Archive for the ‘Mycoplasma’ Category

Mycoplasma and Other Intracellular Bacterial Infections in Rheumatic Diseases: Comorbid Condition or Cause?  by Garth Nicolson, May, 2017  Open Journal of Tropical Medicine

Letter to the Editor

Although the causes of rheumatic diseases have remained relatively unknown, systemic intracellular bacterial infections are commonly found in rheumatic disease patients [1-4]. Because of this, certain infections have been confused with comorbid conditions.

Often patients with rheumatic diseases have co-morbidities, and some authors have concluded that this can include chronic infections. “Infections continue to be a significant cause of morbidity and mortality in patients with rheumatic diseases, and, consequently, early diagnosis and treatment of infection is critical to the successful medical management of these patients” [5].

A link between certain types of infections and rheumatic diseases has been seen by a number of authors. For example, infections with Mycoplasma species, Borrelia species and other intracellular bacteria have been linked to various forms of rheumatic disease [1-4, 6-13]. In addition, animal models of rheumatic disease have been established by infection with Mycoplasma species [13-15]. In one of these contributions experimental arthritis was induced by a clinical isolate from M. fermentans injected into the joints of rabbits [15]. Outbreaks of rheumatic disease, such as polyarthritis, have been traced to infections by Mycoplasma species [16]. Arthritis in animals caused by Mycoplasma species infections closely resemble the signs and symptoms found in patients with rheumatoid arthritis [17]. In addition, reactive arthritis following M. pneumonia infection has been seen in patients [18]. Mycoplasma infections have also been found in the joints of patients with rheumatic disease [19-21]. In a case-control study the presence of antibodies against Mycoplasma pneumoniae have been statistically correlated to the clinical features of rheumatoid arthritis (p<0.001) [21]. Furthermore, genetic analyses and transmission in animals indicate that arthritis is not directly linked to genetic abnormalities [22]. The pathogenesis of rheumatoid arthritis appears to be linked to immunological features of infection(s) involving host recognition of foreign antigens that mimic host antigens or host antigens that are incorporated into microorganism structures and the presence of localized immune complexes and the influences of environmental conditions [22].

Standard treatments of chronic infections like mycoplasma often employ long-term antibiotics, such as but not limited to tetracyclines and other antibiotics [23-26]. The U.S. National Institutes of Health sponsored a double-blind, placebocontrolled, long-term clinical trial that showed that the antibiotic minocycline was safe and effective for the treatment of rheumatoid arthritis. The antibiotic-treated patients showed greater improvements in joint swelling and tenderness (p<0.02), and the treatment group also had better improvements in hematocrit, SED rate, platelet counts and rheumatoid factor with no serious toxicity [27, 28]. A 4-year follow-up indicated that the minocycline-treated patients had fewer relapses and less frequent need for immune-suppressive drugs to control their RA (p<0.02) [29]. Although treatment of arthritis with antibiotics was effective and safe, treatment failures can, just as in any treatment for arthritis, be due to therapeutic failures, resistance and/or mutation of the microorganism [30].

Part of the reason that most rheumatic disease patients do not receive antibiotic treatment may have more to do with the enormous pressure from the marketing and sales of various drugs that do little to address the underlying causes of rheumatic diseases than the effectiveness of various treatments.

In summary, intracellular bacteria are commonly linked to rheumatic diseases, especially rheumatoid arthritis and similar conditions, and these infections can be successfully treated with antibiotics. Treatment often but not always resulted in significant reductions in rheumatic signs and symptoms. Thus chronic infections, such as intracellular bacterial infections, do not appear to be simply co-morbid conditions in rheumatic disease patients. Although there is circumstantial evidence, such as the animal transmission experiments discussed above, that infections like Mycoplasma species may be the cause of rheumatic diseases like rheumatoid arthritis, this has still not been conclusively proven in clinical cases.


1. Ford D (1991) The microbial causes of rheumatoid arthritis. J Rheumatol 18: 1441-1442. Link:

2. Krause A, Kamradt T, Burnmester GR (1996) Potential infectious agents in the induction of arthritides. Curr Opin Rheumatol 8: 203-209. Link:

3. Hyrich KL, Inman RD (2001) Infectious agents in chronic rheumatic diseases. Curr Opin Rheumatol 13: 300-304. Link:

4. Horowitz S, Evinson B, Borer H, Horowitz J (2000) Mycoplasma fermentans in rheumatoid arthritis and other inflammatory arthritides. J Rheumatol 27: 2747-2753. Link:

5. Segal BH, Sneller, MC (1997) Infectious complications of immunosuppressive therapy in patients with rheumatic diseases. Rheum Dis Clin North Amer 23: 219-237. Link:

6. Ponka A (1979) Arthritis associated with Mycoplasma pneumoniae infection. Scand J Rheumato 8: 27-32. Link:

7. Schaeverbeke T, Vernhes JP, Lequen L, Bannwarth B, Bébéar C, et al. (1997) Mycoplasmas and arthritides. Rev Rheumatol Engl 64: 120-128. Link:

8. Schaeverbeke T, Gilroy CB, Bebear C, Dehais J, Taylor-Robinson D, et al. (1996) Mycoplasma fermentans but not M. penetrans detected by PCR in synovium from patients rheumatoid arthritis and other rheumatic disorders. J Clin Pathol 49: 824-828. Link:

9. Hoffman RW, O’Sullivan FX, Schafermeyer KR, Moore TL, Roussell D, et al. (1997) Mycoplasma infection and rheumatoid arthritis analysis of their relationship using immunoblotting and an ultra-sensitive polymerase chain reaction detection method. Arthritis Rheumatol 40: 1219-1228. Link:

10. Haier J, Nasralla M, Franco AR, Nicolson GL (1999) Detection of mycoplasmal infections in blood of patients with rheumatoid arthritis. Rheumatol 1999; 38: 504-509. Link:

11. Lünemann JD, Zarmas S, Priem S, Franz, J, Zschenderlein R, et al. (2001) Rapid typing of Borrelia burgdorferr sensu lato species in specimens from patients with different manifestations of Lyme Borreliosis. J Clin Microbiol 39: 1130-1133. Link:

12. Ford DK (1979) Yersinia-induced arthritis and Reiter’s syndrome. Ann Rheum Dis 38: 127-128. Link:

13. Cole BC, Griffi th MM (1993) Triggering and exacerbation of autoimmune arthritis by the Mycoplasma arthritidis super-antigen MAM. Arthritis Rheumatol 36: 994-1002. Link:

14. Mu HH, Nourian MM, Jiang HH, Justin WT, barry CC, et al. (2014) Mycoplasma super-antigen initiates a TLR4-dependent Th17 cascade that enhances arthritis after blocking B7-1 in Mycoplasma arthritidis-infected mice. Cell Microbiol 16: 896-911. Link:

15. Rivera A, Yanez A, Leon TG, Silvia G, Eduardo B, et al. (2002) Experimental arthritis induced by a clinical Mycoplasma fermentans isolate. BMC Musculoskelet Disord. Link:

16. Agnello S, Chetta M, Vicari Mancuso R, Manno C, Console A, et al. (2012) Severe outbreaks of polyarthritis in kids caused by Mycoplasma mycoides subspecies. Vet Rec. Link:

17. Jansson E, Backman A, Kakkarainen K, Miettinen A, Seniusová B (1983) Mycoplasmas and arthritis. Zeit Rheumatol 42: 315-319. Link:

18. Alvarez LB, Ceballos, BI, Alonso JL (2002) Reactive arthritis following a Mycoplasma infection. Med Clin (Barc).

19. Gilroy CB, Keat A, Taylor-Robinson D (2001) The prevalence of Mycoplasma fermentans in patients with infl ammatory arthritides. Rheumatol 40: 1355- 1358. Link:

20. Ataee RA, Golmohammadi R, Alishiri GH, Esmaeili D, JonaidiJ, et al. (2015) Simultaneous detection of M. pneumoniae, M. hominis and M. arthritidis in snovial fl uid of patients with rheumatoid arthritis by multiplex PCR. Arch Iran Med 18: 345-350. Link:

21. Ramirez AS, Rosas A, Hernandez-Rerain JA, orengo JC, Saavedra P, et al. (2005) Relationship between rheumatoid arthritis and Mycoplasma pneumonia: a case-control study. Rheumatol 44: 912-914. Link:

22. Ford DK (1969) Current views on the pathogenesis and etiology of rheumatoid arthritis. Canad Med Assoc 101: 147-151. Link:

23. Nicolson GL, Nasralla M, Nicolson NL (1999) The pathogenesis and treatment of mycoplasma infections. Antimicrob Infect Dis Newsl 17: 81-88. Link:

24. Nicolson GL, Nasralla M, Franco AR, A. Robert F, Nancy LN, et al. (2000) Diagnosis and integrative treatment of intracellular bacterial infections in chronic fatigue and fi bromyalgia syndrome, Gulf War illness, rheumatoid arthritis and other chronic illnesses. Clin Pract Alt Med 1: 92-102. Link:

25. Baseman JB, Tully JG (1997) Mycoplasmas: sophisticated, reemerging and burdened by their notoriety. Emerg Infect Dis 3: 21-32. Link:

26. Couldwell DL, Lewis DA (2015) Mycoplasma genitalium infection: current treatment options, therapeutic failure and resistance-associated mutations. Infect Drug Resist 8: 147-161. Link:

27. Tilley BC, Alarcon GS, Heyse SP, David ET, Rosemarie N, et al. (1995) Minocycline in rheumatoid arthritis. A 48-week, double-blind, placebocontrolled trial. MIRA Trial Group. Ann Intern Med 122: 81-89. Link:

28. Pillemer SR, Fowler SE, Tilley BC, Graciela SA, Stephen P, et al. (1997) Meaningful improvement criteria sets in a rheumatoid arthritis clinical trial. MRIA Trial Group. Minocycline in rheumatoid arthritis. Arthritis Rheumatol 40: 419-425. Link:

29. O’Dell JR, Paulsen G, Haire CE, Kent B, William P, et al. (1999) Treatment of early sero-positive rheumatoid arthritis with minocycline: four year follow-up of a double-blind, placebo-controlled trial. Arthritis Rheumatol 42: 1691-1695. Link:

30. Razin S, Yogev D, Naot Y (1998) Molecular biology and pathogenicity of mycoplasmas. Microbiol Mol Biol Rev 62: 1094-1136. Link:

For more on Mycoplasma see:

More on Minocycline:

Clinical Association: Lyme Disease and Guillain-Barre

According to this abstract in The American Journal of Emergency Medicine,  the authors state an association between GBS and Lyme is rare; however, the following article states that Epstein-Barr, also known as Mono, is an infection that triggers Guillain-Barre as well as mycoplasma and cytomegalovirus.

Dr. Garth Nicolson states that Mycoplasma is the most common co-infection with Lyme (borrelia).  Cytomegalovirus (herpes virus family) is also a coinfection to LD.

Which leaves EBV.

In Dr. Waisbren’s book, Treatment of Chronic Lyme Disease, the majority of his 51 cases of chronic Lyme had high EBV titers.  He also states,

“As will be seen in other cases, the Epstein-Barr virus may be a candidate for a co-infection associated with LD.”  

Waisbren often treated this co-infected patients that had EBV with 1000mg of Valtrex three times a day with good success.  He also used gamma globulin (4cc twice a week).

I think this is another great example of proclaiming something is rare when little research has been done.  Until Lyme patients are routinely tested for GB, I think it unwise to assume a connection is rare.  Researchers need to tread carefully in all things related to TBI’s, understanding that their words have been used against patients for decades.

Time to admit there’s a lot we frankly just don’t know.


Wolbachia – The Next Frankenstein?

Transmission electron micrograph of Wolachia within an insect cell

Credit:  Public Library of Science/Scott O’Neill

The latest in the effort for world domination over bugs and the diseases they carry is Wolbachia, a Gram-negative bacterium of the family Rickettsiales first found in 1924 and in 60% of all the insects, including some mosquitoes, crustaceans, and nematodes (worms). For those that like numbers, that’s over 1 million species of insects and other invertebrates. It is one of the most infectious bacterial genera on earth and was largely unknown until the 90’s due to its evasion tactics. It’s favorite hosts are filarial nematodes and arthropods.

Wolachia obtains nutrients through symbiotic relationships with its host. In arthropods it affects reproductive abilities by male killing, parthenogenesis, cytoplasmic incompatibility and feminization. However, if Wolbachia is removed from nematodes, the worms become infertile or die. These abilities are what make it so appealing for insect controlcytoplasmic incompatibility, which essentially means it results in sperm and eggs being unable to form viable offering.  (Nifty slide show here)

It also makes it appealing for use in human diseases such as elephantiasis and River Blindness caused by filarial nematodes, which are treated with antibiotics (doxycycline) targeting Wolbachia which in turn negatively impacts the worms. Traditional treatment for lymphatic Filariasis is Ivermectin but they also use chemotherapy to disrupt the interactions between Wolbachia and nematodes. This anti-Wolbachia strategy is a game-changer for treating onchocerciasis and lymphatic filariasis.

Lyme/MSIDS patients often have nematode involvement.  Both Willy Burgdorfer, the discoverer of the Lyme bacterium, as well as Richard Ostfeld, an animal ecologist found nematode worms in ticks. Since then, some provocative research involving nematodes, Lyme/MSIDS, dementia, and Alzheimer’s has been done.  Yet, according to many, Wolbachia is the next eradicator of Dengue Fever and possibly Malaria, chikungunya, and yellow fever because it stops the virus from replicating inside mosquitoes that transmit the diseases. The approach is also believed to have potential for other vector-borne diseases like sleeping sickness transmitted by the tsetse fly.  Evidently, Wolbachia does not infect the Aedes aegypti mosquito naturally, so researchers have been infecting mosquitoes in the lab and releasing them into the wild since 2011. The article states it hopes that the method works and expects infection rates in people to drop and hopes that the mosquitoes will pass the bacterium to their offspring, despite it disappearing after a generation or two of breeding and needing to “condition” the microbes to get them used to living in mosquitoes before injecting them. They also state Wolbachia is “largely benign for mosquitoes and the environment,” and “To humans, Wolbachia poses no apparent threat.” Their work has shown that the bacterium resides only within the cells of insects and other arthropods. They also state that tests on spiders and geckos that have eaten Wolbachia mosquitoes are just fine and show no symptoms. An independent risk assessment by the Commonwealth Scientific and Industrial Research Organizatioin (CSIRO), Australia’s national science agency, concluded that, “Release of Wolbachia mosquitoes would have negligible risk to people and the environment.”

Interestingly, trials are underway in Vietnam, Indonesia, and now Brazil.

They state that scaling up operations to rear enough Wolbachia mosquitoes is too labor-intensive and in Cairns they are going to put Wolbachia mosquito eggs right into the environment. Evidently, other researchers are wanting to release genetically modified (GMO) mosquitoes that carry a lethal gene, and they’ve done it, and it’s causing an uproar:  As of July 14, 2017, Google’s bio-lab, Verily Life Sciences,  started releasing Wolbachia laced mosquitoes in California as part of project, Debug Fresno to reduce the mosquito population.  Numerous studies show unexpected insertions and deletions which can translate into possible toxins, allergens, carcinogens, and other changes.  Science can not predict the real-life consequences on global pattens of gene function.

So, why question the use of Wolbachia as a bio-control?

For Lyme/MSIDS patients, 3 words: worms and inflammation.

Dogs treated for heart worm (D. immitis) have trouble due to the heart worm medication causing Wolbachia to be released into the blood and tissues causing severe Inflammation in pulmonary artery endothelium which may form thrombi and interstitial inflammation. Wolbachia also activates pro inflammatory cytokines. Pets treated with tetracycline a month prior to heart worm treatment will kill some D. immitis as well as suppress worm production. When given after heart worm medication, it may decrease the inflammation from Wolbachia kill off.

The words worms and inflammation should cause every Lyme/MSIDS patient to pause. Many of us are put on expensive anthelmintics like albendazole, ivermectin, Pin X, and praziquantel to get rid of worms and are told to avoid anything causing inflammation due to the fact we have enough of it already. We go on special anti-inflammatory diets and take systemic enzymes and herbs to try and lower inflammation.

Seems to me, many MSIDS/LYME patients when treated with anthelmintics, will have Wolbachia released into their blood and tissues causing wide spread inflammation, similarly to dogs.

And that’s not all.

According to a study by Penn State, mosquitoes infected with Wolbachia are more likely to become infected with West Nile – which will then be transmitted to humans.“This is the first study to demonstrate that Wolbachia can enhance a human pathogen in a mosquito, one researcher said. “The results suggest that caution should be used when releasing Wolbachia-infected mosquitoes into nature to control vector-borne diseases of humans.” “Multiple studies suggest that Wolbachia may enhance some Plasmodium parasites in mosquitoes, thus increasing the frequency of malaria transmission to rodents and birds,” he said.  The study states that caution should be used when releasing Wolbachia-infected mosquitoes into nature.

So besides very probable wide spread inflammation, and that other diseases may become more prevalent due to Wolbachia laced mosquitoes, studies show Wolbachia enhances Malaria in mosquitos. Lyme/MSIDS patients are often co-infected with Babesia, a malarial-like parasite that requires similar treatment and has been found to make Lyme (borrelia) much worse. It is my contention that the reason many are not getting well is they are not being treated for the numerous co-infections.  Some Lyme/MSIDS patients have Malaria and Lyme.

Regardless of what the CDC states, all the doxycycline in the world is not going to cure this complicated and complex illness.

Lastly, with Brazil’s recent explosion of microcephaly, the introduction of yet another man-made intervention (Wolbachia laced mosquitos) should be considered in evaluating potential causes and cofactors. And while the CDC is bound and determined to blame the benign virus, Zika, there are numerous other factors that few are considering – as well as the synergistic effect of all the variables combined. Microcephaly could very well be a perfect storm of events.

I hate bugs as much as the next person, but careful long-term studies of Wolbachia are required here.  “Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.

In short, borrelia (as well as numerous pathogens associated with Lyme/MSIDS), is a smart survivor.

While borrelia have been around forever with 300 strains and counting worldwide, epidemics, such as what happened with Lyme Disease in Connecticut are not caused by genetics but by environmental toxins – in this case, bacteria, viruses, funguses, and stuff not even named yet.

Circling back to Wolbachia.

Hopefully it is evident that many man-made interventions have been introduced into the environment causing important health ramifications: Wolbachia laced mosquitoes and eggs, GMO mosquitoes including CRISPR, and in the case of Zika in Brazil, whole-cell pertussis vaccinations (DTap) for pregnant women up to 20 days prior to expected date of birth, a pyriproxyfen based pesticide applied by the State in Brazil on drinking water, as well as aerial sprays of the insect growth regulators Altosid and VectoBac (Aquabac, Teknar, and LarvX, along with 25 other Bti products registered for use in the U.S.) in New York (Brooklyn, Queens, Staten Island, and The Bronx) to combat Zika. “We feel it’s critical that the scientific community consider the potential hazards of all off-target mutations caused by CRISPR, including single nucleotide mutations and mutations in non-coding regions of the genome … Researchers who aren’t using whole genome sequencing to find off-target effects may be missing potentially important mutations. Even a single nucleotide change can have a huge impact.”

All of this is big, BIG business.

Is the introduction of Wolbachia another puzzle piece in the perfect storm of events causing or exacerbating human health issues?

The jury’s still out, but it’s not looking good – particularly for the chronically ill.

One Tick Bite Could Put You at Risk For at Least 6 Different Diseases by Kevin Loria, June 28,2017

The deer tick, also known as the blacklegged tick, is a fascinating but nasty little creature, and it’s spreading.

The tiny arthropods carry Lyme disease — the serious illness that we most associate them with — but that’s not the only pathogen they spread.

“One thing that people really need to be aware of is that Lyme disease is not the only pathogen that’s out there — there’s quite a few of them, [including] probably quite a few that we haven’t discovered yet,” says Rafal Tokarz, an associate research scientist at Columbia University’s Mailman School of Public Health.

And the deer tick, which as far as we know carries more illnesses than any other tick, “has been expanding its range enormously in the last 30 years,” says Durland Fish, professor emeritus of epidemiology at the Yale School of Public Health. Before the early 70s, it was largely unknown outside the Northeast, but now it has spread north, south, and west.

The diseases that we know deer ticks spread are all serious:

1. Lyme disease, which is transmitted by ticks infected with the bacterium Borrelia burgdorferi, infects roughly 300,000 Americans every year. It can be treated with antibiotics if caught early, but can cause severe inflammation, nerve, and joint pain, among other symptoms, if left untreated.

2. When people are infected with babesiosis, parasites infect and destroy red blood cells. Not everyone shows symptoms but it can be life-threatening for some at-risk patients. It’s “like tick-borne malaria,” says Fish, and is the most important contaminant of the blood bank right now, he says.

3. Anaplasmosis is spread by another bacteria carried by deer ticks. It usually shows up a week or two after a bite and can cause fever, headaches, nausea, and general malaise, among other symptoms. If untreated it can be severe, leading to hemorrhage, renal failure, and for a small fraction of even healthy patients, potentially can be fatal.

4. Deer ticks can also spread the Borrelia miyamotoi bacteria, which Fish says is similar to the one that causes Lyme. Symptoms include joint pain, fatigue, fever, chills, and headache.

5. A relatively recently discovered disease that’s spread by deer ticks as well as dog and Lone Star ticks is ehrlichiosis, caused by a bacteria in the same family as the one responsible for Rocky Mountain spotted fever. Symptoms often present like the flu.

6. Powassan virus has been around for a while but has received more attention recently, especially since the deer tick (which frequently bites humans) started spreading it — the ticks that transmitted the first reported cases in the 1950s rarely bite people. Unlike Lyme, which often takes many hours or even a couple days before it’s transmitted, Powassan infection can occur in as little as 15 minutes. Not everyone who gets bitten by an infected tick gets sick, but if they do, it’s a serious problem since there’s no treatment. In those (still rare) cases, Fish says that there’s about a 50% chance of permanent neurological damage and a 10% chance of death.

The broad range of potential conditions means that doctors don’t even necessarily know what to look for. Even worse, “ticks can frequently be co-infected with more than one pathogen,” says Tokarz. That’s especially true in certain locations, like on Long Island. One bite could transmit both Lyme disease and babesiosis, conditions that would normally be treated quite differently.

It’s also possible that having two or more illnesses could change the way the disease manifests. “We still don’t know whether co-infection exacerbates a disease or doesn’t make a difference,” says Tokarz.”Studies have shown both.”

Unfortunately, we don’t have any good way to control ticks and to stop the ongoing expansion, which will lead to more people getting sick.

In the places where people are at risk of picking up a tick “it is a very important, very severe problem, but the only thing that can be done is to educate people on the dangers of coming into contact with ticks,” says Tokarz.

If you get one on you, pull it off right away — don’t bother with urban legends about needing to burn it off. And protect yourself if you are going to be hiking or spending time in a place where ticks are common. Use permethrin-treated clothing for outdoors work and use insect repellent that contains DEET.


**My letter to the author**

Dear Mr. Loria,

Thank you for your piece on ticks and the pathogens they carry. I just wanted to add to your list; however, as there are many more pathogens carried by ticks. Also, they are discovering a variety of ticks carry pathogens, and if you think about it logically for a moment, ticks have similar habits and mouth parts, and require blood meals to survive, which technically makes every tick suspect. Unfortunately, geographical maps and entomology information (which ticks spread what) have been used to deny patients diagnosis and treatment. A doctor will look at the CDC map and claim, unequivocally, that since such and such isn’t supposed to be in that state, it isn’t TBI’s (tick borne infections). and then eventually they have to admit they are wrong:

How many went undiagnosed through the years?

Borrelia miyamotoi
Bourbon Virus
Colorado Tick Fever
Heartland Virus
Meat Allergy/Alpha Gal
Pacific Coast Tick Fever: Richettsia philipii
Powassan Encephalitis
Q Fever
Rickettsia parkeri Richettsiosis
Rocky Mountain Spotted Fever
STARI: Southern Tick-Associated Rash Illness
Rick Paralysis

I run a physical support group here in Wisconsin, 6th in the nation for TBI’s, and nearly all of us are co-infected, and while Tokarz states he doesn’t know whether coinfection exacerbates a disease, we all do.

Babesia can increase the severity of Lyme disease. Coinfected patients were more likely to have experienced fatigue, headache, sweats, chills, anorexia, emotional lability, nausea, conjunctivitis, and splenomegaly more frequently than those with Lyme disease alone. [7]
Babesia can also increase the duration of illness with Lyme disease. Babesia patients can remain symptomatic for years with constitutional, musculoskeletal, or neurological symptoms. One study found that 50% of coinfected patients were symptomatic for 3 months or longer, compared to only 4% of patients who had Lyme disease alone. [7] Meanwhile, one-third of patients with a history of both Babesia and Lyme disease remained symptomatic an average of 6 years. [2]

“The clinical pictures for 3 out of our 4 coinfected patients included a large number of symptoms, and 1 coinfected patient had persistent fatigue after treatment,” according to a study by Steere and colleagues. [8]”

For a fantastic book on all of this and more, read science journalist and past Executive Editor of Discover Magazine, Pam Weintraub’s work, Cure Unknown: Inside the Lyme Epidemic.

Alicia Cashman
Madison Lyme Support Group




Membrane Lipid Replacement for Lyme/MSIDS

Available online 18 April 2017  Garth L. Nicolsona, , , E-mail author,Michael E. Ash


Membrane Lipid Replacement is the use of functional, oral supplements containing mixtures of cell membrane glycerolphospholipids, plus fructooligosaccharides (for protection against oxidative, bile acid and enzymatic damage) and antioxidants, in order to safely replace damaged, oxidized, membrane phospholipids and restore membrane, organelle, cellular and organ function. Defects in cellular and intracellular membranes are characteristic of all chronic medical conditions, including cancer, and normal processes, such as aging. Once the replacement glycerolphospholipids have been ingested, dispersed, complexed and transported, while being protected by fructooligosaccharides and several natural mechanisms, they can be inserted into cell membranes, lipoproteins, lipid globules, lipid droplets, liposomes and other carriers. They are conveyed by the lymphatics and blood circulation to cellular sites where they are endocytosed or incorporated into or transported by cell membranes. Inside cells the glycerolphospholipids can be transferred to various intracellular membranes by lipid globules, liposomes, membrane-membrane contact or by lipid carrier transfer. Eventually they arrive at their membrane destinations due to ‘bulk flow’ principles, and there they can stimulate the natural removal and replacement of damaged membrane lipids while undergoing further enzymatic alterations. Clinical trials have shown the benefits of Membrane Lipid Replacement in restoring mitochondrial function and reducing fatigue in aged subjects and chronically ill patients. Recently Membrane Lipid Replacement has been used to reduce pain and other symptoms as well as removing hydrophobic chemical contaminants, suggesting that there are additional new uses for this safe, natural medicine supplement. This article is part of a Special Issue entitled: Membrane Lipid Therapy: Drugs Targeting Biomembranes edited by Pablo Escríba-Ruíz.

The article also noted that while glycerolphospholipid absorption in the upper intestines was over 90%, after a large meal, and transported into the blood within 6 hours, dietary MLR polyunsaturated phospholipids are oxidized and degraded during storage, ingestion, digestion, and absorption and need to be protected from acid degradation in the gut and bile salts and hydrolysis from the pancreas and gut microflora in the small intestines.  The researchers found an answer to this problem by complexing MLR phospholipids with specific fructooligosaccharides (Inulins), which protect from oxidation and high temps, acidity, and phospholipases and bile salts.

Plants such as legumes or cabbage are good sources for MLR supplementation but in order to get a daily dose of 1.8 g of membrane phospholipids you’d have to have an intake of 15 kg of beans!

The most convenient, efficient, safe and cost effective method of membrane phospholipid administration in humans has been the use of daily oral lecithin supplements [1]; [2]; [3] ;  [6]. Most oral lecithin supplements are rather crude soy, egg yolk or marine preparations that lack oxidation, bile and phosphatase protection. In addition, most of these oral supplements have not been carefully analyzed for phospholipid composition, and in particular for lipid degradation products. However, there are oral MLR phospholipid supplements, such as NTFactor® and NTFactor Lipids®, that fulfill the requirements for efficacy, oxidation and degradation protection, safety and convenience [1]; [2] ;  [3]. The NTFactor® lipid supplements, and their use in clinical studies, will be discussed in more detail in 8, 9, 10 ;  11. NTFactor®, which also contains probiotic bacteria, growth media and other ingredients, and NTFactor Lipids®, without these additives, come in several oral forms, but almost all contain from 1–2 g of phospholipids per dose [1]; [2] ;  [3]. The recommended optimal daily oral dose of NTFactor Lipids® for most clinical conditions has been estimated at 2–4 g per day, and more recently at least 4 g per day, whereas its anti-aging use has been proposed at 2 g per day [2]. Some updates in these recommendations will be discussed in Section 12.

A table in the article shows uses for MLR supplements such as fatigue, infections, autoimmune, and chemical detox and revised dose levels.  These are issues nearly every Lyme/MSIDS patient has.  The dosages for these issues are upwards of 4g/day, showing the intensive mitochrondrial damage these issues cause in the body.

Due to intense detoxification efforts by the liver, many Lyme/MSIDS patients have high liver titers.  The good news is that patients with advanced liver cirrhosis were given oral MLR phospholipids and after just 3 months had normal blood results for liver function.  They are also safe to use during pregnancy and have in fact been used in high risk pregnancies with success.

**The authors are part-time consultants to Nutritional Therapeutics, Inc. and Allergy Research Group, Inc.



Minocycline for MS and Much More

Canadian researchers have discovered that minocycline, a common acne medication, can slow relapsing-remitting multiple sclerosis in those with initial symptoms.

Standard treatment costs for MS treatment in Canada range from $20,000 to $40,000 per year, with the cost tripled in the U.S.  Treatment using minocycline would cost about $600 per year.  

According to lead author, Dr. Luanne Metz, neurologists will be able to give mino to patients who have MRI results suggesting an MS cause and who are suffering with initial symptoms of demyelination.  

In the study, one group was given 100mg twice a day of minocycline while the other group was given a placebo.  Over six months there was a 27.6% reduction in full blown MS.  (Risk was 61% in placebo group and 33.4% in the mino group).

Minocycline has been used safely and effectively for over 30 years and has many anti-inflammatory and antioxidant properties, chelates calcium and is well-tolerated.  A Tetracycline drug that is bacteriostatic, it is widely used against both gram negative and gram positive pathogens including Rickettsia, Chlamydia, Plasmodium spp., and Mycoplasma pneumoniae.

Minocycline, as most Lyme/MSIDS patients know, is one of the most effective antibiotics which crosses the blood brain barrier, due to its high lipid solubility.  It is one of my personal favorites and the most effective drug for the excruciating occipital (base of the skull) headaches I get due to Tick-borne infections.  If you experience these, please read: as brain infections can cause Chiari.

According to Spanish researchers, Minocycline is much more than just an antibiotic.  Minocycline far beyond an antibiotic  Not only is it antimicrobial and anti-inflammatory, it has also been shown to be neuroprotective, anti-apoptotic, and it inhibits proteolysis, angiogenesis and tumor metastasis.  Preclinical trials have shown it to inhibit malignant cell growth and activation and repletion of HIV, and  prevents bone resorption.  It has helped those with Parkinson’s, Huntington’s, ALS, Alzheimer’s, and spinal cord injury.  The link in blue demonstrates minos effectiveness against dermatitis, periodontal disease, rheumatoid arthritis, and CNS (central nervous system) pathologies, osteoporosis, and autism, as well as has potential to help atherosclerosis, inflammatory bowel disease, and allergic asthma.  The researchers also feel mino is a rational treatment for neuropathic pain, something Lyme/MSIDS patients understand up close and personal.

Mino is inexpensive, has a known side-effect profile, and is well-absorbed (95-100%).  It, along with doxycycline, due to their ability to penetrate the cell wall, is commonly used for Lyme disease treatment:

Hidden Invaders: Infections Can Trigger Immune Attacks on Kids’ Brains Provoking Devastating Psychiatric Disorders  By Pamela Weintraub Wednesday, March 29, 2017

Hidden Invaders:  Infections can trigger immune attacks on kids’ brains, provoking devastating psychiatric disorders.

Please read Weintraub’s detailed article in link above about seven year old Paul who changed over night, due to pediatric acute-onset neuropsychiatric syndrome (PANS).  

“PANS is thought to be an inflammatory condition that results when an infection or some other invasive trigger spurs the body to turn on itself and attack structures in the brain. For years, scientists had focused on a single infection — group A streptococcal disease — that produced antibodies that attacked the part of the forebrain involved in forming habits, resulting in OCD. Today, the paradigm has widened into a much bigger idea that expands our understanding of psychiatric disease: A whole host of infections and other unknown triggers lead to the production of antibodies and immune cells that can cross into the brain. Depending on where these immune responses land and which brain structures they block, erode or destroy, a range of psychiatric ills can result. In one person, it could be OCD; in the next, it could be hyperactivity and inattention, anxiety, restricted eating, even hallucinations or autistic behavior.”

A prominent Wisconsin Lyme literate doctor states that 80% of his PANS children are also infected with Lyme/MSIDS.  They respond and improve with antibiotics, diet change, probiotics, and other supplements to improve immune function. According to Weintraub, researchers are trying to find the right treatment that stops inflammation and immune dysfunction due to rogue antibodies that attack the brain.

Weintraub also reports that strep infections can cause neuropsychiatric symptoms.  One psychiatrist found that some patients right after a strep infection could develop OCD and eating disorders.  She also found that children with OCD from PANDAS had toxic behavior reactions to typical medications that helped those with standard OCD showing the two groups were not equal.  In studying 43 children with acute onset OCD, the infectious triggers were strep and mycoplasma.  She treated them with Azithromycin and the patients improved.

Untreated PANS children can be disabled by their psychiatric symptoms and have, “OCD with severe intrusive thoughts such as suicidal ideation, psychosis, deep anxieties and fears, panic, rage, and are at risk of committing violent acts, ” as well as cognitive problems such as:  “handwriting deterioration, slow processing speed and regressions so frightening that a once-normal 10-year-old might have the skills and behavior of a developmentally slow 3-year-old.”

A pediatric rheumatologist managed to find clusters of children from the same school or neighborhood who had all come down with the condition in the same month as well as other infections besides strep were involved, such as bacterial mycoplasma, influenza, sinusitis, pneumonia and others.  Incredible video by Dr. Marke with written highlights and discussion on PANDAS/PANS.