2 Microarray Analyses of Inflammation Response of Human Dermal Fibroblasts to Different Strains of B. burgdorferi S.S.

This interesting abstract just got posted on PubMed and is in PLoSONE:

Microarray Analyses of Inflammation Response of Human Dermal Fibroblasts to Different Strains of Borrelia burgdorferi Sensu Stricto

Schramm F, Kern A, Barthel C, Nadaud S, Meyer N, Jaulhac B, Boulanger N.

Abstract

In Lyme borreliosis, the skin is the key site of bacterial inoculation by the infected tick, and of cutaneous manifestations, erythema migrans and acrodermatitis chronica atrophicans. We explored the role of fibroblasts, the resident cells of the dermis, in the development of the disease.

Using microarray experiments, we compared the inflammation of fibroblasts induced by three strains of Borrelia burgdorferi sensu stricto isolated from different environments and stages of Lyme disease: N40 (tick), Pbre (erythema migrans) and 1408 (acrodermatitis chronica atrophicans).

The three strains exhibited a similar profile of inflammation with strong induction of chemokines (CXCL1 and IL-8) and IL-6 cytokine mainly involved in the chemoattraction of immune cells. Molecules such as TNF-alpha and NF-κB factors, metalloproteinases (MMP-1, -3 and -12) and superoxide dismutase (SOD2), also described in inflammatory and cellular events, were up-regulated.

In addition, we showed that tick salivary gland extracts induce a cytotoxic effect on fibroblasts and that OspC, essential in the transmission of Borrelia to the vertebrate host, was not responsible for the secretion of inflammatory molecules by fibroblasts.

Tick saliva components could facilitate the early transmission of the disease to the site of injury creating a feeding pit. Later in the development of the disease, Borrelia would intensively multiply in the skin and further disseminate to distant organs.

Link: http://www.ncbi.nlm.nih.gov/pubmed/22768217

Comments:

Take note of that last paragraph:

"Tick saliva components could facilitate the early transmission of the disease to the site of injury creating a feeding pit. Later in the development of the disease, Borrelia would intensively multiply in the skin and further disseminate to distant organs."

Do you think the implications of the above fit in nicely with the mathematical modeling of Borrelia burgdorferi infection cycles mentioned in an earlier entry?

Why or why not?

See:

Abstract: Population Dynamics Of Borrelia burgdorferi In Lyme Disease
http://campother.blogspot.com/2012/04/abstract-population-dynamics-of.html

The implications - for me at least - seem to fit a model where the first wave of infection dies off but then a bigger, immune-resistant subpopulation explodes onto the scene (the site of infection).

Awaiting PLoSONE to publish the full text so I can give a more thorough analysis...

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2 Wormser et al Criticism Launched at Embers' Rhesus Macaque Study

Wormser et al have recently published a critique of Embers' study, "Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection".

Vector Borne Zoonotic Dis. 2012 May 23. [Epub ahead of print]

Critical Analysis of Treatment Trials of Rhesus Macaques Infected with Borrelia burgdorferi Reveals Important Flaws in Experimental Design.
Wormser GP, Baker PJ, O'Connell S, Pachner AR, Schwartz I, Shapiro ED.

Abstract

A critical analysis of two treatment trials of Chinese rhesus macaques infected with Borrelia burgdorferi indicates that insufficient attention was placed on documenting the blood levels, pharmacokinetics, and pharmacodynamic parameters of the antibiotics used in this host. Consequently, it is impossible to conclude that the findings have validity in judging the efficacy of doxycycline or ceftriaxone for the treatment of Borrelia burgdorferi in this animal model.

PMID: 22620495 [PubMed - as supplied by publisher]

Full text of this critique is available here:
http://online.liebertpub.com/doi/full/10.1089/vbz.2012.1012

The full text of the original study which is the focus of this critique is here:
http://www.plosone.org/article/fetchArticle?articleURI=info%3Adoi%2F10.1371%2Fjournal.pone.0029914


Related material on Camp Other blog:

• Paper: Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection
• Debate About Embers Non-Human Primate Chronic Lyme Disease Study Continues
• Embers et al Rhesus Macaque Study Correction Issued
• Embers et al Issues Statement On PLoSONE
• Why Aren't Persisting Spirochetes Enough Evidence Of Infection?

Comments:

For now I am sharing the news that the free full text this critique is available online. Further comments to be made at another time. Comments by readers are welcome.

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0 Babesiosis Fatality In Australia

Earlier this week, the Australian television show Today Tonight aired a story about a 56 year old man from New South Wales who died from Babesiosis. There is some concern by others that the man contracted the infection within Australia and not overseas, though more evidence is needed this is the case.

Babesiosis is a tickborne illness caused by a protozoan parasite, Babesia, which infects red blood cells and produces symptoms which are similar to those found in malaria. It can be subclinical and cause no to mild symptoms - but it can also lead to moderate and severe symptoms. And sadly, as we've seen - even kill people.

People who are most likely to have severe symptoms are the elderly, those with compromised immune systems, and those who do not have a spleen.

I know firsthand what Babesiosis is like because several months after I was bitten by a tick, new symptoms showed up in me which were indicative of an infection with Babesia. I also was fortunate to get a positive blood smear - not something which is easily accomplished in the lab.

The most obvious symptoms I experienced were an ongoing shortness of breath with the sensation of a vice-like grip around my ribs, breaking out into sweats at night, "flash" fevers, and anemia. There were other less known symptoms as well, but these are among the most common. Fortunately, I think (I hope) I have beat this coinfection, and it has not beat me.

As it stands, the United States has seen a number of its own deaths due to Babesia, and according to an article in the New York Times, in coastal Rhode Island, the number of cases of Babesia are around 25% less than those of Lyme disease - in an area which is highly endemic for Lyme disease. And not only is Babesia becoming quite common in northeastern states - it's spreading to the northern midwest as well and was already found on the west coast.

One important thing to be aware of is not only can Babesia be transmitted by ticks - it can be spread through the blood supply via donations and transfusions. Thus far, there are twelve people who have died from Babesia spread through blood transfusions in the US. It is unknown, though, how many people may have been infected with Babesia through the blood supply and currently carry a more subclinical infection that may become more evident later.

There is currently no blood screening test available for donations and transfusions, and research is underway to develop such a test to avoid spreading more Babesia through the blood supply. So I highly recommend that if you have to get surgery and know this in advance, that you blood bank your own blood in preparation in case you need a transfusion.

You can view the dramatic video of the Today Tonight story here [4:46 minutes, plus short ad]:

Read this link for a full transcript of the show:

http://au.news.yahoo.com/today-tonight/latest/article/-/13207421/tick-timebomb/

For more information about Babesia and Babesiosis, check out these links:

Specific to Australia: http://lymedisease.org.au/about-lyme-disease/babesiosis/

About the Lifecycle: http://www.stanford.edu/group/parasites/ParaSites2006/Babesiosis/lifecycle.html

About Treatment: http://emedicine.medscape.com/article/780914-treatment

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2 Обзор Для русских читателей Лайм боррелиоза

Given what I learned about Russian treatment guidelines for Lyme disease - as well as a particular treatment plan from Serbia - I have decided to offer Russian Lyme disease patients (former and current) a survey.  I plan to give a similar survey to readers from other countries after this one...

Дорогие русские читатели этого блога,Благодарим Вас за посещение и чтение других блогов лагерь.Недавно я узнал от читателя, который лечился боррелиоз Лайма в Сербии, что оба вида антибиотиков выбрали и продолжительность лечения была отличной от той, которую мы обычно получают в Соединенных Штатах.

В результате, мне было интересно, о том, что различные руководящие принципы для лечения боррелиоза Лайма в разных странах. Я посмотрел на принципы Сербии лечения, но не могли найти их в Интернете. Потом я посмотрел на принципы лечения России по боррелиозом Лайма, и я нашел их, и разделяет их.

В поисках русских руководящие принципы для лечения боррелиоза Лайма, я узнал немного о том, как Лайм боррелиоза рассматривается врачей и медицинских вузов России. Я знаю, что мое понимание пациентов ограничен, однако.

Поэтому я хотел бы спросить вас, если вы могли бы пожалуйста, ответьте на несколько вопросов для меня о боррелиозом Лайма. Вы можете ответить с именем пользователя блоггер или быть анонимными - либо все в порядке.

Единственным требованием является то, что вы ни были Лайм боррелиоза в прошлом, или у вас есть боррелиоз Лайма сейчас.

Пожалуйста, ответьте на вопросы ниже, используя следующие инструкции:


1) ответы на русском языке первый, так что поисковые системы будут забрать свой комментарий и больше россиян будут видеть и поощрять участие.


2) Далее ваш ответ России, пожалуйста, напишите английский копию ответа так английских читателей, здесь можно понять ваш ответ.(Используйте translate.google.com или иной русско-английский перевод программы вы считаете хорошим, чтобы перевести ваш ответ.)


3) Имейте в виду, что существует предел в 4000 символов для каждого ответа. Если у вас есть длинный ответ, вы можете сделать комментарий.


Пожалуйста, обратите внимание: Все комментарии модерируются, то есть я рассматриваю их, прежде чем отправлять их в Интернете. Там может бытьзадержка между временем, когда вы входите в комментарий, и он показывает на странице. Я делаю это, чтобы избежать случайного спама и маркетинговыхсообщений.



Ну, вот ваши вопросы:


1) Есть ли у вас Лайм боррелиоза в прошлом?


2) Есть ли у вас боррелиоз Лайма сейчас?


3) Какие этапы или шаги Лайм боррелиоза у вас было в прошлом?Сейчас?


4) Было ли у вас укуса клеща и "быки глаз" сыпь?


5) Как долго времени между укусом клеща и лечение антибиотиками?


6) Какие у вас были симптомы?


7) Как долго вы были или вы больны?


8) Какое лечение вы получили для боррелиоза Лайма?


9) Как долго вы используете антибиотики?


10) Какие еще лекарства и методы лечения вы получите за Лайм боррелиоза (не антибиотики)?


11) После лечения, как здорово ты? Есть ли у вас остальные симптомы?Если да, то каковы ваши оставшиеся симптомы?


12) Как вы думаете, боррелиоз Лайма может быть хронической инфекции - даже после лечения антибиотиками? Считаете ли вы, никаких симптомов после лечения антибиотиками, свидетельствуют о аутоиммунное заболевание?


Спасибо за ваши ответы.Я понимаю, это очень много вопросов, но важно знать, какие проблемы у пациентов с Лайм-боррелиозом лица по всему миру. После Лайм боррелиоза является хроническим, то становится труднее лечить, и зная, как другие люди справляются с этой болезнью может быть полезным.


PS: Если вы знаете другие русские, которые пострадали с боррелиозом Лайма, пожалуйста, присылайте их сюда и попросить их ответить на эти вопросы тоже.


PPS: Я прошу прощения за использование Google Translate - это лучшее, что я мог сделать.

Dear Russian readers of this blog,

Thank you for visiting and reading Camp Other blog.

Recently, I learned from a reader who was treated for Lyme Borreliosis in Serbia that both the kind of antibiotics chosen and length of treatment was different from that which we usually receive in the United States.

As a result, I was curious about what different guidelines are for the treatment of Lyme Borreliosis in different countries. I looked for Serbia's treatment guidelines, but could not find them on the internet. Then I looked for Russia's treatment guidelines for Lyme Borreliosis, and I did find them, and shared them.

While searching for the Russian treatment guidelines for Lyme Borreliosis, I learned a little about how Lyme Borreliosis is viewed by doctors and medical universities in Russia. I know that my understanding about patients is limited, though.

So I would like to ask you if you could please answer a few questions for me about Lyme Borreliosis. You may answer with a blogger user name or be anonymous - either is okay.

The only requirement is that you have either had Lyme Borreliosis in the past or you have Lyme Borreliosis now.

Please answer the questions below using these instructions:

1) Respond in Russian first, so that search engines will pick up your comment and more Russians will see it and be encouraged participate.

2) Below your Russian response, please post an English copy of your response so the English readers here can understand your response. (Use translate.google.com or another Russian-English translation program you think is a good one to translate your response.)

3)  Be aware that there is a 4,000 character limit for each response. If you have a long response, you may want to make a new comment.

Okay, here are your questions:

1) Have you had Lyme Borreliosis in the past?

2) Do you have Lyme Borreliosis now?

3) What stages or steps of Lyme Borreliosis did you have in the past? Now?

4) Did you have a tick bite and a "bulls eye" rash?

5) How long was the time between the tick bite and antibiotic treatment?

6) What were your symptoms?

7) How long were you or are you sick?

8) What treatment did you receive for Lyme Borreliosis?

9) How long did you use antibiotics?

10) What other medicines and treatments did you receive for Lyme Borreliosis (not antibiotics)?

11) After treatment, how healthy are you? Do you have any remaining symptoms? If so, what are your remaining symptoms?

12) Do you think Lyme Borreliosis can be a persistent infection - even after antibiotic treatment?  Do you think any symptoms after antibiotic treatment are evidence of an autoimmune disorder?

Thank you for your answers.

I realize these are a lot of questions, but it's important to know what problems patients with Lyme Borreliosis face around the world. Once Lyme Borreliosis is chronic, it becomes harder to treat and knowing how other people are managing this disease could be helpful.

PS: If you know of any other Russians who have suffered with Lyme Borreliosis, please send them here and ask them to respond to these questions, too.

PPS: I apologize for using google translate - it's the best I could do.

Image credit:

English: Tomsk I railway station, Russia

Русский: Вокзал станции Томск I, Россия

by Alexander V. Solomin from Wikimedia Commons

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2 More Thoughts On Birds, Cool Shirts, And My Evil Twin?

More On Ticks And The Atlantic Flyway:

I continue to think about the role of birds carrying ticks to different regions and how Lyme disease (and other tickborne infections) could be spread that way. But much as I found the overlay map I posted earlier this week to be intriguing, I don't think that tracking infected ticks on birds is as simple as following major and principal flyways - even though that could be a reasonable point to start an investigation.

Yale has already done some work in this area, and I have no idea whether or not they've factored the results of this publication, "Do birds affect Lyme disease risk? Range expansion of the vector-borne pathogen Borrelia burgdorferi", into their recently published Lyme disease risk map.

It's important not to discount the role of birds here:

"Although the role of birds in B burgdorferi transmission dynamics is often discounted, data compiled from published studies indicate that the majority (58.6%) of bird species that have been evaluated are capable of infecting larval I scapularis with B burgdorferi. We estimated – for two bird species – that the number of individual birds required to produce one infected I scapularis larva is as low as three, and we conclude that bird-mediated tick movement is an important factor in the range expansion of both I scapularis and B burgdorferi."

Read More: http://www.esajournals.org/doi/abs/10.1890/090062

There are certain behaviors birds engage in and seasonal activities which would lead to a higher likelihood of birds contributing to the spread of Lyme disease on the ground. Specific kinds of birds would be more likely to contribute to infection spread than others - for example, I suspect birds which build their nests on the ground and are ground-based hunters are more likely to contribute to infected tick populations than birds which build their nests in trees. Also, some birds feast on ticks (such as guinea fowl) and they will lower local tick populations.

These are just a few examples - there are many more. I imagine there is no simple algorithm for determining the role for birds in spreading infection. I don't know what all the factors are which would contribute to the spread of Lyme disease via birds, and it's something I continue to look into because it does play an important role in surveillance and determining how infection could spread through different vectors.

Photo credit: Andreas Trepte, www.photo-natur.de

Cool Lyme Disease T-shirts:

While doing a general search for Lyme disease related news the other day, I came across these shirts on Cafe Press:

I think they must have had me in mind as a target demographic, because it's the first Lyme disease related t-shirt that  I've seen which appealed to my appreciation of the TV show, "The Big Bang Theory", and also appealed to my appreciation on word play while mentioning Lyme disease research. It says "More nervous tics than a Lyme disease research facility"- playing on the word "tics" or "ticks".

There are a number of products for sale with this slogan on it (not just t-shirts) at Cafe Press  -  I don't know who is selling them and if they're another Lyme disease patient or not - the product page did not display this information. Check it out if you think it's something you'd like, too.

My Evil Twin?

It's been pointed out to me that I have a doppelganger online named Tom Carolan. He has Lyme disease blog, Tick Borne Diseases Radio, with entries in it which upon reading looked strikingly similar to my own blog at first glance. However, after more examination,  it's clear Tom's blog contains different content and his own unique commentary on the same topics which have grabbed my attention.

(Just so everyone knows, I have no problem with anyone passing on the content I write here as long as you give this blog credit and link to it. That's why I have a Creative Commons license posted at the bottom of each entry - so you know I support a more open source approach to copyright.)

Tom also has a podcast on iTunes on Tick Borne Diseases:
http://itunes.apple.com/us/podcast/tick-borne-disease-radio/id306917344

How about going over there to Tom's site and giving it a good read, and encouraging him to continue to post more podcasts and blog entries? It looks like he has a good thing going on and more content like his would be welcome - particularly more podcasts.

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7 The New Tick Map Vs. The Atlantic Flyway: Things That Make You Go Hmm.

[Ed. - Overlay map revised Feb. 9, 2012.]

Well, I guess everyone has seen this map from Yale University by now...

Yes, it is a map of Lyme disease risk areas based on tick flagging from 2004-2007 in the above regions, followed by an analysis of those ticks. No matter where one looked, the odds of a tick carrying Borrelia burgdorferi were 1 in 5 everywhere... So be careful out there, huh?

While it's good to let people know there are transition areas where Lyme disease is up and coming, it's good not to be too complacent if you fall into a green zone. Today's low risk zone can be tomorrow's transitional area, and these maps must be accurately updated in order to reflect reality.

Thing is, I haven't been thinking of this map as regards tick distribution and Lyme disease so much as I've been thinking about this map:

Because there is evidence that ticks' distribution is spread not only by mammals which hug the ground - but can also be spread geographically by birds. 

So look at the above two maps. Now look at this, after I scale and resize them to overlap (somewhat off-bias, but best I could get with different projections):

Questions for my readers:

• For those of you along the southern principal flyway, how many of you received an infected tick bite near that flyway, either to its north or south?
• For those of you in northeastern and north central Florida, how many of you received an infected tick bite near that flyway passing over your state?
• For those of you in eastern Canada, can you tell me if you received an infected tick bite near that flyway by the Great Lakes?

I'm looking at this and wondering a few other things, too, like I think these flyways would end up moving a little further north as global warming progresses - so I would expect a greater distribution of infected ticks further north as time goes on. Is there any way to confirm this is what is happening?

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0 Poll: Cause Of Post Treatment Lyme Disease Symptoms

A couple months ago, a non-scientific poll was placed on the site which asked readers to select from a number of choices for what they think causes post treatment Lyme disease symptoms: persistent infection, an autoimmune disorder, b-cell dysfunction, all of the above, and none of the above.

During the two months the poll was open, only 18 votes were cast by readers who were given the option to select more than one response. 

This time, the poll will be open again with the same question - and in the interest of collecting more votes,  the poll will be open to voting for one year. Also, additional choices will be given (molecular mimicry, metabolic disorder, and immunosuppression) for readers to select. After the poll is closed, the results will be reported and further discussion of each of these choices will go on.

As it stands, of the 18 responses given in two months' time from the old poll, 10 responses stated that post treatment lyme disease symptoms are caused by a persistent infection, 3 stated that they are caused by an autoimmune disorder, one stated they are caused by a b-cell dysfunction, and 7 stated they are caused by all of the above.

We'll see what kind of responses are received on the new poll as time goes on...

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0 Freedom Of Information Request On Vancouver Complex Chronic Disease Clinic

The Vancouver Sun recently reported on the results of a freedom of information request on the upcoming Complex Chronic Disease clinic in Vancouver, Canada. Gwen Barlee, Lyme disease advocate, was disappointed with the results of her request, saying that she thought "the government appears to be dropping the ball again on taking a proactive approach to managing, diagnosing and treating Lyme disease in British Columbia."

Both pros and cons of the clinic are examined in this article.

Read More Here: http://blogs.vancouversun.com/2011/12/28/freedom-of-information-request-yields-info-about-lyme-other-chronic-diseases-clinic-opening-at-bc-womens-hospital/

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0 Science Article: Oral Bacteria Opens Door To Allow Pathogens In

In today's Science Daily, there is an article on a study showing how one specific oral bacteria, Fusobacterium nucleatum, can provide a gateway for other bacteria to enter human blood vessels and make people sick.

READ MORE Here: http://www.sciencedaily.com/releases/2011/12/111215113521.htm

Original Source:
Yann Fardini, Xiaowei Wang, Stéphanie Témoin, Stanley Nithianantham, David Lee, Menachem Shoham, Yiping W. Han. Fusobacterium nucleatum adhesin FadA binds vascular endothelial cadherin and alters endothelial integrity. Molecular Microbiology, 2011; 82 (6): 1468 DOI: 10.1111/j.1365-2958.2011.07905.x

Reading this reminded me of an earlier post and comments I made about a paper by Judith Miklossy: Alzheimer's disease - a neurospirochetosis.

In my comments there, I stated:

"I think it's possible that infection can be part of the precursor or a cascade effect that gets the ball rolling towards Alzheimer's Disease (AD) - but the question remains: Why do plenty of people have Bb or HSV-1 or any of a number of infections who do not develop AD?"

Maybe this is what makes the difference. Maybe Fusobacterium nucleatum has to cross the endothelium and open the gate for bacteria such as Bb or oral Treponema to cross the blood-brain barrier. If Fusobacterium nucleatum can travel to the brain first, then perhaps these other bacteria will follow on its heels and lead to neurological damage.

It seems further studies to seek Fusobacterium nucleatum in brain biopsies alongside other bacteria could provide some evidence that this is what has happened.

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0 Comments On 2011 Lyme and TBD Conference Summaries

I have a few comments to make as they come up on October's 2011 conference.

I may add and repost to this entry a few times - stay tuned.

1) I looked at this part of the summary on Dr. Reinhard K. Straubinger's talk on “Canine and Equine Lyme Borreliosis” focused on Lyme borreliosis in animals, especially in dogs and horses:

"The highly variable surface protein VlsE is, according to current knowledge, exclusively expressed in the mammalian host. The invariable region IR6, and even a shorter peptide sequence of IR6 called C6 were found having a high potential as specific antigenic components in serologic test systems. This was shown by evaluating sera from infected humans, dogs, monkeys and mice. In experimentally infected dogs, C6-specific IgG antibodies appeared 3 weeks post infection; hence almost one week earlier than antibodies detected with ELISA based whole-cell preparations. Additionally, another benefit became clear when testing sera of people and dogs before and after antibiotic treatment. Contrary to antibodies against whole-cell components, research demonstrates that C6-antibodies declined substantially a few months after treatment. However, in animals with low C6-antibody levels prior to treatment, the decline obviously was minimal post treatment. Despite their high specificity for borrelial contact, C6-antibodies do not necessarily correlate with clinical signs in dogs and false-positive results may result from maternal antibodies in puppies born to infected bitches."

It brought to mind the following paper and a passage within it:

Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation. Stefan S. Tunev, Christine J. Hastey, Emir Hodzic, Sunlian Feng, Stephen W. Barthold, Nicole Baumgarth.

Source: http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1002066

"We did not include the VlsE protein in our studies, a surface-protein thought to subvert the immune response to B. burgdorferi through extensive genetic variation within the host. However, the N40 strain of B. burgdorferi, which we have used here, does not seem to express this protein, based on transcriptional analysis of the IR6 region of vlsE. Moreover, we found no evidence of seroconversion to the C6 antigen of vlsE from strain B31 (S. W. Barthold, unpublished). Recent sequence analysis of the N40 genome has confirmed that N40 vlsE and BBK01 are on different plasmids and that the vlsE locus is indeed significantly different compared to B31, the commonly used VlsE-expressing Borrelia-strain."

So what do we know about C6 tests, briefly?

C6 Lyme ELISAs are based on the synthetic peptide C6, which corresponds to the invariable region IR6 of the surface antigen VLsE.

IR6 is supposed to be highly preserved in all pathogenic strains of Borrelia, and is only expressed in vivo. It evokes a strong immune response.

As a diagnostic antigen, the C6 peptide shows only minor cross-reactivity to other pathogens (e.g. spirochetes for syphilis).

Knowing this, it's interesting to point out that using the C6 ELISA may not work as well for testing a host which is infected with a strain of N40 Borrelia. How can it, when this strain of N40 does not express the vlsE protein?

I have to wonder how many other strains may have vlsE on different plasmids - and not only that - a different locus?

2) Dr. John Aucott’s talk on “Early Lyme disease” reported from the SLICE prospective cohort and his Maryland studies. I want to point out this part of the summary:

"He emphasized that the classic description of a “bull’s eye rash” occurs only 20% of the time – it is not the most common manifestation of the Lyme rash. Rather, a uniformly red or reddish-blue rash, round or oval in shape, with sharply demarcated borders is most common. Most often the rash develops in places such as the knee, groin, or arm pit, occurring at prime tick season, such as the late spring and early summer."

It's important to know that these varied descriptions of so-called "bull's eye" or EM rashes found in Lyme disease are not the only variations found in Lyme disease culture positive lesions.

In an earlier entry about Dr. Vijay Sikand's testimony at an FDA Lymerix Vaccine Review, Dr. Vikand reported this about EM rashes:

"[...] However, erythema migrans is not a single beast. Certainly this is the one which we easily recognize and which I just referred to.Before I continue with further slides, let me point out that the erythema migrans lesions you are about to see are all biopsy lesions which were laboratory proven to be caused by Borrelia burgdorferi.

Sometimes erythema migrans can present as a pustular lesion as is this one in the popliteal fossa inviting the scalpel of a surgeon.

Sometimes the lesions are vesicular in nature, inviting a diagnosis perhaps of herpes simplex infection.

Sometimes our round lesion is actually triangular.

Sometimes it doesn't even look round or red at all and invites a diagnosis of an intertriginous fungal infection in the groin of this patient who was biopsied and proven to have Lyme disease.

Sometimes the lesion is more plaque-like, inviting diagnosis of nummular eczema, psoriasis, or other similar lesions.

Sometimes it is in unusual locations.

Sometimes it is large like this one. Sometimes it is small with satellite areas. Sometimes it is multiple, appearing almost like urticaria or erythema multiform.

Sometimes, as in this individual who was a placebo recipient in the Lyme 008 SmithKline Beecham trial, it presents with other manifestations of early dissemination. This individual came in mainly because he was concerned about his face and it felt kind of funny and it was weak on one side. When I asked him whether he had had any unusual rashes, he said oh do you mean this one, and he showed me his arm with that EM. This is simply to illustrate the infranuclar 7th nerve palsy with which he presented. This patient, by the way, had no history of a tick bite or any unusual antecedent illness which he could remember."

If Sikand's testimony is anything to go on, one has to wonder about the reliability of the "bull's eye rash" as a diagnostic marker.

(For what it's worth, my own EM rash was large, oval, dark red, slightly elevated, and expanding for several days after the bite.)

3) Dr. Karen Newell Rogers presented a talk about novel ways to target chronic inflammation and chronic immune activation among patients with chronic Lyme disease.

Now this part below - especially in bold - really caught my eye:

"[...]Some researchers would argue that chronic inflammation requires the continuous presence of bacteria, whereas others would suggest that continuous presence of bacteria does not always result in inflammation and that exacerbations of chronic symptoms could result from infection with a different organism--or that chronic symptoms could re-cur from unrelated pro-inflammatory events. Potentially reconciling these seemingly conflicting perspectives on the mechanism of Lyme disease may be the effect of Borrelia burgdoreri’s bacterial by-products on Toll Like Receptors, (TLR)-mediated immune activation. TLR appear to be the “gate-keepers” of an inflammatory response. Bacteria, including Borrelia, produce products that, by binding to TLRs on the cell surface, promote leukocyte activation, cytokine production, and acute inflammation. In some genetic backgrounds of mice, acute inflammation is sufficient to fight off infection and resolve disease. In other mouse strains, the pathogens, or in this case the bacteria, get past TLR-induced inflammation and remain symptomatically undetectable in cells and tissues (Barthold, etc); Barthold et al. have found that no matter how severe or mild the disease in any of the genetically inbred strains of mice, there was no more inflammatory disease when the bacteria were eliminated."

Reading this, I reflect back on an earlier entry I made about the combination of genetics effect on individual immune systems AND persistent infection as both leading to ongoing symptoms in hosts:

Immune + Infection = HLA-DR alleles determine responsiveness to Borrelia burgdoferi:
http://campother.blogspot.com/2011/08/immune-infection-hla-dr-alleles.html

Perhaps part of the answer to what is happening with ongoing symptoms lies both in Dr. Newell Rogers' work and Bettina Panagiota Iliopoulou, Mireia Guerau-de-Arellano, and Brigitte T. Huber's research?

It's certainly thought-provoking.

And Barthold's statement implies that ongoing inflammation is intimately tied to persisting infection.

How does one provide evidence this is the case?

Could the answer lie in longer term in vivo GFP and/or iRFP studies on mice and other mammals? Could it lie in maltodextrin enhanced imaging studies? Or something else?

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0 News: Judy Mikovits, CFS Researcher, Has Been Arrested

While not directly about Lyme disease, any news about Chronic Fatigue Syndrome (CFS) can be notable to the Lyme disease community as some patients have been diagnosed with CFS and any research on persisting fatigue and its cause has been of interest.

This is big news. While all the specifics behind the charges are unknown at this time, Retraction Watch just published that Judy Mikovits, a researcher involved in the XMRV controversy, has had a warrant out for her arrest for felony charges and was arrested in Ventura County, California, yesterday.

More information can be found here:
http://retractionwatch.wordpress.com/2011/11/19/chronic-fatigue-syndrome-researcher-judy-mikovits-arrested/

And here:
http://news.sciencemag.org/scienceinsider/2011/11/controversial-cfs-researcher-arr.html?ref=hp

Mikovits' court appearance is scheduled for Nov 22, 2011 at 1:30PM in the Ventura County Superior Court.

More details on this as the story unfolds.

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13 More on Genetic Haplotypes and Lyme Arthritis

So, the more I read, the more unanswered questions there are. Staying on top of all the latest research becomes a job in itself.

Earlier this week, I posted a variety of papers which showed a potential (according to the authors, statistically significant) relationship between haplotype and the development of chronic Lyme arthritis.

Then my attention was drawn to this 2008 paper, and I realized I shouldn't have stopped at papers in 2007 before writing my post about genetic haplotypes...

Human Homologues of a Borrelia T cell Epitope Associated with Antibiotic-Refractory Lyme Arthritis

Source:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2075570

Abstract

Antibiotic-refractory Lyme arthritis, which may result from infection-induced autoimmunity, is associated with HLA-DR molecules that bind an epitope of Borrelia burgdorferi (Bb) outer-surface protein A (OspA165−173) and with T cell reactivity with this epitope. One potential mechanism to explain these associations is molecular mimicry between OspA165−173 and a self-peptide.

Here, we searched the published human genome for peptides with sequence homology with OspA165−173. The two peptides identified with the greatest sequence homology with the OspA epitope were MAWD-BP276−288, which had identity at eight of the nine core amino acid residues, and T-span758−70, which had identity at six residues. MAWD-BP mRNA was expressed by synoviocytes, while T-span7 mRNA was not. However, neither peptide bound all of the HLA-DR molecules associated with antibiotic-refractory Lyme arthritis. Among 11 patients, nine had T cell reactivity with OspA161−170, six had responses to MAWD-BP276−288, and three had reactivity with T-span758−70, but reactivity with the self-peptides was lower than that induced by the spirochetal epitope.

Thus, there remains an association between OspA165−173 and antibiotic-refractory Lyme arthritis, and infection-induced autoimmunity is an attractive hypothesis to explain this outcome. However, molecular mimicry due to sequence homology between OspA165−173 and a human peptide seems unlikely to be the critical mechanism.

---

I suppose I have to keep reading more research?

What's the present model for the cause of chronic Lyme arthritis these researchers are supporting again?

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24 Do Different Genetic Haplotypes Matter?

It seems people are still holding on to the HLA-DR2 and HLA-DR4 concept of subgroup autoimmunity (subgroups of Lyme disease patients who do not respond to additional antibiotic treatment) in the Lyme disease community.

I get the impression that hypothesis has been dropped by a number of researchers in favor of a new one - except in the case of patients with Lyme arthritis. (I don't think HLA-DR2 is associated with Lyme disease, either, and HLA-DR4 is associated with Lyme arthritis.)

I came across this recently:

National Institute of Allergy and Infectious Diseases, NIH: Impact on Global Health (2009) by Vassil St. Georgiev, PhD

Chapter 22.1 Lyme Disease (Lyme Borreliosis, Lyme Arthritis)
Section 22.1.5.4 The Role of Autoimmune Reactivity in Lyme Disease

"In NIAID-supported clinical studies, case subject patients with PTCLD* were compared with control subjects without such symptoms for the presence of several human leukocyte antigen (HLA) class II (DRB1 and DQB1) genetic markers, some of which are known to be associated with the expression of autoimmune reactivity. The results obtained did not support the involvement of an autoimmune mechanism in PTCLD (24). However, because not all autoimmune diseases are associated with specific HLA haplotypes, these findings do not necessarily exclude that possibility. Definitive proof would clearly involve demonstrating the presence of significant levels of relevant autoimmune antibodies and/or autoreactive T cells in patients with PTCLD but not in treated control subjects without such symptoms. A greater frequency of DRB1*0401, which has been reported to be associated with antibiotic-treatment-resistant arthritis, was noted in the case subject patients; although this finding appeared to be nominally significant (p < 0.05), its biological significance is ambiguous because none of the case subjects considered had symptoms of inflammatory arthritis. (http://www3.niaid.nih.gov/research/topics/lyme/research/autoimmune/)"

* In this NIAID-NIH document, PTCLD stands for Post Treatment Chronic Lyme Disease.

24) Klempner MS, Wormser GH, Wade K, Trevino RP, Tang K, Kaslow R, and Schmid C. (2005) A case-control study to examine HLA haplotype associations in patients with posttreatment chronic Lyme disease. J. Jinfect. Dis. 192(6), 1010-1013.

Now this is an interesting piece of information.

This book from the NIAID-NIH is stating following about patients with PTCLD in NIAID-supported studies:

1) Patients with chronic Lyme disease were compared against control subjects with the same genetic markers and the results did not support an autoimmune mechanism for chronic Lyme disease.

2) Not all autoimmune diseases are associated with specific haplotypes.

3) Those patients with chronic Lyme arthritis have had their condition strongly associated with DRB1*0401.

4) None of the case subjects in trials had inflammatory arthritis. None.

I find this particularly interesting since the one statement many patients have made is that some researchers have pegged chronic Lyme disease patients as having an autoimmune disorder, when the research in this regard is fuzzy. What indicates to some researchers today that post-treatment chronic Lyme disease is an autoimmune disorder, if it isn't specific haplotypes which are at risk of developing persisting symptoms?  A different molecular mimicry model than that which leads to Lyme arthritis? A different model of persisting symptoms entirely?

I also find it interesting that none of the case subjects had inflammatory arthritis. I don't know how clinicians defined the criteria for inflammatory arthritis and if they did any serology for inflammation, but I can say that I have had joint swelling, muscle pain, and shooting nerve pain during the course of my illness. That none of the case subjects in trials had inflammatory arthritis comes as a surprise to me.

According to research there is a relationship between a specific haplotype and Lyme arthritis. This is just one such example:

From Persistent arthritis in Borrelia burgdorferi-infected HLA-DR4-positive CD28-negative mice post-antibiotic treatment. Iliopoulou BP, Alroy J, Huber BT. Arthritis Rheum. 2008 Dec; 58(12):3892-901.:

"METHODS:We have previously shown that CD28(-/-) mice develop intermittent monarticular Lyme arthritis that is responsive to antibiotics. Since there seems to be a link in humans between persistent arthritic manifestations post-antibiotic treatment and the HLA-DR4 allele, we generated DR4+/+CD28(-/-)MHCII(-/-) mice, infected them with Borrelia burgdorferi, and subsequently treated them with antibiotics.

RESULTS: Thirty-eight percent of the B burgdorferi-infected DR4+/+CD28(-/-)MHCII(-/-) mice, but none of the B burgdorferi-infected CD28(-/-)MHCII(-/-) mice, remained arthritic post-antibiotic treatment. A significant fraction (36%) of these mice, but none of the mice in which arthritis resolved, had serum antibodies to outer surface protein A of B burgdorferi. After abrogation of active B burgdorferi infection, the inflammatory reaction in mice with persistent joint inflammation was restricted to the joints, since their draining lymph nodes were no longer enlarged. Increased CD20 and interferon-gamma messenger RNA expression in the inflamed joints of these mice suggested a possible role of B cells and inflammatory cytokines in the pathogenesis of persistent arthritis post-antibiotic treatment.

Conclusion: The establishment of this murine model allows, for the first time, the elucidation of the immunologic events that lead to persistent Lyme arthritis post-antibiotic therapy in genetically susceptible individuals."

So according to this, little over a third of the mice with a specific allele remained arthritic after antibiotic treatment, and of this third, about a third of them developed antibodies to OspA.

My questions are: How is it that the remaining roughly two thirds of the mice did not remain arthritic? How is it that two thirds of them did not develop antibodies to OspA?

There are many papers written about the association between specific alleles and development of chronic Lyme arthritis:

1993 - Association of treatment-resistant chronic Lyme arthritis with HLA-DR4 and antibody reactivity to OspA and OspB of Borrelia burgdorferi.

2001 - Autoimmune mechanisms in antibiotic treatment-resistant lyme arthritis. (This is where molecular mimicry as a cause of Lyme arthritis is mentioned.The abstract states: "...only one human protein was identified, lymphocyte function associated antigen-1 (hLFA-1), that had sequence homology with OspA (165-173) and predicted binding in the DRB1*0401 molecule.")

2004 - Molecular characterization of the OspA(161-175) T cell epitope associated with treatment-resistant Lyme arthritis: differences among the three pathogenic species of Borrelia burgdorferi sensu lato. (Borrelia that causes Lyme disease in Europe does not usually lead to chronic Lyme arthritis.)

2006 - Antibiotic-refractory Lyme arthritis is associated with HLA-DR molecules that bind a Borrelia burgdorferi peptide (Concluded that binding of a single spirochetal peptide to certain DRB molecules is a marker for antibiotic-refractory Lyme arthritis and might play a role in the pathogenesis of the disease.)

2007 - Clonal Diversification in OspA-specific Antibodies from Peripheral Circulation of a Chronic Lyme Arthritis Patient

A number of these are Steere's papers - not surprising since he has written so much about the rheumatological aspect of Lyme disease. And some of it is not his research, and I could find a few more by others.

I'm looking for more research on chronic Lyme disease's connection to haplotypes and alleles outside of the Lyme arthritis model. The NIAID-NIH book, written in 2009, states there is no connection.

So to sum up:

1) Particular alleles or haplotypes are not associated with chronic Lyme disease as a whole.

2) Particular alleles or haplotypes are associated strongly with chronic Lyme arthritis.

Hm.

Glossary

allele: is one of two or more forms of a gene.Sometimes, different alleles can result in different traits, such as color. Other times, different alleles will have the same result in the expression of a gene. See more info. at: http://en.wikipedia.org/wiki/Allele

haplotype: a combination of alleles (DNA sequences) at different places (loci) on the chromosome that are transmitted together. A haplotype may be one locus, several loci, or an entire chromosome depending on the number of recombination events that have occurred between a given set of loci.See more info. at: http://en.wikipedia.org/wiki/Haplotype

Additional information: http://en.wikipedia.org/wiki/Category:HLA-DR_haplotypes

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16 Abstract: Chronic Tick Associated Poly-organic Syndrome

Diagnosis and treatment challenges in patients with chronic Tick Associated Poly-organic
Syndrome (TAPOS) - Case series
A. Radulescu, M. Flonta, D. Tatulescu
University of Medicine and Pharmacy, Cluj, Romania,
The Teaching Hospital of Infectious Diseases, Cluj, Romania
Int J Infect Dis 2010;14

Background: Chronic Lyme disease is often considered in case of long lasting miscellaneous symptoms after tick bites. Despite new codified diagnosis algorithm and treatment persistent signs and symptoms frequently occur. The aim of the study was to assess the diagnosis of Tick Associated Poly-organic Syndrome (TAPOS) and to evaluate the treatment’s efficacy.

Methods: A consecutive case series of patients referred to the Cluj-Napoca Teaching Hospital of Infectious Diseases (January 2006 -October 2009) revealed 52 patients with TAPOS. Inclusion criteria were: more than 18 years of age, chronic symptomatology, positive Borrelia burgdorferi serology and/or tick-bite. Data was collected through chart review and medical observation. We used two clinical scores classifying the diagnosis of TAPOS. All patients were seropositive for IgM and/or IgG antibodies to Borrelia burgdorferi (EIA and western blotting). Treatment regimen was established according to the literature data. They received intravenous ceftriaxone, 2 g daily for 21-28 days and doxycyline 200 mg daily for 21 days. Patients with persistent symptoms were retreated with the same regimen.

Results: The baseline assessment documented that the most frequently reported symptoms were neuropsychological (90%), systemic (98%) and articular (23%). The sex ratio was 0.26 (41 women, 11 men), the average age was 43.2 ±12.6 years. Only 7 patients experienced erythema migrans, 57% had tick exposures and Borrelia burgdorferi serology was 92% positive [44 (84%) IgM positive, 19 (36%) IgM and IgG positive]. According to both clinical scores all patients were classified as “very probable” or “probable”. All patients were evaluated at 3 months showing a decrease in the number and intensity of signs and symptoms and the same serologic pattern. Ten patients were 2-3 times retreated due to persistent clinical picture, all presenting mood disorders or depression. No case of clinical aggravation or serious adverse events was reported and Jarish-Herxheimer syndrome was observed just in two cases. Most of the patients remained with at least one neuropsychological complaint.

Conclusion: Diagnosis of miscellaneous Borrelia burgdorferi chronic infection is challenging but should be always considered if prolonged symptomatology or tick related. Treatment regimens are not standardized, we appreciate as reasonable shorter 6 week regimens.

---

Comments: 

First of all, "Tick Associated Poly-organic Syndrome" or TAPOS - is this a new name Romanian doctors have come up with for what Dr. Benjamin Luft was referring to as a "Lyme Borrelia Complex" at the IOM workshop in October 2010 - or instead of Chronic Lyme disease? It's an interesting name, and I'm wondering where the "Poly-organic" part comes in.

The statements "Ten patients were 2-3 times retreated due to persistent clinical picture" and "All patients were evaluated at 3 months showing a decrease in the number and intensity of signs and symptoms and the same serologic pattern", caught my eye. Presumably, those ten patients also experienced a decrease in the number and intensity of symptoms as well as in their serologic pattern - so retreatment was a benefit for them.

So, let's look at the treatment: "They received intravenous ceftriaxone, 2 g daily for 21-28 days and doxycycline 200 mg daily for 21 days." Should one assume based on their report that those ten patients were treated with up to 4 months of  IV ceftriaxone plus 84 days of doxycycline - or is that off? Two to three times the baseline treatment seems to put the upper range in that ballpark.

"No case of clinical aggravation or serious adverse events was reported and Jarish-Herxheimer syndrome was observed just in two cases."

Boy, does that sound very different from the other reports from the American clinical trials on extended antibiotic treatment for chronic Lyme disease. One of the reasons extended treatment with IV antibiotics was recommended against was because of serious adverse events such as line infections. On a large scale, how often do line infections occur in thousands of patients worldwide? It's a risk, but is it that difficult to prevent with proper care?

I find it interesting that these case studies were shown at a poster session at the 14th ICID. An international professional infectious disease conference - pretty much showing a conclusion where chronic infection treatment is mentioned as not being standardized and setting 6 week regimens as being reasonable.

Wait a minute... doesn't this case series treatment study sound very similar to one of the American clinical trials on extended antibiotic treatment for chronic Lyme disease?

[Camp Other goes to new window, googles...]

I guess it is somewhat similar to the 2001 Klempner trials, but the fact that multiple retreatments were permitted under the case studies are a noted difference among other differences. I think for me, I'm wondering what the full text stated, and not just the abstract - in order to see the authors' line of reasoning on the dosage and regimen - but also wondering why there was only a three month followup on patients after treatment? Where are these post-treatment Romanians today, and how are they doing?

I have more questions...

Patients had the following serology at the start of their studies: [44 (84%) IgM positive, 19 (36%) IgM and IgG positive. How was it IgM positive-only patients were included in the study, when other researchers have stated that a sustained IgM response to Bb with no IgG response means the test was a false positive? (I'm not pushing this idea, as I am still working on the whole "how are new and newly intense IgM bands significant" issue - just putting it out there for the overview.)

"All patients were evaluated at 3 months showing a decrease in the number and intensity of signs and symptoms and the same serologic pattern."

Two questions here: What symptoms and signs did they have to begin with, and what changed, objectively and subjectively?

What does it mean to state in the above sentence, "the same serologic patterns"? Did all patients serological results remain the same across the board despite treatment?

"Most of the patients remained with at least one neuropsychological complaint."

What is the cause or what are the causes of the neuropsychological complaints?

Also, even if the authors reported a decrease in the number of signs and symptoms of infection three months post-treatment, how close were patients to their pre-infective state of health? This is always the question for which I want an answer - especially after reading through the results of treatment trials mentioned in the IDSA 2006 Lyme disease treatment guidelines - results which did not always post a clear outcome of cure.

There are a lot of unanswered questions on this abstract - hopefully getting the full text some time will help in answering them.

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13 Lyme Disease Western Blots And Antigen Presentation

I've been thinking of this particular passage on page 504 of the book, Borrelia: Molecular Biology, Host Interaction and Pathogenesis:

"The general picture to have emerged over the years is that IgG and IgM antibodies to the spirochaete develop slowly and are directed against an increasingly diverse array of proteins as infection progresses (Craft et al, 1986; Dressler et al, 1993; Nowalk et al 2006). The earliest responses are to flagellin B (FlaB) and p66, followed by OspC (25kDa) with responses to a number of additional antigens, such as VlsE, fibronectin-binding protein (BBK32), FlaA (37kDa), BmpA (39kDa), and decorin-binding protein A (DbpA) developing as B. burgdorferi disseminates (Coleman and Benach, 1987; Engstron et al, 1995; Bacon et al 2003; Aguero-Rosenfeld et al 2005; Wilske et al, 2007). This temporal pattern is consistent with the notion that the bacterium draws upon an expanding repertoire of differentially expressed proteins once within its vertebrate host, including phased expression of paralogous surface-exposed lipoproteins.
[...]
The clinical ramifications of these observations are significant. Because approximately half of patients with EM do not mount detectable antibody responses to the pathogen, lack of seroreactivity cannot be used to rule out the diagnosis of EM (Steere, 2001; Dananche and Nadelman, 2008). Seroreactivity increases substantially following therapy for EM (Vaz et al, 2001; Dandache and Nadelman, 2008), indicating that killing of the bacterium enhances processing of spirochaetal antigens."

Prior to the 2006 IDSA Lyme disease guidelines, the first set of Lyme disease guidelines which were written contained this specific remark on laboratory criteria for diagnosis:

"Significant change in IgM or IgG antibody response to B. burgdorferi in paired acute and convalescent phase serum samples"

It seems to me that this would still be an important guideline to follow, yet I am aware of a number of stories where patients stated their family doctors gave them an ELISA blood test early after infection, were told it was negative, and because of this, were not given further testing.

This is an inappropriate response, especially given what is known about antibody response in Borrelia burgdorferi infection over time, and given the lack of adequate antibody response early in infection.

Retesting using the western blot several weeks after the initial test - even if negative - makes sense. And if someone is displaying unusually long and moderate-severe flulike symptoms even if there is no EM present, confirmation testing is sensible.

Given this is a serologically progressive infection, why isn't it possible to determine how far long the infection is to some degree (under delayed acute care, at the very least) if the antigens present in a specific order over time? In later infection, it is harder to detect - but doesn't ospA present itself again in neurological infection? Something I have to look into...

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