Saturday, 30 October 2010


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 .

Friday, 29 October 2010


Better Health Guy reports back from ILADS conference here

I was only able to watch a small part through the live Webcast so it was great to read Scott Forsgren's summary.

The slides from the event are available for purchase here for a very reasonable $40. The DVDs (Friday's sessions) and CDs of the presentations can be obtained from ZenWorks Productions.

Below are just a tiny selection that caught my eye from Scott's excellent blog post.

Dr. Richard Horowitz proposed that Chronic Lyme is really MCIDS - Multiple Chronic Infectious Disease Syndrome

Dr. Joe Burrascano shared: New pathogens will likely continue to be discovered such as XMRV / HGRV
In chronic Lyme patients, 100% may be XMRV / HGRV positive

Eva Sapi, PhD talked about the many exciting projects that her team is doing:
They are looking for XMRV in ticks to see if the retrovirus may be transmitted by tick exposure
They did some excellent research showing Samento + Banderol + Serrapeptase (all from NutraMedix) had very significant biofilm eliminating effects

Dr. Joe Brewer spoke on the topic of XMRV:
In one autism study, all mothers tested were XMRV positive and many of them expressed symptoms of Chronic Fatigue Syndrome or Fibromyalgia
In a small sample of MS (4), Parkinson's (1), and ALS (1) patients, 100% of those tested were positive for XMRV
In chronic Lyme disease, over 90% of those tested were positive for XMRV

During Q&A, Dr. Fishman acknowledged the politics involved in Lyme disease. He suggested that XMRV may be the pathway that we should pursue in order to benefit ourselves

But much much more at Better Health Guy here

Thursday, 28 October 2010


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.

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.

In the UK, areas where infection is acquired include:
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
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.

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.
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.

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

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
Infective endocarditis

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 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.

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
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).

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.

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.

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

Tuesday, 26 October 2010


The first video is just a handful of the many thousands of patients suffering with Lyme Disease throughout the World.

For every patient that knows they are suffering with Lyme Disease there will be many more who are unaware that their symptoms or Arthritis, Muscle weakness, peripheral Neuropathies, gastric problems, psychosis, heart block could be connected to an undiagnosed case of Lyme Disease.

They will have been diagnosed with a variety of illnesses Fibromyalgia, ME/CFS, Arthritis, Poly Myalgia Rheumatica, Parkinson's, Multiple Sclerosis, Motor Neuron's, Alzheimer's, Psychosis, Chronn's disease and the list is endless.

Even if their doctors test for Lyme Disease they will say that a negative test means you don't have Lyme when infact even the makers of those test kits say that a negative test can not rule out Lyme Disease.

The second Video made based on the experiences of a ME/CFS patient is in reality something that most of us with Lyme Disease experience to.

Infact about 30% of us actually get diagnosed with ME/CFS before we finally find a doctor that diagnosis Lyme Disease.

This video should be watched by the doctors and therapists who see us so that they can consider what foolish things they say to patients.

Thursday, 21 October 2010



WPI started a study in March 2010 to look for HMRV (Human MLV Related Viruses - both X and P) in UK ME/CFS patients.

The study included 50 patients with ME who met the Canadian Consensus Critera, 50% male and 50% female, along with 50 controls.

It was a blind study.

The 100 samples were tested blindly by two labs who had never worked with MRV or mice (to ensure there was no possibility of contamination).

The labs first tested plasma and 48% of the ME plasma samples were positive for XMRV (all were also tested for mouse DNA and were negative).

Other samples were detectable only after culturing (some sort of special sample preparation).

In some samples, only the virus was detectable; on others, only the antibodies were detectable.

Multiple testing methods were necessary in order to find all of the XMRV positive samples.

In all, 80% of the ME patients in the study were positive for XMRV.

4% of the controls were also positive for XMRV (in line with the original WPI study).

Dr. Mikovitz emphasized that the XMRV was very difficult to find.

They have learned that subtle differences in storage, handling, and testing make a big difference and that multiple methods must be used to find it all.

The above was from Learning to Live with CFS blog here

Read her full post at the above link.

Tuesday, 19 October 2010


'To reduce the potential for inadequate care and assist successful outcomes, physicians need greater knowledge of insidious, intransigent Borrelia burgdorferi.

Without definitive tests, a definitive cure can not be known.

Therefore, while medicine unravels the intricacies of Lyme disease and the coinfections that may accompany it, physicians must have flexibility to treat patients to the best of their ability.

As long as controversy over Lyme disease treatment continues, physicians should be guided by nothing more, and nothing less, than their patient's response to intervention and the principles of informed consent, especially when standard treatment fails.132'

The above is an extract from 'A Patient Looks at Lyme Disease and Guidelines' found

originaly posted on Lyme Works blog

Monday, 18 October 2010


'According to Dr. Brewer, XMRV is potentially associated with Parkinson's, chronic Lyme disease, MS, ALS - as well as ME/CFS. In his practice, 90% of his XMRV+ patients are Lyme Disease. (The Patient Advocate had heard previously that all of Dr. Brewer's Lyme patients are XMRV+) Four our of four of his MS patients are XMRV+, 1 out of 1 ALS patient is XMVR+, and 1 out of 1 Parkinsons patient is XMRV+.'

The above was posted on CFS Patient Advocate blog

(Another great read about Judith Mikovits presentation here
and more here although you may need to follow this on Facebook to read it or follow me on facebook where there is a link.)

Read the full post for more information about the presentation at the recent ILADS conference.

For further posts about ALS or as we call it in UK Motor Neurons, MS, Multiple Sclerosis, or any of the other illnesses mentioned put the name in the search box on the right of this blog for earlier posts.

Saturday, 16 October 2010


Institute of Medicine of the National Academies Webcast
A Workshop on the Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-borne Diseases: the Short-Term and Long-Term Outcomes

Spectrum of Lyme Disease: Approaches to Understanding Multi-factorial and Multidimensional Diseases
Benjamin J. Luft, M.D. (confirmed)
Edmund D. Pellegrino Professor
Division of Infectious Diseases
State University of New York at Stony Brook

here about 54 mins in.

Below is a phonetic translation, sorry about the mistakes but as I am not sure how long the videocam will be available I wanted to save something of this important event.

(Ben Luft's presentation in my opinion was the most important and significant part of this two day workshop.)

Good morning.

I tried to put this together. I was invited only about a week and a half ago and only decided to come about a week ago so it's a
little bit of a last second type of job and I'll apologize in advance

What I wanted to do, I've been working in Lyme Disease for the past 25 years.

I worked on a number of other infectious and noninfectious diseases.

I consider myself to be an academic physician.

I see patients when I find them to be important to my overall
research activity and so my gamut has ranged from working initially about HIV/AIDS and toxoplasmosis to the World Trade Center where I follow 5,500 responders to the World Trade Center disaster for their neuro,psychiatric problems and using epigenetics to try to understand that.

What I would like to do is talk a little bit about Lyme Disease today and part of it comes from my own understanding of this disease from seeing patients over a long period of time and part of it comes from my understanding of other disease entities which I think gives us insight into what is occurring here.

As you heard today by both the previous presenters, you know, Lyme
Disease continues to be an emerging and diverging disease.

What I mean by diverging disease is that it is not purely confined to Borrelia burgdorferi, or at least the original species of Borrelia burgdorferi that we originally heard of.

As we go on and as our knowledge continually expands we realize that
there are more and more organisms that may be playing aplaying a role in this.

And I think as Gary mentioned before, to our patients Lyme Disease
is their disease.

It's what makes them sick.

They're not interested as to whether it's a Borrelia burgdorferi
infection or whether it's, you know,one type of genotype of Borrelia or another genotype of Borrelia.

They're concerned with their illness.

And I think that that's really a very important concept.

I think a lot of the issues in regard to its multi system nature was really well covered in the previous talk.

But I also think it's important to understand that this is a
multi-dimensional disease.

I mean,this is something that I picked up on over the last six years as to what does that mean, multi-dimensionality.

One of my credentials was for 12 years I served as the chairman of the department of medicine and I was very loyal to the department of medicine and thought of everything in this way.

When I began working outside the department I began thinking of more of a patient centered manner and I think you have to think of patients their diseases to understand the multi-dimensionality.

And so you have to understand the various biological, neurological, psychological,economical and other aspects that affect the systems.

Systems don't occur out of that context.

And it also affects responses to therapy and the chronicity of disease and the overall disability that patients may have with Lyme Disease or with any other disease.

So I think that's really an important concept.

Furthermore I think we have to -- you know, I'm giving the end of my talk in the beginning, I think a wise thing to do, we to develop the (indiscernible) and we have to develop a universally accepted phenotype of the disease.

I think as Gary just said everyone has a different idea but, you know, that really doesn't cut it with our patients that 26 years off the onset of our illness that we all have a different idea.

You go to the infectious disease doctor he said one with they be thing, you go to the psychiatrist, he says another thing, you go to the neurologist he saiding on hits thing be you go to your friend
and he or she says another thing.

That doesn't cut it.

We have to know what we're talking about.

We have to define the phenotype.

This is really very important for anyone who wants to
do studies with this disease.

We don't have a universal understanding of what the disease is.

Furthermore, no specialty has developed the conceptual or therapeutic model of dealing with this complex disorder or other infectious or post infectious disorders.

I think it's important for this committee, I'm not going to go into it, to look at what has'd happened in the metherlands with the outbreak of Q fever and there they now have a Q fatigue syndromes.

This happened as a result of an environmental contamination with
Q fever and subsequent developed into acute Q fever and then ubsequently chronic Q fever and the manifestations.

It really mimics Lyme Disease very well.

Few medical centers or any centers of excellence are equipped to deal with the full compendium of medical, psychological and social implications.

The ramifications of this is third party parries are not responsive of needs of this population and there are few practitioners who have been specifically trained to deal with this disease.

There's no expertise out this there.

So there are people who go out there with cam passion but not
very much training and try to deal with this disease and they try to
learn as they goa along sometimes well and sometimes quite frankly not very well and I think that that's a real problem and I think it's a problem with the academy.

It's a problem as to why these types of citieses are so often dismissed and not really dealt with in the manner they should.

So we look at Lyme Disease.

It's kind of looking at the old adage of the blind man with the elephant.

This is from another talk, as you can surmise, but it's like every specialty and every group all have a different idea and they're each describing that entity differently so we're not really talking to one another and there really is no common description.

So we've taken quite honestly over the last 20 some odd years besides doing good amounts of clinical trials and things of that sort for Lyme Disease we've taken a biological approach to try to understand the disease, can he saw the ospb and developed a vaccine
that is now in trial in neuron.

We've been involved in looking at the 36, the multiple pathogens with sticks, the various genotypes, we've been involved in genomic sequencing.

I'm very happy to report that we've recently published together with
(indiscernible) the first ever a series of papers in which we are
releasing the data on three genomes of Borrelia that have been fully
sequenced and this I think will really push the field forward.

And it would be good to have that type of information available to the committee in its full form because it's a very important way, important milestone.

We've been involved with Brett I can't Proteomic and I'll show you some data from that with Dick Smith, north well's national laboratory and we've been involved with a protein arry study.

So this is an early study we did not as early as Dr. Osfeld but what we did originally is we kind of -- I was first, you know, a young person and I liked the idea of going out in the field and we went out and flagged for ticks and we wanted to look at what the OspC variation was within this population and we did a slot blot
which I think is familiar to many of the scientists buff the concept is that as you see more and more dots in the slot blot in each one of those rows, the vertical rows, that indicates the vair Borrelia burgdorferi that were in there, the OSPC we were able to identify.

So can you see in different ticks there were as many as one variant to as many as nine variants of Borrelia burgdorferi found in the ticks.

That was an early study we did and it was inspeak are trying to us that perhaps these ticks are much more -- this infection is a lot more complicated than just Borrelia burgdorferi being all put into one pot and we did a subsequent study which was published in infection and immunity where we were able to identify the various tick ice lats that I just showed you previously and were able to categorize them into different OspC types and those were listed on the top part of the graph, the first horizontal row were the tick
isolates indicating each of them indicating a different -- shown to be a different genotype.

But what we saw was when we looked at patients and their skin isolats, there was a much smaller population that were found in the skin that was causing human disease.

And then the last group, the four isolats that we saw at the bot.

Were the invasive isolats, the ones that were found in the blood of net patients.

So what we were able to show was there raise relatively low
population of Borrelia burgdorferi that was actually causing invasive disease.

So when you look at the complexity of what Dr. Osfeld shows, you know, officers Borrelia burgdorferi being in ticks then you now have to kind of be able to expand that out to looking at 20 different genotypes that might be there and how those might separate
from mouse to chipmunk to squirrel to whatever, you know, whether there's any particular appropriatism.

And I think that's an important area.

Subsequently others have done this.

There was a beautiful study by Wormser and Swartz that really was put out almost con comedantly with this and really showed a very similar finding perhaps using different markers but it just shows the complexity of the problem and that one Borrelia is not like another Borrelia.

When we looked at the invasive strains which is, what we wanted to look as were specifically the OspC types that were associated because that was the marker we were looking at and the OspC
is the major protein of Borrelia burgdorferi at least which is enters the skin.

And so we solved the structure of the OspC pro seen and what we were able to show was the ones that were inhave asive, that they
were -- their structure was identical to the noninvasive strains except at the very head of the structure where the elect static force was different.

It had very high positive level of electro positivity at the head of it and that was something that we hypothesized at the time may be an important indicator for invasiveness.

I recently went to a meeting and was able to show that the CMP protein found in Borrelia hermsa has the exact same characteristic had when it goes to the meninges so perhaps our original finding deserves further study.

But as I said before, Borrelia burgdorferi is an expanding and
diverging process.

There are many species that are now being identified.

At one county saw there were as many as 37 different species throughout the world of Borrelia of which 12 ever believed to cause Lyme Disease one way or the other, some of them cultivated, some of them not cultivated, some of them only by CPR evidence but they're
just there to give a feel for how problem that we deal with it.

But in general Borrelia burgdorferi, as I said, sensu stricto is the
species that causes the strain in the United States of afzelii and garinii in Eurasia as well asberg dory.

Different Borrelia have different capacity to cause human disease.

Not all Borrelia are the same.

And I think that this has important implications for this committee as you decide how the research should go further.

It has implications in terms of thinking about the size of studies,
about the geographic distribution of studies, what is the appropriate power, how appropriate size should be powered.

I think all of these things are very important.

And so here is some data that from some collaboration that did I as well as others with mark issue who is now at Abbott, previously as Ibyss and this was funded originally by Darba.

And what we did is they have developed a system for being able for identify where pathogens or a multiple array of pathogens using a combination of broad range PCR and mass Beck.

I won't go into much detail about that.

But what I wanted to do in this slide was for you to look at the pattern of Borrelia genotype distribution in four different parts of country.

New York, Connecticut, Indiana and California.

And what you see is that there's a good amount of difference in the
proportionality of different genotypes.

And if you take what I said before, that different genotypes have different potential to cause disease, you can see that a variation
or an -- on balancing of different genotypes in one part of the country might give you another disease versus another.

There may be antibiotic responsiveness in one region versus another, depending on what the intrinsic resistance of those
organisms are within those particular areas.

This is just thrown out there.

Do I have a lot of data to say that resistance is different from strain to strain and things of that sort?

No,that hasn't been done yet.

But I do think that this is something that needs to be considered when you're developing appropriate trials.

Here's the genotype did Itressty between regions.

This is New York and Connecticut.

You can see that there are 15 genotypes that are very common
and this is mark Essu's system.

There was where they had 42 different genotypes using the IBA system.

In New York there were 16 distinct ones and in Connecticut there were four distinct ones.

Certainly there's overlap but you can see there are differences.

You can see I'm pushing for the multi centered approach to understanding this disease, okay.

And the other thing that you have to realize is that within a tick, how many different genotypes occur.

I showed you our initial, you know, down and dirty slot block but here's a much more elegant study that was done by Mark using very contemporary techniques.

You can see that there are in 34% of the ticks there are at
least two different genotypes.
And in 5% there were greater than three.

So clearly in about 40% of ticks, they are able to spread the disease,they're infected with multiple genotypes.

Which genotype is causing the disease.

How do they impact one another.

So potentially the immune system is fighting two different infections con comedantly.

What is the impact of that.

Is there synergy, sin tagunism, we really don't know.

And again I think this was mentioned briefly by Gary, the complexity of other microbes.

This is not a simple complexity.

You now have multiple genotypes within that tick and at the same time, look of the tremendous variety of other pathogens that are
there as well.

Pathogens that we know are extremely potent immuno modulators.

Pathogens that can cause a significant amount of disease.

What is the impact of babesiosis?

I can tell you that I study toxoplasma in years and I know the impact of toxoplasma and it's activity in certain circumstances and it's tremendous amount of disthe inflammatory affect is dramatic.

How does that impact the way the disease manifests itself.

How does it impact when you begin trials to try to understand disease how it is when someone is infected with just one Borrelia or three Borrelia or nine Borrelia and babesiosis or a porus
environment or Anaplasma, et cetera, et cetera.

What I'm trying to say is that it's extremely complex.

So the Borrelia burgdorferi sensu stricto has been shown to have
pneumonia are you genotypes present in the areas where it's found.

Some genotypes have been shown to persist longer in mice and affect disease severity in humans.

Mixtures of the genotypes may challenge thein immune system in unknown ways.

What are the implications of this for the development of various types of trials?

Well, I know we're not supposed to talk about they are pew ticks but I'll talk about it a little bit in that I think that multi centered therapeutic trials will be required to assess the efficacy over a broad array of patients exposed to various genotypes and vapor variants swells other pathogens. Some will need to be
placebo controlled and powered.

Underpowered studies which purport to demonstrate unfortunately efficacy need to be viewed with circumspection.

That's very important.

When these patients are coming in to >> Captioner: , they're the rare birds.

Most patients with Lyme Disease I'm able to take care of.

As I try to teach my physicians, 90 to 95% of the patients can be seen by nurse practitioners.

They're only coming to see you for the 5% of patients that are not able to be taken care of that are posing diagnostic did I leam.

Diagnostic tests will need to be consider genotypic various.
Epidemiologic studies need to be appropriately powered and extend over a geographic region as possible to understand the variations of this disease which is caused by a complex infection and I respect fluidize agree that anyone that says 200 patients an
appropriately powered study for this complex disease I think they're wrong.

Not that I'm a statistician but I bet you I can find one to agree with me.

Until appropriately powered studied are performed, smaller studies and observations which show treatment breakthrough and failures should be fullically appreciated.

We did all of these strains and we did a lot of sequencing and we came up with our map, our family free of Borrelia and I'll go over this very quickly.

I'm not going to go over our -- an analysis of our genomic studies.

Some of them haven't been published yet so it wouldn't be fair to the others.

But as you can see, this was the complexity.

And what we did was we again to identify in a very rational way the various strains of Borrelia, and you can see which ones they are,
that we wish to sequence the etire genome.

And we did that with Claire phasier at the -- well, she was at the
venture institute at the time but she's now at the University of Care land. (Indiscernible)

What I wanted to talk to you a little bit about is the whole idea of where we are with that because I think it's an extraordinarily powerful tool what we now have available and that is that
we've been able to have the pangeno.

So what our concept was look, there's the whole confusion.

This is the day of technology.

There shouldn't be any question as to what we did.

Let's do it all.

So what we did was we began to sequence the genomes and we wanted
to know how many scream owns did we need to sequence and to get a complete picture of every gene within the Borrelia family tree.

The reason why we wanted to do that was went wanted to know whether Borrelia was more of a closed genome.

It was an open genome it meant there was a lot of genetic data that it could continually battle and we would never know the complete
Borrelia burgdorferi because we would be getting more information from other strains.

If it was a closed genome and relatively tight we would be able
to do that and we would be much closesser to an answer in terms of
diagnosis and treatment.

And so here I just wanted to give you the data since I think that's
important and I think it's exciting.

So we looked at Borrelia burgdorferi,the sensu stricto, that species.

What we were able to show was that as we were going out to about 14 genomes, that the number of new genes that we were identifying was relatively small.

Every time we sequenced a genome there would be another four genes that we began to identify.

It became a point of diminishing returns and that's why we actually stopped at 17.

We got a good idea of the core genome, the part of the Borrelia that was found in all strains of Borrelia burgdorferi.

We know what is essential to that organism now and we have a pretty good idea of what the pan genome is.

The things that we really don't know -- how many minutes?

My time is up already.

All right.

I'm going to be really quick but -- I'm sorry.

And here basically, basically the take home measures when you use the Borrelia species, what happens is that you have it's morbidity open genome type of problem.

But the real question is how the information is going from beg I can't afzelioo andberg do if I.

If it is fluid, with all of these Borrelia that are out there, it may cause that we may have problems toward the future.

I wanted to just mention one last thing about how we took this
information in regard to the genomic or sequencing and how the practical approach to it.

So as soon as we began to see the data on these 17 different strains we began to look for positively selected genes.

And what I mean by positively selected genes are those genes that
are under a certain amount of immune (President Obama??) and therefore their heterogenius from strain to vein and the reason why they're heterogeneous is because they're continually pushed to be positively selected.

We took those genes and we took the genes that were also, that we could preticket were on the surface of the proteins and we made a protein array.

And the Roe 13 array now is well over 500 different proteins, recomedant proseason that we have each cloned and expressed and put on a chip and we began testing Sierra.

And I just wanted to give you some data on 15 Sierra that we received from the CDC.

These are very well characterized Sierra.

All of them were from patients who had initial arrhythomyagrams.

They were by op acid and cultured so we 93 the genotype.


So they represent a broad away of Borrelia.

And what we were able to show was that when you looked at the western load and ELISA, only 54% of them were Sierra positive.

It was nine out of 15.

However, using the protein nitro array we were able to identify all of them as have been ant body to Borrelia.

I think the important part to this, and this is really just at day zero, at initial time point.

But the important point that I'm trying to make is that when you have the knowledge and when you have the information, you're able to -- the level of Sierra negativity, even in the patient we saw that was 60% negative at the time they are seen, they are antibody.

You have to know where to look.

That will only come to us by doing good science and being receptive to it.

So what -- I'm going to finish this up because they are just my

What is needed to solve the chronic Lyme Disease?

Well,we need a standard operating procedure.

We have to define the patient with Lyme Disease and gather
information on the patient'snist a uniform way.

We have to collect the biological samples in a relislable and
useful way.

We have to reproduce them in a reliable manner and this has to
be done across all centers.

We have to reproduce and validate our results.

And we should utilize -- we are very lucky that we do have a very good animal model.

I think we'll here about it with the talk by Steve

I think it's extremely important and I urge the panel to take
note of that because there are very few animal models out there for
persistent infections.

This is really the opportunity to be able to study this in a way that doesn't require having large numbers of patients.

And I think that this is something you should just take note of.

I canis important to develop a chronic lyme bio bank.

A lyme bio is there to thereside the opportunity to (indiscernible) it's a cost effective resource thorough sides high quality clinical information and biological samples to the research community but
all of this is dependent on developing an accurate methodology for phenotype identification and this has to be done in a very careful manner.

And I just wanted to end with this quote.

"Science is not belief but the will to find out."

And I really want to -- I have been very privileged to work with a very imminent group of scientists throughout my career especially in regard to Lyme Disease.

We went out and recruited a group of people who had really very little idea of knowledge of Lyme Disease and its controversies and I think that they've done an extraordinary job.

Actually I just wish each other every one of them could be here to talk about the work that they did.

Thank you very much.


Later in discussing reinfection and relapsing illness Ben Lufts response was - here 100.30 mins in

>> I want to clarify one point. I think that Peter and Gary were
correct, that you can become reinfected with Lyme disease, after
being -- after having air themea myograms.

But the nature of Lyme disease is it's a relapsing disease.

That's the very nature of you getting infected, very erythema myograms, having dissemination, separated by time, the disease comes back and it can give you cardiac abnormalities or abnormalities in your joint, that's a relapse.

That's a relapsing process.

The period of time is well-being with disease relapses, and that can occur in a cyclical manner.

You can have multiple episodes of relapse, and this can go on for years

That's the natural history of the disease.

The natural history of disease ez is it's a relapsing disease.

It's also very interesting that even though you may have this disease, you can be reinfected with another -- with Lyme disease again, even though you've been previously infected.

I just wanted to clarify that.

Link to earlier post on research on Whole Genome Sequences of 13 isolates of Borellia Burgdorferi here

Thursday, 14 October 2010


Gregg P. Skall, J.D. Counsel, National Capital Lyme and Tick-borne Disease Association Member, Womble Carlyle Sandridge & Rice, PLLC
here about 28 mins in.

A phonetic translation so apologise for mistakes.

Thank you. For sake of brevete and shorthand we will use the term Lyme,to designate all of the diseases we have been talking about and indeed that's important that we do that.

Because we are talking about all of these diseases. About, lets see,
about two years ago, Lyme started working the hill to try to get a full investigative hearing on chronic Lyme Disease.

We never got that hearing,but we did get the ear of congressman
Frank wolf and through his efforts and appropriations committee, I believe,that effort was, at least in part responsible for getting this very,very wonderful workshop together and we are grateful to the committee for putting together a very, very useful and wonderful workshop.

We are and grateful to the congressman for his efforts in making sure that we got this. In fact, you did it almost, the way we would have liked to have seen it done. And you covered a lot of very,very important topics, and we are very interested and they are interesting.

Most important is the fact that Lyme is identified as a national epidemic.

To many of you that may seem like second nature but frankly we have been fighting that battle for a long time.

And we need that recognition. We are only beginning to acknowledge the degree of the complexity of this diseases we are talking about.

And it is crucial that congress, that you,the medical community recognize the complexity of this disease, and the burden it creates on individuals.

From several presentations we were encouraged about the recognition of persistent or chronic Lyme Disease.

Whatever you want to call it. We need more recognition for that.

Most of the presentations really, when you analyze them dealt with acute infection.

We need, and the patients that asked for this proceeding, need
attention to the chronic form or the persistent form of the disease.

To put it a little smart alikey, science of mice is interesting, but while we are studying that we have to know, we have to know that we are still interested in the patient.

We have to keep the focus on the patient.

We were wondering where other studies of the primates? We know there are studies of primates, with respect to this infection.

We would like to see that study and discussed.

In the meantime, while we are doing this studying we need to support the practitioners on the front lines helping the patients, helping our family members, who are afflicted with this disease.

And they are -- they are helping the patients deal with the burden of the disease.

And we did hear, by the way,what we decided to do, because we are
supposed to summarize what we heard, we put quotes in, in the bars here.
I am not going to take the time to read them. But please, review them as we go along. The burden of the disease is enormous, on individuals, on children, children losing their childhood, people losing lives to this disease.

We know that it is a very complex disorder.

And we need better diagnostic tools.

You have heard that discussed by a lot of the people that summarize. I will not go over it again.

But need to recognize and study the fact that we do not have
sufficient diagnostics and particularly with respect to persistent form of the disease.

We need to review the case definition.

The CDC surveillance criteria is inappropriate for application to

But that's exactly what happens, folks.

It is used to deny insurance coverage to individuals.

And it is used to discourage physicians from treating patients with Lyme Disease, and these diseases.

It is much misunderstood in the general medical community.

And frankly, in our experience it is used in the decisions of medical boards to determine how and who to investigate, for the treatment of the diseases with antibiotics.

That needs to stop.

We need a better case definition that is expanded to include all the emerging spectrum of the diseases and recognize that different treatment regimens are appropriate and that the clinician must have the freedom to make an artful decision with respect to how to
practice medicine, in the best interests of their patients.

We need to redefine that criteria, remove the regional biases, how many times have we heard you cannot have Lyme Disease?

We don't have it here in this state.

We need to bring all the information that we heard here, to the general public, and to the general medical community.

We need to include all the diseases in the definition.

We need a better way to report.

Physicians find it too burden somto

We need automated standardized report that covers all states, that is standardized and that includes late manifestations of the disease, or persistent manifestations of the disease and make it easier for the physician to report.

We need a new approach.

Several presenters highlighted the differences in the significant of co-infections and immune suppressing properties.

But like I said most dealt with acute forms of the disease.

We need focus on the persistent forms of the disease.

We need to banish the term post Lyme syndrome.

There is politics folks in how we deal with the labels that we

And when you use post Lyme syndrome you are basically saying you
don't have a disease, you have got a psychological condition. Lets deal with what people really have, lets help them, and find the research that we need to do that.

We need critical research for the 21st century.

Dr. Loft research with the Borellia gene know type, we need to create a database that captures every aspect of the disease.

We need, as we heard, Manhattan like project to deal with this disease.

He was kind enough to say it was hyperbole but that's not
really true.

It is not high ber Boley that's the scope of the kind of project that is needed.

We think that in research we need to look at how the Alzheimers * disease neuro imaging initiative came up with new biomarkers.

Their project leader said that the three-point program they used was extremely important.

They agreed to share the data.

Agreed that every finding would be made public immediately.

And they agreed to renounce ownership in patent rights.

We need T.O. to deal with that issue of the patent rights and whether or not it is inhibiting rather than Fostering research.
So my time is up.

I will try to run through these fast.

Where the research of the focus needs to be, but the important point here is that we need new proposals.

We need fresh blood into this program.

Like I wrote, I am not talking about glass slides. We need new thinking.

We need fresh people coming into the program with new ideas on how to combat these diseases and treat patients.

And we need to replace the CDC surveillance criteria.

Collaboration is extremely important.

That's been emphasized.

I will just let you read the slide.

But we need to find ways to bring all, everybody concerned with this disease, together.

We need the clinicians working with the practitioners, and the
researchers, we need the researchers valuing the information they are getting from the clinicians.

And clinicians and not dismiss ting as anecdotal evidence.

What we have heard here is most of what they have called anecdotal evidence wound up in the slides of a lot of the presenters here as valuable information that demonstrates the consistently see of
the disease across the country.

So while we wait what do we do?

Well, we ask state advocates across the country.

We did also do, I will ask you to read the paper we submitted.

Because we did a national survey of patients but we also have a survey of state advocate leaders and they said these are the most important things.

Doctors are not updated on the existence of Lyme Disease in their
state T needs to be included in the differential diagnosis. So that they have a clue as to how to look at patients when they come to them presenting the diseases, presenting the symptoms, that you have heard about here.

If doctors pursued testing let them know not to simply rely on the alie sacks we have heard all kind of -- it is a decent test.

But it is certainly not the gold standard and we heard a lot about that.

So we need to get doctors to look beyond the simple
serology of the aliza.

And let physicians use the knowledge they have acquired in medical school, through their practice and practice the art, as well as the craft of medicine.

So Lyme Disease is a clinical diagnosis.

Thank you.

Their written presentation to IOM here

Wednesday, 13 October 2010


A Workshop on the Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-borne Diseases: the Short-Term and Long-Term Outcomes

Below is a phonetic transcibing from the Video cast apologies for mistakes but I do not want to change from the original state other than the spacing to assist those with Neuroborreliosis who have difficulties reading.

The video cast link is here and starts at about 23 mins in

Susan O’Connell, M.D.
Consultant Microbiologist
Head of the Lyme Borreliosis Unit
Southampton General Hospital

Thank you very much indeed. I would like to express my great
appreciation, for being invited to this.

I am from the UK, I thought I better express the fact that I don't
have any financial professional conflicts of interest.

Also coming from a different health care
background as well. And insurance companies by and large don't feature it very much at all.

So thank you to the IOM it has been a privilege to be here.

I have heard some wonderful work being talked about
over the last couple of days.

And I would like to say thank you very much
indeed to the patient advocates that are here, because it is really

And I just hope we can go forward in a collaborative spirit from
this whole meeting.

I am afraid I would be repetitive.

Because I will say quite a few of the things that you have heard.

I think one of the things in this area is case definitions and diagnostic criteria,it is obvious that we don't have
agreed definitions at the moment.

I think, we actually need to try and get close to agreements on these areas,very different terms listed here.

Because it is crucial. Both for the diagnosis and the appropriate
management of patients now, patients suffering now.

And also for the research efforts that we want to go with, for the future. Both in basic science and in the diagnosis and proper management of these conditions.

I am thinking particularly of Lyme.But obviously the other conditions as well.

Now, I think, another big area. I come up from both a clinical and
laboratory background so I am going to talk about lab tests for the moment.

And, I think, we all agree we need improved diagnostic tests for all the tick-borne diseases. And I am concern courageed by the progress I have heard.

We should acknowledge also that zero tow logic testing has
improved since the 90s. We need, I do feel strongly, we need now to
review the current state of play as far as 2 tier test sing concerned and time we have a workshop on this.

Things moved on incredibly. I don't think we need to use
immunoballots to the degree that we have been over the years. The new modern recombination peptide base tests have a real place to play here.

And I would urge the IOM to consider seriously promoting the idea of a workshop on this.

I also feel that we need a high volume of sera, from a large number of both patients, normal controls, and Patients' from other
disease groups as well.

To produce a repositor, serum, that we can use, for evaluating new tests. And as they come along, we only have relatively small serum panels at the moment.

And we can do various other things from the point of review of reviewing what is available in the current tests as
well. And I would reiterate,education, education, education from
the point of view of using these tests from the point of view of the disease itself, to health care professionals,
to the communities.

Just if I can just run briefly through clinical aspects. Why do some people do poorly and what proportion of people who gets infections do poorly?

We early diagnosis of treatment is very important.

Again I come back to education. Both for health care professionals and also people that are likely to be exposed. We have heard
wonderful work over the last couple of days B various different possibilities for why patients, some patients do not
do well.

And I would also flag out the point that some patients actually
are misdiagnosed. I do not have Lyme. They have other conditions.

Equally well, we are missing Lyme in patients.

We need to begin considering both the over and under diagnosis of the condition.

Whatever the diagnosis, the patients are sick and they need
help. And I would like to say one idea. And that's that we need to
resort a long-term study of patients.

Who have got -- who have a Lyme label,persistent infection, chronic
infection, call is what you will.

And I wonder if advocate groups could help in the recruitment of this?

To assess accuracy of d possible mechanisms,treatment, management, including and supportive approach.

One thing I would like is patients not shown to have Lyme in this group, don't just shut them away but actually continue
to manage, to care for them. And go ahead.

By repositor as we spoke before. Maintain the various research things,and the prevention.

I am sorry my time is up.

But how will we sell the human behavioral factors as far as
prevention is concerned?

Paul Mead talked about this early on. I really do think we need again education for health care professionals as well as
obviously people living in the community, and I am well out of time.

So I apologize.

Questions and responses

Question from Dr Cameron

Dr. O'Connell had raised a very important question, which is, could we ever get along in a research project that would make advocates, doctors that see chronic manifestations of Lyme and early Lyme and come up with a reasonable design that everybody is happy with?

Never will be anything Beaver but this particular meeting
today, shows that we could all be in the same room and share something, in common. And some goals. So that's encouraging.

But what I want to mention, is that when Dr. Aronowitz
said the case study with the vaccine,is that, you know, if you don't have fairly decent balance between, you know, the community groups, and the doctors that did the vaccine, you can design a study, vaccine, that fell apart over some logistic issues,
definition of early Lyme, late Lyme,definition of effectiveness.

So for a whole, you know, pharmaceutical company to go to that much work and investment and fall apart because of poor communications between different stakeholders, I just think that these
two days show that if we all take, you know, what the different definitions of chronic r acute, co-infection, and,perhaps, instead of having only one out, come and have 2 or 3 important outcomes that are important.

And have different people run it, instead of only one stake holder involved. That we could, you know, probably design something.

We hope to design something.

Dr. Lian, who did a case control study from Massachusetts, that
was pretty good at long-term follow-up. We get something from
every study.

But I think, I am more optimistic after these two days, that
we could, probably, design something as long as stakeholders work together.

So I want to know if you have thoughts about that, about that challenge?

>> I certainly think it is a which I can't speak about how trials get organized, in the U.S.A.. But something that I would throw over to the IOM, to possibly to take forward.

I do think that it should -- I think such a trial should be
multi-specialty, multi-disciplinary as well.

Not just involving medical clinicians, but people coming from
other backgrounds as well.And also,looking to support patients. From the point of view of the other affects on their lives as well.

So that was a suggestion for what it is worth from me.

>> Yeah, I think, just to close on that. If you follow people over time,and more perspective, is find out who had a different diagnosis, and also people that get told they have fibromyalgia or multiple sclerosis, it would be worth looking to see if any
of them Lyme in the end.

Often they have a different diagnosis. That would be a pathosis to add in as a possibility.

So all kind of things.

Patients are concerned that those are not included in the study.

Those that are told they have a different diagnosis.

So lots of creative ideas that patients may bring to the table.
That could be included.

I just want to give a thought about design issues.

>> Well that was the reason I said, if a patient is actually is found not to have Lyme Disease, but is given a diagnosis of something else. Rather than exclude them, from the follow-up.

>> I like that thought.

>> Actually, keep them within the cohort. So we can see what the
long-term outcomes are.

>> The treatment.

>> For all the group.

>> I agree.

>> On that topic, I understand that,NIH, has funded a committee to look into some of those other diseases. Such as chronic fatigue syndrome, and,perhaps, we ought to have a committee on Lyme and tick-borne diseases that would work in conjunction with them,
to exchange data and information, and cause many of the symptoms as I understand manifested by the patients are cross -- whatever you call it as doctors. Cross indicative

>> I am sure there would be a really great benefit from that type of a approach.

Because, a lot of the time we could be looking at final common
pathways, as well.

And with these conditions.

>> So Dr. Gerber glumpy and you are next.

>> Very quick follow-up question for you Dr. O'Connell.

It is wonderful that you come from an environment that doesn't have to worry about a number of things that we have to worry about
in the states.

Who would constitute your ideal clinical management team,for this set of diseases?

>> You don't have to mention rehabilitation. Okay. I mean, that's
my specialty. This is not self serving. I really want to hear what
you have to say.

>> Well, Lyme Disease, affects so many systems, we actually need to bring in a number of different specialists.

You know, for example, in the UK,neuro briloses would be the major
complication to deal with.

And, in fact, rheumatologists in the UK do not tend to see many cases of Lyme arthritis at all. It is not a major feature of Lyme in the UK or most of Europe N what we are looking at here is different.

Strain variations, as much as anything else.

Butba Borrelia Burgdorferi sends you to your home strain, is actually less common than either the other branches are concerned.

So we see less of the manifestations.

So, I mean, I think,we need to bring in yet certainly all the major specialties that would normally be involved in dealing with
the complications that patients with Lyme can have.

I have been tremendously impressed as well by some of the information that Hassett put out yesterday from the point of view
of central pain.

I mean, we have to find ways of managing these symptoms.

And helping patients to get back to --to get their lives back.That's
actually what we are talking about. Rehabilitation can be very major part of that situation.

>> Multi-disciplinary. And multi-special teal teas well

>> It was a very pointed question,that I presented to you.

Because in these repositors, the question is what additional information will enable us, in your view, to understand the
natural history, as well as what are our effective clinical interventions that enable people to be restored.

And so what I am asking is coming from your perspective, management of chronic illness, in a different system, would the contributors, in your view, to these bio repastor res include those things that are much more clinical science driven.

You mentioned the central pain, central fatigue, that sort of stuff.

That's the purpose of my question. I think you have answered T I have an idea of what you have in mine. I appreciate it.

Thank you.

Tuesday, 12 October 2010


Institute of Medicine Talk on The Human Face of Tick-Borne Disease
by Pamela Weintraub (Permission to re post granted)

View the video link here about 43 mins in

Lyme disease entered my life in 1993, when my husband Mark, our two sons, and I moved to Westchester County, New York. At the time I was, as I am now, a science journalist specializing in biomedicine for the national consumer press. Our lovely property in the hamlet of Chappaqua abutted a spruce forest, and we reveled in our new contact with nature—there were deer, squirrels, raccoons, mice and all sorts of other animals and birds.

From that point on, we all became increasingly sick. First there were headaches, joint pains, and an inexplicable weariness. With time, the symptoms intensified and multiplied: My knees became so painful that I had to sit down to descend the stairs in my house on my bottom, one step at a time. I developed dysphagia: I had so much trouble swallowing that I literally choked on my food. I developed peripheral radioneuropathy: My arms and legs buzzed, gently at first, and then increasingly painfully until it felt like electricity was running through me. The headaches became relentless. My eyes were painfully sensitive to light. I spent hours each day in a darkened room, in bed.

Meanwhile Mark, an avid tennis player, began stumbling and bumping into walls. He was an award-winning journalist, but he began struggling with memory and groping for words. Increasingly cognitively impaired, he was forced to leave his job after realizing that he‘d spent hours trying to read a single, simple paragraph.

Our youngest son, David, began to sleep—first so long that he could not do his homework or see his friends; eventually, so much that he could not get to class. In the end he was sleeping 15 hours a day.

Hardest hit was Jason, our oldest, who suffered profound fatigue and shooting pains starting at age nine, late in the summer of ‘93. The doctors called these ―growing pains‖ normal, and my son, though often fatigued, tried to keep going. Then in 1998, he developed a huge erythema migrans rash over his torso. I called the doctor's office and was told not to bring him in—since it wasn't in the shape of a bull's eye, it wasn't Lyme, they said. After that rash, Jason became increasingly ill, and never seemed to get well. By 2000, at age 16, he was functionally disabled. He could not think, walk, or tolerate sound and light. On medical leave from high school, he spent his days in the tub in our darkened main-floor bathroom, drifting in a mental fog while hot water and steam eased his pain. As his condition worsened, as all sorts of lab tests came back negative, a raft of specialists at New York City‘s top teaching hospitals suggested diagnoses from migraine aura to parvovirus. Each diagnosis elicited a treatment, but none of them worked.

“What about Lyme disease?” I asked from time to time.

“There are too many symptoms here and he‘s way too sick for Lyme disease,” responded the pediatrician, who told us he felt it was all psychological. Thankfully the psychiatrist we ultimately consulted –an academic scientist who literally wrote the book on child and adolescent psychiatry—disagreed. At his insistence, the pediatrician drew fourteen vials of blood, testing for hormone imbalance, mineral deficiency, anemia, and a host of infections, including one tick-borne disease -- Lyme. A week later he called to tell us that just one test, a Lyme Western blot from Labcorp, had come back positive, with eight of ten bands highly lit.

Finally the head of infectious disease at Northern Westchester Hospital weighed in: In retrospect, he said, Jason had probably been misdiagnosed for years. I will never forget the way he phrased his grudging diagnosis: “I‘ll give it to you,” he said, as if we had earned some coveted prize that others, whose confusing arrays of multi-system ailments could be explained in some other way, would never get. Unaware of the political turmoil over tick-borne disease, I didn‘t yet understand how rare it was for a doctor like him to diagnose late-stage Lyme disease in New York State. Jason was treated with eight weeks of intravenous Rocephin, but when he didn‘t get well, the Lyme diagnosis was revoked, and that doctor, too, consigned him back to psychiatry.

The situation would stretch any one’s credulity: Our formerly straight-A, basketball-playing son, after contracting Lyme disease, being misdiagnosed for years, and finally receiving antibiotic therapy for two months, had now developed a bizarre, unrelated psychiatric disorder whose symptoms were, coincidentally, exactly the same as those of Lyme disease. Perhaps it is possible to believe this kind of explanation when served up by experts talking about other people‘s children; but it is the rare parent who would accept this decree for a child of his or her own --especially when your psychiatrist has never seen a psychiatric disease like this in his life.

My husband Mark and I, by now both quite ill now ourselves, faced a choice: Accept this unlikely story and give up on our son‘s future, or find one of the Lyme doctors said to treat more aggressively, in opposition to the mainstream views we had followed for years to the current, tragic state of affairs.

So in the summer of 2000 we bundled our boy into the car and headed up to New Haven, and the practice of the embattled pediatrician, Charles Ray Jones. Dr. Jones examined and tested Jason and told us he was so sick because he had contracted not only Lyme disease, but two common co-infections that ticks carry —babesiosis and anaplasmosis. Epidemiologically, it seemed like a reasonable call, given the many vacations we’d taken on Martha‘s Vineyard and Cape Cod, where babesia was rife. Dr. Jones treated Jason with standard doses of doxycycline for anaplasma and Lyme disease, and with mepron and zithromax for babesia. Two weeks later –after years of freefall—our son got out of the bathtub and began throwing a basketball around the family room. Two years later he was playing varsity basketball for his high school, and today he is a graduate of Brown University and earning his MFA in film.

Although my book, Cure Unknown, is in part a memoir, its focus is really what I found after I had dealt with my family's health problems sufficiently for me to sit back and peer through the eyes of the investigative and skeptical science journalist I had been for decades before Lyme swept us away. For almost eight years, from 2000 to 2008, I interviewed patients, the Lyme doctors treating the sickest of them, and dozens of academic scientists, including most of those at the forefront of research and many speaking at this forum. My journey as a patient was contextualized by all this research, and often confirmed. For instance, I met large numbers of patients with classic, incontrovertible presentations of Lyme disease who, like Jason, would probably have been cured with early treatment but who were instead diagnosed late, often very late, in the game. Routinely, patients that I interviewed reported going to their primary care doctors with the tick in hand and being told to throw the tick away and return only if symptoms emerged. Many patients told me of doctors who insisted a Lyme rash had to look like a literal bull‘s eye. Patients reported going to doctors with a tick bite, early flu like symptoms, and sometimes even an erythema migrans rash, and being told to wait for a positive test before they could be treated. When patients tested positive, a significant percent were told they could still not be treated for Lyme disease until they developed gross objective disease signs like swollen knees or inflamed nerves—in other words, until they had advanced into the late stage of disease, when treatment was more likely to fail.

Other patients with known exposure and signs and symptoms of Lyme disease failed to test CDC positive on their Western blots. Take me: I had a positive ELISA and four CDC positive bands plus two additional Borrelia burgdorferi proteins, outer surface proteins A and B. Six bands in all, and the lab was Stony Brook. Still, I had to step outside the bounds of the medical mainstream to find a practitioner who recognized this alternate band pattern as Lyme disease. Patients in the South could have the trademark rash and objective disease signs --but they would be told there was no Lyme or clinically comparable Lymelike disease in their state, and be turned away.

Such patients, in aggregate, constitute what I think of as the chronic Lyme population: They had bona fide Lyme disease that would have been cured with early treatment. Instead of getting that treatment, they were diagnosed months or years too late. They were eventually treated for late stage Lyme disease in accordance with the Guidelines of the Infectious Diseases Society of America. And they failed the treatment.

Completing the community of patients covered by the meeting today are the coinfected—those with babesiosis, anaplasmosis, ehrlichiosis, or some other tick-borne infection. If you look at tick surveys from around the United States these diseases in ticks are widely reported, and they are well-known as human diseases, yet primary care physicians almost never consider or test for them, if indeed the possibility of Lyme itself is seriously considered. I think a real effort needs to be made to determine the whole suite of possible diseases patients with Lyme may be carrying—because having an unknowable, undiagnosable illness can be very much part of the patient experience on the ground. Patients like Jason can be very sick, and their disease can be refractory specifically because it isn‘t just Lyme.

As a group, these patients can be very ill. Mark Klempner of Boston University reports his cohort of chronic Lyme patients was as impaired as those with congestive heart failure or osteoarthritis and more impaired than those with type 2 diabetes or a recent myocardial infarction. Brian Fallon of Columbia reports pain equivalent to post-surgical pain and fatigue as severe as that seen in M.S. Patients can suffer stabbing, boring, shooting pains in their arms and legs, or impaired vision and hearing from damaged nerves. They can suffer heart damage.

Even more devastating, especially to students and knowledge workers, are the cognitive and memory deficits. Testing hundreds of such patients, New York University neuropsychologist Leo Shea found specific deficits in concentration, short-term memory and processing speed. Fallon has objectified these impairments by tracing them to blood flow and metabolism deficits in the brain. Some scientists have called the impact of these impairments mild, but that does not remotely capture the experience for the patient herself —the angst of falling behind in school or feeling perpetually foggy and confused. Many patients report getting lost while driving around their own neighborhoods. Many patients have told me they could no longer remember enough to perform the detailed tasks of their jobs.

For me, the fatigue was the worst of it --during the years I had Lyme disease, I collapsed in a heap every afternoon while my children were in school, my exhaustion overwhelming and profound. Sure, there are studies that minimize these types of “subjective” symptoms as being almost irrelevant. But just because you can see evidence on the outside --for instance the rash or joint swelling-- doesn't mean the devastation on the inside can't also be measured in a reliable fashion or shouldn't be given primary weight as perhaps the most important and clinically relevant outcome of all.

Unresolved Lyme and tick-borne disease can be a nightmare for parents, who bear the heartache of watching their children suffer along with the sense of helplessness and despair that comes from a medical community all too quick to dismiss their complaints: Take it from me. My two boys are better now, but both lost their childhood to Lyme and tick-borne disease. After a child has been allowed to slip through the cracks of early diagnosis and treatment, the stage is set for isolation and alienation as the child drops from clubs, sports teams, friendships and often, even school. In the wake of the child‘s decline, schools often push psychiatric interpretations, foisting inappropriate labels and discipline or help. When the child doesn‘t respond to wrong-headed strategies, the schools may accuse parents of poor skills in parenting or even Munchausen by proxy, a diagnosis that has been called into disrepute by top experts in psychology and psychiatry, but still manages to rear its head as an accusation where mothers and Lyme disease are concerned.

What a chasm I found between the patients I interviewed and some physicians at teaching hospitals in the northeast. One well-known academic told me that virtually all Lyme patients are diagnosed early these days, and for the rare one who slips through the cracks to late stage disease, treatment response is guaranteed. “If the patient doesn‘t respond, he never had Lyme disease,” the doctor said. When, during grand rounds or training sessions, such doctors suggest the patients are bogus --malingerers too wimpy to handle stress, middle-aged suburban women with somatoform disorder, or hypochondriacs in search of the disease du jour-- they have poisoned the chance of timely diagnosis by predisposing front line primary care physicians to seek psychiatric explanations first. With early treatment off the table, such patients wander from family doctor to clinic to teaching hospital, from one specialist to the next --and then off the grid.

My family found our way to doctors who diagnosed infections clinically and treated empirically, all the while using modalities for symptomatic relief of chronic disease: These were the best of the Lyme doctors. They treated our babesiosis and addressed our Lyme relapses and, over the course of years, brought us back to health. We found them compassionate and responsible, but being the patient of such a doctor is stressful: He or she may be under investigation, and rarely takes insurance for fear of being profiled as an outlier and then delisted and further stigmatized, making the financial burden on the patient intense.

Other patients default to outright quackery: dangerous chemicals and mixtures; lethal levels of heat applied to internal tissues; risky doses of salt. Today, some patients are spending life savings on trips to India for a black box therapy said to be based on stem cells. A diaspora of the desperate and broke, many of these patients have come to the end of the line.

It is hard enough to be sick—but to be so sick for so long and also be a suspect—to have your physical pain, your integrity, your very sanity called into question as you travel the medical landscape begging for help, well, let me tell you, that is a crushing course of events. In most other diseases, the sick person can focus on being a patient—on following through with treatment to try to get well. No one suggests the cancer patient is factitious, or the heart patient a sociopath. But in Lyme and tick-borne disease, the brutality of such rejection on top of real physical illness has traumatized the patient community writ large.

No wonder patients are in such turmoil. The three largest patient advocacy organizations have staged a boycott of this forum because they say it is biased against them. To quote their press release, they “remain skeptical that the process will lead to a true understanding of the patients’ needs.” The history of the patient experience has robbed them of faith that anyone in government will understand their pain or address their plight. It has been almost 35 years since Polly Murray reported the strange set of symptoms in her town of Lyme to the Connecticut Department of Health. Back in 1976, Murray noted the loneliness of her journey, but decades later, new patients travel the same lonely path as if Murray had never paved the way. Too many of us still spend years seeking help for what was, in the beginning, incontrovertible and classic Lyme disease, only to reap the whirlwind of late diagnosis and failed treatment—even in the most endemic areas of the United States.

In interviews with hundreds of these patients, I found that relapsing-remitting illness was an overriding hallmark of the chronic disease. Use of antibiotics was overwhelmingly the strategy patients preferred for fighting back, though which drug might work for which person was highly variable, suggesting a scenario that is outrageously complex. I myself had a relapsing-remitting illness. I was infected for some seven years before diagnosis. I was treated and seemed to get better, but every time I stopped antibiotic treatment I relapsed like clockwork over the course of two to three months. I went through draining cycles of relapse followed by retreatment for four years before the recovery was sustained. Can we really dismiss this common experience as coincidence or a psychiatric disease?

I‘ve heard it said that all Lyme patients want are more antibiotics, but that isn’t true. Patients just want to get well, and any therapy that cures them would be embraced. No reasonable person would ever argue that the answer sought by future science should be endless antibiotic treatment for years on end—even if infection remains chronic at low level, as evidence suggests. To help these patients, medicine must acknowledge their pain. And science must deal with the complexity. Anyone who follows bioscience knows what’s happening out in Seattle, where the medical pioneer, Dr. Leroy Hood, is building data-driven P4 medicine --the personalized medicine of the future that any patient group this varied needs. As Dr. Ben Luft suggests, only a systems biology approach can target the full spectrum of infections, strains, and immune cascades for every patient involved.

We are long past the point where we can keep telling patients that they themselves are deluded because the science is state-of-the-art when, clearly, their diagnosis and treatment come from the century past. Yet hearing this bald assertion is part of the patient experience, too. Of course it gets them upset. We’ve all gotten stuck. We have academic scientists embroiled in a broad, dumbed-down fight with patients over the issue of chronicity while a revolution in bioscience has reframed the questions we need to ask.

I’ll end with a paraphrase of Tolstoy: Every early stage Lyme patient is pretty much the same, but each chronic patient takes a singular journey of one. For many years, this discomfiting fact has undermined the patient narrative. But with the advent of proteomics, genomics, and other 21st century tools, with greater powers of vision, the story told by bioscience and the story told by patients might finally converge.


Thank you Pam for your excellent presentation.

Pam Weintraub is Author of the book Cure Unknown Inside the Lyme Epidemic this is a must read for anyone with Lyme Disease as it helps us to understand how doctors can have let us down so much leaving so many to struggle with such chronic illness.

Available through Amazon here