Autism: 2018 Dietrich Klinghardt MD, PhD Infections and Infestations Chronic Infections, Infestations and ASD Infections affect us in 3 ways: 1. Immune reaction against the microbes or their metabolic products Treatment: low dose immunotherapy (LDI, LDA, EPD) 2. Effects of their secreted endo- and exotoxins and metabolic waste Treatment: colon hydrotherapy, sauna, intestinal binders (Enterosgel, MicroSilica, chlorella, zeolite), detoxification with herbs and medical drugs, activation of detox pathways by solving underlying blockages (methylation, etc.) 3. Competition for our micronutrients Treatment: decrease microbial load, consider vitamin/mineral protocol Lyme, Toxins and Epigenetics • In 2000 I examined 10 autistic children with no known history of Lyme disease (age 3- 10), with the IgeneX Western Blot test – after successful treatment. 5 children were IgM positive, 3 children IgG, 2 children were negative. That is 80% of the children had clinical Lyme disease, none the history of a tick bite! • Why is it taking so long for autism-literate practitioners to embrace the fact, that many autistic children have contracted Lyme or several co-infections in the womb from an often asymptomatic mother? Why not become Lyme literate also? • Infections can be treated without the use of antibiotics, using liposomal ozonated essential oils, herbs, ozone, Rife devices, PEMF, colloidal silver, regular s.c injections of artesunate, the Klinghardt co-infection cocktail and more. • Symptomatic infections and infestations are almost always the result of a high body burden of glyphosate, mercury and aluminum - against the backdrop of epigenetic injuries (epimutations) suffered in the womb or from our ancestors( trauma, vaccine adjuvants, work place related lead, aluminum, herbicides etc., electromagnetic radiation exposures etc.) • Most symptoms are caused by a confused upregulated immune system (molecular mimicry) Toxins from a toxic environment enter our system through damaged boundaries and membranes (gut barrier, blood brain barrier, damaged endothelium, etc.). It appears that there is an intentional destruction of human health by poisoning our air, our food and the many direct insults to our body (mercury-amalgam fillings, persistent contrails, herbicides, toxic adjuvants in vaccines, building materials and styles, glyphosate in coffee, etc). A toxic inner milieu turns our symbiotic life-giving microbiome into a pathogenic cesspool with all the oseuees of a hoi ifetio. Microbes achieve dominion over our system by seetig a lage oktail of sall oleules efeed to as biotoxins hih ae responsible for most symptoms. Man-made toxins and microbial toxins have to be cleared via the same biochemical pathways, which are not fully functional in the ASD children for a variety of reasons: genetic SNPs and mutations, epimutations, age at time of injury, EMR exposure, psychological stresses in the family, man-ade isults o the hild’s ai aie adjuvants, medical drugs taken by the mom during pregnancy, ie Tleol, o’s aalga fillings) etc., etc. Literature: Dietrich Klinghardt: iAdvancing Medicine with Food and Nutrients Biotoxins pp 851-868; 2nd edition. CRC Press 2013. Biotoxins from Microbes and Parasites • Bacterial toxins (Exotoxin, Gram positive Bacilli): Clostridium: tetani (Tetanospasmin) · perfringens (Alpha toxin, Enterotoxin) · difficile (A, B) · botulinum (Botox) other: Anthrax toxin · Listeriolysin O • Cocci: Streptolysin · Leukocidin (Panton-Valentine leukocidin) · Staphylococcus (Staphylococcus aureus alpha/beta/delta, Exfoliatin, Toxic shock syndrome toxin, SEB) • Actinobacteria: Cord factor · Diphtheria toxin • Gram negative: Shiga toxin · Verotoxin/shiga-like toxin (E. coli) · E. coli heat-stable enterotoxin/enterotoxin · Cholera toxin · Pertussis toxin · Pseudomonas exotoxin · Extracellular adenylate cyclase • By mechanism: type I (Superantigen) · type II (Pore-forming toxin) · type III (AB toxin/AB5) • Endotoxin: Lipopolysaccharide (Lipid A) · Bacillus thuringiensis delta endotoxin • Virulence factor: Clumping factor A · Fibronectin binding protein A • Mycotoxins: Aflatoxin · Amatoxin (alpha-amanitin, beta-amanitin, gamma-amanitin, epsilon-amanitin) · Citrinin · Cytochalasin · Ergotamine · Fumonisin (Fumonisin B1, Fumonisin B2) · Gliotoxin · Ibotenic acid · Muscimol · Ochratoxin · Patulin · Phalloidin · Sterigmatocystin · Trichothecene · Vomitoxin · Zeranol · Zearalenone • Invertebrates: arthropod: scorpion: Charybdotoxin, Maurotoxin, Agitoxin, Margatoxin, Slotoxin, Scyllatoxin, Hefutoxin, Lq2, Birtoxin, Bestoxin, BmKAEP, Phaiodotoxin · spider: Latrotoxin (Alpha-latrotoxin) · PhTx3 · Stromatoxin · Vanillotoxin · Huwentoxin mollusca: Conotoxin · Eledoisin · Onchidal · Saxitoxin · Tetrodotoxin • Vertebrates: fish: Ciguatera · Tetrodotoxin • amphibian: (+)-Allopumiliotoxin 267A · Batrachotoxin · Bufotoxins (Arenobufagin, Bufotalin, Bufotenin · Cinobufagin, Marinobufagin) · Epibatidine · Histrionicotoxin · Pumiliotoxin 251D · Samandarin · Samandaridine · Tarichatoxin • Reptile/snake venom: Bungarotoxin (Alpha-Bungarotoxin, Beta-Bungarotoxin) · Calciseptine · Taicatoxin · Calcicludine · Cardiotoxin III Nat Rev Neurol 2014 Nov;10(11):643-60. doi: 10.1038/nrneurol.2014.187. Epub 2014 Oct 14. Maternal immune activation and abnormal brain development across CNS disorders. Knuese I, Chicha L, Britschgi M, Schobel SA, Bodmer M, Hellings JA, Toovey S, Prinssen EP Abstract Epidemiological studies have shown a clear association between maternal infection and schizophrenia or autism in the progeny. Animal models have revealed maternal immune activation (mIA) to be a profound risk factor for neurochemical and behavioural abnormalities in the offspring. Microglial priming has been proposed as a major consequence of mIA, and represents a critical link in a causal chain that leads to the wide spectrum of neuronal dysfunctions and behavioural phenotypes observed in the juvenile, adult or aged offspring. Such diversity of phenotypic outcomes in the mIA model are mirrored by recent clinical evidence suggesting that infectious exposure during pregnancy is also associated with epilepsy and, to a lesser extent, cerebral palsy in children. Preclinical research also suggests that mIA might precipitate the development of Alzheimer and Parkinson diseases. Here, we summarize and critically review the emerging evidence that mIA is a shared environmental risk factor across CNS disorders that varies as a function of interactions between genetic and additional environmental factors. We also review ongoing clinical trials targeting immune pathways affected by mIA that may play a part in disease manifestation. In addition, future directions and outstanding questions are discussed, including potential symptomatic, disease- modifying and preventive treatment strategies. Transl Psychiatry 2012 Apr 3;2:e98. doi: 10.1038/tp.2012.24. Effects of maternal immune activation on gene expression patterns in the fetal brain. Garbett KA1, Hsiao EY, Kálmán S, Patterson PH, Mirnics K. Abstract We are exploring the mechanisms underlying how maternal infection increases the risk for schizophrenia and autism in the offspring. Several mouse models of maternal immune activation (MIA) were used to examine the immediate effects of MIA induced by influenza virus, poly(I:C) and interleukin IL-6 on the fetal brain transcriptome. Our results indicate that all three MIA treatments lead to strong and common gene expression changes in the embryonic brain. Most notably, there is an acute and transient upregulation of the α, β ad γ crystallin gene family. Furthermore, levels of crystallin gene expression are correlated with the severity of MIA as assessed by placental weight. The overall gene expression changes suggest that the response to MIA is a neuroprotective attempt by the developing brain to counteract environmental stress, but at a cost of disrupting typical neuronal differentiation and axonal growth. We propose that this cascade of events might parallel the mechanisms by which environmental insults contribute to the risk of neurodevelopmental disorders such as schizophrenia and autism. Lyme and Co-infections The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders Medical Hypotheses, Volume 70, Issue 5, 2008, Pages 967–974 Robert C. Bransfield , Jeffrey S. Wulfman, William T. Harvey, Anju I. Usmand Summary Chronic infectious diseases, including tick-borne infections such as Borrelia burgdorferi may have direct effects, promote other infections and create a weakened, sensitized and immunologically vulnerable state during fetal development and infancy leading to increased vulnerability for developing autism spectrum disorders. A dysfunctional synergism with other predisposing and contributing factors may contribute to autism spectrum disorders by provoking innate and adaptive immune reactions to cause and perpetuate effects in susceptible individuals that result in inflammation, molecular mimicry, kynurenine pathway changes, increased quinolinic acid and decreased serotonin, oxidative stress, mitochondrial dysfunction and excitotoxicity that impair the development of the amygdala and other neural structures and neural networks resulting in a partial Klüver–Bucy Syndrome and other deficits resulting in autism spectrum disorders and/or exacerbating autism spectrum disorders from other causes throughout life. Support for this hypothesis includes multiple cases of mothers with Lyme disease and children with autism spectrum disorders; fetal neurological abnormalities