Author: Laura Alonso Canal, MD

Title: Pediatric Lyme

We are nowadays facing an epidemic of neurodevelopmental problems in our children such as ADHD or autism. Also, gastrointestinal symptoms in the pediatric population are very frequent and are usually labeled as “functional” and benign. The fact that these problems have aroused in conjunction with an epidemic of autoimmune conditions, chronic fatigue syndrome and fibromyalgia in the adult population makes some researchers postulate that a common background could be found in all of these chronic syndromes with a different expression due to a different age of onset.

Scientific evidence has shown a pro-inflammatory state and a dysregulation of the immune system in both autism and fibromyalgia/chronic fatigue syndrome. The possible role of the current Lyme Epidemic and other chronic infections in the pathogenesis of these diseases is a fascinating and hope-giving field.

During my talk I will discuss the importance of a good anamnesis as well as the common findings in physical examination, laboratory studies and medical imaging in the study and treatment of pediatric tick-born-diseases. Children have special peculiarities to take into account, which are feared by some doctors. Especially small children with limited expressive capability who have sometimes been ill since they were born are more challenging.

Author: Marissa Barbieri, BS

Title: Potential Mechanisms of Fatigue in Post Treatment Lyme Disease Patients

Quality of life for Post Treatment Lyme Disease Syndrome patients is poor. Complaints of fatigue is one of the most common symptoms of PTLDS patients. It is known that autoimmune response to self-proteins via molecular mimicry occurs in PTLDS patients. Molecular mechanisms that mediate fatigue in these patients is currently unknown. We hypothesized that potential autoantibodies to mitochondrial proteins may be responsible for fatigue in these patients. We have surveyed Lyme disease patients in Binghamton, New York and have collected serum and urine specimens from 26 patients. We have screened patient serum samples for autoantibodies using HEp2 cells. Many patients showed cytoplasmic granular "strands of beads" suggesting potential anti-mitochondrial antibodies. Screening of an independent group of PTLDS patient sera for potential autoantibodies using ImmuneProfiler™ Biomarker Discovery on HuProtTM Arrays showed presence of antibodies to mitochondrial proteins such as Pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase. Our data indicates a potential link between fatigue and autoantibodies to mitochondrial proteins in PTLDS patients.

Author: Steven J. Bock, MD

Title: Functional Medicine and the Complex Tick-Borne Disease Patient

Tick-borne disease is an epidemic in many parts of the world. Chronic Tick-borne disease can present with multiple symptoms, including chronic fatigue, headaches, joint pains, fibromyalgia, sleep issues, cardiac symptoms, visual symptoms and cognitive dysfunction, to name a few. It can be a persistent infection and /or a chronic inflammation, and it can cause dysregulation of multiple body systems, causing immunological, hormonal, digestive, neurological, metabolic, psychological and energetic dysfunction. These issues can be the result of the tick-borne disease or from underlying predispositions, which need to be identified.

Functional medicine “is a dynamic approach to assessing, preventing and treating complex chronic disease.” Functional medicine helps clinicians identify and ameliorate dysfunction in the physiology and biochemistry in the human body as a primary method of improving patient health. These functions are often for each of us the result of life-long interactions among our environment, including tick exposure, our lifestyles and our genetic predisposition.”

I will discuss the many concepts that comprise functional medicine, including assessment strategies, functional medical testing, medical detoxification, heavy metal, chemical exposure, mold and neurotoxin evaluations, IV and oral nutritional therapy and more. This will enable one to start to determine general and specific treatment modalities that will affect patient outcomes and improve the quality of life in the patient with chronic tick-borne disease.

Author: Magdalena Cubala-Kuscharska, MD, PhD

Title: Immunopsychiatry of Children with Lyme and Co-Infections

Late-stage of borreliosis can manifest as neuroinflamation and mental symptoms, which can easily be misdiagnosed as autism, ADHD, motor diseases, psychosis, schizoaffective disorders, bipolar disorder, depression, anxiety disorders (panic disorder, social anxiety disorder, etc.). Co-infection like bartonella, toxoplasma, Babesia, anaplasma, Erhlichia might aggravate neuropsychiatric symptoms. These pathogens have an ability to evade immune defenses and enter the nervous system, causing direct inflammation in the brain.

Neuroinflammation might be caused by direct infection of the brain but also be a result of immuno-inflammatory cascade and pathophysiological changes associated with oxidative stress, excitotoxicity, changes in homocysteine metabolism and altered tryptophan catabolism. Infected individuals may develop a coordinated set of behavioral changes, known as a sickness behavior. This process is triggered by pro-inflammatory cytokines produced by peripheral phagocytic cells in contact with invading microorganisms. The peripheral immune message is relayed to the brain via a fast neural pathway and a slower humoral pathway, resulting in the expression of pro-inflammatory cytokines in macrophage-like cells, microglia in the brain as well as activation mast cells.

Lyme bacteria causes immune and metabolic effects that result in a gradually developing spectrum of neuropsychiatric symptoms. Antibiotics may help improve functioning and prevent further disease progression. Awareness of the association between LB and neuropsychiatric impairments and studies of their prevalence in neuropsychiatric conditions can improve understanding of the causes of mental illness and violence and result in more effective prevention, diagnosis and treatment. In this presentation, we provide data from our clinic for children with neurodevelopmental disorders, who have been positively tested for borrelia burgdoferi.

Author: Pol De Saedeleer, PharmD

Title: The Affected Th1/Th2/Th17 Immune Response

The lecture starts by detailing our immune response There will be a short overview of how our immune system works under normal conditions. Depending on the circumstances, we develop a Th1, Th2 or Th17 response. However, the lecture will focus on the communication between the innate and the adaptive immune response, especially in a situation in which pathogens have been introduced, resulting in an aberrant immune response.

Next to multi-infectious pathology, the core of this lecture, there is a variety of other circumstances in which the normal immune response is disturbed, such as heavy metal toxicity and pollution, exposure to parasites and stress. These will be briefly covered. Yet, the focus will be on an aberrant immune response as the basis of a multi-infectious pathology, resulting in multisystemic disease.

Author: Kunal Garg, MSc

Title: Challenging the Lyme Monomicrobial Paradigm: Diagnosing Lyme Disease and Beyond

An astounding 83% (2.3 million tests) of all tick-borne diseases (TBD) diagnostic tests performed by the commercial laboratories in the USA accounted for only Lyme disease (LD). However, in the Europe, North America, and Australia 4 - 60% of patients with LD were co-infected with Babesia, Anaplasma, or Rickettsia. Yet, tick-borne diseases (TBD) are not tested simultaneously with LD.

We utilized the enzyme linked immunosorbent assay to test 432 patients suffering at different stages of tick-borne diseases for their immunoglobulin M (IgM) and G (IgG) responses against 20 microbes associated with TBDs. Microbial antigens included three Borrelia species in two distinct morphologies (spirochete and persistent form) and TBD associated co-infections and opportunistic infections. Patients were organized in seven categories according to their respective clinical diagnosis provided by the healthcare professionals. Study outcomes indicated 85% probability that a randomly selected patient will respond to Borrelia and other TBD microbes rather than to just Borrelia. Immune responses to multiple microbes were observed at all stages of tick-borne diseases. Remarkably, 72% of the Centers for Disease Control and Prevention (CDC) negative patients responded to at least one Borrelia species' persistent form. Additionally, the odds that a post treatment Lyme disease syndrome (PTLDS) patient at random will respond to Borrelia persistent forms rather than Borrelia spirochetes is 86%.

Outstandingly large and varied immune responses to Borrelia and multiple TBD associated co-infections and opportunistic infections signified the profound polymicrobial nature of TBDs. Reduced health-related quality of life and increased disease severity in TBD patients could be alleviated by introducing guidelines that recommend early diagnosis of multiple TBD associated microbes for different antibody types (IgM and IgG) simultaneously.

Author: Jack Lambert, MD

Title: Congenital Infections in Pregnancy, with Special Focus on Borrelia

Infections in pregnancy are a risk to both mother and child. Much has been learned from congenital syndrome and infection caused by the treponemal infection T pallidum, which causes congenital syphilis. Much has been learned from studies of the mother to child transmission of HIV, timing of infection, risk factors for HIV transmission, and optimal diagnostic measures used to detect these infections. Little scientific data has been accumulated on Congenital Borreliosis over the years, but there are clear similarities with syphilis, and it will be necessary to put together a scientific plan, similar to has been done with HIV, to be able to tackle and eradicate the mother to child transmission of borrelial infections. This presentation with review available scientific data accumulated to date, and give recommendations for next steps to better understand this infection, with a goal to eradication of congenital infection and disease.

Author: Marie Mas, MD

Title: PATHOTIQUE Study. Multi-site PCR of Vectorial Diseases in Ticks

Current serological tests for Lyme disease may have sensitivity problems and do not detect co-infections. What diagnostic contribution can PCR make?

In 2018 and 2019, 65 patients with a SPPT (polymorphic syndrome persistent after tick bites) table, were included in the PATHOTIQUE 1 research protocol (conducted with Prof. Perronne, Prof. Franck, veterinarian, Dr. Lacout and Dr. Mas).

25 germs (borrelia, bartonnella, babesia, candida, rickettsia, anaplasma, mycoplasma) were investigated, by PCR/metagenomics (sequencing), on four different matrices: venous blood, urine, saliva and capillary blood at D0 and D2 of the intake of an enzyme, bromelaine.

Author: Tatjana Mijatovic, PhD

Title: Neglected Infections and Gastrointestinal Issues in Patients with Late/Persistent/Chronic Vector-Borne Infections

Background : Vector-borne infections are increasing globally - Lyme disease is among the most prevalent vector borne infection in the U.S. and Europe and is reaching epidemic levels. In vector-borne diseases concurrent infections frequently occur. The most known, and most investigating concern borreliosis, bartonelosis, babesiosis, rickettsiosis and anaplasmosis. Many other pathogens can worsen the clinical picture and further complicate differential diagnosis.

Aims: The goal of this contribution is to bring the focus on those neglected infections and to present the associated laboratory data. Furthermore, the present contribution aims to provide a deeper understanding of the gastrointestinal disorders in patients with vector-borne infections.

Methods: Available retrospective data were analyzed in order to show the prevalence of these neglected/less investigated infections. Moreover, associated gastrointestinal issues have been retrieved and analyzed.

Results: Among those neglected infections, there are few that deserve more attention and investigations, like Tularemia, Yersinia, Mycoplasma, Chlamydia, Epstein-Barr virus and Herpesviruses. Our data show that prevalence of these infections is not negligible and they should be more investigated. Different testing options are available and lead to better management of the patients with complex clinical picture. Most of concurrent infections are also characterized by gastrointestinal and hepatic involvement, leading to gut inflammation, opportunistic infections, leaky gut and dysbiosis. Most frequently observed bacterial overgrowth contributing to dysbiosis concern Enterococcus, Streptococcus and Prevotella that are strong hydrogen sulfide (H2S) producers. In excess, H2S acts as a mitochondrial poison and a potent neurotoxin. It can directly inhibit enzymes involved in the cellular production of energy. H2S also interferes with oxygen transport by blocking hemoglobin in the red blood cells. Finally, H2S is lowering gut pH preventing the growth of many beneficial bacteria, like Bifidobacteria. Bacteroides, yet another group of dysbiotic bacterias frequently increased in patients with complex clinical pictures, are significant clinical pathogens and are found in most anaerobic infections with an associated mortality of more than 19 %. Species of the genus Bacteroides have the most antibiotic resistance mechanisms and the highest resistance rates of all anaerobic pathogens. Dysbiosis, associated with leaky gut will enable many toxic metabolites to enter the circulation and further impair immune and neuronal functions.

Conclusion: The overall high failure rate of therapies for vector-borne infections, especially in late/persistent/chronic patients, underscores the necessity to fully investigate different concurrent infections along with resulting gastrointestinal and immune dysregulations.

Author: Robert Miller, ND

Title: Environmental Toxin Detox Weakness from Genetic Variants Found in Those with Chronic Lyme Disease

Background: The NutriGenetic Research Institute’s mission is to discover genetic weakness that predisposes individuals to illnesses caused by environmental factors.

Aims: The aim of the studies was to find if there are genetic variants in pathways that would result in: increased free radical production, less than optimal antioxidant production, and weakness in detoxification pathways, which would allow environmental toxins to have more of an impact on the individuals.

Patients and Methods: To determine if unique genetic patterns exist with chronic Lyme patients, we analyzed the genetic patterns of functional and detoxification pathways from 421 participants, who submitted their 23andme genome for a global contrast to data supplied by the 1000 Genome Phase 3 Project. The reference and alternate alleles for each of the SNPs were determined using the HaploReg v4.1 database.

Results:
Phase I Study showed more genetic variants in genes related to methylation, CYP1A1, CYP1BA (Phase I Detoxification), PON1 (pesticide detox), SOD2 (super oxide dismutase), GSTP1 (Glutathione), CPS1, ASS1, ARG2 (Urea Cycle), and HFE C282Y.
Phase II Study showed more variants in genes related to neurotransmitters. This study found increased variants in the GLS, GOT1, GRIA1, and GAD1 genes, creating the potential for excess glutamate. Studies have shown that glutamate triggers the production of nitric oxide and superoxide, which can create peroxynitrite (ONOO−). High serum levels of total NO, MDA, and nitrotyrosine observed in patients with Lyme borreliosis indicate an enhancement of lipid peroxidation and protein nitration, which may enhance the inflammatory process in Lyme patients.
Phase III illustrated higher genetic variants in SLC40A1, which makes Ferroportin, the only iron exporter, more glutathione genes (GSTA1, GSTA2, GSTA5, GSTM1, GSTM3, and GSTM4), and Nrf2 and Keap1.
Phase IV, illustrated more genetic variants in AMPK, ULK1, ULK2 and ATG13, which are all involved with autophagy, a critical process that enhances the immune system by eliminating intracellular pathogens.
Phase V illustrated weakness in the Phase II detox pathway, acetylation. More genetic variants were found in PANK1, ACAT-2 and NAT2. Weakness of acetylation may impair detoxification of environmental pollutants.
Phase VI showed more variants in the heme pathway. Heme is a cofactor for many detoxification pathways including CYP450, Catalase, SOD, Nitric Oxide and SUOX (sulfite to sulfate conversion). More variants were found in ALAD, CPOX, and FECH in the Lyme group.

Discussion: These studies have shown a genetic predisposition to more free radical production, less antioxidant production, and suboptimal detoxification by weakness in methylation, acetylation, and autophagy, and PON1-pesticide detoxification. Consequently, those with these excess variants may be more strongly impacted by environmental factors. More research is needed to determine the impact these have on those with Lyme disease,

Author: Omar Morales, MD

Title: Complimentary Treatments for Lyme Disease, Babesia, and Other Blood-Borne Diseases

Practical Hematologic Viewpoint of Lyme Disease, Babesia and other blood-borne infections: Explanation of red blood cells, white blood cells and plasma, and how they are affected by Lyme Disease and co-infections.

Comparison: Traditional therapies (i.e., antibiotics, supplements) compared with targeted, modern therapies (i.e. apheresis, dendritic cells, toxin & pathogen removal).

Apheresis: How apheresis targets multiple stages of blood infections. Discussion of the types of apheresis, applicability, what they achieve/outcome and evidence of success.

Immunological Adjuvants for Lyme and Co-Infections: Detox, immune boosters, immunotherapy and immune modulation (i.e., dendritic cell therapy) as complimentary treatments.

Additional Factors to Consider: Lyme life philosophy and basic recap of treatment pillars for the chronically ill.

Author: B. Robert Mozayeni, MD

Title: Bartonella Overlap with Tick-Borne Diseases: Better Diagnosis Supports Better

Outcomes

Bartonella is increasingly recognized as a TBD. It is important to understand the basic biology of Bartonella, the pathogenesis of the illness it may cause, and features helpful for diagnosis, such as Bartonella dermal ‘tracks’, small vessel disease, and neurological manifestations. The proper detection and treatment of Bartonella is important for the successful treatment of patients suspected to have Lyme disease. Social media often cloud the picture and the non-scientific public is focused on the symptoms rather than the cause. As clinicians, we must seek to properly identify the cause of these complex chronic conditions.

Protocols for Bartonella treatment have been in development in my office for over 10 years and lately, they appear to provide lasting results. More work remains to be done to streamline the protocols and improve the clinical management of patients with this infection. Clinical principles and functional medicine skills needed to treat Bartonella will be discussed, including the effects and side effects of various treatments. New diagnostic capabilities will also be discussed.

Author: B. Robert Mozayeni, MD

Title: Mast-Cell Activation Syndrome and the Host Response: Persistent Infectious Disease or Host Response Disease

Though of course not a truly new disease, the recently recognized disorder now termed mast cell activation syndrome (MCAS) presents with confounding extreme heterogeneity and with symptoms that may overlap substantially with the symptoms of tick-borne diseases that may make us thing that the infection persists. The inflammation associated with MCAS may be confused with the persistent infection. It may be that not all cases of what has been thought to be chronic infection; are necessarily persistence of infection -- or even infection at all. Hopefully, the attendee will be able to develop their own new perspective on diagnosis and treatment of TBDs that may help reduce misdiagnosis and help in the care of their patients suspected to have a chronic infection.

Author: Pilar Munoz-Calero, MD

Title: Environmental Contaminants and their Association with Chronic Infectious Diseases, Diagnostic Management and Treatment Difficulty

The environment is one of the determinants of the health status of the population. Environmental pathologies represent a set of disorders caused by exposure to chemical and physical products in the habitual environment. In industrialized countries it is estimated that 20% of the incidence of all diseases can be attributed to environmental factors. Xenobiotics present in the environment can be inhaled or ingested involuntarily. The contamination by heavy metals present in the air, water and food is another very frequent source of contamination to which the human being is exposed and contributes to the alteration of the homeostasis, in diverse aspects of the metabolism and the toxicity of the macrophages.

Xenobiotics tend to deposit in the central and peripheral lymphoid organs, hindering an adequate immune response to infections. In the presence of environmental contaminants, these can act as cofactors of acute or chronic infectious diseases. The enzymatic activity of cytochrome P450 is frequently altered, making it difficult to treat these pathologies. It is also common to see a genetic polymorphism caused by environmental pollution generating immunological, carcinogenic or allergic pathologies.

In this presentation we will emphasize the impact of environmental contamination in patients with environmental pathologies with associated chronic infections and chronic immunosuppression. We will also explain our experience with the treatment of some real cases.

Author: Kanneboyina Nagaraju, DVSc, MVSc, PhD

Title: Screening for Autoantibodies in Post Treatment Lyme Disease Syndrome Patients using HuProt Protein Microarray

Pathogenesis of post treatment Lyme disease syndrome is currently unclear and requires systematic investigation. It has been postulated that some of the PTLDS symptoms could be due to antibacterial immune response that cross-react with host self-proteins (autoantigens), commonly called molecular mimicry. Previous studies have used tandem mass spectrometry, database searches, and manual spectral interpretation to identify MHC class II (HLA-DR)-presented peptides from the synovia of Lyme arthritis patients. While this approach was useful to identify some autoantigens in Lyme arthritis patients, the pathological consequences of immune response (T cells and autoantibodies) remained unclear because of their low affinity interaction with target autoantigens. Here we have screened serum samples from PTLDS, Becker muscular dystrophy and normal control with ImmuneProfiler™ human proteome microarray containing individually purified proteins covering 81% of the human proteome (16,152 genes). This approach has potential to identify disease specific autoantigens in an unbiased manner. We hypothesized debilitating symptoms associated with PTLDS are due to immune response to host self-antigens. We have identified autoantibodies to 93 cellular proteins uniquely in PTLDS patients. We further verified autoreactivity of these samples (nuclear, mitochondrial, golgi, centromere, etc. patterns) using indirect immunofluorescence assay on HEp2 cells suggesting that there is a border autoreactivity that may play a role in in the manifestation of systemic disease phenotype.

Author: Carmen Navarro, MD

Title: Chronic Lyme disease Associated with Environmental Diseases: Multiple Chemical Sensitivity, CFS, Fibromyalgia, and Hyperelectrosensitivity

In my intervention I will try to integrate my individual clinical experience with data that make us think that chronic infections, causing chronic Lyme disease, are the first stressful factor, to which could be added other no less important, potentially causing environmental diseases such as Multiple Chemical Sensitivity, Chronic Fatigue Syndrome, Fibromyalgia and Hyperelectrosensitivity, among others. Link the Dr. Martin Pall's NO/ONOO cycle theory with an etiological theory capable of explaining the association between the above-mentioned diseases.

How the signs and symptoms of these diseases can be generated by high levels of Nitric Oxide and other consequences of this: high levels of oxidative stress and inflammatory cytokines, among others.

How the therapy should be aimed at reducing stressors, including infection, emotional stress, exposure to environmental toxins ... and finally try to justify why therapeutic approaches should be aimed at compensating for excessively high levels of ON, superoxide anion, inflammatory cytokines ... and to repair the oxidative damage caused in cellular structures: plasma membranes, mitochondria ... All of this is ultimately oriented towards the need to achieve a competent immune system.

Author: Wojciech Ozimek, MD

Title: Lyme Disease, Parasites, Protozoans and Microbiome

Parasites and protozoans are the vehicle of bacteriae, viruses and heavy metals and the significant obstacle for Lyme recovery. Most of the LLMDs agree that parasites and protozoans may block Lyme disease treatment. Many consider the parasites and protozoans as an important Lyme disease co-infection since many investigations on bacterial profiles of complex microbial communities associated with the different life-cycle stages of parasites and protozoans were conclusive that parasites and their microbiome may cause diagnostic and therapeutic dilemmas. Parasites’ and protozoans’ bacteriae, viruses and heavy metals are transmitted vertically (from parents), horizontally (from the environment or humans and animals) or in some cases a mixture of horizontally and vertically. The parasites’ and protozoans’ microbiome is constantly exposed to the human intestinal microbiota and reflects also the external micro-organisms of microhabitat [gastro-intestinal tract] and macrohabitat [ food and environment].

Upon deworming, a complex interaction between the anthelminthic drug, helminths and microbiome composition might occur leading to some new symptoms and new therapeutic challenges. Since there are more and more date on growing parasites’ and protozoans’ resistance to standard therapeutic protocols and at the same time papers suggesting an increased risk of autoimmune reactions as a result of deworming- our point- How to remove safely parasites and protozoans to fix Lyme and other chronic illnesses?- remains an open question. The next few years will likely witness an immense number of studies uncovering the exact nature of the human microbiome, parasites and protozoans interaction, and finally reveal the specific molecular mechanisms underlying the parasites’ and protozoans’ microbiome as the true Achilles’ heel of the gastrointestinal parasites. There is abundant room for further progress in investigating the relation between the microbiome of different parasites and protozoans, that has, and will continue to offer an important parallel goal for the removal of a wide-variety of devastating human and animal diseases including Lyme and associated diseases.

Author: Philippe Raymond, MD

Title: How to Make a Clinical Diagnosis of Chronic Lyme Disease or Persistent Polymorphic Syndrome After Tick Bite? (SPPT)

Given the multiplicity of symptoms of SPPT (chronic Lyme), and the poor reliability of biological tests, it is important to be able to make a diagnosis oriented on clinic symptoms. Dr. Raymond will share with us his 13-year experience of managing tick-borne diseases through convenient diagnostic grids. This French experience proved to be superimposable on the clinical signs of the Aucott study on the PTLDS (2018), with the scoring of Richard Horowitz, and allowed to describe the SPPT in the reports of the HCSP 2014 (High Public Health Council) then HAS 2018 (High Authority of Health).

Author: Armin Schwarzbach, MD, PhD

Title: Inflammatory Arthritis, Multiple Sclerosis and Other Illnesses: Associations with Tick-Borne Diseases in the Complexity of Multiple Infections

Lyme disease and coinfections are the chameleon of symptoms, laboratory tests and therapies. Many patients can be infected after tick-bites with several and different bacteria from the ticks. Many symptoms of tick-borne diseases are not high-specific for Lyme disease or other tick-borne diseases. Chronic manifestations of infections are complex interactions between host immunity and stealth bacteria and viruses with emerging evidence for the development of different kinds of illnesses.

There are many evidence-based studies about Borrelia burgdorferi or Ehrlichia/Anaplasma or Chlamydia as the causing agents in patients with inflammatory arthritis or multiple sclerosis.
Additionally, viral infections for example by Epstein Barr Virus or Cytomegalovirus may cause chronic inflammation and weaken the host immune system, resulting in diagnostic difficulties and treatment difficulties. The presentation aims to show correlations of tick-borne diseases in the complexity of other chronic infections with different illnesses and syndromes including modern diagnostic possibilities.

Author: Mariia Shkilna, MD, PhD

Title: Epidemiology of Lyme in Ukraine

Ukraine is a country in Eastern Europe. It has a total area of 603,548 km² and land area of 579,330 km², which makes it the largest country on the European continent after Russia (Basic facts. 2010). The forested area in Ukraine is 9.4 million ha, or 15.6% of the total land area. Forests in Ukraine are distributed unevenly. The largest forested territories are in north and west of the country and encompass Polesie region, the temperate broadleaf and mixed forest biomes and the Ukrainian Carpathians.

Since forests and woods are preferred ecosystems of ticks, the risk of contracting diseases transmitted by ticks is higher among forestry workers, farmers and other people working in wooded areas. Ternopil region (oblast), which located in the western part of Ukraine, is an endemic region for Lyme borreliosis. Territories of Ixodes ricinus ticks borreliosis are educed in 57 settlements of 15 districts of the Ternopil area.

Author: Louis Teulieres, MD, PhD

Title: Chronic Infections, Hormonal Dysfunctions and Heavy Metals Connections in Autism

Because of the complexity of the biochemical disturbances occurring during the maturation of organs during infancy, the studies as well as the variability of the autistic spectrum suggest multiple causes. Recent studies have shown that disturbances of the immune system during pregnancy and early childhood can lead to dysfunctions in the processes of neuronal cell migration and GDNF, their differentiation and synaptic maturation. Disruptions of the immune system have serious neurological consequences; this hypothesis is reinforced by recent studies on differentiation in the development of microglia according to the sex of the individual. This could explain the predominance of male autistics Inflammatory cytokines and chemokines and the cells that produce them within the brain, notably microglia, are critical for normal brain development. Inflammatory events during pregnancy, and infancy e.g. in response to (bacterial) infections, may disrupt the normal expression of immune molecules during critical stages of neural development and thereby contribute to the risk for neurodevelopmental disorders such as autism spectrum disorder (ASD). Nevertheless confirmation of the " infections and immune system" model certainly needs better tests that could demonstrate the long lasting presence of living bacteria.

These immunological/infectious causes may be reinforced by our increasing exposure to heavy metals. The toxic effects of these metals have been demonstrated as well as their impacts on the development of the child. Mechanistic, biochemical, and structural studies have demonstrated the roles these metals play also in hormone functions and responses to maintain healthy homeostasis and biological rhythms. Still the role of heavy metals in the development of autism is still highly debated due to a lack of consensus in diagnostics and toxic load evaluation.
New methods of infections diagnostics by specific bacteriophages as well as proposals for matrix selection and heavy metals dosages will be presented. These novelties could permit to establish the link between heavy metals’ immunotoxicity, disturbances in immune responses and hormonal balance that may explain the dramatic increase in cases of autism spectrum disorders.