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Dr. Holtorf on Infectious Causes of ME/CFS and Fibromyalgia

  [ 69 votes ]   [ 7 Comments ]
By Kent Holtorf, MD* • www.ProHealth.com • May 25, 2011


* Dr. Kent Holtorf, founder of the non-profit National Academy of Hypothyroidism, directs the Holtorf Medical Group in Torrance, Foster City, Pasadena, and Sacramento, CA, Kansas City and Minneapolis. Dr. Holtorf specializes in researching and employing "innovative evidence-based therapies for hard-to-treat and poorly understood illnesses: hypothyroidism, complex endocrine dysfunction, chronic fatigue syndrome (ME/CFS), fibromyalgia and chronic infectious diseases including Lyme and chronic viral illness."

_________________________________

Infectious Causes of ME/CFS and FM Numerous studies have demonstrated a high incidence of chronic infections in chronic fatigue syndrome and fibromyalgia.

These include viral infections of Epstein-barr (EBV), cytomegalovirus (CMV), human herpes virus-6, (HHV-6), and bacterial infections such as mycoplasma, Chlamydia pneumoniae (CP) and Borrelia burgdorferi (Lyme disease).

There is controversy regarding the presence of active infection in these conditions because physicians, including infectious disease specialists, do not understand that the standard way to diagnose acute infections - an elevation of IgG and IgM antibodies - is not a sensitive means of detecting chronic infections in these patients (1-21).

With an acute [new] infection, the body will start producing IgM antibodies against that infection and then start producing IgG antibodies after a few weeks so there is an elevation of both IgG and IgM antibodies.

Chronic reactivating infections, such as those mentioned above, do not stimulate IgM antibodies, as they are not new infections but rather intracellular reactivating infections.

So most doctors, again including infectious disease specialists, will tell patients who have elevated IgG antibodies that they had an old infection or previous exposure and that there is no evidence of, or they do not have, an active infection - because that is what they learned in medical school.

This standard way of detecting active infections has clearly been shown to be inaccurate and misses the overwhelming majority of patients with active infections (1-21).

Polymerase chain reaction (PCR) testing [which can generate thousands of copies of a DNA sequence from one or a few copies] is much more sensitive in a research setting than in the clinical setting, because if the blood sits for more than a few hours, the infectious organism’s DNA degrades and often goes undetected. So in a clinical setting, PCR is a specific test (if it is positive you know you have an active infection), but suffers from low sensitivity (often negative despite an active chronic infection).

Additionally limiting sensitivity is the fact these infections are not concentrated in the blood or serum but rather in the tissues, especially nerves, brain and the white blood cells.

Physicians must have a high incidence of suspicion and look for elevated IgG or early antigen (EA) antibodies along with other signs of chronic infections including low natural killer cell activity, high RNase-L activity, high ACE (> 35), coagulation activation, high tumor necrosis factor (TNF), low melanocyte stimulation hormone (MSH), high interleukin-6 (IL-6), low WBC [white blood cell levels], increased 1,25 vitamin D/25 vitamin D ratio, and elevated or decreased total IgA, IgM or IgG levels.

Chronic infections are almost always present in:

• Those whose symptoms started very acutely, especially with an infection,

• Those whose symptoms were ever associated with swollen lymph nodes or sore throat,

• And those with significant cognitive dysfunction or flu-like symptoms.

It must be remembered that in order to have the highest probability of successful treatment, a multi-system approach should be initiated. (See Dr. Holtorf’s handout, “New Standard for the Treatment of Chronic Fatigue Syndrome and Fibromyalgia.”).

HERPES VIRUSES (Epstein-Barr, Cytomegalovirus and HHV-6)

EBV, CMV and HHV-6 cause or contribute to the symptoms of a large percentage of CFS and FM patients.

As stated previously, the presence of active infections correlates with an elevated IgG antibody, despite the lack of IgM antibodies (10-21).

These infections are generally not acute, but rather intracellular reactivation of an old infection. An elevation of IgM antibodies is typically not seen with active infections of EBV, CMV, HHV-6 (10-21).

Due to the immune dysfunction seen in CFS, in addition to a lack of IgM antibody formation, there may also be a lack of IgG antibodies present despite the presence of an active infection in CFS patients(22,17,23). This has also been demonstrated to be the case with AIDS patients, as demonstrated in the study published in the New England Journal of Medicine entitled “Absence of detectable IgM antibodies during cytomegalovirus disease in patients with AIDS”(22).

It has also been shown that the presence of anti-thyroid antibodies in CFS patients has a significant correlation with active HHV-6 infection (24).

» A study published in Acta Pathologica, Microbiologica et Immunologica Scandinavica entitled “Multiple co-infections (Mycoplasma, Chlamydia, human herpes virus-6) in blood of Chronic Fatigue Syndrome Patients: Association with Signs and Symptoms” found:

• 52% of CFS patients had active mycoplamsa infection,

• 30.5% had active HHV-6 infection,

• And 7.5% had Chlamydia pneumoniae infections,

• Versus only 6%, 9% and 1% of controls, respectively.

They conclude, “The results indicate that a large subset of CFS patients show evidence of bacterial and/or viral infection(s), and these infections may contribute to the severity of signs and symptoms found in these patients (25).”

» A study entitled “A Chronic Illness Characterized by Fatigue, Neurological and Immunological Disorders, and Active Human Herpes virus Type 6 Infection” published in the Annals of Internal Medicine found 70% of patients with CFS had active HHV-6 infection through the use of primary cell cultures and confirmation using assays of monoclonal antibodies specific for HHV-6 proteins and by PCR.

Again, an elevation of IgM antibodies is generally not seen (26).

As summarized below, when specialized testing is used to detect active vs. past infection of HHV-6, the overwhelming number of studies demonstrate a high incidence of active herpes virus infections. These reactivation infections often do not illicit an IgG and especially not an IgM response, so standard serologic testing is specific but not sensitive for such infections.

As mentioned before, PCR testing in a research setting is much more reliable, sensitive and useful than in the clinical setting when the blood is usually not processed for 12 to 48 hours.

» Wagner et al, found that 61% of CFS patients who had elevated IgG antibodies, and 81% with immune deficiency, had confirmed active HHV-6 infection, vs. only 19% of those patients who did not(15). This is regardless of whether or not IgM antibodies were elevated.

Below in Figure 1 is a summary of studies that have looked at the incidence of active HHV-6 infection in CFS/FM patients vs. controls, with 83% of the studies demonstrating a large portion of CFS/FM patients have an active HHV-6 infection.

Figure 1

Assays that differentiated between active and latent virus: 83% positive
(click image to enlarge)

» A study by Lerner [A. Martin Lerner at the Treatment Center for CFS] found that treating patients with 6 months of Valtrex resulted in a significant improvement in symptoms (46).

» In a separate study, Lerner et al found that in CFS patients with elevated IgG antibody against CMV, treatment with the intravenous antiviral ganciclovir, which has a more broad spectrum coverage than Valtrex and anti-CMV activity, resulted in 72% of patients returning to their premorbid health states (total resolution of symptoms) (47).

» A randomized, placebo controlled study published in Clinical Infectious Diseases demonstrated that in CFS patients with elevated IgG antibodies against CMV, a combination of oral Valtrex and intravenous ganciclovir resulted in dramatic improvements with almost complete resolution of symptoms (27).

» Montoya et al. at Stanford University [Infectious Disease Clinic] treated chronic fatigue syndrome patients with 6 months of valganciclovir (Valcyte) if they had elevated IgG tests for HHV-6 and EBV and had at least 4 of the following symptoms: impaired cognitive functioning, slowed processing speed, sleep disturbance, short-term memory deficit, fatigue and symptoms consistent with depression.

Nine of the twelve treated patients (75%) “experienced near resolution of their symptoms, allowing them all to return to the workforce or full time activities.” In the nine patients with a symptomatic response to treatment, EBV VCA IgG and HHV-6 IgG titers significantly dropped. (21)

» Lerner et al collected data on 142 CFS patients treated with antivirals. They found that long-term antiviral therapy was effective unless other untreated coinfections were present.(53)

» We [Holtorf Medical Group] have found that an effective treatment protocol requires the use of an anti-infectious treatment in a significant portion of CFS patients (and the majority of severely affected).

While no single treatment is universally beneficial, we have found that a variety of anti-infectious and immune-modulatory therapies can be very effective. These include Valcyte, Isoprinosine, Kutapressin, gamma globulin (IM or IV), antiviral nutraceuticals, species specific transfer factor, antibiotics, anti-retrovirals, anti-parasitics and low dose naltrexone.

There are a number of markers that indicate that there is an underlying chronic infection as a cause or contributor to the illness. These include:

• Flu-like symptoms or symptoms started with a flu-like illness;

• Elevated IgG or EA against Epstein-Barr virus, Cytomegalovirus and/or HHV-6;

• Low Natural Killer cell activity or number;

• High reverse T3 or low free T3/reverse T3 ratio;

• Low CD57;

• High eosinophilic cationic protein (ECP) or vascular endothelial growth factor (VEGF);

• High RNase-L activity;

• High ACE (> 35);

• Coagulation activation (high D-dimer, thrombin-prothombin complex, high prothrombin fragment 1 & 2, PAI-1 or soluble fragment monomer);

• High tumor necrosis factor (TNF), IL-6 or NFKB;

• Low melanocyte stimulation hormone (MSH);

• Low WBC;

• Increased 1,25 vitamin D/25 vitamin D ratio;

• High C4a or C3a;

• And/or elevated or decreased IgA, IgM or IgG levels;

• Positive XMRV antibody or culture test.

This study contributes more confirmatory evidence that IgM antibodies are not typically elevated in chronic reactivating infections, so most patients are incorrectly told they do not have an active infection based on such testing. This study also demonstrated the lack of sensitivity of standard PCR testing.

There is also evidence that CFS may be due to the above discussed infections with “stealth adaptation” (28-38).

This is primarily due to the deletion of the genes coding for the major antigenic components normally targeted by the cellular immune system.

“Stealth viral adaptation” results in replication that is less efficient than conventional viruses, but has a distinct advantage over conventional viruses in not having to confront the body’s cellular immune defense mechanisms. The virus can, therefore, evade the immune system and create persistent ongoing infections in spite of an individual’s intact immune system (28-38).

A number of studies have also shown dramatic improvement in patients with interferon treatments, especially those with low Natural Killer cell function (39,40,41).

While ganciclovir and interferon may be effective, their toxicity precludes their use and there are less toxic means of eradicating these infections.

MYCOPLASMA

Numerous studies have demonstrated a high incidence of active Mycoplasma infection in CFS and FM (1,44-52). [Mycoplasma are unique fungus-like bacteria that lack a cell wall and aren’t affected by many common antibiotics that keep bacteria from multiplying by interfering with their cell wall formation.]

» Nijs et al. published a study in the journal Immunology and Medical Microbiology entitled “High Prevalence of Mycoplasma Infections Among European Chronic Fatigue Syndrome Patients,” which demonstrated that 68% of CFS patients had an active mycoplasma infection as diagnosed with specialized polymerase chain reaction (PCR) testing where the red and white cells were immediately lysed and centrifuged to concentrate and collect the DNA (1).

Being predominantly intracellular, there is typically not a significant serologic antibody response or just an isolated IgG response with this number of other intracellular infections, so IgG and especially IgM antibodies are almost always in the normal range despite the presence of an active infection (1-9).

This study and others discussed below demonstrated that IGM antibodies are not helpful in the diagnosis of an active infection in CFS and FM.

Nijs et al. stated, “Mycoplasma detection based on antibody testing is characterized by a very high specificity [if IGG and IGM positive], but extremely low sensitivity [active infection almost always present without elevated IgG and IgM an¬tibodies] renders it useless as a diagnostic tool (1).”

» A study by Dylewski et al. in the New England Journal of Medicine demonstrates that in immune compromised patients, such as this patient, active infections correlate with elevations in IgG antibodies without elevations of IgM antibody, and that a lack of elevation of IgM is not useful in these patients as a way to rule-out active infection. A high clinical suspicion must be maintained and implementation of anti-infective treatment should be based on elevated IgG levels (9).

» A study entitled “Diagnosis and Treatment of Chronic Mycoplasmal Infections in Fibromyalgia and Chronic Fatigue Syndrome: Relationship to Gulf War Illness,” published in Biomedical Therapy investigated the presence of active mycoplasmal infection by forensic PCR in patients with CFS and/or FM vs. controls.

They found that 63% of CFS/FM patients had active mycoplasmal species infection compared to 9% of normals, and more specifically the incidence of active Mycoplasma fermentans infection was 50% in CFS/FM patients vs. 0% of controls (2).

» A study published in the International Journal of Medicine Biology Environment tested the blood of 565 CFS and/or FM patients vs. 71 healthy controls. They found 53.1% of patients were positive for mycoplasmal infection vs. only 7 out of 71 controls - and 24.6% of patients had an M. fermentans infection, vs. 2.8% of normals (42).

» A study published in the International Journal of Occupational Medicine, Immunology and Toxicology found that through specialized testing:

• More than half of Gulf War Syndrome/CFS patients had active mycoplasma infections that would not have been detected by standard serological IgG and IgM testing,

• And that 78% of the patients completely recovered with appropriate treatment.

• Additionally, all of recovered patients who were subsequently retested no longer had evidence of infection (7).

» A study and review published in the Antimicrobics and Infectious Disease Newsletter discussed the high incidence of mycoplasma infections in CFS.

• They discuss the fact that the culturing procedures and serological testing are insensitive for detecting intracellular infections due to the fact that there is usually a lack of hormonal response with these infections resulting in “normal” antibody titers or an isolated elevation of IgG antibodies with a lack of IgM antibodies (8).

• Sophisticated PCR testing found multiple species of mycoplasma in the majority of CFS patients.

• They found of the 87 Gulf War illness-chronic fatigue syndrome patients treated with antibiotics, most relapsed after the first 6 week trial and most felt worse, but after up to 6 cycles of 6 weeks of therapy approximately 80% of these patients recovered and were able to return to their normal functional capacity.

This was not a placebo controlled trial, but they discuss the fact that it is unlikely a placebo effect that most patients felt worse during treatment.

They conclude stating that in order to be successful in the treatment of Gulf War Illness-chronic fatigue syndrome, a comprehensive treatment approach must be used that addresses the numerous physiological abnormalities, including chronic infections (8).

» A study by Nasralla et al. published in the European Journal of Clinical Microbiology & Infectious Disease entitled “Multiple Mycoplasmal Infections Detected in Blood of Chronic Fatigue Syndrome and Fibromyalgia Syndrome Patients” investigated the presence of different mycoplasmal species in blood samples from mycoplasma positive patients with chronic fatigue syndrome and/or Fibromyalgia.

They found that the majority of patients had multiple species of mycoplasmal infections, with:

• 59% of patients having active M. pneumoniae infections,

• 48% having active M. fermentans infection,

• 31% having an active M. hominis,

• And 20% having M. penetrans (43).

XMRV (Xenotropic Murine Leukemia Virus-Related Virus)

I was skeptical about XMRV at first and thought it was most likely an opportunistic infection. One reason was that Quest did a pilot study in our office and we found that all the patients who were positive were the chronic Lyme patients. [Quest Diagnostics Clinical Trials in Valencia, CA - See their poster, "A Sensitive Real-time Assay for the Detection and Quantification of XMRV," presented at the recent 2011 Conference on Retroviruses and Opportunistic Infections in Boston.]

Thus my thinking was that Lyme must the primary infection with XMRV being secondary or opportunistic.

Now I think that was too simplistic and think the evidence is showing that having XMRV is a reason that Lyme may not be cleared in some or many patients and may need to be treated.

Our initial treatment with anti-retrovirals has been encouraging. I have been using Isentress [raltegravir] and then adding Viread [tenofovir]. Also using GcMAF ["vitamin D-binding protein," thought to activate immune macrophage response to infectious micro-organisms] in some.

[ProHealth note: As a means of sharing the findings of these anti-retroviral treatments, Dr. Holtorf has indicated he will construct a brief Q&A with one or more of the chronic Lyme patients in his care who may wish to volunteer their experience and observations regarding the therapy. To be included in a future newsletter.]

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References

1. Jo Nijs J et al. High prevalence of Mycoplasma infections among European chronic fatigue syndrome patients. Examination of four Mycoplasma species in blood of chronic fatigue syndrome patients. FEMS Immunology and Medical Microbiology. Volume 34, Issue 3, 15 November 2002, Pages 209-214.

2. Garth L. Nicolson, Marwan Nasralla, Joerg Haier and Nancy L. Nicolson. Diagnosis and Treatment of Chronic Mycoplasmal Infections in Fibromyalgia and Chronic Fatigue Syndromes: Relationship to Gulf War Illness. Biomed. Therapy 1998; 16: 266-271

3. Baseman JB, Tully JG. Mycoplasmas: Sophisticated, reemerging, and burdened by their Notoriety. Emerg Infect Dis 1997 (3): 21-32.

4. Lo S-C, Dawson MS, Newton PB III. Association of the virus-like infectious agent originally reported in patients with AIDS with acute fatal disease in previously healthy non-AIDS patients. Am J Trop Med Hyg 1989 (40): 399-409.

5. Lo SC, Wear DJ, Shih WK, Wang RYH, Newton PB, Rodriguez JF. Fatal systemic infections of non-human primates by Mycoplasma fermentans (incognitus strain). Clin Infect Dis 1993 (17) (Suppl 1): S283-288.

6. Lo SC, Buchholz CL, Wear DJ, Hohm RC, Marty AM. Histopathology and doxycycline treatment in a previously healthy non-AIDS patient systemically infected by Mycoplasma fermentans (incognitus strain). Mod Pathol 1991 (6): 750-754.

7. Nicolson G, Nicolson N. diagnosis and treatment of Mycoplamal Infections in Persian Gulf War Illness-CFIDS Patients. International Journal of Occupational Medicine, Immunology and Toxicology 1996;5:69-78.

8. Nasrala M et al. The Pathogenesis and Treatment of Mycoplasmal Infections. Antimicrobics and Infectious Disease Newsletter 1999;17(!!);81-88

9. Dylewski J et al. Absence of detectable IgM antibody during cytomegalovirus disease in patients with AIDS. New England Journal of Medicine 1985:309:493.

10. Carruthers et al. Myalgic Encepalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols. Journal of Chronic Fatigue Syndrome.Vol 11(1) 2003.

11. Ablashi DV, Zompetta C, Lease C, Josephs SF, Balachandran N, Komaroff AL, Krueger GRF, Henry B, Luka J and Salahuddin SZ. Human herpesvirus-6 (HHV-6) and chronic fatigue syndrome (CFS). Canada Disease Weekly Report 1991; 175E:33-40.

12. Zorenzenon M, Rukh G Botta GA et al. Active HHV-6 infection in chronic fatigue syndrome patients from Italy: New data. J Chron Fatigue Syndr 1996;2(4):3-12.

13. Knox KK, Brewer JH, and Carrigan DR. Persistent active human herpesvirus six (HHV-6) infections in patients with chronic fatigue syndrome. J Chron Fatigue Syndr 1999;5:245-246.

14. Brewer JH, Know KK and Carrigan DR. Longitudinal study of chronic active human herpesvirus 6 (HHV-6) viremia in patients with chronic fatigue syndrome. Abstract. IDSA. 37th Annual Meeting. Nov. 18-21, 1999. Philadelphia, Pennsylvania.

15. Wagner et al. Chronic Fatigue Syndrome: A critical Evaluation of Testing for Active Human Herpesvi¬rus-6 Infection. Review of Data of 107 cases. Journal of Chronic Fatigue Syndorme;2(4) 1996.

16. 15 Krueger GRF, Ablashi DV and Gallo RC: Persis¬tent herpesvirus infections . Current techniques in diag¬nosis. J Virol Methods 21 : 1- 326,1988.

17. Gerhard Rf et al. Clinical Correlates of Infection with Human Herpesvirus-6. In vivo 1994;8:457-86.

18. Ablashi DV et al. Human Herpes virus and chronic fa¬tigue syndrome. Canad Dis Weekly Rep 1991;17S1:33-40.

19. Albashi DV et al. human B lymphotropic virus (hu¬man herpesvirus-6). J Virol Methods 1988;21:29-48.

20. Josephs SF et al HHV-6 reactivation in chronic fa¬tigue syndrome. Lancet 1991;1346-7 21. Montoya et al. Use of valganciclovir (Valcyte) in pa¬tients with elevated antibody titers against Human Her¬pesvirus-6 (HHV-6) and Epstein-Barr Virus (EBV) who were experiencing central nervous system dysfunction including long-standing fatigue. Journal of Clinical Vi¬rology 2006;37:S33-38

22. Dylewski J, Chou S, Merigan TC. Absence of detect¬able 1gM antibody during cytomegalovirus disease in patients with AIDS. N Engl J Med 1985; 309: 493.

23. Krueger GRF et al. Overview of immunopathology of chronic active herpesvirus infection. J Virol Methods 1988;21:11-18

24. Krueger GRF, Klueppelberg U, Hoffmann A, Ablashi DV. Clinical corre¬lates of infection with human her¬pesvirus-6. In Vivo 1994; 8:457-86.

25. Nicolson GL, Gan R, Haier J. Multiple co-infections (Mycoplasma, Chlamydia, human herpes virus-6) in blood of chronic fatigue syndrome patients: association with signs and symptoms. APMIS. 2003 May; 111(5): 557-66.

26. Buchwald D. et al. A Chronic Illness Characterized by Fatigue, Neurological and Immunological Disorders, and Active Human Herpesvirus Type 6 Infection published in the Annals of Internal Medicine 1992;116:103-113.

27. Lerner AM, Zervos M and Chang CH et al. A small, randomized, placebo-controlled trial of the use of antivi¬ral therapy for patients with chronic fatigue syndrome. Clinical Infectious Diseases. 2001;32:1657-58.

28. Martin W.J. Viral infection in CFS patients. in “The Clinical and Scientific Basis of Myalgic Encephalomy¬elitis Chronic Fatigue Syndrome.” Byron M. Hyde Edi¬tor. Nightingdale Research Foundation Press. Ottawa Canada pp 325-327, 1992.

29. Martin W.J. Detection of viral related sequences in CFS patients using the polymerase chain reaction.in “The Clinical and Scientific Basis of Myalgic Encepha¬lomyelitis Chronic Fatigue Syndrome.” Byron M. Hyde Editor. Nightingdale Research Foundation Press. Ot¬tawa Canada pp 278-283, 1992.

30. Martin WJ, Zeng LC, Ahmed K, Roy M. Cytomega¬lovirus-related sequences in an atypical cytopathic virus repeatedly isolated from a patient with the chronic fa¬tigue syndrome. Am. J. Path. 145: 441-452, 1994.

31. Martin W.J. Stealth viruses as neuropathogens. Col¬lege of American Pathologist’s publication “CAP Today” 8 67-70, 1994

32. Martin WJ. Stealth virus isolated from an autistic child. J. Aut. Dev. Dis. 25:223-224,1995

33. Martin WJ, Ahmed KN, Zeng LC, Olsen J-C, Seward JG, Seehrai JS. African green monkey origin of the atyp¬ical cytopathic ‘stealth virus’ isolated from a patient with chronic fatigue syndrome. Clin. Diag. Virol. 4: 93-103, 1995.

34. Martin WJ. Severe stealth virus encephalopathy fol¬lowing chronic fatigue syndrome-like illness: Clinical and histopathological features. Pathobiology 64:1-8, 1996.

35. Martin WJ. Stealth viral encephalopathy: Report of a fatal case complicated by cerebral vasculitis. Pathobiol¬ogy 64:59-63, 1996.

36. Martin WJ. Simian cytomegalovirus-related stealth virus isolated from the cerebrospinal fluid of a patient with bipolar psychosis and acute encephalopathy. Patho¬biology 64:64-66, 1996. 10. Gollard RP, Mayr A, Rice DA, Martin WJ. Herpesvirus-related sequences in salivary gland tumors. J. Exp. Clin. Can. Res. 15: 1-4, 1996.

37. Martin WJ. Genetic instability and fragmentation of a stealth viral genome. Pathobiology 64:9-17, 1996. 12. Martin WJ, Glass RT. Acute encephalopathy induced in cats with a stealth virus isolated from a patient with chronic fatigue syndrome. Pathobiology 63: 115-118, 1995.

38. Martin WJ. Detection of RNA sequences in cultures of a stealth virus isolated from the cerebrospinal fluid of a health care worker with chronic fatigue syndrome. Pathobiology (IN PRESS) NOT

39. See DM, Tilles JG.Immunol Invest. alpha-Inter¬feron treatment of patients with chronic fatigue syndrome.1996 Jan-Mar;25(1-2):153-64.

40. Brook MG, Bannister BA, Weir WR. Interferon-al¬pha therapy for patients with chronic fatigue syndrome. J Infect Dis. 1993 Sep;168(3):791-2.

41. J K S Chia. The role of enterovirus in chronic fatigue syndrome. J. of clin Path 2005;March 14:1126-1132.

42. Marwan Y. Nasralla, Jörg Haier, Nancy L. Nicolson Garth L. Nicolson. Examination of Mycoplasmas in Blood of 565 Chronic Illness Patietns by Polymerase Chain Reaction.. International Journal Medicine Biol¬ogy Environment 2000; 28(1):15-23.

43. Nasralla M, Haier J, Nicolson GL. Multiple mycoplas¬mal infections detected in blood of patients with chronic fatigue syndrome and/or fibromyalgia syndrome.
Eur J Clin Microbiol Infect Dis 1999 Dec;18(12):859-65.

44. Gerhard K. M. Endresen. Mycoplasma blood infec¬tion in chronic fatigue and fibromyalgia syndromes. Rheumatology International Issue: Volume 23, Number 5 September 2003: 211 – 215

45. Marwan Nasralla, Ph.D., Joerg Haier, M.D., Ph.D. and Garth L. Nicolson, Ph.D. Mycoplasmal Infections in Blood from Patients with Chronic Fatigue Syndrome,
International CFS Conference, Sydney, Australia, 1998.

46. Lerner AM, Beqaj SH, and Deeter RG et al. A six-month trial of valacyclovir in the Epstein-Barr virus subset of chronic fatigue syndrome: improvement in left ventricular function. Drugs of Today. 2002;38:549-561.

47. Lerner AM, Zervos M and Dworkin HJ et al. New cardiomyopathy: A pilot study of intravenous ganciclo¬vir in a subset of the chronic fatigue syndrome. Infec¬tious Diseases In Clinical Practice 1997;6:110-117.

48. Vojdani A, Choppa PC, Tagle C, Andrin R, Samimi B, Lapp CW. Detection of Mycoplasma genus and Mycoplasma fermentans by PCR in patients with Chronic Fatigue Syndrome. FEMS Immunol Med Microbiol 1998 Dec;22(4):355-65

49. Vojdani, Aristo, and Al Robert Franco. Multiplex PCRF for the Detection of Mycoplasma fermentans, M. hominis, and M. penetrans in Patients with Chronic Fatigue Syndrome, Fibromyalgia, Rheumatoid Arthritis, and Gulf War Syndrome. Journal of Chronic Fatigue Syndrome Vol. T, No. ¾, 1999, pp. 187-197;

50. Vojdani, A, Franco A. Chronic Fatigue Syndrome: Advance in Epidemiologic, Clinical, and Basic Science Research. 1999, pp. 187-197. The Haworth Press, Inc., 1999

51. Choppa PC, Vojdani A, Tagle C, Andrin R, Magtoto L. Multiplex PCR for the detection of Mycoplasma fer¬mentans, M. hominis and M. penetrans in cell cultures and blood samples of patients with chronic fatigue syndrome. Mol Cell Probes 1998 Oct;12(5):301-8

52. Nicolson G, Nasralla M, Franco R, DeMeirleir K et al. Role of Mycoplamsal Infections in Fatigue Illness: Chronic Fatigue and Fibromyalgia Syndromes, Gulf War Illness and Rheumatoid Arthritis. Journal of Chronic Fatigue Syndrome 2000;6(3/4):23-39.

____

Note: This material is reproduced with kind permission of the author, Kent Holtorf, MD. All rights reserved. It has not been evaluated by the FDA, is general information that should not be construed as medical advice, and is not meant to prevent, diagnose, treat or cure any illness, condition or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.



Please Discuss This Article:   Post a Comment 

Donating Blood Recommended?
Posted by: tplanford
May 25, 2011
Does anyone know of any issues/recommendations about Fibro patients donating blood?
Reply Reply

 
Blood donation
Posted by: aryiella
May 25, 2011
The American Red Cross barred CFS patients from donating blood in Dec 2010. Since CFS and Fibromyalgia often overlap, and the causes are still not known, I would strongly suggest not donating. I have both CFS and FM and I would never donate my blood because I would never want someone to possibly get what I have.

 


Holtorf article
Posted by: spring8
May 25, 2011
This is a most informative, if rather frightening article. Many thanks for the service you are providing to those who suffer these debilitating diseases. Eva Hunter.
Reply Reply

no flu /colds
Posted by: herbqueen
May 25, 2011
I wonder if Dr. Holtorf or others have a theory on why we many of us do not get flu's/colds- I've read this is also true for many with autoimmune diseases such as MS. Is it because our system is so overwhelmed it does not mount an attack?--or if a hyper vigilant state and the virus's never get a chance- perplexing?
Reply Reply

 
Flu/Colds
Posted by: aryiella
May 25, 2011
I've always wondered that myself. Let me know if you figure it out!

 

 
flu/colds
Posted by: JanW
Aug 24, 2012
hi herbqueen,
I realize this is a long time after the article and comment, but I came across it recently and wondered if you were still thinking about this. One possible answer to not getting colds/flu is that we do have them, but by not having an appropriate immune response we don't get many signs/symptoms (which are created by the immune response). One reason for this could be Th2 dominance, which is mentioned in the literature.

bye,
Jan

 


complications from Infectious mono and epstien barr virus
Posted by: tntboys
Aug 11, 2014
I lost my 17 year old son, Tyler Lane Budro, on March 10,2013 to an unknown illness. He was 17 years old and a junior at Hull Daisetta High School. He was sent home from school sick on Tuesday February 19 and went to the doctor that day. They did a mono test and gave him antibiotics. The next day he wasn't any better so he was taken to the doctor again. He received an antibiotic shot and more medicine. On the next day, Thursday, he felt better and ate really good. Friday, February 22, his girlfriend came to check on him and she left him at 1:45 and my dad came home at 4 and found him on the floor. He had been having seizures and was not responsive. He was taken to the ER in Beaumont, TX and was transferred to Pediatric ICU at Memorial Herman hospital in Houston. They were not able to stop him from having seizures and he was put into a medical induced coma to slow down brain activity. Most of his skull was removed to allow room for his brain to swell. They ran test after test to try and find out what was wrong with him, but the only thing he ever tested positive for was mono. After 16 days in ICU we lost him on March 10, 2013, the day before his brothers 16th birthday. It took 10 months before the autopsy was completed and another month to get the report, but they still didn't find anything.
I was just wondering if his case is one that you would want to use in your research. If you are interested, I would be happy for you to. If one person can be saved from having to go through what he went through and the family also, it would mean so much to me.
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