WHAT CAUSES ALZHEIMER'S?

Alzheimer's Disease
Studied with Autopsy demonstrates  that Infection by Borrelia Spirochetes
is regularly present in Autopsy Alzheimer's Disease brains. The Chronic Borrelia Brain Infection is a Cause of Alzheimer's Disease.

The Model  for  Dementia CAUSED by Chronic  brain Infections by Spirochetes is the conclusive Model of Dr. Hideyo Noguchi  who proved that Treponema Pallidum  late chronic Brain Infection is  THE CAUSE  of General Paresis 
[ Syphilis dementia]

21st century tools investigate infection by detection of microbe's DNA at the site of the Disease in human tissue.

DNA of Borrelia is Present in the following areas of the Alzheimer's Brain:
1.  All of the Alzheimer's Plaques
2.  Perfect Spirochetes (Borrelia) are seen under the fluorescent microscope
       in solid brain tissues, in Blood vessels of the Brain, and in the   Alzheimer's Plaques.
3.  All of the Granular bodies which are present in dying nerve cells in the     Alzheimer's Brain
        (Granulo-vacuolar Degeneration: {GVB Lesions]
Autopsy Brain, when placed in Laboratory Cultures produce pure Cultures of Borrelia spirochetes.

My present Research uses DNA Probes , specific for borrelia , to bind to  sites in diseased brain tissues, specifically Alzheimer's Disease Autopsy Brain tissues.

FISH methods (Fluorescence In Situ DNA Hybridization)-  in my research -  utilizes the BEST DNA PROBES available today, specifically Molecular Beacons.  The Molecular Beacons absolutely bind to Target Borrelia DNA ...
but only will bind to a DNA .. if There is a 100% match-
between TheMicrobe Borrelia DNA in diseased tissues - and the DNA structure in My  Molecular Beacon DNA Probes...
            If even a single Base (nucleotide "A"or"T" ,or"G", or "C") Mismatch exists, .. the 100% rule for Molecular Beacon Binding is Violated,.
and no signal will be released by the DNA probe.  A positive signal indicates that the 100% match rule for Molecular Beacon DNA Probe binding has been satisfied.  A Positive FISH Hybridization in Alzheimer's Brain,  is Bulletproof evidence of Borrelia infection - Visualized by the Fluorescent Microscope.
FISH Borrelia Probes Visualize ENTIRE Borrelia spirochetes - at the EXACT sites of Alzheimer's tissue injuries..

In a Series of  cases from the Harvard Brain Bank ,

         [from Alzheimer's Disease Brains]..
my Molecular Beacon DNA Probes bound to Borrelia DNA in ALL CASES STUDIED. (5/5)

The astonishing observation in my DNA probe studies on the Harvard Brain Bank Alzheimer's Disease Cases is the Discovery of not just One Borrelia,  But, Two strains of borrelia in five of five Alzheimer' s brains...
Two different   species of Borrelia spirochetes
(Burgdorferi and Miyamotoi)  were simultaneously present in the Alzheimer's Brain tissues, from Harvard.

The Discovery of Burgdorferi  in Alzheimer's Brain was FIRST published by me in the Journal of the American Medical Association in 1986.  
I demonstrated Borrelia spirochetes from 4 cases obtained from Dr. George Glenner's Brain Bank at the UCSD SanDiego.
I succeeded in a total of 6 Alzheimer's Cases in the culture in the laboratory of Living Borrelia spirochetes from DEAD (Autopsy Brain) tissue., between 1986 to 1988. 
Subsequently, in year 1993,  Cultures for borrelia from Autopsy Alzheimer's disease  was again verified by Dr. Judith Miklossy, in Switzerland.

In year 2015, my research continues, with DNA probes specific for Borrelia DNa in Alzheimer's tissue. I request your support to extend my DNA Probe studies
to connect Chronic Deep Brain Infection with Borrelia Burgdorferi and Borrelia Miyamotoi in Alzheimer's patients. I want to extend my research to study the
Spinal fluid from living Donor patients with Dementia to detect Borrelia DNA in the spinal Fluid.

Early Detection of Borrelia Brain Infection offers the opportunity for the patient to be treated in the hope that ERADICATION of Brain and Spinal Fluid Infection, can Prevent the Development of Dementia.

I thank you for your support.  All of my research has always been FREE for All , and will remain Free for All.
None of my discoveries have been or ever will be patented .  No patient / volunteer will ever be charged for my research on their Behalf.

Respectfully submitted,

Alan B. MacDonald,MD
Fellow, College of American  Pathologists

8427 Benelli Court
Naples. Florida, 34114, USA

Note: Additional Video Lectures on my Alzheimer's Research  are FREEly available on You Tube and Vimeo.

My Website:
www.alzheimerborreliosis.net

I have posted Images /Galleries of Borrelia spirochetes
under Fluorescent Microscopy  using my FISH method
and my Borrelia Specific DNA Probes:

https://www.dropbox.com/s/rlxv1ibmi5jrwf7/Borrelia%20Image%20Gallery%20from%20Alzheimer%27s%20brain%20DNA%20probes%20Hippocampus%20from%20Harvard%20Brain%20Bank.pdf?dl=0

http://alzheimerborreliosis.net/wp-content/uploads/2012/10/PDF-of-Presentation-to-the-Board-of-the-TBDA-October-2012-by-Alan-B.-MacDonald-MD-.pdf

Taken and shared from Dr MacDonald's Fund Raiser - raising funds for further research into the links between various Borrelia species and Alzheimer's.

Please give generously and share this fundraiser among your friends (also at this link Dr MacDonald has updated details and presentations on his important work)
http://www.gofundme.com/z3v2a2k

Link to Poster presentation of Dr MacDonald's research http://f1000research.com/posters/4-631

ALZHEIMER CAUSED BY SPIROCHETES - SYPHILIS, BORRELIOSIS (LYME DISEASE), DENTAL PATHOGENS

Alzheimer Borreliosis Lecture London June 4 2014
Dr Alan MacDonald 

Published on Jul 17, 2014

Infection Induced Human Dementias are briefly reviewed,.Tertiary Syphilitic 
Dementia ( General Paresis) is reviewed and comparisons with Tertiary Spirochetal Human infections , dementing types. (Leptospirosis-NEJM 2014, Treponema pallidum, Borrelia burgdorferi family of spirochetes, and other Oral Treponemes.
The Conclusion Formulation by Dr. Alan MacDonald, MD is that
Alzheimer's disease of the Subtype caused by Tertiary Neuroborreliosis
demonstrates Evidence by Borrelia specific DNA Probe analysis and by 
Microbiologic cultures of Autopsy Alzheimer's Brain tissues producing
live Borrelia in pure culture, that Alzheimer's of the Tertiary Borreliosis type
is a infectious disease. The Plaques in such cases are Borrelia biofilm communities.
Granular Vacuolar lesions of the Hippocampus are granular borrelia
which contain Borrelia DNA and which Bind Borrelia specific DNA tissue
probes with In Situ DNA Hybridization in Autopsy studies.
The Borrelia infection subtype of Alzheimer's, in like manner with with
Treponema pallidum induced Dementia in late disease has the potential to to
be cured by antibiotic therapies. 

The above lecture was given at the Inaugural Meeting of the Spirochetal Alzheimer Association link here

ALZHEIMER'S DISEASE - A NEUROSPIROCHETOSIS

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

Judith Miklossy

• Correspondence: Judith Miklossy judithmiklossy@bluewin.ch

Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90

Published: 4 August 2011

Abstract (provisional)

It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD). Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill. The results show a statistically significant association between spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95% CI = 8-60, N = 247). When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases. Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls. Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies. Importantly, co-infection with several spirochetes occurs in AD. The pathological and biological hallmarks of AD were reproduced in vitro. The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD. Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Support and attention should be given to this field of AD research. Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.

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It is good to see further research by Judith Miklossy to visit her website click here and to read the full paper click here

I have posted about Alzheimer's before here of course those of us who have been following the information about Lyme disease are already aware of the work of Alan Mac Donald interviewed in Under Our Skin Documentary visit their website here or watch a Turn The Corner Foundation U Tube where Alan Mac Donald was interviewed. here

LYME DISEASE AND MENTAL HEALTH

Borreliosis (Lyme Disease) and its known involvement in Mental Health
by Denise Longman

Borreliosis (Lyme Disease) and its known involvement in Mental Health

Scientists and physicians across the world have discovered that the growing numbers of people with mental illness and diseases of the nervous system are being cured or improved by treatment with antibiotics. In other words, it is now known that bacteria can make you mentally ill as well as physically ill!

From Croatia to California, from Sweden to Sicily, conditions such as Schizophrenia and Multiple Sclerosis, even Alzheimer's disease and Stroke, are being found to have common to all one of the most insidiously infective bacteria on the planet, namely Borrelia.

This organism is similar to the bacterium that causes Syphilis, which was once the major cause of mental ill health before the days of penicillin. Both bacteria are large and spiral in shape, but Borrelia is turning out to be far worse than its cousin. Syphilis could be detected fairly easily and then killed with antibiotics, but Borrelia is harder to find, and then it is even more difficult to eradicate. Because it causes such a wide range of symptoms, from mild 'flu-like fever to a rapid onset of psychosis, or from strange rashes to sudden heart-block, this nasty bacterium has spread without most of us realising it, around the world, in what is now being called a pandemic.

Perhaps its most miserable victims are those with hallucinations, panic disorders, manic depressive illness and ADHD, as well as those with the labels of Chronic Fatigue Syndrome and Myalgic Encephalomyelitis; for although the latter two conditions are recognised to be of a bacterial / viral cause by the World Health Organisation, the British medical establishment employees predominantly psychological intervention alone. Imagine being confined to a secure mental hospital, or treated with powerful antipsychotic drugs, or living for decades struggling to maintain normal memory and behaviour patterns, when all along there has been an infection secretly living in your brain and nerves. This bacterium may sometimes be the cause of anorexia, while in some of its victims it has been known to cause episodes of uncontrollable rage.

Other bacteria and viruses can wreak similar havoc: some of the ones that live harmlessly in our throats and on our skin are also able to invade our brains. Doctors and scientists are quite ready to acknowledge and search for things like HIV, Streptococcus and Herpes. But it is only recently that they are becoming aware that the Borrelia bug, one of the hardest to positively identify because of its so-called "stealth " behaviour, must be high on the list for diagnosis.

European countries such as Austria, Germany, Holland and France, have alerted their GPs and specialists to the growing problem of Borrelia. Germany has twice polled every doctor in the country to determine the probable infection rate, and has found that it has doubled in the last 10 years. The Dutch have carried out similar surveys. In Austria, every GP's waiting room has warning signs about Borreliosis. The disease is being spread by ticks that are carried on birds, on wild animals and on pets such as cats and dogs, even on horses. It has been found inside the stomachs of biting flies such as horse flies and cleggs and also in mosquitos and mites.

We present here several medical studies published in recent literature, which link mental illness and brain disease to known Borreliosis infection. There were few to be found that had been carried out in Britain; those quoted here are from the rest of Europe and the United States.

a) In a controlled study undertaken at Columbia University Department of Psychiatry, 20 children were examined following known infection of Borrelia burgdorferi (Bb), and were found to have significantly more psychiatric and cognitive difficulties. Their cognitive abilities were found to be below that of 20 matched healthy control subjects, even taking into account any effects due to anxiety, depression and fatigue during education. The study also discussed the long-term effects of the children’s infection with Borrelia, which had brought about neuropsychiatric disturbances and caused significant psychosocial and academic impairment.

b) An elderly lady treated at the Emperor Franz Josef hospital, Vienna, was initially admitted with suspected Motor Neuron Disease. Testing of fluid from her spinal column indicated the presence of Bb. Following antibiotic treatment, improvement was seen in the patient’s clinical symptoms, and further testing of spinal fluid demonstrated a positive response to the antibiotic treatment. The preliminary diagnosis of amyotrophic lateral sclerosis (ALS) was revised to one of chronic neuroborreliosis, the term given to infection of the central nervous system (CNS) by Bb.

c) A 64-year old woman was admitted to the psychiatric ward of the Sophia Ziekenhuis at Zwolle, in Holland. She was suffering from psychosis, with visual hallucinations, disorientation in time and space, and associative thinking. Psychotropic drugs failed to produce any improvement in her condition and further, neurological, symptoms developed. A lumbar puncture revealed the presence of Borrelia burgdorferi and after treatment with penicillin all of her psychiatric and neurological symptoms were resolved. From the history, which the woman was then able to communicate, it appeared she had been bitten by ticks. Her husband, aged 66, passed through a similar episode of disease

d) In a comparative study carried out at the Prague Psychiatric Center, the blood of 926 psychiatric patients and that of 884 healthy control subjects was screened for four different types of antibodies to Borrelia burgdorferi. Of 499 matched pairs (meaning of similar age and gender but from patient and control group respectively) 166 (33%) of the psychiatric patients and 94 (19%) of the healthy comparison subjects were seropositive in at least one of the four test assays for Bb. This study supports the hypothesis that there is an association between an infection of Borrelia burgdorferi and psychiatric morbidity.

e) It has been well documented in numerous published medical studies of Borrelia’s ability to cause many recognized personality disorders and forms of depression; such as anxiety, depression, confusion, aggressive behaviour, mild to moderate cognitive deficits, fatigue, memory loss, and irritability. As such, the American Psychiatric Associations recommends that specialist doctors and councillors alike should seek to rule out Borreliosis as a possible differential diagnosis before commencing with any form of psychological intervention.

f) At the University of Rostock in Germany, a 42-year old female patient presented with schizophrenia-like symptoms but a complete lack of neurological signs. A brain scan and investigation of the spinal fluid led to the diagnosis of Lyme disease. There was complete relief of symptoms after antimicrobial therapy.

g) In a study of patients at a Boston, MA, hospital, scientists looked at patients with a history of Lyme disease who had been treated with short courses of antibiotics. As well as many physical symptoms, such as musculoskeletal impairment, the Lyme sufferers were found to have highly significant deficits in concentration and memory. Those who had received treatment early in the course of the illness had less long-term impairment.

h) At the Kanazawa University School of Medicine in Japan, a 36-year old woman with severe chronic Encephalomyelopathy was shown to have a very high level of antibodies to Borrelia burgdorferi. She showed severe cerebellar ataxia (walking and balance difficulties due to disease in the cerebellum) and profound mental deterioration. The disease had probably been acquired while she had been in the USA. The autopsy 4 years later showed the presence of spirochaetes throughout the brain and spinal cord, which together with the antibody evidence, demonstrated that the Lyme bacteria had caused this encephalitic form of neuroborreliosis.

i) Dr B. A. Fallon and his team at Columbia University Medical Centre in New York have done extensive studies on both adults and children with Lyme disease. They describe numerous psychiatric and neurological presentations of the disease, and show that it can mimic attention deficit hyperactivity disorder (ADHD), depression and multiple sclerosis. In another study, the same team found panic disorder and mania could be caused by Borrelial infection.

j) Scientists from Vancouver, Canada, and Lausanne, Switzerland, recently looked at post-mortem brain tissue samples from 14 patients who had had Alzheimer’s disease and compared them with 13 controls. All of the Alzheimer’s brains had infection with Borrelia-type organisms, compared to none of the controls. From 3 of the Alzheimer’s cases, they were able to carry out genetic and molecular analyses of these spirochaetes to prove beyond a doubt that they were Borrelia.

k) Following the detailed statistical analysis of all published literature on schizophrenia, (with the criterion that each study had to have detailed histories for at least 3000 patients), Swiss scientist Dr Mark Fritzsche was able to demonstrate that: "globally there is a striking correlation between seasonal and geographical clusters of both Multiple Sclerosis and Schizophrenia with the worldwide distribution of the Lyme bacteria." Yearly birth-excesses of such illnesses were found to mirror, with an intervening nine-month period, both the geographical and seasonal patterns of various types of Ixodes tick. He also went on to further state “In addition to known acute infections, no other disease exhibits equally marked epidemiological clusters by season and locality, nurturing the hope that prevention might ultimately be attainable.”

l) Chronic fatigue syndrome has been found to be associated with infection by Borrelia. A study by the Department of Neurology at the University Hospital of Saarland in Homburg, Germany, investigated blood samples from 1,156 healthy young males, without knowing which ones were suffering from CFS. They saw a significant number with CFS sufferers who had Borrelia antibodies even though there were no other signs of borreliosis symptoms. They state that antibiotic therapy should be considered in patients with Chronic Fatigue Syndrome who show positive Borrelia serology.

m) Dr R. C. Bransfield in New Jersey, has found a significant number of Lyme patients exhibit aggression. Patients were described with decreased frustration tolerance, irritability, and some episodes of explosive anger which he terms “Lyme rage”. In relatively rare cases, there was uncontrollable rage, decreased empathy, suicidal tendencies, suicide, homicidal tendencies, interpersonal aggressiveness, homicide and predatory aggression.

The World Health Organisation has warned that mental illness appears to be increasing globally, and that depression will soon become the second biggest cause of disease on the planet. In Britain, it is estimated that new-onset psychoses have reached the annual level of 30 per 100,000 of the population. According to recent announcements, although there are at present about 900 consultant psychiatrists employed in the UK, with 400 posts vacant, there are plans to recruit 7,500 new psychiatrists in the next 5 years, a massive 5-fold increase.

The European Committee for Action on Lyme Borreliosis (EUCALB) has published epidemiological studies showing that there is a serious problem with tick-borne Borreliosis in Europe. For example, the UK’s nearest neighbour, Holland, has found 73 cases per 100,000 of the population per year, with an unknown number of missed diagnoses. The published figures for England, Ireland and Wales appear to be nearly 2 orders of magnitude lower than this, with only 0.3 cases per 100,000. Are cases of Lyme disease / Borreliosis not being found in Britain because it is still regarded as a rare disease in this country? Or do we genuinely have the lowest incidence in the world? Diagnosis of borreliosis is difficult, with tests for antibodies to the bacteria being the subject of great controversy at present. If a consultant has to look at a suspected case of the disease and believes it to be rare, and blood tests are unreliable, then the diagnosis will be biased, quite understandably, towards the patient having some other condition.

It is hoped that health professionals at all levels, and in all disciplines, will come to realise that Human Borreliosis is the fastest-growing, most prevalent zoonotic disease in the world, and has been called a modern pandemic by several authors, including epidemiologists, rheumatologists, neurologists and infectious disease experts. There seems to be little awareness in the UK at present about this situation, but we urge that it be recognised sooner rather than later, in the hope that both mental and physical illnesses due to Borrelia are successfully diagnosed and treated.


References

a) A Controlled Study of Cognitive Deficits in Children

with Chronic Lyme disease.
Tager, F.A., Fallon, B.A., Keilp, J., Rissenberg, M., Jones, C.R.,
Liebowitz, M.R.
J Neuropsychiatry Clin. Neurosci. 2001; Fall; 13(4): 500-7.

b) ALS- Like Sequelae in Chronic Neuroborreliosis.

Hansel, Y., Ackerl, M., Stanek, G.
Wien. Med. Wochenschr. 1995; 145(7-8): 186-8.

c) Lyme Psychosis.
van den Bergen, H.A., Smith, J.P., van der Zwan, A.
Ned. Tijdschr. Geneeskd. 1993; 137(41): 2098-100.


d) Higher Prevalence of Antibodies to Borrelia burgdorferi in Psychiatric Patients than in Healthy Subjects.
Hajek, T., Paskova, B., Janovska, D., Bahbouh, R., Hajek, P., Libiger, J., Hoschl, C.
Am. J. Psychiatry 2002; 159(2): 297-301.

e) Highlights of the 2000 Institute on Psychiatric Services
Guardiano, J.J., von Brook, P.
Jan. 2001, 52(1): 37-42.

f) Borrelia burgdorferi Central Nervous System Infection
Presenting as Organic Psychiatric Disorder.
Hess, A., Buchmann, J., Zettel, U.K., et al.
Biol. Psychiatry 1999; 45(6): 795.

g) The Long-term Clinical Outcomes of Lyme disease. A Population-based Retrospective Cohort Study.
Shadick, N.A., Phillips, C.B., Logigian, E.L., Steere, A.C. et al.
Ann. Intern. Med. 1994; 121(8): 560-7.


h) Borrelia burgdorferi Seropositive Chronic Encephalomyelopathy: Lyme Neuroborreliosis? An Autopsied Report.
Kobayashi, K., Mizukoshi, C., Aoki, T., Muramori, F.et al.
Dement. Geriatr. Cogn. Disord. 1997; 8(6): 384-90.

i) (1) Late Stage Neuropsychiatric Lyme Borreliosis.
Fallon, B.A., Schwartzburg, M., Bransfield, R., Zimmerman, B. et al.
Psychosomatics 1995; 36(3): 295-300
(2) Functional Brain Imaging and Neuropsychological Testing in Lyme Disease.
Fallon, B.A., Das, S., Plutchok, J.J., Tager, F. et al.
Clin. Infect. Dis. 1997; Suppl.1: 557-63.

j) Borrelia burgdorferi Persists in the Brain in Chronic Lyme
Neuroborreliosis and may be associated with Alzheimer disease.
Miklossy, J., Khalili, K., Gern, L., Ericson, R.L., et al.
J. Alzheimer’s Dis. 2004; 6(6): 639-649.



k) (1) Chronic Lyme Borreliosis at the root of Multiple Sclerosis - is a cure with
Antibiotics attainable?
Fritzsche, M.
Med Hypotheses 2005; 64(3): 438-48.
(2) Geographical and Seasonal Correlation of Multiple Sclerosis to Sporadic
Schizophrenia.
Fritzsche, M.
Int. J. Health Geog. 2002; 1: 5.


l) Chronic Fatigue Syndrome in Patients with Lyme Borreliosis.
Treib, J., Grauer, M.T., Haas, A., Langenbach, J. et al.
Eur. Neurol. 2000; 43(2): 107-9.

m) Aggression & Lyme disease.
Bransfield, R.C.
14th International Scientific Conference on Lyme Disease and other Tick-borne Disorders. April 22-23, 2001, Hartford, Connecticut.

UK ADVICE ON LYME DISEASE

PATIENT UK article on Lyme Disease link here

Lyme Disease

This disease was formally described following the investigation of a collection of patients with rashes and swollen joints occurring in Lyme, Connecticut in 1975, and acquired the name 'Lyme disease' (Lyme arthritis) in 1977.1 The various rashes, however, had been recognised many years previously, as had their association with neurological problems.

Lyme disease is caused by a tick-borne spirochaete, Borrelia burgdorferi2 and others. The infectious spirochetes are transmitted to humans through the bite of certain Ixodes spp. ticks.

The disease is caused by the infection and the body's immune response to infection. Different strains of Borrelia spp. cause different clinical manifestations of Lyme disease and this explains differences between the disease in Europe and the disease in the USA.

Although there is a rising incidence this is likely to be due to better detection and surveillance.3 It is still a rare disease.

Pathophysiology
The spirochete responsible is transmitted from host to host by Ixodes spp. or deer ticks. Understanding the life cycle of these organisms gives better understanding of the epidemiology, other clinical aspects and prevention of Lyme disease.
The Ixodes tick:

Is made up of different species, found in different areas of the world. For example:
Ixodes persulcatus and Ixodes ricinus (European ticks), Ixodes scapularis, Ixodes pacificus.
Emerges in a larval form in the summer and feeds just once on a host animal (often a mouse).
In the spring the larva becomes a nymph and feeds, again only once, from a similar animal host. Humans can be victims in the nymph stage (85% of tick bites in humans occur at this time in spring and early summer).
In the autumn the adult tick finally emerges to feed on deer, again just once. Humans can be hosts at this stage (15% of tick bites in humans are at this stage and occur in the autumn).
The spirochete responsible:

Is transmitted by the tick. The tick must have fed on a host significantly infected with spirochete to pass on the infection to man.

Once it infects, the tick has to go through a particular cycle of multiplication and dissemination to salivary glands within the tick before it can be passed on to the animal victim. Hence a tick must be attached for 2-3 days to a person before infection can be passed on.

Once the spirochete infects the host there may be one of several consequences:

The infection is cleared by host defences. This means the person will have had no clinical manifestations, be asymptomatic but seropositive.
The organism spreads by direct invasion. This is believed to be a feature in early disease. For example, erythema migrans is thought to result from the inflammatory response to direct invasion of the organism in the skin.
The organism excites an immune response in the host which causes a variety of clinical manifestations around the body. In such cases there is no evidence of direct bacterial invasion. Host factors (immunological and genetic) are associated with development of disease in this form. For example, HLA- DR4 and HLA- DR2 are associated with such disease. The manifestations of Lyme disease are also related to the particular Borrelia spp. strain involved. Particular strains are found in different countries. For example:
B. burgdorferi garnii, found in Europe, is associated with neurological disease.
B. burgdorferi afzelii from Europe is associated with acrodermatitis chronica atrophicans.
B. burgdorferi sensu stricto is found on the East Coast of the USA.
B. burgdorferi predominates in the USA4 with an associated pattern of musculoskeletal complications.
B. valaisiana has a relatively high prevalence in British ticks, and does not appear to be associated with manifestations of disseminated borreliosis, which may explain the low incidence of Lyme borreliosis in the UK.
Lyme disease is now becoming global and mixed infections are becoming recognised.

Epidemiology
In the UK, areas where infection is acquired include:
Exmoor
The New Forest
The South Downs
Parts of Wiltshire and Berkshire
Thetford Forest
The Lake District
The Yorkshire moors
The Scottish Highlands

About 20% of confirmed cases are reported to have been acquired abroad:3
The USA
France
Germany
Austria
Scandinavia
Eastern Europe

Laboratory-confirmed reports of Lyme borreliosis have risen steadily since reporting began in 1986. Several factors have contributed to the observed increase, including increased awareness of the disease, access to diagnostic facilities, more sensitive diagnostic methods, the enhanced surveillance scheme (introduced in 1996) and, since 2000, more complete reporting of cases.3 Other possible factors producing a real increase include changes in the geographical ranges of I. ricinus both in the UK and Europe (successive mild winters), more recreational travel to high endemic areas and the increasing popularity of activity holidays (walking, trekking and mountain biking).3

Over 3,000 reports of Lyme borreliosis have been received since 1986, almost 2,800 of which have been reported since the introduction of enhanced surveillance in 1997.3

Mean annual incidence rates for laboratory-confirmed cases have risen from 0.06 per 100,000 total population for the period 1986 to 1992, to 0.64 cases per 100,000 total population in 2002, to 1.1 cases per 100,000 total population in 2005.3 The highest rates in the USA are 69.9 cases per 100,000 persons in Connecticut.

Lyme disease occurs in temperate regions of North America, Europe, and Asia.

In some countries of Europe, the incidence of Lyme disease has been estimated to be over 100 per 100,000 people a year.

Lyme disease infection has occurred in northern forested regions of Russia, in China, and in Japan.

It has not been found in tropical areas or in the southern hemisphere.

Risk of infection is greater if the tick is attached for more than 24 hours.

There is a rise in reported cases in autumn, but the peak occurs in spring and summer.

It is not possible to separate false-positive antibody tests from asymptomatic infection. In endemic areas as many as 10% of the population may have positive serology without any history of symptoms.

Cases of Lyme disease are lowest in urban areas in the eastern states of the USA.
In the USA there are peaks in incidence in the 5-9 year age group and the 50-54 year age group.

Presentation
It should be remembered that some infected people will have no symptoms. In Europe as many as 64% of patients with Lyme disease do not remember being bitten by the often innocuous tick. The presentation depends on the stage of disease at the time of presentation. For example:

Early Lyme Disease (Stage 1 or localised disease):
The characteristic manifestation is erythema migrans:
A circular rash at the site of the infectious tick attachment that radiates from the bite, within 2-40 days.
It expands over a period of days to weeks in 80-90% of people with Lyme disease.
It may be the only manifestation of disease in one third of patients.
In most patients there is only one episode of erythema migrans but, in about 20%, there are recurrent episodes.
About 40% of patients have multiple lesions (not the result of multiple bites).
Pyrexia, arthritis, musculoskeletal symptoms and local lymphadenopathy may occur in about two thirds of patients but one third of patients will develop no further symptoms.

Disseminated Lyme disease (or stage 2 disease ). This disseminated stage is still considered to be early infection and occurs weeks to months later, with:
Flu-like illness, oligoarthralgia (60%). Typically, with myalgia, multiple erythema migrans and sometimes systemic upset. Malaise and fatigue are very marked (particularly in the USA where 80% of patients are affected - about double that recorded in Europe).
Intermittent inflammatory arthritis:
This is more common in the USA.
In Europe joint pains are less often associated with inflammation.
Untreated episodes last about a week.
Most patients have at least 2 or 3 episodes and, even untreated, these resolve over a a few years.
Central nervous system disorders (15%):
These include facial (and other cranial nerve) palsies. These are the most common neurological manifestations in Europe and the USA.
Meningism and meningitis may occur alone or with other neurological manifestations. It is usually at the mild end of the spectrum but can be more severe.
Mild encephalitis producing malaise and fatigue.
Peripheral mononeuritis
Lymphocytic meningoradiculitis (or Bannwarth's syndrome which is more common in Europe than the USA).
Cardiovascular problems (10%):
This usually presents with syncopal episodes associated with fever.
Manifestations include transient atrioventricular block, myocarditis, or chronic dilated cardiomyopathy.
Occasionally hepatitis, orchitis, uveitis and panophthalmitis.
Lymphocytomas:
These are bluish-red nodular lesions infiltrated with lymphocytes.
They typically appear on the earlobe or nipple.
They occur in Europe but not the USA.
Late manifestations of Lyme disease (or stage 3 disease):
Untreated or inadequately treated Lyme disease can cause late disseminated manifestations weeks to months after infection. These late manifestations typically include prolonged arthritis, polyneuropathy, encephalopathy and symptoms consistent with fibromyalgia.

Chronic lyme arthritis - a chronic erosive arthropathy typically involving the knees.
Acrodermatitis chronica atrophicans . This is a bluish discolouration (normally on the lower leg over extensor surfaces) signifying epidermal atrophy, usually with mild sensory neuropathy and myalgia. It is generally seen in Europe not the USA.

Chronic neurological syndromes . Generally these appear to be more common in Europe. These include chronic neuropathies (usually with paraesthesia and occasionally with pain but not with motor deficit). They may even present as chronic fatigue syndromes, spastic paraparesis or depression.

Differential diagnosis

Chronic Lyme disease can be indistinguishable from fibromyalgia and chronic fatigue syndrome and in the assessment of these illnesses B. burgdorferi infection should be considered.

Noninfectious:
Urticaria
Gout
Psoriatic arthritis
Thyroid disease
Degenerative arthritis
Metabolic disorders (vitamin B12 deficiency, diabetes)
Heavy metal toxicity
Vasculitis
Systemic lupus erythematosus
Psychiatric disorders
Localised infections:
Gonococcal arthritis
Meningitis

Infections which can mimic certain aspects of the typical multisystem illness seen in chronic Lyme disease include:
Viral infections, for example:
Parvovirus B19
West Nile virus infection
Bacterial infections, for example:
Relapsing fever
Syphilis
Leptospirosis
Mycoplasma
Infective endocarditis
Investigations5

When to test and when to refer?
It is useful to have clear guidance on when to test and when to refer.

In all cases of suspected Lyme disease seek further advice on when and how to investigate from one or more sources. The following sources of advice are suggested:5
A microbiologist
An infectious diseases consultant
The Lyme Borreliosis Unit

In patients with erythema migrans:
Testing is not usually necessary with a history of tick bite (or possible exposure).
This characteristic rash with a history of tick bite or exposure is enough to make a diagnosis.
In primary care, testing should be considered:
With erythema migrans but with no tick bite (or tick exposure) and no other features of Lyme disease.
When there is isolated unilateral facial palsy (as with Bell's palsy) and Lyme disease needs excluding because of a history of tick bite (or tick exposure).
In patients with other neurological symptoms, joint or cardiac symptoms:
Test in primary care only after specialist advice.
Usually such patients require hospital admission or urgent specialist assessment.

What test?
There is currently no definitive test. Lyme disease is a clinical diagnosis and tests should be used to support clinical judgement. The most useful tests are antibody detection tests. The only national guidelines for testing come from the US Centers for Disease Control and Prevention (CDC).6 They recommend a 2-step testing process:

Lyme disease symptoms (other than erythema migrans) - take a blood sample for antibodies to B. burgdorferi. But note:
If negative and the sample is within 2 weeks of symptoms, repeat the test after 2 weeks.5
The enzyme immunoassay has a high false positive rate (low specificity) and can be positive with other conditions (for example, glandular fever, syphilis, rheumatoid arthritis and some autoimmune conditions).5
If positive or borderline by antibody testing using enzyme immunoassay, then retest using immunoblot or Western blotting to confirm the positive result.
Antibody testing in patients with erythema migrans is unhelpful because the rash develops before the antibodies.

Serology:
Serology may help in cases of endemic exposure where there are clinical features suggestive of disseminated disease.3
Serology - enzyme-linked immunosorbent assay (ELISA) - remains negative for several weeks in the initial phase, but is usually positive in serum and CSF in the disseminated stage. False positives may occur with other spirochaete infections.
Polymerase chain reaction (PCR) may identify very small numbers of spirochaetes in samples, and may influence decisions about whether to treat asymptomatic individuals with positive serology. Usually, however, PCR techniques are not helpful because of the uncertain correlation between positive results and the presence of live organisms in biological fluids.

Management
Discuss management with microbiologist and/or hospital specialists. The early use of antibiotics can prevent persistent, recurrent, and refractory Lyme disease. Antibiotics shorten clinical course and progression. The duration of therapy should be guided by clinical response, rather than by an arbitrary treatment course but guidance is offered.5 Generally speaking, long courses of antibiotics may be required (2-4 weeks or longer).

Management at a glance:
Tick bite- remove tick and consider a single-dose oral antibiotic in high-risk cases (not recommended routinely in UK-acquired tick bites)3
Skin manifestations - (erythema migrans) oral regimen 14-21 days
Arthritis - oral regimen for 30 days, repeated IV if the oral course is unsuccessful
Neuroborreliosis - oral regimen 30 days for all except encephalitis and encephalopathy
Encephalitis/encephalopathy - IV regimen for 28 days
Fibromyalgia - no evidence of benefit from trials with oral or IV treatment



Jarisch-Herxheimer reaction may occur soon after treatment is initiated.
Oral drug therapies for erythema migrans alone can be started in primary care. These are appropriate when:
There is no evidence of neurological, cardiac, or joint involvement.
Patients are not pregnant or breast-feeding.
Doxycycline (and tetracycline), amoxicillin, azithromycin, cefuroxime, and clarithromycin have similar favourable results in studies. For many Lyme disease patients, there is no clear advantage of parenteral therapy.
The following antibiotic regimens have been suggested:5
Adults:
First choice is doxycycline (100 mg twice-daily for 14 days) or amoxicillin (500 mg three times daily for 14 days).7. Some recommend 3 weeks course.6
If both doxycycline and amoxicillin are contra-indicated, use cefuroxime (500 mg twice-daily for 14 days) unless there is a history of anaphylaxis with a penicillin.
When a bacterial cellulitis cannot be excluded use 14 days of either co-amoxiclav alone (500/125 mg three times daily) or cefuroxime axetil alone (500 mg twice-daily) or amoxicillin (500 mg three times daily) with flucloxacillin (500 mg four times daily for 7 to14 days).

Children:
12 years of age or older, give 14 days of either amoxicillin (50 mg/kg per day in three divided doses) or doxycycline (100 mg twice-daily).
Less than 12 years of age, give 14 days of amoxicillin (50 mg/kg per day in three divided doses).
If both doxycycline and amoxicillin are contra-indicated give 14 days of cefuroxime axetil (30 mg/kg/day in two divided doses) unless there is a history of anaphylaxis with a penicillin.
When erythema migrans is indistinguishable from bacterial cellulitis, give 14 days of either co-amoxiclav, cefuroxime axetil or amoxicillin with flucloxacillin in age-appropriate doses.
Intravenous antibiotics are used in severe cases (for example, encephalitis, meningitis, optic neuritis, joint effusions, and heart block); or where there is failure of oral medications - in patients with persistent, recurrent, or refractory Lyme disease. Ceftriaxone, cefotaxime, and penicillin are commonly used intravenous antibiotics. The precise regime will depend on the individual situation but high doses of antibiotics, combination of antibiotics, sequential regimes and prolonged duration (one month or longer) are advocated.
Surgical synovectomy should be reserved for knee pain failing antibiotic treatment. Intra-articular steroid injection may be useful for persistent knee pain but runs the risk of masking persistent infection.
Treatment of Lyme arthritis - cefotaxime, ceftriaxone, doxycycline and amoxicillin plus probenecid are all effective.
Treatment of late neurological Lyme disease - Cefotaxime has been shown to improve neuropathy in patients with late Lyme disease. Intravenous ceftriaxone has been shown to be effective in Lyme encephalopathy.8 Other studies have shown no benefit of antibiotic for late neurological Lyme disease.
A temporary pacemaker may be required where there are carditis and conduction defects.
Prophylactic treatment of tick bite
Prophylactic antibiotics after Ixodes scapularis tick bites in Lyme disease endemic areas in North America have been shown to reduce the risk of developing clinical Lyme disease.9 This article in the New England Journal of Medicine suggests that a single dose of 200 mg of doxycycline within 72 hours of tick removal can prevent Lyme disease developing. The risk in the UK is such that use of prophylactic antibiotics is not recommended. It might be considered in very exceptional circumstances - for example, when a person travelling from an endemic area discovers a tick which has been attached for more than 48 hours.

Prognosis
Lyme disease is rarely fatal.
However, untreated Lyme disease can result in arthritis (50% of untreated people), meningitis or neuropathies (15% of untreated people), carditis (5-10% of untreated people with erythema migrans) and, rarely, encephalopathy. Over 90% of facial palsies due to Lyme disease resolve spontaneously, and most cases of Lyme carditis resolve without sequelae.10
The natural disease course of European borreliosis is not well defined and the effect of antibiotic treatment is unclear.11 There are no UK studies on the outcome of treatment.
Long-term sequelae also include poor concentration and fatigue.10
Recovery is often incomplete if the disease presents late.

Prevention
Measures to reduce infection in areas associated with ticks:

Wear long hair under a hat.
Keep to the middle of paths and avoid unnecessary brushes with foliage where ticks loiter waiting for the next passing mammal.
Avoid wooded areas where possible. Mowed grass areas are less likely to have ticks in them.
Keep legs and arms covered (wear trousers inside socks).
Use insect repellent for humans.
Use tick collars for pets (they can get Lyme disease) and inspect for (and remove) any ticks.
Inspect skin regularly during the day in at-risk areas (especially the groin, axillae and hairline). Remember ticks are unlikely to transmit Lyme disease until attached for several days.

If bitten by a tick:

Remove the tick:
Clean the surrounding skin with disinfectant to prevent bacterial infection.
Gently remove by grasping close to mouth parts with forceps (tweezers).12 The safest, quickest and most reliable method of removal is by using forceps applied to the tick as close to the skin as possible and removed with steady traction (and not twisting).13
Fragments of the mouthparts may be left in the skin, but these are small and rarely cause any problems, especially if the skin is disinfected before and after the procedure.
Note: cigarettes and glowing match heads or suffocating the tick with various agents (for example, petroleum jelly or solvents) are not recommended.13
If tweezers are not available, to avoid delay, find a cotton thread and tie a single loop of cotton around the tick's mouthparts, as close to the skin as possible and pull gently upwards and outwards.
Routine prophylaxis after tick bites is not currently recommended in the UK.3 However, in endemic areas, prophylaxis should be considered if there is a high risk of infection.9

Note: if the tick-bite area does not heal promptly or becomes painful, antibiotics may be necessary to treat other bacteria. Check for a spreading red patch, especially one that appears between 3 and 30 days after removal of the tick. However, remember that the risk of developing Lyme borreliosis from a tick bite is small, even in heavily infested areas and most doctors prefer not to treat patients with antibiotics unless they develop symptoms.13




A vaccine was licensed for use in the USA but later removed from the market.



--------------------------------------------------------------------------------
Document references
Steere AC, Malawista SE, Snydman DR, et al; Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three connecticut communities. Arthritis Rheum. 1977 Jan-Feb;20(1):7-17. [abstract]
Burgdorfer W, Barbour AG, Hayes SF, et al; Lyme disease-a tick-borne spirochetosis? Science. 1982 Jun 18;216(4552):1317-9. [abstract]
Lyme borreliosis/Lyme disease, Health Protection Agency
No authors listed; Lyme disease--United States, 2001-2002. MMWR Morb Mortal Wkly Rep. 2004 May 7;53(17):365-9. [abstract]
Lyme disease, Clinical Knowledge Summaries (January 2010)
Wormser GP, Dattwyler RJ, Shapiro ED, et al; The clinical assessment, treatment, and prevention of lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2006 Nov 1;43(9):1089-134. Epub 2006 Oct 2.; (reviewed 22/4/2010 by IDSA - no changes made to guidelines) [abstract]
British National Formulary; 59th Edition (March 2010) British Medical Association and Royal Pharmaceutical Society of Great Britain, London (link to current BNF)
Logigian EL, Kaplan RF, Steere AC; Successful treatment of Lyme encephalopathy with intravenous ceftriaxone. J Infect Dis. 1999 Aug;180(2):377-83. [abstract]
Nadelman RB, Nowakowski J, Fish D, et al; Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite. N Engl J Med. 2001 Jul 12;345(2):79-84. [abstract]
Seltzer EG, Gerber MA, Cartter ML, et al; Long-term outcomes of persons with Lyme disease. JAMA. 2000 Feb 2;283(5):609-16. [abstract]
Dinser R, Jendro MC, Schnarr S, et al; Antibiotic treatment of Lyme borreliosis: what is the evidence? Ann Rheum Dis. 2005 Apr;64(4):519-23. [abstract]
Correct Method of Tick Removal, Borreliosis and Associated Diseases Awareness UK Website.
EUCALB - European Union Concerted Action on Lyme Borreliosis; A pan-European information site supported by an advisory board comprising an expert group of physicians and biologists from across Europe.
Acknowledgements EMIS is grateful to Dr Richard Draper for writing this article and to Dr Colin Tidy for earlier versions. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2010.
Document ID: 7004
Document Version: 8
Document Reference: bgp442
Last Updated: 30 Jun 2010
Planned Review: 29 Jun 2013

MEDICAL ETHICS TUSKEGEE, GUATEMALA AND NOW LYME DISEASE?

Breaking news, nbc exclusive, frankly a stunning disclosure from the federal government about medical experiments. the u.s. conducted on unknowing patients back in the 1940s. today officials at the very highest levels of government will apologize. robert bazzell is nbc's chief science correspondent. good morning.

>> good morning. the officials that will do the apologizing including secretary of state liquiditien and sebelius. from 1946 to 1948, officials with the u.s. public health service injected gonorrhea and syphilis as part every an experiment in people in guatemala without their permission or consent. these people included people in mental institutions, included prostitutes set loose in prison in an attempt to see how the organisms would spread, all part of an effort to learn more about venereal disease. the records were hidden for many years unless a historic at wesleyan found out about them. we'll hear more about t. but a lot of apologizing all the way around.

>> so bob, this professor found out about it, and presumably brought it to the attention of the u.s. government?

>> she brought it to the attention of the u.s. government. she was studying, and has written extensively about the tuesday ka heee expert on syphilis on african-merican men. this raises comparisons with that horrible incident where from 1932 until press reports revealed it was going on in 1972, u.s. government doctors were telling these african-american men that they were treating them for syphilis when in fact they were withholding treatment. this is a very similar event, though it occurred in guatemala. there will be a lot of apologizing to the nation of guatemala and his spain residents of the united states.

>> good the guatemalan government have any suspicion about this?

>> i think at that time they were fully cooperative, chuck. don't forget there was a lot of politics between guatemala and the united states in that time. 1954, the cia engineered a coup in guatemala.

>> they were hiding this as well?

>> they were hiding this as well. a lot of doctors and nurses were involved in this, but it was under the authority of doctors from the u.s. public health service who was in guatemala. the samples, for instance, of the syphilis organism were taken from a lab in staten island and flown from guatemala to be injected in people without their consent. robert bazzell with the breaks news. secretary sebelius will do a public apology today for experiments that happened back in the '40s. the u.s. government intentionally injecting guatemalans.

>> with cooperation from the guatemalan government. you also heard that secretary of state clinton will you issuing an apology.

http://www.msnbc.msn.com/id/21134540/vp/39456613#39456613

LESTER HOLT, anchor: today from President Obama for something that happened more than 60 years ago. The US conducted secret medical experiments that involved the -- intentionally infecting Guatemalan mental patients with sexually transmitted diseases. Tonight Guatemala is calling it a crime against humanity and says it may take the case to an international court. NBC's chief science correspondent Robert Bazell broke the story this morning. He has this late update tonight.

ROBERT BAZELL reporting: The secret experiments took place in Guatemala between 1946 and 1948, financed by the US government and supervised by US government doctors. Susan Reverby, a professor at Wellesley College, who has studied medical malfeasance extensively, found the evidence in US government records.

Dr. SUSAN REVERBY: I thought that -- frankly, that I wouldn't get shocked but I thought this one was pretty horrific. The details of how they did it were pretty graphic. And I was actually quite surprised.

BAZELL: The doctors inoculated almost 700 prostitutes, institutionalized mental patients and prisoners with the germs that cause either syphilis or gonorrhea.
BAZELL: The subjects did not give their permission and were not told what was happening. They were injected in the skin, the genitals, even the spine. Infected female prostitutes were also sent into the prison and mental hospital to infect men.

Dr. REVERBY: They knew that this wasn't appropriate. The surgeon general even said we couldn't do this in the United States.

BAZELL: The experiments were designed to study the effects of penicillin on sexually transmitted disease. Still, as many as a third of the patients were not properly treated. Today, outrage on the streets of Guatemala's capital and in newspapers online, and from Guatemalan-Americans in Los Angeles.

Mr. RAFAEL CASTILLO (Guatemalan Unity Information Agency): Actually, I'm very surprise, upset. It's like a combination of feelings because it's been a long time already, but it's something outrageous, I would call it.

BAZELL: The incident recalls the infamous Tuskegee, Alabama, syphilis experiment.
nidentified Man: What is now called the Tuskegee experiment began here in 1932.

BAZELL: From 1932 until the research was revealed in the press in 1972, government doctors lied to hundreds of African-American men who were infected naturally. The doctors, some also involved in the Guatemala experiment, told the men they were getting treatment, but in fact they were not. Despite numerous apologies, that incident has left many black Americans weary of the medical establishment.

Dr. BILL RELEFORD (Health Educator): It still resonates after generations and generations. And people still talk about it. So this legacy of mistrust in the African-American community still exists.

BAZELL: Even though the Guatemala experiment took place more than 60 years ago, officials today call on the prestigious Institute of Medicine to launch a full investigation and identify steps to prevent further abuses. Another example of the most vulnerable being victimized and of doctors who ignore their pledge to first do no harm. Robert Bazell, NBC News, New York.

http://www.msnbc.msn.com/id/21134540/vp/39466192#39466192

Prof. Susan M. Reverby website

http://www.wellesley.edu/WomenSt/fac_reverby.html

A detailed report by Prof. Susan M. Reverby

http://www.wellesley.edu/WomenSt/Reverby%20Normal%20Exposure.pdf

Prof. Reverby quotes Thomas Rivers the famed Virologist in which he refers to the law winking when medical science is involved.

The ethics of our Health Departments need careful examination when it comes to Lyme Disease and the denial of Chronic Lyme Disease, methinks there has been too much winking going on over the last 30 years and not enough attention to all the available science.

Ken Liegner's letter to the Institute of Medicine likens the problems over Lyme disease to Tuskegee x 10000.

An earlier post here