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.

-----------------------------------------------------------------

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.

MISTS AND MYTHS SWIRL AROUND INVERNESS

Letter to the ME/CFS/FM community in response to comments under the heading "Lyme disease - let’s dispel the myths", by Dr D. Ho-Yen, October 2006 ME Essential, published by the ME Association, UK.

Mists and Myths swirl around Inverness
By Annie Drummond

Scotland is a land of mists, mountains, and malicious ticks. Sorry Scotland, I love your beautiful country and your hospitable, friendly people, but it is where I was bitten by a tick which gave me Lyme disease (also known as borreliosis.)
Several researchers have found that many patients diagnosed with myalgic encephalomyelitis (ME), Chronic Fatigue Syndrome (CFS), Fibromyalgia (FM) (1,2,3) and Multiple Sclerosis (4,5,6,7) have borreliosis, as do a certain proportion of psychiatric patients (8,9,10).

Scotland has its very own Lyme diagnostic laboratory at Raigmore Hospital in Inverness, while the rest of the British Isles relies on one reference laboratory at Southampton in England. At Raigmore, Dr D. Ho-Yen is the chief microbiologist and has been interested in ME for many years. In fact, he published the first "How to treat ME" book in 1985. He maintains that only a small minority of ME/CFS patients could have Lyme disease as the cause of their illness (11). But is he right?

Lyme disease was brought to worldwide attention in 1975, but its history goes back further (12). However, Ho-Yen in 2006 still feels that he must call Lyme an "emerging disease". Perhaps the pandemic levels (13) that have now been reached have allowed the illness to "emerge" from the cloak of silence that has covered the spread of the disease in the UK. Yet as far back as 1989, i.e. over 17 years ago, the World Health Organisation was aware that the whole of the British Isles, plus Scandinavia, Germany, Austria, half of France, California, areas South of the Great Lakes, and other areas, were endemic for Lyme disease (14).

Ho-Yen has recently admitted that his laboratory missed 33% of Lyme cases (15). He retested old serum samples for the year 2003 to 2004, using different methods of interpretation, and found that previous negative tests were becoming equivocal or strongly positive. One is left to speculate how many suspected victims over the last 30 years have been retested, if any, using these new criteria, and how many patients have been recalled for further investigation. It is admirable that Ho-Yen has published these results, but they sit uncomfortably with his latest pronouncements on the ME/Lyme question.

The ME charities, Action for ME, the ME Association and the TYMES Trust, have relied on Ho-Yen to inform the ME community on the relationship between Lyme and ME in the October and November 2006 issues of their recent magazines. Many scientists and commentators, while not disputing his personal findings and his integrity, would wish to respond to some of the statements he has made in these articles.

There are 6 so-called "myths" that Ho-Yen identifies as current in the Lyme world; each one will be discussed in the light of knowledge available. A very different picture from the one he paints will emerge.

Myth 1: The Internet has the best information on Lyme disease. Verdict: True. This is not a myth. The Internet is the source of millions of archived peer-reviewed scientific reports. We all use the Internet; most of us would be lost without it. The data is more accessible and available to be used more readily; researchers no longer have to physically retrieve dusty documents from medical or university libraries.

To be fair there is a lot of rubbish on the World Wide Web, but it is the easiest place to look for the very latest research. Ho-Yen suggests that it is almost impossible to discern the rubbish from the good material, and at first it can be difficult. However, a recent peer-reviewed paper from 2005, authored by several of the most experienced doctors and scientists working in the Lyme field (16), gives a very useful overview of the data available on the Internet and how this relates to their clinical experience.

Myth 2: Doctors are ignorant of Lyme disease.
Verdict: True. This is not a myth and is definitely true in Britain. Please ask your GPs, whether rural or urban [(Richmond Park, as well as other London parks, has been found to harbour Lyme-carrying ticks (17)] if they have heard of Lyme, or of borreliosis, or of the latest infection rates being reported in Europe?

Most doctors, and members of the public too, think of it as an American disease, (that is, if they have heard of it at all!). But the increasing number of cases across Europe is a cause of concern. For example, in Holland (18), the incidence of the "bull’s eye" rash, Erythema Migrans, (EM), which is pathognomic for Lyme disease, was estimated at 39 per hundred thousand in 1994, which doubled to 74 per 100,000 in 2001, and tripled to 103 per 100,000 in 2005. In southern Sweden (19), the mean annual incidence rate in 2005 was 464 cases of EM per 100,000 inhabitants. The incidence was significantly higher in women than in men, 505 and 423 cases per 100,000 respectively.

These are epidemic rates of infection. Britain’s approximate incidence figures, quoted from the Health Protection Agency (20) are no greater than 1.1 per 100,000. It is difficult to rationalise figures that are 2 orders of magnitude lower than those in Holland for example. The island status of the UK will not have protected it from migratory birds, which are well-documented carriers of Lyme-infected ticks (21,22,23,24). It is also not necessarily true that rural doctors are aware of Lyme disease. There have been several cases in my own rural area of the so-called "well recognised" EM rash being labelled as ringworm and others have been told that they were suffering from shingles or allergies. How many GPs will recognise the condition Acrodermatitis Chronica Atrophicans (25), which is a skin disease associated with Lyme?

Ho-Yen has stated himself that the number of cases in Scotland
is underestimated by as much as a factor of 1 in 10. The point is
• if Lyme is continually labelled as one of "those obscure foreign diseases" doctors will not even bother to test for it. The head of the UK’s Lyme reference lab continues to inform the medical world that the disease is rare in Britain (26) and that positive tests are to be ignored in non-endemic areas.
With the exception of Scotland, Lyme is yet to be made a notifiable disease in Britain. Currently the Health Protection Agency (HPA) website (20) gives the estimated incidence as 1000 to 2000 additional cases per year. This is to be added to the figure for the lab reports for the year, which was 585 cases in England and Wales. The true incidence is unknown.
If the laboratories testing for Lyme are not aware of the many reasons for negative antibody tests in the presence of the disease, and do not inform consultants that the patient could still have Lyme, despite the serology being negative, then the situation is perpetuated.

Myth 3: Most ME is Lyme disease.
Verdict: Open. But it is likely to be true for a high proportion of ME/CFS/FM cases, and not a myth at all, according to many Lyme specialists (27,28,29). Most open-minded people agree that not all cases of ME/CFS/FM would be due to Lyme but there are now thousands of people with these conditions who are finding out that they have Lyme borreliosis or other tick-borne infections.
Recent research in the UK points to the fact that biochemical and immunological markers are very similar in Lyme and ME. In a presentation to the Edinburgh ME group in September 2005, Professor John Gow of Glasgow University stated that gene expression regulation in those with ME is identical to that seen in Lyme patients.

In contrast to Ho-Yen’s assertion that the EM rash of Lyme is an easily recognised indicator, half of those bitten do not show the rash and those that do may have atypical presentations (30,31). Seventy percent of Lyme patients who responded to a poll by the Internet group EuroLyme stated that they were previously diagnosed with ME/CFS. The UK government has stated that Lyme can cause Chronic Fatigue Syndrome, but has not broadcast this statement as an important issue. While there is a heated dispute between specialists who believe that Lyme infection is easily cured by a short course of antibiotics and those who say it persists, nevertheless, both sides agree that the "post Lyme syndrome" often presents as fibromyalgia and chronic fatigue syndrome. However, many studies have shown that there is persisting infection, and that this is treatable (32,33,34,35).

Late Lyme is also hard to distinguish from many other diseases, and is more often under-diagnosed than over -diagnosed (36,37,38,39). Most importantly, although Ho-Yen has listed cardiac, joint and skin manifestations of Lyme, he has omitted to mention the devastating neurological symptoms manifest both in ME/CFS/FM and Lyme (40), unless he is implying that the term "fatigue state" encompasses all of the central and peripheral nervous system deficits that may occur in neuroborreliosis, (e.g. encephalopathy, facial paralysis, vertigo, light and sound sensitivity, tinnitus, meningitis). Ho-Yen fails to state the source of his belief that only 10% of late Lyme patients show this "fatigue state". Most people with late Lyme are crippled by a "fatigue state", as are most people with ME/CFS/FM.

Ho-Yen contends that only 5% of Scottish ME patients studied by him had Lyme. However, he does not state which criteria were used for diagnosing Lyme (as mentioned earlier, blood tests cannot be relied upon to rule out Lyme.) Neither does he mention the length of time of follow up of these patients, despite the fact that Lyme, like ME, is known to be a relapsing-remitting disease (41).

Myth 4: Antibiotics can cure Lyme disease.
Verdict: True. This is not a myth. Antibiotics and other drugs in combination or in series can cure many cases of Lyme disease. The treatment needs to be under the supervision of an experienced Lyme specialist and sometimes must be carried out for months or even years.
According to Ho-Yen "the very need for such prolonged treatment with antibiotics suggests that the success rate is not good". Applying his criteria we would refuse to treat TB patients and leave them to their misery. The longer that Lyme disease remains untreated or under-treated, the worse the potential for permanent damage. In some cases, antibiotics may merely lessen the progress of the disease. However Lyme patients across the world who can access appropriate medical care may recover their health or at least have partial remission. (42).

Ho-Yen states "Indeed, it is difficult to separate the natural improvement that occurs with chronic disease from the effects of antibiotic treatment". His solution is to treat ME/CFS as if it were a viral illness, but this is not appropriate knowing the bacterial causation of Lyme. Viruses and bacteria are quite different biologically, needing completely different treatment approaches.

Myth 5: All laboratories produce dependable results. Verdict: False. This is perhaps the only myth on which we have a point of agreement: if all laboratory tests were reliable, Ho-Yen would not have published his 2005 paper, saying that his lab had had to reinterpret a third of its own tests.
Two comprehensive reviews of the accuracy of standard tests for Lyme, in Europe (43) and the US (44), showed that the same sample of blood could test positive or negative depending on which lab it was sent to, or even if tested again in the same lab. Worse still for those with suspected Borrelia infections, the Polish National Institute of Health has reported that patients with low or negative antibody levels have tested positive using other more sensitive techniques. Specific DNA capture and culturing showed that there were live bacteria in their body fluids (45) indicating that those with negative blood tests could be even more ill than those who have circulating antibodies. The problem of co-infections with other organisms is another complicating factor.

In 2003 Dr Lowes, head of microbiology at Southampton, where the Lyme reference laboratory is housed, promised that an internal audit would be conducted into the lab’s operations. He made that promise following complaints that inaccurate testing and interpretation procedures were being carried out at the Lyme lab. The results of that audit have never been made public to this day.

We agree with Ho-Yen that commercial motives could compromise the quality of lab diagnostics. However, nowhere is this more reflected than in the vested interests of the Lyme committee of the Infectious Disease Society of America (IDSA), which as mentioned below, is currently the subject of an anti trust investigation by the Attorney General in Connecticut, where there is one of the highest rates of Lyme infection in the world.

Dr Susan O’Connell, the head of the UK’S Lyme Reference Laboratory, was a consultant to that committee, and both she and the Department of Health promote its viewpoint as a model for diagnostic and treatment policy in this country. Ho-Yen’s recent article demonstrated that he too has adopted much of that view.

Myth 6: There is misleading expert comment
Verdict: True. This is definitely not a myth. As alluded to earlier, in November 2006, Connecticut Attorney General Richard Blumenthal ordered a Civil Investigative Demand under the anti-trust laws concerning the recently published guidelines produced by the Lyme committee of the IDSA. This group of 14 scientists have been the most vociferous in stating that Lyme disease is never chronic and that treatment, beyond a few weeks of antibiotics, is not indicated. (46).

In a press interview (47) Blumenthal voiced his fear that the guidelines were being used by the powerful US insurance industry to deny health coverage to Lyme patients. In addition to the close ties with the insurance industry held by some members of the committee, a number of them have significant conflicts of interest due to their involvement with companies producing Lyme vaccines or test-kits.

Two of the members, Gary Wormser, lead author of the guidelines, and Allen Steere, admit to receiving money from the multi-national Baxter corporation, which is currently developing a vaccine for the European market. A restrictive approach to Lyme diagnosis serves the interests of vaccine manufacturers as it can cover vaccine failure. It is also difficult to conduct clinical testing of vaccines without using antibody tests to rule out the disease. However, all the evidence indicates that the tests are not sensitive enough to be used in this way. The end losers are the patients.
Clinicians associated with the International Lyme and Associated Diseases Society (ILADS) oppose the IDSA, and treat thousands of patients in the US and across the world with long-term antibiotics if necessary (48).

How many Infectious Disease experts in the UK know about the many reasons (49) why both chronic and early Lyme disease can show no antibodies in blood tests (seronegative)? Why does the Health Protection Agency’s Lyme Reference Laboratory inform doctors that a negative ELISA test rules out Lyme in all but the earliest stages, when there is documented evidence (50) that this is not the case?

Conclusion
A combination of the facts above, and the lack of openness surrounding the topic of Lyme borreliosis, has left many thousands of Lyme patients undiagnosed and untreated.

There are many people who suffer for long periods of time, decades in some cases, who have never been tested for Lyme or who have had negative tests. Years later, they find that the antibodies can be seen in their blood or that other more precise tests reveal the DNA of borrelia in their bodies.

A Lyme diagnosis means virtually nothing here in Britain since there are very few doctors who know how to proceed. The persistence of borrelia infections (51,52) means that antibiotic therapy must be extended in order to reduce the bacteria to a low enough level for the immune system to take over.

There is also the problem of co infections, with growing evidence that many Lyme patients may be infected with anaplasma, babesia, bartonella and mycoplasma species (53,54,55,56).

If the patient has been ill for years, thousands of generations of bacteria will have multiplied and spread throughout the body. They may then lie dormant until the immune system is challenged by other events - perhaps by toxicological insult from organophosphates and other poisonous chemicals in the environment, or by catastrophic life events such as automobile accidents etc.

In other patients, the bacteria may rampage continuously and may cause ME/CFS/FM, heart disease, arthritis, MS, ALS, thyroid disease, and visual defects. They may endure pain and vertigo and brain fog, arthralgia and arthritis, endocrine problems, endometriosis, irritable bowel and bladder disease, skin rashes, rapid heart beats, heart failure, hearing loss, seizures, temporary or permanent paralysis, muscle spasms, tendonitis, memory loss and panic attacks. There is even some evidence to suggest that borrelia infection may lead to bipolar disorder, schizophrenia and Alzheimer’s disease (6, 57,58).

On and on the list goes, making many doctors certain that it is an impossible mixture of symptoms to have and therefore must be all in the patient’s mind. Victims of Lyme disease, like those with ME/CFS/FM, have consequently been called over-emotional yuppies with personality problems, stressed-out under-achievers, or over-anxious and depressed individuals.

Now Ho-Yen has exacerbated this situation by accusing British Lyme patients of hysteria. Lyme victims are hysterical, and demand antibiotics. They are hysterical, and say they know more than doctors. Worse still, people with ME/CFS/FM are catching the hysteria, and phoning him up in hundreds to ask if they have Lyme.

Patients with ME/CFS/FM are advised to beware of this hysterical label and to remember how the two hundred or so nurses, doctors and patients in the Royal Free Hospital came down with a nasty epidemic of so-called "hysteria" in 1955. Many of them never recovered from the disease, and never recovered from the stigma attached to that label.

Over the last 30 years Lyme patients have received the same sort of treatment as people with ME/CFS/FM, - ridicule, contempt, disbelief, denial of investigations and treatment, and the ignominy of a psychosomatic label.

Unfortunately, over the last 20 years, there has been a concerted effort by a small but very influential group of psychiatrists to inundate both the scientific literature and the ordinary press with tales of "psychosocial" causes of ME/CFS/FM (59).

We are all being confused by myths, according to Ho-Yen, but is it possible that he has himself been myth-taken? His suggestions that "fatigue" is only shown by the minority of Lyme patients; that antibody tests can rule out the disease; and that chronic Lyme responds to palliative rather than antimicrobial therapy, are all unproven. They are especially unhelpful in the present situation.

Now the common sense of decent people and the integrity and honesty of certain doctors and scientists, such as Kenneth Liegner (60), will unearth the truth about the causes of ME/CFS/FM. These may be multiple. However, in every case, patients are entitled to full information about their diagnosis and prognosis.

Ho-Yen concludes with "In the end, it is a matter of what makes you better" and urges patients to take responsibility for their own illness. We contend that ME/CFS/FM patients struggle heroically to cope with their condition and are forced to take responsibility for their illness every day. Patients will never get better until there is clarity (61) over the issues surrounding Lyme, ME/CFS/FM and other chronic infections.

References
(1.) Treib, J., Grauer, M.T., Haas, A., Langenbach, J., Holzer, G.,Woessner, R. Chronic Fatigue Syndrome in patients with Lyme borreliosis Eur Neurol. 2000; 43(2): 107 - 9
(2) Nicolson GL, and Nicolson NL. Chronic infections as a common etiology for many patients with chronic fatigue syndrome, fibromyalgia, and Gulf War Illness. Intern J Med. 1998; 1:42-6.
(3.) Taylor, S. Lyme disease (borreliosis). A plague of ignorance
regarding the ignorance of a plague.
http://www.autoimmunityresearch.org/lyme-disease/
(4.) Fritzsche, M. Geographic and seasonal correlation of multiple sclerosis to sporadic schizophrenia. Int J Health Geogr.2002; 1(1): 5
(5.) Fritzsche, M. Seasonal correlation of sporadic schizophrenia to Ixodes ticks and Lyme borreliosis. Int J Health Geogr. 2002; 1(1): 2
(6.) Chmielewska-Badora, J., Cisak, E., Dutkiewicz, J. Lyme borreliosis and multiple sclerosis: any connection? Ann Agric Environ Med. 2000; 7: 141 - 3
(7.) Brorson, O., Brorson, S.H., Henriksen, T.H., Skogen, P.R.,Schoyen, R. Association between multiple sclerosis and cystic structures in cerebrospinal fluid. Infection 2001; 29(6): 315 - 9
(8.) Fallon, B.A., Nields, J.A. Lyme disease: a neuropsychiatric illness. Am J Psychiatr. 1994; 151(11): 1571 - 83
(9.) Sherr, V.T. Panic attacks may reveal previously unsuspected chronic disseminated Lyme disease J Psychiatr Pract. 2000; 6(6): 352-6
(10.) Hajek, T., Paskova, B. Janovska, D., Bahbou, R., Hajek, P., et al. Higher prevalence of antibodies to Borrelia burgdorferi in psychiatric patients than in healthy subjects. Am J Psychiatr. 2002; 159(2): 297 - 301
(11.) Ho-Yen, D. Lyme Disease - let’s dispel the myths. October 2006 ME Essential. Published by the ME Association.
(12.) Schaltenbrand, G. Durch Arthropoden übertragene Erkrankungen der Haut und des Nervensystems Verhandl Dtsch Ges Inn Med.1967; 72:975-1006
(13.) Harvey, W.T., Salvato, P. Lyme disease: ancient engine of an unrecognised borreliosis pandemic? Med Hypotheses 2003; 60(5): 742 - 759
(14.) World Health Organisation Epidemiology of Erythema Lyme borreliosis http://www.ciesin.org/docs/001-613/map25.gif
(15.) Evans, R., Mavin, S., Ho-Yen, D.O. Audit of the laboratory diagnosis of Lyme disease in Scotland. J Med Microbiol. 2005 Dec; 54(Pt 12): 1139 - 41
(16.) Stricker, R. B., Johnson, L.J.D., Harris, N., Burrascano, J.J. Inaccurate information about Lyme disease on the Internet Pediatr Infect Dis J., 2005 Jun; 24(6): 577 - 8
(17.) Rees, D.H., Axford, J.S. Evidence for Lyme disease in urban park workers: A potential new health hazard for city inhabitants. Br J Rheumatol. 1994 Feb; 33(2): 123 – 8
(18.) Hofhuis, A., van der Giessen, J.W.B., Borgsteede, F.H.M., et al. Lyme borreliosis in the Netherlands: strong increase in GP consultations and hospital admissions in past 10 years. Euro Surveill. 2006; 11(6): E060622.2
(19.) Bennet, L., Halling, A., Berglund, J. Increased incidence of Lyme borreliosis in southern Sweden following mild winters and during warm, humid summers. Eur J Clin Microbiol Infect Dis. 2006-11-21
(20.) Health Protection Agency website.
http://www.hpa.org.uk/infections/topics_az/zoonoses/lyme_borreliosis/enhanced.htm
(21.) Poupon, M-A., Lommano, E., Humair, P-F, Douet, V., Rais, O.,et al. Prevalence of Borrelia burgdorferi sensu lato in ticks collected from migratory birds in Switzerland. Appl Environ Microbiol. 2006; 72(1): 976 – 79
(22) Olsen, B., Jaenson, T.G., Bergstrom, S. Prevalence of Borrelia burgdorferi sensu lato-infected ticks on migrating birds. Appl Environ Microbiol. 1995; 61(8): 3082 - 7
(23.) Hoogstraal, H. Birds as tick hosts and as reservoirs and disseminators of tick borne infectious agents. Wiad Parazytol 1972; 18(4): 703 - 6
(24.) Smith, R.P., Muzaffer, S.B., Lavers, J., Lacombe, E.H., e al. Borrelia garinii in seabird ticks (Ixodes uriae), Atlantic coast,North America. Emerg Infect Dis. 2006; 12(12): 1909 - 12
(25.) http://www.emedicine.com/derm/topic4.htm
(26.) Aliyu, S.H., Ludlam, H., O’Connell, S. Lyme borreliosis – a preventable disease? CPD Infect. 2002; 3(2): 54 - 8
(27.) Donta, S. Lyme disease as a model of Chronic Fatigue Syndrome. CFS Res Rev. 2002; 3(2): 1 - 4
(28.) Goldenberg, D.L. Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome. Curr Opin Rheumatol. 1995; 7(2): 127 - 35
(29.) Nicolson GL, and Nicolson NL. Chronic infections as a common etiology for many patients with chronic fatigue syndrome, fibromyalgia, and Gulf War Illness. Intern J Med 1:42-6, 1998.
(30.) Gustaw, K. Chronic fatigue syndrome following tick-born diseases. Neurol Neurochir Pol. 2003; 37(6): 1211 - 21
(31.) Lesniak, O.M., Belikov, E.S. The classification of Lyme borreliosis (Lyme disease). Ter Arkh. 1995; 67(11): 49 - 51
(32.) ILADS position papers on diagnosis and treatment of Lyme disease.http://www.guidelines.gov/summary/summary.aspx?ss=15&doc_id=4836&nbr=3481
(33.) Priem, S., Munkelt K., Franz, J.K., Schneider, U., Werner, T. et al. Epidemiology and therapy of Lyme arthritis and other manifestations of Lyme borreliosis in Germany: results of a nation-wide survey Z Rheumatol. 2003; 62(5): 450 -8
(34.) Stricker, R.B., McNeil, E. Duration of antibiotic therapy for Lyme disease. Ann Intern Med.2004; 140(4): W6
(35.) Bransfield, R., Brand, S., Sherr, V.T. Treatment of patients with persistent symptoms and a history of Lyme disease. N Engl J Med. 2001; 345: 1424 - 5
(36.) Frey, M., Jaulhac, B., Piemont, Y. et al. Detection of Borrelia burgdorferi DNA in the muscle of patients with chronic myalgia related to Lyme disease. Am J Med. 1998; 104: 591 - 4
(37.) Stricker, R.B., Lautin, A., Burrascano, J.J. Lyme disease: point/counterpoint. Exp Rev Anti Infect Ther. 2005; 3(2): 155 - 65
(38.) Fallon, B.A., Kochevar, J.M., Gaito, A., Nields, J.A. The
underdiagnosis of neuropsychiatric Lyme disease in children
and adults. Psychiatr Clin North Am 1998; 21(3): 693 - 703,viii
(39.) Bachman, D.T., Srivastava, G. Emergency department
presentations of Lyme disease in children. Pediatr Emerg Care
1998; 14(5): 356 – 61
(40.) Shadick, N.A., Phillips, C.B., Logigian, E. L., Steere, A.C. et al. The long-term clinical outcomes of Lyme disease. A population-based retrospective cohort study. Ann Intern Med. 1994; 121: 560 - 7
(41.) Omasits, M., Seiser, A., Brainin, M. Recurrent and relapsing course of borreliosis of the nervous system. Wien Klin Wochenschr. 1990; 102(1): 4 - 12
(42.) The ILADS Working Group: Cameron, D. et al. Evidence-based guidelines for the management of Lyme disease. Expert Rev Anti Infect Ther. 2004; 2(1): S1 - S13
(43.) Hunfeld, K.P., Stanek, G., Straube, E., Hagedorne, H-J., et al. Quality of Lyme serology. Wien Klin Wochenschr. 2002; 114(13-14): 591 - 600
(44.) Bakken, L.L., Callister, S.M., Wand, P.J., Schell, R.F.
Interlaboratory comparison of test results for detection of Lyme
disease by 516 participants in the Wisconsin State Laboratory
of Hygiene/ College of American Pathologists
proficiency-testing program. J Clin Microbiol. 1997; 35:537 – 43
(45.) Tylewska-Wierzbanowska, S., Chmielewski, T. Limitation of serological testing for Lyme borreliosis: Evaluation of ELISA and Western blot in comparison with PCR and culture methods. Wien Klin Wochenschr. 2002; 114(13-14): 601 - 5
(46.) Wormser, G. et al. IDSA Guidelines Clin Infect Dis. 2006; 43: 1089 - 1134
(47.) http://pqasb.pqarchiver.com/courant/access/1164183821.html?dids=1164183821:11641\83821&FMT=ABS&FMTS=ABS:FT&type=current&date=Nov+17%2C+2006&author=ELIZABETH+HAMI\LTON&pub=Hartford+Courant&edition=&startpage=B.1&desc=LYME+DISEASE+GUIDELINES+FO\CUS+OF+ANTITRUST+PROBEArticle by Elizabeth Hamilton. Lyme disease guidelines focus of antitrust probe. Connecticut News November 17th 2006 edition.
(48.) ILADS op cit.
(49.) Harris. N. An understanding of laboratory testing for Lyme disease Journal of Spirochetal and Tick-borne Diseases. 1998;Volume 5, Spring/Summer http://www.igenex.com/labtest.htm
(50.) http://www.lymeinfo.net/medical/LDSeronegativity.pdf
(51.) Lawrence, C., Lipton, R.B., Lowy, F.D., Coyle, P.K.Seronegative chronic relapsing neuroborreliosis. Eur Neurol.1995; 35: 113 - 7
(52.) Bradley, J.F., Johnson, R.C., Goodman, J.L. The persistence of spirochetal nucleic acids in active Lyme arthritis.Ann Intern Med. 1994; 120: 487 - 9
(53.) Krause, P.J., McKay, K., Thompson, C.A. et al. Disease-specific diagnosis of co-infecting tickborne zoonoses: babesiosis, human granulocytic Ehrlichiosis and Lyme disease.Clin Infect Dis. 2002; 34: 1184 - 1191
(54.) Benach, J., Coleman, J.L., Habicht, G.S., Grunwaldt, E.,Giron, J.A. Serological evidence for simultaneous occurrences of Lyme disease and babesiosis. J Infect Dis. 1985; 152(3): 473
(55.) Eskow, E., Rao, R.V., Mordechai, E. Concurrent infection of the central nervous system by Borrelia burgdorferi and Bartonella henselae: evidence for a novel tick-borne disease complex. Arch Neurol. 2001; 58(9): 1357 - 63
(56.) Nasralla, M., Haier, J. Nicolson, G.L. Multiple mycoplasma infections detected in blood of patients with CFS and/or Fibromyalgia. Eur J Clin Microbiol Infect Dis. 1999; 18: 859 - 65
(57.) MacDonald, A.B., Miranda, J.M. Concurrent neocortical borreliosis and Alzheimer’s disease. Hum Pathol. 1987; 18(7): 759 - 61
(58.) Miklossy, J., Khalili, K., Gern, L., Ericson, R.L., Darekar, P.,
Borrelia burgdorferi persists in chronic Lyme neuroborreliosis
and may be associated with Alzheimer disease. J Alzheimers
Dis. 2004; 6(6): 639 – 49
(59.) Document prepared for the Countess of Mar by Malcolm Hooper, Emeritus Professor of Medicinal Chemistry, University of Sunderland UK, in collaboration with members of the ME community. The mental health movement: persecution of patients? A consideration of the role of Professor Simon Wessely and other members of the "Wessely school" in the perception of myalgic encephalomyelitis (ME) in the UK. Background briefing for the House of Commons Select Committee. December 2003.
(60.) Kenneth B. Liegner, M.D., P.C. Remarks before the NYS Assembly Committee, chaired by Richard Gottfried. Albany, 2001, November 27th.
(61.) Stricker, R.B., Lautin, A. The Lyme Wars: time to listen. Expert Opin Investig Drugs 2003; 12(10).

_________________________

Not a lot has changed in how patients are left undiagnosed and undertreated since this was written although there has been considerable research published that supports ILADS views. This is still ignored by our so called experts as they continue to put their personal spin when they publish papers that illustrate their view rather than a comprehensive view of all the research.

TIME TO EDUCATE OUR NHS CONSULTANTS

I don't generally post personal stories of patients with Lyme disease but this one particularly touched me.

With permission I am only going to post a small section of it but do go to the full details here

Apart from highlighting patients' struggle with the disease and getting a diagnosis for their multi system problems it so highlights the crass comments our 'esteemed' medical professionals come out with, it is time they were taken to task over their behaviour and held to account for their comments to patients when clearly they are not informed of the complexities of Tick borne illness. Lyme Disease and the many co infections that can also affect us.

***************************************************************************** the ----establishment had so badly let me down and basically left me for dead at 36 years old !!

I went to London to the Infectious Disease clinic and the journey itself was hard as I am so poorly.

We were seen and told from the offset that, "we were there to listen to his opinion and that we would not be discussing Lyme until we had heard what he had to say" and i felt like a naughty schoolgirl that had been pulled up in front of the headmaster and was really tired of being treated so awfully when I was sick .

He asked about where I had traveled to tropically and then in Europe and then in the UK.... I reeled of the list of many places as I had travelled to all of these in my youth through bar work.

He then said "well you haven't been anywhere that is tick endemic and so its not Lyme" ..I, this time, had no patience to argue ,as the last time had taught me I was banging my head up a brick wall so I just sat there and silently disagreed with him in my head.

So he preceded to examine me which was very different to the previous 20 or so examinations I'd had by other doctors...and consisted of my lymph glands down my body and my spleen....he had said he would check my eyes as I was wearing the sunglasses but after he had done his tests he told me to go back and sit down and did not again look at toenails,rash or the eyes .

My husband then played him the video footage of me and my attack ...he watched about 10 seconds of it and said" that's enough "and then showed him the positive test results and he asked ..".who done these..."my husband replied "Igenex" and he said "well i can get a positive result for any test I want if I send it to the right place "and then told me that the "Americans are all mental and blame every symptom they have on Lyme" ....he said "don't get fixated with Lyme "...

to which I replied "I'm not fixated ..its just I have every symptom ..even definitive ones of Lyme ..positive test results that are non biased .. and the most important thing is ...if its not then what is it ??..

because I have seen nearly 20 doctors now ...who either tell me they don't know.. or we can tell you what its not ...or its a headache.... or a stiff neck ... or I may never get a diagnosis for this...or the last doctor who had the cheek to tell me there was NOTHING wrong with me...or its all in your head ....so believe me, I'm not fixated, I just haven't even been given anything else that it realistically could be ...and the fact that this is capable of evading normal routine tests, which is what's happened with me is surely proof enough to give antibiotic treatment a go

""He then said that, as this is an infectious disease clinic then he was going to run 3 tests of diseases that are of African nature..... and although the timing is out as to when I should have got ill with these after my return from Africa..... and the chances of me having them are next to none... he needed to rule them out anyway ....

to which I agreed ,but wondered why this wasn't checked for in the hospital on my admission on that first night ..as they were made fully aware of the fact we had not long returned from a tropical country and they did tell my husband that all possibilities had been checked for ...

Then we had the punchline delivered to us..in a very sinister way indeed ... considering he had just told me that if he wanted to ,then he could get a positive result for any test if he sent it to the right place.

..one of the tests that he was running was for an African borne disease that's VERY ,VERY RARE.. but the only treatment for it is to pump arsenic into your blood ..which results in 3 out of 5 death rate anyway...

I couldn't believe it ...one of the possible options that he'd managed to come up with rather than even acknowledging there is even a slight chance that it might be Lyme was of a rare disease that you had hardly any chance of surviving from the treatment..

.and it had sounded more like a threat ...

and I wondered why he had no worries about putting arsenic into me but I was having such a tough time getting antibiotics ..

I had also, before I'd found Lyme gone through, like I said every disease going ..and had studied African diseases especially hard, as we had spent a lot of time in Africa in the last two years and the symptoms and timing didn't match any of the diseases. .

So I'd agreed to his tests (or death sentence )that he had given me... and then I continued talking about Lyme .

This is when I believe ...he used the sentence that it had taken the doctors all these months to come up with ...of how to get around this situation, without actually telling me they would not treat me long term.

He said I am going to put you on a course of doxycycline for 3 weeks..if you get better then it was Lyme and you are cured...if not then it wasn't Lyme.

Here's how this interprets ...3 weeks course of doxycycline does treat and cure Lyme disease if caught in the early stages ..ie after the bite of an infected tick ..or the trademark rash being present ...after that if left untreated it grows in your body and will eventually turn into stage 2 which is harder to treat... and if still not detected it will go to stage 3 ...when it crosses the blood borne barrier and enters the brain and internal organs and this is where I am at and is extremely difficult to treat

and the NHS are not willing to invest the time or money to see if long term IV antibiotics make a difference...even though it has been proved by real people suffering with the disease at late stage... who have had to raise money and sell there homes .beg and borrow to find theirself a LLMD (Lyme Literate Medical Doctor) who specialises in the treatment of Lyme and its co infections and understands the complexity of the disease and of the treatment plan ,for life .

This is the aim of this appeal... I need to find myself a LLMD who will treat me and this will be outside the NHS and possibly outside the UK ...

Thankyou for reading my story ..please educate yourself and your family and friends on Lyme....... because if I can stop this happening to someone else it will do some good ...please if you are on facebook join the group that was my daughters idea and my husband set up ...called Would you pay a £1 to help save my mummy's life?..pass it on to your friends and ask them to pass it on and so on ...the more people that join ..the more awareness there is and it also gives my little girl some hope and makes us not feel not so totally alone in this situation http://www.facebook.com/profile.php?id=1109650270&ref=search#!/group.php?gid=134675306560444&ref=mf thankyou so much if you would like to donate click on the link below or if you would like to send a cheque ..please make payable to ...The Sonia Smith Appeal Fund 29 St Johns Rd
Bletchley
Milton Keynes
MK3 5DU
England
or for further queries contact soniasmithappeal@aol.com

****************************************************************

Initially Sonia was admitted to hospital with a suspected Brain Tumour or stroke but when tests showed nothing she was dismissed with 'It's all in your head' despite symptoms of paralysis, Bells Palsy, verbal stuttering and difficulties speaking, light and sound sensitivity to mention just a few of her symptoms.

As most of us find with Lyme Disease here in the UK like elsewhere in the World getting diagnosis even with positive Igenex tests is no guarantee that NHS will treat with antibiotics. Quite remarkable that this ID specialist would consider IV arsenic for some rare African Disease and yet simple antibiotics even oral antibiotics have significantly improved the lives of many patients with a clinical diagnosis of Lyme Disease let alone a serological diagnosis.

All these consultants in denial should listen to the recent presentations at the Institute of Medicine Workshop showing how complex all these tick borne diseases are to test for let alone to treat. Click here

HOW TO PREVENT HEALTH CARE COSTS

'Dementia and stroke as a consequence of Treponema and Borrelia infections also occur in the tertiary or late stages of these spirochetal diseases.

In meningovascular neurosyphilis and neuroborreliosis the leptomeninges and leptomeningeal arteries are involved leading to Heubner's arteritis and arterial thrombosis with secondary cerebral infarct (indirect parenchymal involvement). When Treponema or Borrelia spirochetes invade the nervous tissue (direct parenchymal involvement) there is a meningo-encephalitis or encephalitis. With respect to the direct parenchymal involvement, which corresponds to a meningoencephalitis, two different forms are distinguished. In the infiltrative form there is a severe lymphoplasmacytic infiltration and in the atrophic form, a poor or absent lymphoplasmacytic infiltration, but severe microgliosis, neuronal loss and cortical atrophy are present. The pathology of both, the infiltrative and atrophic forms were clinically and pathologically documented in both neurosyphilis and Lyme neuroborreliosis.

The cases with chronic or late Lyme neuroborreliosis, illustrated in the chapter, were published in per reviewed, internationally recognized medical journals. Some of them more than 15 years ago. Chronic or late Lyme neuroborreliosis was confirmed by clinical, pathological and serological examinations and the spirochetes, their antigens or their genes were detected in the tertiary lesions of the brain. Improvement of late or chronic neurosyphilis and neuroborreliosis following antibiotic treatment was repeatedly reported both in syphilis and Lyme disease, however the treatment of late or chronic cases are more difficult. Syphilis was virtually eradicated by the use of Penicillin, indicating that we can also eradicate Lyme disease.


Newer approaches to the treatment of Lyme disease should take into account the frequent co-infection with other pathogens and the need for a more prolonged combination therapy, as it is the case in the treatment of tuberculosis. Even in the doubt of tuberculosis the treatment of the patients with "tritherapy" is necessary for 6 months. It should be an example for the future treatment of Lyme disease. Such treatment, in analogy to tuberculosis and syphilis will substantially prevent extensive healthcare costs in the future.'

************************************************************
The above was posted on Judith Miklossy's website here

I have long since been a fan of the outstanding work Judith Miklossy has done in the field of Lyme Disease but also in Alzheimer's and it was a privilege to meet her in 2009 at the Lyme Disease Action conference.

Those of us unfortunate enough to get Lyme Disease who are lucky enough to get diagnosed and find a good knowledgeable Lyme Doctor who is able to tailor treatments to suite us are testament to Miklossy's recommendation about treatments.

Sadly there are many thousands more who go undiagnosed and untreated because not enough attention is being paid to this formidable disease.

I was browsing through an earlier post I did on the UK figures for Lyme Disease 2009 here

1467 in the UK

but according to Dr Ho Yen HPA Scotland ten times the figure of serologically positive tested cases is more likely.

14670 likely Lyme Disease cases in the UK in 2009

As many of us have been sick several years even on the conservative side say 5 years mean that is still an incredibly high number of 73000 people here in the UK many of whom will be unable to work full time due to their illness.

Just imagine how much our Government could save if only there was more awareness and early adequate treatment as well as appropriate treatment for late stages of Lyme Disease.

CHRONIC FATIGUE, ARTHRALGIAS, MYALGIAS, DYSESTHESIA, DEPRESSION

This recent research article is a start in the right direction looking at Chronic Lyme Disease, so far most research concentrates on the early acute form only.

The recent Institute of Medicine workshop highlighted that more studies need to be done in this later chronic state of illness with or without positive serology.

Abstract can be found on Pub med here

The diagnostic spectrum in patients with suspected chronic Lyme neuroborreliosis - the experience from one year of a university hospital's Lyme neuroborreliosis outpatients clinic.

Most common symptoms in all categories were arthralgia, myalgia, dysaesthesia, depressive mood and chronic fatigue. Conclusion:  Patients with persistent symptoms with elevated serum antibodies against BB but without signs of cerebrospinal fluid inflammation require further diagnostic examinations to exclude ongoing infection and to avoid co-infections and other treatable conditions (e.g. autoimmune diseases). One patient with acute LNB, who was treated with ceftriaxone for 3 weeks suffered from LNB with new headaches and persistent symptoms 6 months later. These data should encourage further studies with new experimental parameters.

details also found on Prohealth here

I found the above interesting because it highlights that Borrelia infection may not be ruled out by lack of Cerebrospinal fluid inflamation, something that many Neurologists tend to do with people with Neurological illness or Multiple Sclerosis.

Also the study talks about 122 patients in one year with suspected Chronic Lyme Neuroborreliosis that in itself is interesting because 114 of these people had tested positive for Lyme Disease and all had received antibiotic treatment.

To have such a number suffering with Arthralgias, myalgias, Dysesthesia, Depression and Chronic Fatigue after the standard treatment has to raise some serious questions beyond what this study was aiming at.

Because current guidelines adopted from the IDSA guidelines suggest that these remaining symptoms are rare, all in your head or the aches and pains of daily life it would seem they are not so rare after all.

One has to wonder with the poor state of reliable testing for Lyme Disease how many more people with the above symptoms could infact be suffering from an undiagnosed case of Lyme Disease and may benefit from antibiotic treatment following such as the ILADS guidelines .

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