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too bad this ILADS document is in timesnewroman making illegible for neuro patients like me that runsallwordstogether like this for me!
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DebAz
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I am sorry... about that.
I can not change that but for anyone who can read it ..
Depending on what software you use to view pdf's, you may be able to select the text and copy it into a word processor for font manipulation.
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My pdf software is able to select and copy the text in the doc. PM me with your email addy and I can send it to you Betty if you want it. I can't do it tonight because my gift wrapping is over the top (thank you secret santas), but after the holidays I can do it!
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DebAz
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I know you have great newbie links but for some reason i have found a couple I wish i had before.
If Jeanie can create them for you maybe that will work for posting or archiving??
-------------------- You never know how strong you are until being strong is the only choice you have. Posts: 807 | From South Dakota | Registered: Jul 2005
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METALLlC BLUE
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Her name is at the very top of the article. She's the author of the paper but she's not an M.D. nor does she prescribe antibiotics. She's safe.
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
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Chronic Lyme Disease and Co-infections: Clinical Overview
Rebecca Snow, MS, RH (AHG), CNS, LDN This paper summarizes the major clinical issues surrounding chronic Lyme disease and the underlying pathophysiology of the disease.
This information will serve as a foundation for the herbal practitioner's clinical approach to chronic Lyme disease. The corresponding presentation at the AHG conference will focus on specific case studies and the nuts and bolts of seeing clients with Lyme disease.
Introduction to Lyme Disease
Lyme disease or Lyme borreliosis, is a multi-system infectious disease caused by a tick-transmitted spirochete, Borrelia burgdorferi. Although the disease was named for Lyme, Connecticut, where an outbreak of rheumatoid arthritis was initially misdiagnosed in the late 1970's and later discovered to be caused by an infectious agent, the first reported case was in Germany in 1883.
Borrelia burgdorferi is the most common species in the United States; there are 100 strains in the US alone and 300 strains worldwide. There are actually several other infectious species of Borrelia in the US and abroad.
There are 15 species that are infectious to man, including B. garinii, B. afzelii, B. japonica, B miyamoto, B lonestari, and B andersonii. From this point forward I will use the abbreviation (Bb) to refer to Borrelia burgdorferi and related species.
Generally acute and early-disseminated Lyme disease is marked by fever and bulls-eye rash and yet in many cases transmission may be asymptomatic or atypical.
!!!***** If the infection goes untreated or even if the infection is treated it may become chronic. *****!!!
The organism can lay dormant for many years and be reactivated (Rubel, 2006). Symptoms are diverse and elusive. ``Initially thought to be a disorder beginning in the skin and progressing to involve the joints, Lyme disease is now ranked as one of the great mimickers of other diseases, in a manner similar to that once ascribed to syphilis,'' (Duray, 1989).
The complex nature of the disease is elucidated later in this paper. Bb is the most genetically complex bacteria identified to date. Bb contains 132 functional genes, compared to the syphilis spirochete Treponema pallidum's mere twenty-two. Ninety percent of these genes are novel to all bacteria.
Bb's genome is 2/3 the size of the human genome. Bb contains 21 plasmids, more than any other bacteria. This characteristic allows the organism to be highly adaptive to its environment, with the ability to survive in a number of different hosts (Stricker, 2006; Wikel, 2006; Porcella & Schwan, 2001).
!!!!--Lyme disease is the fastest growing vector-borne disease; found on 5 continents (Sigler, Kershaw et al., 1997; Stricker, 2006). Reported cases are estimated to represent 10% of the actual number of cases in the United States.---!!!
The Centers for Disease Control and Prevention (CDC) reported 24,000 cases in 2002. With vast underreporting, the actual number of cases was likely to be 240,000 that year (Stricker, 2006). The reason for the growth and spread of Lyme disease is multifaceted. Plausible reasons include degradation of natural habitats, climactic changes, suburban sprawl, increase in vector populations, human, animal and bird migration, and genetic and evolutionary changes of pathogenic organisms, which may be triggered by the misuse of antimicrobial agent (Ranga, Trivedi, et al. 1997; Stricker, 2006).
!!!__ Infected ticks have been found on migratory birds that travel between states, countries and continents__!!!
(Gardner, 2001). Since 1900 the US deer population has multiplied 70-80 times from 500,000 to 35-40 million. (Ranga et al., 1997; Stricker, 2006). Using Baltimore County, Maryland as a microcosm of geographic correlations with disease incidence, Glass et al. found a higher incidence of Lyme disease with proximity to forest edge, moderate altitudes, and soil type, in particular soil suited for conifers but not herbaceous vegetation (Glass, Schwartz, et al., 1995).
Issues of Diagnosis and Treatment
Numerous issues complicate the treatment and diagnosis of chronic and pervasive Lyme disease (see Box 1 for a summarized list).
Understanding these issues will help the herbalist and health care practitioner to more effectively support their clients with Lyme disease.
!!!_Issue #1: There is no definitive test for the presence of Bb; chronic Lyme disease is a clinical diagnosis. Direct detection of Bb through laboratory tests is not commonly available._!!!
Bb is a slow growing organism and is difficult to culture from tissue samples. According to the CDC, Lyme disease is a clinical diagnosis.
Aside from acute or early-disseminated infection, the existence of chronic and/or persistent Lyme disease (active infection with or without 14-21 days of antibiotics) is not commonly recognized by medical professionals, largely due to lack of reliable testing.
TBC....
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The Lyme-literate clinician reviews symptoms, available laboratory tests, history of rash and tick bite(s), exposure, place of residence and response to treatment.
Unfortunately the gold star diagnostic, an Erythema Migrans (EM) rash occurs in less than 50% (possibly as low as 30%) of positively diagnosed patients. It often presents in an atypical fashion, not the typical bulls-eye rash (Stricker, Lautin, et al., 2005). The tests commonly used in Lyme-literate practices are the Polymerase Chain Reaction (PCR) and antibody detection methods.
A PCR detects small strands of Bb DNA in tissue and blood samples. This form of testing has a high rate of false negatives and low diagnostic value, largely due to Bb's affinity for body tissue rather than fluids. But with close to 100% specificity, false positives are rare (Aguero-Rosenfeld, Wang et al., 2005). PCR is the preferred method of testing for acute infection (Schmidt, Muelleger et al., 1996).
Antibody detection methods include both the Enzyme-Linked Immuno-Sorbant Assay (ELISA) and the Western Immunoblot. ELISA has a lower specificity and sensitivity than the Western blot. The latter is the preferred antibody detection method and the most commonly used lab test in Lyme-literate medical practices.
The Western blot measures both IgG and IgM antibodies to several Bb specific antigens.
Diagnosing chronic and persistant infection is more challenging. The implications of a positive Western blot with persistent IgG and/or IgM antibodies after antibiotic treatment is unclear. Is it chronic infection, indicative of past infection or cross-reactive antibodies?
Asymptomatic individuals can test positive and clinically diagnosed patients can test negative. It is estimated that 30% of clinically positive patients test negative on the Western blot (Harris, 2006; Jones, 2004). In one study, of 55 patients with EM, 20% were seronegative with Western Blot (Aguero-Rosenfeld et al., 2005).
There are several possible explanations for negative tests in clinically positive individuals aside from potential misdiagnosis:
Antibodies could be bound in circulating immune complexes, there is a diversity of antigenic profiles due to multiple strains, evasion of immune recognition by the organism, intracellular location of organisms, and/or the hosts immune system may be suppressed (Harris, 2006; Taylor, 2004).
It is interesting to note, that clinically positive yet seronegative patients will often test positive on the Western blot after a course of antibiotic treatment (Burrascano, 2006). A negative test does not rule out chronic Lyme disease, and a positive test does not diagnose Lyme disease. Ultimately it is a clinical diagnosis; the presence of antibodies is weighted against clinical picture and response to treatment.
Other Clinical Tests
Two less conventional laboratory tests used to measure progress and treatment are levels of CD57+ NK cells and Vitamin D 1,25 (active form of D in the body) and Vitamin D ,25 (inactive form). CD57 is a particular glycoprotein marker found on the cell surface of certain aggressive Natural Killer cells.
Labcorps is the only lab currently running this test. Normal levels are > 200, but there is a standard deviation of +/- 30. Preliminary research and empirical data suggest that low levels are correlated with clinical diagnosis of chronic Lyme & elevated pro-inflammatory cytokines.
It is a potential marker for differential diagnosis, as low levels are not commonly seen in Multiple Sclerosis (MS), Systemic Lupus Erythematosus (SLE), Lou Gehrig's Disease (ALS) (Savely, 2006). It is unclear if low levels of this NK cell contribute to the disease state or simply serve as a marker of unresolved infection.
Researcher Trevor Marshall, author of the Marshall protocol for Lyme disease, demonstrated that Vitamin D 1,25 and Angiotensin II (A-II) are key players in a self-perpetuating cycle of inflammation and Th1 cytokine production in chronic Lyme disease.
A standard blood test, the ratio of 1,25-D and ,25-D can be useful clinical marker for inflammation and Th1 activation (Mozayeni, 2007; Marshall, Lee et al., 2006). Issue #2: Treatment response to long-term and short-term antibiotics is variable. The Infectious Diseases Society of American (IDSA) recommends a treatment course of 10 - 21 days in acute infection (Wormsler, Dattwyler et al., 2006). According to ILADS this approach is insufficient. Failure rates are significant and acute infection often goes undetected due to atypical presentation.
--- As an example, one study demonstrated 74.2% of patients with previous EM rash, treated with 3 weeks to 2 months of oral or intravenous antibiotics had positive urine PCR (Bayer, Zhang et al. 1996). Treatment failure occurred in 32/165 of patients with three months of antibiotics and of those who relapsed 40% were seropositive for Lyme (Oksi, Marjamaki, et al., 1999). A review of antibiotic treatment for Lyme disease is available at www.lymeinfo.net/medical/LDPersist.pdf.---
Mixed reviews of antibiotics' benefits have several implications: clients are confused by treatment choices; length of treatment is ambiguous; it's unclear if symptomology post-treatment is reflective of persistent infection or post-infectious immune dysregulation; and lastly, there is a need for a more holistic and broader treatment approach. No clinical trials, to date, have studied the use of antibiotics in conjunction with herbs and nutritional supplements to support immune function and body terrain.
Issue #3: The Borrelia organism is pleiomorphic and evasive. Many of the issues of testing, diagnosing, and treating Lyme disease stem back to the very nature of Bb. Under stress, in the presence of antibiotics or cerebro-spinal fluid, the organism changes morphology.
Currently identified morphological variations include: Spirochetal form (coiled & uncoiled), cystic form or spheroplasts, blebs and granules, and the cell wall deficient or L form (MacDonald, 2006; Rubel, 2003b).
TBC.......
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These forms have been identified in vitro and in symptomatic patients (Mursic et al1996); they enable the organism to become latent for long periods of time, resist treatment, evade immune recognition, and trigger an immune response (MacDonald, 2006; Brorson, 2006; Brorson & Brorson, 2006; Rubel, 2003b).
The cystic form, a non-replicating form of the organism, can evade immune recognition by turning the cellular membrane insideout and presenting a different antigenic profile (Brorson, 2006; Rubel, 2003b; Brorson & Brorson, 1997), helping to explain negative spinal fluid PCR seen in patients with neuroborreliosis (Brorson & Brorson, 1998). The cystic form has demonstrated the ability to convert back to a spirochetal form in vivo (Gruntar & Malovrh, 2001); and even after 6 years of dormancy the cystic forms are able to convert back to spirochetal form in vitro (Brorson & Brorson, 2006).
Skin biopsies of symptomatic yet seronegative patients with dermatological manifestations of Lyme have demonstrated small granular structures of Borrelia among collagen fibers (Aberer, 2006; Aberer & Kerston, 1996). These granules are likely to be infective. They can penetrate cell membranes and possibly transfer DNA (Rubel, 2003b; Beermann, Wunderli-Allenspach, et al., 2000). Kersten, Poitschek et al. ``identified intact spirochetal parts,'' with transmission electron microscopy, ``mostly situated in cysts ... seen up to 96 h after exposure with ... three antibiotics (penicillin, doxycycline, and ceftriaxone),'' (1995). For a pictorial review of diverse Bb morphology see http://www.molecularalzheimer.org/files/Spirochetal_diversity_3_pages.pdf.
Issue #4: Presence of co-infections Borreliosis may be co-transmitted with other tick-borne infections. The most common co-infectious organisms are Babesia microti (Babesiosis), Ehrlichia spp & Anaplasma phagocytophila (Ehrlichiosis), and Bartonella spp Rates of co-infections vary.
DeMartino, Carlyon et al. found that one out of every five individuals who were seropositive for Bb also showed immunological evidence of exposure to Ehrlichiosis (2001). Prevalance of Babesiosis can range from 10% to 60% in individuals who are seropositive for Borrelia (Rubel, 2003c; Kraus, McKay et al, 2002). In a random selection of Ixodes scapularis ticks in New Jersey, 33.6% were positive for Borrelia burgdorferi, 8.4% for Babesia, 1.9% Anaplasma, and 34.5% Bartonella (Adelson, Rao et al., 2004).
Distinguishing individual infections in the clinic is challenging as the clinical manifestations overlap. For instance, acute Babesiosis and Ehrlichiosis can manifest in a nondescript flu-like illness.
Testing for co-infections is limited. For instance, of the 13 strains of Babesia found in ticks, clinical tests are only available for B. microti, WA1, and B. duncani. Testing should not rule out co-infections. Patients with Bb and one or more co-infections often have more complex, severe, and persistent symptoms along with longer recovery periods. Further research is needed to clarify how co-infections affect disease dissemination (Kraus et al, 2002).
Babesia is a protozoa not a bacteria. It is a distant cousin to the infectious agent of malaria, Plasmodium spp. Clinical signs and symptoms include a high fever at the time of acute infection, chronic low grade fever, chills, night and day sweats, low RBC, hematocrit, and hemoglobin counts, thrombocytopenia, air hunger and migraine-like headaches (Burrascano, 2006; Horowitz, 2006; Kraus et al 2002).
Two random screenings of residents in Sonoma County, California found that 16-19% of residents were positive for B. microti WA1 (Jerant & Arline 1999; Persing & Herwaldt, 1995).
Co-infection with Bartonella may present as CNS symptoms that are out of proportion to the physical, including anxiety, insomnia, agitation, and confusion, with eye manifestations, sore soles and/or fevers upon waking (Burrascano, 2006; Horowitz, 2006).
Clinically, Ehrlichiosis can be mild or severe, and commonly is associated with acute onset of symptoms, leucopenia and thrombocytopenia, elevated liver enzymes, knife-like headaches, muscle aches predominant over joints (Burrascano, 2006; Horowitz, 2006). TBC..............
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Issue #5: Other modes of transmission The deer tick (Ixodes dammini) and the black-legged tick (Ixodes scapularis) are not the only ticks able to transmit Bb.
Others include Lone Star ticks (Ammblyoma americanum), western black-legged ticks (Ixodes pacificus) and dog ticks (Dermacentor variabilis) (Taylor, 2004). The prevalence of these vectors is largely underreported.
!!!-- In addition to ticks, both mosquitos and flies have been found to be carriers of Bb (Magnarelli, Anderson et al., 1986). Empirical data suggests that transmission from biting flies may occur (Fishman, 2007; Luger, 1990).---!!!!!
New evidence continues to emerge which demonstrates that Lyme and co-infections are not solely tick-borne diseases.
!!!-- Animal and human models demonstrate that Bb is present in semen, vaginal fluid, breast milk, and the placenta of pregnant women (Rubel , 2006; Bach, 2001)
Peer reviewed literature offers evidence of gestational transmission in humans and animals (Silver,Yang et al. 1995, Duray & Steere, 1988).
!!!!!-- ``It is clear that B. burgdorferi can be transmitted in the blood of infected pregnant women across the placenta into the fetus. This has now been documented with resultant congenital infections... Spirochetes can be recovered or seen in the infant's tissues including the brain, spleen and kidney,'' (Duray & Steere, 1988). ---!!!!!!!!!
Several well know Lyme-literate doctors have devoted their practice to children born with gestational Lyme disease.
!! In an unpublished clinical review of 102 children born of mothers who were either seropositive or infected at the time of pregnancy, Dr. Jones found that over 60% of the mothers had difficult pregnancies. In the same study, of the 102 children born with 4
Box 2 Internationa l Lyme and As soc iated Diseases Soc iety (ILADS) Guidelines for Treatment from www. ilads. com TBC....................
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Several well know Lyme-literate doctors have devoted their practice to children born with gestational Lyme disease.
In an unpublished clinical review of 102 children born of mothers who were either seropositive or infected at the time of pregnancy, !!!! Dr. Jones found that over 60% of the mothers had difficult pregnancies. !!!! In the same study, of the 102 children born withgestational Lyme, 80% of the children had cognitive problems, 72% fatigue, 69% chronic pain, 59% low grade chronic fever.
Over 50% of the children tested positive with the Western blot (Jones & Gibb, 2006). Empirical data and one pilot study demonstrate that Borrelia organisms may be transmitted sexually. At Optimal Health Physicians and other clinics around the country, it is common for both sexual partners to test positive with PCR and/or Western Blot.
In a presentation at the 14th Annual International Scientific Conference on Lyme Disease, Bach presented that 14 out of 32 Lyme patients tested (44%) had Borrelia DNA nucleotide sequences in semen samples identified with PCR tests.
!!!-- 100% of those individuals with sexual partners, had partners test positive as well (Bach, 2001). ---!!!!!!
More than 40 cases of Babesiosis from blood transfusion have also been reported (Lux, Weiss et al., 2003), and a screening of blood donors reported a 3-8% prevalence of Babesiosis in the general population (Homer, Aguilar-Delfin et al., 2000). Borrelia spirochetes are viable after 6 weeks of cold storage in blood banks; transfusion of Borreliosis is a theoretical possibility (Nadelman, Sherer et al., 1990).
Issue #6: Conflicting Medical Opinions
The existence of chronic and persistent Lyme disease is debated in medical communities. The recently published guidelines of the IDSA (www.idsociety.org) deny a need for long-term treatment, recommending no more than 21-28 days of antibiotic treatment.
The lead author states, ``There is no convincing biological evidence for the existence of symptomatic chronic B. burgdorferi infection among patients after receipt of recommended treatment regimens for Lyme disease,'' (Wormsler, Dattwyler et al., 2006).
Many health professionals and researchers in this camp claim that chronic Lyme disease is over-diagnosed. On the other hand, the International Lyme and Associated Diseases Society (ILADS www.ilads.com) takes a progressive approach to treatment and diagnosis (see the recently published recommendations in Box 2), claiming under-diagnosis is prevalent among medical professionals and that long-term antibiotic treatment may be necessary.
For the patient, these conflicting medical opinions often drive them to the Internet for medical answers, some find themselves without medical coverage for ongoing treatment.
Part II: Overview of Pathophysiology and Clinical Presentation
The pathophysiology of chronic Lyme disease is complex and difficult to convey in a short paper. It can be roughly divided into cytopathic (direct cytotoxic effects of the organism) and immunopathic (physiological changes that are immunologically mediated) aspects of disease progression (see Diagram 1).
This diagram is a mind map of physiological processes that will be discussed in this section. These pathways are not clearly delineated, for instance vasculitis may be promoted by intracellular invasion of epithelial cells as well as immune-mediated inflammation in the blood vessels.
CYTOPATHIC EFFECTS
Bb is both an intracellular and extracellular organism. Bb is not commonly found in body fluids but rather has an affinity for collagenous tissue, such as the bladder wall, synovium, myelin sheath of nerve fibers, and the meninges (Stricker, 2006).
Bb uses various techniques to bind to proteins and proteoglycans of the ECM to travel to distant sites of the body often far from the original site of injury. In this process, the organism causes tissue damage and ECM remodeling (Sricker, 2007; Lagal, Portnoi et al., 2006; Wikel, 2006, Buhner, 2005; Coleman, Roemer et al., 1999).
Bb has been found in practically every tissue and organ in the body (Rubel, 2006). A tissue culture in mice, found the bladder to be the most frequent site of appearance: Bladder 94%, Kidney 75%, Spleen 61%, Blood 13%, Urine 0% (Oksi, Marjamaki et al., 1999). Bb can coat itself with plasmin and fibrin helping it evade immune recognition (Horowitz, 2006; Colemen et al., 1999; Coyle, Deng et al., 1993).
!!!-- Patients with neuroborreliosis commonly have signs of cortical atrophy and demyelination (Oksi et al., 1996). MRI scans can present lesions and/or cerebral atrophy (Rubel, 2006). --!!!!!!
Bb DNA can be found at the site of tissue inflammation, suggesting direct tissue invasion of the organism. It has been shown that Bb can cross the blood-brain barrier and hide from the immune system in this ``immunoprivileged'' site (Stricker 2007, Oksi et al., 1996).
Along the same lines, Borrelia burgdorferi cysts and DNA segments have been discovered in brain tissue and cerebrospinal fluid (CSF) samples from patients diagnosed with AD and MS.
TBC.......................
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The DNA discovered in AD patients was often at the site of tissue injury and beta amyloid plaque formation (MacDonald, 2006a; MacDonald, 1988).
Cystic forms of Borrelia discovered in the cerebral spinal fluid of 10 randomly selected MS patients in Norway were still viable and reemerged as spirochetal forms when placed in culture (Brorson & Brorson, 2001). The implication of this research is unclear.
Is this misdiagnosis or is Bb a causative factor these neurodegenerative conditions? Neuroborreliosis can mimic AD, MS, ALS, and many other conditions.
Borrelia-induced neurological changes are comparable to the chronic inflammation, dementia, amyloid deposition and corticol atrophy in late stage syphilis (MacDonald, 2006a; Miklossy et al., 2004; MacDonald, 1988). As an intracellular organism, Bb demonstrates the ability to induce cell death via multiple mechanisms (MacDonald, 2006b; Dorward, Fischer et al., 1997).
The organism has the ability to invade many types of cells in the body, including endothelial cells, lymphocytes, macrophages including kupffer cells, fibroblasts, neuroglial and cortical neuronal cells (Stricker 2006; Livengood & Gilmore, 2006).
Lyme disease is a risk factor for cardiovascular disease and events. In 35 of 39 Bb infected non-human primates, carditis and spirochetal infiltration in cardiac tissue was evident. It is estimated that carditis occurs in 25% of humans with Bb infection (Cavidad, Bai et al, 2004).
In addition, multiple factors of the disease process promote vasculitis, including infection and invasion of the endothelial cells, influx of inflammatory mediators, and circulating immune complexes (Horowitz, 2006; Taylor 2004; Coleman et al., 1999; Oksi et al., 1996; Coyle et al., 1993).
!! Vasculitis may be one of the primary mechanisms of Lyme pathology (Oksi et al., 1996), contributing to impaired peripheral and cerebral blood flow and compounding neurodegenerative effects of the disease process--!!!!!!!! (Fallon, Keilp et al., 2003; Oksi et al., 1996). TBC..............
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Borrelia burgdorferi dynamically interacts with the host's immune system. At the time of initial infection in humans, the organism demonstrates several mechanisms for immune suppression including inhibition of the complement cascade (Stricker,2007, Wikel, 2006).
An initial strong Th1 cytokine response helps reduce severity of tick-transmitted infection acutely (Wikel,2006) and helps to reduce chronicity (Zhang, 2007).
Bb lipoproteins are potent activators of pro-inflammatory cytokines, including IFNγ, IL-12, TNFα, and IL-6. These cytokines can remain elevated, tending to a predominance of Th1 type cytokines in chronic infection (Kumradt, 2002; Ghosh, Seward et al.,2006). Interleukin-4 and Il-10 (Th2 cytokines) tend to be decreased in the chronic state.
IL-10 is recognized as a potent antiinflammatory cytokine, and Mice deficient in IL10 developed more severe arthritis after acute infection with Bb (Brown, Zachary et al., 2006). In animal models, Bb infection is also characterized by elevated expression of COX2, associated up-regulation of inflammatory eicosanoids and subsequent arthritis (Ghosh et al., 2006; Anguita, Samanta et al., 2002).
Another explanation for persistent symptoms is autoimmunity. Individuals with persistent Lyme arthritis more commonly carry the genetic marker HLA-DR4 that is associated with rheumatoid arthritis. Molecular mimicry is a proposed mechanism of autoimmunity in Lyme arthritis, in particular where Bb DNA is not evident in the synovial fluid or tissue.
Bb surface proteins OspA and OspC are potential triggers for cross-reactive T cells and several auto-antigens have been proposed (Ghosh et al., 2006; Kamradt, 2002). Molecular mimicry is also proposed in neuroborreliosis; autoreactive B cells have been found in the CSF of patients with persistent neuroborreliosi(Oksi et al., 1996). .................
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One of the most confusing aspects of Lyme disease for the new clinician is addressing neurocognitive symptoms such as insomnia, mental agitation and anxiety. Patients are often unresponsive to a standard approach, whether it is SSRIs prescribed by their physician or skullcap (Scutellaria lateriflora) recommended by their herbalist.
The client's symptom presentation is often due to an underlying immune dysregulation from chronic infection. Needless to say, skullcap may have undiscovered immunomodulating properties, considering the pharmacology of its relative Baikal skullcap (S. baicalensis), but the key point here is that altered immune function and cytokine dysregulation has multisystem effects and may be a key underlying factor in symptomology.
Potential secondary effects
Secondary effects due to immunological and tissue changes of chronic Lyme include increased insulin resistance, HPA axis dysfunction, weight gain, thyroid dysfunction, and altered liver detoxification (Fishman, 2007; Burrascano, 2006).
Patients with disseminated Lyme are more likely than the general population to have elevated liver function tests (Rubel, 2006) Symptoms and Clinical Presentation Lyme disease offers a complex symptom picture for the clinician. Infection with Bb may be overlooked due to common misperceptions about disease presentation and pervasiveness (Stricker et al., 2005).
Lyme disease can be misdiagnosed a fibromyalgia, CFIDS, Multiple Sclerosis, Lupus, Parkinson's, Alzheimer's, Rheumatoid Arthritis, ALS, and a number of neuropsychiatric disorders (Taylor, 2004).
Disease onset and progression is varied with multisystem involvement and diverse clinical presentation. ``Symptoms can be surprisingly variable, so that days of near normality can alternate with days of profound debility,'' (Pachner, Dail et al., 1995). Bb's reputation is surpassing that of the syphilis spirochete, Treponema pallidum as the ``Great Imitator,'' able to mimic many common conditions.
It is becoming more imperative to rule out Lyme in a variety of presenting cases. Unlike syphilis, stages of disease development do not follow a clear or chronological pattern. In particular, neurocognitive symptoms can show up in early or late phases of the disease process. The Canadian Lyme Disease Foundation provides a great symptom checklist compiled from peer-reviewed literature (See Box 3).
Box 3 Symptoms of Lyme Disease, www.canlyme.com _________________________________________________
Tick Bite Rash at site of bite Rashes on other parts of the body Rash basically circular and spreading out (or generalized) Raished rash disappearing and recurring Unexplained hair loss Headache, mild or severe Seizures Pressure in head, white matter lesions in head (MRI)
Twitching of facial or other muscles Facial paralysis, Bell's Palsy Tingling of nose, (tip of) tongue, cheek or facial flushing Stiff or painful neck Jaw pain or stiffness Dental problems (unexplained) Sore throat, clearing throat a lot, phlegm, hoarseness, runny nose Double or blurry vision Increased floating spots Pain in eyes, or swelling around eyes Oversensitivity to light Flashing lights/Peripheral waves/phantom images in corner of eyes Decreased hearing in one or both ears, plugged ears Buzzing in ears Pain in ears, oversensitivity to sounds Ringing in one or both ears
Diarrhea Constipation Irritable bladder (trouble starting, stopping) or Interstitial cystitis Upset stomach (nausea or pain) or GERD (gastroesophageal reflux disease) Bone pain, joint pain or swelling, carpal tunnel syndrome Stiffness of joints, back, neck, tennis elbow Muscle pain or cramps, Fibromyalgia
Shortness of breath, can't get full/satisfying breath, cough Chest pain or rib soreness Night sweats or unexplained chills Heart palpitations or extra beats Endocarditis, Heart blockage Tremors or unexplained shaking Burning or stabbing sensations in the body Fatigue, CFIDS,weakness, peripheral neuropathy or partial paralysis Pressure in the head Numbness in body, tingling, pinpricks Poor balance, dizziness, difficulty walking Increased motion sickness Lightheadedness, wooziness
Mood swings, irritability, bi-polar disorder Unusual depression Disorientation (getting or feeling lost) Feeling as if you are losing your mind Over-emotional reactions, crying easily Too much sleep, or insomnia Difficulty falling or staying asleep Narcolepsy, sleep apnea
Panic attacks, anxiety Memory loss (short or long term) Confusion, difficulty in thinking Difficulty with concentration or reading Going to the wrong place Speech difficulty (slurred or slow) Stammering speech Forgetting how to perform simple tasks Loss of sex drive Sexual dysfunction Unexplained menstral pain, irregularity Unexplained breast pain, discharge Testicular or pelvic pain Unexplained weight gain, loss Extreme fatigue Swollen glands/lymph nodes Unexplained fevers (high or low grade) Continual infections (sinus, kidney, eye, etc.)
Symptoms seem to change, come and go Pain migrates (moves) to different body parts Early on, experienced a "flu-like" illness, after which you have not since felt well Low body temperature Allergies Chemical sensitivities Increased effect from alcohol and possible worse hangover _________________________________________________
It is important to be familiar with the Jarisch- Herxheimer Reaction (herx) when working with clients with Lyme disease. Commonly, individuals experience a temporary flare of symptoms with treatment geared to eliminating the pathogen. This reaction can be attributed to a phenomenon first identified by Jarisch and Karl Herxheimer in 1895.
The phenomenon is common to other complex organisms, such as those causing leprosy and tuberculosis. One explanation of the phenomenon is that inflammatory endotoxins are released from the dying organism (The Roger Wyburn-Mason and Jack M. Blount Foundation for the Eradication of Rheumatoid Disease, 1991).
During the reaction, eosinophils are not elevated suggesting it is unlikely to be an allergic reaction to antibiotics (RWM & JMB Foundation, 1991).
The author was skeptical of such reactions at first, associating them with harsh therapies. However, the author has found herxheimer reactions to be less severe with herbs and concurrent herbal antiinflammatories but unavoidable in many cases.
It is noted by other herbal practitioners, strength of reaction often correlates with clinical improvement and organism load (Zhang, 2007).
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This is the best article and most complete on that I've ever seen!! Thank you so much for posting it!!!
I tried to post the article and break it up a little so that it is easier to read. I don't know if this will help or not. It is a long, but wonderful article.
The above is only 7 of 14 pages of this article!!!! I'm sorry,------I got tired!!!!
If this, ( breaking up the text some ), does make it easier for anyone, please let me know. I will do the other 7 if it is helpful.
Just by doing this, it was MUCH eisier for me. Although I've still pretty much scanned a lot of it.
Thanks again Deb!!!!!!!
Posts: 351 | From Georgia | Registered: Feb 2008
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bettyg
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posted
scared, thx for taking time/effort to break this up and post it here.
i'll attempt to copy it all over to ms word this weekend for my neuro lyme.
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