Archive for the ‘Lyme’ Category

Integrated Tick Management Reduces Ticks by 93% Study Finds

https://www.ncbi.nlm.nih.gov/pubmed/31853763

2019 Dec 18. doi: 10.1007/s10493-019-00452-7. [Epub ahead of print]

Evaluating the effectiveness of an integrated tick management approach on multiple pathogen infection in Ixodes scapularis questing nymphs and larvae parasitizing white-footed mice.

Little EAH1,2, Williams SC2,3, Stafford KC 3rd1,2, Linske MA1,2, Molaei G4,5,6.

Abstract

We investigated the effectiveness of integrated tick management (ITM) approaches in reducing the burden of infection with Borrelia burgdorferi, Babesia microti, and Anaplasma phagocytophilum in Ixodes scapularis. We found a

  • 52% reduction in encountering a questing nymph in the Metarhizium anisopliae (Met52) and fipronil rodent bait box treatment combination as well as a
  • 51% reduction in the combined white-tailed deer (Odocoileus virginianus) removal, Met52, and fipronil rodent bait box treatment compared to the control treatment.
  • The Met52 and fipronil rodent bait box treatment combination reduced the encounter potential with a questing nymph infected with any pathogen by 53%.
  • Compared to the control treatment, the odds of collecting a parasitizing I. scapularis infected with any pathogen from a white-footed mouse (Peromyscus leucopus) was reduced by 90% in the combined deer removal, Met52, and fipronil rodent bait box treatment and by
  • 93% in the Met52 and fipronil rodent bait box treatment combination.
Our study highlights the utility of these ITM measures in reducing both the abundance of juvenile I. scapularis and infection with the aforementioned pathogens.

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For more:  https://madisonarealymesupportgroup.com/2019/04/12/tick-prevention-2019/

https://madisonarealymesupportgroup.com/2019/07/18/frequent-prescribed-fires-can-reduce-risk-of-tick-borne-diseases/

https://madisonarealymesupportgroup.com/2018/04/03/fire-good-news-for-tick-reduction/

https://madisonarealymesupportgroup.com/2018/05/27/study-conforms-permethrin-causes-ticks-to-drop-off-clothing/

https://madisonarealymesupportgroup.com/2019/06/16/study-shows-effectiveness-of-factory-treated-permethrin-impregnated-clothing-works/

https://madisonarealymesupportgroup.com/2019/08/09/military-eyes-bug-repellent-coating-to-replace-permethrin-in-uniforms/

 

Category:

Anaplasmosis, Babesia, Lyme, research, Testing, Ticks

Lyme: The Differential Diagnosis

https://globallymealliance.org/lyme-the-differential-diagnosis/

By Jennifer Crystal

WITH OVERLAPPING SYMPTOMS, HOW DO YOU KNOW THAT YOU HAVE LYME AND NOT ANOTHER DISEASE? IT’S IMPORTANT TO CONSIDER ALL HEALTH FACTORS

A patient recently asked me, “How do you know you have Lyme and not multiple sclerosis or chronic fatigue syndrome? It sounds to me like you have chronic fatigue syndrome.”

I understand such questions. They come up because Lyme is considered the “great imitator.” Many of its symptoms are similar to those of other illnesses such as multiple sclerosis (MS) and chronic fatigue syndrome (CFS), as well as rheumatoid arthritis (RA), Lou Gehrig’s disease or amyotrophic lateral sclerosis (ALS), lupus, and fibromyalgia. If a doctor is not well-versed in tick-borne disease, they might have difficulty making a differential diagnosis—differentiating between Lyme and other diseases.

However, there are important distinctions between these conditions. For example, Lyme arthritis can affect one, few, or many joints, whereas RA tends to affect most. While synovitis (inflammation of a synovial membrane) can mean Lyme or RA, only Lyme would show fluid in the sub-patella area.[1]A good Lyme Literate Medical Doctor (LLMD) understands such nuances.

I know I have Lyme because I had an unequivocal CDC-positive test. I also tested positive for two tick-borne co-infections, babesia and Ehrlichia. I presented with specific clinical symptoms of these diseases and the tests corroborated my LLMD’s clinical assessment. He knew that my low CD-57 test was indicative of Lyme, because ALS and MS don’t usually have low CD-57 counts. He knew that my hallucinogenic nightmares and other sleep disturbances were a sign of neurological Lyme and babesia (later confirmed by a SPECT scan), and he knew that my migratory on-and-off aches were typical for Lyme, not RA (which are more symmetrical and persistent). Moreover, he recognized that my crushing fatigue was a result not just of my tick-borne illnesses, but also of my underlying Epstein-Barr virus.

Yes, you read that right: I write primarily about my tick-borne diseases, but they’re not my only medical conditions. So in some ways, the patient who questioned me was not incorrect; I do have CFS, or a version of it called chronic fatigue immune deficiency syndrome. It stemmed from a case of mono that became chronic Epstein-Barr virus (EBV) because I had underlying tick-borne infections that prevented me from adequately fighting the mono.

Here’s the rub with these umbrella diseases, diseases under which a number of symptoms fall: often patients have more than one of them, or their symptoms fall under the broad spectrum of more than one, because what they’re battling is actually a multi-system immunological breakdown from years of health issues. As Richard Horowitz, an LLMD, states in his book Why Can’t I Get Better? Solving the Mystery of Lyme & Chronic Disease, “Identifying the multifactorial causes of chronic illness is the next most important paradigm shift in medicine.”[1]

To consider all health factors in making a differential diagnosis, Dr. Horowitz uses a detailed Lyme multi-system infectious disease syndrome (MSIDS) questionnaire based on one originally created by another prominent LLMD, Joseph Burrascano. This health map looks at Lyme disease, co-infections, other bacterial infections, viral infections, parasitic infections, and fungal infections, and takes into account immune dysfunction, inflammation, environmental toxicity, allergies, nutritional and enzyme pathways, mitochondrial dysfunction, neuropsychological issues, autonomic nervous system dysfunction, endocrine abnormalities, sleep disorders, gastrointestinal abnormalities, abnormal liver functions, issues with pain, drug use, and physical conditioning.[2]

As Dr. Horowitz notes, “This process ensures that no symptoms are left out and gives the provider an initial opportunity to develop a broad range of differential diagnoses…It provides the health-care provider with clues that point to whether the patient has a high probability of having Lyme disease, a possible case of Lyme disease, or is unlikely to have Lyme disease.”[3]

Other LLMDs use similar broad-spectrum evaluations to make differential diagnoses. Dr. Bernard Raxlen explains in his book Lyme Disease: Medical Myopia and the Hidden Global Pandemic that he looks for “red flags” or “common themes,” listing two full pages of symptoms that are specific to tick-borne illnesses. These include including air hunger, purple/red streaks or scratches, constant sweating on one side of the body, psychogenic or emotionally driven seizures, loss of reading ability, and migrating pain, particularly in joints, muscles, and nerves.[4]

I spent two years treating EBV before seeing an LLMD and realizing I was only fighting half the battle. I know now to ask, what else could be going on? Am I treating all of my symptoms? Does my diagnosis speak to all of them? The patient who questioned me probably only read one of my articles that described my fatigue, and made a quick assumption that I have CFS. Had this person read more of articles describing my specific experiences with neurological Lyme disease, they may have drawn a different conclusion. It’s important for patients and for doctors to get the full picture before drawing conclusions or making diagnoses. Lyme may be the great imitator, but it is not a catch-all diagnosis, and we must understand what differentiates it from other diseases.

[1]Gaito, Andrea, MD. “Clinical Evaluation and Treatment of Lyme Arthritis; An Autoimmune Perspective.” ILADS, 2012.

[2]Horowitz, Richard I., MD. Why Can’t I Get Better? Solving the Mystery of Lyme & Chronic Disease. New York: St. Martin’s Press, 2013 (29).

[3]Horowitz, 58.

[4]Horowitz, 33.

[5]Raxlen, Bernard, MD with Cashel, Allie. Lyme Disease: Medical Myopia and the Hidden Global Pandemic. London: Hammersmith Health Books, 2019 (26-7).

jennifer crystal_2Opinions expressed by contributors are their own.

Jennifer Crystal is a writer and educator in Boston. Her memoir about her medical journey is forthcoming. Contact her at lymewarriorjennifercrystal@gmail.com.

 

 

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**Comment**

Great article pointing out the blatant fact that Lyme is often not “just Lyme,” but a complex illness caused by many factors working together.

The first thing I tell patients to do is print and fill out the Horowitz questionnaire.  If you have a preponderance of symptoms, it’s likely you have Lyme/MSIDS.  Go here for the questionnaire:  https://madisonarealymesupportgroup.com/wp-content/uploads/2016/01/symptomlist.pdf

This questionnaire has been validated: https://madisonarealymesupportgroup.com/2017/09/05/empirical-validation-of-the-horowitz-questionnaire-for-suspected-lyme-disease/

It’s also quite helpful to print and fill out other checklists for coinfections:

https://madisonarealymesupportgroup.com/2011/09/25/the-babesia-checklist-copyrighted-2011-james-schaller-md-mar-version-20/

https://madisonarealymesupportgroup.com/2011/09/25/the-bartonella-checklist-copyrighted-2011-james-schaller-md-version-11/

Category:

Lyme

Lyme Disease: Multifaceted & Misunderstood!

https://www.linkedin.com/pulse/lyme-disease-multifaceted-misunderstood-darin-ingels-nd/?

Lyme Disease: Multifaceted & Misunderstood!

Darin Ingels, ND

Darin Ingels, ND

Public awareness of Lyme disease is largely overlooked by healthcare professionals and the public at large. As a general community, we know that Lyme disease is on the rise.

We also know that it is a very difficult disease to properly diagnose and treat. It is primarily transferred from tick bites, although new evidence suggests mosquitos and other insects may be carriers as well. It’s a disease that is often misunderstood. At one point, it was used as an excuse for the poor behavior of a contestant on a reality show.

There is a plethora of information on the complexities of Lyme disease. However, it can be extremely misleading and somewhat confusing for the average person to grasp. Understanding Lyme disease is very important because it can lead to a more informed and better treatment plan with your health care practitioner.

1. Lyme Disease is known as a bacterial infection, which is different from illnesses caused by viruses.

An example of a viral infection is the common cold or flu. A bacterial infection requires a different response from the human immune system and therefore may require powerful herbs and even specific antibiotics to treat. These antibiotics can be effective against Lyme disease, but sometimes the side effects from these can outweigh the benefits.

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2. Lyme Disease is not be caused by a single species of bacteria.

Lyme Disease is generally thought of an infection from a single bacterial species, primarily Borrelia burgdorferi. Why this may be the causative agent in most cases of Lyme disease, there are actually many other species of bacteria that also contribute to Lyme disease symptoms. There are over 300 known species of Borrellia in the world, so it is unlikely than one is the sole cause of Lyme disease.

Additionally, tick bites can also transmit other bacteria, called coifections. Coinfections can be transmitted along with Borrelia burgdorferi and can cause additional symptoms associated with Lyme.

Coinfections are also diverse in the ways that they hide in the body from the immune system, so getting a comprehensive test to evaluate for these coinfections is important.

These tests allow us to have better insight as to which specific co infection an individual may have. This way, we can be more prepared at devising treatment protocols on a case-by-case basis.

3. Ticks might not be the only carrier of Lyme disease.

Ticks are referred to as “vectors” for Lyme disease. This means that the tick is a specific route, or pathway, for Lyme disease to reach the human body. Vectors, therefore, are delivery systems for viral or bacterial infections.

Lyme can be transferred primarily through tick bites and secondarily through other insect bites.

Though there is less research done on other insects, there are cases where patients have presented with Lyme disease symptoms after getting bitten by fleas and mosquitos. However, there still isn’t enough information at this time.

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4. One disease, many different symptoms.

Lyme is multifaceted. There is no one set of symptoms that it follows, although brain fog, muscle soreness and joint stiffness, fatigue, anxiety, higher levels of stress, lack of sleep, headaches and even cardiac issues are just some of the more common ones I hear from patients.

Symptoms tend to come on gradually and can build up over time. This makes it difficult to get a proper diagnosis early on.

Lyme Disease has an impact on the nervous system and endocrine system, which is why so many symptoms exist. Lyme and its coinfections look for weaknesses in the body and try to magnify the impacts of those weaknesses.

5. Lyme Disease can be treated.

There are ways to lessen the impact of Lyme disease and in some cases, get rid of the infection altogether.

Nutrition, herbal therapies, low dose immunotherapy, homeopathy and pulsed electromagnetic frequency devices can help the body get over the hump of Lyme disease. An effective strategy can be developed to support the body & immune system in order to combat Lyme disease.

If you think you might have Lyme disease or you have been suffering from multiple unexplained symptoms for a long time, seek a Lyme-literate healthcare provider to get tested and proper treatment.

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**Comment**
My only comment is that the treatments suggested may not be enough.  This is a complex illness with many pathogens often involved.  It takes a nuanced, open minded approach that is willing to try many modalities to achieve wellness.  Serious antimicrobials should be a part of this treatment plan.
You can look up other treatments by scrolling down the website and looking on the right hand side of the page.  There are articles for Babesia, Bartonella, Mycoplasma, parasites, viruses, Anaplasmosis and more.

Category:

Lyme, Treatment

CDC Lyme Disease Research Funding to Increase by $2 Million

https://www.whec.com/news/lyme-disease-funding-cdc/CDC Lyme disease research funding to increase by $2 millionPhoto: MGN.

WHECTV
Created: December 20, 2019 

WASHINGTON, D.C. (WHEC) — $14 million in federal funding is set aside in next year’s spending bill to combat Lyme disease.

According to U.S. Senators Chuck Schumer and Kirsten Gillibrand, that’s a $2 million increase.

They say Upstate New York is the number one target for tick-borne diseases in the nation.

The funding will be used to study, identify and prevent exposure to pathogens that cause Lyme disease and other tick-borne illnesses.

The Kay Hagan Tick Act is also included in the bill. It requires HHS to develop a national strategy for vector-borne illnesses and reauthorizes the Regional Centers of Excellence in Vector-Borne Disease for five years at $10 million per year.

 

Category:

Activism, Lyme, Uncategorized

Borrelia Detection & Lyme Disease: The Current UK Situation

https://www.linkedin.com/pulse/borrelia-detection-lyme-disease-current-uk-situation-chris-newton/?

Borrelia detection and Lyme disease: the current UK situation

Chris Newton
Chris Newton
Research Director CIMMBER (Center forImmuno-Metabolism, Microbiome… See More
66 articles 

Part 2. Anatomy of a serology test system: antigen selection, sensitivity and specificity

(This article continues from the one published at the end of November 2019)

Laboratory confirmation of Borrelia infection in the UK is based around the protocol laid down in 1995 by the Centres for Disease Control (CDC) in the US. The concept developed at this time was that a two-tier systems should be used, where the first-tier test should be a high sensitivity assay, such as an ELISA, followed by a more specific, but less sensitive, immunoblot. It would appear that in the UK, some of the regional hospital laboratories use the DiaSorin Liaison XL auto-analyser as a screening approach. If positive or equivocal, a further patient sample should be sent to the reference laboratory, where the first-tier assay is the C6 ELISA and the second tier is a microarray immunoblot assay (ViraChip from Viramed; Theel et al., 2018), a more robust version of the previous line blot system (itself a replacement for the Western blot.

It would appear that in effect, a three-tier system is operated to provide laboratory confirmation of Lyme disease in some regions of the UK. From the recent PHE meeting held in Liverpool on the 22nd November, an abstract was presented where analysis performed by the Bristol NHS Trust using the DiaSorin methodology, was compared to C6 ELISA results obtained by the RIPL at Porton Down. Out of 3131 tests performed at the Bristol laboratory, 296 samples tested positive for IgM antibodies to Borrelia and 195 tested positive for IgG antibodies.

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As the first screening of samples was performed by the Bristol lab., one must assume that the -ve category (for Bristol) in the above table (reproduced from Albur et al., 2019) arrises as a result of the medical professional having enough clinical suspicion of Lyme disease for another blood sample to be tested at Porton Down.

By considering the positive tests in the table above, it would appear that the DiaSorin test is more sensitive for both IgM and IgG detection than the C6 (considerably more so for IgM than IgG). For samples from patients who previously had a negative test result in Bristol, half the samples are now positive with the C6 (74/149) for IgM, and 19.6% of samples that were originally negative at Bristol are now positive for IgG with the C6. These re-test results possibly provide evidence of seroconversion (the development of an antibody response to Borrelia), as the repeat sampling would have been performed at least two weeks after the first, giving more time for an antibody response to develop. This observation suggests that the difference between the two test systems is even more significant in terms of test sensitivity- a difference that favours of the DiaSorin test.

So what might explain the difference in sensitivity between the two test systems? In an attempt to answer this we must return to where we left off in Part 1, namely the effect of antigen selection on sensitivity and specificity.

As discussed in the previous article, as a methodology, serology for Lyme disease screening determines the presence of antibodies to proteins on the outside of the Borrelia microorganism. Antibody detection is achieved by selecting an appropriate antigenic protein (a protein that activates the immune system) on the surface of the microorganism. A traditional approach to find such antigens is to prepare a protein extract from the organism and then to run these proteins on a polyacrylamide gel and perform a Western blot. In this process, proteins from a gel are transferred to nitrocellulose paper (blotted) and the paper is exposed to patient sera. Once excess serum is washed away, a second enzyme-labelled antibody specific to human IgM or IgG is incubated with the paper and after washing off excess, a substrate for the enzyme is added that allows proteins recognised by antibodies in the patient serum to be identified. A typical example of a western blot is shown below.

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The Western blot above is from the 1988 paper by Hansen et al. This paper describes the development of a Borrelia ELISA based around the p41 antigen. Proteins are often described by their molecular weight in kDaltons; p41 is flagellin, the major component of the Borrelia flagellum. The p41 protein is highly antigenic and the figure above shows that purified p41 strongly reacts to antibodies in serum from an individual with Lyme disease. Hansen and colleagues then tested how much p41 was needed in comparison to the crude protein extract to give the highest difference between a control serum and serum from a Lyme patient. Their original graph is shown below.

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The y-axis shows colour development in the ELISA wells (see Part 1 for outline of ELISA design), whilst the x-axis is the dilution of both protein extract and the p41 protein. To establish the assay with p41 as antigen, a dilution of 3200 was used as this gave the highest differential between 1, values for a control serum and 4, values for serum from a Lyme patient. For the control serum of curve 2, it is clear that there is more non-specific binding with the crude protein extract from the Swedish strain of Borrelia burgdorferi.

This dilution of p41 was then used to coat plastic wells of multi-well plates and these plates were used to test serum from uninfected individuals (controls), from those with symptoms of Lyme disease and from individuals infected with other spirochaetes (that have flagella and thus may cross-react). A section from one of the original figures from the Hansen et al. paper is reproduced below.

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In comparison to wells coated withe the total protein extract from Borrelia (left), for p41 as antigen, there is reasonably clear differentiation between controls and patient samples (LMR). Samples from Syphilis-infected individuals (SY1/2) show some cross-reactivity but much less so than for wells coated with the crude protein extract. These studies clearly demonstrate how the choice of antigen changes both sensitivity and specificity. The cut-off, or assay threshold for positivity has to be raised for the crude extract (horizontal line). Due to such a lack of specificity, sensitivity is lost, meaning that many more patients with symptoms of Lyme disease fall below the threshold for positivity.

Whilst p41 would appear to be ideal for fist-tier screening of suspected Lyme cases, the perception of wide ranging cross-reactivity to other organisms meant that throughout the 1990s other Borrelia antigens were considered in preference (the unfortunate dismissal of p41 as a screening antigen will be returned to in Part 3 of this article).

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The search for antigens since the the mid 1980s has given rise to a spectrum of antigenic proteins for antibody detection. On the right is a list of proteins identified by Roger Evans and colleagues (2010) from a MedLine search for protein bands on Western blots. From the 1990s onwards, at least 20 companies have developed assay systems based on a number of these proteins.

Returning now to the issue of antigen choice and the difference between the two ‘first-tier’ screening systems used in the UK. The DiaSorin system for IgM detection uses two recombinant antigens, OspC, an outer surface protein that appears to show specificity for IgM detection in the early phase of infection, and the VlsE protein. For IgG, the DiaSorin test system uses a recombinant VlsE alone. In contrast, for both IgM and IgG detection, the C6 of Immumetics uses a short sequence of 25 amino acids corresponding to an invariant region in the protein.

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This is not the only difference between the two systems. The DiaSorin LIAISON test uses a chemoluminescent assay format where the second antibody is labelled with a light-emitting probe (see diagram above taken from the paper of Cinquanta et al., 2017). Chemiluminescent immunoassays (CLIA) have the potential for analytical sensitivity many orders of magnitude greater than ELISA (Cinquanta et al., 2017). As described in Part 1 of this article, an increase in sensitivity will decrease the analytical detection limit for antibodies. For Borrelia antibody detection, a decrease in cut-off or working detection limit, will only be realized if by choice of the most appropriate antigen, specificity also increases (the figure concerning p41 detection above is an example of how antigen selection determines specificity, that in turn, determines the assay cut-off and hence clinical sensitivity).

Although both the DiaSorin and C6 tests use the VlsE antigen, DiaSorin use a full length recombinant protein whereas the C6 uses a 25 amino acid sequence of the VlsE protein (Liang et al., 1999). So it would appear that in the UK we have a screening assay for Borrelia that is rather different to the true first-tier test used in the reference laboratory at Porton Down.

From these data provide by the Bristol NHS trust (Table at beginning of this article) it would appear that the DiaSorin CLIA is more sensitive than the C6, especially so for IgM. With respect to further comparison of assay systems, a significant study was published last year by Pegalajar-Jurado et al. The CDC recommended two tier-test paradigm of ELISA, EIA (enzyme immunoassay) or CLIA before an immunoblot, was compared to a first-tier with an EIA or CLIA followed by a second tier with a similar type of assay. These algorithms are described in the figure below (taken from Pegalajar-Jurado et al., 2018).

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This study used well characterised samples from the CDC (Molins et al., 2016) and made comparisons of several assay types including the DiaSorin CLIA and the C6 from Immumetics. Although complex, the major table from this study is reproduced in its entirety below.

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Whilst the distinction between IgM and IgG positivity has not been made in the above table, it of high significance that particularly for Early Lyme disease with EM, the MTTT algorithm outperforms the STTT algorithm for all assay combinations. Also significant, is the inclusion of data from the DiaSorin VlsE/C6 combination showing no loss in specificity, as noted by the control samples tested.

Currently testing within some regions of the UK conforms to the VlsE/C6 algorithm with the exception that the DiaSorin CLIA for VlsE is performed several weeks before a repeat test with the C6 at the reference laboratory. Also, samples that are positive with the C6 in reference laboratory at Porton Down, are re-tested with the ViraChip system. This three-tier algorithm doesn’t fit into either the MTTT or the STTT paradigm.

So what can we conclude from all this?

Primarily, a review of the current serological testing paradigm for Lyme disease within the UK is urgently needed.

Although data provided by the Bristol NHS trust suggest that the DiaSorin CLIA in UK format is more sensitive than the C6, it is essential that further studies are conducted where the same serum samples are tested in both assay systems (DiaSorin CLIA and C6). Whilst data provided by Pegalajar-Jurado and colleagues (2018) suggest that the VlsE/C6 MTTT algorithm is more effective than the STTT algorithm for early laboratory diagnosis of Lyme disease, we cannot make the same assumption for a UK cohort of samples/patients. The same format of study as reported by Pegalajar-Jurado and colleagues must be conducted in the UK.

Also, it is not know whether all suspected cases of Lyme disease are tested within the local hospital trust and therefore give rise to a three-tier protocol (DiaSorin CLIA, followed some weeks later by a C6 and a Virotech Line blot). Unless it is experimentally investigated, it cannot be assumed that a three-tier protocol will give the same overall sensitivity as a two-tier protocol.

Centers for Disease Control and Prevention. (1995) Recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR Morb Mortal Wkly Rep 44:590 –591

Theel ES, Sorenson M, Grangera D. (2018) Evaluation of a Novel Microarray Immunoblot Assay for Detection of IgM- and IgG-Class Antibodies to Borrelia burgdorferi. J. Clin. Microbiol 56 (11) e00992-18

Albur M, Hamilton F, MacGregor K (2019) Serodiagnosis of Lyme disease: Cheese and Chalk or Peas in a Pod? Lyme and tick-born disease research in the UK. PHE conference. Liverpool, 21-22nd November 2019

Hansen K, Hindersson P, Pedersen NS (1988) Measurement of Antibodies to the Borrelia burgdorferi Flagellum Improves Serodiagnosis in Lyme Disease. J Clin Microbiol. 26 (2): 338-346

Evans R, Mavin S, McDonagh S, Chatterton JM, Milner R, Ho-Yen DO. (2010) More specific bands in the IgG western blot in sera from Scottish patients with suspected Lyme borreliosis. J. Clinical Pathol. Doi:10.1136/jcp.2010.076307

Cinquanta L, Fontana DE, Bizzaro N (2017) Chemiluminescent immunoassay technology: what does it change in autoantibody detection? Autoimmun Highlights 8:9 https://doi.org/10.1007/s13317-017-0097-2

Liang FT, Alvarez AL, Gu Y, Nowling JM, Ramamoorthy R, Philipp MT (1999) An Immunodominant Conserved Region Within the Variable Domain of VlsE, the Variable Surface Antigen of Borrelia burgdorferi. J Immunol November 163 (10) 5566-5573

Pegalajar-Jurado A, Schriefer ME, Welch RJ, Couturier MR, MacKenzie T, Clark RJ, Ashton LV, Delorey MJ, C Molinsa CR. (2018) Evaluation of Modified Two-Tiered Testing Algorithms for Lyme Disease Laboratory Diagnosis Using Well-Characterized Serum Samples. Journal of Clinical Microbiology 56 (8) e01943-17

Molins CR, Delorey MJ, Sexton C, Schriefer ME. (2016). Lyme borreliosis serology: performance with several commonly used laboratory diagnostic tests and a large resource panel of well-characterized patient samples. J Clin Microbiol 54:2726–2734. https://doi.org/10.1128/JCM .00874-16

Branda JA, Strle K, Nigrovic LE, Lantos PM, Lepore TJ, Damle NS, Ferraro MJ, Steere AC. 2017. Evaluation of modified 2-tiered serodiagnostic testing algorithms for early Lyme disease. Clin Infect Dis 64:1074–1080. https://doi.org/10.1093/cid/cix043.

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Go here for part 1:  https://www.linkedin.com/pulse/borrelia-detection-lyme-disease-chris-newton/

Category:

Lyme, Testing