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Thursday, November 20, 2003 10:36 AM

Fw: [asthma] Fw: Mycoplasma #2 why we are sick!

 

 

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Mycoplasma #2 why we are sick!

 

 

Mycoplasmal Infections in Chronic Illnesses:

Fibromyalgia and Chronic Fatigue Syndromes,

Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis

 

Garth L. Nicolson, PhD, Marwan Y. Nasralla, PhD, Joerg Haier, MD, PhD,

Robert Erwin, MD, Nancy L. Nicolson, PhD, Richard Ngwenya, MD

 

 

ABSTRACT Invasive bacterial infections are associated with several acute and

chronic illnesses, including: aerodigestive diseases such as Asthma,

Pneumonia, Inflammatory Bowel Diseases; rheumatoid diseases, such as

Rheumatoid Arthritis (RA); immunosuppression diseases such as HIV-AIDS;

genitourinary infections and chronic fatigue illnesses such as Chronic

Fatigue Syndrome (CFS), Fibromyalgia Syndrome (FMS) and Gulf War Illnesses

(GWI). It is now apparent that such infections could be (a) causative, (b)

cofactors or © opportunistic agents in a variety of chronic illnesses.

Using Forensic Polymerase Chain Reaction we have looked for the presence of

one class of invasive infection (mycoplasmal infections) inside blood

leukocyte samples from patients with CFS (Myalgic Encephalomyelitis), FMS,

RA, and GWI. There was a significant difference between symptomatic CFS,

FMS, GWI, and RA patients with positive mycoplasmal infections of any

species (45-63%) and healthy positive controls (~9%) (P<0.001). This

difference was even greater when specific species (M. fermentans, M.

hominis, M. penetrans, M. pneumoniae) were detected. Except for GWI, most

patients had multiple mycoplasmal infections (more than one species of

mycoplasma). Patients with different diagnoses but overlapping signs and

symptoms often have mycoplasmal infections, and such mycoplasma-positive

patients generally respond to multiple cycles of particular antibiotics

(doxycycline, minocycline, ciprofloxacin, azithromycin, and clarithromycin).

Multiple cycles of these antibiotics plus nutritional support appear to be

necessary for successful treatment. In addition, immune enhancement and

other supplements appear to help these patients regain their health. Other

chronic infections may also be involved to various degrees with or without

mycoplasmal infections in causing patient morbidity in various chronic

illnesses.

 

 

 

Introduction --- Chronic Illnesses

 

 

There is growing awareness that many chronic illnesses may have an

infectious nature that is either responsible (causative) for the illness, a

cofactor for the illness or appears as an opportunistic infection(s) that is

responsible for aggravating patient morbidity.(1) There are several reasons

for this notion, including the nonrandom or clustered appearance of an

illness, often in immediate family members, the course of the illness, and

its response to therapies based on infectious agents. Since chronic

illnesses are often complex, involving multiple, nonspecific, overlapping

signs and symptoms, they are difficult to diagnose and even more difficult

to treat. Most chronic illnesses do not have effective therapies, and

patients rarely recover from their conditions,(2) causing in some areas of

the world catastrophic economic problems.

 

Some chronic illnesses, such as Rheumatoid Arthritis (RA), are well

established in their clinical diagnosis,(3) whereas others, such as Chronic

Fatigue Syndrome (CFS, sometimes called Myalgic Encephalomyelitis),

Fibromyalgia Syndrome (FMS), and Gulf War Syndrome or Gulf War Illnesses

(GWI), have rather nonspecific but similar complex, multi-organ signs and

symptoms that overlap or are almost identical.(1) In the case of CFS, FMS

and GWI these include: chronic fatigue, headaches, muscle pain and soreness,

nausea, gastrointestinal problems, joint pain and soreness, lymph node pain,

cognitive problems, depression, breathing problems and other signs and

symptoms.(4) The major difference between these illnesses appears to be in

the severity of specific signs and symptoms. For example, FMS patients have

as their major complaint muscle and overall pain, soreness and weakness,

whereas CFS patients most often complain of chronic fatigue and joint pain,

stiffness and soreness, but otherwise their complaints usually overlap.

Often these patients have increased sensitivities to various environmental

irritants and enhanced allergic responses. Although chronic fatigue

illnesses have been known for several years, most patients with CFS, FMS,

GWI and in some cases RA have had few treatment options. This may have been

due to the imprecise nature of their diagnoses, which are based primarily on

clinical observations rather than laboratory tests, and a lack of

understanding about the underlying causes of these illnesses or the factors

responsible for patient morbidity.(1) These illnesses could have different

initial causes or triggers but similar cofactors or similar opportunistic

infections that cause significant morbidity.

 

 

Chronic Illnesses --- Overlapping Signs and Symptoms

 

 

The multiple signs and symptoms of FMS, CFS and GWI are complex, nonspecific

and completely overlapping (Figure 1), suggesting that these illnesses are

related and not completely separate syndromes.(1,6) In this figure only

differences in the signs and symptoms after the onset of illness are shown,

and the data for FMS and CFS have been combined, because previous studies

indicated that with the exception of muscle pain and tenderness, there was

essentially no difference in patient signs.(4) Illness Survey Forms were

analyzed to determine the most common signs and symptoms at the time when

blood was drawn from patients. The intensity of patient signs and symptoms

prior to and after onset of illness was recorded on a 10-point rank scale

(0-10, extreme). The data were arranged by 38 different signs and symptoms

and were considered positive if the value after onset of illness was two or

more points higher than prior to the onset of illness. The data in Figure 1

indicate that patients diagnosed with CFS or FMS had complex signs and

symptoms that were similar to those reported for GWI. In addition, the

presence of rheumatoid signs and symptoms in each of these disorders

indicates that there are also similarities to RA.(7) Moreover, it is not

unusual to find immediate family members who display similar signs and

symptoms. For example, there is evidence that GWI has slowly spread to

immediate family members,(8) and it is likely that it has also spread to

some degree in the workplace.(1) A preliminary survey of approximately 1,200

GWI families indicated that approximately 77% of spouses and a majority of

children born after the war had signs and symptoms similar or identical to

veterans with GWI.(8)

 

In the absence of laboratory tests to the contrary, chronic illnesses are

often misdiagnosed as somatoform disorders caused by stress and other

nonorganic factors.(9) Patients with CFS, FMS and GWI usually have cognitive

problems, such as short term memory loss, difficulty concentrating and other

problems, and physicians who find psychological or psychiatric problems in

these patients often decide that these conditions are caused by somatoform

disorders, not organic problems.(1) Stress is often mentioned as an

important factor or the important factor in these disorders. Indeed, GWI

patients are often diagnosed with Post Traumatic Stress Disorder (PTSD) in

veterans' and military hospitals.(10) The evidence that has been offered as

proof that stress or PTSD is the source of GWI sickness is the assumption

that veterans must have suffered from stress by virtue of the stressful

environment in which they found themselves during the Gulf War,(10) but the

veterans themselves do not feel that stress-related diagnoses are an

accurate portrayal of their illnesses. Most testimony to date refutes the

notion that stress is the major factor in GWI,(11) suggesting that stress,

albeit important, is not the cause of GWI.(12) But most physicians would

agree that stress can exacerbate chronic illnesses and suppress immune

systems, suggesting that stress plays a secondary not primary role in

chronic illnesses, such as GWI, CFS, and FMS.(1) However, in the absence of

physical or laboratory tests that can identify possible origins of FMS, CFS

or GWI, many physicians accept that stress is the cause of these chronic

illnesses. It has been only recently that other causes were seriously

considered, including chronic infections.(13)

 

 

Mycoplasmal Infections in CFS, FMS and GWI

 

 

We have been particularly interested in the association of certain chronic

infectious agents in CFS, FMS and GWI, because these microorganisms can

potentially cause most or essentially all of the signs and symptoms found in

these patients.(1,14) One type of infection that elicited our attention was

microorganisms of the class Molecutes, small bacterial mycoplasmas, lacking

cell walls, that are capable of invading several types of human cells and

are associated with a wide variety of human diseases.(14)

 

We have examined the presence of mycoplasmal blood infections in GWI, CFS,

and FMS patients. The clinical diagnosis of these disorders was obtained

from referring physicians according to the patients' major signs and

symptoms. Since the signs and symptoms of CFS and FMS patients completely

overlapped, these patients were therefore considered together (CFS/FMS).(1)

Blood was collected, shipped over night at 4°C and processed immediately for

PCR after purification of DNA using a Chelex procedure.(1,7) Patients' blood

was analyzed for the presence of mycoplasmal infections in blood leukocytes.

Positive PCR results were confirmed if the PCR product was 717 base pairs in

size using the genus-specific primers (or 850 base pairs for M. fermentans

specific primers, etc.) along with a positive control of the same size in

the same gel, and if a visible band was obtained after hybridization with

the internal probe.(15) The sensitivity and specificity of the PCR methods

were determined by examining serial dilutions of purified DNA of M.

fermentans, M. pneumoniae, M. penetrans, M. hominis and M. genetalium.

Amounts as low as 10 fg of purified DNA were detectable for all species

using the genus primers. The amplification with genus primers produced the

expected fragment size in all tested species, which was confirmed by

hybridization with an inner probe.(16)

 

Mycoplasma tests were performed on all patients as described previously

(1,7,17) either from Chelex-purified DNA or DNA prepared from whole blood

using a commercial kit. The targeted Mycoplasma spp. sequence was amplified

from DNA extracted from the peripheral blood of 144/203 CFS or FMS patients

(~70%). In 70 healthy subjects positive results for Mycoplasma spp. were

obtained in 6 samples (<9%). The difference between patient and control

groups was significant (p<0.001).(17) In addition, two of the 70 controls

were positive for M. fermentans. The ratio between positive and negative

patients was comparable in female and male patients. These results are quite

similar to the results recently published by others.(18) Similarly, using

Nucleoprotein Gene Tracking to analyze the blood leukocytes from GWI

patients we found that 91/200 (45%) were positive for mycoplasmal

infections.(19,20) In contrast, in nondeployed, healthy adults the incidence

of mycoplasmal infections was 4/62 (~6%).(19,20)

 

Patients with FMS or CFS often have multiple mycoplasmal infections and

probably other chronic infections as well. When we examined CFS/FMS patients

for M. fermentans, M. pneumoniae, M. penetrans, M. hominis infections,

multiple infections were found in over one-half of 93 patients (Figure 2).

CFS/FMS patients had double (over 30%) or triple (over 20%) mycoplasmal

infections, but only when one of the species was M. fermentans or M.

pneumoniae.(17) Higher score values for increases in the severity of signs

and symptoms were also found in patients with multiple infections. CFS/FMS

patients infected with different mycoplasma species generally had a longer

history of illness, suggesting that patients may have contracted additional

infections with time.(17)

 

In the course of our studies we found that DNA preparation and blood storage

was extremely important in preserving the test samples. Storage of blood

frozen or at 0-4°C resulted in reproducible assay results, whereas storage

at room temperature resulted in loss of PCR signal over time. Within 1-2

days at room temperature, most of the positive samples reverted to negative

results.(1) Also, blood drawn in tubes (blue-top) containing citrate and

kept at 0-4°C before the assay yielded better results than other

anticoagulants, unless the samples were frozen in EDTA (purple-top) tubes.

 

 

Mycoplasmal Infections in Rheumatoid Diseases

 

 

The underlying causes of rheumatoid diseases are not known, but RA and other

autoimmune diseases could be triggered or exacerbated by infectious agents.

It has been known for some time that infectious diseases in some animal

species result in remarkable clinical and pathological similarities to RA

and other rheumatoid diseases. Aerobic and anaerobic intestinal bacteria,

viruses and mycoplasmas have been proposed as important agents in RA.(21)

Recently there has been increasing evidence that mycoplasmas may play a role

in the initiation or progression of RA.(22) Mycoplasmas have been proposed

to interact nonspecifically with B-lymphocytes, resulting in modulation of

immunity, autoimmune reactions and promotion of rheumatoid diseases.(23) M.

pneumoniae, M. salivarium and U. urealyticum have also been found in the

joint tissues of patients with rheumatological diseases, suggesting their

pathogenic involvement.(24)

 

When we examined RA patients' blood leukocytes for the presence of

mycoplasmas, we found that approximately one-half were infected with various

species of mycoplasmas.(7) The most common species found was M. fermentans,

followed by M. pneumoniae and M. hominis and finally M. penetrans. Similar

to what we found in CFS/FMS patients, there was a high percentage of

multiple mycoplasmal infections in RA patients when one of the species was

M. fermentans.(7)

 

Although the precise role of mycoplasmas in RA and other rheumatoid

inflammatory diseases remains unknown, mycoplasmas could be important

cofactors in the development of inflammatory responses and for progression

of the disease. As an example of the possible role of mycoplasmas in

rheumatological diseases, M. arthritidis infections in animals can trigger

and exacerbate autoimmune arthritis.(25) This mycoplasma can also suppress

T-cells and release substances that act on polymorphonuclear granulocytes,

such as oxygen radicals, chemotactic factors, and other substances.(26)

Mycoplasmal infections can increase proinflammatory cytokines, such as

Interleukin-1, -2, and -6,(27) suggesting that they are involved in the

development and possibly progression of rheumatological diseases.

 

In addition to mycoplasmal infections, other microorganisms have been under

investigation as cofactors or causative agents in rheumatological diseases.

The discovery of EB virus(28) and cytomegalovirus(29) in the cells of the

synovial lining in RA patients suggested their involvement in RA, possibly

as a cofactor. There are a number of bacteria and viruses that are

candidates in the induction of RA or its progression.(30) In support of

bacterial involvement in RA, it has been known for some time that

antibiotics like minocycline can alleviate the clinical signs and symptoms

of RA.(31) Although this has been proposed to be due to their

anti-inflammatory activities, these drugs are likely to be acting to

suppress infections of sensitive microorganisms like mycoplasmas.

 

 

Mycoplasmal Infections in Immunosuppressive and Autoimmune Diseases

 

 

Mycoplasmas have been implicated in the progression of HIV-AIDS. It has been

known for some time that some species of mycoplasmas are associated with

certain terminal human diseases, such as an acute fatal illness found with

certain Mycoplasma fermentans infections in non-AIDS patients.(32) Recently,

mycoplasmal infections have attracted attention as a major source of

morbidity in AIDS patients. For example, M. fermentans can cause renal and

CNS complications in patients with AIDS,(33) and M. penetrans has also been

found in the respiratory epithelial cells of AIDS patients.(34) Other

species of mycoplasmas have also been found in AIDS patients where they have

been associated with disease progression, such as M. prium and M.

hominis.(32) Blanchard and Montagnier(35) have proposed that mycoplasmas are

cofactors in HIV-AIDS, accelerating progression and accounting, at least in

part, for increased susceptibility of AIDS patients to additional

infections. In addition to immune suppression, some of this increased

susceptibility may be the result of mycoplasma-induced host cell membrane

damage from toxic oxygenated products released from intracellular

mycoplasmas.(36) Also, mycoplasmas may regulate HIV-LTR-dependent gene

expression,(37) suggesting that mycoplasmas may play an important regulatory

role in HIV pathogenicity.

 

There is some preliminary evidence that mycoplasmal infections could be

associated with autoimmune diseases. In some mycoplasma-positive GWI cases

the signs and symptoms of Multiple Sclerosis (MS), Amyotrophic Lateral

Sclerosis (ALS or Lou Gehrig's Disease), Lupus, Graves' Disease and other

complex autoimmune diseases have been seen. Such usually rare autoimmune

responses are consistent with certain chronic infections, such as

mycoplasmal infections, that penetrate into nerve cells, synovial cells and

other cell types. These autoimmune signs and symptoms could be caused when

intracellular pathogens, such as mycoplasmas, escape from cellular

compartments and incorporate into their own structures pieces of host cell

membranes that contain important host membrane antigens that can trigger

autoimmune responses. Alternatively, mycoplasma surface components

('superantigens') may directly stimulate autoimmune responses,(38) or their

molecular mimicry of host antigens may explain, in part, their ability to

stimulate autoimmunity.(39)

 

 

Mycoplasmal Infections in Other Clinical Conditions

 

 

Asthma, airway inflammation, chronic pneumonia and other respiratory

diseases are known to be associated with mycoplasmal infections. For

example, M. pneumoniae is a common cause of upper respiratory

infections,(40) and severe asthma is commonly associated with mycoplasmal

infections.(41) Recent evidence has shown that certain mycoplasmas, such as

M. fermentans (incognitus strain), are unusually invasive and often found

within respiratory epithelial cells.(34)

 

Heart infections (myocarditis, endocarditis, pericarditis and others) are

often due to chronic infections, such as Mycoplasma,(42,43) Chlamydia(44)

and possibly other infectious agents.

 

Other species of mycoplasmas are also associated with various illnesses: M.

hominis infections were first found in patients with hypogammaglobulinemia,

and M. genitalium was first isolated from the urogenital tracts of patients

with nongonococcal urethritis.(45,46) Although mycoplasmas can exist in the

oral cavity and gut as normal flora, when they penetrate into the blood and

tissues, they may be able to cause or promote a variety of acute or chronic

illnesses. These cell-penetrating species, such as M. penetrans, M.

fermentans and M. pirum among others, can probably result in complex

systemic signs and symptoms. Mycoplasmas are also very effective at evading

the immune system, and synergism with other infectious agents can occur.(14)

Similar types of chronic infectious agents may occur.(14) Similar types of

chronic infections caused by Chlamydia, Brucella, Coxiella or Borrelia may

also be present either as single agents or as complex, multiple infections

(see Figure 2) in many of the diseases discussed above.

 

 

Mycoplasmal Infections --- Treatment Suggestions

 

 

Once mycoplasmal infections have been identified in the white blood cell

fractions of subsets of CFS, FMS, GWI, RA and other patients, they can be

successfully treated. Appropriate treatment with antibiotics should result

in patient improvement and even recovery.(6,19,20) The recommended

treatments for mycoplasmal blood infections require long-term antibiotic

therapy, usually multiple 6-week cycles of doxycycline (200-300 mg/day),(47)

ciprofloxacin (1,500 mg/day), azithromycin (500 mg/day) or clarithromycin

(750-1,000 mg/day).(48) Multiple cycles are required, because few patients

recover after only a few cycles, possibly because of the intracellular

locations of mycoplasmas like M. fermentans and M. penetrans, the

slow-growing nature of these microorganisms and their relative drug

sensitivities. For example, of 87 GWI patients that tested positive for

mycoplasmal infections, all patients relapsed after the first 6-week cycle

of antibiotic therapy, but after up to 6 cycles of therapy 69/87 patients

recovered and returned to active duty.(19,20) The clinical responses that

were seen were not due to placebo effects, because administration of some

antibiotics, such as penicillins, resulted in patients becoming more not

less symptomatic, and they were not due to immunosuppressive effects that

can occur with some of the recommended antibiotics. Interestingly, CFS, FMS

and GWI patients that slowly recover after several cycles of antibiotics are

generally less environmentally sensitive, suggesting that their immune

systems may be returning to pre-illness states. If such patients had

illnesses that were caused by psychological or psychiatric problems or

solely by chemical exposures, they should not respond to the recommended

antibiotics and slowly recover. In addition, if such treatments were just

reducing autoimmune responses, then patients should relapse after the

treatments are discontinued.(1)

 

Patients with CFS, FMS, RA or GWI usually have nutritional and vitamin

deficiencies that must be corrected.(48) These patients are often depleted

in vitamins B, C, and E and certain minerals. Unfortunately, patients with

these chronic illnesses often have poor absorption. Therefore, high doses of

some vitamins must be used, and others, such as vitamin B complex, must be

given sublingual. Antibiotics that deplete normal gut bacteria can result in

over-growth of less desirable flora, so Lactobacillus acidophillus

supplementation is recommended. In addition, a number of natural remedies

that boost the immune system are available and are potentially useful,

especially during antibiotic therapy or after therapy has been

completed.(48) One of us (R.N.) has been involved in the development of

ancient African and Chinese natural immune enhancers and cleansers help to

restore natural immunity and absorption. Although these products are known

to help AIDS patients, their clinical effectiveness in GWI/CFS/FMS/RA

patients has not been carefully evaluated. They appear to be useful during

therapy to boost the immune system or after antibiotic therapy in a

maintenance program to prevent relapses.(48)

 

Why aren't physicians routinely treating mycoplasmal and other chronic

infections? In many cases they are treating these infections, but it has

been only recently that such infections have been found in so many

unexplained chronic illnesses. These infections cannot be successfully

treated with the usual short courses of antibiotics due to their

intracellular locations, slow proliferation rates and inherent insensitivity

to most antibiotics. In addition, a fully functional immune system may be

essential to overcoming these infections, and this is why vitamin and

nutritional supplements are so important.

 

 

Conclusions

 

 

We have proposed that chronic infections are an appropriate explanation for

the morbidity seen in a rather large subset of CFS, FMS, GWI and RA

patients, and in a variety of other illnesses. Not every patient will have

this as a diagnostic explanation or have the same types of chronic

infections, and additional research is necessary to clarify the role of such

infections in chronic diseases.(1,7) Some patients may have chemical or

radiological exposures or other environmental problems as an underlying

reason for their chronic signs and symptoms. In these patients, chronic

infections may be opportunistic. In others, somatoform disorders or

illnesses caused by psychological or psychiatric problems may indeed be

important. However, in these patients antibiotics, supplements and immune

enhancers should have no lasting effect whatsoever, and they should not

recover on such therapies. The identification of specific infectious agents

in the blood of chronically ill patients may allow many patients with CFS,

FMS, GWI or RA and other chronic diseases to obtain more specific diagnoses

and effective treatments for their illnesses. Finally, patients with

cardiopathies, AIDS, respiratory illnesses, and urogenital infections are

often infected with Mycoplasma, Chlamydia, Brucella or other chronic,

invasive bacterial and parasitic infections, and these patients could

benefit from appropriate antibiotic and neutraceutical therapies that

alleviate morbidity.

 

 

 

References

 

 

 

1. Nicolson GL, Nasralla M, Haier J, Nicolson NL. Biomed. Therapy

1998;16:266-271.

2. Hoffman C, Rice D, Sung H-Y. (1996) JAMA 1996;276:1473-1479.

3. Hochberg MC, et al. Arthritis Rheumatol. 1992;35:498-502.

4. Nicolson GL, Nicolson NL. J. Occup. Environ. Med. 1996;38:14-16.

5. Murray-Leisure K. et al. Intern. J. Med. 1998;1:47-72.

6. Nicolson GL. Intern. J. Med. 1998;1:42-46.

7. Haier J, Nasralla M, Nicolson GL. Rheumatol 1999;38:504-509.

8. Senate Committee on Banking, Housing and Urban Affairs, U. S. Congress

(1994) U.S. chemical and biological warfare-related dual use exports to Iraq

and their possible impact on the health consequences of the Persian Gulf

War, 103rd Congress, 2nd Session, Report: May 25, 1994.

9. N.I.H. Technology Assessment Workshop Panel. The Persian Gulf experience

and health. JAMA 1994;272:391-396.

10. Nicolson GL, Nicolson NL. Med. Confl. Surviv. 1997;13:140-146.

11. House Committee on Government Reform and Oversight, U. S. Congress

(1997) Gulf War veterans': DOD continue to resist strong evidence linking

toxic causes to chronic health effects, 105th Congress, 1st Session, Report:

105-388.

12. U. S. General Accounting Office (1997) Gulf War Illnesses: improved

monitoring of clinical progress and reexamination of research emphasis are

needed. Report: GAO/SNIAD-97-163.

13. Nicolson GL, Nicolson NL. Townsend Lett. Doctors 1996;156:42-48.

14. Baseman JB, Tully JG. Emerg. Infect. Dis. 1997;3:21-32.

15. Van Kuppeveld FJM, et al. Appl. Environ. Microbiol. 1992;58:2606-2615.

16. Erlich HA, Gelfand D, Sninsky JJ. Science 1991;252:1643-1651.

17. Nasralla M, Haier J, Nicolson GL. Clin. Microbiol. Infect. Dis. 1999; in

press.

18. Vojdani A, Choppa PC, Tagle C, Andrin R, Samimi B, Lapp CW. FEMS

Immunol. Med. Microbiol. 1998;22:355-365.

19. Nicolson GL, Nicolson NL. Intern. J. Occup. Med. Immunol. Tox.

1996;5:69-78.

20. Nicolson GL, Nicolson NL, Nasralla M. Intern. J. Med. 1998;1:80-92.

21. Midvedt T. Scan. J. Rheumatol. Suppl. 1987;64:49-54.

22. Schaeverbeke T, et al. Rev. Rheumatol. 1997;64:120-128.

23. Simecka JW, Ross SE, Cassell GH, Davis JK. Clin. Infect. Dis. 1993;17

(Supp. 1):S176-S182.

24. Furr PM, Taylor-Robinson D, Webster ADB. Ann. Rheumatol. Dis.

1994;53:183-184.

25. Cole BC, Griffith MM. Arthritis Rheumatol. 1993;36:994-1002.

26. Kirchhoff H, et al. Rheumatol. Int. 1989;9:193-196.

27. Mühlradt PF, Quentmeier H, Schmitt E. Infect. Immunol.

1991;58:1273-1280.

28. Fox RI, Luppi M, Pisa P, Kang HI. J. Rheumatol. 1992;32:18-24.

29. Takei M, et al. Int. Immunol. 1997;9:739-743.

30. Krause A, Kamradt T, Burnmester GR. Curr. Opin. Rheumatol.

1996;8:203-209.

31. Tilley BC, et al. Ann. Intern. Med. 1995;122:81-89.

32. Savio ML, et al. New Microbiol. 1996;19:203-209.

33. Bauer FA, Wear D J, Angritt P, Lo S-C. Hum. Pathol. 1991;22:63-69.

34. Stadtlander CT, Watson HL, Simecka JW, Cassell GH. Clin. Infect. Dis.

1993;17 (Suppl. 1):S289-S301.

35. Blanchard A, Montagnier L. Ann. Rev. Microbiol. 1994;48:687-712.

36. Pollack J D, Jones MA, Williams MV. Clin. Infect. Dis. 1993;17 (Suppl.

1):S267-S271.

37. Nir-Paz R, Israel S, Honigman A, Kahane I. FEMS Microbiol. Lett.

1995;128:63-68.

38. Kaneoka H, Naito S. Jap. J. Clin. Med. 1997;6:1363-1369.

39. Baseman JB, Reddy SP, Dallo SP. Am. J. Respir. Crit. Care Med.

1996;154:S137-S144.

40. Balassanian N, Robbins FC. N. Engl. J. Med. 1967;277:719.

41. Gill JC, Cedillo RL, Mayagoitia BG, Paz MD. Ann. Allergy 1993;70:23-25.

42. Prattichizzo FA, Simonetti I, Galetta F. Minerva Cardioangiol.

1997;45:447-450.

43. Hofner G, et al. Zeit. Kardiol. 1997;86:423-426.

44. Bowman J, et al. J. Infect. Dis. 1998;178:274-277.

45. Tully JG, Taylor-Robinson D, Cole RM, Rose DL. Lancet 1981;1:1288-1291.

46. Risi GF Jr, Martin DH, Silberman JA, Cohen JC. Mol. Cell. Probes

1987;1:327-335.

47. Nicolson GL, Nicolson NL. JAMA 1995;273:618-619.

48. Nicolson GL. Intern. J. Med. 1998;1:115-117 and 123-128.

 

 

Prof. Garth L. Nicolson, Drs. Marwan Nasralla, Joerg Haier, Robert Erwin and

Nancy L. Nicolson are affiliated with The Institute for Molecular Medicine,

15162 Triton Lane, Huntington Beach, CA 92649-1401, (714) 903-2900, Fax

(714) 379-2082, website: www.immed.org, email: gnicimm; Dr.

Richard Ngwenya is affiliated with the James Mobb Immune Enhancement

Clinics, 132 Josiah Chinamano Ave., Harare, Zimbabwe, Fax: +263-4-739-832.

 

Dr. Nicolson et al's article is hereby published as one view of the possible

cause(s) of the Gulf War Syndrome and other chronic illnesses and because a

federal grant has been earmarked to evaluate his thesis, but its publication

should not be construed as an endorsement of that thesis by the Medical

Sentinel or the AAPS---Editor.

 

 

This article was published in the Medical Sentinel, Volume 4, Number 5,

September/October 1999, pp. 172-175, 191.

 

 

 

 

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