Autovaccine therapy, summary and Literature

On this site you can find video and text testimonies by a number of patients that show that we can achieve very positive, even spectacular, results using autovaccine therapy. This therapy has a broad application for conditions that regular medical practice does not yet have an answer for. Below you will find a complete - but compact - summary. An extended literature list will show that this therapy, which is still new in the Netherlands, is solidly based on scientific knowledge and research. 

Autovaccine therapy is a relatively unknown therapy to effectively treat chronic inflammatory diseases, autoimmune diseases. Barger, Horgan and Horgan [1] described how they had successfully treated hundreds of patients suffering from colitis ulcerosa with autovaccination in the Journal of the American Medical Association back in 1929. They had made sterile culture filtrates prepared from the patient’s own gut bacteria and injected those patients with it, successfully treating most patients. The advent of sulphur drugs and shortly afterwards the development of antibiotics, coupled with the high expectations ascribed to them, pushed these experiments – and autovaccination as a potential therapy – almost completely out of the picture.

In the last couple of decades there has been a renewed interest in autovaccination by diverse international centres for the treatment of cancer. They use various techniques to implement this therapy [2,3,4]. Medical literature also describes the successful use of autovaccination for chronic infections, particularly in cases of resistance to antibiotics, such as the MRSA bacteria [5,6]. Using pathogens taken from the infected organ or from infected tissue, which have been identified by cultivating samples in a culture medium, sterile vaccines are prepared according to the De Vito method to address a specific pathogen. The method is a precisely formulated combination of steps: incubation, treatment with formaldehyde, and dilution [7].

Repeated autovaccination using the patient’s own blood has also been shown to have a healing effect in cases of allergies in dogs that are difficult to treat, as published by M. Klein in Biologische Tiermedizin [8]. These and other similar own-blood treatments are utilized quite frequently in Germany by GPs to treat the symptoms of illnesses caused by immune system dysfunction – such as allergies, recidivist infections, auto-immune system diseases and habitual abortion. These therapies involve intramuscular injections of small amounts of the patient’s own blood at intervals of between two weeks and a month, after the blood has been taken and then held in vitro for a few hours at room temperature. In cancer surgery circles, it is recognized that blood transfusions using the patient’s own blood, can measurably strengthen the immune system and has a positive effect on post-operative recovery. The usual transfusion using donor blood has the reverse effect [9,10,11].

The assumption that blood taken from healthy individuals contains no micro-organisms is now outdated. Advanced research techniques (PCR and FISH) have shown that so-called “sterile blood” can still contain microbiological DNA remnants from previous infections [12-17]. Micro-organisms can escape the deadly effects of the immune system or antibiotics by disguising themselves. Any number of exterior shapes are possible - such as illustrated here. IThe axioms of Robert Koch no longer apply to them in this form. Worse still, the use of antibiotics actually exacerbates this process. Treatments using antibiotics - mostly a spectacular therapy for infections in the short term - actually increase the chance of a chronic inflammatory disease in the long term. This effect caused by Cell Wall Deficient Bacteria (CWDB) is a phenomenon known for at least half a century, but it is not universally accepted. In scientific studies, (see below) these mutated bacteria have been associated with chronic illnesses, are unrecognizable to the immune system, cannot be seen using classical culture methods, and carry intact bacterial DNA that can transform back into virulent bacteria at any given time. CWDBs are also known in the literature as L-forms.

Chronic illnesses such as arteriosclerosis and rheumatism can be explained by making the link between previous infections and these CWDBs. There is a great deal of scientific evidence that bacterial DNA can be found in arteriosclerotic plaques or in pathological joint fluid and that there is a relationship with oral flora – particularly in cases of periodontitis [18-38]. The connection between CWDB and diverse chronic illnesses in humans and animals has been revealed as a result of thorough research documented by microbiologist, Lida H. Mattman [39]. Recent research indicates the possibility that whole sequences of bacterial DNA are able to penetrate the human genome and in this way increase malignity and pass it on to future generations [40]. A meta-analysis published in the Journal of Alzheimers’ Disease in 2015, has shown that Alzheimer’s Disease is increasingly seen as a delayed result of infections undergone earlier in life [41].
“If pathogens are indeed the cause behind the development of plaques, then we should be able to vaccinate ourselves against those infections,” writes Robert D. Moir, assistant professor at Harvard Medical School [42], “but it will not be easy to develop a vaccine for Alzheimer because there are apparently so many different pathogens involved in plaque formation,” according to Jacobus Jansen, researcher at Maastricht University [43].

As it is not necessary to determine precisely what microorganism is causing the problem when using autovaccine therapy, the diagnostic problem raised by Jansen is not an issue. However, it is of supreme importance to follow the correct procedures when making the vaccine. Many years of research and testing has gone into the preparation of this protocol. The goal of the autovaccine therapy is (a) to train the immune system to recognise the pathogenic nucleus of the Cell Wall Deficient Bacteria (CWDB-DNA) as an antigen, so that (b) this new information is stored in the adaptive part of the immune system and (c) the antigen is then neutralised by the immune system as soon as it leaves the body cells. This happens during extra-cellular cell division of the CWDB. The autovaccine prevents new CWDBs forming and gradually ensures that the chronic illness heals.

Blood that is stored in vitro will disintegrate into its various parts. This is not only true for blood cells, but also for the CWDB. Because of this process, the pathogenic DNA is also released from the L-form (CWDB) as free bacterial DNA. In this state, the denaturated blood has itself become an antigen and can be used to treat chronic inflammatory disease. Once injected with the autovaccine, the production of antibodies against the bacterial DNA is triggered, preventing the development of new populations of the pathogenic DNA. The new cells formed in the body are no longer subject to infection and the healing process can gradually get underway. This last step can take some time. It has to be noted that the desired result of autovaccine therapy can be hindered by all sorts of external factors such as illness caused by genetic disorders, high stress levels, hormonal imbalance, gut dysbiosis, dental infections, heavy metal poisoning, certain medications, etc. Further research in the future will help clarify how to deal with these obstacles for successful treatment.

 

References

1. Barger J A, Horgan E, Horgan J. De behandeling der chronische ulceratieve colitis met autovaccins en cultuurfiltraten van enterococcen in Referaten A.J.L. Terwen: N Tijdschr Geneesknd 1929;73.II.44.
2. Foon KA. Immunotherapy for colorectal cancer. Current Oncology Reports 2001;3(2):116-26.
3. Besser MJ et al. Clinical Responses in a Phase II Study Using Adoptive Transfer of Short-term Cultured Tumor Infiltration Lymphocytes in Metastatic Melanoma Patients. Clin Cancer Res. 2010;16(9):2646-55.
4. Rosenberg SA et al. Use of tumor-infiltrating lymphocytes and interleukin-2 in the Immunotherapy of patients with metatstatic Melanoma. N Engl J Med 1988;319:1676-80.
5. Caterina Rizzoa, Gianluca Brancacciob, Danila De Vitoc and Giovanni Rizzod. Efficacy of autovaccination therapy on post-coronary artery bypass grafting methicillin-resistant Staphylococcus aureus mediastinitis. Interact CardioVasc Thorac Surg 2007;6:228-29.
6. Wilczyński K, Koźmińska J, Biliński A. The testing of auto-vaccination of patients with chronic purulent otitis media. Otolaryngol Pol. 1995;49(23):183-185.
7. De Vito D, Rizzo G. Il ritorno di una pratica trascurata: la terapia con autovaccini. Igiene Moderna 1999; 112:1245–51.
8. Klein, M. Atopische Dermatitis des Hundes: Behandlung mit der Auto-Sanguis-Stufentherapie. Biol Tiermedizin 2009;26 (2): 31-35.
9. Busch O.R.C., Hop W.C.J., van Papendrecht M.A.W.H. et al. Blood transfusions and prognosis in colorectal cancer. N Engl J Med 1993;328:1372-76.
10. Vamvakas E.C., Moore S.B. Perioperative blood transfusion and colorectal cancer recurrence: a qualitative statistical overview and meta-analysis. Transfusion 1993;33:754-65.
11. Heiss M.M., Jauch K.W., Delanoff C. et al. Blood transfusions modulated tumor recurrence—a randomized study of autologous verusus homologous blood transfusion in colorectal cancer. J Clin Oncol 1994;12:1859-67.
12. Haranaga S, Yamaguchi H, Leparc GF, Friedman H, Yamamoto Y; Detection of Chlamydia pneumoniae antigen in PBMNCs of healthy blood donors. Transfusion 2001; 41(9):1114 – 19.
13. Yamaguchi H, Yamada M, Uruma T, Kanamori M, Goto H, Yamamoto Y, Kamiya S. Prevalence of viable Chlamydia pneumoniae in peripheral blood mononuclear cells of healthy blood donors. Transfusion. 2004; 44(7):1072-8.
14. Boman J, Söderberg S, Forsberg J, Birgander LS, Allard A, Persson K, Jidell E, Kumlin U, Juto P, Waldenström A, Wadell G. High prevalence of Chlamydia pneumoniae DNA in peripheral blood mononuclear cells in patients with cardiovascular disease and in middle-aged blood donors. J Infect Dis. 1998;178(1):274-7.
15. Karimi Gh, Samiei Sh, Hatami H, Gharehbahian A, VafaiyanV, Tabrizi Namini M. Detection of Chlamydia pneumoniae in peripheral blood mononuclear cells of healthy blood donors in Tehran Regional Educational Blood Transfusion Centre. Transfusion Medicine Volume 2010; (4): 237-43.
16. Grayston JT. Background and current knowledge of Chlamydia pneumoniae and atherosclerosis. J. Infect. Dis. 2000; 181 (3): 402-10.
17. Boman J, Söderberg S, Forsberg J, Birgander LS, Allard A, Persson K, Jidell E, Kumlin U, Juto P, Waldenström A, Wadell G. High prevalence of Chlamydia pneumoniae DNA in peripheral blood mononuclear cells in patients with cardiovascular disease and in middle-aged blood donors. J Infect Dis. 1998;178(1):274-7.
18. Martinez-Martinez, RE et al. Detection of periodontal bacterial DNA in serum and synovial fluid in refractory rheumatoid arthritis patients. J Clin Periodontol. 2009; 36(12):1004-10.
19. Témoin, S et al.Identification of oral bacterial DNA in synovial fluid of patients with arthritis with native and failed prosthetic joints. J Clin Rheumatol. 2012;18(3):117-21.
20. Moen, K. Oral bacterial DNAs in synovial fluids of arthritis patients. Microbial Ecology in Health and Disease. 2005; 17: 2-8
21. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM. Dental disease and risk of coronary heart disease and mortality. BMJ 1993; 306: 688–691
22. Amar S, Gokce N, Morgan S, Loukideli M, Van Dyke TE, Vita J. Periodontal disease is associated wtih brachial artery endothelial dysfunction and systemic inflammation. Arterioscler Thromb Vasc Biol. 2003;23(7):1245-9.
23. Seymour, G. J., Ford, P. J., Cullinan, M. P., Leishman, S. and Yamazaki, K. (2007), Relationship between periodontal infections and systemic disease. Clinical Microbiology and Infection 2007, 13: 3–10.
24. Beck JD, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol 1996; 67: 1123–1137.
25. Hung H-C, Willet W, Merchant A, Rosner BA, Ascherio A, Joshipura KJ. Oral health and peripheral arterial disease. Circulation 2003; 107: 1152–1157.
26. Desvarieux M, Demmer RT, Rundek T et al. Relationship between periodontal disease, tooth loss, and carotid artery plaque. The oral infections and vascular disease epidemiology study (INVEST). Stroke 2003; 34: 2120–2125.
27. Jansson L, Lavstedt S, Frithiof L, Theobald H. Relationship between oral health and mortality in cardiovascular diseases. J Clin Periodontol 2001; 28: 762–768.
28. Janket S-J, Baird A, Chuang S, Jones JA. Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. Oral Surg Oral Med Oral Pathol 2003; 95: 559–569.
29. Khader YS, Albashaireh ZSM, Alomari MA. Periodontal diseases and the risk of coronary heart and cerebrovascular diseases: a meta-analysis. J Periodontol 2004; 75: 1046–1153.
30. Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Periodontal disease and risk of coronary heart disease. JAMA 2000; 284: 1406–1410.
31. Periodontal disease is associated with brachial artery endothelial dysfunction and systemic inflammation. Arterioscler Thromb Vasc Biol 2003; 23: 1245–1249.
32. Mercanoglu F, Oflaz H, Oz O et al. Endothelial dysfunction in patients with chronic periodontitis and its improvement after initial periodontal therapy. J Periodontol 2004; 75: 1694–1700.
33. Tonetti MS, D'Aiuto F, Nibali L et al. Treatment of periodontitis and endothelial function. N Engl J Med 2007; 356: 911–920.
34. Sheu JJ, Lin HC. Association between multiple sclerosis and chronic periodontitis: a population-based pilot study. Eur J Neurol. 2013; 20(7):1053-9.
35. Fitzpatrick SG, Katz J. The association between periodontal disease and cancer: a review of the literature. J Dent. 2010; 38(2):83-95.
36. Li L, Messas E, Batista EL, Levine RA, Amar S. Porphyromonas gingivalis infection accelerates the progression of atherosclerosis in a heterozygous apolipoprotein E-deficient murine model. Circulation 2002; 105: 861–867.
37. Lalla E, Lamster IB, Hofmann MA et al. Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null mice. Arterioscler Thromb Vasc Biol 2003; 23: 1405–1411.
38. Ford PJ, Gemmell E, Timms P, Chan A, Preston FM, Seymour GJ. Anti-P. gingivalis response correlates with atherosclerosis. J Dent Res 2007; 86: 35–40.
39. Mattman LH. Cell Wall Deficient Forms, Stealth Pathogens 2001; 3rd ed; CRC Press Washington DC
40. David R. Riley, Karsten B. Sieber, Kelly M. Robinson, James Robert White, Ashwinkumar Ganesan, Syrus Nourbakhsh, Julie C. Dunning Hotopp. Bacteria-Human Somatic Cell Lateral Gene Transfer Is Enriched in Cancer Samples. PLoS Computational Biology, 2013; 9 (6).
41. Maheshwari P, Eslick GD. Bacterial infection and Alzheimer’s disease: a meta-analysis: J Alzheimers Dis 2015;43(3):957-66.
42. Moir RD et al. The Alzheimer’s Disease-Associated. Amyloid-beta Protein Is an Antimicrobial Peptide. PLoS ONE 2010; 5 (3): 1-10.
43. Anil Ananthaswamy, 3 juni 2016; www.newscientist.nl

Print Email

Copyright © 2018 Art of Medicure (Leendert Kunst M.D.). All Rights Reserved.