All Posts Tagged With: "borrelia burgdorferi"

F.I.G.H.T. L.I.M.E.S.

It is time to rename LYME;  if we call it LIMES it will change the paradigm and help many more people on the road to recovery than if IV antibiotics suddenly were free for everyone, as often as they wanted them. That is not the best answer for most patients today.  Oxidative treatment would make more sense (UVB/OZONE).

Lyme is all around us but I believe we will help many more if we give up on blaming everything on the tick related introduction of more pathogens than we had the day before we are bit.  Continued

Reduced immune response to Lyme

Linda’s comment:  We previously observed that γδ T cells in vitro are activated by Borrelia burgdorferi in a TLR2-dependent manner. We now observe that the activated γδ T cells can in turn stimulate dendritic cells in vitro to produce cytokines and chemokines that are important for the adaptive immune response.

 This paralleled greater Borreli a burden in
γδ-deficient mice as well as more cardiac inflammation. These findings
are consistent with a model of γδ T cells functioning to promote the
adaptive immune response during infection.

Bells Palsy and Lyme Neuroborreliosis

Linda’s Comment:   Bell’s palsy and Lyme neuroborreliosis are the two most common diagnoses in patients with peripheral facial palsy in areas endemic for Borrelia burgdorferi.\

Excerpt:

CONCLUSIONS: We found that the time of the year, associated neurological
symptoms and mononuclear pleocytosis were strong predictive factors for
Lyme neuroborreliosis as a cause of peripheral facial palsy in an area
endemic for Borrelia.

Lyme bacteria hides out in lymph nodes

Linda’s comments:  What amazes me is they have said for years that those who suffered from MONO ended up having Lyme disease.  So now they feel they have made a discovery that many doctors and patients have known about in the alternative arena….Bottom-line, at least they are now publishing about these issues…

Link: http://www.healthtalkandyou.com/uc-davis-finds-lyme-disease-bacteria-in-lymph-nodes/

Excerpt:

UC Davis Finds Lyme Disease Bacteria in Lymph Nodes
by Maejoy Tutor in Diseases on Jun 15, 2011 

One of the most significant and considered as threatening and rising diseases in US is the Lyme disease. The bacteria which causes this seems to be hiding particularly in lymph nodes. University of California Davis researchers have reported that this can trigger a considerable immune response, except that it is not too strong to defeat the infection.

BB & host derived proteases

Linda’s comment: in vitro model of the human BBB mimics many of the important features of in vivo B. burgdorferi interactions with the BBB. Hence, this model should be an important tool for identifying the cellular and molecular elements implicated in B. burgdorferi interactions with the BMEC, as well as for helping characterize the biochemical mechanisms by which the bacteria cross the BBB.

Link: http://iai.asm.org/cgi/content/full/73/2/1014

Excerpt:

Our in vitro model of the human BBB mimics many of the important features of in vivo B. burgdorferi interactions with the BBB. Hence, this model should be an important tool for identifying the cellular and molecular elements implicated in B. burgdorferi interactions with the BMEC, as well as for helping characterize the biochemical mechanisms by which the bacteria cross the BBB.

Banderol + Samento for Lyme

Linda’s comment:  This is EXCELLENT read….I have taken ALL of these products and they WORK!!

Full aritcle: http://www.newhaven.edu/news-events/82773.pdf

Excerpt:

 Our results demonstrated that both herbal agents, but not doxycycline, had very significant effects on all forms of B. burgdorferi, especially when used in combination, suggesting that herbal agents could provide an effective therapeutic approach for Lyme disease patient. 

Lyme in the central nervous system

Excerpt:

Lyme disease, the multi-system infection caused by the tick-borne
spirochaete Borrelia burgdorferi, can involve the nervous system, most
commonly causing, alone or in combination, lymphocytic meningitis or
abnormalities of cranial or peripheral nerves, the latter most typically
presenting as a painful radicular syndrome. Diagnosis is based on
appropriately used, standard serological tests; in instances where the
central nervous system is involved, cerebrospinal fluid assessment for
organism-specific antibodies can be useful. Treatment with any of several
standard regimens of oral or parenteral antimicrobials is highly effective.
Prolonged treatment beyond four weeks is rarely if ever warranted, and
carries significant risk.

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21127770&retmode=ref&cmd=prlinks

ELISA Lyme test evaluation for Lyme & Co-infections

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21117995&retmode=ref&cmd=prlinks

Excerpt:

Results-Sensitivity and specificity of the in-clinic ELISA for detection of
heartworm antigen (99.2% and 100%, respectively), antibodies against B
burgdorferi (98.8% and 100%, respectively), and antibodies against E canis
(96.2% and 100%, respectively) were similar to results for a similar
commercial ELISA. In samples obtained from dogs in the northeast and upper
Midwest of the United States, sensitivity and specificity of the in-clinic
ELISA for antibodies against Anaplasma spp were 99.1% and 100%,
respectively, compared with results for an immunofluorescence assay. Samples
from 2 dogs experimentally infected with the NY18 strain of A
phagocytophilum were tested by use of the in-clinic ELISA, and antibodies
against A phagocytophilum were detected by 8 days after inoculation.
Antibodies against Anaplasma platys in experimentally infected dogs
cross-reacted with the A phagocytophilum analyte. Coinfections were
identified in several of the canine serum samples. 
Conclusions and Clinical Relevance-
The commercially available in-clinic ELISA could be used by veterinarians to
screen dogs for heartworm infection and for exposure to tick-borne
pathogens.

Borrelia in mice – no symptoms?

Link: http://www.liebertonline.com/doi/abs/10.1089/vbz.2009.0215

Excerpt:

 The epidemiology of vector-borne zoonotic diseases is determined by
encounter rates between vectors and hosts. Alterations to the behavior of
reservoir hosts caused by the infectious agent have the potential to
dramatically alter disease transmission and human risk. We examined the
effect of Borrelia burgdorferi, the etiological agent of Lyme disease, on
one of its most important reservoir hosts, the white-footed mouse,
Peromyscus leucopus. We mimic natural infections in mice using the vector
(Black-legged ticks, Ixodes scapularis) and examine the immunological and
behavioral responses of mouse hosts. Despite producing antibodies against B.
burgdorferi, infected mice did not have elevated white blood cells compared
with uninfected mice. In addition, infected and uninfected mice did not
differ in their wheel-running activity. Our results suggest that infection
with the spirochete B. burgdorferi has little impact on the field activity
of white-footed mice. Lyme disease transmission appears to be uncomplicated
by pathogen-altered behavior of this reservoir host.

Borrelia burgdorferi surface proteins

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21217173&retmode=ref&cmd=prlinks

Excerpt:

Antibiotic-refractory Lyme arthritis may result from Borrelia
burgdorferi-induced autoimmunity in affected joints. Such patients usually
have certain HLA-DRB1 molecules that bind an epitope of B. burgdorferi
outer-surface protein A (OspA), and cellular and humoral immune responses to
OspA are greater in patients with antibiotic-refractory arthritis than in
those with antibiotic-responsive arthritis. Recent work in a mouse model
suggests that, during B. burgdorferi infection, OspA in genetically
susceptible individuals stimulates a particularly strong T(H)1 response,
which may be one of several factors that can help set the stage for a
putative autoimmune response in affected joints. However, vaccination with
OspA did not induce arthritis in this mouse model, and case and control
comparisons in human vaccine trials did not show an increased frequency of
arthritis among OspA-vaccinated individuals.
Thus, a vaccine-induced immune response to OspA does not replicate the
sequence of events needed in the natural infection to induce
antibiotic-refractory Lyme arthritis.