Monday, 14 October 2013

What if you have Lyme Disease, EBV in your system and Candida, it's quite feesable to have all 3 plus Atlas misalignment


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.
Parallel Symptom Patterns
Dr. Donta presented the symptom lists for chronic Lyme disease, chronic fatigue syndrome (CFS), fibromyalgia (FM), and Gulf War Illness (GWI).  He pointed out the similarities between them, and found there were few differences.  He has treated hundreds of patients with these illnesses.  He found that CFS and GWI have identical symptoms, and FM is only distinguished by a positive tender point exam, that is often positive in CFS and GWI as well.  Clinically it is almost impossible to distinguish or differentiate these illnesses. 
He has concluded that chronic Lyme disease is remarkably similar to CFS, FM, and GWI.  These multi-symptom disorders have similar symptom patterns consisting of fatigue and neurocognitive dysfunction, along with numerous other symptoms that probably relate to altered neurological function.  Musculoskeletal symptoms may be more frequent in FM and in some patients with chronic Lyme than in CFS, but the definition of CFS and GWI also includes muscle aches (myalgias) and joint aches (arthralgias).
Lyme Disease Symptoms
Flu-like illness, fever, malaise, fatigue, headache, muscle aches (myalgia), and joint aches (arthralgia), intermittent swelling and pain of one or a few joints, "bull's-eye" rash, early neurologic manifestations include cognitive disorders, sleep disturbance, pain, paresthesias (including numbness, tingling, crawling and itching sensations), as well as cognitive difficulties and mood changes.  
The only symptom difference in Lyme disease is the expanding circular rash with a clearing area and center resembling a "bull's eye."  He pointed out that Lyme has multiple types of rashes and half of the rashes are not typical, they may not even include the "bull's eye" rash.  They can appear from two day after the bite, then go on for a week or so.  Patients who are infected may not develop or see the rash, and may not develop any future symptoms.  In studies, only one third of the patients were actually aware of their tick bites. 
30-50% of acute Lyme disease patients went on to develop chronic Lyme disease.  Additionally, some previously asymptomatic patients may reactivate their infection following various stressors such as trauma, surgery, pregnancy, coexisting illness, antibiotics treatment, or severe psychological stress.  The Lyme vaccine can also reactivate their infection.  Similar triggers such as trauma, surgery etc. are known to precipitate CFS, FM and GWI as well.  This is not a new phenomenon with infectious diseases.  We know infectious diseases (i.e. TB) will reactivate after illnesses or surgery-- any stressor.
Dr. Donta reported on the effects of gender on host susceptibility in Lyme disease, CFS, FM and other multi-symptom diseases.  In all these disorders, women appear to be more affected than men, usually at about 2:1 ratios.  He noted that neural cells contain estrogen and progesterone receptors, and that herpes viruses can utilize estrogen receptors to gain access to the reservoir in the cell nucleus.  Treatment of chronic Lyme disease also seems to be gender-dependent to some degree, with men generally having more speedy and complete recoveries compared to women.  He concluded that gender relationships are known for a number of infectious diseases, so it would not be surprising that such a relationship exists for chronic Lyme disease, CFS, FM and other multi-symptom disorders.
Etiology
Lyme Disease: A distinct difference between Lyme disease, CFS and FM is that the origin of Lyme is clear.  Lyme disease is caused by spirochetal bacteria transmitted by the bite of an infected deer tick.  This bacteria is the Borrelia burgdorferi bacteria.  It was identified in the late 1900s in Europe.  The US was late to recognize what Europe had described.  Lyme disease was not formally identified by the CDC until 1977 when arthritis was observed in a cluster of children in and around Lyme, CT.  Since that time Lyme disease has been identified in many states.  The CDC reports that it causes more than 16,000 infections per year in the US.  Some researchers feel that the prevalence is higher than that. 
CFS and FM: Dr. Donta feels that Lyme disease is an important cause of CFS and FM.  In addition to Lyme, there are a number of other possible causes.  The evidence is still circumstantial though.  Epstein-Barr virus (EBV), the major cause of infectious mononucleosis, continues to be debated as a cause of CFS.  It is uncertain whether EBV can cause symptoms other than fatigue, such as myalgias and arthralgias that are not seen during acute or reactivated EBV infection in patients who are being immunosuppressed, but it remains possible that EBV could cause one type of chronic fatigue disorder.  There are also other herpes viruses i.e. HHV6 that are being evaluated as potential culprits.

Dr. Donta reported that recently recognized species of Mycoplasma (Mycoplasma fermentans, Mycoplasma genitalium) have been implicated in CFS, FM and GWI.  These same bacteria have also been implicated as causative agents of rheumatoid arthritis, based on PCR-DNA evidence in patients with these disorders in which 50 percent are found to have the DNA of the Mycoplasma in circulating white blood cells, compared to 5-10 percent of a normal population.  Whether the presence of this DNA represents past exposure or ongoing infection remains to be resolved.  No long-term studies have yet been performed in patients with CFS and FM to determine whether the finding of Mycoplasma DNA persists over months or years or whether such patients have any evidence of other infection such as Lyme disease or infection with Chlamydia species.
Central Nervous System Involvement
Dr. Donta reported that in Lyme disease, the nervous system seems to be the primary target for the bacteria causing the disease.  Patients with Lyme disease express many neurologic symptoms such as pain, paresthesias including numbness, tingling, crawling and itching sensations, as well as cognitive difficulties and mood changes.  Even the joint pains and occasional arthritis appear to be neuropathic in origin, as anti-inflammatory agents such as ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAID) have little if any effect on the pain.  Experimental evidence from animal models also affirm the localization of B. burgdorferi DNA to the nervous system.  Dr. Donta postulates that the disease mechanisms could involve inflammatory responses, autoimmune responses or toxin-associated disruption of neural function.  Any inflammatory responses appear to be weak, and there is no compelling evidence that Lyme disease is a result of immunopathologic mechanisms.
Commenting on his research, Dr. Donta speculated that if they are correct, and lyme bacteria is a nerve toxin that interferes with the transmission of the nerve impulse, then that is all you need to impede the normal flow of information.  There is a lot of cross-talk in the nervous system.  This toxin will decrease that cross-talk causing delayed responses resulting in cognitive problems-- the brain fog so commonly described in all these multi-symptom disorders. 
Although the disease pathways for other possible causes of CFS and FM have not been defined, Dr. Donta postulates that the central nervous system would appear to be a logical target for other pathogens or other disease processes.  These illnesses clearly affect the brain and are bound to cause many neurological manifestations.  Any changes in immunologic function would not appear to be sufficient to explain the various symptoms, and are likely to be secondary to other disease processes.
He feels we have been thinking too simplistically about finding whole organisms replicating in chronic diseases.  It is highly likely that there is no single cause for these illnesses.  It's more likely that there are multiple causes-- different organisms causing the same final set of symptoms.  Researchers need a better algorithm to study these fatiguing illnesses.  We need to be more inclusive, rather than trying to separate the illnesses.  Sometimes in medicine, if an illness is too complex to study, research interest dwindles.  We have the technology to do the research, but there hasn't been the will and the momentum to get it done.
Clinical Diagnosis

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