Collection of articles below related to Lyme & ME/CFS..
Is it Lyme or ME?
This excellent article explores the similarities between Lyme & ME.
Extracts are inserted below – full text is available at the link above (I suggest reading the full article if you have been diagnosed with ME!)
Many people in the United Kingdom with M.E. who are now being tested privately are finding they are infected with bacteria from the Borrelia Burgdorferi species that cause Borreliosis or Lyme disease. It wouldn’t be surprising if a very significant percentage of those currently with a diagnosis of M.E. are actually infected with Borrelia or similar bacteria. An e-mail group poll showed that 80% of those with a diagnosis of Borreliosis or Lyme disease had a previous diagnosis of M.E.
Many UK doctors don’t know that you can get infected with Borrelia from ticks in the UK. The Natural History Museum tested many of its UK specimen ticks (PCR testing) and found between 8 and 97% were infected depending on the species of the tick. Some of the specimens were 100 years old. Another study from Swansea showed 30% of ticks in woods in South Wales were infected with Borrelia and 7% with a co-infection erlichosis. It can only take one tiny tick bite from an infected tick for a human to become infected – a bite that goes totally unnoticed more often than not.
Diagnosis & Testing
• The illness should be diagnosed by clinical evidence rather than by tests alone since these are not reliable enough.
• If a bull’s eye rash occurs, treatment should start immediately without testing, as tests may be negative in the very early stages.
• An active infection can exist when there is a negative serology test.
Antibody tests for Borreliosis/Lyme are highly unreliable for a number of reasons some of the main ones being:
• Borrelia infections cause malfunctioning of the immune system. Co-infections only add to this.
• The infection can go into cyst form which reduces the immune response.
• In a recent infection – the immune response may not have taken hold.
• If the disease is in the late stage – those who are chronically infected very often have negative antibody tests.
Irish M.E. Trust
Members of the organisation will receive a quarterly magazine produced by ME Action UK plus supplemented courses on pain management, Alexander technique, EFT etc. that take place around Ireland. Once a year they hold an ME therapy week & also have regular writer’s club meetings.
The role of infectious agents in ME (CFS)
Many CFS patients report an infectious-like onset of their illness, and much research has thus been conducted to identify a possible causative infectious agent for CFS. The fact that outbreaks of CFS have occurred in the past—and the observation that there seems to be a higher rate of onset during the cold season—also supports the hypothesis that an infectious illness can trigger the onset of CFS.
In a review of the scientific literature published before the year 2002, Evengard and Klimas6 conclude that various infectious agents may trigger the onset of CFS. Epstein Barr virus (EBV), the causative agent of IM and Borrelia burgdorferi (the spirochete causing Lyme disease) were most commonly cited.
Both of these agents are polyclonal immunologic activators, and could thus trigger the disease through activation of the immune system. Other possible triggering agents suggested included cytomegalovirus (CMV), human herpesvirus (HHV) type 6 and 7, Borna Disease virus (BDV), various enteroviruses, as well as Chlamydia and Mycoplasma species. Evidence for a persistent chronic infection in CFS sufferers was only found for two agents, however, HHV-6 and possibly Mycoplasma species.
Several studies published after 2002 reported results that might shed some more light on the possible role of infectious agents in the pathogenesis of CFS.
• A study involving 150 subjects with a history of IM found support for the
existence of two discrete post IM chronic fatigue syndromes, one of which was still demonstrable 4 years after onset.
• Lane et al reported the detection of enterovirus sequences in muscle biopsy
samples from 20.8% of CFS patients, but not in any of their control samples.
• Nicolson et al found a high prevalence of mycoplasmal (52%), Chlamydia
pneumoniae (7.5%), and active HHV-6 (30.5%) infections in 200 CFS patients.
Parts of those findings were in agreement with a number of previous studies that had consistently found evidence of chronic mycoplasmal infection in about 50% of CFS sufferers.
• Another study (including 22 monozygotic twin-pairs discordant for CFS),
however, found no evidence of an increased prevalence of active HHV-6, HHV-7, HHV-8, CTV, EBV, herpes simplex virus, varicella zoster virus, JC virus, BK virus, or parvovirus B19 infections in CFS sufferers.
• Gustaw reported the development of CFS in as many as 71% of borreliosis
patients and in 24% of subjects with a history of tick-borne encephalitis.
In summary, it thus appears that the presence of chronic mycoplasmal infections might play a role in the perpetuation and/or development of CFS, while several viruses and bacteria (especially B. burgdorferi) may trigger the onset of the disease, but do not seem to be consistently associated with its perpetuation.
All Roads Lead to Rome – Why do Misdiagnosed Illnesses Respond to Lyme Treatment?
NB: link now broken but have left for informational purposes..
by Dawn Irons, Editor
Recently the Centers for Disease Control and Prevention (CDC) have recognized Chronic fatigue Syndrome (CFS) as an actual disease, and not just a multitude of symptoms. This is a major breakthrough for those who have suffered from the disease for many years. More often than not, CFS patients have endured the scorn of both doctors and the general public. For ages, those who have battled CFS have been called lazy, hypochondriacs, and leeches to the social service system, for the help they needed and received, due to their illnesses.
It is estimated that more than 40 million Americans suffer from Chronic Fatigue Syndrome—now classified as an authentic disease. The CDC believes that only 20% of CFS sufferers actually get diagnosed. This is due, in part, to the lingering belief that CFS is a psychological illness and somehow imagined. CFS is characterized by incapacitating fatigue, sleep difficulties, problems with shortterm memory and concentration, and typically accompanied by flu-like symptoms.
In August 2006, Dr. Kenny De Meirleir, Professor of Physiology and Internal Medicine at Free University of Brussels in Belgium, released a new study on the advances of CFS testing and treatment. The study showed a wealth of confirmed biochemical abnormalities in CFS patients. Dr. De Meirleir’s research showed that CFS patients could be differentiated from healthy people with 99% accuracy based on his test of low molecular weight (LMW) RNase L in the blood.
Dr. Jonathan Forester, of Pineville, Louisiana has been studying CFS in his medical practice for over 20 years. At one point in his medical practice he began noticing the striking parallels between his CFS patients and his Lyme disease patients. He began testing his CFS patients for Lyme disease and over 90% came back positive for Lyme. Of those 90%, when he began treating them for Lyme disease, 80-90% were able to get into complete remission of the disease.
Dr. Forester said, “Until proven otherwise, Chronic Fatigue Syndrome is Lyme Disease.”
Lyme Disease has been given the nickname of “The Second Great Imitator”. The original “Great Imitator” was syphilis, which is a spirochetal disease just as Lyme disease is a spirochetal disease. Lyme Disease is notorious for being difficult to diagnose and treat due to its similar symptoms to other diseases such as Multiple Sclerosis, ALS (Lou Gherig’s Disease), Lupus, CFS, Fibromyalgia, Alzheimer’s disease, and Parkinson’s disease. Many a Lyme patient has received one or more of those diagnoses prior to getting their Lyme diagnosis.
In recent studies it has been shown that Multiple Sclerosis has been thought to be of a bacterial origin. When treated with long-term antibiotics, many of the MS patients had a significant return of bodily function. Many who had been in wheelchairs are now walking after treating with long-term antibiotics. New studies in Alzheimer’s patients are showing the borrelia spirochete in both spiral and cyst forms in almost 95% of the autopsied brain tissue samples. Similar results have been shown in studies involving ALS and Parkinson’s disease.
I just find it curious that all these diseases that Lyme sufferers were misdiagnosed with having, prior to getting their Lyme diagnosis and treatment, are now actually responding to the Lyme treatments of long-term antibiotics with great results and return of bodily functions!
Could it be that there may be one common denominator? Could the borrelia spirochete possibly be behind all of these? I suppose only time and more research will tell. At least for now, we know through research that ALL of these diseases are responding to one common treatment…the long-term antibiotic treatment used for Lyme disease. Shakespeare wrote in Romeo and Juliet, “What’s in a name, that which we call a rose, by any other name would smell as sweet…”. Shakespeare makes a good point! Call it what you want…ALS, MS, Parkinson’s, Lupus…. but if it responds to Lyme treatment…give me the antibiotics and call it want you want! I prefer to keep my ability to walk and form clear thoughts. Let the scientists argue over what to name it…just give me the treatment that works!
After all, it should be an issue of informed consent, right? In a perfect world, patients would be made aware of these new research findings and given the chance to make the choice of available treatment options…but alas, we live in a day where every research foundation wants to collect dollars for their particular designer name disease, while the patients are left of suffer. Let the researchers call a rose “a daffodil” if they like, just give us the water for the roots!
Late and Chronic Lyme Disease: Symptom Overlap with Chronic Fatigue Syndrome & Fibromyalgia
May 15, 2002
By Sam Donta,M.D.
DISCRIMINATING BETWEEN CHRONIC FATIGUE AND IMMUNE DYSFUNCTION SYNDROME AND LYME
By Dana Wiseman, MD, Glastonbury, Connecticut
A currently available and cost-effective way to discriminate between bacterial illness, such as Lyme Disease, and viral illness, as Chronic Fatigue and Immune Dysfunction Syndrome is suspected to be, is the antibiotic trial. It not only has diagnostic value, but can be therapeutic as well.
In Lyme Disease, as in syphilis, patients on antibiotics will usually have Jarisch-Herxheimer reactions; one would not expect these in a viral illness. A Herxheimer, or die-off, reaction is a worsening of symptoms that occurs when spirochete antigens are released and cause immune activation.
This immune activation is similar to the proposed mechanism for symptoms in Chronic Fatigue and Immune Dysfunction Syndrome. These symptoms include: headache, body pain, sweating, insomnia, fever, confusion; in short, a flare-up of earlier symptoms. Herxheimer reactions usually appear in the first week of taking oral antibiotics and within the first three days on intravenous antibiotics.
They can occur for many weeks and return at any time as more organisms are killed, usually with an escalation or a change in therapy. Often, a similar phenomenon of symptom flare-up occurs every fourth week, when large numbers of organisms are dividing and therefore susceptible to the destructive action of antibiotics.
Again, it is the release of spirochete antigens responsible for the symptom flare-up. Withholding antibiotics for two days will reduce the intensity of Herxheimer symptoms, and may be especially necessary during the fourth week of treatment.
The appearance of the Herxheimer reaction is cause for optimism, because it indicates that the organism is antibiotic-responsive and therefore drugs are available to treat the syndrome.
No drugs are currently available to cure viral Chronic Fatigue and Immune Dysfunction Syndrome. Because the Herxheimer reaction has been viewed as a necessary evil to be endured in order to rid the body of Lyme Disease, the process has been likened to an exorcism.
I have offered antibiotic trials to over 100 patients presenting with Chronic Fatigue and Immune Dysfunction Syndrome and negative Lyme serologies. Although there were no control groups for comparison, their responses have been of three types with the third group representing nearly half:
1. No Herxheimer or other response to antibiotics given over 1 to 2 months. These patients were presumed to have a viral infection an antibiotics were stopped.
2. Apparent Herxheimer reactions, usually mild, for 1 to 2 months, but without any improvement in symptoms. In these cases, antibiotics were continued for 4 to 6 months, then discontinued when it was apparent health status had not improved.
Attempts to terminate antibiotics prior to the four month mark led to a slight relapse in some cases, so they were restarted, but no relapses occurred if antibiotics were stopped after the six month mark.
These patients were presumed to have a mixed infection. Broad spectrum antibiotics cleared the bacterial superinfection, leaving the primary viral infection.
3. Longer and more severe Herxheimer reactions with progressive improvement to a near fully-functional level. Continued medium-dose, prophylactic antibiotics helped to ensure continued success. I observed some relapses with overactivity, inadequate rest, or life stresses, but with rest and an increase in antibiotic dosages, remission followed promptly. These patients were presumed to have seronegative Lyme Disease, or a similar antibiotic-responsive illness as their primary infection.
It is undetermined whether patients in this third category have seronegative Lyme Disease, a related spirochete infection or an unrelated bacterial illness. If the patient has a past history of Lyme Disease, as evidenced by a prior positive serology, culture or documented erythema migrans, then the current illness is likely to be Lyme Disease, rather than a new illness, such as Chronic Fatigue and Immune Dysfunction Syndrome.
If Lyme serologies have always been negative and there is no history of erythema migrans, then either this patient is not infected with Borrelia burgdorferi, or the antibody response has been attenuated such that no free antibody exists. In either case we could aptly describe this disease as antibiotic responsive Chronic Fatigue and Immune Dysfunction Syndrome. If a reliable antigen detection test showed evidence of Borrelia burgdorferi, however, then a diagnosis of seronegative Lyme Disease should be entertained.
Many persons with Chronic Fatigue and Immune Dysfunction Syndrome believe that antibiotics are harmful to them and should be avoided at all costs. Clearly, high doses of antibiotics, as are needed for a Lyme trial, can lead to diarrhea and yeast overgrowth, yet these are the only untoward side effects commonly encountered. I have heard persons with Chronic Fatigue and Immune Dysfunction Syndrome say that antibiotics will worsen their symptoms.
Since one quarter of my patients had no effect whatsoever from high doses of single agent antibiotics, there is no rationale to universally avoid them. Instead, I would argue that patients who feel worse from antibiotics are having Herxheimer reactions, and this is a reason to continue, not stop them.
Finally, I would like to suggest ways to minimize problems with Lyme antibiotic trials. Patients should stagger doses of acidophilus or primadophilus between their antibiotic doses to limit yeast overgrowth.
In the event of persistent vaginal yeast infection, thrush or increased intestinal gas and diarrhea, nystatin tablets or powder may be added four times daily. Alternatively, one can use ketoconazole (Nizoral), fluconazole (Diflucan) or itraconazole (Sporanox) tablets, but these are expensive and potentially hepatotoxic.
With persistent diarrhea, stools should be checked for Clostridium difficile toxin.
Initial drugs of choice are doxycycline and amoxicillin because of their lower cost. Doxycycline should be avoided in children and pregnant women, and patients taking it should be cautioned to avoid prolonged sun exposure.
RESPONSE TO ANTIBIOTICS:
Often do well on antibiotics if given concurrently with acidophilus or primadophilus, even at the higher “Lyme” dosages. May contribute to overgrowth of candida necessitating antifungal medication. If symptoms intensify on antibiotics consider the Jarisch-Herxheimer reaction and a longer antibiotic trial.
Jarisch-Herxheimer reaction often within 10 days on oral antibiotics, and much more rapid and pronounced on IV antibiotics. Symptoms are a worsening of the pretreatment ones, especially fatigue, headaches, pains and sweats. Improvement may take weeks. Relapse is common when antibiotics are discontinued.
When risk factors exist for Lyme Disease, and the clinical picture fits, a diagnostic trial of antibiotics is warranted regardless of Lyme serology status. A Herxheimer response to high dose oral antibiotics is suggestive of Lyme disease, and warrants continued aggressive antibiotic therapy.
ANTIBIOTIC TRIAL: [NB – for info only]
Doxycycline 100 mg po tid
Amoxicillin 1000 mg po tid with Probenecid 500 mg po tid
Amoxicillin 1000 mg po q6 hr
When at a plateau, replace the above with Zithromax or Biaxin, or combine any of the above regimens with one of the following:
Biaxin 500 mg 2-3 times a day
Zithromax 250 mg 1 tab a day, may alternate with 2 tabs
Erythromycin 1-2 grams a day in divided doses
Bactrim DS bid
Suprax 400 mg bid
Ceftin 500 mg bid
LIMITING YEAST OVERGROWTH:
In order to limit yeast overgrowth with antibiotic trials, give acidophilus or primadophilus 2 tabs bid between antibiotic doses. A two-drug antibiotic regimen may require antifungal therapy with Nystatin 500,000 units qid, Sporonox 100 mg 1-2 times a day or Diflucan 100 mg a day in addition to lactobacillus supplementation.
[In Lyme disease] patients on antibiotics will usually have Jarisch-Herxheimer reactions; one would not expect these in a viral illness. A Herxheimer, or die-off, reaction is a worsening of symptoms that occurs when spirochete antigens are released and cause immune activation.
This immune activation is similar to the proposed mechanism for symptoms in Chronic Fatigue and Immune Dysfunction Syndrome. … The appearance of the Herxheimer reaction is cause for optimism, because it indicates that the organism is antibiotic-responsive and therefore drugs are available to treat the syndrome ~
Ticks do not need to be attached for days in order to transmit the disease, but actually can do so in less than 24 hours, especially if improperly removed. Squeezing the body of the tick during a removal attempt can actually force the bacteria out of the tick and into the host.
Fibromyalgia, Chronic Fatigue Syndrome and Lyme Disease
by Bonnie Gorman RN
Dr Sam Donta presented a comprehensive, compassionate, cutting-edge lecture to Mass. CFIDS/FM Association members on November 3rd, 2002. His topic was “The Interface of Lyme Disease with CFS and FM: Diagnostic and Treatment Issues.” Dr. Donta is a nationally recognized expert on Lyme disease. He is the Director of the Lyme Disease Unit at Boston Medical Center and a Professor of Medicine at BU Medical School. He is a bacteriologist and an infectious disease specialist, who views CFS and FM from that vantage point. He is also a consultant to the National Institutes of Health (NIH), and presented at NIH’s scientific meetings on CFS research.
What does Lyme disease have to do with CFS and FM you might be asking? Some people believe that Lyme disease may be one of the causative factors in both CFS and FM. Others believe that some CFS and FM patients are really misdiagnosed chronic Lyme disease patients and vice versa. Some believe that there is no such thing as chronic Lyme disease, instead these patients actually have CFS or FM. We asked Dr. Donta to help sort all this out….
DIAGNOSIS AND THERAPY OF CHRONIC SYSTEMIC CO-INFECTIONS IN LYME DISEASE AND OTHER TICK-BORNE INFECTIOUS DISEASES
Prof. Garth L. Nicolson
The Institute for Molecular Medicine (Website http://www.immed.org)
16371 Gothard Street H, Huntington Beach, CA 92647
About Lyme: This disseminated disease can become persistent or chronic and involve the central and peripheral nervous systems as well as ophthlamic, cardiac, musculoskeletal and internal organ invasion. At this late persistent phase chronic arthritis, neurologic impairment with memory and cognitive loss, cardiac problems (mycocarditis, endocarditis causing palpitations, pain, bradycardia, etc.) and severe fatigue are often apparent [2-4]. Unfortunately, the signs and symptoms in the late persistent phase of the disease usually overlap with other chronic conditions, such as Chronic Fatigue Syndrome, Fibromyalgia Syndrome, Rheumatoid Arthritis, among others , causing confusion in the diagnosis and treatment of the late persistent phase in Lyme Disease patients.
RETROSPECTIVE ANALYSIS OF A COHORT OF INTERNATIONALLY CASE DEFINED CHRONIC FATIGUE SYNDROME PATIENTS IN A LYME ENDEMIC AREA
Samuel Shor1, MD, FACP
1Samuel Shor, MD, FACP
Associate Clinical Professor
George Washington University Health Care Sciences
Internal Medicine of Northern Virginia
1860 Town Center Drive #230
Reston, Virginia 20190
Of the total 210 included in the analysis, 209 or 99% were felt to represent a high likelihood of “seronegative Lyme disease.” Initiating various antimicrobial regimen, involved at least a 50% improvement in clinical status in 130 or 62%. Although not achieving the 50% threshold according to the criteria discussed, another 55 patients subjectively identified a beneficial clinical response to antimicrobials, representing a total of 188 or 88% of the total identified as having a high potential for seronegative Lyme disease.
There are multiple plausible explanations to explain this phenomenon of seronegativity using present technology in the diagnosis of Lyme disease. Recognizing that it is the organism’s immunogenicity to which the host amounts a response, any mechanisms that may alter this immunogenicity has the potential to decrease that response. In so doing, the sensitivities by which this serologic response could be detected would likely be diminished. Bburgdorferi has in fact evolved a number of mechanisms by which this is a likely occurrence. Adapting to changes in its environment, Bburgdorferi has been shown to have the capacity to change its physical characterististics, such as modulating the composition of its outer membrane. (51-56) Variable gene expressions have been well characterized. (57-60) Different structural forms of Bburgorferi have been described. Cystic structures (61,62) and “cell wall deficient spheroblasts and L-forms have been described. (63-67)
Sanctuaries or areas of the body in which sequestered viable spirochetes reside, may lead to internal cycles of acute infection that evade the body’s immune response.(68,69) This has been detected in the CNS.(70-73) as well as the synovium. (74) Residence in an intracellular location confers several survival advantages to Bb through protection from cellular and humoral responses. (75-78) Multiple researchers have demonstrated in vitro evidence of Bb within endothelial cells, myocardium, fibroblasts, ligamentous tissue, synovial cells, keratinocytes, lymphocytes, neurons and glial cells. (79-91)
Lastly, Stricker and Winger have characterized the potential decrease in a subset of NK cells in some with Lyme disease. (33) Thus, there is evidence for immune dysfunction to contribute to the attenuation of the aforementioned serologic response.
Recognizing that the infectious process to which we are alluding is often polymicrobial [including Borrelia, Babesia, Bartonella species and others], several antimicrobials were often employed. In addition, there were frequently relapses in many cases when antimicrobials were entirely withdrawn. The duration of treatment was generally adjusted by the patient’s clinical response and was quite variable.
(Above includes only selected parts of the article – full report at the following link..)
What is Chronic Fatigue Syndrome?
by Lesley Ann Fein MD, MPH
Both patients and physicians continue to think of chronic fatigue syndrome as a “wastebasket” diagnosis, or one of exclusion. This is complete misconception.
CFS or ME (Meningo-encephalopathy) is very well studied both in the U.S., Europe and Japan. The current estimate is 1 million cases in the U.S. and 2 million in Europe. The actual numbers most likely greatly exceed these estimates.
This is a “syndrome”. In other words, a collection of symptoms and manifestations, rather than a diagnosis based upon a specific test.
The primary event is an infection. Infectious agents that have been associated with CFS/ME are Borrelia, EBV, CMV, HHV6, HHV7, Parvovirus, Chlamydia pneumonia, Mycoplasma species, Q fever, Ross River syndrome and herpes virus 1.
The role of the newly discovered XMRV virus as a common denominator is still being debated.
There have been studies suggesting genetic predisposition to developing CFS in the face of these infections.
This is a small summary of the myriad of physiological and metabolic dysregulations that have been established:
1. Cardiac abnormalities: elevated resting heart rate, decreased cardiac output, abnormal T waves, biopsy evidence of fibrosis and muscle disruption, and patients hearts have to work 50% harder than normal hearts. In addition, many patients have POTTs syndrome, or autonomic neuropathy. This results in dizziness and fainting in the upright position, because the heart is not sensing that it needs to adapt to working harder against gravity, and ultimately the brain is not adequately perfused, and patients have top lie down before they pass out.
2. Exercise response: patients with CFS are unable to tolerate aerobic activity. As opposed to “normal” people, these patients do not respond by improving aerobic capacity, but rather get premature anaerobic metabolism, and post-exertional pain and malaise. These symptoms are associated with elevation of multiple inflammatory substances. Part of the poor exercise capacity could be related to low red blood cell counts and low blood volumes documented in these patients as well.
3. Cellular dysfunction: low ATP levels and Glutathione depletion. Markers of increased oxidative stress. This is most likely why there is an inability to exercise as these are the “energy” blocks of the cell. The “fuel” of the cells is inadequate to generate energy required to function normally, let alone the up-regulation required for exercise.
4. Sleep disorders are almost universal: PLMS (periodic limb movements), restless leg syndrome, myoclonic jerking, “alpha intrusion waves” not allowing the brain to go into a deep sleep and wake people up when they reach stage 2 sleep, UARS (upper airway resistance syndrome) similar to sleep apnea, non restorative sleep resulting in “dysania”-foggy, stiff, tired and sore in the morning
5. Probably the most key issue is brain dysfunction, as was so elegantly presented by Hirohiko Kuratsune at the 2007 IACFS conference in his brilliant talk: “Brain Dysfunction is a key abnormality for understanding the state of chronic fatigue.” Brain SPECT scanning is abnormal, and even the brain goes in to anaerobic metabolism. In other words, after trying to read or “exercise” the brain, there is accumulation of lactic acid showing metabolic dysfunction in the brain as well. The cascade effect of brain dysfunction affects neuroendocrineimmune systems throughout the body. Elegant studies from Georgetown show findings in the spinal fluid unique to CFS patients.
The treatment must be tailored to each individual patient. One needs to identify as much as possible which organisms are being implicated and target those organisms. In addition, we need to address all the “fallout” effects, i.e. the sleep, the pain, the metabolic dysfunction, the autonomic dysfunction, the serotonin depletion always associated with chronic pain syndromes, nutrition, hydration, stress avoidance etc. The studies have clearly demonstrated a direct inverse relationship between stress and immune function. Since you are already dealing with a syndrome associated with poor immune function, adding stress is devastating to recovery.
The research is fast and furious, and hopefully this will no longer be a diagnosis without a cure. It is certainly a diagnosis with potential treatments, and the usual response to “just go home, see a psychiatrist and take anti-depressants” is not the answer. Also, many patients have been made to feel lazy. They need to be reassured that it is not their fault that they are unable to perform even daily tasks without exhaustion. This sense of guilt is not only completely undeserved, but often implied when physicians, friends and families tell the patients to just “push through” while not understanding how difficult it is to get out of bed every day. These patients need a lot of compassion and emotional support. They have been misunderstood and poorly treated for many years, and deserve a huge apology from a medical community who has been dismissive and condescending.
NB: link now broken but have kept for informational purposes..
Lyme borreliosis: perspective of a scientistpatient Ron Hamlen
Hengge and colleagues state: “Since Lyme borreliosis is a popular explanation for many poorly understood symptoms, such as arthralgias or chronic fatigue syndrome, proper instruction to physicians is key to prevent misdiagnosis or overdiagnosis”. Conversely, the fact that symptoms of persistent B burgdorferi infection overlap those of chronic fatigue syndrome, fibromyalgia, multiple sclerosis, and motor neuron disease contributes to the misdiagnosis and inadequate treatment of this spirochetal illness.[2, 17, 18 and 19]
(requires password to access)
Fibro, CFS, MS, etc., could it be Lyme disease?