Guest guest Posted February 21, 2004 Report Share Posted February 21, 2004 suzy this is what cindy sent, it's a load of info! claudia I would think the reverse would be true as well. Immune activation in the absence of infection contributes to autoimmune disorders. Infection with Mycobacterium bovis BCG Diverts Traffic of Myelin Oligodendroglial Glycoprotein Autoantigen-Specific T Cells Away from the Central Nervous System and Ameliorates Experimental Autoimmune Encephalomyelitis. Sewell DL, Reinke EK, Co DO, Hogan LH, Fritz RB, Sandor M, Fabry Z. Department of Pathology and Laboratory Medicine, University of Wisconsin. Department of Microbiology, Medical College of Wisconsin, Milwaukee, Wisconsin. Infectious agents have been proposed to influence susceptibility to autoimmune diseases such as multiple sclerosis. We induced a Th1-mediated central nervous system (CNS) autoimmune disease, experimental autoimmune encephalomyelitis (EAE) in mice with an ongoing infection with Mycobacterium bovis strain bacillus Calmette-Guerin (BCG) to study this possibility. C57BL/6 mice infected with live BCG for 6 weeks were immunized with myelin oligodendroglial glycoprotein peptide (MOG(35-55)) to induce EAE. The clinical severity of EAE was reduced in BCG-infected mice in a BCG dose-dependent manner. Inflammatory-cell infiltration and demyelination of the spinal cord were significantly lessened in BCG-infected animals compared with uninfected EAE controls. ELISPOT and gamma interferon intracellular cytokine analysis of the frequency of antigen-specific CD4(+) T cells in the CNS and in BCG-induced granulomas and adoptive transfer of MOG(35-55)-specific green fluorescent protein-expressing cells into BCG-infected animals indicated that nervous tissue-specific (MOG(35-55)) CD4(+) T cells accumulate in the BCG-induced granuloma sites. These data suggest a novel mechanism for infection-mediated modulation of autoimmunity. We demonstrate that redirected trafficking of activated CNS antigen-specific CD4(+) T cells to local inflammatory sites induced by BCG infection modulates the initiation and progression of a Th1-mediated CNS autoimmune disease. Naturally occurring anti-IFN{gamma} auto-antibody and severe infections with Mycobacterium cheloneae and Burkholderia cocovenenans. Hoeflich C, Sabat R, Rosseau S, Temmesfeld B, Slevogt H, Docke WD, Gruetz G, Meisel C, Halle E, Goebel UB, Volk HD, Suttorp N. Institute for Medical Immunology, University Hospital Charite, Humboldt University, Berlin, Germany. Recently various genetic defects in IFNgamma mediated immunity have been described including mutations in the interferon-gamma receptor 1 (IFNgR1) and receptor 2 (IFNgR2), Stat1 and IL-12 receptor beta 1 (IL-12Rb1) and IL-12 p40 genes. These mutations are associated with the occurrence of severe infections with intracellular pathogens especially nontuberculous mycobacteria and vaccine-associated BCG. Here we report on a previously healthy adult patient primarilary presenting with severe infections with Burkholderia cocovenenans and subsequently Mycobacterium cheloneae. We found a strong inhibitory anti-IFNgamma activity in the patient's plasma and identified a high-affinity neutralizing anti-IFNgamma autoantibody. Unfortunately, the patient died due to severe sepsis before knowing the nature of the inhibitory activity. The application of alternative therapeutic approaches such as IVIG or immunoadsorption may have been beneficial in this case. Screening for neutralizing anti-IFNgamma autoantibodies should supplement testing for IFN-gamma and IL-12 pathway defects in patients with recurrent infections with intracellular pathogens, especially with NTM. Ann N Y Acad Sci. 2003 Nov; 1005: 404-8. Related Articles, Links Vaccinations may induce diabetes-related autoantibodies in one-year-old children. Wahlberg J, Fredriksson J, Vaarala O, Ludvigsson J; Abis Study Group. Division of Pediatrics, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linkoping University, Linkoping, Sweden. Vaccinations have been discussed as one among many environmental candidates contributing to the immune process that later may lead to type 1 diabetes. ABIS (All Babies in Southeast Sweden) is a prospective cohort study following a nonselected birth cohort of general population. In a randomly selected sample collection from 4400 children, GADA and IA-2A have been determined at the age of 1 year. The information on vaccinations was collected from questionnaires answered by the parents and was related to beta cell autoantibodies. When studying the induction of autoantibodies using the autoantibody level of 90th percentile as cutoff level, hemophilus influenza B (HIB) vaccination appeared to be a risk factor for IA-2A [OR 5.9 (CI 1.4-24.4; p = 0.01)] and for GADA [OR 3.4 (CI 1.1-10.8; p = 0.04)] in logistic regression analyses. Furthermore, the titers of IA-2A were significantly higher (p < 0.01 in Mann-Whitney test) in those children who had got HIB vaccination. When 99th percentile was used as cutoff to identify the children at risk of type 1 diabetes, BCG vaccination was associated with increased prevalence of IA-2A (p < 0.01). We conclude that HIB vaccination may have an unspecific stimulatory polyclonal effect increasing the production of GADA and IA-2A. This might be of importance under circumstances when the beta cell-related immune response is activated by other mechanisms. PMID: 14679101 [PubMed - indexed for MEDLINE] Messages Messages Help Reply | Forward | View Source | Unwrap Lines | Delete | Remove Author | Ban Author Message 11670 of 11999 | Previous | Next [ Up Thread ] Message Index Msg # From: Sheri Nakken <vaccineinfo@...> Date: Wed Jan 7, 2004 6:08 am Subject: More: Disease/Vaccine Charts & info var trv_lrec_formUrl = " http://rd./SIG=12e9vmc30/M=220133.4478820.5655239.2772263/D=egroupweb/\ S=1705043011:LREC/EXP=1076812363/A=1986196/R=0/id=formurl/*http://shop.store.yah\ oo.com/cgi-bin/clink?travelocity2+shopping:dmad/SIG=12e9vmc30/M=220133.4478820.5\ 655239.2772263/D=egroupweb/S=1705043011:LREC/EXP=1076812363/A=1986196/R=1/107672\ 5963+http://us.rmi./rmi/http://www.travelocity.com/rmi-framed-url/http:\ //dps1.travelocity.com/cannonball.ctl " ; From: Dewey Ross Duffel <duffel@...> April I too have wanted, when spare time permits, to develop a web page just for the links that show that the vaccinated always have more disease than the unvaccinated, and that this includes the target disease. I have not even started this 'little' project but just now collected a few for flu and smallpox and tuberculosis. Please share what you find. Thanks, Dewey. Here are a few snips for you: see: http://www.vaclib.org/intro/present/overview.htm (for an introduction to vaccination) see: http://www.vaclib.org/intro/present/index3.htm#4 for a graph showing a large smallpox epidemic in 1871-72, inspite of compulsory vaccination. http://www.vaclib.org/basic/fluindex.htm Do flu shots work? - - - Why Japan ended compulsary School age flu shots ... 60% Vaccination twice annually, or dropping to 20% coverage made no difference in flu incidence. Two large studies with cities with vaccination rates between 1% and 90% showed little difference in incidence. In fact, vaccinated incidence rates were slightly higher. " From 1972 to 1979 , a total number of 142 children and families sued the government for damages. The total number of deaths were 50, severe developmental retardation were 65, and intractable epilepsy were 35. " http://www.vaclib.org/basic/smallpoxindex.htm thompson2.htm " Professor Dick, speaking at an environmental conference in Brussels in 1973, admitted that in recent decades, 75% of British people who contracted smallpox had been vaccinated. This, combined with the fact that only 40% of children (and a maximum of 10% of adults) had been vaccinated, clearly shows that vaccinated people have a much higher tendency to contract the disease. " http://www./vaclib.org/chapter/wysmallpox.htm#quotations " I have been a regular practitioner of medicine in Boston for 33 years. I have studied the question of vaccination conscientiously for 45 years. As for vaccination as a preventative of disease, there is not a scrap of evidence in its favor. Injection of virus into the pure bloodstream of the people does not prevent Smallpox. Rather, it tends to increase its epidemics and makes the disease more deadly. Of this we have indisputable proof. In our country (U.S.) cancer mortality has increased from 9 per 100,000 to 80 per 100,000 or fully 900 per cent increase, within the past 50 years, and no conceivable thing could have caused this but the universal blood poisoning now existing. " Dr. E. Page http://www.vacliborg/basic/quotes.htm " It was similar with the measles vaccination. They went through Africa, South America and elsewhere, and vaccinated sick and starving children...They thought they were wiping out measles, but most of those susceptible to measles died from some other disease that they developed as a result of being vaccinated. The vaccination reduced their immune levels and acted like an infection. Many got septicaemia, gastro-enteritis, etcetera, or made their nutritional status worse and they died from malnutrition. So there were very few susceptible infants left alive to get measles. It's one way to get good statistics. Kill all those that are susceptible, which is what they literally did. " --Dr. Kalokerinos, M.D. Read Dr. Kalokerinos book, " Every Second Child " for worst case example of vaccines killing children. Early in this century, the Philippines experienced their worst smallpox epidemic ever after 8 million people received 24.5 million vaccine doses; the death rate quadrupled as a result. (Physician Hay's address of June 25, 1937; printed in the Congressional Record) Whale.to site: Wonderful MMR vaccine quotes http://www.whale.to/vaccine/mmr49.html The last " safe " MMR vaccine " I believe the documents clearly reveal how the central government hid undesirable data and delayed discontinuation of the (MMR) vaccine, " lawyer Tatsuro Shigemura said. " --Media 2002 " The conclusion of the research report was: Children who received all of the AAP recommended vaccinations were 14 times more likely to become learning disabled and 8 times more likely to become autistic compared with children who were never vaccinated. http://www.vaclib.org/basic/evidence.htm EVIDENCE AGAINST VACCINES by Jon Rappaport " Smallpox, like typhus, has been dying out (in England) since 1780. Vaccination in this country has largely fallen into disuse since people began to realize how its value was discredited by the great smallpox epidemic of 1871-2 (which occurred after extensive vaccination). " W. Webb, A Century of Vaccination, Swan Sonnenschein, 1898. " The world's biggest trial (conducted in south India) to assess the value of BCG tuberculosis vaccine has made the startling revelation that the vaccine 'does not give any protection against bacillary forms of tuberculosis.' The study said to be 'most exhaustive and meticulous,' was launched in 1968 by the Indian Council of Medical Research (ICMR) with assistance from the World Health Organization (WHO) and the U.S. Centers for Disease Control in Atlanta, Georgia. " The incidence of new cases among the BCG vaccinated group was slightly (but statistically insignificantly) higher than in the control group, a finding that led to the conclusion that BCG's protective effect 'was zero.' " New Scientist, November 15, 1979, as quoted by Hans Ruesch in Naked Empress, Civis Publishers, Switzerland, 1982. " Between 10 December 1929 and 30 April 1930, 251 of 412 infants born in Lubeck received three doses of BCG vaccine by the mouth during the first ten days of life. Of these 251, 72 died of tuberculosis, most of them in two to five months and all but one before the end of the first year. In addition, 135 suffered from clinical tuberculosis but eventually recovered; and 44 became tuberculin-positive but remained well. None of the 161 unvaccinated infants born at the time was affected in this way and none of these died of tuberculosis within the following three years. " Hazards of Immunization, . " We conducted a randomized double-blind placebo-controlled trial to test the efficacy of the 14-valent pneumococcal capsular polysaccharide vaccine in 2295 high-risk patients... Seventy-one episodes of proved or probable pneumococcal pneumonia or bronchitis occurred among 63 of the patients (27 placebo recipients and 36 vaccine recipients)... We were unable to demonstrate any efficacy of the pneumococcal vaccine in preventing pneumonia or bronchitis in this population. " New England Journal of Medicine, November 20, 1986, p. 1318, Simberkoff et al. Arerugi. 2000 Jul;49(7):585-92. Related Articles, Links [The effect of DPT and BCG vaccinations on atopic disorders] [Article in Japanese] Yoneyama H, Suzuki M, Fujii K, Odajima Y. Department of Pediatrics, Tokyo Metropolitan Government Hiroo General Hospital. METHODS: To examine the relationship between DPT and BCG vaccinations and development of atopic diseases, we studied on 143 children resident of the island of Kodushima, Tokyo Japan. This study dealt with the entire population of 0-3 years old (82), all of the first graders of the elementary school (31) and all of the first graders of the junior high school (30) on the Island. RESULTS: Among the 82 children aged 0-3, out of the 39 who received DPT vaccination, 10 (25.6%) suffered from bronchial asthma and this ratio was significantly higher than among the children who have not received DPT vaccination (1 in 43, 2.3%), (p < 0.01). This was also the case concerning atopic dermatitis (7 in 39, 18.0% vs 1 in 43, 2.3%) (p < 0.05). The same trend was also observed if three diseases (bronchial asthma, allergic rhinitis and atopic dermatitis) were combined (22 in 39, 56.4% vs 4 in 43, 9.3%) (p < 0.01). As to the context of BCG vaccination, there were no cases with atopic disorders among the tuberculin positive first graders of the elementary school. No such relations, however, were observed among the first graders of the junior high school at all. FINDINGS: From these results we conclude that DPT vaccination has some effect in the promotion of atopic disorders, while successful BCG vaccination inhibits the development of atopic disorders, although the preventive effect of BCG may not last for many years. PMID: 10944825 [PubMed - indexed for MEDLINE] http://www.blackwell-synergy.com/links/doi/10.1046/j.1440-1843.2003.00489.x/abs/ Respirology Volume 8 Issue 3 Page 376 - September 2003 doi:10.1046/j.1440-1843.2003.00489.x SHORT COMMUNICATION Control of an outbreak of BCG complications in Gaza Objective: We aim to describe Bacille Calmette Guerin (BCG) complications in Gaza using two studies: one during an outbreak and the other after control of the possible contributing factors to this outbreak. Methodology: The first study was conducted on 6145 newborn infants vaccinated in 21 primary care centres in Gaza with BCG vaccine, Pasteur Paris, batch number 5122 from July to October 2001. The study was repeated after changing the BCG vaccine and training 63 nurses from November to December 2001. The training program included theoretical lectures on BCG and tuberculosis and practical training in strict intradermal injection. The second study included 6877 newborn infants vaccinated with BCG vaccine, batch number 101023, Denmark, from January to April 2002. Results: During the outbreak, BCG complications occurred in 225 infants with a complication rate of 36.61 per 1000 vaccinations. The mean age at presentation was 4 months. The commonest complications were regional lymphadenitis in 138 (61.33%) infants, local abscess in 48 (21.33%) infants, local ulcer in 26 (11.56%) infants, keloid scar in 12 (5.33%) infants and one (0.44%) infant who died from disseminated disease had severe combined immunodeficiency. In the follow-up study, BCG complications occurred in 43 infants with a complication rate of 6.25 per 1000 vaccinations, which is significantly lower (P < 0.001) than that during the initial outbreak. Conclusion: The study supports the use of a less virulent vaccine and proper vaccination techniques to minimize the incidence of BCG complications. The training of nurses in strict intradermal injection should be maintained and the proper selection of those receiving the vaccines should be considered to avoid the vaccination of any infant with immunodeficiency. Received 8 August 2002; revised 31 January 2003; accepted for publication 13 February 2003. Affiliations Chest Department, Shifa Hospital and Al Azhar University-Gaza, Palestinian Authority Correspondence Correspondence: Walid Daoud, College of Applied Medical Sciences, Al Azhar University-Gaza, PO Box 1277, Palestinian Authority Via Israel. Email: <A HREF= " mailto:wdaoud@... " > wdaoud@...</A> To cite this article DAOUD, Walid (2003) Control of an outbreak of BCG complications in Gaza. Respirology 8 (3), 376-378. doi: 10.1046/ j.1440-1843.2003.00489.x Perhaps one of the most interesting and controversial observations on the role of Th1 stimuli on Th2 _expression is found when examining the effect of the antituberculosis vaccine Bacillus Calmette-Guerin (BCG) on the development of atopy. Japanese schoolchildren, who routinely undergo BCG vaccination, had a significant inverse relationship between delayed hypersensitivity to Mycobacterium tuberculosis and incidence of asthma and elevation of IgE (46). As with many studies of environmental influences on atopic disease, there are confounding data. Studies in Britain fail to show a relationship between response to BCG vaccination and atopy (46). Furthermore, whether the observations by Shirakawa et al. (45) result from the effect of the vaccine itself or the innate ability of that child to respond to that vaccine is open to debate (46). However, experiments in mice, which demonstrate that immunization with BCG blunts development of allergen-specific IgE and eosinophilic responses to allergen after allergen challenge, support the idea that BCG vaccine is a potent Th1 stimulus (47). Taken together, these observations support the notion that BCG stimulates increased Th1 function and is associated with decreased Th2 immune responsiveness. It has also been argued that decreased incidence of infection and frequent use of antibiotics may also be contributing to the development of atopy. The hypothesis is that by decreasing exposure to Th1 stimuli (either by active infection or by alteration of bacterial colonization, which may stimulate Th1 immune responses), the Th2 immune responsiveness expressed by the fetus has a better chance of being maintained, thus allowing for _expression of the immune phenotype. The use of antibiotics in the early years of life correlates with the subsequent development of atopy. Similarly, in societies in which antibiotic use is decreased and natural infections are more frequent, atopy occurs less frequently. However, despite these data, it seems unlikely that children at very high risk for asthma (inner-city African Americans) have increased exposure to antibiotics compared to more affluent populations at lesser risk (31,37). In addition to antigen-specific immune responses, it has been suggested that accessory molecules expressed by bacteria (classic Th1 stimuli) may contribute to immune maturation such that Th1 responses are emphasized (31,48). Lipopolysaccharide (LPS) is a molecule expressed on all gram-negative bacteria that interacts with antigen-presenting cells and other immune effector cells via the CD14 receptor. Treatment of APCs with LPS results in secretion of IL-12, which in turn blunts Th2 responses and stimulates interferon- secretion. It has been argued that mucosal colonization with bacteria, including LPS- bearing organisms, allows for nonspecific deviation toward the Th1 phenotype. Recently, it was found that the gene for CD14 colocalizes with genes for IL-3, IL-4, and GM-CSF on the chromosome region 5q31.1. Furthermore, a specific polymorphism has been identified (a C-to-T transition at base pair -159) in which those children homozygous for the T allele have significantly higher levels of soluble CD14 than do heterozygotes or those who are homozygous for the C allele (48). In turn, serum levels of CD14 (which could mediate LPS interaction with APCs) have a significant positive correlation with interferon- and a negative correlation with IL-4 (48). This observation supports the hypothesis that an imbalance between Th1 and Th2 influences the development of atopic disease Superimposed on any genetic predisposition that may exist is the role of environmental influences that might induce either Th1 responses (certain immunizations such as BCG, bacterial infections and stimuli, and colonization with bacteria) or Th2 responses (early exposure to allergens, especially food allergens and indoor aeroallergens). Other influences may be important as well, including toxicological stimuli that may shift the immune response toward a Th2 response. Another important question is if the timing of exposure to potential environmental stresses is important in subsequent postnatal _expression of an atopic/asthmatic phenotype (Table 2). Other than carrying genes that predispose an individual to developing atopic responses, preconceptional exposure of parents to environmental factors is unlikely to be an important window of exposure for the development of atopy in subsequent offspring. However, it is likely that an even more important window of exposure for the impact of environmental agents is during the first year of life. This could include allergen exposure (food and airborne), natural or vaccine stimulation of Th1 responses, and the potential for agents such as PAH to modify Th1 or Th2 responses during this period. Several studies indicate that the risk of developing atopic disease and maintaining it throughout life is greatest if it occurs during the first year of life. Many atopic infants lose a significant degree of atopic _expression from 2 to 5 years of age and it is a well-recognized phenomenon that children may grow out of asthma by puberty. It is interesting that one of the hallmark features of Th1 immune maturation is an ability to mount an adequate IgG response to polysaccharide antigens, usually occurring by 2 years of age. This suggests that avoidance of pro-Th2 environmental stressors (allergen avoidance and the avoidance of environmental adjuvants of Th2 responses such as diesel exhaust and ETS) during the toddler years is important. Also, it suggests that potentially inappropriate removal of Th1 stimuli (such as gut flora), perhaps by the inappropriate use of antibiotics, might also promote persistence of atopy. Although unique and very strong environmental exposures might induce allergy during adulthood, this is relatively rare. The best examples of such adult- onset allergies are occupational diseases, some of which are " typical " Th2-based IgE responses to naturally presented antigens, whereas others are unique sensitizing agents that cause immunologically unique disorders. Taken together, it seems that the exposures to environmental stressors during the perinatal, neonatal, and toddler years are of the most importance. Likewise, maternal rather than paternal influences during perinatal life could be significant. Environmental stresses that support Th2 inflammation are obviously important. However, the impact of stresses that decrease Th1 responses (including the production of interferon- and IL-12) cannot be ignored. Finally, better understanding of the molecular basis for the development of atopy, including production of relevant cytokines and their receptors, antigen presentation, T-cell influence on B-cell function and direct alteration of B-cell function, are essential to appropriately identify immune processes that may be targets for the action of known and as yet unappreciated environmental agents which influence the development of atopy and asthma in susceptible people. This article has been edited. For full article please see; http://ehpnet1.niehs.nih.gov/members/2000/suppl-3/475-482peden/peden- full.html TI: Mestnye privivichnye reaktsii i tuberkulinovaia allergiia u detei posle vnutrikozhnoi vaktsinatsii BTsZh [Local reaction and tuberculin allergy in children after intradermal BCG vaccination] AU: Rostomashvili,-S-G SO: Probl-Tuberk. 1974; 65(4): 7-10 JN: Problemy-tuberkuleza IS: 0032-9533 LA: Russian; Non-English AN: 74251566 TI: Dynamika alergii poszczepiennej BCG i zwiazanego z nia mechanizmu obronnego. [Evolution of BCG post-vaccination allergy and related defense mechanisms] AU: Norska,-I SO: Gruzlica. 1966 Feb; 34(2): 121-9 JN: Gruzlica-i-choroby-pluc IS: 0017-4955 LA: Polish; Non-English AN: 66163296 TI: Alergia poszczepienna u dzieci szkolnych szczepionych dawka 0,05 mg i dawka 0,1 mg BCG Moreau. [Postvaccination allergy in school children vaccinated with 0.05 mg and with 0.1 mg of BCG Moreau vaccine] AU: Krzyszkowska,-A SO: Gruzlica. 1965 Jun; 33(6): 471-5 JN: Gruzlica-i-choroby-pluc IS: 0017-4955 LA: Polish; Non-English AN: 66030658 TI: BCG et surveillance de l'allergie post-vaccinale: constat d'echec? [bCG and the monitoring of post-vaccinal allergy: a proven failure?] AU: de-Cornulier,-M; Picherot,-G SO: Arch-Fr-Pediatr. 1989 Oct; 46(8): 628 JN: Archives-francaises-de-pediatrie IS: 0003-9764 LA: French; Non-English AN: 90103784 Abstract <A HREF= " http://www2.us.elsevierhealth.com/scripts/om.dll/#top " > TOP </A> We report the case of a 2-year-old boy with juvenile sarcoidosis, in whom the cutaneous lesions first arose at the site of and soon after a BCG vaccination. Juvenile sarcoidosis is rare, and the pattern of clinical features is distinct from the adult form of sarcoidosis, possibly related to immunologic development. The cause of sarcoidosis is unknown, although there is much interest in the possibility of mycobacterial species operating as antigenic stimuli to initiate the disease. This case suggests that the Mycobacterium bovis present in the BGC vaccination may have been etiologically important in the development of sarcoidosis. (J Am Acad Dermatol 2003;48:S99-102.) Publishing and Reprint Information <A HREF= " http://www2.us.elsevierhealth.com/scripts/om.dll/#top " > TOP </A> This supplement is made possible through an unrestricted education grant from Stiefel Laboratories to the American Academy of Dermatology. From the Department of Dermatology, Imperial College School of Medicine, Chelsea and Westminster Hospital. Reprint requests: Dr G. E. N. Osborne, Specialist Registrar in Dermatology, St 's Institute of Dermatology, St ' Hospital, Lambeth Palace Road, London, SE1 7EH, United Kingdom. Copyright © 2003 by the American Academy of Dermatology, Inc. 0190-9622/2003/$30.00 + 0 doi:10.1067/mjd.2003.158 A DGReview of :<A HREF= " http://www.docguide.com/gpc.nsf/doc?CreateDocument & n=95 & id=03E05ADF052F2F3\ \ E852568C000807CA5 & cond=Vaccinology & t=08-06-40;AM & l=News & u=/news/content.nsf/Pape\ \ rFrameSet?OpenForm & id=03E05ADF052F2F3E852568C000807CA5 & newsid=8525697700573E1885\ \ 256CD9004D6914 & u=http://jama.ama-assn.org/cgi/content/abstract/289/8/1012 & ref=/n\ \ ews/content.nsf/news/8525697700573E1885256CD9004D6914?OpenDocument & id=03E05ADF05\ \ 2F2F3E852568C000807CA5 & c=Vaccinology & count=10 " > " BCG Vaccination and Risk of Atopy " </A> Journal of the American Medical Association (JAMA) 02/27/2003 By Elda Hauschildt Infants who receive Bacille Calmettee Guerin (BCG) vaccination do not experience a reduction in risk of developing atopy, research in Greenland indicates. Until 1990, BCG vaccination was given routinely to newborns in Greenland but the procedure was withdrawn in 1990/1991. Because of local outbreaks of tuberculosis, however, it was re-introduced in 1997 and administered to newborns in the routine vaccination program. Investigators from the Statens Serum Institut in Copenhagen, Denmark, and Sisimiut Hospital in Sisimiut, Greenland, studied BCG- vaccinated children and unvaccinated children from the northwest coast of Greenland. " No significant differences in the risk of atopy was found according to age at BCG vaccination, " they say. " Overall, these results do not support the hypothesis that BCG vaccination has a protective effect on the development of atopy. " The cross-sectional study included 1,686 children (79%) living in the towns of Sisimiut, Ilulissat, Aasiaat and Maniitsoq. These towns have a similar number of inhabitants (3,500 to 5,200) and similar climate, infrastructure and living conditions. Complete information on vaccination status was found for 1,575 of the children. Participants were aged 8 to 16 years. Blood samples were drawn and BCG vaccination information obtained during two periods, November 1998 and November 2001. Atopy was defined as a positive result in an assay testing for immunoglobin E (IgE) specific against the most common inhalant allergens. The investigators say they that cannot say the effect of BCG vaccination will be the same in populations with other genetic constitutions. Almost all of the Greenland children studied were born there, and Greenland has a large Inuit population. " Furthermore, our primary focus was on the effect of early BCG vaccination. Thus, we had limited data regarding children vaccinated at ages outside the general recommendations. " JAMA, 2003;289:1012-1015. & u=/news/content.nsf/PaperFrameSet?OpenForm & id=03E05ADF052F2F3E852568C000807CA5 & \ \ newsid=8525697700573E1885256CD9004D6914 & u=http://jama.ama-assn.org/cgi/content/a\ \ bstract/289/8/1012 & ref=/news/content.nsf/news/8525697700573E1885256CD9004D6914?O\ \ penDocument & id=03E05ADF052F2F3E852568C000807CA5 & c=Vaccinology & count=10 " > " BCG Vaccination and Risk of Atopy " </A> ===== http://www.himalayasalt.co.uk http://www.stores.ebay.co.uk/thealternativeway http://www.freeyurko.bizland.com/ http://www.he-ed.org.uk " The mind is like a parachute. In order to function, it first has to open. " -- Dewar ___________________________________________________________ Messenger - Communicate instantly... " Ping " your friends today! Download Messenger Now http://uk.messenger./download/index.html Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 16, 2008 Report Share Posted December 16, 2008 is bcg for bladder an alternative ie. good or another one of the established procedures? what test can i take to know if cancer is still there or not? Quote Link to comment Share on other sites More sharing options...
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