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One of the most disabling symptoms for the patient with Lyme-MSIDS is chronic pain. Over the counter medications only provide minimal really. By the time they seei lyme aware physicians some of the patients are on high dose narcotics to control pain. These patients frequently have seen rheumatologists and, depending on the clinical presentation, they may have been told that they suffer from sero-negative rheumatoid arthritis or from a non-specific auto immune disease. They are then placed on steroids such as prednisone, or disease modifying antirheumatic drug regimens, such as methotrexate. These agents might give temporary relief but can have significant side effects.Pain can be so debilitating that some people lose their ability to function in a meaningful and productive way. Many turned the pain management specialist, who then often prescribe multiple drug regimens to provide pain relief. Despite these physicians best attempts, patients may still have pain, and as the narcotics wear off, higher and higher doses are required to control and discomfort.-the end result is that pain sufferers and up on disability, and are unable to work or go to school.
Lyme disease can cause pain in every part of the body. Although this pain may be limited to one of two areas, and be more or less constant, one particular hallmark of tick areborne disease, and particularly Borrelia Bergdorferi , is that pain comes and goes and migrates.
This includes arthritis pain, myalgia’s (Muscle pain), and neuropathic pain (nerve pain), all of which normally do not tend to migrate. In women the pain is also influenced by hormonal cycles, since women usually flare several days right before, during, and after the Menses.We can also suspect a tick-borne disorder when antibiotic use increases pain (From a Jarisch-Herxheimer reaction) or decreases pain. This will occasionally happen in patients treated for a unrelated bacterial infection such as sinusitis or urinary tract infection, who are unaware that they have lime disease.If pain is associated with multiple systemic symptoms, especially the ones listed in the Horowitz questionnaire, then it is quite likely that it is cause by lyme –MSIDS. A patient who just presents with neck pain or an isolated pain in a joint might simply have a herniated disk with neuropathy, or osteoarthritis.If the patient circles many of the symptoms on this sheet one should suspected tick-borne disorder and order the appropriate tests. Establishing a proper pain aetiology can be difficult, because as we have seen above Lyme – MSIDS can mimic most common pain syndromes.
Simultaneously treating the three I’s of lyme disease- infection inflammation and immune dysfunction may be the key to alleviating chronic pain. Finally inadequate phase I and phase II liver detoxification, with inadequate production or over utilisation of glutathione, and the subsequent inability to remove Neuro toxins and cytokines often seen with lyme– MSIDS, will also result in pain. Many different medical problems that are listed on the MSIDS Map can cause pain, and may be contributing overlapping factors. Each of these different factors can increase free radical production and increase cytokines, and may need to be simultaneously addressed to achieve adequate pain control in both lyme– MSIDS and non-lyme– MSIDS.
These will include
1. Detoxification problems
2. endocrine abnormalities
3. food allergies
4. heavy metals and environmental toxins
5. nutritional and enzyme deficiencies
6. other infections including bacteria parasites viruses and opportunistic infections(Candida)
7. sleep disorders
Psychological disorders may also increase discomfort, as the amygdala is the part of the brain deals with the emotions and pain sensation when patients suffer from depression and anxiety, their pain thresholds can be lowered, leading to increased perception of pain.
Early diagnosis and treatment are important to stop the progression of the Lyme disease. If untreated, the disease can result in neurological disorders such as peripheral neuropathy, including Bell’s palsy, as well as pain, numbness or weakness in the limbs. The onset of peripheral neuropathy typically develops weeks, months or years later, if the disease is left untreated.
While potentially serious, Lyme disease can be treated, especially in the early stages. It is important to take preventive measures when outdoors in areas known to have infected deer ticks. Some helpful steps include: wearing enclosed shoes and light colored clothing; checking clothing and exposed skin frequently for ticks; and using insect repellant containing DEET (Diethyl-meta-toluamide) on skin or clothes.
SYMPTOMS (Not all symptoms and signs may be present.)
Lyme disease progresses in three stages of severity:
• Fever and chills
• Muscle and joint pain
• Red circular rash
• Stiff neck
• Swollen lymph nodes
• Facial paralysis (Bell’s palsy)
• Irregular heartbeat
• Meningitis (fever, stiff neck, severe headaches)
• Numbness and pain in arms and legs
• Stiff neck
• Poor coordination
• Chronic arthritis and swelling in large joints, especially the knees
• Chronic pain in muscles
• Problems with sleeping
• Numbness and pain in arms and legs
• Nervous system problems
• Difficulty concentrating
• Memory loss
• Numbness and tingling
• Peripheral neuropathy
• Pain, numbness and tingling in limbs
• Paralysis of facial muscles (Bell’s palsy)
EVALUATION AND TESTS (Not all evaluation and tests may be necessary.)
• Neurological exam
• Nerve conduction velocity test
• Blood tests, including tests for antibody against the agent that causes Lyme disease and tests to detect the agent itself.
TREATMENT AND THERAPY (Not all treatments and therapies may be indicated.)
• Intravenous therapy For Bell’s palsy (facial paralysis)
• Eye drops for affected eye
• Medications such as steroids to reduce inflammation of nerve and decrease
• Surgery (in rare cases to improve appearance)
• Treatment of underlying inflammatory condition, if present
If experiencing weakness, pain, or inflammation (in limbs or knees)
• Ask your doctor about special therapeutic shoes or a knee brace (which may be covered by Medicare and other insurance)
• Take safety measures to compensate for loss of sensation
• Lyme disease is curable, if treated early
Free pathology test for Lyme/MSIDS: email@example.com
Possible related medical conditions:
1. Lyme disease
3. autoimmune disorders
4. carpal or cubital tunnel or any nerve entrapment syndrome
8. heavy metal toxicity
9. other environmental toxins
10. vitamin deficiencies
11. immune deficiency
12. mitochondrial dysfunction
14. strokes or TIAs
15. anxiety with hyperventilation
Shifting numbness is a classic symptom of Lyme disease.
Mayo Clinic: Neurological problems. Weeks, months or even years after infection, you might develop inflammation of the membranes surrounding your brain (meningitis), temporary paralysis of one side of your face (Bell’s palsy), numbness or weakness in your limbs, and impaired muscle movement.
The Foundation for Peripheral Neuropathy:
Early diagnosis and treatment are important to stop the progression of the disease. If untreated, the disease can result in neurological disorders such as peripheral neuropathy, including Bell’s palsy, as well as pain, numbness or weakness in the limbs. The onset of peripheral neuropathy typically develops weeks, months or years later, if the disease is left untreated.While potentially serious, Lyme disease can be treated, especially in the early stages. It is important to take preventive measures when outdoors in areas known to have infected deer ticks. Some helpful steps include: wearing enclosed shoes and light colored clothing; checking clothing and exposed skin frequently for ticks; and using insect repellant containing DEET (Diethyl-meta-toluamide) on skin or clothes.
SYMPTOMS (Not all symptoms and signs may be present.)
Lyme disease progresses in three stages of severity:
Fever and chills
Muscle and joint pain
Red circular rash
Swollen lymph nodes
Facial paralysis (Bell’s palsy)
Meningitis (fever, stiff neck, severe headaches)
Numbness and pain in arms and legs
Chronic arthritis and swelling in large joints, especially the knees
Chronic pain in muscles
Problems with sleeping
Numbness and pain in arms and legs
Nervous system problems
Numbness and tingling
Pain, numbness and tingling in limbs
Paralysis of facial muscles (Bell’s palsy)EVALUATION AND TESTS (Not all evaluation and tests may be necessary.)
Nerve conduction velocity test
Blood tests, including tests for antibody against the agent that causes Lyme disease and tests to detect the agent itself.TREATMENT AND THERAPY
(Not all treatments and therapies may be indicated.)
Free pathology test for Lyme/MSIDS: firstname.lastname@example.org
Is it normal to be losing your memory as you get older? Is it normal to have an Alzheimer’s
epidemic affecting not only the United States and also the rest of the world? Or is it possible that there are multiple etiologies at the root of these conditions? We find that the majority of lyme patients with co- infections have severe memory and concentration problems.
Evidence of the connection between infection and dementia can be found in a report from pathologist Dr Alan MacDonald who examined brain biopsies from the McLean hospital (an affiliate of Harvard University) data bank from patients with confirmed Alzheimer’s disease.
His PCR analysis show that 7/10 of these patients had the DNA of Borrelia Bergdorferi in their brain, the ETO logic agent of lyme disease. We also fine at The majority of our chronically ill patients with lyme disease and co- infections have been exposed to high levels of heavy meals, such as Mercury and lead, and occasionally to aluminium. These also can cause memory and concentration problems, and can cause the production of elevated levels of free radicals, which can increase inflammation.
Similarly we are exposed to hundreds of environmental chemicals every day that are fat-soluble and therefore are deposited in brain. These can and do affect cognitive processing. We have enough causes for an epidemic of dementia in the general population. Drugs prescribed for Alzheimer’s only slow down the cognitive decline. Horowitz has seen the improvements in cognitive functioning after treating these patients for chronic tick borne infections, by detoxifying them of fat-soluble toxins with glutathione, by using oral chelation agents to remove mercury lead and aluminium, and by identifying and treating B12 deficiencies and/or hypothyroidism.Horowitz screened 50 lyme patients for co- are infections with Ehrlichia, Babesia microti, Mycoplasma, and Bartonella henselae. He reported that treatment with two drugs was better than treatment with one drug, especially where intracellular bugs are concerned.
Horowitz tests for a broad range of co-infections including different strains of babesiosis, Ehrlichia, Anaplasma, Bartonella, Rickettsial infections such as Rocky Mountain spotted fever, Q fever, and typhus, tularemia, Brucella, chlamydia pneumonia, Mycoplasma species, viruses such as EBV, CMV, HHV 6, and parasites such as toxoplasmosis.
And increase in neuropsychiatric symptoms also takes place when a patient has contract in co- infections, such as a babesiosis, where Babesia you can exacerbate underlying lyme disease symptoms including depression.
Other co- infections also can influence psychiatric symptoms. Ehrlichiosis can cause central nervous system symptoms, as can viruses and intracellular infections with Mycoplasma spp. And Chlamydia pneumonia, which are frequently found in MSIDS patients.
Often the patients with the worst neurological symptoms have lyme disease, mycoplasma and/ Bartonella simultaneously, with or without the other co- infections . Bartonella henselae, organism that causes cat Scratch fever, exacerbates many of the neurological and neuropsychiatric symptoms we see with lyme disease, and has been linked to anxiety disorders and depression, as well as various central nervous system abnormalities.
These include encephalomyelitis ( involving inflammation in both the brain and spinal cord, leading to difficulties with cognition and motor function) ; transverse myelitis(inflammation and demyelination of the spinal cord, leaving to difficulty walking); spastic para paresis(stiffness and spasm in the lower extremities, affecting walking); seizures with hemiparesis (Weakness on one side of the body); cerebellar syndromes (Primarily defined by symptoms of dizziness and poor balance) and movement disorders (which can cause a variety of symptoms, including spasms twitching and involuntary movements).
Bartonella can also be transmitted to the foetus. Therefore resistant neuropsychiatric symptoms in children might be linked to maternal transmission of the organism, and should be suspected of the patient is living in a lyme endemic area or has cats at home.
Some patients with Bartonella have other severe neurologic manifestations with a ophthalmologic involvement i.e. inflammation VI manifesting as optic neuritis, episcleritis, conjunctivitis, uveitis or iritis.
Bartonella can also cause an oculoglandular syndrome with preauricular adenopathy and conjunctivitis, neuroretinitis, branch retinal artery occlusion and vision loss. Bartonella should therefore be considered when patients present with particularly severe opthalmological symptoms.
If we look at the symptom complex used to define CFS, we see that the symptoms overlap those seeing in lyme disease and associated co-infections and it explains why lyme disease is frequently misdiagnosed. Apart from the results of a spinal tap, one of the primary differences is the symptoms of persistent lyme disease tend to come and go, fluctuating with good and bad days, and the symptoms tend to migrate.
Free pathology test for Lyme/MSIDS: email@example.com
The first most essential tool for the medical detective is therefore compassion and proper motivation.
Most Lyme patients have a long history of chronic complex illnesses and bring a stack of medical records and a long list of complaints. By meticulously reviewing their records and using the Horowitz questionnaire we can ensure a proper history.
The Horowitz questionnaire also provides the opportunity to formulate the most probable differential diagnosis while interviewing the patient. Taking a history from these patients usually takes an hour.
It usually takes between two and three hours with each new patient to complete a social history, family history, and environmental exposure history and to review their symptoms,conduct a complete physical exam, and assessment, and devise a treatment plan.
This model is quite comprehensive in its scope, and it has the potential to lead to diagnosis and treatment in the shortest period of time while costing the health-care system the least amount of precious resources.
One of the essential problems with the current medical model is that doctors are taught in medical school that there is generally only one a areetiology for each illness. One implication of this model is that if a doctor can’t find a single answer to your host of problems, then they assert that the problem must be in your head, since the sophisticated laboratory tests and imaging studies in modern day clinics and hospitals surely are reliable and comprehensive.
The majority of Lyme patients generally do not have one sole cause for their symptoms. They often have an overlapping set of medical problems.
Horowitz identified sixteen likely categories of illnesses that can occur simultaneously with Lyme disease ‘Lyme-MSIDS’, or exacerbate the symptoms of other diseases that occur without Lyme disease (non-Lyme-MSIDS).
The difficulty in establishing a diagnosis is that Lyme disease can cause symptoms that are seen with each of these sixteen separate medical conditions. Lyme disease like its cousin syphilis, can mimic many illnesses commonly seen in modern day medical practice and exacerbate previous medical problems. For example, if you were always prone to headaches, you may begin to have migraines.
Laboratory Testing to diagnose Lyme disease:
According to the CDC surveillance case definition, late manifestations require laboratory confirmation. This may involve obtaining a positive culture for Borrelia burgdorferi from, blood, skin, a joint or cerebral spinal fluid, or by identifying antibodies to the bacterium in the CSF: the most common method, however, known as the two tier testing algorithm, uses a specific sequence of blood tests. The first is the ELISA, the second is a Western blot.
These are indirect tests of infection because instead of identifying the organism itself, they look for antibodies to Borrelia burgdorferi that were made by the immune system.
ELISA tests measure the total amount of anti Borrelia Bergdorferi antibodies present, while Western blots identify individual antibodies and look for specific proteins patterns that are unique to Borrelia. If enough of Borrelia proteins are present the test is considered to be positive.The CDC points out that there are problems with testing, and that a patient with lime disease may not be diagnose using these criteria. The presently used two tiered testing missed 81% of the lyme cases, especially when the patient did not have a Bullseye rash.One of the most comprehensive reviews of the standard lyme tests comes from a 2005 Study at John’s Hopkins University confirming the poor sensitivity of the ELISA.Another study published in 2007 in the British medical Journal by Ray Stricker MD found that the overall sensitivity of the combined Eliza Western blot was only 56%.
Polymerase Chain Reaction (PCR), a DNA test, is an important diagnostic tool for patients who have negative blood tests, at Many require multiple samples over time, using specimens from different body compartments(Such as serum, aspirated joint fluid, synovial tissue, urine, cord blood, placenta, and/or spinal fluid), and it must be performed at a reliable laboratory. The PCR has an overall sensitivity of around 30% when any individual specimens, with a specificity of over 99% (It is highly specific for the disease, with a few false positive results). New tests increased the sensitivity to 62% in early lyme disease. Horowitz says that he may need to send off several sets of PCRs on blood or urine before getting back a positive result.
Other tick borne diseases such as the Babesia and Bartonella can be transmitted with the same tick bite the transmits lyme disease. These diseases complicated clinical presentation often making the symptoms of lyme disease much worse.
Horowitz created the differential diagnostic system as a roadmap for identifying multiple components of MSIDS. Health care providers finally have a single tool that organises the list of seemingly unrelated symptoms that a chronically your patient brings to the doctor.
Chronic inflammation lies at the heart of most chronic illnesses, and addressing the underlying causes of inflammation, using the MSIDS Map, has the potential to decrease inflammation and improve health.
The initial inflammation may have developed as a direct effect of lime disease and associated coinfections, or it could be a response to an over stimulated immune system, environmental toxins, food allergies, or an associated sleep disorder.
The MSIDS model offers an intelligent and sensible path to help diminish the cost and the burden of disease for Lyme and associated co-infections. By not driving lyme patients to search relentlessly and fruitlessly, year after year, for other diseases that might be responsible for symptoms, it provides the methodology for processing diagnosis and treatment options that can save millions of dollars annually.
MSIDS: overlapping factors contributing to chronic illness
1. Lyme disease and co- infections
2. Immune dysfunction
4. environmental toxins
5. functional medicine abnormalities with nutritional deficiencies
6. mitochondrial dysfunction
7. endocrine abnormalities
8. neurodegenerative disorders
9. neuropsychiatric disorders
10. sleep disorders
11. autonomic nervous system dysfunction and pots
13. gastrointestinal disorders
14. liver dysfunction
15. pain disorders/ addiction
16. lack of exercise/ deconditioning
Horowitz on page 68 of his text describes the appropriate laboratory testing for medical conditions associated with his 16 point MSIDS Map. This approach allows us to combine different intracellular medications simultaneously to maximise the effect and reduce possible side-effects.
Perhaps the patient has not gotten well because he/ she suffers from adrenal fatigue with a low cortisol levels. This condition is quite commonly soon in patients with MSIDS. These patients may need adrenal supplements and/or hydrocortisone. Often we will see clinical improvements once a patient’s adrenal function is normalised.
Poor sleep can be the reason the patients fatigue and memory and concentration problems processed. Or perhaps they have nutritional deficiencies in magnesium, iodine or zinc, which are needed for proper hormone production, detoxification and immune function.
Other possibilities include mitochondrial dysfunction from oxidative stress which has not been corrected, or perhaps they have a parasite that has not yet been discovered and are decondition from a lack of exercise, which could account for their ongoing fatigue.
Free pathology test for Lyme/MSIDS: firstname.lastname@example.org
Bio Resonance: This circuit solves 90% of Lyme disease phenotype changes: contact Us for details:
Changing phenotypes complicate Western Medicine diagnosis and treatment of Lyme disease!
A phenotype results from the expression of an organism’s genes as well as the influence of environmental factors and the interactions between the two.
Because the physical characters (phenotypes) of the infections associated with Lyme disease are constantly changing it is not possible to have precise testing and treatment of these organisms through traditional pathology.
Persister organisms with their changed phenotypes are the most significant reason that Western medicine cannot reliably test & treatLyme disease:
Lyme disease caused by Borrelia burgdorferi and co-infections is the most common vector borne disease in the United States and Europe.1,2 The current treatment for Lyme disease is a 2-4 week antibiotic monotherapy with doxycycline, amoxicillin or cefuroxime.3 While this treatment is effective for Lyme disease patients, if treated in the 6weeks following infection, about 10%-20% of patients still have persisting symptoms such as fatigue, muscular pain, and neurological impairment even six months after the treatment,1 a collection of symptoms called Post Treatment Lyme Disease Syndrome (PTLDS).4 While the cause of PTLDS remains unclear and controversial, several hypotheses have been proposed to explain PTLDS, including host response to continued presence of bacterial debris,5 autoimmunity,6 co-infections,7 and presence of bacterial persisters not killed by the current Lyme antibiotics.7Consistent with the persisting organisms not killed by current antibiotics, experiments in various animal models such as mice, dogs and monkeys have shownB. burgdorferi could still be detected after treatment with different Lyme antibiotics though viable organisms could not be cultured.8,9,10In vitro studies also demonstrated that B. burgdorferi could develop antibiotic tolerant persisters.11 Although persister mechanisms have been reported in the model organism E. coli,12 the mechanisms of B. burgdorferi persisters remain unknown.
Our findings not only shed new light on the mechanisms of B. burgdorferi persisters but also have practical applications. For example, the upregulated genes identified in B. burgdorferi persisters may not only serve as targets for developing new drugs for more effective treatment but also antigens for developing diagnostic tests for persistent Lyme disease, and finally for developing therapeutic vaccines for improved treatment. Future studies are needed to address these possibilities for more effective control of Lyme disease.
Dr Horowitz summed it up:-
Major universities are finally taking an interest in persister bacteria and their role in contributing to chronic symptoms in patients with Lyme disease. Dr Ying Zhang and researchers from Johns Hopkins University just published on Borrelia persisters in Emerging Microbes and Infections where they identified the gene expression profile for Bb persisters that survived antibiotic treatment with doxycycline and amoxicillin. They found differences in transporter genes, bacterial envelope protein coding genes, DNA repair related genes, bacterial chemotaxis genes, bacterial secretion genes, and genes encoding proteases. Comparison of the pathways of the doxycycline persisters and amoxicillin persisters revealed that they share several common features where some genes were up regulated and some down regulated. “These gene expression changes may play important roles in facilitating survival of B. burgdorferi persisters under antibiotic stress…and the upregulated genes identified in B. burgdorferi persisters may not only serve as targets for developing new drugs for more effective treatment but also antigens for developing diagnostic tests for persistent Lyme disease, and finally for developing therapeutic vaccines for improved treatment”. The MSIDS map identifies up to 16 different reasons why patients may stay ill after classical treatment for Lyme disease. Persistent infection with borrelia species and co-infections certainly plays a large role in chronic illness, but we must also treat associated inflammation, autoimmune reactions, detoxify internal and external biotoxins, repair the damage caused by free radicals and oxidative stress which damage mitochondria, nerves, brain cells and internal organs, while balancing cytokines, hormones, and the microbiome. Once all of the associated factors on the 16 point MSIDS map have been adequately addressed, the vast majority of my patients improve. A large thanks goes out to the Global Lyme Alliance for their support of this research, and to Dr Zhang and his colleagues at Johns Hopkins for continuing to search for answers for this debilitating illness.
The tick is one carrier of the disease:
How is it possible that an epidemic of tick-borne diseases could be spreading without getting the proper attention from Western Medicine and politicians ? How could patients throughout the world continue to be desperate for help?
Sixty years ago, Nobel Prize-winning scientist Joshua Lederberg first described a biological mystery. He showed how bacteria could lose the cell walls that define their shapes, potentially becoming less visible to the immune system, only to later revert back to their original form and regain their full infectious potential.
Click on Dr Klinghardt’s name at the top of this page
for his scientific approach to Lyme disease.
This disease can spread throughout the body from the site of the initial bite, and even within 24 hours can invade the central nervous system.
The most common Lyme related inflammation causes:
optic neuritis: inflammation of the optic nerve
iritis: inflammation in the anterior chamber of the eye
Meningococcal disease is an uncommon, unpredictable, and serious disease that can include meningitis (infection of the lining of the brain and spinal cord) and/or sepsis (blood infection). Even with appropriate treatment, roughly 1 in 10 people who contract meningococcal meningitis or sepsis diewithin 24 to 48 hours from the start of symptoms, and those who survive may face severe consequences, such as loss of arms or legs, brain damage, or hearing loss.1,2
encephalitis: inflammation in the sac, surrounding the brain and in the brain tissue itself: inflammation of the brain and spinal cord
carditis: inflammation of the heart
Lyme arthritis: inflammation of the joints
multiple sclerosis:numbness in body, tingling, pin pricks
Burning/stabbing sensations in the body, burning in the feet
Weakness or paralysis of the limbs
Tremors or unexplained shaking: stroke
Poor balance, dizziness, difficulty walking
Increased motion sickness, wooziness
Encephalopathy (cognitive impairment from brain involvement)
Academic or vocational decline
Difficulty with organisation and planning
Auditory processing problems
Word finding problems
Slowed speed of processing
Head Face Neck
Facial paralysis (like Bell’s Palsy)
Tingling of nose, cheek or face
Sore throat swollen glands
Heightened allergic sensitivities
Twitching of facial/ other muscles
Change in smell, taste
Skin: Benign tumour-like nodules
Erythema Migrans (rash)
Night sweats or unexplained chills
Diminished exercise tolerance
Heart block, murmur
Chest pain or rib soreness
Ringing or buzzing in ears
Pain in ears
Forgetfulness, memory loss (short or long term)
Poor school or work performance
Attention deficit problems, distractibility
Confusion, difficulty thinking
Difficulty with concentration, reading, spelling
Disorientation: getting or feeling lost
Mood swings, irritability, agitation and anxiety
Depression, anxiety, personality changes, malaise
Aggressive behavior impulsiveness
Suicidal thoughts, rare cases of suicide
Over emotional reactions crying easily
Disturbed sleep, too much, too little, difficulty falling asleep or staying asleep
Suspiciousness, paranoia, hallucinations
Feeling as though you are losing your mind
Obsessive compulsive behavior
Bi-polar disorder/ manic behavior
Schizophrenia like state including hallucinations
Lyme disease (LD) is the world’s leading tick borne infection caused by the spirochete,Borrelia burgdorferi (Bb). This infection is a global health concern and is associated with numerous cardiologic, dermatologic, rheumatologic neurologic, and psychiatric manifestations (Bratton et al., 2008). Only a few epidemiologic studies have evaluated the frequency of antibodies to Bb in psychiatric patients; one study found only 1/517 (0.2%) of all adult psychiatric patients had Lyme titer seropositivity (Nadelman et al., 1997) and the other larger study found that 322/926 (35%) of psychiatric inpatients had seropositivity to antibodies to Bb (Hajek et al., 2002).
If you would like a copy of the Hajek paper please contact us through the ‘Free testing’ tag at the top of this page,
Joint pain swelling or stiffness
Shifting joint pain: Fibromyalgia
Muscle pain or cramps
Poor muscle coordination, loss of reflexes
Loss of muscle tone, muscle weakness
General Well Being
Upset stomach (nausea, vomiting)
Unexplained weight loss or gain, loss of appetite, anorexia
To understand the answer to this dilemma, you need to understand the intricacies of Lyme disease and the conditions controlling doctors and health authorities.
Treating Lyme Disease:
Doctors have been forced to enter the battle against Lyme Disease. Many have already been forced out of medicine, lost their licences, or been forced to undergo medical monitoring, because they have not followed guidelines sanctioned by medical licensing boards.
They have spent hundreds of thousands of dollars in legal fees to uphold their licences.
Antibiotics for Lyme Disease:
Consequently, many states, including Rhode Island and California, have formally recognised that it is not professional medical misconduct to use longer term antibiotics to treat Lyme disease.
The ineffectual testing and ineffective paradigms that modern medicine offers provide no satisfactory answers.
Without a paradigm shift, the present approach to this epidemic ensure that the suffering will continue.
Dr Horowitz believes that the identification of MSIDS, multiple systemic infections disease syndrome, may prove to be the missing link to end this war once and for all.
One year it was the clue that led to the identification of a strain Babesia microti, a malaria like illness that could explain the fevers, chills, and day & night sweats and that account for some of their resistant symptoms.
Once treated, some patients using wheel chairs could stand and walk.
Next was the discovery of cat scratch disease symptoms, or Bartonella, which could explain their resistant neurological symptoms, such as treatment-resistant neuropathy or encephalopathy.
Next was the uncovering of Mycoplasma fermentans, the organism suspected in Gulf War syndrome and possibly a contributor to some patient’s ALS-type symptoms.
More recently we have been able to link the presence of heavy metals, such as mercury, lead, arsenic, cadmium, and aluminium, with patient’s overlapping symptomatology.
These can be treated with IV glutathione and oral chelation regimens such as DMSA to detoxify treatment resistant patients.
The results have been astounding. You need to know that your symptoms are not only real and identifiable, but they are treatable.
Treating Chronic Lyme:
Many people who have received treatment for Lyme disease do not feel well either during treatment or once the courses of antibiotics are completed.
For these patients, the Horowitz sixteen point differential diagnostic map is the best way to determine if they are suffering from MSIDS (multiple systemic infection disease syndrome).
Patients with complex chronic illnesses, no matter which diagnosis they receive, often have simultaneous bacterial, parasitic, viral and fungal causes for their illness.
Many times they also have associated immune dysfunction, large environmental toxic loads, hormonal dysfunctions, mitochondrial dysfunction, allergies, sleep disorders, or underlying psychological dysfunction.
The history of Medicine:
Medicine is a continuously changing and expanding field.
It is said that almost half of what is learnt at Medical School will usually be proven to be wrong every five to ten years. But along the way to modern medicine, some medical pioneers have been dismissed or even attacked for what others believed were their heretical ideas.
Semmelweiss discovered that washing his hands before delivering a child prevented puerperal sepsis that kills women after giving birth. When he shared his findings with colleagues he was ridiculed. As patients abandoned his colleagues and begged to deliver in his clinic, he was ostracized by his medical society and driven out of medicine. He was committed to an asylum, where ironically, he died of septicemia after being severely beaten by his guards.
Dr Louis Pasteur who was ridiculed and it was years before his germ theory causing illness was proven to be correct.
Australian doctors Barry Marshall and Robin Warren discovered Heliobacter pylori in the stomachs of patients with gastritis and stomach ulcers. They also proposed that treatment with antibiotics rather than stomach removal, were best for ulcer patients. Their discovery was ignored for 20 years, until proof led to Nobel prizes in medicine .
Many of these pioneers pushed the boundaries until the paradigm of that specific disease process was transformed. Are things different today? Have we learnt to listen to those challenging the medical establishment? Certainly not with respect to Lyme Disease and associated tick-borne disorders.
History of Lyme Disease:
In the mid 1970s, when portrait painter Polly Murray first noticed an outbreak of what had been called “juvenile rheumatoid arthritis” in the town of Lyme, Connecticut, that had affected her and her children from decades earlier.
Dr Alan Steere, a rheumatologist at Yale University, was called in to investigate the epidemic, as were researchers from the National Institutes of Health (NIH) and Rocky Mountain Labs.
Dr Willy Burgdorfer, a researcher at Rocky Mountain Labs, identified a microscopic spirochete, a spiral shaped bacteria that resembles the one that causes syphilis. This was eventually identified as the causative agent of the newly identified disease, and the spirochete was named Borrelia burgdorferi (Bb) after Dr Burgdofer’s discovery, and the related disease was caused Lyme, after its initial outbreak in the town of Lyme, Connecticut.
By 1977 Dr. Steere was reporting a whole host of specific and often bizarre signs of this new disease, including fever, fatigue, headache, migratory joint pains, as well as multiple cardiovascular and neurological abnormalities.
If a Lyme disease patient presents with 35 different symptoms, the established paradigm would be to try and explain these complaints according to the accepted medical model: one primary diagnosis.
If the doctor could not find a single aetiology, or cause, for your symptoms, it must be because it is psychological in nature, and you are crazy.
Or the answer maybe elusive because the symptoms can’t be understood in the HMO-dictated fifteen minute time frame.
Getting to the source of chronic illness:
The Horowitz Lyme-MSIDS Questionnaire:
This essential questionnaire is based on one developed by Dr joseph Burrascanowhen he started treating Lyme disease patients. You can use the following questionnaire to determine the probability of a Lyme MSIDS diagnosis for yourself.
All of the points on the list in section 1 are symptoms that can be seen with lyme disease. They are not specific to lyme disease in and of themselves, and can be found in many other illnesses. However the advantage that can be perceived by looking at all of the symptoms simultaneously helps the clinician reach a probability as to whether the patient may suffer from Lyme disease and associated tick-borne disorders.
At the same time this list can also be used to identify simultaneous overlapping disease states, so that the true source of the patient suffering is discovered.
These multifactorial causes of illnessare often at the heart of most chronic diseasestates, and this led Dr Horowitz to create the MSIDS model.
Sections 2 and 3 of the questionnaire represent those signs and symptoms complexes most associated with Lyme and MSIDS, which Dr Horowitz has compiled after examining hundreds of our patients charts over the last decade.
Section 4 is based on two of the four questions in the healthy days core module used by the CDC to track population trends nationally and identify healthcare disparities, and it helps us identify the frequency of physical and mental health problems in the preceding month.
Talk to your doctor about the results of this questionnaire. Depending on your score you may want to follow up with blood tests for lyme disease or electrotherapytesting with Hope Australia (0412 994 001).
Do not just rely on the CDC criteria of using Eliza in a two tiered testing protocol as this is not sensitive enough to confirm the diagnosis. You can use this questionnaire as the starting point of the decision-making detective work that will lead you to the proper diagnosis.
Remember, Lyme disease is a clinical diagnosis and the blood tests only help to confirm your clinical suspicion.
Answer the following questions as honestly as possible stop think about how you have been feeling over the previous month and how often you have been bothered by any of the following problems. Score the occurrence of each symptom on the following scale none, mild, moderate, severe.
Lyme Disease Symptoms:
Section 1: Symptom frequency score: circle your score number:
32. difficulty with concentration or reading0 1 2 3
33. forgetfulness poor short term memory0 1 2 3
34. disorientation getting lost going to the wrong places 0 1 2 3
35. difficulty with speech or writing0 1 2 3
36. mood swings irritability depression0 1 2 3
37. disturbed sleep too much too little early awakening 0 1 2 3
38. exaggerated symptoms or worse hangover from alcohol 0 1 2 3
Add up your totals from each of the four columns . This is your first score.
Section 2 : Most common Lyme symptoms score:
If you rated a three for each of the following in section 1, give yourself five additional points :
Forgetfulness poor short-term memory
joint pain or swelling
tingling numbness burning or stabbing sensations
disturbed sleep too much too little early awakening
Section 3 lyme incidence score
Now please circle the points for each of the following statements you can agree with:
1. You have had a tick bite with no rashor fluke symptoms 3 points
2. You have had a tick bite, an erythema migrans, or an undefined rash, followed by flu like symptoms 5 points
3. You live in what is considered a Lyme-endemic area2 points
4. You have a family member who has been diagnosed with Lymeand/or other tick borne diseases 1 point
5. You experience migratory muscle pain4 points
6. You experience migratory joint pain4 points
7. You experience tingling/burning/ numbness that migratesand/or comes and goes 4 points
8. You have received a prior diagnosis of chronic fatigue syndrome or fibromyalgia3 points
9. You have received a prior diagnosis of a specific autoimmune disorder (lupus, MS, or rheumatoid arthritis), or of a nonspecific autoimmune disorder3 points
10. You have had a positive Lyme test(IFA, ELISA, Western blot, PCR, and/or borrelia culture) 5 points
Score for Section 3 ( )
Section 4: Overall health score:
1. Thinking about your overall physical health, for how many of the past thirty days was your physical health not good? __________Days
Award yourself the following points based on the total number of days:
0-5 days = 1 point
6-12 days = 2 points
13-20 days = 3 points
21-30 days = 4 points
2. Thinking about your overall mental health, for how many days during the past thirty days was your mental health not good? _________days
Award yourself the following points based on the total number of days:
0-5 days=1 point
6-12 days=2 points
13-20 days=3 points
21-30 days=4 points
Score for Section 4.2
Record your total scores for each section below and add them together to achieve your final score:
Section 1 Total:______
Section 2 Total:______
Section 3 Total:______
Section 4 Total:______
This is a published example of Phenotype switching which has limited the capability of Western Medicine to diagnose and treat the infections associated with Lyme disease:
Melanoma switches phenotypes to become metastatic and drug-resistant
Phenotype switching may be involved in changing the appearance of melanoma tumors by altering the number and type of protein receptors that dot the surface of the individual melanoma cells within a tumor. Identifying the phenotype that patients exhibit may help determine which patients are more likely to benefit from existing medications while also providing an opportunity to create new targeted therapies.
“We were able to demonstrate for the first time that different receptors within a single signaling pathway—in this case, the Wnt signaling pathway—can guide the phenotypic plasticity of tumor cells, and increased signaling of Wnt5A in particular can result in an increase in highly invasive tumor cells that are less sensitive to existing treatments for metastatic melanoma,” said Ashani Weeraratna, PhD, of The Wistar Institute in Philadelphia, Pennsylvania.
While melanoma accounts for less than 5% of all cases of skin cancer, it is the deadliest form of the disease, resulting in the majority of deaths related to skin cancer, according to the American Cancer Society. The 5-year survival rate for patients with metastatic melanoma is about 15% to 20%, and although new, targeted therapies designed to combat the disease based on a person’s genetics have become available in recent years, some of these drugs are not effective in many patients, and many who do respond well to the drugs often eventually become resistant to them.
Weeraratna’s team focused on Wnt5A, a Wnt signaling molecule that has been found in increased levels in metastatic melanomas. In order for Wnt5A to promote the phenotype switch from early in the tumor’s formation to the time it becomes metastatic, the tyrosine kinase receptor ROR2 is required. When ROR2 is not present, Wnt5A is unable to promote tumor metastasis. The only other member of the family that has been identified is ROR1, and this research was done to determine what role ROR1 might play in the progression of melanoma.
The researchers were able to determine that ROR1 inhibited the invasion of melanoma cells, and ROR1 was targeted for degradation by Wnt5A and ROR2. When ROR1 was silenced, the researchers observed that there was an increased rate of invasion of melanoma cells both in vitro and in vivo.
In addition to laboratory studies in cells and mice, the researchers tested their hypotheses in a small cohort of patients. They found that seven out of nine patients who demonstrated less than a 33% clinical response to vemurafenib had a positive expression of Wnt5A, and only two of the remaining 15 patients who had a 38% or greater clinical response to vemurafenib exhibited any Wnt5A expression.
Additionally, in eight patients who had undergone BRAF inhibitor therapy, the levels of Wnt5A were much lower in tumor cells prior to therapy compared to cells that were tested for Wnt5A after those same patients had relapsed. The study was published in Cancer Discovery (2013; doi:10.1158/2159-8290.CD-13-0005).
How cells change their phenotype
David Tosh & Jonathan M. W. Slack
Recent attention has focused on the remarkable ability of adult stem cells to produce differentiated cells from embryologically unrelated tissues. This phenomenon is an example of metaplasia and shows that embryological commitments can be reversed or erased under certain circumstances. In some cases, even fully differentiated cells can change their phenotype (transdifferentiation). This review examines recently discovered cases of metaplasia, and speculates on the potential molecular and cellular mechanisms that underlie the switches, and their significance to developmental biology and medicine.
How do infections change their phenotypes? Huang
Now, using time-lapse microscopy and other new techniques, Stanford bioengineering professor K.C. Huang and colleagues at Stanford and Princeton have created a forensic account detailing exactly how bacteria pull off this shape-shifting trick.
The experiments they describe in Molecular Microbiology now offer a step-by-step explanation of this curious behavior, and also shed light on one of the ways bacteria may develop antibiotic resistance.
Huang’s team experimented with E. coli, one of the bacteria that can cause food poisoning. It’s also a favorite of laboratory scientists, who have studied the organism for over 100 years.
Their experiments focused on the rigid cell wall that gives E. coli its characteristic rod-like shape.
In the wild, the cell wall exists to protect the bacterium, but it also send out signals that can alert our immune system to the presence of a potentially infectious intruder.
“A bacterial cell that’s growing is also constantly shedding parts of its cell wall, similar to how a snake sheds its skin every so often,” Huang said. “If a bacterium could get rid of its cell wall, it could effectively go undercover and avoid giving off the signals that its infected host might use to try to mount a response against this invader.”
When the rigid cell wall is dissolved, the bacterium becomes a shapeless blob called an L-form.
In the 1950s, Lederberg, who later founded the genetics department at Stanford, showed that E. coli could survive for a time as L-forms and then recover their rod-like shapes in a process called reversion.
Huang’s team created a molecular-level understanding of the process that Lederberg first observed. They used high-resolution microscopes to record time-lapse images of rod-shaped E. coli cells becoming L-form blobs and then reverting to rod-shaped again.
Follow the proteins:
E. coli’s cell wall is knitted together by proteins, a class of molecules that work together to perform many biological functions.
Using time-lapse microscopy, Stanford bioengineer K.C. Huang and colleagues reveal how bacteria lose the cell walls that define their shapes, become less visible to the immune system, then revert to original form and regain full infectious potential. Credit: Tom Abate and Vignesh Ramachandran
“It’s like an orchestra in which several proteins perform different roles required to build the cell wall,” Huang said.
But those studies focused on normal, rod-shaped E. coli. In this experiment, Huang’s team wanted to understand how MreB factored into the process by which L-forms reverted back to normal.Previous research has shown that one protein, MreB, acts like the conductor, coordinating the efforts of several other proteins.
“We had a suspicion that as the conductor of this orchestra during regular growth, MreB might also be critical for reversion,” Huang said.
Under the tireless gaze of their time-lapse microscope, the researchers grew E. coli cells dosed with the antibiotic cefsulodin. A relative of penicillin, cefsulodin prevents E. coli from building cell walls.
The cefsulodin did not kill the E. coli, but as the cells divided and created successive generations, the bacteria lost their rod-shaped walls and became blob-like L-forms.
The bioengineers let the L-forms grow and reproduce for a few hours before flushing out the cefsulodin. All the while they kept these blobs under microscopic surveillance. As the cells continued to reproduce, the time-lapse images showed that later generations slowly regained their rod-like shape.
That experiment documented the process of reversion to standard form. But it did not prove that MreB was essential.
To demonstrate the link between the rod shape and MreB, the engineers performed a variation on this experiment.
After adding cefsulodin and letting the rod-shaped E. coli reproduce to become shapeless L-forms, they once again flushed out the antibiotic.
But this time, they added a different antibiotic that specifically suppressed MreB function.
Two hours later, the cell walls returned, as a rigid structure protecting the cell.
But this time the cells were still shaped like blobs, and eventually all of these misshapen cells died.
“What we found was very stark: MreB was critical for this reversion process to occur, and without MreB what would happen is that the cells would just expand in size without any notion of their normal shape,” Huang said.
In addition to offering fundamental insights into how cells maintain their structures, Huang said the findings could help researchers understand how some bacteria adapt to stressful environments.
Many antibiotics, including penicillin, target the cell wall. But bacteria can lose their cell walls and then later recover their shapes. This process of reversion might explain how bacteria develop resistance to bacteria and establish chronic infections. The populations that survive in L-form and revert to their original shape may not be as susceptible to the next dose of antibiotics.
“Better understanding of cell wall construction could lead to better antibiotic strategies,” Huang said. “And I’m always amazed to discover ways in which biology is programmed so robustly.”
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