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This virtual medical conference is sponsored by Georgetown University and The Foundation for Total Recovery, Autoimmune Encephalopathy Secondary to Infectious Disease: A New Perspective on the Pathogenetic Interaction of the Immune System, Infection, Stress, and Chronic Disease. Read more about the conference below the Selected Lecture Recaps. Register today – https://www.sw-online.com/vhalls/welcome-to-foundation-for-total-recovery
Select Lecture Recaps
- The Impact of Childhood Adverse Events, Chronic PTSD and The Risk of Developing Autoimmune Disease – Robert C. Bransfield, MD, DLFAPA
- Neuropsychiatric Lyme Disease, Immune Markers, and the Vagus Nerve – Brian Fallon, MD, MPH
- Treatment for Various Disease Entities – Bruce Patterson, MD, CEO IncellDX
- Treatment for Sleep Disorders and Psychological Manifestations of AEIE – Robert C. Bransfield, MD, DLFAPA
- Immune-mediated Mechanisms Driving Neurovascular and Neuronal Circuitry Dysfunction in Post-infectious Autoimmune Encephalitis – Dritan Agalliu, PhD
- Developing Treatments for Lyme Disease – Kim Lewis, Professor, Director Antimicrobial Discovery Center Northeastern University
Epidemiology: How Big is the Problem? Immune Dysregulation Secondary to Infections as a Cause of Chronic Disease – Gary Kaplan, DO, DABFP, DABPM, FAAMA
Approximately 20 million people in the United States have an autoimmune disease, many with an infectious ideology. These conditions include ME/CFS, Fibromyalgia, Chronic Lyme, post covid syndrome, PANS/PANDAS, and other neuropsychiatric diseases. Neuroinflammation is common to all these conditions, and at least in a subset of all these conditions, there is evidence for an infectious etiology and immune dysregulation.
The Impact of Childhood Adverse Events, Chronic PTSD and The Risk of Developing Autoimmune Disease – Robert C. Bransfield, MD, DLFAPA
Childhood adverse events and chronic Post Traumatic Stress Disorder (PTSD) can contribute to
- chronic stress
- compromised immunocompetency
- persistent inflammation
- a failure of adaptive immunity
- psychiatric illness
Internal or external events can cause the danger response and be adaptive or maladaptive. A maladaptive response to danger can cause physical or psychiatric illnesses.
When an unexpected and overwhelming traumatic event undermines a basic sense of safety and security, memory of the event(s) may be suppressed. These suppressed memories can create intrusive thoughts. Intrusive symptoms are a core component of PTSD pathophysiology resulting in hyperarousal, avoidance, and emotional numbing. Intrusive symptoms can be associated with a high level of distress, and sometimes suicide and aggressive behavior. PTSD patients are 6 times more likely to attempt suicide than the general population
There is a reciprocal causal relationship between PTSD and Autoimmune Encephalopathy Secondary to Infectious Disease (AEIE). It is essential to acknowledge this pathophysiology in patients and consider treatment options.
PTSD or Adverse Childhood Events (ACE) have a profound negative impact socially, medically, and psychologically. The more adverse events in childhood, the higher the risk of chronic illness, including autoimmune disease. Recovery from trauma requires changing the maladaptive danger response to an adaptive response. Treatment utilizes psychosocial and pharmacological approaches to address infections, immune modulation, and psychiatric symptoms.
Neuropsychiatric Lyme Disease, Immune Markers, and the Vagus Nerve – Brian Fallon, MD, MPH
Post Treatment Lyme (PTLD) affects the brain in several ways:
- Microglia are activated
- Brain metabolism is decreased
- Blood flow is decreased
- Autoantibodies are often present
Borrelia can cause autoantibodies against neuronal tissue, which can trigger psychiatric symptoms. Psychiatric disorders seen in PTLD include anxiety, OCD, panic attacks, mania, suicidality, psychosis, Tourettes, and sensory hyperarousal. Up to 90 percent of people with PTLD complain of cognitive difficulties. Some (7-30%) have objective measurable problems, including short-term memory, verbal fluency, and processing speed problems.
In patients after Lyme disease, the rate of affective disorders increased by 42%. The rate increased two-fold if there was more than one episode of Lyme disease. The highest rate of affective disorders (2.6x higher) was seen within 6-12 months after the first diagnosis of Lyme. Some studies have shown depression is 4x more common in PTLD. Microglial activation and inflammation in Lyme disease can cause depression. The rate of suicide after Lyme disease was increased by 75%. The rate of suicide was increased 2-3x if there was more than 1 episode of Lyme.
Vagal Nerve stimulation (VNS) may be a helpful treatment. Studies have shown VNS can decrease pain, fatigue, and depression. It also reduces inflammation and other biomarkers. Some case studies have shown improvement in Covid symptoms with VNS.
Treatment for Various Disease Entities – Bruce Patterson, MD, CEO IncellDX
Many post-infectious chronic immune disorders share several same symptoms, including fatigue, post-exertional malaise, and muscle/joint pain. It can be challenging to establish a correct diagnosis with significant symptom overlap. The IncellKINE™ diagnostic test measured 14 cytokines and chemokines directly involved in COVID-19. The test results can help to differentiate between different post-infectious immune disorders. Immune profiles were developed for acute Covid, long Covid (Post Acute Sequela of Covid – PASC), post-vaccination PASC, EBV, ME/CFS, and post Lyme. Cytokine biomarkers also correlate with fatigue, shortness of breath, dysautonomia, cardiac function, and neurologic disability. Cytokines can also be used to categorize autoimmune diseases by the pathophysiology rather than the organ affected, which allows the possibility of targeting the cytokines involved to treat the disorder.
The pathophysiology of PASC was studied and may be attributed to a persistent S1 protein subunit of Covid in CD16+ monocytes, which is present up to 15 months after infection. CD16+ monocytes express both CCR5 and fractalkine receptors which contribute to vascular inflammation in Covid. Monocytes typically die after 1 week, but when binding to Fractalkine or a foreign protein, they don’t die. Interrupting this process, so the monocytes die allows recovery.
Medications were selected and tested based on this cytokine profile. Maraviroc is a CCR5 inhibitor, and statins function as a Fractalkine inhibitor. PASC and post vax PASC patients treated with Maraviroc and statins typically improved within 6-12 weeks. Patients saw an improvement in fatigue, shortness of breath, dysautonomia, cardiac function, neurologic disability, and exercise tolerance. The return of exercise tolerance often marked the point of full recovery.
Treatment for Sleep Disorders and Psychological Manifestations of AEIE – Robert C. Bransfield, MD, DLFAPA
Autoimmune encephalopathy secondary to infectious disease can cause a variety of sleep disorders. Poor sleep quality is associated with impaired immunocompetence and contributes to disease progression. Untreated insomnia can lead to depression, anxiety, hyperarousal, or Alzheimer’s disease. A decrease in depth of sleep is associated with a 70 to 100% greater chance of having Alzheimer’s disease 9 years later.
REM sleep is needed for memory reorganization. Sufficient delta sleep is necessary for regeneration and the proper functioning of the immune system. Delta sleep is also necessary for growth hormone, which helps modulate the immune response. Sleep initiates the Th1 response in lymph nodes and promotes immune-supportive hormones such as GH & prolactin, which suppress anti-inflammatory hormones such as cortisol, norepinephrine, and epinephrine. Sleep also promotes clearance of B-amyloid and other waste products from the brain. Cytokines produced by cells of the immune and nervous systems, particularly interleukin-1beta and tumor necrosis factor-alpha, help regulate sleep. Sleep deprivation increases IL-6 and pain-related symptoms in healthy volunteers.
Insomnia is a disorder of hyperarousal and blunting of the circadian rhythm. Insomnia can be caused by medical, physical, cognitive, or emotional issues. Studies have demonstrated a prevalence of sleep-related complaints in 66-100% of Lyme disease patients. Narcolepsy and sleep apnea are also common in Lyme disease.
Poor sleep quality is associated with impaired immunocompetence and contributes to disease progression. Psychological and physical symptoms that impact sleep must be treated. Good sleep habits are also crucial in the treatment of sleep disorders. Doctors should aim to improve restorative sleep by giving sleep-promoting aids at night and activating agents in the morning. Several drugs promote slow-wave sleep, but many can cause dependence and tolerance issues. Treating sleep disorders improves immune competency and is one of the most effective approaches to aid recovery.
Immune-mediated Mechanisms Driving Neurovascular and Neuronal Circuitry Dysfunction in Post-infectious Autoimmune Encephalitis – Dritan Agalliu, PhD
In Basal Ganglia Encephalitis, the antibodies target dopaminergic receptors. D1 and D2 receptor antibodies and antibodies to cholinergic interneurons have been identified in causing inflammation in the Basal Ganglia, leading to specific neuropsychiatric symptoms after GAS Infection.
The BBB protects the central nervous system from pathogens, immune cells, and drugs and is essential for maintaining hemostasis. Repeated GAS infections trigger an innate and adaptive immune response leading to the generation of Th17 lymphocytes in the nasal-associated lymphoid tissue in mice, equivalent to the tonsils and adenoids in humans. Th17 lymphocytes are implicated in virtually every autoimmune disease and trigger vascular and central nervous system pathology, including BBB damage.
Studies show that immunoglobulin G (IgG) readily crosses the BBB with repeated GAS infections in wild-type mice compared to Th17 deficient mutant mice. Microglial activation and macrophage infiltration were significantly reduced after 48 hours in the brain of the Th17 deficient mutant mice compared to the wild-type mice, implicating Th17 as a major factor in BBB pathology. In the absence of Th 17 cells, all the pathology is reduced, showing that Th17 cells cause BBB damage, activation of microglia, loss of excitatory synapses, and neuronal function.
Single-cell RNA sequencing studies identify the shift in transcriptomic states in each cell type in the brain after repeated infections with GAS infection. The disease state versus healthy state was associated with higher numbers of macrophages, T cells, endothelial cells, and microglia.
Dr. Agalliu identified unique cytokines only secreted by the microglia in GAS infections but not in other modes of inflammation. His research concludes that the central nervous system pathology is complex and driven by myeloid-derived cytokines in post-infectious Basal Ganglia Encephalitis.
- Th17 cells are critical for pathology in the mouse brain.
- Th17 cells are critical for damage to the BBB.
- Th17 cells are critical for up-regulating antigen presentation and leukocyte migration in activated microglia.
- Th17 cells are critical in leading to activated microglial secretion of several unique inflammatory cytokines and chemokines, which are detected in patients with PANS/PANDAS in the active stage of the disease.
- In vitro data suggests these inflammatory cytokines break down the BBB. The data also indicates that the sustained BBB damage allows the antibodies to enter the brain, entry to which is regulated by relay mechanisms in the state of microglial activation.
Developing Treatments for Lyme Disease – Kim Lewis, Professor, Director Antimicrobial Discovery Center Northeastern University
Lyme disease affects an estimated 500,000 people in the US. About 10% of Lyme patients develop chronic symptoms known as Post Treatment Lyme Disease Syndrome (PTLDS). Borrelia burgdorferi, the bacteria that causes Lyme disease, increases gut permeability which causes translocation of gut bacteria into GI lymph nodes and alters immune function.
Two-thirds of PTLDS patients have a dysbiotic microbiome characterized primarily by high levels of Blautia or Enterobacteriaceae. The changes to the microbiome are distinctive and could be used as a diagnostic tool to identify PTLDS patients. Dr. Lewis hypothesizes that changes to the microbiome from Borrelia bacteria and the antibiotics used to treat Lyme disease alter immune function and lead to PTLDS symptoms. Soil organisms were studied to search for new antibiotics that might be less damaging to the microbiome while still effective against spirochetes.
The compound Hygromycin A has very low activity against the microbiome or human cells and is still very effective against spirochetes. Mice infected with Borrelia had a 100% clearance of Borrelia burgdorferi when treated with Hygromycin A, and it did not disrupt the microbiome. Studies are underway to see if Hygromycin A is an effective treatment for Lyme disease. There is some evidence of Borrelia persistence in biofilms. So, pulsed dosing with Hygromycin A may be an effective treatment strategy for Lyme patients. Pulsing allows time for the persister cells to become more active and, therefore, more susceptible to the antibiotic. Since Hygromycin A does not lyse or break open the Lyme bacteria, it may not cause Lyme patients to have a herxheimer or die-off reaction.
- CME Registration: 19.5 credit hours of CME is $375
- General Public Registration (non-CME): $99.00
- This also includes a post-conference bonus – Access to “Translating the Science into the Practical” – a separate, Q&A session at no additional cost. This session provides the opportunity to ask questions in a more informal environment.
At this online event, you will hear from more than 15 of the world’s foremost specialists from universities around the world including Oxford, Columbia, Duke, and even the leading medical center in the Middle East—Sheba Medical Center in Israel. Speakers will address a range of topics covering immune dysregulation resulting in neuroinflammation. Key conference questions: What if these diseases aren’t distinct? What if they are different manifestations of the same root cause—immune dysregulation resulting in neuroinflammation? And if they are, how do we successfully treat it?
Partial Speaker List
- Yehuda Shoenfeld – Post COVID-19 Syndrome, Vaccine and Autoimmunity
- Brian Fallon – Neuropsychiatric Lyme Disease, Immune Markers, and the Vagus Nerve
- Susan Swedo – PANS/PANDAS-Post-infectious Basal Ganglia Encephalopathies
- Craig Shimasaki – Molecular Mimicry and Common Infections: A Biological Basis for Autoimmune Basal Ganglia Encephalitis Associated with Antineuronal Antibodies and Neuronal Cell Stimulation in Neurologic Lyme, PANS/PANDAS and Long-Covid
- Amiram Katz – Treatment for AEIE-Lessons Learned from Lyme Disease
ASPIRE Virtual Sponsor Booth
ASPIRE is proud to sponsor the Autoimmune Encephalopathy Secondary to Infectious Disease conference. We will have a virtual booth with live chat during the lunch breaks. Stay tuned for special guests and details. So, register today!
More about this conference
To truly help patients like you return to full health, we need better ways of understanding, diagnosing, and treating these illnesses. We need to explore what predisposes an individual to such illnesses, analyze the emerging research, and get input from medical and research leaders who share the same passion for finding a path to total recovery. This conference will address all that—and more.
The Autoimmune Encephalopathy Secondary to Infectious Disease: A New Perspective on the Pathogenetic Interaction of the Immune System, Infection, Stress and Chronic Disease conference is being jointly sponsored by the International Center for Interdisciplinary Studies of Immunology (ICISI) at Georgetown University Medical Center and the Foundation for Total Recovery. They join efforts to help a very specific patient population representing more than 20 million Americans and tens of millions of people around the world – those suffering from a group of chronic disabling disorders and diagnosed without a clear path forward to healing and often misunderstood or overlooked by the broader medical community. Fibromyalgia, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), PANS/PANDAS, neuropsychiatric illnesses, post-Lyme syndrome, and most recently the post COVID-19 long haul syndrome are but a few of these conditions.
The organizers understand that digesting complex science and research can be challenging. Since they can’t address every single question during the actual conference, participation will also include VIP access to a special, separate Q&A session on March 5th, 2022, three-weeks post-conference at no additional cost. This follow-up focuses on translating the science to the practical and provides patients a roadmap to healing.