Autovaccine therapy®

1. What it is and how it works

Autovaccine therapy is a relatively unknown method of effectively treating chronic inflammatory diseases, autoimmune diseases. To understand how it works, it is necessary to have a bit of background information about infections.

Although it is generally accepted that acute inflammations and infections can be caused by viruses or bacteria, it is not generally known that there is evidence that the cause of most chronic illnesses can be traced back to bacterial DNA left in the body after the acute symptoms have gone. This DNA hides in tissue or blood in a state which circumvents the immune system, and is unrecognizable using standard diagnostic tests like blood culture, staining and microscopic diagnosis. The manner in which we use autovaccine therapy is designed to release the malignant DNA from its disguise in order to enable the immune system to recognize it and then deal with it. We do this by removing a number of phials of blood from the patient. This blood is stored for a length of time under specific conditions in which the encapsulated – and thus hidden – DNA is released from the blood. This process turns the patient’s own blood into a vaccine which once injected back into the patient, triggers the immune system to effectively deal with the malignant bacterial DNA.

The true elegance of this system lies in the fact that it is not necessary to do any of the very expensive and time consuming tests that are sometimes available to determine the true nature of the DNA. The immune system does not need a name, it just deals with any foreign bodies that are revealed by the autovaccine therapy.

2. More background on autovaccine therapy

Autovaccine therapy is not a new phenomenon. 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.

At that time, they could not have been aware that they had inadvertently inoculated the patients with bacterial DNA, nor could they have foreseen the enormous potential of this successful experiment. ['Read more about the implications of their work…'] 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. Both these alternatives seemed to be “miracle” drugs. They worked swiftly and there was nothing to indicate that there could be possible disadvantages in using them.

Nowadays, our view of antibiotic drugs has become more realistic as research reveals more and more of how they work. We know that they are only useful for treating acute infections. We know that they can damage the intestinal flora, that bacteria can become resistant to them and – most importantly of all in this context – they are useless for treating chronic inflammatory disease.

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 [2-4]. 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 and 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].

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, recidivistic 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 [9-11]. 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].

The assumption that blood taken from healthy individuals contains no micro-organisms is now outdated. Advanced research has 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 – although still retaining their original DNA. They can alter their (external) membranes in any number of ways – as illustrated at the beginning of this article. These Cell Wall Deficient Bacteria (CWDB) do not behave like normal bacteria. The 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.

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].

The problem of determining the pathogens, as raised by Jansen, is not an issue in autovaccine therapy. The goal of the therapy is to (a) enable the immune system itself to recognize the pathogenic nucleus of the CWDB (CWDB-DNA) as an antigen, so that (b) the new information can be filed in the adaptive part of the immune system enabling it (c) to neutralize these antigens as soon as they are released from the cell. This occurs during the extracellular cell division of the CWDB. The nature of autovaccine therapy then ensures that no new pathogens can be formed and allows a gradual recovery from the chronic illness to take place.

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. In this way, the pathogenic DNA-nucleus is released from its ‘disguise’. In this new state, the blood becomes an antigen and can be used as a vaccine against the chronic inflammation caused by the pathogenic DNA. The production of antibodies against this essential protein particle is set off by the injection of the vaccine with the result that no new pathogens are formed and healing can gradually take place. This is a slow process and can take a long time.

Initially, the idea of injecting even a small amount of “old” blood might seem bizarre – and that is probably why it is never done. Doctors recoil from the suggestion. The question is, is this a reflection of scientific reality or of is it just a gut reaction? Are there real risks involved in autovaccine therapy using your own blood? The answer is no. This is because of the long incubation time that is involved when preparing the blood. This period is six weeks or more and has the advantage that the only living thing left in the preparation is DNA. This means that all other bioactive molecules have been neutralised. The risk of undesirable side effects, such as auto-immune reactions which are caused by autoreactive T-lymphocytes does not exist as there is nothing recognizable for the body to react against – other than the DNA – which is the crux of the whole therapy. This has been confirmed in crossover tests done using autovaccines and patients’ blood. After treating many patients – some of them having had more than 30 injections, there have been no adverse reactions to the injections. This is no accident, there is no known scientific basis for any fear of a negative result.

The desired positive result can be limited or even blocked by various other factors such as a genetically determined illness, severe stress, hormonal imbalance, intestinal dysbiosis, (hidden) dental infections, heavy metals poisoning, conflicting medicines, etc. It is therefore necessary to undertake a thorough examination of the patient prior to applying the autovaccine therapy in order to eliminate those things that can render the therapy ineffective.

Without resorting to the use of pharmaceuticals, the therapy described above can achieve not only positive, but often spectacular results in patients with diverse chronic inflammatory diseases that have (until now) been deemed as untreatable by regular medical practice.

3. Scientific 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. 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. 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, 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; newscientist.nl

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