Archive for the ‘Testing’ Category

Juvenile Tick Attachment on Mice Significantly Greater in Japanese Barberry Shrubs

https://www.ncbi.nlm.nih.gov/m/pubmed/29850912/

Indirect Effects of Japanese Barberry Infestations on White-Footed Mice Exposure to Borrelia burgdorferi.

Linske MA, et al. Environ Entomol. 2018.

Abstract
Japanese barberry (Berberis thunbergii de Candolle; Ranunculales: Berberidaceae) is an exotic shrub that has invaded woodland understories in the northeastern United States. It forms dense thickets providing ideal structure and microclimate for questing blacklegged ticks (Ixodes scapularis Say; Acari: Ixodidae). While there have been studies on the favorable habitat barberry provides blacklegged ticks, little has been studied on the relationship between barberry, vectors (ticks), and reservoirs (white-footed mice; Peromyscus leucopus Rafinesque; Rodentia: Cricetidae); specifically, the influence Japanese barberry has on the abundance of blacklegged ticks and Borrelia burgdorferi infection (Johnson, Schmid, Hyde, Steigerwalt, and Brenner; Spirochaetales: Spirochaetaceae) in mice.

We studied the impacts of barberry treatment over the course of 6 yr to determine influence on encounter abundance with white-footed mice, encounter abundance with B. burgdorferi-infected mice, and juvenile blacklegged ticks parasitizing mice.

Results from our study suggest that while both white-footed mouse and B. burgdorferi-infected mouse encounters remained similar between barberry treatment areas, juvenile tick attachment to mice was significantly greater in intact barberry stands (X¯ = 4.4 ticks per mouse ± 0.23 SEM) compared with managed (X¯ = 2.8 ± 0.17; P < 0.001) or absent (X¯ = 2.2 ± 0.16; P < 0.001) stands. Results of this study indicated that management of barberry stands reduced contact opportunities between blacklegged ticks and white-footed mice. Continued efforts to manage Japanese barberry will not only allow for reestablishment of native plant species, but will also reduce the number of B. burgdorferi-infected blacklegged ticks on the landscape

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For More:  https://madisonarealymesupportgroup.com/2018/01/20/manage-barberry-lower-ticks/  (Other links after article)

 

Category:

Lyme, research, Testing, Ticks, Transmission

Success of Blood Test For Autism

https://www.sciencedaily.com/releases/2018/06/180619122434.htm

Success of blood test for autism affirmed

First physiological test for autism proves high accuracy in second trial

June 19, 2018
Rensselaer Polytechnic Institute

One year after researchers published their work on a physiological test for autism, a follow-up study confirms its exceptional success in assessing whether a child is on the autism spectrum. A physiological test that supports a clinician’s diagnostic process has the potential to lower the age at which children are diagnosed, leading to earlier treatment. Results of the study, which uses an algorithm to predict if a child has autism spectrum disorder (ASD) based on metabolites in a blood sample, published online today, appear in the June edition of Bioengineering & Translational Medicine.

“We looked at groups of children with ASD independent from our previous study and had similar success. We are able to predict with 88 percent accuracy whether children have autism,” said Juergen Hahn, lead author, systems biologist, professor, head of the Rensselaer Polytechnic Institute Department of Biomedical Engineering, and member of the Rensselaer Center for Biotechnology and Interdisciplinary Studies (CBIS). “This is extremely promising.”

It is estimated that approximately 1.7 percent of all children are diagnosed with ASD, characterized as “a developmental disability caused by differences in the brain,” according to the Centers for Disease Control and Prevention. Earlier diagnosis is generally acknowledged to lead to better outcomes as children engage in early intervention services, and an ASD diagnosis is possible at 18-24 months of age. However, because diagnosis depends solely on clinical observations, most children are not diagnosed with ASD until after 4 years of age.

Rather than search for a sole indicator of ASD, the approach Hahn developed uses big data techniques to search for patterns in metabolites relevant to two connected cellular pathways (a series of interactions between molecules that control cell function) with suspected links to ASD.

“Juergen’s work in developing a physiological test for autism is an example of how the interdisciplinary life science-engineering interface at Rensselaer brings new perspectives and solutions to improve human health,” said Deepak Vashishth, CBIS director. “This is a great result from the larger emphasis on Alzheimer’s and neurodegenerative diseases at CBIS, where our work joins multiple approaches to develop better diagnostic tools and biomanufacture new therapeutics.”

The initial success in 2017 analyzed data from a group of 149 people, about half of whom had been previously diagnosed with ASD. For each member of the group, Hahn obtained data on 24 metabolites related to the two cellular pathways — the methionine cycle and the transsulfuration pathway. Deliberately omitting data from one individual in the group, Hahn subjected the remaining dataset to advanced analysis techniques and used results to generate a predictive algorithm. The algorithm then made a prediction about the data from the omitted individual. Hahn cross-validated the results, swapping a different individual out of the group and repeating the process for all 149 participants. His method correctly identified 96.1 percent of all typically developing participants and 97.6 percent of the ASD cohort.

The results were impressive and created, said Hahn, a new goal: “Can we replicate this?”

The new study applies Hahn’s approach to an independent dataset. To avoid the lengthy process of gathering new data through clinical trials, Hahn and his team searched for existing datasets that included the metabolites he had analyzed in the original study. The researchers identified appropriate data from three different studies that included a total of 154 children with autism conducted by researchers at the Arkansas Children’s Research Institute. The data included only 22 of the 24 metabolites he used to create the original predictive algorithm, however Hahn determined the available information would be sufficient for the test.

The team used their approach to recreate the predictive algorithm, this time using data of the 22 metabolites from the original group of 149 children. The algorithm was then applied to the new group of 154 children for testing purposes. When the predictive algorithm was applied to each individual, it correctly predicted autism with 88 percent accuracy.

Hahn said the difference between the original accuracy rate and that of the new study can likely be attributed to several factors, the most important being that two of the metabolites were unavailable in the second dataset. Each of the two metabolites had been strong indicators in the previous study.

Overall, the second study validates the original results, and provides insights into several variants on the approach.

“The most meaningful result is the high degree of accuracy we are able to obtain using this approach on data collected years apart from the original dataset,” said Hahn. “This is an approach that we would like to see move forward into clinical trials and ultimately into a commercially available test.”

Hahn was joined on the research by Rensselaer doctoral students Troy Vargason and Daniel P. Howsmon; Robert A. Rubin of Whittier College; Leanna Delhey, Marie Tippett, Shannon Rose, and Sirish C. Bennuri of the Arkansas Children’s Research Institute and the University of Arkansas for Medical Sciences; John C. Slattery, Stepan Melnyk, and S. Jill James of the University of Arkansas for Medical Sciences; and Richard E. Frye of Phoenix Children’s Hospital. The research was partially funded by the National Institutes of Health.

Materials provided by Rensselaer Polytechnic Institute. Note: Content may be edited for style and length.

Journal Reference:

Daniel P. Howsmon, Troy Vargason, Robert A. Rubin, Leanna Delhey, Marie Tippett, Shannon Rose, Sirish C. Bennuri, John C. Slattery, Stepan Melnyk, S. Jill James, Richard E. Frye, Juergen Hahn. Multivariate techniques enable a biochemical classification of children with autism spectrum disorder versus typically-developing peers: A comparison and validation study. Bioengineering & Translational Medicine, 2018; DOI: 10.1002/btm2.10095

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**Comment**

Autism like Lyme/MSIDS is an epidemic and according to one Wisconsin LLMD, 80% of his Autistic patients are also infected with Lyme/MSIDS.

For more:

https://madisonarealymesupportgroup.com/2018/06/15/canadian-data-more-autism-where-vaccine-coverage-is-highest/

https://madisonarealymesupportgroup.com/2018/06/01/immunoexcitotoxicity-as-the-central-mechanism-of-etiopathology-treatment-of-autism-spectrum-disorders-a-possible-role-of-fluoride-aluminum/

https://madisonarealymesupportgroup.com/2017/10/26/clinical-trial-shows-most-kids-with-autism-are-not-born-with-it/

 

Category:

Activism, Autism, research, Testing

Reclassification of Borrelia spp. Isolated in South Korea Using Multilocus Sequence Typing

https://www.ncbi.nlm.nih.gov/m/pubmed/29848848/

Reclassification of Borrelia spp. isolated in South Korea using Multilocus Sequence Typing.

Park KH, et al. Jpn J Infect Dis. 2018.

Abstract
Using Borrelia isolated from South Korea, we evaluated by MLST and three intergenic genes (16S rRNA, ospA, and 5S-23S IGS) typing to analyze the relationship between host and vector and molecular background. Using the MLST analysis, we identified B. afzelii, B. yangtzensis, B. garinii, and B. bavariensis. This study was first report of the identification of B. yangtzensis using the MLST in South Korea.

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**Comment**

This recent paper:  https://www.sciencedirect.com/science/article/pii/S0890850816300652 shows that the Borrelia genus is expanding and that there are “misfit” members that can not even be defined by conventional criteria.  The paper also discusses members that challenge the “existing dogma” that Lyme-disease inducing strains are transmitted by hard ticks, while relapsing fever-inducing spirochetes are transmitted by soft ticks.

This argument about soft-bodied ticks being able to transmit Lyme and/or a Lyme-like disease has been raging for decades:  https://madisonarealymesupportgroup.com/2017/10/06/remembering-dr-masters-the-rebel-for-lyme-patients-who-took-on-the-cdc-single-handedly/

https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-016-1353-4  This article states that out of 20 spirochete species from Borrelia burgdorferi  sensu lato (s..l.) complex recognized to date, a live spirochete strain found in the U.S. patient has revealed close relatedness to Borrelia bissetti.  The authors state that “the potential of B. bissettii to cause human disease, even if it is infrequent, is of importance for clinicians due to the extensive range of its geographic distribution.”  Yet, in the discussion the authors state that when B. bissetti was investigated in mice, it was sufficient to induce disease within the heart, femorotibial joint, and bladder.  European studies also suggest potential human disease as well.

The potential for human disease could be said about every single genus – yet current testing tests for 1 strain from 1 spirochete from 1 lab tick.  See the problem here?  The other problem is that many researchers don’t even report “rare” cases of transmission as they feel them unimportant.  I was told this exact thing to my face.  All I could say was, “What if you happen to be the poor, sorry sucker that is that ONE “rare” case?  Does rare even matter when the potential is there?”  

Patients could very well be infected with pathogens that testing can’t even pick up.  They don’t even know the potential for human disease yet…..This is why I say to take each and ever tick bite as seriously as a heart attack.  It only takes one bite to sideline you and testing won’t even pick it up.

Category:

Lyme, research, Testing, Ticks

The Role of Retroviruses in Chronic Illness – A Clinician’s Perspective

https://klinghardtinstitute.com/wp-content/uploads/2018/05/IHCAN-Dr-K-article-HERV-05.1.pdf

The Role of Retroviruses in Chronic Illness- Dietrich Klinghardt, MD, PhD

The role of retroviruses in chronic illness is greatly disputed in academic circles. However, at the Sophia Health Institute Dr DIETRICH KLINGHARDT, MD, PhD, reports seeing significant improvement in treatment outcomes – in the most severely affected patients with chronic illness – when anti- retroviral strategies are included.

The results we are seeing at the Sophia Health Institute at our locations in Seattle and Marin County would not have been possible without the brilliant work of Judy Mikovits, PhD.

What is published and what illnesses are potentially caused by, or have as a contributing factor, activated retroviruses?

  • CNS-related illnesses: ME/CFS, Gulf War Syndrome, Autism, MS, Parkinson’s, ALS, Schizophrenia
  • Auto-immune diseases: Lupus, Crohn’s, Hashimoto’s Thyroiditis, Polymyositis, Sjogren’s syndrome, Bechet’s Disease, primary biliary cirrhosis
  • Cancer: prostate, breast, non-Hodgkin’s lymphoma, chronic lymphocytic leukaemia, mantle cell lymphoma, hairy cell leukaemia, bladder, colorectal, kidney, ovarian.

To that I am adding a list of other illnesses that have responded under my care to retroviral interventions: intractable Lyme disease, mold illness, insomnia, brain fog and all stages of a deteriorating brain, most childhood illnesses including ADHD and behavioural problems, asthma, breast cancer, lung cancer and many more.

Working backwards

What are retroviruses? The more familiar DNA viruses such as those from the “herpes family” – and many others – work their way from DNA over to RNA and from there to the manufacture of viral proteins. Retroviruses work their way backwards – from the RNA to the DNA – and then forward again from there.

Retroviruses are subdivided into different- lettered classes – Beta Retroviruses: HERV-K. Gamma Retroviruses: HERV-H and HERV-W.

The generally accepted key contributors to chronic illness are inflammation, oxidative stress and microbial infection. All of these are known triggers for retroviral activity, and in turn are also caused by retroviral activity.

Both human and animal retroviruses can infect the central nervous system (CNS). These are associated with many diseases of the CNS and cause neurological disease by several mechanisms:

1. Directly through infection of immune cells which traffic to the brain;

2. Indirectly through increases in proinflammatory cytokines and chemokines, or

3. In the absence of detectable brain inflammation indirect effects known as “bystander effects”- causing chronic retroviral replication of immune cells.

A retrovirus works via the enzyme “reverse transcriptase”. Once inside the cell, it uses the enzyme to force the cell to create viral DNA. This viral DNA becomes integrated into the host cell DNA. A retrovirus integrated into our genome may be passed from mother to child during pregnancy (Sakuma et al, 2012).

Only 2% of our DNA is protein-coding, but 6-8% of our DNA is retroviral DNA – passed down to us from our ancestors as scars from our constant encounter with an often hostile microbial and virus-rich environment (Stoyle, 2006, Mayer et al, 2011; Li et al, 2001). These viruses are referred to as Human Endogenous Retroviruses or HERVs.

However, not all embedded retroviral DNA is bad. Some sections have become a functional part of our genome because they have given us an evolutionary advantage, such as the formation of the p53 gene regulatory network (Shin et al, 2013; Barbusecu et al, 2001). Other retroviruses have to be silenced throughout life, mainly through DNA methylation and acetylation.

The transcription of retroviral DNA makes the infected person susceptible to numerous de-novo genetic mutations, including MTHFR, DNMT and other genes which control methylation. Many other illness-producing effects are known, implicating HERV-K in the pathogenesis of neuroinflammatory and autoimmune illnesses. For a patient to get well today, it is rarely enough to just interpret the genomic testing and to substitute accordingly.

Acquiring infection

How do we become infected? Retroviruses can be acquired (inhalation, blood-based products, physical contact) or the viruses already present in our DNA can be activated through influences such as a viral infection or chronic inflammation (Manghera and Douville, 2013).

For example, the Epstein Barr virus induces expression of the HERV-K envelope gene and the transactivation of MSRV, the Multiple Sclerosis retrovirus (Mameli et al, 2007; Sutkowski et al, 2001). Herpes simplex type-2 activates members of the HERV-W family. These and other mechanisms are likely responsible for the activation of HERVs seen in rheumatoid arthritis, SLE, Sjorgens disease, schizophrenia, autism, MS and cancer. Cell phone radiation has disabled many of our protective proteins (Fragopoulou et al, 2012) and so have many of the food-based toxins such as glyphosate (Seneff et al, 2017) and air-based inhalants (aluminium etc).  An unintended source of retroviruses are some vaccines as reported in Frontiers in Microbiology in January 2011).

Diagnosis

Currently PCR testing is only available to
the research community. We have to rely on indirect parameters:

  • decrease of CD56 NK cells (CD56 is involved in adhesion, migration, growth, differentiation and other cellular functions); down regulation of IL-13, IL-2, IFN gamma, TH-1 cytokines (J. Mikovits et al, 1998)
  • upregulated levels of TH-2 cytokines: IL-4, IL-10 and pro-inflammatory cytokines: IL-1, IL-6, IL-8 and TNF-alpha.
  • elevated levels of TGF beta-1: has profound effects on innate and adaptive immunity through stimulation of mast cells (often mistaken as mould-related). This may be the true cause of mastocytosis.

Other practical markers from my experience: low wbc (white blood count below 4500), low CD 56. I always include the CD 57 to rule out an active Borrelia burgdorferi infection as compounding factor.

Treatment

When the retroviruses are effectively addressed early in the treatment of chronic illness, other issues such as bacterial infections (Borrelia, Mycoplasma, Bartonella etc), mould illness, EBV, CMV, HHV-6, silent inflammation, parasites, heavy metal toxicity and many other problems become less symptomatic and often undetectable – and respond much better to treatment, even to interventions that have failed before.

Plants have been exposed to the same retroviruses as us, but for 300 million years longer – and many have developed potent adaptogens. Even though drugs like Truvada and AZT can be successfully used, I prefer the use of plant-based products that have unique anti-retroviral properties. A few examples with the key references:

  • Scutalaria root (Ruscetti et al: “Inhibition of HIV infection by baicalin – a flavonoid compound purified from Chinese herbal medicine”, Cellular & Molecular Biology Research 39, 2 (1993): 119-124).
  • Cistus incanus (Rebensburg et al: “Potent in vitro antiviral activity of Cistus incanus extract against HIV and Filoviruses targets viral envelope proteins”. Scientific Reports 6 (2016): 20394).
  • Broccoli sprouts (Furuya et al: “Sulforaphane inhibits HIV infection of macrophages through Nrf2.” PLoS Pathogens, 12.4 (2016): e1005581)
  • St John’s Wort (Meruelo, Lavie and Lavie: “Therapeutic agents with dramatic anti- retroviral activity and little toxicity at effective doses: aromatic polycyclic diones hypericin and pseudohypericin.” Proc Nal Acad Sci 85.14 (1988): 5230-5234).

In addition, I like to put my patients on a high dose of seleno-cysteine (commonly 800mcg, a dose that has been established as safe (Yang, G.; Zhou, R. (1994) “Further Observations on the Human Maximum Safe Dietary Selenium Intake in a Seleniferous Area of China”. Journal of Trace Elements and Electrolytes in Health and Disease. 8 (3–4): 159–165. Baum et al. “High risk of HIV- related mortality is associated with selenium deficiency.” JAIDS 15.5 (1997): 370-374).

Suramin, an old anti-parasitic, has turned out to be one of the most effective anti- retroviral agents. Retroviruses activate the “cell danger response” and the P2 purinergic receptor on each cell. Suramin downregulates this receptor and inhibits the binding of growth factors TGF-beta, EGF, PDGF to their receptors and thus antagonises the ability of these factors to stimulate growth of tumour cells. It can be given iv every six weeks.

I prefer giving daily homeopathic doses (Mitsuya et al: “Suramin protection of T cells in vitro against infectivity and cytopathic effect of HTLV-III.” Science 226.4671 (1984): 172-174).

When we use suitable liposomal extracts of plants in proper dose and frequency, together with selenium and “energetic copies” of immune modulators like suramin, olmetarsan (vitamin D receptor), rapamycin (mTOR), significant results can be achieved in the treatment of chronic illness that were not possible before. This new therapeutic approach should always be combined with the synergistic use of EMR protection, treatment of Lyme and co-infections, mould and metal detox.

• On June 10, Dr Klinghardt will present a one-day seminar on the correct and effective use of anti-retroviral interventions in chronic illness. For more information and to book see news story on page 9 and visit www. Klinghardtinstitute.com.

About the author

Dr DIETRICH KLINGHARDT studied medicine and psychology in Freiburg, Germany, completing his PhD on the involvement of the autonomic nervous system in autoimmune disorders. Early in his career he became interested in the sequelae of chronic toxicity (especially lead, mercury, environmental pollutants & electromagnetic fields) in the course of illness.

While working in India he encountered Eastern concepts of disease aetiology and blended them with his Western training. This laid the foundation for his 5-level system of Integrative Medicine. In the US he spent three years as a full-time emergency physician before becoming Medical Director of the Santa Fe Pain Centre.

Increasingly aware of the limitations of conventional medicine when dealing with chronic conditions, he trained in Ericksonian hypnotherapy and began to include body-oriented psychotherapeutic and counselling approaches in his work, along with neural therapy, mesotherapy injection techniques and applied psychoneurobiology. Dr Klinghardt has contributed significantly to the understanding of metal toxicity and its connection with chronic infections, illness and pain. He has been instrumental in advancing various fields within biological medicine – non-invasive pain management, injection techniques for pain and orthopaedic dysfunction, anti-ageing medicine, toxicology, paediatrics (neuro-developmental disorders), energy psychology, biological dentistry and others. He has also developed Autonomic Response Testing, a comprehensive diagnostic system that has helped many practitioners to become accomplished holistic physicians. He founded Sophia Health Institute in 2012, and is actively involved in patient care at his clinic.

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**Comment**

For more on Mikovitz’s work:  https://madisonarealymesupportgroup.com/2017/10/15/vaccines-and-retroviruses-a-whistleblower-reveals-what-the-government-is-hiding/

https://madisonarealymesupportgroup.com/2018/03/01/vaccines-could-contribute-to-disease-epidemics-due-to-retrovirus-contamination/

To hear the audio of the talk & slides, go here:  http://simplymimi.net/archives/1151

 

 

 

 

 

 

 

 

 

 

Category:

Activism, Herbs, Inflammation, Lyme, research, Supplements, Testing, Transmission, Treatment, vaccines, Viruses

Northern & Southern CA Cats have Bartonella and Rickettsia – Proven by 16S rRNA Next Gen Sequencing

https://www.ncbi.nlm.nih.gov/m/pubmed/29893631/

Assessing Cat Flea Microbiomes in Northern and Southern California by 16S rRNA Next-Generation Sequencing.

Vasconcelos EJR, et al. Vector Borne Zoonotic Dis. 2018.

Abstract
Flea-borne diseases (FBDs) impact both human and animal health worldwide. Because adult fleas are obligately hematophagous and can harbor potential pathogens, fleas act as ectoparasites of vertebrates, as well as zoonotic disease vectors. Cat fleas (Ctenocephalides felis) are important vectors of two zoonotic bacterial genera listed as priority pathogens by the National Institute of Allergy and Infectious Diseases (NIAID-USA): Bartonella spp. and Rickettsia spp., causative agents of bartonelloses and rickettsioses, respectively.

In this study, we introduce the first microbiome analysis of C. felis samples from California, determining the presence and abundance of relevant pathogenic genera by characterizing the cat flea microbiome through 16S rRNA next-generation sequencing (16S-NGS). Samples from both northern (NoCal) and southern (SoCal) California were assessed to expand current knowledge regarding FBDs in the state. We identified Rickettsia and Bartonella, as well as the endosymbiont Wolbachia, as the most abundant genera, followed by less abundant taxa. In comparison to our previous study screening Californian cat fleas for rickettsiae using PCR/digestion/sequencing of the ompB gene, the 16S-NGS approach applied herein showed a 95% level of agreement in detecting Rickettsia spp. There was no overall difference in microbiome diversity between NoCal and SoCal samples. Bacterial taxa identified by 16S-NGS in this study may help to improve epidemiological investigations, pathogen surveillance efforts, and clinical diagnostics of FBDs in California and elsewhere.

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**Comment**

Bartonella and Rickettsia spp. are also diseases Lyme/MSIDS patients have to contend with.  There is no good, solid research studying the ability of ticks to transmit Bartonella, yet most of us out here in Lyme land have it.  Rickettsia’s out here too in plenty.  I would think this important issue would be dealt with.  Somehow patients are getting these diseases and its either happening by direct transmission or by being activated once they get Lyme and their immune systems become compromised.

Either way, this issue MUST be studied, resolved, and appropriately death with.

Mainstream medicine is completely lost when it comes to tick borne illnesses such as these.  Lyme is finally getting acknowledged due to shear numbers, but don’t kid yourself, thousands upon thousands have Bartonella and Rickettsia as well.  The one drug, one pathogen paradigm needs to be forgotten like a bad dream and researchers and doctors need to become educated on this complex 21st Century plague.

BTW:  Wolbachia is being widely used as a biocontrol.  Here’s why that may not be such a great idea:  https://madisonarealymesupportgroup.com/2017/07/10/wolbachia-the-next-frankenstein/

https://madisonarealymesupportgroup.com/2018/02/12/wolbachia-laced-mosquitoes-being-released-why-lyme-msids-patients-might-be-negatively-affected/

https://madisonarealymesupportgroup.com/2018/05/22/mosquito-spit-alone-may-significantly-alter-your-immune-system-for-days-after-a-bite/

https://madisonarealymesupportgroup.com/2018/05/02/tick-mosquito-and-flea-diseases-more-than-tripled-since-2004/

It is my strong opinion that ALL of these factors are a perfect storm of events causing human suffering and disease.  Researchers need to zoom out and look at the big picture and the interconnection of things or we are doomed.

Category:

Activism, Bartonella, Lyme, research, Rickettsia, Testing, Transmission