current info here: www.91outcomes.com/The Pentagon hides behind Executive Order 13292 so that the bulk of what happened in the Gulf remains hidden from the public. Except this is criminal intent to withhold information of neglect, misconduct, mishandling, and much worse during the Gulf War. The very same people who say nothing happened are the ones with full knowledge of those records, and vow to conceal them at all cost. The same people who lead us back to Iraq again under false terms, and created yet another disaster to live down. There should be FULL public disclosure, and we have the right to know what really happened in Iraq from 1990 to present. www.gulflink.org/Skyship
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