Lyme disease, science, and society: Camp Other
Showing posts with label immunoblot. Show all posts
Showing posts with label immunoblot. Show all posts

Tuesday, July 17, 2012

3 NOTES: House Subcommittee Hearing On Lyme Disease

Here are some very rough notes from today's hearing on Lyme disease in Washington, DC. Please be aware that notes on about 5 minutes of testimony are missing towards the end of the day's hearing. If the webcast is archived, viewers may wish to refer to it to make their own notes.

House Committee on Foreign Affairs, Subcommittee on Africa, Global Health, & Human Rights hearing

2PM EDT
Tuesday, July 17, 2012
2172 Rayburn HOB
Washington, DC, USA

"Global Challenges in Diagnosing and Managing Lyme Disease - Closing Knowledge Gaps"

OPENING REMARKS

CHRIS SMITH - CHAIR - NJ Rep

We have a missed decade on Lyme disease research
Chris mentions chronic Lyme disease controversy
Mentions bill to establish tickborne disease committee and take fresh look at all the scientific approaches to Lyme disease
Mentions some history about Lyme disease including Borreliosis in Europe and discovery in Lyme, CT
2010 - 20,000 cases reported, but actual number of maybe 300,000 cases in US in 2010
North America Borrelia burgdorferi s.s.
Different species = different manifestations of disease
Clinical manifestations come in three stages
Mentions two distinct views of Lyme and research conflicting
Hard to catch, easy to cure vs. easy to catch, hard to cure
IDSA states short course of abx ok - anything else is risky
ILADS says the science is unsettled
One or more cause of chronic Lyme disease symptoms is possible, including persistent infection
Persistent symptoms could be due to a combination of persistent infection and immune problems

Three areas we need to took at:
1) diagnostics
2) post treatment symptoms
3) available treatments in light of science

CDC: 2 tier serological testing, but should be used for surveillance not diagnosis -unfortunately it is used for diagnosis by some doctors instead of clinical diagnosis
Europe: 8 immunoblots were shown to have a wide range of sensitivity and specificity
Bolen/NIAID: Lyme multistage disease is difficult to diagnose at any stage
Dr. Eshoo: Has exciting info on new diagnostic tools

Persistence: IDSA says Lyme disease cannot be persistent
Chris Smith says there is plenty of evidence that it can persist past antibiotic treatment
Mentions Barthold's studies and persistence in animal model studies
Mentions possible mechanisms of persistence studies: morphological changes (cell wall deficient, biofilms, etc)

Counterargument by IDSA: there are no convincing arguments that post treatment persistent Lyme disease infection is possible.
Chronic Lyme disease is a misnomer according to IDSA.
IDSA treatment guidelines should be based on best science - Smith argues they don't take into consideration possibility of persistent infection and deny patients needed treatment.

Chris Smith reports that the IDSA, NIH, and CDC were invited to the hearing today. The IDSA representative had scheduling conflict, and they were requested to testify at a very near future date before the subcommittee.

MS. BASS

Mentions the serious concern of missing early diagnosis
States few cases of LD in CA - MS. Bass says she thinks Lyme disease is under reported in CA especially in Central Valley
"Deer ticks" aptly named, as deer can carry 1000 ticks on their back on average.
But white footed mice are now known to be major carriers of the disease.
Other animals are now suspected including birds.
Need new solutions and explorations.
Changes in temperature, weather, and precipitation and their role in spread of Lyme disease should be examined.
Improved detection of early disease is contributing to higher reported numbers to some degree.
Local health departments are increasing awareness in spring and summer.
How can we improve awareness with limited budgets and resources?
Work with WHO to prioritize the disease esp in emerging areas such as Asia.

Rep. GIBSON

This is constituent driven. Major issue in upstate NY. (After he retired from army, so many people are suffering from LD and are confused and medical community is divided over its treatment. A Lyme disease task force would resolve this. Need more awareness about disease and diagnosis. Need to make sure money goes to right place. Money has gone into similar place before and the results were the same.

Most encouraging is research to be published in next year about role of confections in persistent symptoms.

WITNESS TESTIMONY

DR. STEPHEN BARTHOLD, UC DAVIS

Borrelia persists normally in immune competent host
i.e. mice rats hamsters gerbils guinea pigs dogs nonhuman primates
antibiotics are likely to fail under some circumstances if not many circumstances
finds self in contentious field - is somewhat of a pariah
we know in pre-immune stage animals can be cured
in immune stage, animals are not easily cured by antibiotics
Only a few places are really studying post antibiotic treatment Lyme - my group, Finland, NY, Louisiana... [?]
Ceftriaxone, Tigecycline, Amoxicllin, Zithromax: spirochetes are shown to survive these antibiotics in animal models
clonal population of Lyme disease spirochetes -> given antibiotic treatment -> results in non cultivable but living spirochetes
Transcribing RNA = metabolically alive spirochetes
exoplant -> carries infection from Bb infected animal to naive animal

Completed study, hope to publish it soon: 12 month post treatment resurgence of spirochetes found in mice.
what is significance of these spirochetes?
viruses can re-ignite and cause disease - question is: can spirochetes?
The answer is not known yet; something unique is going on with Bb and needs further study

DR. RAPHAEL STRICKER
San Francisco, CA - LLMD

speciality in internal medicine, ILADS Vice President
has 2,000 LD patients
number of patients has grown exponentially in past 15 yrs
patients all over the world Canada Brunei Costa Rica UK even NJ
reflects an increasing rate of LD around the world
Lyme disease is the most common TBD

patients develop muscle, joint, neurological, and cardiac symptoms
despite common disease, doctors are ignorant of how to diagnose and treat:
a bulls eye rash may be absent (50% not seen)
patient may be unaware of tick bite (some bitten by poppy seed size tick)
patients have a wide range of symptoms - doctors are often unaware of this wide range

testing remains problematic (not standardized and insensitive)
treatment has evolved in haphazard fashion (IDSA guidelines only address acute infection; standard guidelines ignore more chronic and severe form)
LD has become international medical disaster
thousands of patients suffer from undiagnosed and untreated Lyme disease
and even though it is all over media
the IDSA sits by and does nothing

State of California is grateful to state health board for forming a state Lyme disease advisory board
for requiring mandatory laboratory reporting of Lyme disease to Department of Health just like system for reporting STIs
California has a physician protection law which allows doctors to treat Lyme disease patients as they deem appropriate
Stricker thinks a model for a Lyme disease national advisory board could stem from CA state model

We need CDC and NIH to abandon failed Lyme disease research programs
need them to have targeted research for better tests just as they did for AIDS
need to have more research on treatment of chronic Lyme disease
need to get them to look at evidence and discard dogma about what chronic Lyme disease is
we need for them to listen to patients and how they are affected

Almost 2 decades ago Dr. Joe Burrascano testified before the Senate. He said, "The very existence of 100s of LD support groups, etc underscores many problems which exist in real world of LD." Two decades later and it's the same story.

DR. MARK ESHOO
IBIS Biosciences, Abbott Labs

Need to develop better diagnostic tests
number cases steadily increasing
Lyme disease is severely under reported
Babesiosis is also important
Babesiosis can be mistaken for malaria (Babesia looks similar to malaria under the microscope, too)
Other TBDs are also present

Lyme spread by ticks to mice, and then ticks infect more mice
mice become chronically infected with Lyme disease
bacteria evolved to evade immune system, especially immune privileged sites (e.g. skin, joints)
humans can have long lasting or chronic infection
those infected develop neurological and joint problems
best time to treat is early in infection
most typical early symptoms are bulls eye rash, flu-like, fatigue, aches

CDC 2 tier test - involves indirect detection of antibodies; has 3 problems:
1) can take Lyme patient more than 3 wks for immune system to detect infection
2) interpretation of 2 tier tests can be subjective and change outcome
3) even after treatment, patient can remain positive… controversy over how long to treat patient (weeks? months? years?)

Abbott Labs is looking directly at presence of DNA of pathogens
Sensitive direct assay of organism is historically very difficult because spirochetes are present in small numbers
Abbott made an assay with 8 independent tests to detect the presence of bacteria in blood
they use large volume of blood
and find way to amplify the presence of small numbers of bacteria (bacterial DNA) in blood

Eshoo et al did a study which could find organism very early in infection in doctor's office (refer to abstract) in 62% of patients

Another area of research Eshoo is working on:
variations of strains may determine type and severity of disease
need to study 100 different strains of Bb and what makes them different in terms of impact of disease

We need more government research and funding
- sensitive test for direct detection early in infection before dissemination (monitor responses to treatment
- find out cause of PTLDS. A direct diagnostic tool would be useful
- need to increase research into diff Borrelia strains differences and their role in human infection

PAT SMITH, LDA USA

LD called yuppie or housewife disease
patients have been referred to by some doctors as being paranoid, hysterical, hypochondriac, etc. without any evidence and without looking that something else could be wrong
many advocacy organizations in the world have been victimized in peer reviewed publications
Many patients confide they'd rather have cancer than Lyme disease due to the misunderstanding and controversy over the disease
Patients want studies which solve their dilemmas (such as doctors don't believe they're sick, answer the question "Why isn't the government doing anything?")
The outcome of small clinical trials/studies put a coffin the nail for treatment of chronic Lyme disease and for a number of reasons, these studies were inadequate.
The conclusion was that no treatment is effective for long term Lyme.

Lyme in the south - there are many myths. Myths that:
No lyme disease can be found in south or west
No reservoir hosts in the south
Deer ticks on lizards prevent Lyme disease in ticks all throughout the south
Deer ticks in south do not bite people (?!)
These claims are not scientifically backed.

Patients are overburdened with medical problems.
There are cutbacks in public health depts. so number of cases are unknown.
Pharmacists who won't fill prescriptions for Lyme disease patients in some places.
Munchausens by proxy charges are made toward mom's who treat kids with Lyme disease with long term antibiotics.

Guidelines that are written by researchers and not clinicians are problematic
IDSA is against any sort of treatment for CLD - either antibiotics, alternative treatment, or the use of supplements
CDC surveillance criteria for Lyme disease has formed basis of IDSA guidelines and this is problematic
patients can die of Lyme disease: study of 114 patients who had Lyme disease who died. After they died, most terminal events for which LD was known as the underlying cause have listed on their death certificate a reported cause of death which researchers stated were thought to be unrelated to Lyme disease. Only one patient was said to have died of complications of Lyme disease directly. Question that.

Has seen recorded 22 point IQ drop in kids with Lyme disease due to infection affecting brain
kids have killed themselves due to Lyme disease - due to pain and due to disbelief by peers and others of their having the disease

Pat Smith has had 2 daughters affected by Lyme disease

CDC, NIH, IDSA were absent at hearing and she thinks they are avoiding responsibility when they were invited to be part of the process to help patients.

EVAN WHITE, NYC
Patient - Had Chronic Lyme Disease

(wife just had baby, he is on SKYPE  - his life is now normal being part of point of his testimony)

20 yr advocate borne out of very tragic case of his own Lyme disease due to being given limited antibiotic treatment
at end he is now well because of conscientious doctors
today is father and practicing attorney and employer.

he says his case is an illustration: if not for long term treatment, none of this would be possible

so many people do not have benefits he had
if they had access to treatment, they would be contributing members of society
his story has happy ending
he is fighting for fellow Lyme patients to have same access to treatment
he is advocating for change in limited guidelines

his case study is that short term treatment did not work
long term treatment helped him recovered
he was ill at 11 yrs old
missed school due to flu-like symptoms
doctor did diagnose Lyme disease and he was given 1-2 wks of antibiotics
after 2 weeks he did not get better
the response to not recovering after 2 wks was that PT and psych therapy was needed after those 2 weeks
daily his condition deteriorated
he was a 12 yr old who trusted his doctor
but 6 months later so bad could not do anything
could not go to school, had trouble getting out of bed
blood test showed Lyme disease and confections were very much present months later

here is devastating result of un (or under treated) Lyme disease
6 months of no treatment sent him into tailspin
he vastly deteriorated, went from active athletic child to one who couldn't care for himself
had muscle atrophy, neurological problems
60 lbs at age 13, called a vegetable, and doctors were confused by his state
doctors put him in children's rehabilitation care
did brain scan
it revealed Lyme disease's affect in its passing the BBB: hypoperfusion
he had trouble reading and talking
and was surrounded by doctors who had no idea why he was in condition he was in
2 yrs bounced from hospital to hospital
6 months in children's hospital

went home and parents arranged for appt with LLMD
the LLMD "got it" and had their own personal experience with the disease - not just treating other patients
he had long road ahead for recovery but this was his turning point
he was on long term antibiotics coupled with supplements
2 year crawl to get out of that place
even if it were 10 yr crawl that would have been ok with him
stopped using wheelchair
got out of bed
began to take care of self
began to read again
began to be able to communicate again
got him on trajectory to become person he is today and fully recovered

hoping through this testimony that patients who are affected can get treatment they need to recover from chronic Lyme disease
the net effect of current guidelines restricting treatment deprives so many if not all from having health care option to seek long care treatment that does work for many patients so that they can recover and live long healthy lives

Rep. SMITH

intro Stella in UK

STELLA HUYSHE-SHIRES
Lyme Disease Action (UK)

UK doctors not taking patients seriously
Department of Health accreditation of Lyme Disease Action, Lyme Disease Action is now considered an unbiased source of information on Lyme disease in the UK
papers say Lyme Disease is overdiagnosed
public say it is underdiagnosed
what is the evidence?
we don't know incidence of Lyme disease in the UK
One GP practice finds it 20x greater than numbers which are reported
1300 cases found in one year may mean there are really more like 26,000 cases in UK

survey:
23% patients found ot have Lyme disease but the rest with similar symptoms were diagnosed with CFS
there is concern CFS patients are misdiagnosed and have Lyme disease
on the flip side maybe
100 people year in clinics in UK may be misdiagnosed with Lyme disease
But in a CFS clinic - 40% patients were misdiagnosed with CFS

Why is LD difficult to diagnose and what can be done about it?
we need unequivocal tests and clear guidelines
none exist in UK
most doctors haven't seen Lyme enough and rely on blood tests for diagnosis in UK

unreliable info on internet, certain labs, etc only part of story even if there is an element of truth in it
European challenge of more than one strain of Bb adds to complexity of test issue
Scotland uses more bands in its lab than other locations - leading to different line drawn for positive test results and access to treatment

Most treatment recommendations based on opinion not evidence
need other stakeholders to investigate Lyme disease
Lyme Disease Action (UK) is working with James Lind Alliance to engage doctors in more awareness of LD in patients and in general

The biggest challenge globally is recognition of unknowns in Lyme Disease
All across Europe there is a polarization of opinions along IDSA/ILADS poles
and there may be reluctance to climb out of one's entrenched view of Lyme disease

In Northern Europe doctors rely heavy on test results - similar issues found there.
In Central Europe, doctors have more experience: Lyme is a big problem, doctors say the tests are not good enough; doctors say they don't know how to effectively treat all patients.

Politics are a problem.
Uncertainty of the science is a problem.
Politics prevents recognition of the uncertainties.

QUESTION AND ANSWER SESSION (Rep Smith/Rep Gibson ask questions)

HUYSHE-SHIRES

A: HPA guidelines come from IDSA
Worse thing when patients are told symptoms are in their head
IDSA only recognizes visible arthritis then patient may get further tx
HPA does follow IDSA guidelines
indiv doctors sometimes make indiv clinical decision
case studies London school of hygiene (4-5 yr period) - some patients did not recover after initial course of abx, then some not after second, then some had a third. Between each treatment, patients were believed and found rising antibody levels.
Doctors will say adequate tx occurred, but it's adequate in terms of meeting guidelines but not in terms of effectively treating patient

BARTHOLD

Q: Are proposals being rejected for research at NIH?

A: Peer review is an issue. Peers are divided just are anyone else in Ld community
have direct exp in prejudicial statements in grant application reviews - peer view of applications does not get over the barrier
NIH is struggling to fund investigators
young people are not entering science, old people are leaving
in that environment combination of things - anything controversial having difficulty being funded
made NIH call for application on research on persistence after antibiotic treatment
only suggestion is his
we scientists are always looking for money. Follow the money.
NIH invests in biodefense then people gravitate towards biodefense research.

STRICKER

Q: Rep.brings up conflicts of interest and suppression of data in IDSA guidelines review.

A: IDSA hearing was organized by IDSA and no treating physicians were on the committee
Even though guidelines were flawed they were ruled acceptable.
Stricker encouraged by Dr Eshoo's research and development of advanced early testing.

["To date no antibiotic treatment treats biofilms." - attribution?]

Q: Rep comments to Barthold: issue of "mopping up" after antibiotics
host immune system must mop up remaining spirochetes... Explain.

BARTHOLD

A: using biofilm analogy: there is a population of microorganisms, some of which are dormant
dormant non-dividing bacteria are universally tolerant of antibiotics and are not dividing or active metabolically
Borrelia: we know it is dividing and disseminating and susceptible to antibiotics early on but during the immune phase in animals there is a 10 fold reduction in population (not necessarily in biofilms) and what is found are non-dividing spirochetes; they are dormant and antibiotics are not touching them
What is unique is they grow out but they cannot be cultured - they may be attenuated.


STRICKER

A: Borrelia has molecular machinery to make biofilms according to Dr. Stricker.
Stricker states cell wall deficient form evades antibiotics and it needs to be researched more.

Q: Rep. Asks Dr. Eshoo: How close are you to coming up w new test and why is Big Pharma not getting further involved?

ESHOO

A: It's a small market according to BP and takes lots of money and time to invest.
Lot of people in medical community say current test is good enough.

Eshoo thinks sensitivity needs to be improved and tests need to be improved to end the controversy.

Who wants to be infected for 3 weeks or more untreated waiting for a positive blood test? Nobody.

Rep. Q to Stricker:

Are there people outside the IDSA guidelines panel who notice there's a problem [with testing]?
Does Dr. Francis Collins (NIH director) say "What is wrong here? Why is this a persistent bone of contention?"

STRICKER

A: Blumenthal investigation found there are 14 people in the IDSA who control guidelines, testing, and diagnostic guidelines of Lyme Disease. The rest of the IDSA (8,000 people) defer to this group.

PAT SMITH, Lyme Disease Association

LDA has Scientific and professional review board
It is voluntary board
If issues need to be addressed or LDA is considering funding research, the board is asked to comment on it using their expertise
CALDA, LRA, etc also rely on this board

STRICKER

Q: Rep. [?]: you have 2,000 patients. What is your takeaway from this huge patient number and how are they when they find you?

A: Number of patients exceeds CDC reporting. That's one thing it tells me. Number of those affected may be 10 fold higher.
Many come after yrs of misdiagnosis and no treatment.
70% of patients get better. He finds this gratifying and he turns a deaf ear to the controversy because of outcome.
Uses long term antibiotic treatment.
Published study last year on neurological patients needing 6-12 months of antibiotic treatment to improve.

[5-6 minutes of testimony notes missing]


COMMENTS NEAR END

8.75 million dollar research fund Chris Smith says has been put forward. Chronic Lyme is supposed to be included in this research. How should the wording for the law be improved and how can there be better oversight to get money to the right place?

Barthold said: Follow the money.
If you enlarge the pot and spend it on research that's already been done, we get nowhere.
If we and NIH recognize persistence after treatment as an issue, then new research would be done on this issue.
A more narrowly focused call for applications would help if NIH would agree with that - research on chronic symptoms and the biology/pathology of the organism.

Dr. Eshoo said the field needs support to get off the ground and that RFAs must be specifically targeted toward solving narrowly defined problems.

PAT Smith has concern research money goes to post Lyme disease syndrome and not chronic Lyme disease - which is a different condition.
Patient perspectives on issues of the disease is important and knowing how it's affecting them is important.
Advocates, treating physicians, and patients need to be involved in the process of determining what needs to be researched.

Q: Rep. Gibson: How do you expand Lyme literacy among old and new doctors?

STRICKER

A: ILADS has preceptorship program. Can learn about diagnosis and treatment of Lyme disease. Program is funded privately. Mentor doctors who want to get involved sign up.

Stricker has trouble finding physicians willing to get involved due to controversy. This has had a chilling effect on mentorship.


Q: Rep Gibson: is that because state med board may censor them?

A: Yes. Though state has protection law, the risk censoring by board and other doctors may still go on.

Has 27 studies in table in written testimony (table 2) showing persistence in humans after IDSA guidelines-based treatment.

BARTHOLD

We need to know what is happening in humans but animals allow us to extrapolate models. Many people are using animals but looking only at acute early phase of infection. Not many people are looking at chronic persistent infection in animals. Fewer than five labs worldwide are studying this but it is the most important aspect of the disease.

HUYSHE-SHIRES

Borrelia has been isolated in patients after initial treatment - there are some cases recorded in published papers.
Some people improve after longer treatment
We need more investigation to determine how to better diagnose and treat Lyme disease

IDSA guidelines are accepted in the UK
Summary of recommendations for treatment by European Federation of Neurology Specialists (organization name needs fact checking) - make the point that in neurological Lyme there are no good trials of more than 28 days antibiotic treatment for neuroborreliosis.
They base this on opinion because there is no trial in Europe for longer term treatment of neuroborreliosis.

There are some trials which show good recovery, but at most 60-70% patients experience a good response. A patient does not consider 7 of 10 people responding to treatment as being a rate that is excellent.

PAT SMITH

Children are most affected by Lyme. They have more complications and are greatly impacted by their peers and teachers and what they are saying about them.

It is appalling what comments are being made about students who are ill with Lyme who cannot make it to school because they are too sick. No one wants to stay at home with their mother from school for four years.

One problem is inadequate early antibiotic treatment may lead to a poor antibody response and negative tests, which then put child at further risk for being disbelieved for having Lyme disease.

Some family services will take kids away from parents if those parents treat one child with antibiotics for chronic Lyme disease. This is serious and kids are psychologically damaged by the disease as well as the response from society and their community towards their illness.

We have the knowledge and tools in this country to stop this.

HUYSHE-SHIRES

1-3 people in UK are believed to have expertise on Lyme in UK, and those 1-3 apply IDSA guidelines and support them
NHS did not make any needed changes to their guidelines even though they should be made to suit the UK patient population

ETHAN WHITE

If sick, seek out people who will lead you to knowledgeable doctors who will offer treatment for Lyme disease.

SOME CLOSING COMMENTS

Barthold thinks people on both sides are good people, and he thinks we need to move past contentiousness and work together to help those affected by Lyme disease.

We need to work to get out of entrenched positions and get to the bottom of what's happening using science.

It's time for people to get together and show their cards and be willing to act in the best interest of patients and work past this contentiousness.



Comments:

Will be adding links relevant to this testimony soon.

If anyone who gave testimony at the hearing reads these notes and sees a correction that needs to be made, please request correction in comments and I will revise this post.

UPDATE - July 17:

Original testimonies are now available for download including additional materials from each of the witnesses. Scroll down this page for pdf files: http://foreignaffairs.house.gov/hearings/view/?1455

UPDATE - July 19:

Ustream has two streaming video archives of the hearing available at the following links:

http://www.ustream.tv/recorded/24058724

http://www.ustream.tv/recorded/24060689


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Tuesday, July 3, 2012

0 WBUR Series: Living With Lyme

On June 26, 2012, WBUR, Boston's NPR (National Public Radio) station, 90.9, began publishing a series, "Living With Lyme", on their website.

The series of articles are accompanied by free downloadable podcasts and sometimes photos and slideshows. In addition to these articles, a live streaming video discussion on Lyme disease was broadcast on June 28 and is available online in its archives.

Additional Lyme disease related articles continue to be published on WBUR after the initial series was posted.

Here is a comprehensive list of all the articles published in the "Living With Lyme" series, from the oldest to the newest post:

Resource List - Lyme Disease:
http://www.wbur.org/2012/06/25/lyme-disease-resources

In Lincoln, It's Town Vs. Ticks:
http://www.wbur.org/2012/06/25/lyme-disease-lincoln

Map: Lyme Disease Cases In Mass., By Town:
http://www.wbur.org/2012/06/25/massachusetts-lyme-disease-map

A Long, Painful Battle With Lyme Disease:
http://www.wbur.org/2012/06/26/barbara-macleod-lyme-disease

The Debate Over 'Chronic' Lyme Disease:
http://www.wbur.org/2012/06/26/chronic-lyme-disease

What To Do If You Think You've Been Exposed To Lyme Disease:
http://www.wbur.org/2012/06/26/lyme-what-to-do

Why Your Dog Can Get Vaccinated For Lyme Disease And You Can't:
http://www.wbur.org/2012/06/27/lyme-vaccine

Some Cape Residents Worry Tourists Aren’t Taking Precautions To Prevent Lyme:
http://www.wbur.org/2012/06/27/cape-cod-lyme

How Much Lyme Disease Are We Living With?:
http://www.wbur.org/2012/06/28/lyme-prevalence

Lyme Disease Complicates Doctor-Patient Relationship:
http://www.wbur.org/2012/06/29/lyme-science-controversy

The Complexities Of Diagnosing Lyme Disease:
http://www.wbur.org/2012/06/29/diagnosing-lyme-disease

Emerging Tick-Borne Diseases Causing Concern In Mass.:
http://www.wbur.org/2012/06/29/tick-borne-diseases

For a series on Lyme disease, it is surprising how few patients have left comments on a number of these posts to date. It's been my observation that most of the time, patients participate in commenting on articles about Lyme disease and ticks far more frequently than this series has been responded to so far.

There are a few exceptions, such as the vaccine thread, which I commented on some days ago and which is still receiving more new comments. Sometimes the comments are more informative than the article itself, so they are worth a look. (Other times, they are educational only as a magnifying lens under which one can view other people's psychology... use your judgment, do your own research, and weigh the evidence linked to what people have to state.)

Here is the link to the Special Lyme Disease Panel Discussion (online streaming video):
http://www.wbur.org/2012/06/28/lyme-disease-panel

Panelists include:
  • Dr. Thomas N. Mather, a.k.a. the TickGuy, conducts public education programs on tick-borne illnesses
  • Rep. David Linsky, sponsored the bill that created a state commission on Lyme disease
  • Dr. Sheila Statlender, a clinical psychologist and advocate for Lyme disease patients
And just today, an additional article was posted about tracking Lyme disease:

http://onpoint.wbur.org/2012/07/03/tracking-lyme-disease

A lot of thought-provoking articles to read at WBUR, with some thought-provoking comments in response. Check it out...


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Friday, February 3, 2012

2 Paper: Course of Antibody Response In Lyme Borreliosis Patients Before And After Therapy


ISRN Immunology Volume 2012 (2012), Article ID 719821, 4 pages doi:10.5402/2012/719821 Research Article

Course of Antibody Response in Lyme Borreliosis Patients before and after Therapy

Elisabeth Aberer1 and Gerold Schwantzer2

1Department of Dermatology and Venereology, Medical University of Graz, Auenbruggerplatz 8, 8036 Graz, Austria

2Institute for Medical Informatics, Statistics and Documentation, Graz, Medical University of Graz, 8036 Graz, Austria

Received 27 September 2011; Accepted 27 October 2011

Academic Editors: A. Clayton and S. Devi

Copyright © 2012 Elisabeth Aberer and Gerold Schwantzer. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The early immune response (IR) in European Lyme borreliosis patients has not yet been studied in detail. The aim of the study was to analyse retrospectively the antibody development in 61 erythema migrans (EMs) patients depending on the duration of infection from tick bite by using a whole-cell lysate B. garinii immunoblot. The evolution of antibodies proved to be undulatory in untreated patients with two peaks for IgM at weeks 5 and 9 and for IgG at weeks 4 and 8. The analysis of IR courses after therapy identified patients constantly seropositive or seronegative and patients with repeated seroconversions with a switch, disappearance, or reappearance of anti-23 kD or anti-39 kD antibodies during the one-year period. We suggest that the antibody production in EM patients may be missed due to an undulatory IR. This phenomenon might be an as yet insufficiently researched aspect in Lyme borreliosis.

1. Introduction

Serological testing aids in the diagnosis of Lyme borreliosis (LB). IgM antibodies develop during the first 3 weeks after infection followed by IgG antibodies after 4–6 weeks [1]. However, to our knowledge, the early immune response (IR) in European patients has not yet been studied in detail.

In routine clinical practice, we observed patients whose IR switched from positive to negative and vice versa in the course of time. The aim of this study was to analyse the development and the course of the IR in European erythema migrans (EMs) patients with known duration of disease from tick bite and to follow up their antibody profile during a 12-month period after treatment.

2. Patients, Materials, and Methods

One hundred and two patients with EM were enrolled for clinical and serological diagnosis. Their mean age was 50 (SD16) years. Forty-seven patients were male and 55 female. The mean duration of EM was 23 (1–210) days. Eighty-seven patients had EM without and 15 patients EM with extracutaneous symptoms. As sixty-one (28 males and 33 females aged between 22 and 78 years) remembered their tick bite, the onset of their infection was known and only these patients were included in the study. These patients received antibiotic treatment with phenoxymethylpenicillin 1500 000 IE threetimes a day, 26 patients for 14 days and 35 patients for 20 days. No statistical difference in the clinical outcome of the differently treated groups was observed during the 12-month observation period as described in a previous study [2].

Blood samples were obtained from all 61 patients for serological testing at the initial visit before therapy and then thereafter at 3 weeks after first blood withdrawal. Sera were available from 46 patients 3 months after therapy, from 52 after 6 months, and from 53 after 12 months (Table 1).

tab1
Table 1: Number of investigated patients’ sera.
Patients’ sera that had been stored at −20°C were retested at the same time and antibody response was measured by a whole-cell lysate immunoblot (IB) according to the manufacturer’s instruction (Borrelia garinii, MRL Diagnostics, Cypress, CA). Interpretation of the IB bands was performed by a single technician. Criteria for a positive IB, as indicated in the manufacturer’s manual, were 1 of 2 bands (23 and 39 kD) for IgM and 4 of 7 bands (21, 23, 37, 39, 41, 45, and 93 kD) for IgG. Data obtained were entered in a computerized database and graphically displayed.

3. Results and Discussion

3.1. Development of Immune Response

Twenty-five of 61 (41%) sera showed IgM antibodies in IB before therapy. The IR started in week 1 after tick bite and peaked in week 5, when 5 of the 7 tested sera (71%) reacted positively (Figure 1).

In the following weeks there was a wavelike decrease of seropositive reactions. Furthermore, from week 8 there was a second increase in seropositivity peaking at week 9. IgG antibodies were positive in 13/60 (21%) patient sera (one serum could not be analysed because of a smear). The IR started from week 2 and peaked at week 4, where 75% (3 of the 4 tested sera) reacted positively (Figure 1).

Similar to the IgM antibody trend, the IgG IR decreased in the following weeks. However, there was a second increase of IgG IR that peaked in week 8.

719821.fig.001
Figure 1: Development of immune response from tick bite (weeks).


The development of the IR to an infection with B. burgdorferi (Bb) s.s. in EM patients from the United States was studied by Aguero-Rosenfeld and showed that 43% of the patients had positive IgM antibodies before therapy [3].

Due to the heterogeneity of borrelia strains in Europe, differences between IR on the two continents are expected since the Bb s.s. species provokes a stronger immune reaction than the dominant European species B. afzelii. Patients with culture-confirmed B. burgdorferis.s. erythemas from the USA were more often seropositive (35.3%) at presentation compared with 22.4% culture-confirmed B. afzelii erythemas [4].

In another European study with recombinant ELISA, German Lyme borreliosis patients yielded positive IgG antibodies in 22% and IgM antibodies in 61.5% for phase I of LB [5].

Both the IgM and IgG IR showed an undulatory distribution with antibodies coming and going in untreated patients over weeks. A similar periodicity is known in other bacterial infections, like relapsing fever with recurrent bacteraemias [6].

Syphilis can be reactivated by different conditions like HIV infection, showing seroconversion of the unspecific VDRL [7].

3.2. Course of Immune Response after Treatment

With respect to the course of IR after therapy, 21 of 61 (34%) patients did not show IgM seroconversion (constantly negative), whereas 12 (20%) were constantly positive. In the remaining 28 patients, different kinds of IgM seroconversion occurred. Nine patients (15%) (Figure 2, patients 1–9) seroconverted from positive to negative and 6 (11%) (Figure 2) (Figure 2, patients 16–22) seroconverted to positive and than back to seronegative during the 12 months. Six patients (10%) (Figure 2, patients 23–28) showed repeated seroconversions of IgM antibodies that presented as a switch of anti-23 kD to anti-39 kD antibodies and vice versa or the dis- or reappearance of either anti-23 kD or anti-39 kD antibodies.

719821.fig.002
 Figure 2: IgM antibody response in immunoblot before and  up to 12 months after therapy. Filled circles: positive IgM antibody response; empty circles: negative IgM antibody response; blank spaces: no serum available. BT: before therapy; AT: after therapy; 3, 6, 12 months after start of therapy.


Thirty-eight of the 60 patients (63%) were constantly IgG negative and 3 patients (5%) constantly positive in IB. Nineteen patients seroconverted within the observation period. Their data are presented in Figure 3. Six patients (10%) (patients 1–6) seroconverted from initially positive to negative and 2 (3%) (Figure 3, patients 7 and 8) from negative to positive.

Seven patients (12%) (Figure 3, patient 9–15) who were primarily negative seroconverted to positive and then back to seronegative during the observation period.

719821.fig.003
Figure 3: IgG antibody response in immunoblot before and up to 12 months after therapy. Filled circles: positive IgG antibody response; empty circles: negative IgG antibody response; blank spaces: no serum available. BT: before therapy; AT: after therapy; 3, 6, 12 months after start of therapy.


Four patients (7%) (Figure 3, patients 16–19) showed repeated seroconversion with at least 2 changes. The seroconversion itself presented as a loss of detectable antibodies from a previous maximum of up to 5 bands (23, 37, 39, 41, 45, and 93 kD) to 1 band.

When observed closely, none of the patients with a repeated seroconversion had any features that could distinguish them from the other patients with either persistent antibodies or seronegative individuals. There was also no relation between IgM and IgG seroconversion. Clinically, no correlation to the duration of treatment or to the presence of extracutaneous signs could be drawn.

A recent survey on the development of the IR, measured by ELISA, in Austrian EM patients over a minimum of 1 year after treatment showed 3 distinct courses: persistent positive, persistent negative, and positive to negative patients [8]. In this study, there were also patients with a change from negative to positive antibodies (3% IgM, 4% IgG), but this was not attributed to the original EM as seroconversion occurred after a median of 350 (for IgM) and 349 days (for IgG) after EM. In our study, IB was found to be more sensitive than ELISA; therefore only IB results were analyzed and the IR could be studied in more detail.

In our patients, the appearance of IgM antibodies only detected after 6 months (patients 21 and 22) and IgG antibodies only at 3 months (patients 9 and 10) cannot be related to the previous infection. Moreover, an isolated IgM seroreaction has been observed to be unspecific [910].

Isolated positive serum IgM titers were seen in about 20% of children with a febrile illness, enterovirus meningitis, or headache [9]. In another article 2,6% of sera submitted for B. burgdorferi serology expressed unspecific anti-p41 IgM antibodies by ELISA. Confirmation test with IB showed that some sera also reacted with p39 or OspC antigen. No conclusive evidence for borrelia infection could be drawn [10].

The first appearance of antibodies after 6 and 12 months in our study (patients 14 and 15 for IgM, and 7 and 8 for IgG) might indicate a new infection in these patients.

Although the undulatory character of the IR before therapy in our patients could not be determined in every single patient, the findings after treatment might reflect a similar situation also in untreated patients before therapy. So, we suggest that a single serological finding is a snap shot and gives evidence of an infection. On the other hand, the true infection might be missed by negative IR, as might be the case in the ~40% seronegative EM patients.

Serological findings do not distinguish between active and previous disease. Borrelia DNA can persist in urine for even 1 year after treatment [11], and antibodies to Bb may persist for up to 20 years after appropriate therapy [12]. Bearing in mind the characteristics of cyclic patterns in other bacterial infections, the undulatory IR noted in our study may be an as yet insufficiently researched aspect in Lyme borreliosis.

Conflict of Interests

The authors declare that there is no conflict of interests.

Acknowledgments

The authors greatly acknowledge Jasmina Custovic, M.D., for collecting and analysing the data which were also partly shown in her thesis (development of the immune response in erythema migrans with special significance of the p18 antigen) and Mrs. Ingrid Krainberger for her excellent laboratory support during the study.

References

  1. B. Wilske, “Serodiagnosis of lyme borreliosis,” Zeitschrift fur Hautkrankheiten, vol. 63, no. 6, pp. 511–514, 1988.
  2. E. Aberer, P. Kahofer, B. Binder, T. Kinaciyan, H. Schauperl, and A. Berghold, “Comparison of a two- or three-week regimen and a review of treatment of erythema migrans with phenoxymethylpenicillin,” Dermatology, vol. 212, no. 2, pp. 160–167, 2006.
  3. M. E. Aguero-Rosenfeld, J. Nowakowski, S. Bittker, D. Cooper, R. B. Nadelman, and G. P. Wormser, “Evolution of the serologic response to Borrelia burgdorferi in treated patients with culture-confirmed erythema migrans,” Journal of Clinical Microbiology, vol. 34, no. 1, pp. 1–9, 1996.
  4. F. Strle, R. B. Nadelman, J. Cimperman et al., “Comparison of culture-confirmed erythema migrans caused by Borrelia burgdorferi sensu stricto in New York State and by Borrelia afzelii in Slovenia,” Annals of Internal Medicine, vol. 130, no. 1, pp. 32–36, 1999.
  5. K. P. Hunfeld, M. Ernst, P. Zachary, B. Jaulhac, H. H. Sonneborn, and V. Brade, “Development and laboratory evaluation of a new recombinant ELISA for the serodiagnosis of Lyme disease,”Wiener Klinische Wochenschrift, vol. 114, no. 13-14, pp. 580–585, 2002.
  6. C. Larsson, M. Andersson, J. Pelkonen, B. P. Guo, A. Nordstrand, and S. Bergström, “Persistent brain infection and disease reactivation in relapsing fever borreliosis,” Microbes and Infection, vol. 8, no. 8, pp. 2213–2219, 2006.
  7. A. McMillan, H. Young, and J. F. Peutherer, “Influence of human immunodeficiency virus infection on treponemal serology, in patients who have been treated for syphilis,” Journal of Infection, vol. 21, no. 1, pp. 95–103, 1990.
  8. M. Glatz, M. Golestani, H. Kerl, and R. R. Müllegger, “Clinical relevance of different IgG and IgM serum antibody responses to Borrelia burgdorferi after antibiotic therapy for erythema migrans: long-term follow-up study of 113 patients,” Archives of Dermatology, vol. 142, no. 7, pp. 862–868, 2006.
  9. R. Bennet, V. Lindgren, and B. Zweygberg Wirgart, “Borrelia antibodies in children evaluated for Lyme neuroborreliosis,” Infection, vol. 36, no. 5, pp. 463–466, 2008.
  10. E. Ulvestad, A. Kanestrøm, L. J. Sønsteby et al., “Diagnostic and biological significance of anti-p41 IgM antibodies against Borrelia burgdorferi,” Scandinavian Journal of Immunology, vol. 53, no. 4, pp. 416–421, 2001.
  11. E. Aberer, A. R. Bergmann, A. M. Derler, and B. Schmidt, “Course of Borrelia burgdorferi DNA shedding in urine after treatment,” Acta Dermato-Venereologica, vol. 87, no. 1, pp. 39–42, 2007.
  12. R. A. Kalish, G. McHugh, J. Granquist, B. Shea, R. Ruthazer, and A. C. Steere, “Persistence of immunoglobulin M or immunoglobulin G antibody responses to Borrelia burgdorferi 10–20 years after active Lyme disease,” Clinical Infectious Diseases, vol. 33, no. 6, pp. 780–785, 2001.
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Wednesday, September 28, 2011

0 Blog Log: Spirochetes Unwound on Flawed Study of Topical Antibiotics

Remember that article on topical azithromycin I posted earlier this month?

Our favorite spirochete blogger has some criticism about the research on which it was based here:

http://spirochetesunwound.blogspot.com/2011/09/flawed-study-claiming-prevention-of.html

A flawed study claiming prevention of Lyme spirochete infection with topical antibiotics

Two recent papers tested the effectiveness of topical antibiotics in preventing Borrelia burgdorferi infection in mice following a tick bite. Infection by the Lyme disease spirochete was successfully halted in the Knauer et al. study from Germany1 but not in the Wormser et al. study conducted in New York.2 However a flaw in the Knauer study may have unfairly tipped the outcome in the antbiotic's favor. (I'll save the Wormser study for another post.)

READ MORE HERE >>>


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Friday, August 5, 2011

12 Antibodies linked to long-term Lyme symptoms

Nature has just published an article today on research which shows a relationship between post-Lyme disease syndrome and persistent infection.

Armin Alaedini at Weill Cornell Medical College in New York and his colleagues have found that patients diagnosed with post-Lyme disease syndrome have antibodies that suggest they carried the infection for an unusually long time. The finding, published in Clinical Immunology, might help the syndrome to be better understood, diagnosed and treated.

Bockenstedt is quoted in the article, saying, "This is the first study I've seen that shows some immunologic difference between someone who resolves their Lyme and someone who develops post-Lyme disease syndrome."

I highly recommend everyone checks it out, supporters and naysayers alike: The finding suggests that patients with chronic symptoms have experienced a prolonged infection.

Original Research:
Epitope mapping of antibodies to VlsE protein of Borrelia burgdorferi in post-Lyme disease syndrome. Abhishek Chandra, Norman Latov, Gary P. Wormser, Adriana R. Marques, and Armin Alaedini. Clin. Immunol. http://dx.doi.org/10.1016/j.clim.2011.06.005 (2011)

Comments:

I'm withholding any further comments on the content of the paper until I read the full text, but am open to discussing the contents and context of the article from Nature in comments.

READ MORE: http://www.nature.com/news/2011/110805/full/news.2011.463.html

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Wednesday, April 27, 2011

0 IOM Summary Report: Neuroborreliosis Notes #2

This is Part 2 of part 1, IOM Summary Report: Neuroborreliosis Notes...
(Read that first...)

After Dr. Stephen Barthold's presentation, the following discussion came up:

"Another participant questioned how neurologic symptoms occur if the bacterium is just in collagen,even if it is associated with neural tissue. Barthold noted that mice do not get central nervous system disease, possibly because they don’t have much connective tissue in their brain. However, central nervous system disease is seen in larger mammalian species that have more collagen in their meninges and perivascular spaces. Under those circumstances, Barthold has observed spirochetes in the collagenous areas and along the perivascular spaces into the brain. Because there is a dearth of good analysis of human neuroborreliosis cases, it is not known if the spirochetes are located in other areas.  He noted that a tissue bank or biorepository would be very valuable to allow for these types of analysis."

Has Dr. Barthold talked to Dr. Alan MacDonald at all? I have to wonder... aren't there other tissue banks out there which already have neuroborreliosis samples?

So all these people - a portion of which knew they were bitten by ticks - have cognitive and neurological symptoms, but there is little good analysis of human neuroborreliosis cases.

Why is that?

Does it have anything to do with how difficult it is to determine whether or not a patient has neuroborreliosis, especially once you're read the European data on testing the CSF for IgG antibodies and realize that the initial positive rate is at it's best within two weeks of clinical presentation (assuming this means symptom onset)?

When they say there isn't enough data on human neuroborreliosis... let's start with this chart:


No news is good news?

I note that there also is no independent measurement for Late disease-Neuroborreliosis  in this table, either. Just arthritis and the measure for culture is labeled "anecdotal". So data is lacking there, too. (I have to wonder why the author used "ancedotal".)

But then there is always two-tier testing, which is indirect detection testing (does not test for the organism itself, but tests for antibodies to it):


As you can see from this chart, depending on which kind of testing you use (ELISA, two-tier Western Blot, or this other proposed test), supposedly serological testing for early Lyme disease is poor, and early disseminated neurological infection is better. Not perfect, but better.

Is that late neurological and arthritis disease detection rate correct? I want to see the cited research (this requires finding the original full text publication) before commenting more on it. But I will say that even with the correct distribution of findings here,  neuroborreliosis that occurs within the first week after being bitten is not going to show up in the early group, and 13-37% of early disseminated neuroborreliosis cases are missed, depending on the test set.

Note on page 7-4 that:

"The C6 testing protocol has performed comparably in accurately detecting the presence of antibodies to B. burgdorferi in sera of patients with acute EM, but was slightly less effective in the case of neurological Lyme disease."

And also, this is an important point, related to the first chart at the top and information in my previous neuroborreliosis notes post:

"One scientific gap is the testing of cerebrospinal fluid for antibodies. Europeans measure intrathecal production of antibodies by measuring antibodies in CSF and comparing these results against the concentration of antibodies in the serum to produce a ratio. U.S. Scientists have not had a sufficiently large population in which to evaluate the efficacy of this approach because fewer cases of neuroborreliosis are documented in the United States as compared to Europe and CSF sampling is not routinely done in patients with Lyme disease. The absence of this type of testing is a gap in diagnostics for neuroborreliosis caused by B. burgdorferi in the United States."

Is this the case - that the gap in diagnostics for neuroborreliosis is to be blamed on the bacteria? I think that's unfair to the bacteria. As far as I can see, what's happened is that the fact of neuroborreliosis is not something that has been discussed or emphasized when pathogenic Borrelia are neurotropic to varying degrees. Neurological symptoms should be included when educating doctors, nurses, and patients about the disease, and not sidelined to "that only happens in European strains". It doesn't, and besides, Americans do sometimes visit Europe. And hey, if B. garinii and B. afzelii are beginning to show up in southern ticks, well, maybe in a while you'd be seeing more cases of early neuroborreliosis anyway.

I don't know about you, but many Lyme disease patients I've spoken with only got an ELISA test for Lyme disease from their primary care physician, and when that came back negative, there was no further testing.

CSF testing when I had early neurological symptoms is not something I was offered, either.

Which is ludicrous when early serological testing is especially prone to not detecting an infection. What should happen is if the person has a lot of neurological symptoms shortly after a tick bite, they should have a LP. And also the Western Blot. Repeated Western Blot testing which shows an increasing and changing serological profile would be useful in demonstrating antibody response.

It is also stated elsewhere in the summary report:

"An increment in immunoreactive bands is observed in the IgG immunoblots of sera of patients with neuroborreliosis and Lyme disease arthritis."

Saying that Borrelia burgdorferi doesn't cause neuroborreliosis isn't true. Saying it's rare isn't a helpful statement, and aside from utility, it's not even clear how rare it is because we simply lack that data. We don't know. What we have is a guess.

Referring to some studies (there are more studies on neuroborreliosis in the paper):

Page 7-15

"Turning to the literature pertaining to patients with chronic persistent symptoms, Fallon noted a number of areas need additional research. A European study compared patients with neurologic Lyme disease to those with erythema migrans 3 years later and found that 50 percent of those with neuroborreliosis experienced persistent symptoms versus 16 percent of the EM patients (Vrethem et al., 2002). These results suggest that follow up studies on chronic symptoms, rather than focusing solely on early EM, should focus on the subpopulation of patients who present with neurologic or other disseminated symptoms."

Page A-94:

"In a study of 60 U.S. patients with neuroborreliosis (16 with early and 44 with late neuroborreliosis), the sensitivity of PCR in CSF was 38% in early and 25% in late neuroborreliosis, and an inverse correlation was found between duration of antimicrobial treatment and PCR results (Nocton et al., 1996)."

So clearly, PCR isn't so great at detecting neuroborreliosis in early or late stage infection.

Page 7-16
"With respect to pathophysiology, Borrelia act directly and can invade neural cells in vitro (Livengood and Gilmore, 2006); there are also indirect actions, such as the induction of local cytotoxins or inflammatory mediators (reviewed in Fallon et al., 2010). European studies show that pro-inflammatory cytokines are increased, and chemokines, excitotoxin, and quinolinic acid are increased in patients with neuroborreliosis (Weller et al., 1991; Halperin and Heyes, 1992; Widhe et al., 2004; Rupprecht et al., 2005)."

(An aside: For all of those readers getting excited about the excitotoxin, it's not produced by the Lyme Borrelia spirochete - it's produced by your own body. If you're thinking about detoxing that, I'll be discussing it in a different post.)

A discussion item on this was noted at some point during the workshop:

"...Dumler noted that large-scale human clinical studies that have sufficient statistical power are needed. As discussed by previous panelists, such studies would allow the acquisition of large numbers of subjects and potentially bring together all of the involved communities — patients,advocate groups, physicians, academicians—to address research uncertainties on a large scale. These clinical trials for tick-borne diseases could easily be assimilated into modern high-throughput methods that may make whole genome surveys feasible.There would need to be some discussion on how many patients would be needed for a single-nucleotide polymorphism (SNP) analysis for neuroborreliosis. A large-scale clinical study would be intense and difficult, but it would rely on the communities coming together. These clinical trial groups could provide critical corroborated subjects and a biorepository of samples for pathogenesis studies. Within the group, one could create and validate the next generation of diagnostics. It would also provide a critical structure for the assessment of the new diagnostics, clinical interventions, and therapeutics.

Here's one action item: Organize a large-scale human clinical study involving single-nucleotide polymorphism (SNP) analysis.

But is this the most relevant test for people who are ill and have persistent symptoms? I wish Dumler would outline the process for patients as to what he sees in the future for patient treatment using this data.

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