Borrelia – F.I.G.H.T for your health! http://lymebook.com/fight Linda Heming describes her Lyme disease healing journey Wed, 06 Nov 2013 05:54:37 +0000 en-US hourly 1 https://wordpress.org/?v=4.9.25 Lyme emergence in Brazil & IDSA denial http://lymebook.com/fight/lyme-emergence-in-brazil-idsa-denial/ http://lymebook.com/fight/lyme-emergence-in-brazil-idsa-denial/#respond Tue, 14 Jun 2011 04:59:23 +0000 http://lymebook.com/fight/?p=2514 Linda’s comment:  Where will it all end…..Lyme has become a world-wide epidemic, yet the ISDA boys/girls say there is not such thing as chronic Lyme!!  I don’t know where they went to medical school but they need to ask for a refund from their medical school.  Many of the IDSA members have written published studies on Lyme and the co-infections, yet they deny treatment to suffering people….

Link: http://www.scielo.br/pdf/bjmbr/v40n4/6497.pdf 

Excerpt:

An emerging clinical entity that reproduces clinical manifestations
similar to those observed in Lyme disease (LD) has been recently
under discussion in Brazil. Due to etiological and laboratory particularities
it is named LD-like syndrome or LD imitator syndrome. The
condition is considered to be a zoonosis transmitted by ticks of the
genus Amblyomma, possibly caused by interaction of multiple fastidious
microorganisms originating a protean clinical picture, including
neurological, osteoarticular and erythema migrans-like lesions. 

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Cell Fusion in Lyme http://lymebook.com/fight/cell-fusion-in-lyme/ http://lymebook.com/fight/cell-fusion-in-lyme/#respond Mon, 07 Mar 2011 16:31:33 +0000 http://lymebook.com/fight/?p=2225 Link: http://www.ncbi.nlm.nih.gov/pubmed/21276171

Excerpt:

Using cryo-electron tomography, we observed closely associated Borrelia cells. Some of these showed a single outer membrane surrounding two longitudinally arranged cytoplasmic cylinders. We also observed fusion of two cytoplasmic cylinders and differences in the surface layer density of fused spirochetes. These processes could play a role in the interaction of Borrelia species with the host’s immune system.

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Arthrobacter mysorens & skin reaction http://lymebook.com/fight/arthrobacter-mysorens-skin-reaction/ http://lymebook.com/fight/arthrobacter-mysorens-skin-reaction/#respond Mon, 14 Feb 2011 16:27:40 +0000 http://lymebook.com/fight/?p=2157 Link: http://www.biomedcentral.com/content/pdf/1471-2334-10-352.pdf

Excerpt:

Background

Skin erythemas of unknown origin are a frequent reason for consulting the general practitioner or dermatologist.

Case presentation

Here we report a case of an erythema resembling the erythema migrans manifestation of Lyme disease, but with atypical symptoms like persistent pruritus. The patient had no history of a recent tick-bite but displayed a positive serology for an advanced stage of Lyme borreliosis, which stood in contrast to the clinical manifestation of erythema migrans as a symptom of early Lyme disease. Three skin swabs and soil samples, collected in the area where the patient possibly acquired the infection, were examined by bacterial and fungal culture methods. Microorganisms were identified by using 16S rRNA gene sequencing and bioinformatics. The patient and soil isolates were compared by employing RAPD analysis. The serum samples of the patient were examined by immunoblotting. Arthrobacter mysorens, a soil bacterium, was isolated from the collected skin and soil samples. The identity of both isolates was determined by molecular fingerprinting methods. A.mysorens was proven to be causative for the erythema by direct isolation from the affected skin and a positive serology, thus explaining the atypical appearance of the erythema compared to erythema migrans caused by Borrelia infection.

Conclusions

Infections with A.mysorens might be underreported and microbiological diagnostic techniques should be applied in cases of patients with unclear erythemas, resembling erythema migrans, without a history of tick bites.

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Borrelia and inflammation http://lymebook.com/fight/borrelia-and-inflammation/ http://lymebook.com/fight/borrelia-and-inflammation/#respond Mon, 10 Jan 2011 00:31:00 +0000 http://lymebook.com/fight/?p=2018 Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21182088&retmode=ref&cmd=prlinks

Excerpt:

Borrelia burgdorferi spirochetes cause Lyme disease, which can result in
severe clinical symptoms such as multiple joint inflammation and
neurological disorders. IFN-gamma and IL-17 have been suggested to play an
important role in the host defense against Borrelia, and in the
immunopathology of Lyme disease.
The caspase-1-dependent cytokine IL-1beta has been linked to the generation
of IL-17-producing T cells, whereas caspase-1-mediated IL-18 is crucial for
IFN-gamma production. In this study, we show by using knockout mice the role
of inflammasome-activated caspase-1 in the regulation of cytokine responses
by B.
burgdorferi. Caspase-1-deficient cells showed significantly less IFN-gamma
and
IL-17 production after Borrelia stimulation. A lack of IL-1beta was
responsible for the defective IL-17 production, whereas IL-18 was crucial
for the IFN-gamma production. Caspase-1-dependent IL-33 played no role in
the Borrelia-induced production of IL-1beta, IFN-gamma or IL-17. 
In conclusion, we describe for the
first time the role of the inflammasome-dependent caspase-1 activation of
cytokines in the regulation of IL-17 production induced by Borrelia spp. As
IL-17 has been implicated in the pathogenesis of chronic Lyme disease, these
data suggest that caspase-1 targeting may represent a new immunomodulatory
strategy for the treatment of complications of late stage Lyme disease.
Copyright (c) 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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ILADS 2010 Conference Takeaways from Scott Forsgren http://lymebook.com/fight/ilads-2010-conference-takeaways-from-scott-forsgren/ http://lymebook.com/fight/ilads-2010-conference-takeaways-from-scott-forsgren/#respond Wed, 10 Nov 2010 05:22:27 +0000 http://lymebook.com/fight/?p=1867 Full article: http://betterhealthguy.com/joomla/blog/216-ilads-2010-conference-takeaways

Excerpt:

In October 2010, I attended the ILADS 2010 Annual event.  The event was packed.  Almost 400 people attended in person and over 1,000 people watched on the live webcast.  It is exciting to see so many people taking an interest in this controversial area of medicine.  The event was full of great information and people working hard to help us all find answers.

In this blog entry, I will share a few of the key takeaways that I learned at the event.  The slides from the event are available for purchase here for a very reasonable $40.  The DVDs (Friday’s sessions) and CDs of the presentations can be obtained from ZenWorks Productions.  Thus, I am not going to attempt to repeat information that is available elsewhere, but I will focus on some of the key things that caught my attention.

  • The 2011 ILADS event will be in Toronto, Canada – October 28-30, 2011
  • Dr. Richard Horowitz proposed that Chronic Lyme is really MCIDS  MultipleChronic Infectious Disease Syndrome
  • Biofilm treatment may be with EDTA or a Banderol/Samento combination.  There may be a strong antigen release with biofilm treatment which may make it a good candidate for pulsed therapy
  • Dr. Steve Harris mentioned that yeast may cannibalize dying Borrelia and that yeast is not always the result of antibiotic therapy alone.  He suggested up to 100 billion probiotic organisms daily.  In terms of diet, he said, “If it’s white, it ain’t right”
  • Minocycline may have longer toxic effects than doxycycline but has better CNS penetration.  Mino also has less sun sensitivity than doxy.  That said, Dr. Joe Burrascano commented that the effectiveness of minocycline may be regional as he never observed it working well in his patients

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Established and emerging pathogens in Ixodes ricinus ticks on an exotic island http://lymebook.com/fight/established-and-emerging-pathogens-in-ixodes-ricinus-ticks-on-an-exotic-island/ http://lymebook.com/fight/established-and-emerging-pathogens-in-ixodes-ricinus-ticks-on-an-exotic-island/#respond Thu, 04 Nov 2010 06:24:15 +0000 http://lymebook.com/fight/?p=1840 Article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20868431&retmode=ref&cmd=prlinks

Excerpt:

Tick-borne pathogens such as Lyme borreliosis spirochaetes,
Anaplasma phagocytophilum, Rickettsia spp. and Babesia spp. cause
a great variety of diseases in animals and humans. Although their
importance with respect to emerging human diseases is increasing,
many issues about their ecology are still unclear. In spring
2007, 191 Ixodes ricinus (Acari: Ixodidae) ticks were collected
from 99 birds of 11 species on a bird conservation island in the
Baltic Sea in order to test them for Borrelia spp., A.
phagocytophilum, Rickettsia spp. and Babesia spp. infections.
Identification of the pathogens was performed by polymerase chain
reaction (PCR), restriction fragment length polymorphism and
sequence analysis. The majority of birds with ticks testing
positive were European robins and thrushes. Borrelia DNA was
detected in 14.1%, A. phagocytophilum in 2.6%, rickettsiae in
7.3% and Babesia spp. in 4.7% of the ticks. Co-infections with
different pathogens occurred in six ticks (3.1%). The fact that
11 ticks (five larvae, six nymphs) were infected with Borrelia
afzelii suggests that birds may, contrary to current opinion,
serve as reservoir hosts for this species. Among rickettsial
infections, we identified Rickettsia monacensis and Rickettsia
helvetica. As we detected five Rickettsia spp.
positive larvae and two birds carried more than one infected
tick, transmission of those pathogens from birds to ticks appears
possible.

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Birds carry a multitude of infections on island near Baltic Sea http://lymebook.com/fight/birds-carry-a-multitude-of-infections-on-island-near-baltic-sea/ http://lymebook.com/fight/birds-carry-a-multitude-of-infections-on-island-near-baltic-sea/#respond Wed, 03 Nov 2010 17:10:48 +0000 http://lymebook.com/fight/?p=1836 Full article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20868431&retmode=ref&cmd=prlinks

Excerpt:

Tick-borne pathogens such as Lyme borreliosis spirochaetes,
Anaplasma phagocytophilum, Rickettsia spp. and Babesia spp. cause
a great variety of diseases in animals and humans. Although their
importance with respect to emerging human diseases is increasing,
many issues about their ecology are still unclear. In spring
2007, 191 Ixodes ricinus (Acari: Ixodidae) ticks were collected
from 99 birds of 11 species on a bird conservation island in the
Baltic Sea in order to test them for Borrelia spp., A.
phagocytophilum, Rickettsia spp. and Babesia spp. infections.
Identification of the pathogens was performed by polymerase chain
reaction (PCR), restriction fragment length polymorphism and
sequence analysis. The majority of birds with ticks testing
positive were European robins and thrushes. Borrelia DNA was
detected in 14.1%, A. phagocytophilum in 2.6%, rickettsiae in
7.3% and Babesia spp. in 4.7% of the ticks. Co-infections with
different pathogens occurred in six ticks (3.1%). The fact that
11 ticks (five larvae, six nymphs) were infected with Borrelia
afzelii suggests that birds may, contrary to current opinion,
serve as reservoir hosts for this species. Among rickettsial
infections, we identified Rickettsia monacensis and Rickettsia
helvetica. As we detected five Rickettsia spp.
positive larvae and two birds carried more than one infected
tick, transmission of those pathogens from birds to ticks appears
possible.

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Diversity of Borrelia Species in Ticks in Sweden http://lymebook.com/fight/diversity-of-borrelia-species-in-ticks-in-sweden/ http://lymebook.com/fight/diversity-of-borrelia-species-in-ticks-in-sweden/#respond Mon, 18 Oct 2010 06:02:53 +0000 http://lymebook.com/fight/?p=1768 Full article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20844223&retmode=ref&cmd=prlinks

Excerpt:

Members of the genus Borrelia are among the most common
infectious agents causing tick-borne disease in humans worldwide.
Here, we developed a Light Upon
eXtension(TM) (LUX) real-time PCR assay that can detect and
quantify Borrelia species in ticks that have fed on humans, and
we applied the assay to 399 such ticks. Borrelia PCR-positive
ticks were identified to species by sequencing the products of
conventional PCR performed using Borrelia group-specific primers.
There was a 19% prevalence of Borrelia spp. in the detached
ticks, and the number of spirochetes per Borrelia PCR-positive
tick ranged from 2.0 x 10(2) to
4.9 x 10(5) with a median of 7.8 x 10(3) spirochetes. Adult ticks
had a significantly larger number of spirochetes with a median of
8.4 x 10(4) compared to the median of nymphs 4.4 x 10(4). Adult
ticks also exhibited higher prevalence of Borrelia (33%) compared
to nymphs (14%). Among the identified species, Borrelia afzelii
was found to predominate (61%), followed by B. garinii (23%), B.
valaisiana (13%), B. burgdorferi sensu stricto (1%), B.
lusitaniae (1%), and B. miyamotoi-like (1%). Also, 3% of the
ticks were co-infected with multiple strains of B. afzelii.
Notably, this is the first report of B.
lusitaniae being detected in ticks in Sweden. 

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Insanity virus — a crazy idea? http://lymebook.com/fight/insanity-virus-a-crazy-idea/ http://lymebook.com/fight/insanity-virus-a-crazy-idea/#respond Sun, 03 Oct 2010 05:20:59 +0000 http://lymebook.com/fight/?p=1706 This research about the “insanity” virus has not stopped, and in fact, the more you read up on endogenous retrovirus the more you will see that this all further reinforces my FIGHT4yourhealth concept. The June Discover magazine on the newsstands brings this story up to date but the more you become interested in the infection component of today’s epidemic of impaired health, the more you will see how this infection from endogenous retroviruses found in what we used to call our JUNK DNA, helps explain Bipolar and MS as well as Schizophrenia.

Maybe we all need to get toxins out so our immune system can handle these inborn infections better, and more of us will need to lower the total body burden of all infections fungal bacterial and viral using ACS 200 Silver that is proven to efficiently lower even Borrelia and Candida.

This is worth really understanding, as this is real and when we begin to understand how these virus that are in our DNA are kept under control, until certain things happen, like a severe viral infection during pregnancy, and then years later the child starts to hear voices
etc. I have covered on my website with 8 hours of webinars, the topics of Food, Infection, Genetics, Hormones, Toxins, etc but this aspect of infection was not covered. If we think about it, there could be some tie in here to the live virus given children when they receive their MMR, and subsequent development of Autism. There could be a HERV-W involved in that condition too.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Excerpt:

 #1: http://discover.coverleaf.com/discovermagazine/201006/?pg=64#pg65

#2: http://articles.sfgate.com/2002-08-05/news/17557040_1_mental-illness-mental-health-dr-e-fuller-torrey

Insanity virus — a crazy idea? / Mainstream psychiatric outcast ponders parasitic mental illness
August 05, 2002|By Keay Davidson, Chronicle Science Writer

#3: New Findings Boost Theory That Infection Causes Schizophrenia 

Psychiatric News March 19, 2010 
Volume 45 Number 6 Page 1 
© American Psychiatric Association 
1.   Mark Moran

A review of studies of maternal exposure to infectious agents and schizophrenia in their offspring suggests that eliminating certain infections could prevent as many as 30 percent of schizophrenia cases. 

Call it an instance of science being stranger than science fiction, and of nature’s unintended consequences.

In 2000, a team of British researchers published a remarkable paper in the journal of the Royal Society titled “Fatal Attraction in Rats Affected With Toxoplasma Gondii.” It seems that rodents infected with Toxoplasmosis gondi (T. gondii), a parasite that normally thrives in cats, become fatally attracted to cat urine, causing them to shed their normal avoidant behavior in the presence of a cat. 

Naturally, cat catches rodent and devours it, with the result that the parasite T. gondii is again where it belongs: in a feline host. 

Observing this case of attraction gone fatally wrong, the researchers, from the University of Oxford, postulated that T. gondii, one of nature’s most successful organisms, had developed an ingenious evolutionary mechanism for manipulating the behavior of the rodent—in whom the parasite would have reached a dead end—so that the rodent seeks out, suicidally, the feline host in which the parasite can thrive and complete its life cycle. 
Fast forward to 2009 when another group of researchers seeking to explore the neurochemical mechanisms for the parasite’s behavioral manipulation of its host discover a likely culprit. In a paper published in the March 2009 PLoS One, Glenn McConkey, Ph.D., and colleagues at the University of Leeds found that the genome of the T. gondii parasite encodes the enzyme tyrosine hydroxylase, the central enzyme in dopamine synthesis. 
“Intriguingly, dopamine is the most logical neurotransmitter candidate for altering the avoidant behavior of the rodent,” McConkey told Psychiatric News. “So it would make sense for the parasite to increase dopamine. For the parasite, this is an ideal way to manipulate the behavior of the host.” 

New Credibility for Infectious Etiology
And this strange cat-and-mouse story has yet another wrinkle.
For decades, an excess of dopamine has been implicated in schizophrenia. And so last year’s discovery that T. gondii synthesizes dopamine has lent new credence to an intriguing, though not universally accepted, theory—that at least some forms of schizophrenia may be caused by infection. 

Among researchers inclined to the theory, T. gondii has been one, among several, of the most prominent candidates. 

“Humans infected with T. gondii will form the same cysts on the brain as are found in infected rodents when high levels of the gene involved in dopamine synthesis are expressed,” McConkey said. “While production of dopamine in the rodents could be an evolutionary mechanism devised by the parasite, in humans it would be merely accidental. But now suddenly, this provides a possible link to the observed correlation of T. gondii with some forms of schizophrenia.” 

The theory of an infectious etiology for at least some forms of schizophrenia has a long history, though it is still outside the mainstream. As far back as the 1960s, British epidemiologist Edward Hare, Ph.D., documented a marked increase in late-winter and early-spring births of people with schizophrenia, a finding that pointed to an infection, possibly acquired during winter months in utero. 

Psychiatrist E. Fuller Torrey, M.D., a long-time proponent of the theory, published a paper in the Lancet as early as July 1973 titled “Slow and Latent Viruses in Schizophrenia.” 
Since then, Torrey has published a number of papers with Johns Hopkins University pediatrician and virologist Robert Yolken, M.D., showing increased antibodies to T. gondii—possibly acquired in utero or early childhood through exposure to cat feces, undercooked meat, or contaminated water, dirt, or sand—among people with schizophrenia. 
Meanwhile, infectious agents have been implicated in other diseases—the heliobacter pylori virus in peptic ulcers, the papilloma virus in cervical cancer—that had been considered unlikely candidates for infection. “It’s no longer a theory from Mars,” Torrey told Psychiatric News. “We’ve arrived on planet Earth.” 

Epidemiologic Data Accumulate
Now, a report published online in AJP in Advance on February 1 by Alan Brown, M.D., of Columbia University and colleagues, reviews more than 40 studies looking at seroepidemiologic findings, ecologic data, and maternal reports on prenatal exposure to influenza and other infectious agents and the development of schizophrenia. 

They found that odds ratios for associations between schizophrenia in offspring and serologically documented maternal influenza, elevated levels of antibody to T. gondii, and other peri-conceptional genital or reproductive infections ranged between 3.0 and 5.0. 
The study, “Prenatal Infection and Schizophrenia: A Review of Epidemiologic and Translational Studies,” was done in collaboration with Catherine Schaefer, Ph.D., director of the Kaiser Permanente Research Program on Genes, Environment, and Health, and Barbara Cohn, Ph.D., director of the Child Health and Development Studies, funded primarily by the National Institutes of Health. 

In a study published in the April 2005 American Journal of Psychiatry, titled “Maternal Exposure to Toxoplasmosis and Risk of Schizophrenia in Adult Offspring,” Brown and colleagues conducted serological assays for Toxoplasma antibody on maternal serum specimens from pregnancies giving rise to 63 cases of schizophrenia and other schizophrenia spectrum disorders and compared them with assays from 123 matched healthy subjects. 

They found that the adjusted odds ratio of schizophrenia/schizophrenia spectrum disorders for subjects with high maternal Toxoplasma IgG antibody titers was 2.61. 
“The infectious theory has garnered more interest in the research community,” Brown told Psychiatric News. “This is being driven in part by accumulating data from epidemiological studies of schizophrenia and translational neuroscience in which offspring exposed prenatally to immune challenge and infection show evidence of neurobiological abnormalities found in schizophrenia.” 

A Gene-Environment Interaction
Still, the pathogenic theory of schizophrenia runs counter to years of orthodox thinking that schizophrenia is a congenital, organic brain disorder. Maternal and intrauterine infections are notably common, so one question is that if schizophrenia is infectious in origin, why aren’t more offspring born with schizophrenia? 

But proponents acknowledge that infection alone is unlikely to cause schizophrenia. “Infections are almost certainly interacting with susceptibility genes and other environmental factors,” Brown explained. “So gene-environment interactions likely play a very important role.” 

Nor do proponents of the pathogenic theory insist that infection is necessarily the cause of all schizophrenia.

“While replication in independent samples is warranted, the data from our sample suggest that up to approximately 30 percent of schizophrenia cases could be prevented in the offspring of the pregnant population [in the review appearing in AJP in Advance] if we were to completely eliminate three of the infections we studied—influenza, elevated Toxoplasma antibody, and peri-conceptional genital-reproductive infections,” Brown told Psychiatric News. 

While complete eradication is highly unlikely, Brown says, the finding has implications for prevention and treatment (see Can Infection-Related Schizophrenia Be Prevented?). 
More “orthodox” researchers acknowledge that infection may be a factor in a more expansive research vision looking at “domains of psychosis” in which schizophrenia-like symptoms stem from different gene-environment interactions. 

“Most people acknowledge today that schizophrenia is never going to be found to have a single etiology,” said psychiatric researcher and AJP deputy editor Carol Tamminga, M.D., of the University of Texas Southwestern Medical Center. “It’s more likely a syndrome like congestive heart failure than a disease like Parkinson’s with a single molecular lesion. So we can assume that schizophrenia is a diagnosis with multiple etiologies and overlapping risk factors. 

“We know genetics and environmental factors are risks,” she continued. “Keeping an open mind, I think we will find a list of risk genes and a list of environmental factors, and we will have to see how both of those play out in producing symptoms of a brain disease like schizophrenia.” 

An abstract of “Fatal Attraction in Rats Infected With Toxoplasma Gondii” is posted at <www.ncbi.nlm.nih.gov/pubmed/11007336>. “A Unique Dual Activity Amino Acid Hydroxylase in Toxoplasma Gondii” is posted at <www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004801>. “Prenatal Infection and Schizophrenia: A Review of Epidemiologic and Translational Studies” is posted at <http://ajp.psychiatryonline.org/cgi/reprint/appi.ajp.2009.09030361v1>. “Maternal Exposure to Toxoplasmosis and Risk of Schizophrenia in Adult Offspring” is posted at <http://ajp.psychiatryonline.org/cgi/content/full/162/4/767>.  
http://pn.psychiatryonline.org/content/45/6/1.2.full 

Related articles
Clinical & Research News: Can Infection-Related Schizophrenia be Prevented? Psychiatr News March 19, 2010 45:19

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IDSA knows that chronic Lyme exists http://lymebook.com/fight/idsa-knows-that-chronic-lyme-exists/ http://lymebook.com/fight/idsa-knows-that-chronic-lyme-exists/#respond Tue, 10 Aug 2010 04:21:05 +0000 http://lymebook.com/fight/?p=1469 Full article: http://sci.tech-archive.net/Archive/sci.med.diseases.lyme/2008-06/msg00078.html

Excerpt:

IDSA knows that chronic Lyme exists

The IDSA is aware that chronic Lyme exists. We know this because
members of the 2000 and 2006 Lyme disease guideline panels wrote, in
research articles and patents, that chronic Lyme exists.

Evidence about the existence of chronic Lyme borreliosis has increased
since the 2006 LD guidelines were published.

Scientists in California recently reported that not only can Bb persist
in mice despite treatment with ceftriaxone, but the Borrelia can also
infect other ticks and mice. (1) This study buttresses previous
studies that showed that Borrelia can persist in mice (2, 3), dogs (4,
5, 6), and ponies (7).

Studies have also shown that Bb can persist despite antibiotic
treatment in the following human cells, tissues, organs, and body
fluids:

* Fibroblasts (8; Mark Klempner, an IDSA LD guideline panel member in
2006, is an author of this study)

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