The REAL Cause of CFS

We are convinced (along with many others) that the real cause of most CFS is Lyme disease and/or Herpes Epstein-barr virus. Herpes, we discuss in other articles.  Here, Lyme disease is called “The Great Imitator” for a reason – it imitates, and often is, CFS.  Fortunately, we have the best, most complete natural protocol for Lyme disease available!  Following is a clinical study showing the CFS / Lyme disease connection.  We have edited it to make it more readable (our comments are italicized.)

Excerpts, and our thanks, from:
Samuel Shor, MD, FACP, George Washington University Health Care Sciences.  Journal of Chronic Fatigue Syndrome, Vol. 13(4) 2006.  The Haworth Press, Inc. doi:10.1300/J092v13n04_06 67 ABSTRACT.

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   Chronic Fatigue Syndrome (CFS) and late stage or “Chronic Lyme” infection, with or without “co-infections”, are difficult diagnosis to establish.  The symptom complex of both conditions can be very similar.  This case study supports serious consideration for patients otherwise diagnosed with “CFS,” as actually representing chronic Lyme disease.

   It includes a case study of a 33-year-old man, who for two years, was being managed as having CFS.  However, after 2 years of treatment with limited success, the diagnosis of Lyme disease was reconsidered.  More aggressive testing confirmed the diagnosis of Lyme disease.  Changes in treatment had an improved level of functioning that was far in excess of “CFS” treatment was able to achieve.

   The features of CFS and chronic Lyme disease can be very similar and include the following. Profound fatigue often associated with cognitive impairment.  Other common symptoms related to both of these conditions include sleep disturbances and fibromyalgia.

Conclusion: Being aware of the possibility that Lyme disease can misinterpreted as CFS is very important!

Introduction

   Because there are no consistent markers for CFS, it is considered a “diagnosis of exclusion.”  This means they simply rule out other possibilities to establishing this diagnosis.  (That is a confidence builder.  Why not just say “we don’t know”?)

   Lyme disease or Lyme borreliosis is a well-accepted disease that, unfortunately, can manifest in many different ways.  That means there is also a significant degree of controversy as to the diagnosis and management of Lyme disease.  In the last 10 years, two medical standards of care have evolved for the diagnosis and treatment of Lyme disease. These two medical standardsare:

1.  The guidelines of the Infectious Diseases Society of America (IDSA), (1) and,

2.  The guidelines of the International Lyme and Associated Diseases Society (ILADS).(2)

   As a result of this confusion, the identification of Lyme disease has problems that can contribute to missing seeing chronic fatigue syndrome as one of the infectious syndromes of chronic Lyme!  We include a case study of a 33-year-old male who was supposed to have CFS but who actually had Lyme disease.

   “DB” described “severe fatigue” and “aches.”  By the time he was seen by me, he was unable to function at all at work.  He had described several “crashes” that left him bed-bound.  Other symptoms included “profound unrefreshing sleep, cognitive fog, mild headaches, and nausea.”

   Exams had included testosterone levels, HCV, HHV6 by PCR, HIV and tests for Borrelia burgdorferi, in keeping with CDC “two-tiered” analysis by ELISA, and were all negative.  He had had some mild temporary clinical benefits that were not lasting (many CFS people we talk to have been there).

   Years later, a reevaluation for the potential of tick/B. burgdorferi exposure was checked into and the patient’s diagnosis at that point was changed from CFS to chronic Lyme – with “CFS-like” features (except we can treat Lyme disease!!!).

Discussion

   There are no “markers” that have been consistently established to definitively make the diagnosis of CFS.   However, Lyme disease is also considered a complicated multi-system disorder caused by the spirochete B. burgdorferi complex(3,4), transmitted by Ixodes dammini and other related ixodid ticks.(5,6)

   It can be 4-6 weeks (or longer) before the first systemic symptoms (other than multiple rashes) occur in some patients, usually in the form of “flu”.(7)  Soon after the flu, fatigue, arthralgias and/or myalgias may begin.  In fact, as previously described, chronic or “late stage” Lyme disease can clinically be indistinguishable from chronic fatigue syndrome.

   Lyme B. burgdorferii has evolved multiple ways to elude immune recognition.  It is not surprising that present technology is far from ideal in having a definite description of Lyme disease.  Tests are often falsely negative and Lyme disease is often missed.(8-11)

   Over 75% of patients with chronic Lyme disease are negative by the ELISA test, but positive by Western blot test.(12-14)  The Western blot is recognized by the National Institute of Allergy and Infectious Diseases (NIAID), a division of the National Institutes of Health (NIH), as the most useful method for detecting B. burgdorferi antibodies currently available.(15).  (A new test is now coming out and offers better diagnosis.)

   Lyme disease is believed to be in a virtually immune protected environment.  In doing so, the likelihood of the host’s immune system (or antibiotics) mounting a consistently reliable immune response is minimized (the biofilms we can dissolve).(16)  Lyme can even burrow in and reside within cells.(17-19)

   Lyme B. burgdorferi has been shown to change to a cyst form (spheroplast L-forms) when exposed to a hostile environment such as antibiotics.(20)  In addition, cysts have been shown to change back to spiral forms in vivo (21).  Reports also suggest that co-infections with one or more of these agents can both exacerbate the presenting symptoms of Lyme disease and decrease response to therapeutics. (All of which we can deal with.)

Conclusion

   Patients with symptoms that are consistent with chronic fatigue syndrome should be seriously evaluated for the potential of chronic Lyme infection.  Common features in both conditions include profound fatigue, sleep, and cognitive impairment, along with fibromyalgia and dysautonomias.

   In addition, if chronic Lyme is determined to be present, then evaluation for the potential of co-infections with Ehrlichia sennetsu, Bartonella henselae or Babesia microti should be undertaken.  In doing so, we are more likely to effectively reverse the chronic, often debilitating processes with which our patients are so often presenting.

   Our 3 Step CFS Answer.

References

1. Wormser GP, Nadelman RB, Dattwyler RJ et al. Practice guidelines for the treatment of Lyme disease: The Infectious Diseases Society of America. Clin Infect Dis 2000; 105(4pt 1): 855-857.

2. The ILADS Working Group. Evidence-based guidelines for the management of Lyme disease. Expert Rev Anti-Infect Ther 2004; 2(suppl): S1-S13. 8. Shah J. Igenex publication July 6, 2005.

3. Barbour AG. Linear DNA of Borrelia species and antigenic variation. Trends Microbiol 1993; 1: 236-239.

4. Postic D, Assous MV, Grimont PA, Baranton G. Diversity of Borrelia burgdorferi sensu lato evidenced by restriction fragment length polymorphisms of rrf(5S)-rrl (23S) inter-genic spacer amplicons. Int J Syst Bacteriol 1994; 44: 743-752.

5. Steere AC. The Borellia burgdoerferi sensu lato is transmitted by Ixodes dammini and other related ixodid ticks. Lyme disease.NEngl JMed 1989; 321: 586-596.

6. Steere AC, Grodzicki RL, Kornblatt AN et al. The spirochetal etiology of Lyme disease. N Engl J Med 1983; 308: 733-740.

7. FederHMJr, Gerber M, Krause PJ. Early Lyme disease: A flu-like illness without erythema migrans. Pediatrics 1993; 91: 456-459.

8. Logigian EL, Kaplan RF, Steere AC. Chronic neurologic manifestations of Lyme disease. N Engl J Med 1990; 323: 1438-1444.

9. Rawlings JA, Fournier PV, Teltow GJ. Isolation of Borrelia burgdorferi from patients in Texas. J Clin Microbiol 1987; 25(7): 1148-1150.

10. Aguero-Rosenfeld ME, Nowakowski J, Bittker S, Cooper D, Nadelman RB, Wormser GP. Evolution of the serologic response to Borrelia burgdorferi in treated patients with culture-confirmed erythema migrans. J Clin Microbiol 1996; 34(1): 1-9.

11. Aguero-Rosenfeld ME, Nowakoski J, McKenna DF, Carbonaro CA, Wormser GP. Sero-diagnosis in early Lyme disease. J Clin Microbiol 1993; 31(12), 3090-3095. Original Research 73

12. Donta ST. Tetracycline therapy of chronic Lyme Disease. Clin Infect Dis 1997; 25: S52-56.

13. Donta ST. Treatment of chronic Lyme disease with macrolide antibiotics. In: Program and abstracts of the VIIIth International Conference on Lyme Borreliosis; June 20-24, 1999; Munich, Germany. Abstract P. 193.

14. Donta ST. Late and chronic Lyme disease. Med Clin North Am 2002; 86(2): 341-349.

15. National Institutes of Allergy and Infectious Diseases (National Institute of Health) profile, fiscal year 2001 HYPERLINK “http://www.niaid.nih.gov/publications/NIAIDProfile” (accessed January 2006).

16. Schwan TG, Piesman J, Golde WT, Dolan MC, Rosa PA. Induction of an outer surface protein on Borrelia burgdorferi during tick feeding. Proc Natl Acad Sci USA 1995; 92: 2909-2913.

17. Georgilis K, Peacocke M, Klempner MS. Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro. J Infect Disease 1992; 166: 440-444.

18. Klempner MS, Noring R, Rogers RA. Invasion of human skin fibroblasts by the Lyme disease spirochete, Borrelia burgdorferi. J Infect Disease 1993; 167: 1074-81.

19. Haupl T, Hahn G, Rittig M, Krause A, Schoerner C, et al. Persistence of Borrelia burgdorferi in ligamentous tissue from a patient with chronic Lyme Borreliosis. Arthritis Rheum 1993; 36: 1621-1626.

20. Murgia R, Piazzetta C, Cinco M. Cystic forms of Borrelia burgdorferi sensu lato: Induction, development and the role of RpoS. Wien Klin Wochenschr 2002; 114(13-14): 574-579.

21. Gruntar I et al. Conversion of Borrelia garinii cystic forms to motile spirochetes in vivo. APMIS 2001; 109(5): 383-388.