Natural Lyme Disease Cure and Treatment

Lyme Strategies

This latest updated text, in digital eBook form and available for immediate download, has been expanded nearly eightfold over the original guide of 2004 in terms of the exact, step-by-step lue-print and essential information designed to maximize this protocol. Just some of the valuable information contained in this 193-page guide includes: How to do the protocol, including the exact, specific method or procedure that is critical to its success. Schedule chart, measurements guide, tips and recommendations. The basic elements of the protocol are actually five, not just salt and vitamin C what these are and why Understanding what a Jarisch-Herxheimer reaction (or Herx) is. Particular djunct items found to be extremely helpful and particular items for special issues. A Technical Section detailing why the protocol works (posited mechanisms), including scientific citations and and studies. The right salt versus wrong salt and why. the low-salt, no-salt myth and scientific truth. the historical, medicinal use of natural salt. Did you know salt was used to treat syphilis, caused by Lyme's bacterial cousin, in the 1800s? Why Vitamin C and what does it do? The protocol and specific body considerations (heart, adrenals, etc.) Key Characteristics of the Lyme bacterium (Borrelia burgdorferi), including nearly 20 extraordinary mechanisms and features it uses to elude the immune and proliferate in the body

Lyme Strategies Summary


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Contents: 193 Pages EBook
Author: M. Fett
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Recently several visitors of blog have asked me about this manual, which is being advertised quite widely across the Internet. So I purchased a copy myself to find out what all the fuss was about.

All the modules inside this ebook are very detailed and explanatory, there is nothing as comprehensive as this guide.

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Autoimmunity In Chronic Lyme Disease

It is not clear if persistence of the organism is necessary for ongoing disease, since antibiotic therapy may not be as effective in late disease as it usually is at an early stage (38). Indeed, the presence of B. burgdorferi at local sites of inflammation is difficult to demonstrate (37). These findings are compatible with the premise that an autoimmune mechanism may be active in the pathogenesis of chronic Lyme disease. Although an immune response to heat shock proteins in patients with Lyme disease has been demonstrated in the various studies cited above, there is no evidence that molecular mimicry between the homologous B. burgdorferi and host heat shock proteins leads to an autoimmune response. Three lines of evidence will be presented to demonstrate that neurological Lyme disease may be an autoimmune disease resulting from molecular mimicry between B. burgdorferi flagellin and human hsp 60. These include (1) immunostaining of nerve tissues and neuroblastoma cells, (2)...

Brief Review Of The Clinical Features Of Lyme Disease

Lyme disease (LD) is a multisystem inflammatory disease caused by B. burgdorferi. As reviewed (29,30), the clinical features of the disease can be divided into three categories early localized (31), early disseminated (32,33), and chronic or late disease (34,35). The immunology of Lyme disease has been reviewed previously (36,37).

Discovering therapeutic targets

Despite the availability of so many complete genome sequences, the functions of many genes remain unclear, in particular if they share little sequence similarity with genes of known function. Expression profiling can be an efficient way to functionally characterize such genes. Co-expression of functionally uncharacterized genes across many experiments with others, of which the functional roles are known, indicates that the corresponding gene products are likely to be involved in the same pathway or protein complex. For instance, genes involved in motility and chemo-taxis are controlled by an alternative sigma factor in many bacteria, which is part of the RNA polymerase complex. In the model bacterium B. subtilis the corresponding regulatory network could be comprehensively mapped by the identification of genes that are co-expressed with this sigma factor 13 . Using this approach, genes of unknown function could be functionally characterized. Similarly, expression profiles of bacteria...

The Vector Human Body Louse Introduction

The threat posed by lice is not only associated to the louse infestation considered as a disease in itself known as pediculosis. Indeed, the human body lice, Pediculus humanus humanus, or P. h. corporis (Fig. 3), are recognized as vectors of three human infections that are reemerging epidemic typhus, relapsing fever (caused by Borrelia recurrentis) and trench fever (caused by Bartonella quintana). Only the human body lice can transmit human pathogens. They live in clothes and multiply when conditions such as cold weather, lack of hygiene, or war are present. Its prevalence reflects the socioeconomic level of the society (52). Currently, the infestation by the human body louse is reemerging, and it is increasingly described in the poorest populations of developed and industrialized countries (26-29).

Associated Medical Findings

Proptosis or periorbital fullness suggests an orbital process such as Graves' disease, orbital meningioma, or orbital pseudotumor. The patient's general appearance may suggest an underlying chromosomal, endocrinological, or metabolic disorder. For instance, the disfiguring frontal bossing and enlargement of the mandible and hands are characteristic of acromegaly associated with a growth hormone-secreting pituitary adenoma. The heart rate, blood pressure, and carotid and cardiac examinations are important in any patient with a possible ischemic event. Patients with pseudotumor cerebri tend to be young females with obesity or a history of recent weight gain. Skin lesions such as erythema migrans (Lyme disease) or malar rash (systemic lupus erythematosus), and abnormal discolorations, such as cafe(c)-au-lait spots and axillary freckling (neurofibromatosis), or hypopigmented ash-leaf spots (tuberous sclerosis) also may be helpful in guiding the evaluation of patients with visual...

Dermatologic Parasitology

Arthropod dermatoses are divided into those caused by two classes of organisms the arachnids (spiders, scorpions, ticks, and mites) and the insects (lice, bugs, flies, moths, beetles, bees, and fleas). Lyme disease is caused by a spirochete that is transmitted by a tick and is discussed in Chap 16.

Polyamines and Life Strategy

Polyamines are now considered essential for cell proliferation. Bacteria contain putrescine and spermidine, but may contain some 30 other di- and polyamines. Their patterns have been used as a phylogenetic tool (Hamana and Matsuzaki, 1992). What can be learned on the enzymes of polyamine synthesis from the genomic sequences Genes for enzymes producing putrescine and spermidine are absent in M. genitalium, Borrelia burgdorferi, and Treponema pallidum. Haemophilus influenzae can produce putrescine, and Helicobacter pylori, Mycobacterium tuberculosis, and E. coli can produce both putrescine and spermidine. Some Archaea, Methannococcus (M. jannaschii) and Halococcus, lack synthesis of polyamines and lack them in direct analysis (Hamana and Matsuzaki, 1992). Nanobacteria do not have putrescine or spermidine, but contain a compound having similar mobility with cadaverine in high pressure liquid chromatography. Cadaverine, a special polyamine used by several eubacteria as a covalently linked...

Microbiology Pathology And Pathogenesis Taxonomy and Nomenclature

Human granulocytic anaplasmosis (HGA) is a tick-borne zoonotic infection that is caused by A. phagocytophilum (4). HGA has become increasingly recognized in the United States and in several European countries. The increased desire of humans to pursue outdoor recreational activities during the summer months has also amplified their potential exposure to pathogenic bacteria, for which a portion of the lifecycle occurs in nonvertebrate bloodsucking enzootic hosts. Just like Borrelia burgdorferi, the agent of Lyme borreliosis, A. phagocytophilum cycles within hard-bodied ticks that are members of the Ixodes persulcatus complex.

The Insect Connection

Another characteristic of many permanent CWD organisms is that insects typically transmit them. The classic example is Lyme disease caused by Borrelia burgdorferi, a disease that is transmitted by ticks. This suggested a correlation for the evolution and the way of life of CWD organisms and their pathogenesis. I have, therefore, proposed (Koch, 2003b) a connection between CWD organisms and their historical or current existence within an insect vector this suggestion is made even if the microorganisms may no longer live only in insects.

Abridged Dictionaryindex

Pustular Bacterid

Acrodermatitis chronica atrophicans, 173, 260. A chronic, biphasic disease seen rather commonly in western Europe. The first phase begins with an erythematous patch on an extremity, which, in weeks or months, develops the second phase of skin atrophy. The cause is believed to be a mixed infection with group B arboviruses, transmitted by the wood tick Ixodes ricinus, and a penicillin-sensitive bacterium or spirochete. Can be a chronic late stage of Lyme disease.

Chronic Progressive External Ophthalmoplegia and Kearns Sayre Syndrome

Conditions to exclude include other mitochondrial diseases, primarily MERRF and MELAS any disease causing ophthalmoplegia when that is the sole presenting symptom, especially myasthenia gravis other diseases that cause multisystem involvement, such as collagen vascular diseases, particularly systemic lupus erythematosus and in the appropriate setting, Lyme disease (caused by infection with Borrelia burgdorferi) or Whipple's disease. Ihe ultimate diagnosis is made by muscle biopsy and mtDNA analysis. Ihere is no proven specific treatment, although coenzyme Q10 and carnitine have been used. Implanted cardiac pacemakers can be used for conduction defects. Associated endocrine abnormalities--growth hormone deficiency, diabetes mellitus, or hypoparathyroidism--can be treated medically. Although these conditions are considered chronic, complete heart block may result in sudden death.

Reviews And Selected Updates

In Roos KL (ed) Central Nervous System Infectious Diseases and Therapy. New York, Marcel Dekker, 1997, pp 213-236. Marra CM Neurosyphilis. In Roos KL (ed) Central Nervous System Infectious Diseases and Therapy. New York, Marcel Dekker, 1997, pp 237-252. Roos KL Meningitis 100 Maxims in Neurology. London, Arnold, 1997, pp 1-208.

Ecology And Epidemiology Ecology

Ticks in the Ixodes genus are known vectors for A. phagocytophilum, and are also vectors of B. burgdorferi (Lyme borreliosis) and Babesia microti (human babesiosis) (37,43,44). The most important tick vector of A. phagocytophilum in North America is I. scapularis that is distributed broadly across the east to the midwestern region of the United States (45,46) a smaller region on the Pacific coast of northern California, Oregon, and Washington is endemic for I. pacificus that are also competent vectors (47). Transmission in Europe is largely by the bites of I. ricinus ticks, and a role for I. persulcatus in Eastern Europe and Asia is also supported by increasing data (48,49). Although A. phagocytophilum is occasionally identified within other tick genera, no evidence exists to show that non-Ixodes spp. ticks are competent vectors (50). A. phagocy-tophilum is very inefficiently transmitted by transovarian passage from adult female ticks to eggs and larvae, but transstadial transmission...

Management Of Neuropathy Associated With Nucleoside Reverse Transcriptase Inhibitor Therapy

Compared with HIV-associated DSP, toxic neuropathies appear more abruptly and progress more quickly, thus, an individual who develops such progressive symptoms within several months after the introduction of a potentially neurotoxic antinucleoside agent is more likely to have a toxic neuropathy. The diagnosis, however, can be confirmed only if symptoms resolve on discontinuation of the agent (18,29). Because some subjects in clinical trials experience only transient paresthesias (36), minor symptoms may not necessarily require immediate change in therapy. Furthermore, in some instances, it may be preferable to continue the agents despite minor neuropathic symptoms because of a robust antiretroviral response. A detailed neurological examination to assess the extent of sensory and reflex impairment, and a detailed neurological history to pursue other causes of neuropathy is an important measure, which should be obtained at the onset of symptoms and is also a...

RLS Associated with Spinal Cord Lesions

There are numerous case reports describing the onset of RLS in close temporal association with spinal pathologies such as lumbosacral radiculopathy (73), borrelia-induced myelitis (74), transverse myelitis (75), vascular injury of the spinal cord (76), multiple sclerosis (77), traumatic lesions (77), cervical spondylotic myelopathy (77), or syringomyelia (77). After spinal anesthesia, 8.7 of 161 patients developed transient new onset RLS (78). Many subjects in these reports responded to dopaminergic treatment (74,75,77,79), while in one subject (76) relief was obtained by a combination of tilidin and zolpidem.

Sauer notes syphilis

Because diagnosis of Lyme disease is difficult, treatment may be indicated, especially in endemic areas, based on history and clinical findings. Lyme Disease Abele DC, Anders KH. The many faces and phases of borreliosis I. Lyme disease. J Am Acad Dermatol 1990 23 -167. Abele DC, Anders KH. The many faces and phases of borreliosis II. J Am Acad Dermatol 1990 23 401. Burlington DB. FDA public health advisory Assays for antibodies to Borrelia brugdorferi Limitations, use, and interpretation for supporting a clinical diagnosis of lyme disease. FDA, July 7, 1997. Golde WT. A vaccine for Lyme lisease Current progress. Infections in Medicine 1998. Lyme Disease-United States, 1996. Arch Dermatol 1997 133. Stere AC, Taylor E, McHugh GL, et al. The overdiagnosis of Lyme disease. JAMA 1993 269 1812. Treatment of Lyme disease. Med Lett 1997 39. Trevisan G, Cinco M. Lyme disease. Int J Dermatol 1990 29 1.

Relapsing Fever

Relapsing fever is a disease characterized by one or more relapses after the primary febrile paroxysm has subsided. Various types of relapsing fever are caused by blood parasites of the Borrelia group. There are two chief forms of the disease endemic relapsing fever, transmitted to humans by various ticks of the genus Ornithodoros and maintained among a variety of rodents and epidemic relapsing fever, caused by a parasitic spirochete, Borrelia recur-rentis, which is transmitted by human head and body lice. B. recurrentis is less virulent than the tick-borne forms. Under favorable conditions,


Ehrlichia are small gram-negative pleomorphic coccobacilli that primarily infect circulating leukocytes and other cells derived from the hematopoietic system. 1041 There are two species of ehrlichia that cause human disease. Ehrlichia chaffeensis is the causative organism of human monocytic ehrlichiosis, and an organism that is closely related to or nearly identical to E. equi and E. phagocytophila is the causative agent of granulocytic ehrlichiosis. 1041 1051 1061 E. chaffeensis infects mononuclear phagocytes in the blood and tissues, and the granulocytic Ehrlichia species infects granulocytic phagocytes in blood and tissues. 104I The infectious agents of human ehrlichiosis and Lyme disease are both transmitted by tick bites. Most cases of human granulocytic ehrlichiosis have been identified in Wisconsin, Minnesota, New York, Connecticut, and Massachusetts, and most cases of human monocytic ehrlichiosis have been identified in the southeastern and south-central United States. 1061...

Rickettsia helvetica

R. helvetica was first isolated in I. ricinus (the vector of Lyme borreliosis) in Switzerland in 1979 (35,36). Because transstadial and transovarial transmission of this rickettsia has been demonstrated in I. ricinus, this tick represents both a potential vector and natural reservoir of R. helvetica. No animal reservoirs were found, although wild deer were intensively studied (37). R. helvetica has been identified in I. ricinus in many European countries, including France, Germany, Sweden, Hungary, Slovenia, Portugal, Spain, Italy, and Bulgaria (38-43) where the average infection rate is approximately 10 . Recently, it has been shown that the distribution of R. helvetica is not limited to Europe, but extends to Asia. Rickettsiae identical with or closely related to R. helvetica have been isolated from I. ovatus, I. persulcatus, and I. monospinosus ticks collected in Japan (8,11). By polymerase chain reaction (PCR), it has also been found in H. japonica (8). R. helvetica has also...

Acquired atrophies

A moderately rare idiopathic atrophy in older adults, particularly women, characterized by the presence of thickened skin at the onset, with ulnar bands on the forearm, changing into atrophy of the legs below the knee and of the forearms. In the early stages this is to be differentiated from scleroderma. High doses of penicillin may be effective. Late stage of Lyme disease. Borreliosis. See Lyme disease


The major genera of spirochetes include Spirocheata, Treponema, Borrelia, and Leptospira. These genera include the causative agents of syphilis, yaws, Lyme disease, African relapsing fever, periodontal disease, and leptospirosis. All these organisms have a flexible wall and can exist in tight spiral shapes. As they rotate they can move through a viscous medium. These cells grow as coiled filaments because they have rotating axial fibrils. The latter are the equivalent of the flagella found in other species but are located inside the periplasmic space. One (or more) is attached near each pole. The base of the flagella is inserted into the cytoplasmic membrane and the structure enclosing the end of the flagellum is the motor that can rotate it in either direction powered by the protonmotive force. This directionality probably happens as it does in the well-studied case of E. coli. For E. coli, the power delivering mechanism is anchored in both parts in the inner and outer membranes and...

Clinical Features

The differential diagnosis of hypochondriasis is important to keep in mind when evaluating the patient. First, a medical condition must be excluded. Given that some medical diseases may be hard to exclude completely because their early stages are less apparent or because adequate laboratory diagnostic tools are unavailable for them (e.g., multiple sclerosis, systemic lupus erythematosus, Lyme disease, occult malignancies), the physician working with a patient whose hypochondriasis does not improve with psychiatric treatment should reconsider the possibility that a diagnosis of medical illness has been missed. Similar to somatization disorder, hypochondriasis is characterized by the presence of unexplained symptoms or sensations. However, the patient with hypochondriasis takes these symptoms one step further by leaping to a catastrophic cognitive misinterpretation of the significance of these symptoms.

Infectious disease

Linfocitoma Cutis

LYME DISEASE. (See also Chap 16.) Lyme borreliosis (Fig 26-10), a vector-borne infection, can affect several organ systems. Cutaneous manifestations include erythema chronicum migrans (ECM), borrelial lymphocytoma (BL), and acrodermatitis chronica atrophicans (ACA). ECM is the principal cutaneous hallmark of Lyme disease. An initially homogenous erythema starts at the site of the tick bite and spreads in centrifugal fashion. The center may fade or clears leaving an annular erythema. BL, also known as lymphadenosis benigna cutis, often starts at or near the site of the tick bite. Some patients have a preceding or concomitant lesion of ECM. The classic lesion of BL is a solitary bluish-red nodule with regional lymphadenopathy. Sites of predilection include the earlobe, nipple and areola, scrotum, and nose. Lesions of ACA usually develop 6 months to 10 years after a tick bite. The connection between the two is rarely suspected by patients. ACA is a chronic dermatitis of the acral sites....

Spinal Cord Strokes

Spinal infarcts can also develop in relation to infections in the meninges and parasitic invasion of the spinal arteries. Syphilis, tuberculosis, and lyme borreliosis can involve the spinal arteries. Adhesive arachnoiditis can also cause obliteration of spinal arteries and lead to cord ischemia, especially in the central portion of the spinal cord. Schistosomiasis can involve feeding spinal arteries. Hypoxic-ischemic injury to the spinal cord also develops in patients with severe systemic hypotension and shock. In these patients, brain damage usually is more severe than spinal injury and makes it difficult to identify the spinal pathology clinically.