Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
In the Jan-Feb 2011 issue of Discover Magazine on page 62 there is an article about the "13 faces of lyme"...page 62.
Basically...13 strains of Bb have a
different capacity
to cause disease...
Some cause nerve damage, some heart block, some swollen joints, 20% fatigue, etc...(I don't agree...more like 100% fatigue from what I've read from you all - melatonin up?)
"We now have a more complete picture of the pathogen and the genes that may be related to the disease."
Future:
"Diagnostic tests could be tailored to
different strains
or stages of the disease",
and vaccines could be designed to
SKIRT THE INTERACTION WITH THE HUMAN BODY."
*********
Me...sorta sounds like current testing might not be picking up all strains of Bb
or results may depend on the STAGE of the disease.
Me...like many viruses, it appears to me that Bb counts on our immune reaction to survive (esp. inflammation).
(Many viruses count on our histamine response to help them to invade, for example).
If we can stop the "normal" response to Bb (primarily a lot of inflammation) AND at the same time "hit it"...perhaps...
***
Personal note...just back home (FL) from a 2" white Christmas in Charlotte. Enough to make a snowman.
Happy New Year ya all.
BELIEVE in miracles. ALWAYS.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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Carol in PA
Frequent Contributor (5K+ posts)
Member # 5338
posted
Here, so that people can read it:
Top 100 Stories of 2010 #58: The 13 Faces of Lyme by Pamela Weintraub From the January-February special issue; published online December 16, 2010 http://discovermagazine.com/2011/jan-feb/58
Lyme disease, the most prevalent tickborne infection in the United States, can vary greatly from one person to the next. The hallmark is said to be a bull’s-eye rash, yet the rash can take other shapes or not appear at all. Some patients suffer nerve damage, others heart block or swollen joints.
Almost 20 percent report a flu-like condition marked by myalgia, arthralgia, and fatigue. Intensity veers wildly too: In one patient symptoms may be barely discernible; in another so incapacitating that life is derailed.
Now the reason for this inconsistency is becoming clear. In October a team of scientists published the sequences of the genomes of 13 strains of Borrelia burgdorferi, the bacterium that causes Lyme disease.
“Different strains have different capacity to cause disease,” explains infectious-diseases physician Benjamin Luft of the State University of New York at Stony Brook. “We now have a more complete picture of the pathogen and the genes that may be related to the disease.”
For patients the payoff could be great. Scientists have had to develop diagnostic tests and vaccines without information from the genomes.
But now “the approach can be reset using the bacterial and human genomic data,” says immunologist Steven Schutzer of the University of Medicine and Dentistry of New Jersey. “For instance, diagnostic tests could be tailored to different strains or stages of the disease,” and vaccines could be designed to skirt interaction with the human body.
These results, along with imaging technologies that capture pathogens in the living host, form a “scaffold” for future research into Lyme disease, says Joseph Breen, bacteriology program officer at the National Institute of Allergy and Infectious Diseases, which funded the work.
Posts: 6947 | From Lancaster, PA | Registered: Feb 2004
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Good find! Thanks for posting it! I saw mention of this in the paper back in November.
FYI - This is a copy of someone's transcription of L's IOM presentation in October, taken from a mailing list:
NSTITUTE OF MEDICINE 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
11 OCTOBER 2010
9:30 am Spectrum of Lyme Disease: Approaches to Understanding Multi-factorial and Multidimensional Diseases L, M.D. (confirmed)
Worked in Lyme past 25 yrs. Worked on other diseases, infections and non-infectious. Is academic physician, has worked w HIV and Toxoplasmosis to WTC assistance for 9/11.
Has seen patients over long period of time and looked at other diseases that give him insight.
Lyme continues to be emerging and diverging disease. Diverging in that it also comes with coinfections from different organisms. To patients Lyme Disease is their disease regardless of genotypes - they�re concerned w their illness.
It is multisystem and multidimensional.
What does multidimensional mean? I was once chairman of dept of medicine and then became more patient-centred. Had to begin to grasp the different facets of Lyme that affected patients and how that affects their disability and their recovery.
We have to develop biological and clinical instruments to qualify this disease. We need universal phenotype for the disease. There are too many definitions out there, we don�t have a universal description for this disease.
Look at the outbreak in the Netherlands with Q Fever. They now have a disease known as Q Fever Syndrome or a chronic Q Fever -- similar to Chronic Lyme Disease.
No-one is trained to deal with either situation, there�s no real expertise out there or training; people try to learn as they go along.
This is a problem with the academy and why these diseases are often dismissed and not dealt with as they should be.
Adage: Old blind men with the elephant -> specialists looking at different things when it�s all Lyme and TBIs.
Vaccine is in trials in Europe Looking at multiple pathogens in ticks Looking now at Genomic Sequencing
We just published papers on genomes in Borrelia that will be very useful esp to the IOM committee We are involved w (Dick Smith, WA) proteomics study
Our studies:
We flagged for ticks and wanted to see OspC within population of ticks More dots in slot blot = variance of Bb that were in the population Different ticks had 1 variant up to 9 variants of Borrelia in each tick This infection is a lot more complicated than Bb alone.
Another study:
Various tick isolates identified into diff OspC types (diff genotypes) Looked at patient skin isolates have much smaller population in skin causing diseases Last isolates were most invasive isolates found in blood A relatively small population of Borrelia are infectious agents.
We wanted to expand this to 20 different genotypes Others have worked on this (Wormser and Schwarz) using different markers This shows complexity of problem: One strain of Borrelia is not like the others.
OspC is the major OSP of Bb when it enters the skin. We looked at its structure. Showed invasive ones had structure identical to non-invasive ones, except at the very head. Had very high electropositivity at the head (asked if this was a sign of its invasiveness... apparently hermsii has this too).
Bb is an expanding and diverging process. There are as many as 37 diff species of Bb throughout the world, 12 believed to cause Lyme Disease.
What is the variation of Borrelia? Diff Borrelia have different capacity to cause human disease. This has important implications for this committee in thinking of size of study, geographic region of study, and more.
DARPA funded study:
RE Mark Eshoo Can identify multiple arrays of pathogens using broad PCR and mass spectrometry.
NY, CT, IN, CA - studied for genotypes Genotype prevalent in one part of country gives antibiotic response in one part of country but different response in another. Needs more study and to be considered when developing appropriate trials.
NY and CT 15 common genotypes 4 distinct ones in CT
How many genotypes are there? We gathered ticks and looked at what they carried... In 34% of ticks, at least 2 diff genotypes 5% >3 In 40% of ticks there are multiple genotypes. Which is causing disease? How do they impact one another?
Potentially immune system is fighting more than one infection concurrently. We don�t know. Is there synergy? Antagonism? We don�t know.
Then there�s the complexity of other microbes... Yes, multiple Borrelia genotypes and then other pathogens on TOP of this.
What is the impact of Babesia? I know about Toxoplasmosis. What about Babesia? How does it impact trial design if someone has just one Borrelia or three, or anaplasma, or Powassan? It�s extremely complex.
Numerous genotypes in areas where it is found. Some genotypes persist longer in mice and cause greater problems for humans.
Multicentred therapeutic trials will be needed with many patients. we need double blinded controlled studies that show universal efficacy These studies need to be looked at in a circumspect way
Most patients w Lyme Disease I can take of, and 90% can be taken care of by my nurses or nurse practitioners - but the other 5% have problems posing diagnostic dilemma, requiring more testing, and they�re more complex (his experience)
Epidemiological studies need to cover a wider area and examine all the genotypes and organisms present.
Is 200 patients an appropriate number for study design? I don�t think so. Until we have larger studies, more smaller studies with treatment breakthroughs and failures need to be appreciated.
We did a lot of sequencing and now have a map or family tree of Borrelia (genomic study) to be published soon.
(shows slide)
We began to identify various strains where we wish to sequence the entire genome. (Claire Fraser, U of MD, Steve Schutzer, others...)
Where are we with this? We�re able to have a pan genome. There�s so much confusion, so let�s try to get as much info as we can. We wanted to know how many genes we needed to sequence to get a complete picture of the Borrelia family tree.
Wanted to know if it�s a closed or open genome. Could it be open and continually acquire new genetic material from other species and other strains? Or is it closed, where it�s easier to come closer to an answer for diagnosis and treatment?
Looked at Bb ss Going out about 14 genomes, number of new genes identified were small. With each round of sequencing, 4 new genes were found, same with next... we stopped at 17 genomes or strains. We think we�ve found the core genetic material or core genome and know what is common to all Borrelia. Good idea of pan genome, too.
The genome is more of an open genome type of process though. How much exchange is there between genotypes? We don�t know how fluid it is. It needs more study. It may cause problems.
Data on 17 diff strains looked for pos selected strains, heterogeneous from strain to strain pushed to be positively selected, also looked at genes predicted to be on surface of organism came up w 500 recombinant proteins and begin testing them
got 15 sera from the CDC from patients who had EM and many diff cultured Bb were taken from their EM. Only 54% of these folks were serum positive With the protein array we have, ALL of them had antibody response to Borrelia When you have the knowledge, the tools, the information, you don�t have seronegativity. This comes with good science.
We have to gather patient info and history in reliable way We have to test in reliable and reproducible way. We have to reproduce and validate our results. We need a chronic Lyme bio databank.
But all this requires accurate methodology for phenotype identification which has to be done very carefully.
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Fellow researchers...
IgG2 deficiency at play?
"Immunoglobulin G2 confers
protection against Borrelia burgdorferi
infection in LSH hamsters." PMID: 1612738
"The observed distribution suggested the presence of a
***subpopulation with low IgG2 concentration.***
Because apparently healthy individuals in a general population have low IgG2 concentrations, IgG2 measurements alone may have a limited clinical usefulness as an index of immune function against
No "formal" LPS (only "LPS-like")- so we "fry" Bb's Osps (proteins) via ROS?
Then what...cell wall deficient form remains capable of rebuilding UNLESS - step #2: osmotic pressure changes or ultrasound are used to rid the CWD form to "finish it off" (basics of how to rid a gram negative pathogen i.e., hit the cell wall/prevent it from forming and then go to step #2).
Get this:
Man-made IgG2?!!!
"Denosumab (Prolia): A human IgG2 monoclonal antibody that binds to RANKL (or receptor activator of nuclear factor kappa-B ligand), preventing RANKL from activating its receptor (RANK) on the surface of osteoclasts."
Test level of IgG2 first? If low...indicated?
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Pinelady
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posted
I just love how they keep changing words/diseases/proteins around to confuse. There ought to be a law against it.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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