Borrelia – In the Lymelight

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Joel (Snowathlete) continues his series on zoonotic pathogens with a thorough examination of Borellia and Lyme disease - and their possible relevance for ME/CFS patients.


Borrelia spirochete
by Tina Carvalho, University of Hawaii at Manoa


Borrelia is the bacterium that causes borreliosis. It is a microscopic spiral-shaped parasite. There are many different species of Borrelia, some of which cause Lyme borreliosis, otherwise known as Lyme disease.

Borrelia is a zoonotic pathogen transmitted via a vector, usually a tick. There is evidence that other arthropods such as fleas, biting flies, mites and spiders also carry it, but so far there is only limited - mainly anecdotal - evidence of transmission to humans by non-tick arthropods.

Transmission from ticks appears to be the most common and important method of transmission, perhaps because ticks have a salivary protein called Salp15 which the Borrelia attaches to and which is thought to have immunosuppressive effects [1]. Following transmission, Borrelia can travel through the body quite rapidly, including into the central nervous system [2, 3].


How common is it?

Borreliosis, including Lyme and Lyme-like diseases, is one of the most prevalent infectious diseases in the world. In the USA it is the most commonly-reported vector-borne disease and the sixth most common disease nationally. It is more prevalent in the northeast and upper Midwest of the US; in Massachusetts, only hepatitis and HIV-AIDS are more common, despite under-reporting.


Deer Ticks (Ixodes scapularis)
Photo by Sandy__R


In the past there has been a view that tick-borne infections, particularly Borrelia, are only common in the US and that other parts of the world don’t have a problem. This is simply not the case, with the UK, mainland Europe and Asia/Oceania also affected. The disease is the same, the ticks (and often the species of Borrelia) are different.

The existence of Lyme disease in Australia is controversial. The government has strict border controls to stop foreign insects and pathogens from entering the country, and the government have been reluctant to accept that there is a local problem, claiming that Borrelia infection occurs outside the country when people travel abroad. Most Lyme organizations in Australia dispute this and so does some of the medical literature [4].


Different strains

In North America, the predominant strain that causes Lyme disease is Borrelia burgdorferi. This strain also occurs in Europe and Asia, though B. garinii and B. afzelii are more common in these areas. Many other strains are known to infect humans and cause disease, some being suspected of causing Lyme, or Lyme-like illness. In particular, two other strains; B. spielmanii and B. bavariensis (both closely related to B. burgdorferi) are now widely acknowledged to cause Lyme disease.

Some strains have only been confirmed to cause borreliosis in the last few years, but have possibly been doing so for much longer[5].


Co-infections

Those diagnosed with Lyme disease often have co-infections, usually transmitted by the same tick that gave them Borrelia, and these co-infections can complicate disease and treatment. Some of the more common co-infections are Babesia, Rickettsia, Ehrlichia and Bartonella, and they can be serious in their own right. It is common for ticks to transmit multiple pathogens in one bite. Some of these other pathogens will be discussed in detail in future articles in the zoonotics series.


Symptoms


Borrelia spirochete agglomeration into colony-like masses.
Image courtesy of BioMed Central.

When you peruse a list of symptoms caused by Lyme disease or other borreliosis, you can’t help but notice that most of the symptoms in the list are the same, or similar, to those belonging to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and fibromyalgia.

As with ME/CFS the disease tends to get worse over time with new symptoms developing. A quick Google search will return many pages with information on symptoms. As most readers will be familiar with the majority of these symptoms already, I won’t try to list them here. Instead, I will focus on those symptoms that are usually distinguishable from ME/CFS, though not everyone with Lyme disease will have these symptoms.
  • Lyme can cause paralysis of facial muscles, sometimes called Bell’s palsy. It tends to be on only one side of the face and often is not permanent.
  • Meningitis may also develop from Lyme, or from other forms of borreliosis, and is another symptom which is not as common in ME/CFS.
  • Atrophy of the skin may occur, especially with treatment as the Borrelia rise to the peripheral circulation to avoid antibiotic contact.
Having any of the above may signal that you have Lyme rather than ME/CFS, though not having them doesn't necessarily rule out Lyme.

The other species of Borrelia that cause non-Lyme borreliosis tend to produce milder symptoms, the main presentation being relapsing fever or short-term virus-like illness, but some strains such as B. miyamotoi can, in some cases, cause severe disease [5].


Borrelia's effect on the immune system and its ability to change form


Borrelia cysti, covered by a thick membrane masking the contents of the cyst.
Image courtesy of BioMed Central.

Borrelia is reported to spread quickly to the central nervous system [2, 3] where it is harder to touch, and it is thought that the longer you’ve had it, the harder it is to get antibiotics to these places to kill it.

Genetically speaking, Borrelia is a very advanced bacterium [6]. It is pleomorphic, which means that it can change form from a spirochete to a cell-wall-deficient L-form [25] which is thought to be a mechanism of defense and antibiotic resistance [7, 8]. There is also evidence that Borrelia is able to create biofilm[9] which is thought to provide resistance to antibiotics and immune cells.

Borrelia is the only bacterium with 21 plasmids (B. burgdorferi), which gives it a diverse arsenal. Plasmids are pieces of DNA separate from the chromosomal nucleus of the cell, and they express surface-proteins that are essential to the bacteria’s pathogenicity [10].


Ötzi the Iceman

The remains of Ötzi the Iceman, a deceased human discovered in the Alps in 1991, were found to be infected with Borrelia burgdorferi [11, 12], showing that the bacteria has been infecting humans for at least 5300 years.

Nevertheless, there is some suggestion that Lyme disease has become more pathogenic recently as cases have increased so much in the last 50 years. This may in fact be down to improved recognition and reporting, but there is another theory that it is related to changes in the environment that have favored ticks.

Another interesting view is that Lyme may cause autoimmunity [13,14,15], which is interesting because autoimmune diseases appear to have been on the increase in the modern age as well, and some people believe ME/CFS to be an autoimmune disease (see my previous article here). Perhaps it is possible that Borrelia may be a trigger for ME/CFS autoimmunity?


How is it tested?


Otzi the Iceman - not your typical Lyme disease sufferer

You’d think that as they managed to detect Borrelia in Ötzi, a guy who’s been dead for more than five millennia, it should be a simple matter to detect it in living patients in the here and now, but it isn’t, and as a result the testing of Lyme disease is controversial.There are many who believe that Lyme tests often produce false-negatives, though some disagree about this, and then there is the question of false-positives too... So who is right?

A recent argument for the reliability of tests (at least with established infections) is made by John J Halperin et al [16].However,there are those in the Lyme community that disagree with the science behind many of the conclusions in this article, and they may be right on some points. A key fact, I think, is that the Centers for Disease Control and Prevention (CDC) still says that Lyme diagnosis should not be based solely on test results, which does support the view that the tests are not reliable enough.

Questions aside over the reliability of the approved tests, there is evidence that those who are immunocompromised are more likely to turn up false-negatives for Lyme as the FDA approved tests look for antibodies. The problem is that those with a compromised immune system may not produce antibodies properly [17]. This could therefore be relevant for those of us with ME/CFS because of the evidence of immune dysfunction.


The FDA approved tests

The FDA currently recommends a two-step test process using two different types of test. If the patient is positive or equivocal in the first test then the second test is carried out. If either test is negative then the tests indicate that the patient does not have Lyme disease.

The first test is an enzyme-linked immunoassay (ELISA), which looks for antibodies against Borrelia in the blood. The second test is known as a western blot and looks for immunoglobulin M (IgM) and/or immunoglobulin G (IgG) antibodies.

The results of the approved western blot tests are themselves contentious, as the results that are returned have to be interpreted and the CDC seems to be quite conservative about what constitutes a positive result. Therefore, some people believe that some results that the CDC would deem negative should in fact be read as positive.


Non-approved tests

There are several non-approved tests, some using blood, some using other fluids, some looking for DNA, others for antibodies or antigens. But what is consistent is that they all cost money and because they are not FDA approved you may question their reliability, and even if you don’t, your doctor probably will. Some of the alternative tests on the market have at least been formally assessed and so you may find such published papers [18] useful in making your own judgment on the value of such tests.

Rather than trying to make such a judgment for you or trying to produce an exhaustive list, instead I am just going to mention some of the more commonly recommended tests, though I personally have no experience with any of these tests myself.

Infectolabs in Germany are often suggested, and seem to find a number of people positive who had previously tested negative using the FDA approved tests. Another lab often recommended is IgeneX in the US which also offers a variety of different tests for Borrelia.


Chronic Lyme

Chronic Lyme (or ‘post treatment Lyme disease syndrome’ as the CDC prefers to call it) is controversial. At the heart of it are two opposing organizations and the only thing they have in common is the letters they share in their acronyms. Although it may sound like the title of a bad B movie, a paper titled “Lyme disease: the next decade” [19] does a good job of explaining the differences between these two groups, but I will briefly summarize it here:

Representing the dark-side in our little B movie, we have the Infectious Diseases Society of America (IDSA) who essentially state that chronic Lyme doesn’t exist and have tried to limit treatment of the condition. Representing the light-side you have the International Lyme and Associated Diseases Society (ILADS – remember: the one with the L in the acronym is on the light-side) who speak up for the many thousands of people who have difficulty recovering from Lyme, even after treatment.

This study [20], which supports the views of the IDSA, claims that chronic Lyme doesn’t exist. Nevertheless, the evidence to the contrary is not insignificant, and there has even been litigation against the IDSA alleging conflicts of interest that may have influenced their position on chronic Lyme.

The thing is, it’s all too easy to dismiss an illness like this, isn’t it? That is, unless you're the guy suffering from it, in which case you know all too well how real it is.

Whatever the reason - unidentified infection, bacterial remnants, autoimmunity, irreversible damage - I believe these people are sick, and just like ME/CFS, the illness is not given the attention it deserves.


How is Lyme disease treated?


lone-star tick (Amblyomma americanum)
by Elizabeth Nicodemus

Unsurprisingly, treatment is controversial too, with some believing that longer and stronger treatment is needed, especially in long established illness.

One of the important factors here is that Borrelia is known to replicate slowly, often only once or twice in 24 hours, whereas a bacterium such as staphylococcus (mentioned in my first article on zoonotics) would replicate around 70 times in 24 hours. This is important because many antibiotics target the cell wall of bacteria when they are dividing.

Antibiotics are bactericidal (they kill bacteria) or bacteriostatic (they inhibit replication), so bacteriostatic antibiotics given in short courses may not reduce Borrelia infection very much. Bactericidal antibiotics are probably better against Borrelia, but still the argument is made that low dose and short-course treatments are insufficient to kill most of the infection. This leads to some experts stating that long-term antibiotic treatment is required to control or eradicate Borrelia.

Those that are immunosuppressed by another illness can have more difficulty eradicating Borrelia and so it seems reasonable to suspect that anyone with both Borrelia and ME/CFS would have difficulty with treatment. Additionally, someone with Lyme may be more susceptible to ME/CFS and probably other illnesses, due to the immune impact of Lyme.

Different antibiotic treatments may be given to target Borrelia in its various guises and stages of illness. The treatment of choice is usually doxycycline, but other antibiotics including penicillin, amoxicillin and cefuroxime axetil are also commonly prescribed. In more stubborn cases cefotaxime or ceftriaxone may be given intravenously. Treatment in pregnancy is usually with erythromycin.

As well as ceftriaxone, minocycline or metronidazole may be used where infection of the brain is suspected as it crosses the blood-brain barrier. Additionally, there is evidence that metronidazole may be more effective against Borrelia in its cyst form [21].


What has this to do with ME/CFS?

Some people think that ME/CFS is actually undiagnosed Lyme. There is some limited evidence for that, such as a study from Poland which found that 50 percent of patients diagnosed with borreliosis or tickborne encephalitis could be identified as having CFS, concluding: "The findings suggest that the chronic fatigue syndrome is frequent among patients with a history of borreliosis."[22]. This illustrates that tickborne zoonotics may be implicated in ME/CFS. Alternatively, it could be argued that this is just a result of the two illnesses presenting with similar symptomology.

Another study looked at gender differences and found that women were significantly more likely to develop chronic Lyme compared to men [23]. This is interesting, given the higher ratio of women to men with ME/CFS. Of course, correlation does not constitute evidence, and the finding may support other conclusions, such as the higher degree of women with autoimmune diseases.

A recent study provides evidence which suggests the two diseases are distinct by demonstrating that the cerebrospinal fluid was different in the two conditions [24].

As you can imagine, both sides continue to argue over whether the two illnesses are the same, related, or completely separate. I’m not sure there is enough evidence either way yet, but what is certain is that some people with ME/CFS do later turn out to have Lyme disease. In the last two months on the Phoenix Rising forum I have noticed at least three recent posts (Jan-Feb 2013) from ME/CFS sufferers who have been tested for Lyme and come up positive.

Then you have to bear in mind that Lyme is caused by several different species of Borrelia, as explained above, and several other species are suspected of causing Lyme. Each comes with its own flavor of Lyme disease, where symptoms differ slightly. Additionally, as stated earlier, some people infected with Borrelia don’t get Lyme disease but get other borreliosis illnesses, some of which come with overlapping symptoms to ME/CFS, or which may be present as co-infections.

And importantly, if the illnesses are distinct, then there is still no rule that says you can’t have ME/CFS and Lyme disease at the same time.

Not all species of Borrelia are tested for, and probably not all are even discovered yet, as most have only been discovered in the last two decades. Indeed, the Australian government agree that another pathogen infecting Australian ticks, either a novel Borrelia or some other zoonotic, may be the cause of Lyme-like disease in the country, so there is still room for a greater number of people to have Lyme, borreliosis, or some other tick-borne pathogen as the cause of their ME/CFS, or at least as a co-infection.

Whereas there is some scope for ME/CFS to turn out to be caused by Borrelia, I don’t think anyone can reasonably make that kind of claim yet. For the moment it is categorized as a different illness. Nevertheless, I think the similarities are quite intriguing and at the very least some people labeled as having ME/CFS do have Lyme either instead of, or as well as, ME/CFS. I think it is good, therefore, that some ME/CFS doctors do test for it, and adjust their treatment protocols accordingly. Lerner, De Meirleir, probably one or two others, but it does appear that some ME/CFS doctors overlook it.


What should I do then? Get tested?

With the symptoms being similar and with the knowledge that some people with a diagnosis of ME/CFS do later test positive for Lyme, it has to be said that there is a case for getting tested. Most of us would probably bite your Borrelia-infested arm off if we could swap from an illness of unknown etiology to one of proven etiology, with some prospect of treatment.

The level of testing you go to is of course a different topic and there are no easy answers on how far you should pursue it, but it would seem prudent to at least have the standard FDA approved tests, and if you live in a region where Lyme is endemic, or you think you have some other reason to suspect that you might have been bitten, then you may want to explore test options further.

Joel was diagnosed with ME/CFS in 2009 but struggled with the illness for some time prior to this. He loves to write, and hopes to regain enough health to return to the career he loved and have his work published.


OTHER ARTICLES BY THIS WRITER:
REFERENCES:
  1. Joppe W.R. Hovius, et al. Tick–host–pathogen interactions in Lyme borreliosis. 2007.
  2. Steer AC, et al. The Emergence of Lyme disease. 2004.
  3. Pachner AR, et al. Lyme neuroborreliosis: infection, immunity, and inflammation. 2007.
  4. Mayne PJ. Emerging incidence of Lyme borreliosis, babesiosis, bartonellosis, and granulocytic ehrlichiosis in Australia. 2011.
  5. Platonov AE, et al. Humans infected with relapsing fever spirochete Borrelia miyamotoi , Russia. 2011.
  6. Frazer, et al. Genomic sequence of a Lyme disease spirochaete, Borrelia burgdorferi. 1997.
  7. Elizabeth Fuller, et al. β-Lactam Resistance in Staphylococcus aureus Cells That Do Not Require a Cell Wall for Integrity. 2005.
  8. A Kersten, et al. Effects of penicillin, ceftriaxone, and doxycycline on morphology of Borrelia burgdorferi. 1995.
  9. Sapi E, et al. Characterization of Biofilm Formation by Borrelia burgdorferi In Vitro. 2012.
  10. Chan K, et al. Detection of established virulence genes and plasmids to differentiate Borrelia burgdorferi strains. 2012.
  11. Iceman Autopsy – National Geographic. 2011.
  12. Kean WF. The musculoskeletal abnormalities of the Similaun Iceman ("ÖTZI"): clues to chronic pain and possible treatments. 2013.
  13. Aberer E, et al. Molecular mimicry and Lyme borreliosis: a shared antigenic determinant between Borrelia burgdorferi and human tissue. 1989.
  14. Elizabeth S. Raveche, et al. Evidence of Borrelia Autoimmunity-Induced Component of Lyme Carditis and Arthritis. 2005.
  15. A M Ercolini, et al. The role of infections in autoimmune disease. 2009.
  16. John J Halperin et al. Common Misconceptions About Lyme Disease. 14 January 2013.
  17. van Dop WA, et al. Seronegative lyme neuroborreliosis in a patient using rituximab. 2013.
  18. Volker von Baehr et al. The Lymphocyte Transformation Test for Borrelia Detects Active Lyme Borreliosis and Verifies Effective Antibiotic Treatment. 2012.
  19. Raphael B Stricker, et al. Lyme disease: the next decade. 2011.
  20. Henry M Feder, Jr., et al. A Critical Appraisal of “Chronic Lyme Disease”. 2007.
  21. Brorson O et al. An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to metronidazole. 1999.
  22. Gustaw K. Chronic fatigue syndrome following tick-borne diseases. 2003.
  23. Wormser GP, et al. Implications fo gender in chronic Lyme disease. 2009.
  24. Steven E Schutzer, et al. Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome. 2011.
  25. Mursic VP, et al. Formation and cultivation of Borrelia burgdorferi spheroplast-L-form variants. 1996.
IMAGES
Figures B and H originally published by BioMed Central. Journal of Neuroinflammation. Judith Miklossy, et al. 25 Sep 2008. Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis.
B. Dark field microscopy of Borrelia burgdorferi showing the usual spiral form of spirochetes and their agglomeration into colony-like masses.
H. Cystic form of Borrelia burgdoferi spirochetes, entirely covered by a thickened membrane masking the contents of the cyst.


FURTHER READING:
  1. A History of Cell Wall Deficient Bacteria: A Selection of Researchers Who Have Worked with the L-form.
  2. Vaccination against Lyme disease: past, present, and future. 2013.
  3. FDA recorded webinar on Lyme disease diagnostic research. 2012.





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Comments

Ive printed off the "Bartonella: A new frontier in chronic disease" thing to take to doctors to try to convince one to test me next time I get to go to one. It says on that sheet "recommendations for medical practioners: . Consider testing patients at high risk who present with general rheumatic or neurological symptoms for Bartonella infection" (I get a ton of neuro symptoms including what appear to be seizures). It lists the Symptoms for bartonella as being "may range from reincuring fever, headaches, insomina, joint/muscle aches and pains, myalgia, neurocognitive dysfunction, seizures, vasculitis and vaso-proliferative tumors or lesions as well as more common lymphdenopathy and splenomegaly" (Ive italics all the symptoms there I get at times with the ME). One thing which is different to my ME then what many get was the VERY HIGH reincurring fevers I used to get (I still do get fevers at times but they are mild now) also the seizures (not related to the fevers, I think the seizure incidences thou may be related to the POTS).

The article says Bartonella has also been documented to cause osteomyelitis. I used to be in agony due to pain which felt like it was inside my bones (the doctors ignored it but it was very severe.. I used to cry from the pain in my bones so I think I probably had osteomyelitis at the time. Im not having much issues with the Bartonella symptoms now as my ME has changed (predominant POTS now).

I used to do a lot of animal rescue stuff with my main love being cats.. so been scatched a lot, not just that deep puncture cat bite which got infected). Hopefully I can convince a dr to get a test (not sure thou even if there is tests for this in Australia. The lab Im going to be doing my lyme test throu.. didnt have Bartonella on its list it sent out). I can do the lyme test in 1 week (been waiting for antimicrobial herb to get out of my body before doing the test).
One of the sad things is that the standard tests only test for a couple of the strains of Bartonella and don't test for a strain that has been found in many ME patients. Not much you can do about it though without access to a lab that tests more strains.

Sushi

Sushi
Hello Tania
All strains of bartonella can be tested at Himmunitus in Belgium and Galaxy in the USA.
I had a bone tumor in '99 and the bone is still not healed, glomus tumor, thrombocytopenic purpura when I was pregnant, my newborn nearly died in IC due to an unknown infection (ahum) in 1995, my face looks as if I have lupus due to overvascularisation caused by bartonella, my bones hurt all the time as well, I lost weight as if I had aids, my chest hurts horribly, ... I tested positive for bartonella in 2008 but the doctor said it was nothing because all other infections (Pfeiffer, CMV, ...) were positive as well.
I know now that bartonella deadlocks your immune system and hell breaks loose. My last pregnancy was did the trick. Bartonella got the chance to break out again.
 
Ive printed off the "Bartonella: A new frontier in chronic disease" thing to take to doctors to try to convince one to test me next time I get to go to one. It says on that sheet "recommendations for medical practioners: . Consider testing patients at high risk who present with general rheumatic or neurological symptoms for Bartonella infection" (I get a ton of neuro symptoms including what appear to be seizures). It lists the Symptoms for bartonella as being "may range from reincuring fever, headaches, insomina, joint/muscle aches and pains, myalgia, neurocognitive dysfunction, seizures, vasculitis and vaso-proliferative tumors or lesions as well as more common lymphdenopathy and splenomegaly" (Ive italics all the symptoms there I get at times with the ME). One thing which is different to my ME then what many get was the VERY HIGH reincurring fevers I used to get (I still do get fevers at times but they are mild now) also the seizures (not related to the fevers, I think the seizure incidences thou may be related to the POTS).

The article says Bartonella has also been documented to cause osteomyelitis. I used to be in agony due to pain which felt like it was inside my bones (the doctors ignored it but it was very severe.. I used to cry from the pain in my bones so I think I probably had osteomyelitis at the time. Im not having much issues with the Bartonella symptoms now as my ME has changed (predominant POTS now).

I used to do a lot of animal rescue stuff with my main love being cats.. so been scatched a lot, not just that deep puncture cat bite which got infected). Hopefully I can convince a dr to get a test (not sure thou even if there is tests for this in Australia. The lab Im going to be doing my lyme test throu.. didnt have Bartonella on its list it sent out). I can do the lyme test in 1 week (been waiting for antimicrobial herb to get out of my body before doing the test).
With your history of cat scratches, if you can tolerate antibiotics, it might just be worth skipping the somewhat unreliable testing and doing an antibiotic challenge for a few months to see if you saw any improvement.

(Yes, long term antibiotics are not good for the gut but neither is a long standing untreated infection.)

Ema
 
Back to Borrelia, it was very interesting what I think dr. Ostfeld said at the TBDA forum this week. That Borrelia changes its outer proteins over time in your body. So you wont make the 'typical' antibodies anymore, but maybe other antibodies. Thought he said they were looking for this in monkeys. It would explain the whole negative antibodytesting in chronic patients. And better testing could be developped. Happy to see this is investigated. It would be easier to acknowledge by stubborn doctors than the 'not making antibodies anymore due to impairment of the immunesystem' which is hard to prove.

Because it is hard to find Borrelia in humans they are also doing a study where they let 'clean' thicks feed on humans ith lyme to see if they can detect Borrelia in the thick afterwards. Yuck! Scary testing method!
 
Back to Borrelia, it was very interesting what I think dr. Ostfeld said at the TBDA forum this week. That Borrelia changes its outer proteins over time in your body. So you wont make the 'typical' antibodies anymore, but maybe other antibodies. Thought he said they were looking for this in monkeys. It would explain the whole negative antibodytesting in chronic patients. And better testing could be developped. Happy to see this is investigated. It would be easier to acknowledge by stubborn doctors than the 'not making antibodies anymore due to impairment of the immunesystem' which is hard to prove.

Because it is hard to find Borrelia in humans they are also doing a study where they let 'clean' thicks feed on humans ith lyme to see if they can detect Borrelia in the thick afterwards. Yuck! Scary testing method!
My bolding.

Seriously? Who is going to sign up for that?! :eek:
The tick may be clean off Borrelia, but what about other tick-borne pathogens, known and un-known?
Besides, even a 'clean' tick still passes you substances that affect your immune system, and thats shorly the last thing you need if you already have Lyme.
 
That clean tick stuff is for the birds. It is criminal they are doing that to humans. BTW - who trusts researchers anymore anyway?
 
As a silly comment can I add that the scientists involved in the various autopsies of the 5000 year old virtual mummy man in the Alps a little while ago found he suffered from Lyme disease. One feels bound to add if he can be tested so easily why not me !
 
Sorry Snowathlete I see Otzi is part of your article (hadn't read through completely), nevertheless it might be more prevalent than they think.
 
Tick conference
http://karlmcmanusfoundation.org.au/files/KMF_TBD2013_Booklet.pdf

I think that in the US at least 95% of CFS patyients have Lyme infections!!!
just a thought
Big happenings at the tick conference
looks like some good treatment options
think the worm may have turned
spoke to most of the Lyme doctors
Government committee formed with 3 big pinch hitters from the Lyme community
direct link straight to the cheif medical officer
will update when i can
 
Mualla Mcmanus
Dear all,
I would like to say that TBD2013 was a success. We had more Drs turning up and wanting to learn how to treat Lyme Disease in Australia. More have emailed me about not being able to attend but that they are interested in purchasing the DVD. It is very positive. AIMA and KMF are in partnership. We will be working to get as many Drs as possible to join an learn about Lyme. AIMA has 300 Drs as members. Revolution is underway!!!!! Change is happening!!!. Having Prof Baggoley at the conference was also a sign to Drs not to be afraid of being deregistered if they treat Lyme disease. In addition we were able to get the conference RACGP approved for CPD points. That means we are on the way of being accepted. So soon big changes will be underway.

From Mualla McManus
 
Mualla Mcmanus
Dear all,
I would like to say that TBD2013 was a success. We had more Drs turning up and wanting to learn how to treat Lyme Disease in Australia. More have emailed me about not being able to attend but that they are interested in purchasing the DVD. It is very positive. AIMA and KMF are in partnership. We will be working to get as many Drs as possible to join an learn about Lyme. AIMA has 300 Drs as members. Revolution is underway!!!!! Change is happening!!!. Having Prof Baggoley at the conference was also a sign to Drs not to be afraid of being deregistered if they treat Lyme disease. In addition we were able to get the conference RACGP approved for CPD points. That means we are on the way of being accepted. So soon big changes will be underway.

From Mualla McManus
Thanks for the update!

Do you have specifics about what treatments are being used in Australia?

Sushi
 
Thanks for the update!

Do you have specifics about what treatments are being used in Australia?

Sushi
yes i am trying to collate everything
a small byte here
vitamin C, large doses - try increasing slowly until get like loose bowels
then just drop back a dose
diatomaceous earth which helps kill parasites- 4 days on then 3 days off
 
I'd really love more info from the conference if you have any GC, I've just tested positive for Lyme and beginning abx treatment.
 
I'd really love more info from the conference if you have any GC, I've just tested positive for Lyme and beginning abx treatment.
This is not my work so I have no opinion on its success
It does contain some pertinant points though.
For example from John Coleman
Patients diagnosed with Lyme disease and coinfections have a number of protocols to choose from for reducing the bacterial load; most will have significant antimicrobial activity. Lysed bacteria release endotoxins that may be as dangerous as the original infection unless all detoxification pathways are optimised.
Many Lyme Borreliosis treating doctors consider Herxing to be a sign that detoxification is inadequate, the antimicrobial program is too vigorous, or both. In my own practice, I gain better results by beginning with quite robust detoxification activities, primarily patient driven.
A strict dietary regimen and clearing environmental toxins in the home are a first step. Efficient bowel function is very important and constipation may be ameliorated with vitamin C titrated to bowel tolerance (usually combined with magnesium), which also assists as an anti-inflammatory, antimicrobial, antioxidant and immune booster.

Dry skin brushing, Epsom salts baths or foot baths, oil pulling, soaked chia seeds, warm lemon water and cautious use of infrared saunas have been found to help. Detox therapies that I have effectively used while treating neurodegenerative and autoimmune disorders (where systemic toxicity is an exacerbating factor) include Heel Galium-Heel and Heel Detox Kit at extremely low doses (beginning at about 1/30 of the recommended
doses), and MH Enhance P2 Detox powder. Byron White Formulas (BWF) Selective detox formulas are proving to be very efficacious at enhancing detoxification and reducing Herx effects when started at very low doses and titrated to individual requirements.
The BWF have the advantage of being aimed at specific infections (Borrelia, Bartonella, etc), so are effective at removing endotoxins as those bacteria are lysed. Optimising detoxification pathways allows more vigorous antimicrobial activity with less distress; patient compliance is increased and health improvements more assured.

Clinical observations with those diagnosed with advanced neurodegenerative and autoimmune disorders had already shown the advantage of using vastly reduced doses of these remedies to provide effective therapy with little or no
aggravation. Indicative dosing comparisons include:
Aqua Hydration Formulas:
Recommended starting dose: 7 drops bd
My starting dose: 1 drop bd
Heel Galium-Heel:
Recommended starting dose: 10 drops tid
My starting dose: 1 drop daily
Herbal mixes:
Recommended starting dose: 5ml tid
My starting dose: 5 drops tid
Byron White Formulas:
Recommended starting dose: 1-2 drops bd
My starting dose: 1 drop daily

10-15% of debilitated patients will aggravate/ herx on even these low starting doses. For homeopathic remedies, the most effective dilution is K dilution (to be explained) while, with herbal remedies, the choices are either quantity
dilution or K dilution (to be compared)