Guest guest Posted December 15, 2001 Report Share Posted December 15, 2001 ---------- From: Ishgooda <ishgooda@...> Date: Sun, 16 Dec 2001 01:02:50 -0500 " karaka.j@... " <janclarke@...> Subject: Re: FW: " First, Do No Harm " excerpt http://hepatitis-central.com/hcv/vaccines/forced.html ... CDC director Satcher admitted in a June 17 LA Times article that a National Institutes of Health (NIH) investigation of the 1990-1991 Los Angeles study found that informed consent regulations had been violated because parents were not told their babies would be injected with an experimental vaccine that had never been licensed by the FDA for use in America. Both Kaiser and the CDC have denied that any of the LA babies were harmed by the high potency EZ vaccine, but did admit that one child died from a bacterial infection they maintain is unrelated to the vaccine. The high-potency EZ measles experiment began at four major sites in the mid-1980's, including Haiti, Senegal, Guinea Bissau and Mexico. Other trials followed in Cameroon, Gambia, Bangladesh, Togo, Iran, New Guinea, Peru, Rwanda, Sudan, South Africa, Egypt, Philippines, Uzbekistan, Thailand, Zaire and Los Angeles. Primary funding came from the U.S. Agency for International Development and the World Health Organization (WHO). In Haiti, infants were given the experimental vaccine at 10 to 500 times the usual dose levels. In a June 1996 article in the Journal of Infectious Diseases, s Hopkins " researchers " report that infants with the highest antibody to high titer measles vaccine have the most profound immune suppression. At 06:34 PM 12/16/2001 +1300, you wrote: I noticed that the letters from Desmond and Dr Bobby Tsang have appeared in a number of community newspapers recently, promoting the measles vaccination campaign. Published in a South African medical journal - and in other studies - shows that just one single dose of vitamin A given to children under the age of 2 years old reduced the morbidity and mortality in measles by 30 and 50 percent respectfully. At around $85 each for a vaccine, with a population of 3.8 million, it's no rocket science to work out which is the cheaper health option. However, vaccination remains big business, the success of which depends on sales. Those who research and develop vaccines, doctors, and providers, are monetarily rewarded for pumping them into our children from birth to prevent normal childhood illnesses developing.Those multi-national pharmaceutical companies which promote immunisation at the beginning of our lives and cures at the end, profit the most. The Ministry of Health has prioritised vaccination for Maori children. There is significant funding for those who deliver these 'services'. Iwi health providers hold 'tamariki ora' contracts that require them to fulfill the service to a set number of tamariki. Comments in government documents such as " parents need to have all information to make an informed decision to immunise their children and to have children immunised as recommended by the well child / tamariki ora schedule " show that there is an embedded assumption that immunisation is not under debate. The question is that while our own health providers may have the best interests of our babies at heart, they are 'informed'’ from a single source (ie government). So that the question is not " should we immunise? " ’ but " of course immunisation is right so HOW do we get all our tamariki immunised? " There is also no discretion between one innoculation and another as the government has created a package deal’ as part of it's 'well child' strategy and that again assumes children have the whole range of vaccinations rather than a selection. The well child book (or plunket book) that is handed out to new mothers clearly facilitates the innoculation of babies and children through the whole range. How many of you are aware that in order to fulfill his contract, Tamihere chose an 'opt off' method of immunising children who attended Waipareira Health in Auckland? This meant that unless a care-giver expressly said their child should NOT be immunised, the tamaiti got the jab anyway. The opt off method was a shrewd way to get the job done because many of our people don't answer letters or fill out forms if no-one is actively pushing it. This decision may not have been just about funding but a Waikato Kohanga reo expelled a child, (whose mother, in the face of aggressive coercive blackmail steadfastly refused vaccination on cultural and religious grounds) as the government funding for that Kohanga was tagged in favour of vaccination. (How many of you are aware that vaccines are manufactured on the cell tissue culture of choice, diploid tissue, otherwise known as aborted foetal cell culture?) In the late 1950's early 1960's all pupils in schools throughout the country (2,500,000 children) were vaccinated against polio. Later through the media, we learned that some were injected with a batch of highly dangerous contaminated monkey based polio vaccine. This substance left some children crippled for life, and the rest of us facing threats of possibly developing brain, kidney, breast and other tumours and multiple sclerosis (to mention a few). In 1973 Professor. Classen, (Director of the Institute of Preventative medicine at the University of Odense in Denmark) warned the medical establishment : " Millions of people have been inoculated with anti-polio vaccine contaminated with tumoural SV40 virus (present in green monkey cells ground to produce the vaccine). It is possible that it will take 20 or more years before the eventual harmful effects of the vaccine manifest itself " . A decade later our Minister of Health Dr A Malcolm stated: " It cannot be ruled out that two million New Zealanders could not be suffering in 30 years time from cancerous brain tumours as a result of vaccinations " . The Evening Post (24/7/87), the Dominion (dated July 29/87), and the NZ Listener (Aug 29 1987) reported that some New Zealand children given a polio vaccine from Connaught Lab in USA suffered alarming neurological effects and viral meningitis. the mass immunisation campaign was called off. Many of us believed the propaganda that to be good, responsible adults we had to vaccinate children. With a family of nine, Maori friends immunised a couple of their tamariki then discovered that the children still contracted measles, despite being told that the jabs were to protect them. Concerns as to why the tamariki contracted measles were fobbed off with; " oh some children still get a mild dose. " The woman being a lawyer, our friends began studying vaccine labels, questioning doctors, reading books, finding out about alternatives such as nutrition, homeopathy, and looking at our recent history to see how our forebears and mothers dealt with illnesses such as dysentery, measles, flu, smallpox and so on. They looked at diet and qualities of certain foods such as garlic, honey, oranges, kumara, puha and shark oil. (Captain Cook stopped scurvy by feeding citrus - vitamin C - to his crew). Some years ago, indigenous babies in Australia - every second aboriginal child - began dying following the introduction of an vaccination programme. Dr Cilento found by feeding them vitamin C before innoculation, they survived. We have been born with an immune system which has to recognise invaders and protect the body against diseases, many of which are linked to poverty. Maori people had access to good food - kai which is needed to keep the immune system strong - food that is now packaged and sold (for exorbitant prices) off the shelf, such as fish oils, seaweed, kutai, puha, kumera, riwai or kanga. Once the family had educated themselves, they decided not to vaccinate their children. Naturally the public nurses, plunket nurses and doctors continued to pressure them to conform, mainly using fear tactics such as " if your child gets measles, they could be brain damaged " . The whanau waited for their tamariki to catch all of the usual childhood illnesses - ones which we were exposed to as children - and nursed their children that caught mumps, chickenpox, measles, through in the same way their parents did - including resting in a darkened room, food rich in vitamins C and A, sufficient hydration, some sponging down, keeping warm and resting. The mother was later told by a Chinese practitioner that if the children didn't catch the diseases at a young age, it was unlikely that they would get them later as they might have already developed an immunity by having been in contact with someone who had had the disease. She believes the push for inoculation of common childhood illnesses over the last 30 or so years has diverted our attention from healthy eating and living. It has also undermined our confidence to use basic nursing skills to deal with illnesses which happen with or without vaccination. The Immunisation Awareness Society, ( http://www.ias.org.nz/ ) Vaccine Information Network, newspapers and some books comment on the devastating effects of vaccinations which are not highly publicised. (eg 'The Dangers of Compulsory vaccinations How to avoid them Legally', by US Attorney Tom Finn.) In the book, 'Animal Research Takes Lives' by Bette Overell is discussed (in chapter 5) the Vaccination conspiracy and the research and findings into all major childhood immunisations. If the authorities want to improve Maori health then governments need to begin with the basics and ensure that their policies will provide access to jobs and resources which will allow us to feed our tamariki a balanced diet, and adequately house them. Housing New Zealand has recognised the proven fact that insulating houses can improve the health of people living in substandard dwellings and are taking steps to meet insulation needs of some of their tenants (who, from recent media accounts may be better housed than some of our people). My friend says that the currently highlighted third world conditions that some Northland people are living under contribute significantly to ill health and set up pre-existing conditions which ensure that in the absence of good food and housing, vaccination against diseases is the only other option. If you want to banish measles you may wish to consider reading a South African medical journal about vitamin A therapy. It was found that one dose of vitamin A given to children under two years old reduced morbidity and mortality by 30 and 50 percent respectfully - just one single dose, of a simple cheap nutrient. Compared to the cost per vaccine of around $85, vitamin A dosing may save enough money to provide better housing to ensure healthier New Zealanders. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 15, 2001 Report Share Posted December 15, 2001 ---------- From: Ishgooda <ishgooda@...> Date: Sun, 16 Dec 2001 01:00:32 -0500 " karaka.j@... " <janclarke@...> Subject: Re: FW: " First, Do No Harm " http://www.jorsm.com/~binstock/vacc-let.htm Research document and recommendation for Dan Burton, Representative from Indiana, House Government Reform Committee, regarding: Vaccines: finding a balance... MECHANISMS OF VACCINATION SEQUELAE a sampling from scientific literature August 3, 1999 final by Binstock Researcher in Developmental and Behavioral Neuroanatomy email: aspergerian@... Introduction This letter does not recommend that all vaccinations be discontinued; instead, this document offers a sampling of scientific evidence delineating mechanisms by which vaccination-induced neuropathy and vaccination-induced intestinal problems occur in some individuals, including children plunged into the autism-spectrum soon after a vaccination. For reasons set forth hereinbelow, my conclusion is as follows: In light of a growing body of scientific information, vaccination- exemption criteria ought be expanded, especially in regard to infants, toddlers, and women of childbearing age. Despite using restrictive criteria, many studies have documented a relationship between vaccinations and adverse neurologic sequelae (eg, 1-8). Some of these studies focused upon febrile seizures during short time periods after various vaccinations. More recent studies have documented brain regions that are affected by febrile seizures (9-11); and these brain regions correspond to brain regions implicated in autism-spectrum disorders (eg, 12). In the very least, these two research domains offer a mechanism whereby some children's deterioration into the autism-spectrum may have occurred. Interferon gamma When a child is vaccinated, a complex physiological process is initiated. For instance, a 1997 article documented that in human infants, a primary effect of the MMR vaccination is a prolonged pulse of endogenously created interferon gamma (13). This finding, in conjunction with other studies about interferon gamma, supports the anecdotal documentation by numerous parents of children whose gastrointestinal and/or neurologic function deteriorated subsequent to a vaccination. One of interferon gamma's most important effects is that of increasing permeability of tissues that normally have highly restricted permeability. Two such tissues are the intestinal tract and the blood-brain barrier. Interferon gamma is now realized to increase permeability in both of these tissues (eg, 14- 17); and the increased permeability can have pathological significance. Intestinal permeability increased by interferon gamma can lead to increased translocation of pathogens (eg, 18); and increased permeability of the blood- brain barrier is associated with a variety of pathologic states, ranging from CNS-infiltration of peripheral pathogens, to CNS-entry of activated B-cells and T-cells of the human immune system (19-24). Measles virus and measles vaccination impair immunity For nearly two decades, Diane E. and colleagues at s Hopkins have been documenting the mechanisms by which measles and measles vaccinations impair immunity, thereby increasing risk of reactivation of current infections and increasing the likelihood that a newly acquired infection will be more serious (25-29). By subjecting an an infant to an MMR around the time of his or her 1st birthday, a physician not only causes the pre-toddler to have impaired immunity for several weeks or months thereafter, but this impairment in immunity occurs during what for some children is an extended period of normally occurring " transient hypogammaglobulinemia of infancy " , ie, a time between (a) the decline of maternal antibodies in the infant's blood, and ( the gradual strengthening of the infant's own immune defenses (eg, 30-32). In other words, a naturally occurring period of increased susceptibility to infection in some pre-toddlers is the very time at which the MMR and its immune-impairment are mandated. To administer the MMR during a time of naturally lower immunity (in some children) means that those children would be at increased risk of having an increased pathogen load in peripheral tissues as the MMR-induced pulse of interferon gamma increased permeability in the intestinal and blood-brain barriers. Cytomegalovirus (CMV) provides an example, because infants can be congenitally or neonatally infected but remain asymptomatic even though the CMV remains within the child (33). For some such children, a vaccination that impairs immunity would be permissive for increased viral replication. Furthermore, that same vaccination (eg, the MMR), via its pulse of endogenous interferon gamma, would increase blood-brain barrier and gastrointestinal permeability concurrently with increased viral replication occurring in the presence of vaccination-impaired immunity. Conclusion A large number of parents are convinced that their child's descent into the autism-spectrum began soon after a major vaccination such as the HepB, DPT, or MMR. Increasingly, medical literature is documenting the vaccination-related mechanisms by which immunity is impaired by vaccinations and by which neurologic and gastrointestinal sequelae may ensue. As examples, this document offers citations (a) about vaccination-induced interferon gamma and its effects upon permeability of intestinal tissue and of the blood-brain barrier, and ( about how a measles vaccination induces prolonged impairment of immunity. In addition, other concerns regarding advense vaccinal events ought be addressed by the committee. Specifically, A. The post-vaccination time-periods studied for negative effects have been too brief, especially (i) since the mechanisms by which vaccination sequelae can occur are diverse and, (ii) since, given the epidemiology of childhood pathogens, when combined with effects induced by a vaccination-induced pulse of interferon gamma, there is likely to be much inter-individual variation in vaccination-induced pathology and related data. B. Febrile seizures and their sequelae are important, but they are not the only mechanism by which vaccination-induced neuropathy or gastroinestinal difficulty can occur. Interferon gamma's effects upon MHC-I and MHC-II presentation should also be considered in regard to not uncommon " asymptomatic " infections common in infants (33). C. Some individuals have impaired antibody responses to a vaccinal antigen (34). When a child or woman of childbearing age is found to have missing antibodies for a common vaccinal antigen, there are at least two possibilities to be considered: One, that the person's vaccinal immunity has subsided, or Two, that he or she has an immune weakness specific for that pathogen-specific antigen ought be watched more closely for vaccinational responses or infectious episodes that might have neurologic or other adverse effects (35-36). For a child or woman with seemingly low vaccinal antibodies, additional immune testing ought preceed hasty decisions to vaccinate, especially since at least some vaccines impair immunity, thereby creating the possibility of a woman of childbearing age acquiring an infection she might otherwise have successfully immunosuppressed. D. This document is but a preliminary sketch, the proverbial tip of a very large iceberg. In other words, solidly researched findings of the last ten years are revealing numerous mechanisms by which vaccination-induced pathologies can occur. Vaccination guidelines need revision. Recommendations to the Committee As a researcher who listens to parents of autism-spectrum children and who has perused medical literature regarding various mechanisms by which negative vaccination-induced sequelae can occur, my suggestions to the Committee are as follows: 1. In studying vaccination-induced pathologies, longer post-vaccination time periods and a variety of vaccination-pathology mechanisms ought be considered. 2. US infants and toddlers are receiving too many vaccinations too soon. 3. Sick kids or recently sick kids ought not be vaccinated. 4. The criteria for vaccination-exclusion and vaccination-delay ought be expanded significantly. Sincerely and respectfully, Binstock Researcher in Developmental and Behavioral Neuroanatomy Denver A series of autism-related webpagesContents email to: Binstock References 1. Tonz O, Bajc S. [Convulsions after whooping-cough vaccination]. [Article in German] Schweiz Med Wochenschr 1980 Dec 20;110(51):1965-71. ab: Convulsions or status epilepticus in 11 infants after pertussis vaccination are reported. In 3 cases grand mal epilepsy persisted and 2 children developed infantile epileptic encephalopathy (Lennox syndrome). On the basis of our own experience, the incidence of seizures approximates 1:4800 infants vaccinated or 1:12 800 vaccinations. According to a recent prospective study from the USA, the incidence of seizures may be closer to 1:600 infants... 2. Hirtz DG et al. Seizures following childhood immunizations. J Pediatr 1983 Jan;102(1):14-8 1983. ab: In 1.4% of children who experienced a seizure during the first seven years of life, the seizure followed within two weeks of an immunization procedure. We report 40 postimmunization seizures in 39 children enrolled in the Collaborative Perinatal Project. Ten seizures followed diphtheria-pertussis-tetanus (DPT) immunization, and 10 followed measles immunization. All but one of the seizures were associated with fever, often high. Thirty-seven seizures lasted less than 30 minutes. More than half of the children had a personal or immediate-family history of febrile seizures. One of the children had a right focal seizure lasting six hours after DPT immunization and had a significant speech deficit on long-term follow-up... 3. JV et al. Recurrent seizures after diphtheria, tetanus, and pertussis vaccine immunization. Onset less than 24 hours after vaccination. Am J Dis Child 138(10):908-11 1984. ab: Twenty-two patients with recurrent seizures that started less than 24 hours after immunization with diphtheria, tetanus, and pertussis (DTP) vaccine were retrospectively studied. The initial seizure generally occurred after one of the first three DTP vaccine immunizations, and followed that immunization by less than 12 hours... 4. son V et al. Relationship of pertussis immunization to the onset of epilepsy, febrile convulsions and central nervous system infections: a retrospective epidemiologic study. Tokai J Exp Clin Med 13 Suppl:137-42 1988. Department of Neurology, UCLA School of Medicine. ab: A change in the pertussis immunization schedule in Denmark allowed a retrospective study examining the relationship of the time of onset of selected neurologic disorders with the time of pertussis immunization in two core cohorts of children. Records of 2,199 children with febrile seizures were reviewed and a significant association between first febrile seizures and the scheduled age of pertussis immunization was noted (p = 0.004)... 5. Baraff LJ et al. Infants and children with convulsions and hypotonic-hyporesponsive episodes following diphtheria-tetanus-pertussis immunization: follow-up evaluation. Pediatrics 81(6):789-94 1988. Department of Pediatrics, University of California, Los Angeles, School of Medicine. ab: In a prior prospective study, we evaluated the nature and rates of adverse reactions occurring within 48 hours following 15,752 diphtheria-tetanus-pertussis (DTP) immunizations. Nine children had convulsions, and nine had hypotonic-hyporesponsive episodes... No child had significant neurologic deficit, although four had minor neurologic abnormalities... 6. MR et al. Risk of seizures and encephalopathy after immunization with the diphtheria-tetanus-pertussis vaccine. JAMA 263(12):1641-5 1990. Department of Preventive Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232-2637. ab: We evaluated the risks of seizures and other neurological events following diphtheria-tetanus-pertussis (DTP) immunization for 38,171 Tennessee Medicaid children who received 107,154 DTP immunizations in their first 3 years of life. There were 2 children with encephalitis; both had disease onset more than 2 weeks following DTP immunization. There were 277 children who had febrile seizures, 42 with afebrile seizures, and 37 with seizures associated with other acute neurological illness (acute symptomatic). The risk of febrile seizures in the 0 to 3 days following DTP immunization (n = 6) was 1.5 (95% confidence interval, 0.6 to 3.3) times that of the control period 30 or more days following DTP immunization... 7. MR et al. Risk of seizures after measles-mumps-rubella immunization. Pediatrics 1991 Nov;88(5):881-5 1991. ab: To evaluate the risks of seizures and other neurologic events following measles-mumps-rubella (MMR) or measles-rubella (MR) immunization, a retrospective cohort study was conducted among 18,364 Tennessee children enrolled in Medicaid who received MMR or MR immunizations in their first 3 years of life. One hundred children had seizures at some time between immunization and 36 months; there were no encephalopathies during this period. Four children had febrile seizures in the 7 through 14 days following MMR or MR immunization compared with 72 in the interval 30 or more days following MMR or MR immunization yielding a relative risk (95% confidence interval) of 2.1 (0.7 to 6.4). Although not statistically significant, this increase in febrile seizures in the 7- through 14-day interval following MMR immunization is coincident with the occurrence of fever following MMR immunization and is consistent with reports of other investigators. 8. Cherry JD et al. Pertussis immunization and characteristics related to first seizures in infants and children. J Pediatr 122(6):900-3 1993. Department of Pediatrics, University of California Los Angeles School of Medicine. ab: In a previous study in which we examined the relationship of pertussis immunization to the onset of neurologic disorders during 1967 and 1968 and during 1972 and 1973 in Denmark, there were 554 children with initial onset of epilepsy and 2158 children with first febrile convulsions... The cause of increased severity of febrile seizures apparently associated with pertussis immunization is unknown. 9. Tuunanen J et al. Decrease in somatostatin-immunoreactive neurons in the rat amygdaloid complex in a kindling model of temporal lobe epilepsy. Epilepsy Research. 26(2):315-327, 1997. 10. Tuunanen J et al. Status epilepticus causes selective regional damage and loss of gabaergic neurons in the rat amygdaloid complex. European Journal of Neuroscience. 8(12):2711-2725, 1996. 11. Chen K et al. Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits. Nat Med 1999 Aug;5(8):888-94. Department of Anatomy and Neurobiology, University of California, Irvine 92697-1280, USA. 12. Bachevalier J. Medial temporal lobe structures and autism: a review of clinical and experimental findings. Neuropsychologia. 32(6):627-48, 1994. 13. Pabst HF et al. Kinetics of immunologic responses after primary MMR vaccination. Vaccine. 15.1.10-4 1997. ab: To study the kinetics of humoral as well as cellular immunity to measles and to test for associated immunosuppression 124 12 month old children were studied twice, before routine MMR and either 14, 22, 30, or 38 days after vaccination... Interferon-gamma was the principal cytokine produced after primary measles immunization... 14. Madara JL, Stafford J. Interferon-gamma directly affects barrier function of cultured intestinal epithelial monolayers. Journal of Clinical Investigation 83.2.724-7 1989. 15. Huynh HK, Dorovini-Zis K. Effects of interferon-gamma on primary cultures of human brain microvessel endothelial cells. American Journal of Pathology 142.4.1265-78 1993. " The results of these studies indicate that human brain microvessel endothelial cells respond to in vitro cytokine stimulation by undergoing profound morphological, functional, and permeability changes. We conclude that cerebral endothelium may play an important role in the initiation and regulation of lymphocyte traffic across the blood-brain barrier in inflammatory disorders of the human central nervous system. " 16. Planchon SM et al. Regulation of intestinal epithelial barrier function by TGF-beta 1. Evidence for its role in abrogating the effect of a T cell cytokine. Journal of Immunology 153.12.5730-9 1994. " Maintenance of the integrity of the single-cell-thick intestinal epithelium as an in vivo barrier between environmental Ags and mucosal immunocytes is pivotal for health. The T cell cytokine IFN-gamma consistently disrupts this epithelial barrier in vitro... " 17. RB et al. IFN-gamma modulation of epithelial barrier function. Time course, reversibility, and site of cytokine binding. Journal of Immunology 150.6.2356-63 1993. " ...we suggest that IFN-gamma-induced changes in epithelial permeability may be a major cause of altered intestinal barrier function in vivo. " 18. Berg RD. Bacterial translocation from the gastrointenstinal tract. Journal of Medicine 23.217-244 1992. 19. Banati RB, Graeber MB. Surveillance, intervention and cytotoxicity: Is there a protective role of microglia? Developmental Neuroscience 16.114-27 1994. 20. Benveniste EN. Inflammatory Cytokines within the central nervous system: sources, function, and mechanism of action. American Journal of Physiology 263.C1-C16 1992. 21. Hickey WF et al. T-lymphocyte entry into the central nervous system. Journal of Neuroscience Research 28.54-260 1991. 22. Cserr HF, Knopf PM. Cervical lymphatics, the blood-brain barrier and the immunoreactivity of the brain: a new view. Immunology Today 13.507-512 1992. 23. Stoll G, Jander S. The role of microglia and macrophages in the pathophysiology of the CNS. Prog Neurobiol 58.233 1999. 24. Matyszak MK. Inflammation in the CNS: balance between immunological privilege and immune responses. Prog Neurobiol 56.19-35 1998. 25. Karp CL et al. Mechanism of suppression of cell-mediated immunity by measles virus. Science 1996 Jul 12;273(5272):228-31. 26. Hussey GD et al. The effect of Edmonston-Zagreb and Schwarz measles vaccines on immune response in infants. J Infect Dis 1996 Jun;173(6):1320-6. " ...measles immunization resulted in suppression of lymphoproliferation, which was most evident in infants with the highest antibody responses and most immune activation. " 27. Auwaerter PG et al. Changes within T cell receptor V beta subsets in infants following measles vaccination. Clin Immunol Immunopathol 1996 May;79(2):163-70. " Measles produces immune suppression which contributes to an increased susceptibility to other infections. Recently, high titered measles vaccines have been linked to increased long-term mortality among some female recipients. " 28. Ward BJ, DE. Changes in cytokine production after measles virus vaccination: predominant production of IL-4 suggests induction of a Th2 response. Clin Immunol Immunopathol 1993 May;67(2):171-7. Department of Medicine, s Hopkins University School of Medicine, Baltimore, land 21205. 29. Wu VH et al. Measles virus-specific cellular immunity in patients with vaccine failure. J Clin Microbiol 1993 Jan;31(1):118-22. 30. Dressler F et al. Transient hypogammaglobulinemia of infancy. Acta Paediatrica Scandinavia 78.767-74 1989. 31. Cano F et al. Absent specific viral antibodies in patients with transient hypogammaglobulinemia of infancy. Journal of Allergy & Clinical Immunology 85.510-3 1990. 32. Glassman M et al. High incidence of hypogammaglobulinemia in infants with diarrhea. Journal of Pediatric Gastroenterology and Nutrition 2.465-71 1983. 33. Pass RF et al. Specific lymphocyte blastogenic responses in children with cytomegalovirus and herpes simplex virus infections acquired early in infancy. Infect Immun 34.1.166-70 1981. ab: Cell-mediated immune responses in 27 infants and children with cytomegalovirus (CMV) infection acquired between birth and 1 year of age were compared with responses in 13 children who had neonatal herpes simplex virus (HSV) infection. Infection was asymptomatic in 25 of 27 CMV-infected children... 34. Hayney MS et al. The influence of the HLA-DRB1*13 allele on measles vaccine response. J Investigative Medicine 44.261-3 1996. Mayo Clinic and Foundation, Rochester, MN. 35. McCusker C et al. Specific antibody responses to diptheria/tetanus revaccination in children evaluated for immunodeficiency. Ann Allergy Asthma Immunol 79.145-50 1997. 36. Epstein MM, Gruskay F. Selective deficiency in pneumococcal antibody response in children with recurrent infections. Ann Allergy Asthma Immunol 75.125-31 1995. A series of autism-related webpagesContents email to: Binstock copyright 1999 At 06:34 PM 12/16/2001 +1300, you wrote: >I noticed that the letters from Desmond and Dr Bobby Tsang have >appeared in a number of community newspapers recently, promoting the measles >vaccination campaign. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 15, 2001 Report Share Posted December 15, 2001 ---------- From: Ishgooda <ishgooda@...> Date: Sun, 16 Dec 2001 00:46:36 -0500 " karaka.j@... " <janclarke@...> Subject: Re: FW: " First, Do No Harm " Subject: MEASLES AND CROHN'S DISEASE Content-Type: text/plain; charset=iso-8859-1 X-MIME-Autoconverted: from 8bit to quoted-printable by ns1.access1.net id HAA01620 ken and meryl dorey wrote: The Lancet 13/12/97 Measles vaccination and inflammatory bowel disease Sir--Mark Feeney and colleagues (Sept 13, p 764)1 are to be commended on their efforts to investigate a possible link between measles vaccine and inflammatory bowel disease (IBD). However, as they themselves acknowledge, the potential difficulty of poor ascertainment of vaccination status could blur any relation between vaccination and the risk of IBD. and co-workers,2 who used the Royal College of General Practitioners (RCGP) database covering a nationally representative 1% of the UK population, found that, at a time when national vaccine uptake rates exceeded 55%, general practitioners recorded having given measles vaccine in only 8% of patients in the appropriate age-group. According to the RCGP, recording was only improved when general practitioners were remunerated for achieving vaccination targets. On the basis of 's study,2 ascertainment of vaccination status from general-practitioner records covering the relevant period1 could have underestimated measles vaccination rates by as much as 47% among either cases or controls. Absence of a record of measles vaccination cannot be taken as absence of vaccination. Poor ascertainment of measles vaccination status is likely to reduce the statistical significance of any relation between vaccination and subsequent disease, so that a small systematic bias is more likely to obliterate any such relation. There is a risk that by replacing controls, but not patients with IBD who had inadequate vaccination records, systematic bias may have been introduced into this study. Feeney and colleagues have attempted to address the issue of unobserved heterogeneity by looking at the uptake rates for vaccination against pertussis and diphtheria/tetanus. Although examination of vaccinations other than against measles provides more evidence about reliability of these data, it cannot provide conclusive evidence of homogeneity among cases and controls. The significantly higher uptake rates for pertussis and diphtheria/tetanus indicate that there could be a less significant relation between socioeconomic circumstances and vaccine uptake when compared with vaccination against measles. When this is coupled with the uncertainty of vaccination records, it renders them inadequate as indicators of childhood circumstances and characteristics. It is important that trials such as this are conducted and reported, but they cannot be a substitute for adequate safety trials of procedure that might cause severe iatrogenic damage, even if only in a few cases. * M Montgomery, D L , R E Pounder, A J Wakefield ---------------------------------------------------------------------- University Department of Medicine, Royal Free Hospital School of Medicine, University of London, London NW3 2PF, UK 1 Feeney M, Clegg A, Winwood P, Snook J. A case control study of measles vaccination and inflammatory bowel disease. Lancet 1997; 350: 764-66. 2 NP, Flemming DM,Pounder RE, Wakefield AJ. Crohn's disease, measles, and measles vaccination: a case control failure. Lancet 1996; 347: 263. Authors' reply Sir-- Montgomery and colleagues raise important questions about the accuracy of the data on which our study is based, and suggest some possible sources of bias. In our discussion we set out the reasons why we feel that the data are sufficiently reliable to justify the conclusions drawn. On the basis of national vaccination figures and the age distribution of our study population, we would have expected a measles vaccination prevalence of 54·2% in the control group--in fact the observed figure was 57·1%. It therefore seems most unlikely that we failed to identify vaccine recipients in appreciable numbers. It remains unclear why this apparently did happen in the study of et al,1 although the numbers concerned were small. Unfortunately, this study is difficult to interpret because it was published in brief letter format. In particular, it is not clear how rigorously health-care records were searched for the relevant information, a key determinant of successful data retrieval. Subgroup analysis does not support the suggestion that replacing controls with reserves when records were inadequate introduced bias into our study. Of 45 reserve controls, 25 (56%) had received measles vaccine, compared with 24 (53%) of matched cases. Finally, the suggestion that there is a " less significant relation between socioeconomic circumstances and vaccine uptake " for pertussis or diphtheria/tetanus than for measles is unsubstantiated. Evidence does not support this view.2 We share Montgomery and colleagues' sentiments about the importance of adequate safety trials. However, in the case of measles vaccine a trial with an unvaccinated limb would now be ethically questionable because the vaccine has proved so effective. In the absence of this type of trial, our finding of no link between measles vaccination and the later development of inflammatory bowel disease is reassuring,3 especially since this conclusion has recently been supported by a smaller case-control study.4 *Mark Feeney, Clegg, Winwood, Jonathon snook --------------------------------------------------------------------- Poole Hospital, Dorset BH15 2JB, UK 1 NP, Fleming DM, Pounder RE, Wakefield AJ. Crohn's disease, measles and measles vaccination: a case-control failure. Lancet 1996; 347: 263. 2 Clegg AJ. Childhood immunisation uptake: geographical perspectives. PhD Thesis, Portsmouth University, 1993. 3 Baxter T, Radford J. Measles vaccination as a risk factor for inflammatory bowel disease. Lancet 1995; 345: 1363. 4 DL, Montgomery SM, Ebrahim S, Pounder RE, Wakefield AJ. Measles vaccination and inflammatory bowel disease in the 1970 British cohort study. Gut 1997; 41(suppl3): A37. Sir--The case-control study by Mark Feeney and colleagues1 is an important contribution in the search for possible links between measles and Crohn's disease. The study shows that for individuals born in the 1970s and vaccinated during their second year of life, no increased risk of developing Crohn's disease could be demonstrated during over 20 years of follow-up. The purported basis for an association between measles and Crohn's disease is persistent measles virus or measles vaccine virus infection. Explaining Crohn's disease through association with measles vaccination requires a mechanism for the development of such persistent infection. We have proposed such a mechanism on the basis of an immunological tolerance window (unpublished data). We postulate that in the absence of maternal antibodies against measles, and before the maturation of the child's immune system, during the immunological tolerance window, exposure to measles virus (be it wild virus or vaccine virus) could result in tolerance to measles antigen and therefore persistent infection. Individuals with tolerance to measles antigen would consequently be at high risk of Crohn's disease. A large immunological tolerance window is most obviously present in the few children born to mothers without measles antibodies; from the in-utero period until immunological maturity at, say, 6 months of age. A shorter window is also present in some children in whom maternal antibodies wane early, before maturation of their immune system. Several studies2,3 back up the existence of such a mechanism. Of particular interest are non-boostable primary non-responders to live attenuated measles vaccine. This non-response is much more frequent in the case of vaccination at very young age (6-9 months), and may indicate such induced tolerance. The study by Feeney does not invalidate the measles tolerance hypothesis, since the individuals studied were vaccinated during their second year of life, when maturation of most children's immune system is reached. According to the measles tolerance hypothesis, an association between measles vaccination and Crohn's disease would only be expected in case of vaccination of a child who is (a) not protected by maternal antibodies anymore, and ( not yet immunological mature. The discussion thus remains open. If the measles tolerance hypothesis were to prove correct, it could contribute to the explanation of the increase in Crohn's disease in western countries. More important though, are the potential consequences for developing countries. A combination of vaccination as young as 6 months of age (the practice in Kinshasa, Congo, for the past 10 years), and reduced protection by maternal antibodies of children born to mothers who derive their immunity from vaccine, would multiply the opportunities for developing immune tolerance. The prospect of an epidemic of Crohn's disease in African countries 20 years from now, induced by vaccination at too young an age today, would be gloomy indeed. To clarify the possible link between measles and Crohn's disease, two research tracks should be explored. First we need to demonstrate, or refute, the existence of immunotolerance to measles virus. The non-boostable primary non-responders to measles vaccine identified in several studies could be a good starting point.4 Second, we should test the link between immunotolerance to measles virus and Crohn's disease. Studies of links between measles vaccination and Crohn's disease should then focus on vaccination at very young ages. In view of the potential high stakes, this would constitute a worthwhile contribution to the debate. *Wim Van Damme, Lut Lynen, Guy Kegels, Wim Van Lerberghe ---------------------------------------------------------------------- Department of Public Health, Institute of Tropical Medicine, 2000 Antwerpen, Belgium 1 Feeney M, Clegg A, Winwood P, Snook J. A case-control study of measles vaccination and inflammatory bowel disease. Lancet 1997; 350:764-66. 2 NP, Montgomery SM, Pounder RE, Wakefield AJ. Is measles vaccination a risk factor for inflammatory bowel disease? Lancet 1995; 345: 1071-74. 3 Ekbom A, Daszak P, Kraaz W, Wakefield AJ. Crohn's disease after in-utero measles virus exposure. Lancet 1996; 348: 515-17. 4 Mendelson E, Duvdevani P, Varsano N, et al. Measles immunity and response to revaccination of a young adult population in Israel. J Med Virol 1996; 50: 249-53. Sir--Persistent measles virus infections is implicated in Crohn's disease.1,2 This measles hypothesis is based mainly on immunohistochemical1 and epidemiological findings.2 However, Mark Feeney and colleagues' case-control study3 has provided evidence against this hypothesis. Immunohistochemical evidence derives essentially from the observation that both a monoclonal antibody and polyclonal hyperimmune serum specific for measles-virus-stained measles antigen are present in the intestine of Crohn's disease. We confirmed this observation with the same monoclonal antibody (MAS 182r: Harlan Sera-lab, Crawley Down, UK) that Wakefield and colleagues1 used (figure). However, we failed to identify measles virus genome, even with a highly sensitive reverse-transcriptase (rt)-PCR.4 Measles-specific monoclonal antibody MAS 182r was used to screen 1·5 million clones in a [(lambda)]gt11-expression library constructed from the intestinal tissue surgically excised from a 38-year-old patient with typical Crohn's disease. We thus identified and sequenced one positive clone to find that it was not a part of any measles virus genome but that it was 99% homologous with an undefined human gene deposited in the DNA data bases (AA449055). A Southern blot analysis further confirmed the host origin of this protein. This unexpected result led us to produce a monoclonal antibody (4F12) against this protein. When the intestinal tissues from the patients with Crohn's disease were doubly-stained with the monoclonal antibodies MAS 182r and 4F12, virtually all MAS 182r-positive cells were stained with 4F12. Although the possibility still remains that the antigen recognised by MAS 182r was a measles virus antigen, we assume that such a possibility is slight since none of measles-virus related clones were identified in the cDNA library. Thus, our findings, together with earlier rt-PCR results,4 are not in accord with the hypothesis that persistent measles virus infection is the cause of Crohn's disease. Previous immunohistochemical observations can be accounted for by antigen mimicry between measles virus and an undefined host protein found in the intestine of Crohn's disease. *Masahiro Iizuka, Osamu Masamune ---------------------------------------------------------------------- First Department of Internal Medicine, Akita University School of Medicine, Akita 010, Japan 1 Wakefield AJ, Pittilo RM, Sim R, et al. Evidence of persistent measles virus infection in Crohn's disease. J Med Virol 1993; 39: 345-53. 2 Ekbom A, Daszak P, Kraaz W, et al. Crohn's disease after in-utero measles virus exposure. Lancet 1996; 348: 515-17. 3 Feeney M, Clegg A, Winwood P, et al. A case-control study of measles vaccination and inflammatory bowel disease. Lancet 1997; 350: 764-66. 4 Iizuka M, Nakagomi O, Chiba M, et al. Absence of measles virus in Crohn's disease. Lancet 1995; 345: 199. Meryl Dorey, President The Australian Vaccination Network, Inc. PO Box 177 02 6687 1699 Phone Bangalow NSW 2479 02 6687 2032 FAX van@... http://www.ozemail.com.au/~shotinfo " All truth goes through three stages. First it is ridiculed. Then it is violently opposed. Finally, it is accepted as self-evident. " (Schopenhauer) ____________________________________________________________________________ ______ Any information obtained here is not to be construed as medical OR legal advice. The decision to vaccinate and how you implement that decision is yours and yours alone. ********************************************************* Karin Schumacher Vaccine Information & Awareness (VIA) 12799 La Tortola San Diego, CA 92129 619-484-3197 (phone/voicemail) 619-484-1187 (fax) via@... (email) http://www.909shot.com (NVIC website) http://www.access1.net/via (VIA website) ********************************************************* We Must Have The Freedom To Choose & Respect Everyone's Choice ********************************************************* Any information obtained here is not to be construed as medical OR legal advice. The decision to vaccinate and how you implement that decision is yours and yours alone. ******************************* Quote Link to comment Share on other sites More sharing options...
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