Friday, 30 November 2012


Despite that future research is still needed, some data of the literature suggest a possible relationship between ALS and Lyme disease.

References with respect to ALS and Borrelia burgdorferi

Lancet. 1987 Aug 8;2
Borrelia burgdorferi antibodies and amyotrophic lateral sclerosis.
Waisbren BA, Cashman N, Schell RF, 
Johnson R.

Muscle Nerve. 2009 Oct;40(4):626-8.
Lyme disease serology in amyotrophic lateral sclerosis.
Qureshi M, 
Bedlack RS, Cudkowicz ME.
Neurology Clinical Trials Unit, Massachusetts General Hospital, Harvard Medical 
School, 13th Street, Building 149, Room 2274, Charlestown, Massachusetts 02129,

Lyme disease is sometimes part of the differential diagnosis for amyotrophic lateral sclerosis (ALS). Herein we report on 414 individuals with ALS at the Massachusetts General Hospital who underwent laboratory testing for Lyme disease. 
Twenty-four (5.8%) were seropositive, but only 4 (0.97%) had confirmed past immunoreactive infection. Two of these patients received ceftriaxone for 1 month without clinical improvement. Lyme disease was rare in 414 patients with ALS and is not likely to be causative.

Wien Med Wochenschr. 1995;145(7-8):186-8.
[ALS-like sequelae in chronic 
[Article in German]
Hänsel Y, Ackerl M, Stanek G.
Neurologischen Abteilung des Kaiser-Franz-
Josef-Spitals, Wien.
CSF investigation in a 61-year old female patient with clinical picture of motoneuron 
disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.

Rev Neurol (Paris). 2006 Jun;162 Spec No 2:
[What is the role of other complementary examination in amyotrophic lateral sclerosis?].
[Article in French]

Tranchant C.
Département de Neurologie, Hôpitaux Universitaires, Strasbourg. Christine.Tranchant@chru-strasbourg.
Amotrophic lateral sclerosis diagnosis is based on clinical and electrophysiological findings. Transcranial 
magnetic stimulation and MRI can show abnormalities which are not specific, but which can confirm upper motor neuron involvement. The other tests are performed to exclude differential diagnosis. Tests which should be performed in every cases are: medullar MRI, blood counts, erythrocyte sedimentation, serum protein electrophoresis, calcium, phosphore, 
serological tests for HIV, siphylis, Lyme disease. Other tests are made in some clinical circonstances to exclude genetical disease or metabolic disorders (SMN gene, Kennedy gene, Hexosaminidase A, very long chaine fatty acids), haematological or paraneoplasic disorders (anti-neurons antibodies, PSA, CT of chest and abdomen, mammography, bone 
marrow biopsy) or inclusion myositis (muscle biopsy).

Wien Med Wochenschr. 1995;145(7-8):186-8.
[ALS-like sequelae in 
chronic neuroborreliosis].
[Article in German]
Hänsel Y, Ackerl M, Stanek G.
Neurologischen Abteilung des Kaiser-
Franz-Josef-Spitals, Wien.
CSF investigation in a 61-year old female patient with clinical picture of motoneuron disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.
PMID: 7610670 [PubMed - 
indexed for MEDLINE]

Arch Neurol. 1990 May;47(5):586-94.
Immunologic reactivity against Borrelia burgdorferi in 
patients with motor neuron disease.
Halperin JJ, Kaplan GP, Brazinsky S, Tsai TF, Cheng T, Ironside A, Wu P, Delfiner 
J, Golightly M, Brown RH, et al.
Department of Neurology, State University of New York, Stony Brook 11794.

Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi; 4 of 38 matched controls were seropositive. Eight of 9 seropositive patients were male (8 of 12 male patients vs 2 of 24 controls). Rates of seropositivity were lower among patients with ALS from nonendemic areas. All patients had typical ALS; none had typical Lyme disease. Cerebrospinal fluid was examined in 24 ALS patients--3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti-B burgdorferi antibody. Following therapy with antibiotics, 3 patients with predominantly lower motor neuron abnormalities appeared to improve, 3 with severe bulbar dysfunction deteriorated rapidly, and all others appeared unaffected. There appears to be a statistically significant association between ALS and immunoreactivity to B burgdorferi, at least among men living in hyperendemic areas.

Wednesday, 28 November 2012


Lyme Disease treatment on the NHS has been a very controversial area for those patients who fail the usual couple of weeks antibiotics usually given by NHS doctors following the HPA guidance. That is when they are treated in the early stages of the illness, because so many of us missed that window of opportunity despite seeking medical attention for tick bites, bulls eye rashes, summer flu' and migrating arthralgias.

Lyme Disease Action charity has been working with the James Lind Alliance reviewing the available research on diagnosis and treatment of Lyme disease looking for areas of uncertainties. 

The James Lind Alliance is funded by the National Institute for Health.

Links to the Lyme disease Action website here

Links to more than 39 uncertainties here

Doctors and patients or their carers can vote on the top ten priorities for research before the 9th December 2012 here

Hopefully this research will be brought to the attention of doctors who frequently fail to even recognise the certainties of Lyme Disease such as the EM Rash -

'Does EM provide an ‘accurate’ clinical diagnosis of LD? 

Yes it does. See Stanek G, Fingerle V, Hunfeld K, Jaulhac B, Kaiser R, Krause A, et al. Lyme 
borreliosis: clinical case definitions for diagnosis and management in Europe. Clinical 
Microbiology and Infection. 2011 Jan;17(1):69–79.

In correspondence from the Dept of Health, Earl Howe, 12.12.2011 via my MP Anne Milton .The Dept of Health says 'The Department is working with Lyme Disease Action (LDA) and I am aware that you as Health minister, have met with LDA representatives. We are supporting its initiative with the James Lind Alliance and await the findings of their review.'

I look forward to more information about these uncertainties being relayed to our treating doctors and consultants and changes to existing guidance from the Dept of Health via the Health Protection Agency reflecting that there are many uncertainties, instead of the current restrictive guidance based more on opinion than scientific data. 

By identifying uncertainties in the research hopefully in time research will be directed into these areas that need more detailed investigation. 

Saturday, 24 November 2012


Sharing from a friend with a link to a post on my blog about him here

The translation is thanks to Google so apologise for errors but you get the idea.

Dear Joanne 
would you please translate this to English? Its a column to have been underwritten wooden i will send to ILADS guys! borreliasyk I've been in 12 years. 

Like many others, I have not been believed that the Norwegian health care system that diagnosed me with ALS. I've driven trial twice. Lost both. This despite the fact that I tested positive on the Western Blot test, tested positive at the Vestfold Hospital and found Borrelia DNA in my blood in 2009. 

I sometimes have a feeling of being involuntary participant in an academic parlor game. It's as if most of the health care system sees this as a game - and not as a prolonged, intense and bitter struggle for life and health. , we have a large group of seriously ill patients who have good reason to believe that a Borrelia infection is the underlying cause - but are banned from using the device with a negative antibody test (often Elisa) as justification. 

In 12 years I have accumulated knowledge about the disease, but it seems that doctors have a monopoly on qualified opinions. Because of their status, they can decide what is the scope for credible evidence to justify saying their opinions. 

If they encounter documentation that goes across their opinions, they may with ease doubt about it. Or so they know not to studies and publications that make their arguments fall through. The latter is probably hard to recognize, so it will be easier to call documentation implausible. 

I refer to the magazine's story about how Borrelia among others Dr. Jon Sundal attended. He was also an expert witness against me in the trial. I'm not looking for the actual content of the program, but there are general attitudes Sundal have, I want to life! 

One tries to persuade public opinion that good western blot tests often give false positive responses, which is incorrect tests based on several numerical markers that identify Borrelia bacterium. Some markers are nonspecific and may cross react with other bacteria, while some markers are specific borrelia "fingerprint" - markers. Mon. require a certain number of markers to be regarded as positive for declaring the test as positive. 

This will make it easier to evaluate the tests. requirement to have a positive test, three of these specific markers. 

The American Health Authority (CDC) has recognized my test as secure positive. micrograms recombinant western blot (immunoblot) containing antigen that captures all strains of Borrelia bacteria. It does not Elisa! . Recommended Vestfold Hospital (SIV's) MIKROGEN recombinant western blot that is the best test.

 The problem is again money. The test is expensive and time consuming. This must be funded! SIV has expertise and a highly skilled specialists! 

Sundal also claims that one must have inflammatory cells in the spinal fluid of having neuroborreliosis. This Slovenian researcher Franck Strle proven wrong. He is with Hunfeld Fingerle Wilske and Stanek among tungtvektekterne in Europa.Også laboratories in Norway have discovered this! Unfortunately, doctors are not updated for this No, absolutely no Norwegian attending their seminars! Only a retired doctor, Per Bjarke. 

False negative tests dominate. Therefore, it is dangerous to allude that Elisa tests are good enough. Lori Bakken conducted a double-blind study showed that not only was Elisa inaccuracies between competing laboratories, but the same laboratory showed different results on the same sample. Only 45 laboratories had a score of 55 percent.

 Another study was conducted by the College of American Patholigists. The result was terrible. It was similar to the same number of false positives as false negatives. Only 45 percent of the 516 laboratories that tested showed the correct answer. It entered that stage I of the disease discovers Elisa 20-50 percent of cases and in stage II / III 70-100 percent, depending on the tests used. 

Some argue that sensitivity in stage II / III is not more than 20-80 per cent. The tests used in the cerebrospinal fluid in Norway today finds no more than 50 percent: 70 percent for garinii and 10 percent for afzelii, which is the most common borrelia strain circulating in Norway due to false negative results are numerous. 

The bacteria manipulate our immune system so that we do not produce antibodies. Antibodies are very late in forføpet. The bacteria can lie in niches inside the cells of the organs where it is hidden from the immune system. The bacterium converted to cyst forms with new antigens that are not found in the tests available today. 

The tests used today are quite specific as false positive is not a big problem. False negatives, however, problematic. This is why clinic and patients' own history is so important in the overall assessment. I think Western blot should be emphasized rather than as indirect Elisa test. The sensitivity has been discussed regarding western blot, but specific band in the test should be a clear indicator of Borrelia infection. 

ANTIBIOTICS For chronically ill have a pulsating regime (periodic time) high doses of ceftriaxone IV has been a success. This was published in the early 90's and was confirmed on MLDA Lyme congress in 2002. treatment should be individualized on both the dosage and length. 

Stricker refers to studies where long-term antibiotic treatment is far better than the standard treatment. Klempners standard (Dr Mark Klem opens conducted a study on the treatment of patients. Though the study had clear deficiencies, it has been accepted as standard. Probably why we have several cases of illness due under treatment) in a month ceftriaxone IV and two months of oral doxycycklin, had little effect on chronic borrelia or come late disease. 

Increased improvement the longer treatment duration was noticeable. This is published in the CID that is a IDSA (Infectious Disease Society of America). Looks like IDSA turns when they choose to publish this. So in these cases must be treated for months and even years with antibiotics. 

Change of combination treatments may be necessary. Must be individualized. It is vital to acknowledge this since late come and chronic Borrelia ill probably have chronic infection combined with additional infections. Therefore, required prolonged treatment. Therefore I genuinely sorry when doctors refuse patients treatment! There is no reason to doubt that prolonged treatment helps some. 

According to statistics I should have been dead 10 years ago! I'm probably the only one in the world who has lived with ALS diagnosis in 12 years, which can stand on their feet and do not need a respirator! Court, the appeal board patient and their experts find it more probable than that I have borrelia. 

Fortunately rescued antibiotics I received in the USA for 03 my life! I had to go. Here at home did not help! Health care is often concerned with the ethical dimension. As I see it, it is the exclusion of Lyme disease patients is the greatest ethical challenge. These patients (assuming they indisputably have very severe disease) are invited ME diagnosis or ALS without other evidence than that it can not be anything else. 

It may NOT be ethically problematic to make treatment studies in this group of patients. They get anyway no qualified help. I will fight for us, as long as there is life in me.

Eivind Markhus

Friday, 23 November 2012


'Any therapy which is capable of reversing the untreated

natural history of Motor Neuron Disease is Press-worthy.'

User avatar
Posts: 548
Joined: Fri 13 Jan 2012 22:32

by inmacdonald » Fri 23 Nov 2012 17:22

ALS-like Lyme and ALS not related to Lyme Neuroborreliosis:

Let us reduce the discussion to progressive incapacitating Motor Neuron Disease.
Dr William Harvey ,now deceased from a Heart Attack in year 2012 an buried with honor at the Cemetery of the US Air force Academy, developed Motor Neuron disease,progressive type.
He diagnosed himself ..He started a course of Long term antiborrelia antiBabesial antimicrobialtherapy.
Dr. William Harvey experienced a reversal of his motor neuron disease after long term antibiotic therapy.

Dr David Martz developed progressive motor neuron disease. He was diagnosed by several consultant neurologists as "most consistent with Amotropic Lateral Sclerosis. His children searched the Internet
and found the newspaper reports of Dr William Harvey's results with the success of long term antibiotic
and antibabesia therapy in motor neuron disease. Dr David Martz became a patient of Dr Bill Harvey.
Long term Therapy with antiborrelia/antibabesial medications produced a reversal of his disease. but from time to time, Dr David Martz must restart the Dr Harvey Protocol to maintain his recovery.

Dr. David Martz and I had a conversation on Nov 3, 2012 in Boston. We discussed our "MarkTwain" moments. Dr.Martz has since his recovery, treated multiple patients with Antibiotics/antibabesial medications and has noted reversal of motor neuron disease in his patients. He is drafting a manuscript
to report these patients. It is likely that the completed manuscript will be published in a Scandinavian Neurology Journal, just as his case report was published. It is noteworthy that previous to the acceptance of
the Harvey Martz manuscript in a Scandinavian Journal, it was reviewed and rejected by multiple journals based in the USA and in the United Kingdom.

Any therapy which is capable of reversing the untreated natural history of Motor Neuron Disease is Press-worthy. The untreated natural history of Motor Neuron Disease is a short pathway to death by suffocation.
Above all , do no harm.
Alan B> MacDonald MD

Motor neuron disease recovery associated with IV 
ceftriaxone and anti-Babesia therapy
We have documented the full neurological recovery in a patient 
with an unrecoverable MND. Thesuccessful clinical outcome was 
associated with antibiotic therapy in response to evidence of two 
concurrent infections. 
We suggest that MND may be associated with an infectious trigger
in certain cases. The use of antibiotic therapy in MND merits further evaluation.
The above comments by Dr MacDonald was posted on 
Lymenet Forum here  in response to my comments about 
an ALS/MND forum post.
Earlier posts about Dr Martz and his research can be found here  

Wednesday, 21 November 2012


Early signs of Multiple Sclerosis were thought to be lesions in the white matter of the brain, new research  discusses disease progression and finds that it is a process starting outside of the brain.

Multiple sclerosis (MS) may progress from the outermost layers of the brain to its deep parts, and isn’t always an “inside-out” process as previously thought, reported a new collaborative study from researchers at the Mayo Clinic and the Cleveland Clinic. The traditional understanding is that the disease begins in the white matter that forms the bulk of the brain’s inside, and extends to involve the brain’s superficial layers, the cortex. Study findings support an opposite, outside-in process: from the cerebrospinal fluid-filled subarachnoid space, that cushions the outside of the brain and the cortex, into the white matter. The new findings will guide researchers as they seek to further understand and treat the disease. The study was published in the December 8th, 20011 issue of the New England Journal of Medicine.

Link to these research findings here
It says 'the early lesions were highly inflammatory'

It has been recognised for some time that some MS cases can be caused by infections such as Chamydia Pneumonia  websites here and here  
and Lyme Disease.

Microbiologist Thomas Grier has lectured extensively on Lyme disease and Multiple Sclerosis, links to several of his lectures are posted in the right hand column of this blog. 

Below was Tom's response to the new MS research :-

Thomas Grier says:
The observation that early MS begins with inflammation in the outer cortical regions of the brain seems to fit with the physiology of the location of the BBB and the close proximity to microglia cells, an arrangement that suggests something is crossing the BBB to initiate inflammation and vessel infiltrate.
It is also interesting that white matter lesions later on seem to aggregate around or near the central ventricles often with micro-vessel inflammation/infiltrate seen in the ependyma membrane of the ventricles. This also suggests some outside factor is entering from the “Outside-In” through the CSF.
The spirochete hypothesis of sclerosing pathology suggested by myself, suggests that Borrelia (various species) enter through the BBB and inflame the vessels and activate microglia. Some motile bacteria may also enter the subarachnoid space a place spirochetes cannot thrive and then find their way to the ventricles-ependyma and back into blood vessels where spirochetes can find a more favorable environment. Increases in quinolinic acid levels from BBB-junction inflammation may also contribute to white matter destruction without the direct presence of the bacteria in the white matter lesions. (Spirochetes are more often found in the gray-matter)
This is born out by the lack of spirochetes found in white matter lesions, but classical forms when found, are almost always in the gray matter. This can be seen by using silver stains combined with microwave deflation of the fresh brain cells allowing the spirochetes from many levels becoming visible as the metal coated bacteria rise through the collapsed brain tissue.
This spirochete sclerosing model addresses
1) cortical gray-matter inflammation,
2) rise of an inflammatory toxin of demyelination Quinolinic Acid
3) a mechanism that explains periventricular inflammation and lesions secondary to BBB breakdown and gray-matter inflammation.
4) A possible reason for heterogeneous plagues prevailing
5) The increased incidence of MS in Lyme endemic areas
6) Intracellular infection in neurons explains lack of positive serology tests and patient relapses after antibiotics.
It seems that if spirochetes play a role in forming some plaques similar to MS plaques, then in order to get good data for treatment research we must consider trying to separate the Spirochete Sclerosing componant from the rest of the data.
For example an immune modulating drug might help true MS but if the data is mixed with patients from Lyme endemic areas that have not been separated in these trials, then treatment may have brief improvement and then a worsening without knowing which patients have an infectious component.
In the hundreds of biopsies used in this study were any also stained with anti-Borrelia antibody fluorescent stains or silver stains? If not we can make no conclusions that spirochetes did not play a role in the gray-matter pathologies.
Tom Grier (A survivor a primary progressive MS)

Earlier this year research by Sam Donta here

SPECT Brain Imaging in Chronic Lyme Disease

Conclusions: Brain SPECT scans are abnormal in most patients with chronic Lyme disease, and these scans can be used to provide objective evidence in support of the clinical diagnosis. The use of certain antibiotic regimens seems to provide improvement in both clinical status and SPECT scans.

Figure 2
FIGURE 2. SPECT scan of the brain before (A) and after (B) antibiotic treatment. These transaxial images are from a 51-year-old man diagnosed with Lyme disease with a recent change in memory. Representative pretreatment images show hypoperfusion within the mid posterior and mid temporoparietal cortex bilaterally. Representative posttreatment images (14 months later) reveal improved perfusion to the posterior temporoparietal cortex bilaterally, correlating with improved symptoms. Perfusion within the remaining cerebral cortex, basal ganglia, thalamus, and cerebellum was normal.

Sunday, 18 November 2012


Why does my arthritis get better when I take antibiotics but deteriorate when I stop?
Why does my muscle weakness get better on antibiotics but deteriorate when I stop?
Why does my fatigue and Fibromyalgia get better when I take antibiotics but deteriorate when I stop?
Why do my chronic symptoms improve on antibiotics for urinary tract infection and then deteriorate when antibiotics stop?
Why do my neurological symptoms get better on antibiotics and deteriorate when I stop?

I hear these questions all the time from people with RA, ME/CFS, Fibromyalgia, MS, Parkinson's - read any Facebook site for these illnesses and you see it over and over.

Well in my case it turned out that I had Lyme Disease but no doubt there are other bacterial infections that are not cleared by just a couple of courses of antibiotics.

Biofilms is one reason why Borrelia ( Lyme Disease) can persist despite long term antibiotics. 

Dr MacDonald pathologist and researcher of Lyme Borreliosis gives us a good lesson on Biofilms of Borrelia- from Lymenet Europe here

We now have entered a third era in Lyme Borreliosis - namely the Biofilm Era. 
Biofilms of borrelia burgdorferi were undreamed of until year 2006 and proven to exist in vitro and recently In ViVO in human skin biopsies of Erythema Migrans and in living Ixodid Tick midguts.
Biofilm science is radically different from Planktonic microbiology. Biofilms are part of the 
repertoire of over 99.9% of microbes. Biofilms form from planktonic microbial forms, but
biofilms provide mechanisms for microbial survival under adverse conditions which would eliminate
planktonic microbes. Biofilms explain Chronic antibiotic resistance. Biofilms are the mechanism
for Chronic Infections of many organ systems. The diagnostic names - infected artificial medical
device, bacterial endocarditis, Helicobacter pylori chronic gastritis, Dental root canal infections,
and may more- have the concept that these infections are solely due to biofilmsand the persistence of 
biofilms in humans despite administration of antibiotics/

In biofilms the microbes {planktonic forms} undergo specialization and are no longer
identical to Planktonic [single free living microbes]. Biofilm microbes are biochemically specializing
(ie have a different biochemistry, different cell wall structure, have cell to cell intercommunications
[nanowires and nanotubes] which enable cell to cell communication between the cytoplasmic compartments, and form water channels to facilitate the flux of nutrients and the removal of waste
from the biofilm community. An envelope of Extracellular matrix invests biofilm communites. This matrix is derived from once living --now dead members of the biofilm community. For Borrelia biofilms
the matrix investment includes Sloughed Outer Surface Membrane {slime layer} of Bb, Extruded 
DNA [eDNA], alginate-like material, and liposomes {micro vesicles} [blebs].

Biofilm communities may be and often are POLYMICROBIAL.

Biofilm communities spread from their sessile site of naissance to the body sites by
two mechanisms:
1. pieces of the Sessile community [Matrix invested specialized microbes] actually break apart
from the parent community and METASTASIZE to other sites.
2. Planktonic Showers rain from the sessile community from time to time and these
planktonic showers re-establish new communities in the mammalian host.

So in the year 2102, we have now entered into the 3rd era of Borrelia pathobiology;
namely the Biofilm Era.

Implicit in the biofilm concept is the ability of DNA transfer/exchange
[lateral DNA Transfer/ horizontal DNA transfer] among specialized members of the biofilm.
With DNa exchange, there is a mechanism for transfer of new virulence factors and new
modalities in antibiotic resistance. Persistence of biofilm infection in mammalian hosts
is in part due to PERSISTER microbes, which may reside within biofilm communities or which may reside intracellularly, or which may reside in so called "Sanctuary Sites"

The clinical spectrum of Lyme borreliosis continues to expand into areas of medicine
in which NAMED diseases of unknown cause [idiopathic diseases] are now incorporated within
the Lyme borreliosis disease complex. The number of skin conditions which are now Lyme disease
cutaneous manifestations has increased, thanks to the work of Dr Klaus Eisendle and Dr Bernhard Zelger to include many new entities, [ and more to be added with the use of FFM techniques]
I summarize these in my lecture on the International Cutaneous and Molecular Dermatopathology
of Lyme Borreliosis [attached , Boston Mass , Date November 4,2012]

In parallel with the expansion of cutaneous Borreliosis conditions, is the expansion of lymphoid
neoplasias linked to chronic Borrelia infections [ analogy with Helicobacter pylori induced
Malignant Lymphomas], Sarcoidosis in China as a borreliosis infection, Idiopathic lethal fibrosing
illnesses [Retroperitoneal Fibrosis, and Mediastinal fibrosis], borrelia to human Tranfections
mimicking human spontaneous gene mutations, Cardiomyopathies secondary to chronic Lyme borreliosis, giant cell arteritis [temporal arteritis] due to borrelia infection, Abdominal aortic aneurysms due to borrelia aortitis, and various intra-ocular inflammations {uveitis, optic neuritis},
Demyelination syndromes secondary to borrelia infections, and transplacental transmission of borrelia with possible lethal outcomes in the fetus in untreated conditions. The list above is only partial and will be added 
to as future medical research utilizing molecular Tools such as DNA probes fleshes out the full spectrum of
Lyme borreliosis and related co-infections.

It is truly a great time to be alive.

With all good wishes,

An earlier post on biofilms and Borrelia here

Dr Alan B MacDonald has already earned a Nobel Prize several times over in my view for the services he has done to the science and medicine in the field of Lyme Borreliosis I hope I am still around to see him recognised for those services.

Saturday, 10 November 2012


Most doctors are unaware of the many ways that Lyme Disease can affect patients so I am copying and posting this open letter that Dr Alan B MacDonald sent to Carter Blakely on Wellness Guidelines which includes a comprehensive list of conditions that can be related to an infection of Lyme Disease. Thanks to Dr MacDonald for posting on Lymenet Europe link here

Carter Blakey
I write to support the inclusion of the ILADS Lyme Disease
Objectives for inclusion in Healthy People 2020.

ILADS is an international society of physicians, researchers,and concerned
health care professionals whom are expert in the theory and in the practice
of Lyme Disease and Related Disorders ( Co-Infections which exist simultaneously
in some Lyme Patients). Lyme Disease has the potential to cause tissue 
in multiple organ systems of the human body. The first systems to be recognized
namely skin [Erythema Migrans], Joint [Lyme arthritis] , nervous system 
[Borrelia meningitis and Borrelia induced Bell's {facial nerve} Palsy], and 
Cardiac [ Borrelia induced Bradycardias and Tachycardias- with or without
Atrioventrio-ventricular conduction system "Heart block"] were all described
in the Pre Spirochetal Era [ in the era 1975-1980] before Dr Willy Burgdorfer
described the etiologic infectious agent of Lyme disease, namely Borrelia
burgdorferi. The expansion of Medical complications of Lyme disease
has burgeoned in the Post-Spirochetal Era to now include such diseases as
Mononeritis mutiplex, a Lyme Multiple Sclerosis-like demyelination illness,
a Lyme Amytrophic Lateral Sclerosis-like Motor Neuron Disease, Lyme 
disease in pregnancy with transplacental transmission of the spirochete
across the placenta from Mother to unborn fetus causing Miscarriage , stillbirth
at term pregnancy, and linked to several congenital malformations in the 
developing fetus, Lyme disease associated Neurocognitive disorders including
a Lyme disease Dementia closely resembling Alzheimer's disease, Lyme Disease
Parkinson's disease like illness, Lyme disease Cardiomyopathy, Lyme disease
Temporal arteritis-like illness with blindness, Lyme disease of the Eye with Uveitis,
Optic neuritis, and Ossifying myositis of the extra ocular muscles of the eye,
Lyme disease related Malignant lymphomas [similar in evolution to the
Lymphomas consequent to chronic Helicobacter pylori infection of the gastric 
mucosa] , Lyme disease Autonomic Nervous System Dysfunction, Lyme Disease
Endocrine dysfunction, Specially prominent in the thyroid gland and in the
Pituitary Adrenal Gland systems, Lyme Disease related Chronic Fatigue Illness,
Lyme Disease Myalgic Encephalomyelitis, Lyme disease Transverse Myelitis,
Lyme disease Muscle wasting Illness,Lyme Disease related Hepatitis, Lyme disease associated Hepatitis, Lyme Disease associated Destructive and deforming arthritis, Lyme Disease associated Squamous cell Carcinoma as a consequence of Acrodermatitis chronica Atrophicans, and Lyme Disease Neuropsychiatric Disorders.

Investigators in China have published evidence that the Lyme Disease spirochete
[chinese strain] is recoverable from some cases of Sarcoidosis in Chinese patients.
Investigators in Europe have published evidence that Lyme disease associated
Abdominal Aortic aneurysm exists in Europe.

Lyme Disease is more properly called Lyme borreliosis, because a variety of Borrelia
strains from all continents [except Antarctica] are now isolated, each with a different
strain name and each with a different potential to cause disease and or death
in human and mammalian patients.

Babesia infections [similar to Malaria- but tick transmitted] are co-travellers with
Lyme borreliosis. Borrelia exist as different strains, each with a potential to threaten
the safety of the human blood supply. Babesia infections may be diagnosed by blood smear examination by an expert pathologist. Alternatively, the detection of
antibodies which are specific to each of the strains of Babesia is possible if and only
if the test kits utilized are a perfect match for the suspected Babesia strain,based
on the geographic location where Tick transmitted Babesia infection was acquired.
For example, in the United States of America, Babesia infections on the East coast
are usually Babesia Microti, and on the West Coast Babesia duncani. In Missouri, babesia infections are Babesia strain MO. In Europe, Babesia infections may be due to a number of strains such as[but not limited to] Babesia strain Eo, strain divergens, and strain bigemina. In detection of blood antibodies - which are strain specific, the use of the proper test kit [ kit specificity restricted to one strain at a 
time] is essential to avoid missing the diagnosis of Babesiosis. For example,
test kits designed to detect antibodies to Babesia microti will produce NEGATIVE
results if the patient has Babesia Duncani in his/her blood. Undetected Babesia in Blood bank units , when transfused into human hosts may produce Fatal results. A
Registry of human fatalities due to Transfusion transmitted Babesiosis is on file
at the Centers for Disease Control and prevention. Over 100 cases of transfusion
transmitted babesiosis with a Fatal outcome in the recipients have been recorded
in a 10 year interval by the CDC.Ongoing surveillance for contamination of Blood
donor units from Asymptomatic Blood donors is aggressively being conducted
in New York State . Other States in the USA may have an unrecognized
threat to the blood supply because Babesiosis screening programs are not
in place in All of the 50 states. It is well known that residents of the USA
relocate their residence to other states every 6-7years. It is therefore a real concern that Babesia infections acquired in one state may produce potential blood supply
safety issues when Blood donors relocate their residence.

In addition to Babesiosis ,other Lyme Disease complex co-infections include:
Anaplasmosis,Human granulocytic Ehrlichiosis, Human Monocytic Ehrlichiosis,
Bartonellosis (various strains), and for the Amblyomma american tick [Lone Star Tick] vector: Francisella tularenesis {Tularemia}, Rocky Mountain spotted Fever, Coxiella burnetti infection.

Tick Transmitted infections to man are the fastest growing category of
infectious diseases in the United States of America today. The Statistical 
compilation of such infections, by the CDC, is admittedly an underestimate
of the true numbers of Tick tick transmitted infections in USA citizens and
in immigrants to the USA.


Alan B. MacDonald MD, FCAP, FASCP
November 9,2012
User avatar
Posts: 522
Joined: Fri 13 Jan 2012 22:32