Archive for the ‘Treatment’ Category

Chronic LD Summit #2

http://chroniclymediseasesummit2.com/?idev_id=11577&idev_username=Summit3  Please register at link.

Lyme disease is quickly spreading across the entire globe — very few are enlightened on this troublesome condition — that’s why Dr. Jay Davidson has urgently created the second summit on this topic (with only 2 repeat speakers from 2016). 300,000+ people per year contract Lyme, and 2017 is predicted by some to be an incredibly risky year!

The Chronic Lyme Disease Summit 2 is online and FREE from June 19-26, 2017.

Speakers and Topics:

Wayne Anderson, ND
Overview of Lyme and Its Evolution

James Maskell
Evolution of Medicine and Lyme

Scott Forsgren, FDN-P
Maximizing Lyme Disease Recovery

Philip Blair, MD
Col. US Army, ret.
Lyme Recovery with CBD

Jay Davidson, DC, PScD
Improving Lyme Disease Protocols

Jonathan Streit, DC
Testing for Functional Neurological Issues

Tyna Moore, ND, DC
Strength Training to Optimize Stem Cells

Sarah Ballantyne, PhD
Diet/Lifestyle as a Complementary Approach

Leslie Douglas, PhD
DNA Connexions PCR Assay

Greg Lee, MAc, BS
GoodbyeLyme™ Treatments and Remedies

Dave Ou, MD
Things Missed in the Treatment of Lyme

Evan H. Hirsch, MD, ABOIM
Coinfection Bartonella Treatment

Katie Dahlgren, ND
Helping Lyme Through Parasites

Shayne Morris, PhD, MBA, CNS
The Omics of Borrelia
Dietrich Klinghardt, MD, PhD
Latest on Lyme Testing and Treatments

Amy Derksen, ND
Non-Antibiotic Approaches to Treating Children

Dan Pompa, DPSc
Is Chronic Lyme Linked to Heavy Metals?

Todd Watts, DC
Killing Parasites to Kill Lyme Disease

Isaac Eliaz, MD, MS, LAc
Biofilm and Galectin-3 Breakthrough Strategies

Darin Ingels, ND
Herbal Therapy and Low Dose Immunotherapy (LDI)

Jerod Bergman, DC, CCSP, CSCS
Stopping EMFs and Geopathic Stress

Izabella Wentz, PharmD, FASCP
Thyroid and Lyme Disease

Tim Jackson, DPT, CNS(c)
Mitochondrial Dysfunction and Inflammatory Cytokines

Joette Calabrese, HMC, CCH, RSHom
Homeopathic Approach to Lyme Disease

David A. Jernigan, DC
Unique Approach to Healing

Gerry Curatola, DDS
Microbiome of Your Mouth

Jonathan Landsman
Fixing Toxic Teeth and Gums

Jill Carnahan, MD, ABFM, ABIHM, IFMCP
CIRS and Lyme Disease

Christine Schaffner, ND
Healing Your Brain from Lyme Disease

Diane V. Capaldi, MAP
Consciousness as It Relates to Healing

Jon Butcher
Repairing Relationships After Illness

Keesha Ewers, PhD, ARNP
Feeling Betrayed by Your Body?

Kim D’Eramo, DO
Mindsets That Impair Immune Function

Dana Walsh & Brent Martin
How to Lyme Less and Live More!

Sarah Schlichte Sanchez
Fighting as a Mindset

Category:

Activism, Detoxing, diet and nutrition, Herbs, Lyme, Psychological Aspects, Treatment, Viruses

Chronic Lyme Disease – A Case Definition at Last

fulltext_chronicdiseases-v4-id1025  Published: May 03, 2017 Stricker RB and Fesler MC.   Chronic Lyme Disease: A Working Case Definition. Chronic Dis Int. 2017; 4(1): 1025.

Abstract

Although Lyme disease is the most common tickborne illness in the USA and Eurasia, the pathophysiology and clinical course of chronic Lyme disease (CLD) have not been formally defined. The purpose of this paper is to present a working case definition of CLD based on analysis of more than 700 peerreviewed publications. According to this definition, CLD is a multisystem illness with diverse musculoskeletal, neuropsychiatric and/or cardiovascular manifestations that result from ongoing infection with pathogenic members of the Borrelia spirochete complex often associated with other tickborne disease (TBD) pathogens. To qualify for the diagnosis of CLD, patients must have Lyme compatible symptoms and signs that are either consistently or variably present for six or more months. Two subcategories of CLD include untreated chronic Lyme disease (CLD-U) and chronic Lyme disease following a limited course of antibiotic treatment (CLD-T). The symptom patterns and optimal therapy of CLD require further study.  ______________________________________________________________________

While a relatively short course of appropriately directed antimicrobials may be adequate for individuals who are treated early in the Lyme disease process, treatment is frequently not curative, raising the possibility of TBD pathogen survival [88-96]. Persistent TBD infection in animals and humans involves potential roles for multiple mechanisms: (1) Immune evasion via physical seclusion of pathogens within immunologically protected tissue sites such as the central nervous system, joints, eyes, connective tissue and genital tract [88-96]. (2) Alterations in Outer surface protein (Osp) profiles of pathogens through antigenic variation [95-99] and alteration in pathogen morphology (including cell-wall deficient forms, spherocytes, round bodies and biofilm aggregates) [100-107]. (3) Immune modulation via complement interference, neutrophil and dendritic cell dysfunction and cytokine/chemokine alterations [108-115]. (4) Generation of antibiotic-tolerant “persister cells” in some pathogen populations [116-118].

Clinical Manifestations of CLD Lyme disease is a multisystem illness that is often referred to as the “new great imitator” due to the diversity of its clinical manifestations that are reminiscent of syphilis [119-123]. The wide spectrum of clinical features can range from an EM rash to severe arthritis, carditis or neuropsychiatric symptoms [4,5]. Another clinical feature often associated with this condition is the Jarisch- Herxheimer reaction whereby symptoms increase after exposure to antimicrobials [124-131]. This is a phenomenon associated with the treatment of spirochetal diseases such as syphilis, louseborne relapsing fever, leptospirosis and Lyme disease [124-131]. Recent studies suggest that the Jarisch-Herxheimer reaction is triggered by rapid uptake of damaged spirochetes by neutrophils and mononuclear cells with release of lipoproteins and pyrogens that increase inflammatory cytokines [131]. To date, the complete mechanism of this phenomenon remains undefined. Since clinical features of Lyme disease may change following exposure to antimicrobials, we have proposed two categories for this working case definition of CLD, as outlined above.

**For CLD-U, the natural course without antimicrobial intervention has been described by Steere et al. in the USA [19,132]. Prior to recognition of the importance of antimicrobial therapy, untreated patients with EM rash displayed the following clinical characteristics over six years of follow-up: 62% developed intermittent or persistent arthritis; 18% developed arthralgias; 11% developed neurologic abnormalities; 4% developed cardiac complications; 33% developed fatigue; and 33% developed other symptoms and signs including headache, stiff neck, morning stiffness, myalgias and abdominal pain [132]. Further characteristics of CLD-U patients have been described by Wormser et al. in the 2006 IDSA Lyme guidelines [4]. Based on clinical diagnosis with serological confirmation using CDC surveillance criteria, later stages of Lyme disease may feature prominent multisystem symptoms and signs as described above [1,4,5].

**In contrast to CLD-U, CLD-T is a term used to describe individuals who have been treated for TBDs with a limited course of antibiotics (generally < four weeks) and within six months develop persistent or recurrent and functionally significant fatigue, musculoskeletal pain, cardiovascular disease and/or neuropsychiatric dysfunction that persists for six months or more [133,134]. CLD-T acknowledges the extensive published evidence for persistent TBD infection despite a limited course of antibiotic therapy. In contrast, the research case definition for PTLDS proposed by IDSA includes the following statement: “There is no convincing biologic evidence for the existence of symptomatic chronic B. burgdorferi infection among patients after receipt of recommended treatment regimens for Lyme disease” [4]. Based on animal models and human studies, however, we propose that treatment with limited antibiotic regimens may not consistently clear the infection, and we have provided evidence to support potential mechanisms by which this persistent infection occurs (see above). Thus Lyme patients who remain symptomatic following a limited course of antibiotic therapy likely have an ongoing, active TBD infection similar to CLD-U patients. We characterize this group as having CLD-T. Other conditions that can mimic the clinical presentation of CLD must be ruled out. However, the diagnosis of “idiopathic” conditions such as multiple sclerosis, motor neuron disease, fibromyalgia or chronic fatigue syndrome is insufficient to rule out the presence of CLD. We analyzed more than 700 peer-reviewed publications featuring symptoms and signs associated with both forms of CLD from a MEDLINE search (Appendix A). From this list, we chose 16 studies that describe symptoms and signs in patients with CLD-U and 13 studies that describe symptoms and signs in patients with CLD-T (Appendix B). In these 29 studies, persistent Bb infection was documented by culture, PCR and/or microscopy, while other studies without this stringent documentation were excluded. The symptom profiles in patients with persistent Bb infection are indicative of the protean manifestations of CLD. In our representative sample, patients with CLD-U appeared to have relatively more musculoskeletal and cardiovascular symptoms and signs, while patients with CLD-T appeared to have relatively more neuropsychiatric symptoms and signs (Tables 1 and 2). The broader pathology in untreated patients versus more restricted pathology following limited treatment is reminiscent of the immunopathology patterns in untreated versus initially-treated syphilis [134]. To date, however, the number of studies with stringent documentation of persistent Bb infection is too small to draw definitive conclusions about patterns of symptoms and signs in CLD patients. Further comparison of symptom profiles associated with the two forms of CLD is warranted.

Co-Infections

In both categories of persistent Bb infection, the presence of of other TBD pathogens may complicate the diagnosis and treatment of Lyme disease. Ixodes ticks are known to carry more than 237 types of bacteria and at least 26 viruses [136,137]. Some of these organisms, frequently referred to as co-infections, may alter the manifestations of Lyme disease and make it more difficult to eradicate the spirochete.  The interplay of other infectious agents with Bb may complicate the clinical presentation of Lyme disease and prolong the duration of infection, as noted in animal models [145-147].

Functional Impact of CLD

A community-based study of CLD patients found that the Quality of Life (QoL) of these patients was the same or worse compared to that of individuals with depression, diabetes, heart disease, osteoarthritis and rheumatoid arthritis [148]. Using a CDC metric of health-related QoL, a second survey of more than 5,000 respondents with CLD supported this analysis, revealing that 71.6% rated their health as fair or poor. The functionality scores of CLD patients were worse than those of other chronic diseases including congestive heart failure, fibromyalgia, post-stroke syndrome, post-myocardial infarction, diabetes and multiple sclerosis [149]. Further support for the adverse health impact of CLD was recently provided by Adrion et al [150]. Based on retrospective data from medical claims over five years in the USA, 52,795 individuals treated for Lyme disease were compared to 263,975 matched controls with no evidence of TBDs. The study found that as many as 63% of treated Lyme disease patients had persistent symptoms of CLD, and that Lyme disease was associated with $2,968 higher total health care costs (95% CI: $2,807- $3,128, p<0.001) and 87% more outpatient doctor visits (95% CI: 86%-89%, p<0.001) over a 12 month period compared to TBD-negative controls [150,151]. A more recent study from the Netherlands found that the annual cost of treatment for CLD was €5700 (about $6300) per patient or a total of €19.3 million ($21 million) per year in that country [152].

We recognize that there may be other contributing and at times independent causes for persistent symptoms in CLD patients. In essence, not all patients who remain symptomatic after being treated for Lyme disease suffer from an active, ongoing infection. Proposed mechanisms of persistent symptoms include immune dysregulation of various types, tissue injury, infection-induced secondary conditions and unrelated diseases [153,154]. Based on the clinical evidence, however, we assert that a potentially large number of individuals with CLD are adversely impacted by persistent TBD infection associated with significant functional limitations and financial burdens [148- 151]. We hope that technological advances in the characterization of ongoing TBD infection will improve our ability to deal with this condition.

Clinical Judgment

Until technological advances provide reliably sensitive and specific diagnostics, some patients will continue to have a diagnosis that remains unclear. Under these circumstances, the value of clinical judgment will remain an important component in treating these individuals. According to the American Medical Association Code of Medical Ethics, the primary responsibilities of clinical medicine are to alleviate patient suffering and prevent disease [155]. As previously described by Johnson et al [149] and Cameron et al [156,157]. patients with CLD are often quite ill, and physicians are charged with finding balanced and effective management strategies for such patients. Uncertainty about a CLD diagnosis may confound clinical decision making, but clinical uncertainty should not exclude that diagnosis. This process involves both inclusionary and exclusionary criteria. Patient care is dynamic, and clinical judgment requires vigilance in assessing clinical outcomes. As described by Kienle and Kiene, “Clinical judgment is a central element of the medical profession, essential for the performance of the doctor” [158]. Thus given the current absence of a “gold standard” test for Lyme disease, it is essential that healthcare providers should consider this condition if symptoms and/or clinical signs occur in patients with a history consistent with CLD, as summarized in the guidelines of the International Lyme and Associated Diseases Society (ILADS) [5].

**Please see link for Table 3 which outlines the proposed diagnostic criteria for CLD.

Conclusions

This is the first study that provides a working case definition of chronic Lyme disease (CLD) and its subcategories. We propose that CLD is the result of persistent, active infection by pathogenic members of the Borrelia spirochete complex often associated with other TBD pathogens. Infection with these organisms produces a wide array of symptoms and signs that may be expressed in a given individual during the course of the chronic illness [5,122]. Whether due to delayed diagnosis (CLD-U) or as a result of persistence after a limited course of antibiotic treatment (CLD-T), these symptoms and signs may fluctuate but are required to have cumulatively persisted for at least six months.

At this time, clinically available diagnostic testing does not consistently allow for identification of the pathogen(s) affecting individuals with CLD. As such, a hallmark feature of our working case definition is reliance on clinical judgment. This process includes the use of supportive diagnostics, but it does not require laboratory confirmation in light of present technological limitations of TBD testing. We recognize that as diagnostic testing evolves, the ability to define this entity should improve.

We also recognize that other diagnoses may be responsible for symptoms and signs that are similar to CLD and need to be considered in CLD patients. We hope that this outline will provide the clinician with a framework to weigh management options for these often significantly debilitated patients. We also hope to provide additional impetus for public policy to recognize the growing risk of the Lyme disease epidemic. Lastly, we encourage researchers to use the proposed definition of CLD to improve laboratory methodology for identifying patients with this condition, and to facilitate the development of new treatment options for CLD patients.

** See Link for references.

Category:

Lyme, research, Treatment

The Reality of Lyme Disease, Not Just Two Camps Anymore

http://whatislyme.com/the-reality-of-lyme-disease-not-just-two-camps-anymore/    Written:  5/4/2017 by Lisa Hilton, Wisconsin Lyme Advocate and patient

Lyme Disease

Camp A, B, C & D

I remember when I first finally got diagnosed with Lyme disease. I literally started screaming out of excitement to know what was wrong with me. For about fifteen long years I had been getting sicker and sicker and no one could figure out my ever changing symptoms. I went from panic attacks to joint pain to neurological symptoms throughout the years. Who would of known they were all connected? It sure didn’t seem like doctors thought they were since they were sending me from specialist to specialist depending on what symptoms I had and what part of my body that symptoms happened to be in.

Anyways, fifteen years into it, I finally had a positive Lyme test. I knew nothing about Lyme. I came to be tested after calling my doctor saying, “Now my hands and feet are going numb.” After a long line of symptoms such as fevers, low blood pressure, random pain that moved around, anxiety, gastro issues, cardiac issues… for some reason, when I told her this she responded quickly with, “Have you ever gotten tested for Lupus or Lyme disease.”

Honestly, I had no idea. I had no idea which tests all these doctors had performed. I just knew they had ruled out MS and Lupus through blood tests and MRIs. So she repeated the Lupus test and added in a Lyme test. The next day, a nurse from her office called and said, “Congratulations, we finally figured it out, you have Lyme disease. Go pick up three weeks of Doxy at the pharmacy and you will be ok.”

This started a long journey. When I was not ok in three weeks, and the doctor and their office seemed weary of my calls as I grew sicker on the Doxy, (none explained to me what a Herxheimer Reaction was) I was dismissed as a patient and told to go elsewhere for help. They referred me to an infectious disease doctor, which seemed upset I was “wasting his time” and asked me outright, “What do you want from me? You do not have Lyme disease.”

I was so confused. I said but you are the one that told my doctor I did. He responded by telling me that my Elisa was positive but  my western blot was equivocal and he told her just to be safe to put me on Doxy, and if I got better it meant I had Lyme and if I didn’t I should go see a psychiatrist.

After many horrible doctor experiences like this, I eventually found an online support group called, “LymeNet.” It was a life saver for me! I could not believe the stories I read on there. I was not the only one going through this. I was not crazy. This was a real disease and tests were inaccurate and doctors seemed clueless around the world about Lyme disease. I was in shock that this could be happening in this day and age. I could not believe patients could be turned away and denied and ridiculed.

One of the blog posts that struck me the most on LymeNet was called, “CAMP A and CAMP B, The Lyme Disease Controversy,” written by a user going by the pseudonym, “Tin Cup.” It explained the controversy of Lyme disease. It spelled out the different “sides” of the Lyme battle. There were two camps, Camp A and Camp B, one being IDSA doctors with their set of treatment guidelines and one being ILADS doctors and their set of treatment guidelines.

Camp A

Camp A consisted of the rules for treating Lyme disease put forth by the Infectious Disease Society of America (IDSA.) The Centers for Disease Control (CDC) uses these guidelines to tell doctors how they recommend you treat an illness. The problem is, insurance companies also use these guidelines to decide what medicines they will approve or not.

The IDSA recommends short course of antibiotics for Lyme disease. They give the impression that Lyme disease is easy to diagnose and treat. They do go into longer treatments for severe cases but go on to say that those cases are very rare and long term antibiotic treatment is usually not necessary. They seem to insinuate that Lyme disease is not a persistent infection and when patients still have symptoms after treatment they coin it, “Post Lyme Syndrome.” This gives the idea that it is just left over damage instead of a continuing infection.

Because of the CDC using the IDSA guidelines, insurance companies deny patient long term treatment even when symptoms persist. Another travesty of this set up is that doctors that are willing to try to treat their patients long term with antibiotics or any alternative treatments beyond the scope of the IDSA treatment guidelines get turned in by insurance companies, investigated and many have lost their licenses over this.

Camp B

Camp B is pertaining to doctors that believe that Lyme patients need to be treated with long term treatments, usually antibiotics. Although, as time goes by these “Lyme Literate” doctors are starting to add in more and more alternative treatments. But for the most part, over the years, “Lyme doctors” or Lyme Literate MDS, or LLMDs as Lyme patients call them have mostly used long term antibiotics usually via route of oral, picc lines or ports. You can find more information on the antibiotic use, picc lines and ports here. 

ILADS became the super hero for Lyme patients. They believed us, they understood we were truly sick and wanted to help us, despite pressure to conform to the IDSA and CDC views. They were the first organization to truly come out and say, Lyme disease is a chronic infection. It can persist even after short courses of antibiotic and it is not just damage, it is a persistent infection. See the ILADS Lyme Disease Guidelines Here.

ILADS also believes you cannot rely on the current faulty testing we have for Lyme disease. They believe your need specialty labs, such as Igenex or others listed here. http://whatislyme.com/different-lyme-tests-available-which-ones-are-worth-paying-for/ There are many reasons for this.  First, the Elisa is notoriously inaccurate http://whatislyme.com/why-lyme-tests-arent-always-accurate/ leaving over half the people who have Lyme disease with an incorrect negative test. Laws have even been passed, such as HB 962 in Virginia, in some states now insisting that doctors tell their patients that a negative Lyme test does not mean you do not have Lyme disease.

Secondly, the current tests have removed Lyme specific bands that are important when testing for Lyme disease such as bands 31 and 34 due to complications with the Lyme vaccine causing everyone to test positive for Lyme disease who had received the LYMErix vaccine. http://whatislyme.com/why-was-the-lyme-vaccine-pulled-from-the-market/  So instead of just asking people if they got the Lyme vaccine before having a Lyme test, they just removed these important bands from all current Lyme tests. Specialty labs still use those bands giving more accurate results.

Since this original post came out, I believe more camps have been added. Long term antibiotics have helped some. Others it’s hurt or not had any affect on. So, new camps of people trying to get better with new treatment options were born. 

Camp C

Camp C is a new camp emerging from a group of Lyme patients who are just not getting better with Camp A or Camp B Lyme treatment protocols. This camp is the “alternative” camp. This group of patients has done the IDSA short term antibiotic route. They have also usually done the long term ILADS antibiotic route. They are still not better.

This group of patients is turning to what mainstream medicine considers alternative, even through ironically, much of it was the “original” medicine used for years. In some cases it’s like, “back to the basics.” People are changing their diets to cleaner, organic, raw, grass fed, natural foods. Other alternative treatments are more extreme or “New Age,” such as turning to Rife machines, energy testing, biofeedback machines. And then there is going back to traditional old fashioned Chinese medicine, acupuncture, chiropractor, homeopathic, herbs and supplements.

Of course some patients will combine Camp B and Camp C. Many Lyme doctors are now doing the same. Most of these patients have become scholars in their own right on anything from supplements to pharmaceuticals to any illness that comes along with Lyme disease such as co infections, adrenal and thyroid conditions. We know about organ systems, body chemistry, dietary influences, side affects from anything from medicine to histamine producing foods. We remind our pharmacists of interactions, we tell our doctors about the latest research, we know when  a doctor is lying to us or being condescending. We are educated.

This was not to sound cocky. This is just what we have had to do to survive.

Camp D

Camp D is the “self-treaters.”  The lost ones in the Lyme community. Most are either self treating, or not treating at all. Insurance companies won’t pay for many of the alternative treatments. Most LLMDs cannot take insurance at all for risk of the insurance companies turning them in for treating outside the IDSA and CDC guidelines. So this group of patients is left to self treat if they can even afford to do that.

This camp of patients tends to research and learn about all sorts of treatments, supplements, protocols online. They are forced to. They are sick, usually have lost everything, many are homeless or living with family or friends. They have lost friends, jobs, houses, marriages, even their children to the court systems. They have no way to get to doctor appointments or to pay for them if they do make it there. If they make it to a Lyme doctor or specialist once, it’s hard to get back a second time to follow up.

Many times meds, and almost always supplements are totally out of pocket costs. It is nearly impossible for Lyme patients to get on disability as it is not recognized as a chronic or disabling disease. Treatments like chiropractic, acupuncture and energy testing can really benefit a Lyme patients but will usually not be covered by insurance,

We lose many to suicide in this group. 

This article is sad, might make one feel hopeless. This is not the intent of this article. It is really the opposite. I am writing this article to plea with “the powers to be” whoever hold the power to change things, to please do so. We are desperate. We are sick. We are losing people in our community. We are asking for someone to notice, for the IDSA, CDC or whoever has the control or power to stop the ignorance and denial and make change happen. 

Until then, we will continue to raise our voices, rally, protest, educate ourselves, educate the public, turn to the media, write songs, write poems, take pictures, make videos, do blog posts and Facebook statutes for Lyme awareness.

We will not give up until things have changed. 

For more information please see Lisa’s website:  Whatislyme.com

Category:

Activism, Lyme, Treatment

Mast Cell Activation Syndrome & Lyme/MSIDS

The path to health leads many Lyme/MSIDS patients down numerous rabbit holes.  A pathogen invasion of various bacteria, funguses, viruses, and nematodes depletes the body of many important things.  We are literally being feasted upon, and patients find that they need to supplement their deprived bodies of many things after becoming infected.

Pathogen invasion also causes autoimmunity, where the body attacks itself. Cytokine cascades are continually being set off and the body is in a state of immunoconfusion with a pro-inflammatory response.  The immune system can no longer identify bad guys from good guys.  For many, getting the immune system straightened out is at least half the battle.

Mast Cell Activation Syndrome (MCAS) can cause these things as well.

Dr. Lawrence Afrin, M.D. wrote about MCAS in his book, Never Bet Against Occam.  In reading the book, it becomes clear there are as many nuances with MCAS as there are with Lyme/MSIDS.  Every patient is truly, uniquely different. In treatment, there is much trial and error, with each patient responding to differing things.

Our personal experience with MCAS stems from my daughter who developed allergy-type symptoms over years which came to a head when she developed severe Epstein Bar Virus (EBV).  Prior to that she would frequently have to stop running or walking due to severe itching (exercise induced urticardia).  http://www.mayoclinicproceedings.org/article/S0025-6196(11)63475-7/fulltext  Our LLMD uses LDA/LDI for those with immunoconfusion with success.  Although, she thankfully doesn’t present with Lyme/MSIDS, she definitely struggles with a confused immune system and EBV.  Read here for more on LDA/LDI:  https://madisonarealymesupportgroup.com/2016/05/30/new-kids-on-the-block-ldaldi/  In her case, she reacted strongly to the LDA.  The injections are  somewhat separated so you can visibly see what your issues are.  She developed a facial rash which was deep and painful.  Within a day of her shot it resolved completely, showing how skin symptoms can definitely be caused by allergens and immunoconfusion.

IMG_0475

https://www.linkedin.com/pulse/mast-cell-activation-syndrome-mcas-when-histamine-carnahan-md?trk=v-feed&lipi=urn%3Ali%3Apage%3Ap_flagship3_search_srp_content%3BH0Gf8FqaKVxrspeojT9VVA%3D%3D

Mast Cell Activation Syndrome (MCAS): When Histamine Goes Haywire…

Published on October 31, 2016
Jill C. Carnahan, MD – Used with permission
Founder, Medical Director, Flatiron Functional Medicine

Mast cells are present in most tissues throughout the human body, especially connective tissue, skin, intestinal lining cardiovascular system, nervous system, and reproductive organs. They are part of the allergic response designed to protect us from threat and injury. When the body is exposed to a perceived threat, the mast cells secrete chemical mediators, such as histamine, interleukins, prostaglandins, cytokines, chemokine and various other chemicals stored in the cytoplasm of the cell. These chemical messengers produce both local and systemic effects, such as increased permeability of blood vessels (inflammation and swelling), contraction of smooth muscle (stomach cramps and heart palpitations), and increase mucous production (congestion, sneezing, etc). Historically, we thought of mast cells only in relation to an allergic or anaphylactic response. We now know they play a profound role in immune activation, development of autoimmunity and many other disorders, such as POTS (postural orthostatic hypotension). Sadly we are seeing a large increase in patients presenting with mast cell disorders and MCAS. I believe it is in part do to the onslaught of more pervasive environmental toxins, molds and chemicals.

Without mast cells, we would not be able to heal from a wound. They protect us from injury and help the body to heal. Unfortunately, overactive mast cells can cause a variety of serious symptoms.

Symptoms of overactive mast cells may include:

skin rashes/hives
swelling/edema
flushing
itching
abdominal pain
nausea/vomiting
diarrhea
wheezing
shortness of breath
heart palpitations
anxiety, difficulty concentrating
headaches
brain fog
low blood pressure
fatigue

Mast cell activation syndrome (MCAS) is a condition symptoms involving the skin, gastrointestinal, cardiovascular, respiratory, and neurologic systems. It can be classified into primary (clonal proliferation or mastocytosis), secondary (due to a specific stimulus), and idiopathic (no identifiable cause). Proposed criteria for the diagnosis of MCAS included episodic symptoms consistent with mast cell mediator release affecting two or more organ systems with hives, swelling, flushing, nausea, vomiting, diarrhea, abdominal pain, low blood pressure, fainting, heart palpitations, wheezing, red eyes, itching, and/or nasal congestion.

Triggers may be medications, foods, supplements, hormones, opioids, stressors (physical or emotional), cold temperature, heat, pressure, noxious odors, chemicals, insect bites, trauma or environmental toxins.

We commonly see mast cell activation syndromes associated with CIRS (chronic inflammatory response syndrome) in response to biotoxins, such as mold, inflammagens, and lyme-related toxins.

Low MSH and Mast Cell Disorders?

As mentioned above, we frequently see histamine intolerance and MCAS in patients with mold-related CIRS (chronic inflammatory response syndrome). It is interesting to note that a common finding in CIRS is low MSH. According to this study in the Journal of Investigative Dermatology, alpha-MSH plays an immunomodulatory role during inflammatory and allergic reactions of the skin. In addition, there is evidence that MSH induces mast-cell apoptosis (cell death).

Definition of Mast Cell Activation Syndrome (MCAS)

Typical clinical symptoms as listed above
Increase in serum tryptase level or an increase in other mast cell derived mediators, such as histamine or prostaglandins (PGD2), or their urinary metabolites,
Response of symptoms to treatment

Diseases Associated with Mast Cell Activation Syndrome (MCAS)

Allergies and Asthma
Autism
Autoimmune diseases (Hashimoto’s thyroiditis, systemic lupus, multiple sclerosis, bullous pemphigoid, rheumatoid arthritis and others.                                            Eczema
Celiac Disease
Chronic Fatigue Syndrome
CIRS (chronic inflammatory response syndrome)
Eosinophilic Esophagitis
Fibromyalgia
Food Allergy and Intolerances
Gastroesophageal reflux (GERD)
Infertility (mast cells in endometrium may contribute to endometriosis)
Interstitial Cystitis
Irritable Bowel Syndrome (IBS)
Migraine Headaches
Mood disorders – anxiety, depression, and insomnia
Multiple Chemical Sensitivities
POTS (postural orthostatic hypotension)

Mast cells are known to be the primary responders in allergic reactions, orchestrating strong responses to minute amounts of allergens. Several recent observations indicate that they may also have a key role in coordinating the early phases of autoimmune diseases, particularly those involving auto-antibodies.

Lab tests specific to mast cell activation for suspected MCAS may include:

Serum tryptase (most famous mast cell mediator)
Serum chromogranin A
Plasma histamine
Plasma PGD2 (chilled)
Plasma heparin (chilled)
Urine for PGD2 (chilled)
PGF2a
N-methylhistamine

Tryptase is the most famous mast cell mediator. Serum tryptase value is usually normal in MCAS patients, but sometimes it is elevated. Tryptase values that show an increase of 20% + 2 ng/ml above the baseline level are considered diagnostic for MCAS.
Chromogranin A is a heat-stable mast cell mediator. High levels can suggest MCAS, but other sources must first be ruled out, such as heart failure, renal insufficiency, neuroendocrine tumors and proton pump inhibitor (PPI) use.
Heparin is a very sensitive and specific marker of mast cell activation. However, due to its quick metabolism in the body, it is very difficult to measure reliably.
N-methylhistamine is usually measured in a 24 hour urine test to account for the variability in release over the course of the day.
Prostaglandin D2 is produced by several other cell types, but mast cell release is responsible for the dominant amount found in the body. PGD2 is less stable than histamine and metabolized completely in 30 minutes.
Other less specific mast cell mediators that are sometimes abnormal in MCAS patients include Factor VIII, plasma free norepinephrine, tumor necrosis factor alpha, and interleukin-6.

Treatments to reduce MCAS symptoms and lower histamine

H1 Blockers – hydroxyzine, doxepine, diphenhydramine, cetirizine, loratadine, fexofenadine
H2 Blockers Famotidine (Pepcid, Pepcid AC), Cimetidine (Tagamet, Tagamet HB) Ranitidine (Zantac)
Leukotriene inhibitors: Montelukast (Singulair), Zafirlukast (Accolate)
Mast cell stabilizers -Cromolyn, Ketotifen
Tyrosine kinase inhibitors – imatinib
Natural anti-histamines and mast-cell stabilizers
Ascorbic Acid
Quercetin
Vitamin B6 (pyridoxal-5-phosphate)
Omega-3 fatty acids (fish oil, krill oil)
Alpha Lipoic Acid
N-acetylcysteine (NAC)
Methylation donors (SAMe, B12, methyl-folate, riboflavin)
Certain probiotics decrease histamine productionLactobacillus rhamnosus and bifidobacter species
DAO Enzymes with meals – Xymogen HistDAO or Histamine
Decrease consumption of high histamine foods (more on histamine-restricted diet)
Avoid alcoholic beverages
Avoid raw and cured sausage products such as salami.
Avoid processed or smoked fish products. Use freshly caught seafood instead.
Avoid pickles
Avoid citrus fruits.
Avoid chocolate
Avoid nuts
Avoid products made with yeast and yeast extracts
Avoid soy sauce and fermented soy products
Avoid black tea and instant coffee
Avoid aged cheese
Avoid spinach in large quantities
Avoid tomatoes, ketchup and tomato sauces
Avoid artificial food colorings & preservatives
Avoid certain spices: cinnamon, chili powder, cloves, anise, nutmeg, curry powder, cayenne pepper

Specific Symptom Treatment in MCAS

(Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options)

Headache⇒ paracetamol; metamizole; flupirtine
Diarrhea⇒ colestyramine; nystatin; montelukast; ondansetron
Colicky abdominal pain ⇒ metamizole; butylscopolamine
Nausea⇒ metoclopramide; dimenhydrinate; 5-HT3 receptor inhibitors; icatibant
Respiratory symptoms (mainly increased production of viscous mucus and obstruction with compulsive throat clearing) ⇒ montelukast; acute: short-acting albuterol
Gastric complaints⇒ proton pump inhibitors
Osteoporosis, bone pain⇒ biphosphonates, Vitamin D plus calcium
Non-cardiac chest pain⇒ H2-histamine receptor antagonist; proton pump inhibitors
Tachycardia⇒ verapamil; AT1-receptor antagonists; ivabradin
Neuropathies ⇒ a-lipoic acid
Interstitial cystitis⇒ pentosan, amphetamines
Sleep-onset insomnia/sleep-maintenance insomnia⇒ triazolam/oxazepam
Conjunctivitis⇒ preservative-free eye drops with glucocorticoids for brief course
Elevated prostaglandin levels, persistant flushing⇒ incremental doses of acetylsalicylic acid (50-350 mg/day; extreme caution because of the possibility to induce mast cell degranulation)

For more on MCAS, Lyme/MSIDS, and parasites:  https://madisonarealymesupportgroup.com/2017/03/23/rebecca-keith-on-mcas-parasites-lymemsids/

References

Mast Cell Activation Syndrome, A Review http://www.jillcarnahan.com/downloads/MCASReview.pdf
Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options  http://jhoonline.biomedcentral.com/articles/10.1186/1756-8722-4-10
Presentation, Diagnosis and Management of Mast Cell Activation Syndrome by Dr. Afrin  http://www.jillcarnahan.com/downloads/MCAS-Afrin.pdf
Histamine and Gut Immune Mucosal Regulation  http://www.jillcarnahan.com/downloads/Histamine-gut.pdf
Dr. Theoharides presents “Mast Cell Disorders”  https://www.youtube.com/watch?v=92nrFwcNSwc&feature=youtu.be
Diagram of Histamine Symptoms  https://mastcellblog.files.wordpress.com/2013/11/mast-cell-symptoms.jpg
Mast Cell Aware  http://www.mastcellaware.com
A Tale of Two Syndromes  http://www.dysautonomiainternational.org/blog/wordpress/a-tale-of-two-syndromes-pots-and-mcas/
Mold Histamine Connection  https://healinghistamine.com/the-mold-histamine-link/

Category:

Lyme, Treatment, Viruses

Ocular Bartonellosis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318637/
J Trop Med. 2017; 2017: 7946123.
Published online 2017 Feb 7. doi:  10.1155/2017/7946123
PMCID: PMC5318637

Clinical Profile and Visual Outcome of Ocular Bartonellosis in Malaysia
Chai Lee Tan, Lai Chan Fhun,  Evelyn Li Min Tai, Nor Hasnida Abdul Gani, Julieana Muhammed, Tengku Norina Tuan Jaafar, Liza Sharmini Ahmad Tajudin, and Wan-Hazabbah Wan Hitam 

Abstract

Background. Ocular bartonellosis can present in various ways, with variable visual outcome. There is limited data on ocular bartonellosis in Malaysia. Objective. We aim to describe the clinical presentation and visual outcome of ocular bartonellosis in Malaysia. Materials and Methods. This was a retrospective review of patients treated for ocular bartonellosis in two ophthalmology centers in Malaysia between January 2013 and December 2015. The diagnosis was based on clinical features, supported by a positive Bartonella spp. serology. Results. Of the 19 patients in our series, females were predominant (63.2%). The mean age was 29.3 years. The majority (63.2%) had unilateral involvement. Five patients (26.3%) had a history of contact with cats. Neuroretinitis was the most common presentation (62.5%). Azithromycin was the antibiotic of choice (42.1%). Concurrent systemic corticosteroids were used in approximately 60% of cases. The presenting visual acuity was worse than 6/18 in approximately 60% of eyes; on final review, 76.9% of eyes had a visual acuity better than 6/18. Conclusion. Ocular bartonellosis tends to present with neuroretinitis. Azithromycin is a viable option for treatment. Systemic corticosteroids may be considered in those with poor visual acuity on presentation.

In the results section we learn that 19 patients with ocular bartonellosis were followed from 3-68 weeks. Neuroretinitis is an inflammation of the neural retina and optic nerve which can be caused by viruses, autoimmune disease, or bacteria including: syphilis, Rocky Mountain Spotted Fever, toxoplasmosis, toxocariasis, histoplasmosis, leptospirosis, and Lyme Disease. Tuberculosis and Tularemia can also present similarly. The most common ocular complaint was blurred vision with around 60% reporting headaches as their initial symptom.

We also learn that the treatment of choice was Azithromycin followed by Doxycyline, ciprofloxacin, ceftazidime, and cotrimoxazole, with 60% receiving systemic corticosteroid therapy. The discussion section states that the treatment of Bartonellosis is still controversial and that they had to resort of isolated case reports for information.

http://webeye.ophth.uiowa.edu/eyeforum/cases/36-CatScratchBartonella.htm In this case study a 44 year old woman had non-specific blurriness of vision in her left eye. After they went through about every other possibility, they asked about pets at which she showed multiple cat scratches on her arms.

Laboratory results showed:
*White blood cell count: 18,200 with left shift (12,194 segmented neutrophils and 3276 bands)
*Bartonella Henselae IgG 1:1024 (strongly positive)

According to this study, a literature review suggested that a one month course of doxycycline or erythromycin (with or without rifampin) is adequate to treat the organism and hasten recovery. They chose a one month course of doxycycline 100 mg twice daily. The patient returned for follow-up appointments one and two months after this initial diagnosis. Vision improved to 20/60 in the affected eye, improving visual fields, decreased optic disc edema, and resolving sub-retinal fluid.

The case study also states that diagnosis officially requires 3 out of 4 criteria:
• Lymphadenopathy in the absence of other reason (can be missed because it is not present yet or subclinical)
• Positive Bartonella H. titer or skin test
• Known cat contact, preferably with pustule or papule at the site
• Lymph node biopsy with bacilli present, necrosis

They admit this woman met only 2 of the criteria. They also state it is well documented patients will almost always get better on their own but that hundreds of reports give various treatment regimens including doxycycline, erythromycin, rifampin, azithromycin, ciprofloxacin, later addition of steroid drop, and many others.

The unfortunate thing about both of these reports is they make Bartonellosis out to be a benign pathogen, which for Lyme/MSIDS patients couldn’t be further from the truth.

As to the criteria to diagnose:

Thankfully, this woman didn’t present with swollen lymph nodes so they had to find a reason and state it was either subclinical or hadn’t presented yet.

*Hardly anyone I know with Bartonella has swollen lymph nodes.

*The testing for Lyme and every coinfection, including Bartonella, is abysmal.

*They emphasize the cat’s role but don’t even mention ticks, mites, biting flies, other arachnids, sand flies, mosquitoes, fleas and flea feces, the human body louse, potentially from needles and syringes in the drug addicted, as well as bites and scratches from other reservoir hosts.

*As to node biopsy, even this NIH study shows a lack of specificity and lack of typical micro abscesses in almost half of the cases and may mimic other lymphadenopathies.
https://www.ncbi.nlm.nih.gov/pubmed/26551620

*https://wwwnc.cdc.gov/eid/article/22/3/15-0269_article This CDC article states that Bartonella spp. may be the cause of unclear and undiagnosed chronic illness in humans previously bitten by ticks.

*They also fail to mention there are 15 species and counting of Bartonella known to infect humans and that Dr. Ricardo Maggi states, “This case reinforces the hypothesis that any Bartonella species can cause human infection.”
http://townsendletter.com/July2015/bartonellosis0715_3.html  Besides the cat (including bobcats, mountain lions, and other large cats), rats, dogs, rabbits, deer, cattle, small woodland animals, rodents, coyotes, foxes, and elk were found to harbor Bart.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88941/ The question really should be, “What doesn’t carry Bartonella?”

https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/  Here, Dr. Mozayeni states about 60% of Lyme patients tested positive for Bartonella and that it is one of the major coinfections. This link also has treatments, explanation of Bartonella including what it does and how it can present, along with a link for a checklist you can print out and take to your doctor to discuss.

I appreciate Dr. Breitschwert’s and Dorsey Kordick’s comment in the concluding remarks,

“Not too long ago, many were taught during microbiology courses (or medical school training) that blood is generally a sterile medium. Increasingly, this assertion must be qualified with regard to Bartonella spp. as well as other intracellular pathogens that have coevolved with humans and animals to persist in circulating blood cells such as erythrocytes or macrophages for months to years and perhaps longer.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88941/

I wish more researchers were this transparent, then perhaps patients would be taken more seriously.   And, don’t kid yourself, Bartonella is a formidable foe to the immunocompromised.

Category:

Bartonella, Lyme, mosquitoes, research, Ticks, Transmission, Treatment