Archive for the ‘research’ Category

Retinal Vessel Occlusion Caused by Bartonella Infection

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236082/

. 2018 Nov 19; 33(47): e297.
Published online 2018 Oct 29. doi: 10.3346/jkms.2018.33.e297
PMCID: PMC6236082
PMID: 31044568

A Case of Retinal Vessel Occlusion Caused by Bartonella Infection

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A 29-year-old female visited the emergency room with sudden visual loss in the right eye started on the same day. She had been suffering from fever for two days. A best-corrected visual acuity (BCVA) was 0.5/0.7 in the Snellen chart. Fundus examination (Fig. 1) showed multiple retinal hemorrhages. Severe vascular sheaths around the optic disc area were present in the right eye. Candle-wax-dripping sign in the superior hemisphere were found in the left eye.

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On systemic examination, erythema of the lower extremities (Fig. 1C) and right inguinal lymph node enlargement were discovered. With systemic doxycycline (100 mg) and gentamicin (90 mg) administration, fever subsided after three days. Bartonella infection was confirmed after 10 days with in-house indirect immunofluorescent assay (IFA) analysis (immunoglobulin G; cutoff points for seropositive titer at 1:64). Lymph node biopsy showed necrotizing granulomatous lymphadenitis (Fig. 1D). On the same day, the BCVA decreased to hand motion in the right eye. When asked, she could not specify when the vision loss began. The candle-wax-dripping sign in the left eye had progressed to vascular sheath with flame-shaped hemorrhages. Fluorescein angiography shows a rack of filling of the retinal arteries. Blocked fluorescence by retinal hemorrhage was found in the whole area of right eye and in the superotemporal quadrant of left eye. Inner-retinal hyper-reflectivity of the right eye and cystoid macular edema in the left eye were revealed (Fig. 2). The impression was central retinal artery and vein occlusion for the right eye and branch retinal artery and vein occlusion for the left eye, associated with severe vasculitis secondary to Bartonella infection. The patient was treated with a systemic methylprednisolone 500 mg, anticoagulant (Enoxaparin sodium 60 mg) and Rifampin (300 mg). Three month after disease onset, the BCVA in the right eye improved to 0.1. For photographs and medical records that consisted possible identification of the patient, a consent form was obtained from the patient for use of publication.

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ACKNOWLEDGMENTS

The authors thank Professor Jin-Soo Lee, Department of Internal Medicine, Inha University School of Medicine, for his help with the in-house IFA analysis.

Footnotes

Funding: This research was supported by the Bio & Medical Technology Development Program of the National Research Foundation of Korea (NRF), funded by the Korean government, the Ministry of Science and ICT (MSIP) (NRF-2017M3A9E2056458).

Disclosure: The authors have no potential conflicts of interest to disclose.

Contributed by

Author Contributions: Conceptualization: Woo M, Kim SW. Investigation: Woo M, Ahn S. Writing – original draft: Woo M. Writing – review & editing: Ahn S, Song JY, Kim SW.

References

1. Kwon HY, Im JH, Lee SM, Baek JH, Durey A, Park SG, et al. The seroprevalence of Bartonella henselae in healthy adults in Korea. Korean J Intern Med. 2017;32(3):530–535. [PMC free article][PubMed] []
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Breakthrough Paves Way For New Lyme Disease Treatment

https://www.newsleader.com/story/news/2019/06/17/new-lyme-disease-treatment-cure-ticks-virginia/1456187001/

Breakthrough paves way for new Lyme disease treatment

A Virginia Tech biochemist has discovered the cellular component that contributes to Lyme arthritis, a debilitating and extremely painful condition that is the most common late stage symptom of Lyme disease, a press release said.

According to the release from Virginia Tech, the biochemist, Brandon Jutras, found that as the Lyme-causing bacteria borrelia burgdorferi multiplies, it sheds a cellular component called peptidoglycan that elicits a unique inflammatory response in the body.

“This discovery will help researchers improve diagnostic tests and may lead to new treatment options for patients suffering with Lyme arthritis,” said Jutras, lead author on the study. “This is an important finding and we think that it has major implications for many manifestations of Lyme disease, not just Lyme arthritis.”

Lyme disease is the most reported vector-borne disease in the country, and in Virginia reports have increased by more than 6,000 percent in the last fifteen years. The Centers for Disease Control, estimates that approximately 300,000 people are diagnosed with Lyme disease annually in the United States. Scientists predict that the number of people who become infected Lyme will increase as our climate continues to change.

Jutras — an assistant professor of biochemistry in the College of Agriculture and Life Sciences and an affiliated faculty member of the Fralin Life Sciences Institute — and his collaborators recently published their findings in the Proceedings of the National Academy of Sciences.

According to the release, the PNAS paper was four years in the making, and Jutras began this research during his post-doctoral fellowship in the lab of Christine Jacobs-Wagner, a Howard Hughes Medical Institute Investigator and professor at Yale University.

“Nowadays nothing significant in science is accomplished without collaboration,” said Jutras. Co-authors on this paper ranged from bench scientists to medical doctors and practicing physicians. Dr. Allen Steere, a Harvard doctor who originally identified Lyme disease in the 1970s, assisted Jutras with his research and provided access to patient samples.

The research could provide a new way to diagnose Lyme disease and Lyme arthritis for patients with vague symptoms based on the presence of the cellular component called peptidoglycan in synovial fluid.

Read: Every spot in Virginia is a hotspot for ticks

The press release said, the team found peptidoglycan is a major contributor to Lyme arthritis in late-stage Lyme disease patients. Peptidoglycan is an essential component of bacterial cell walls. All bacteria have some form of peptidoglycan, but the form found in the bacteria that causes Lyme, borrelia burgdorferi, has a unique chemical structure. When the bacteria multiply, they shed peptidoglycan into the extracellular environment, because its genome does not have the appropriate proteins to recycle it back into the cell.

“We can actually detect peptidoglycan in the synovial fluid of the affected, inflamed joints of patients that have all the symptoms of Lyme arthritis but no longer have an obvious, active infection,” said Jutras in the release.

Peptidoglycan elicits an inflammatory response and the molecule persists in the synovial fluid, which means that our bodies continue to respond, without mounting a counter response.

Receptors in our immune system sense bacterial products and, depending on the individual’s genetic predispositions, may determine how strongly a patient’s body reacts to peptidoglycan.

The next phase of Jutras’ work is to use methods to destroy the peptidoglycan, or intervene to prevent a response, which could get rid of Lyme disease symptoms. According to the release, Jutras predicts that with either therapy patients would start recovering sooner.

Breakthrough paves way for new Lyme disease treatment, as discussed in this video provided by Virginia Tech. Video provided by Virginia Tech, Staunton News Leader

Clinical samples included in this study were obtained from patients that had confirmed cases of Lyme disease under the guidelines of the CDC, but virtually all did not respond to oral and/or intravenous antibiotic treatment, the release said. The presence of peptidoglycan in these patients’ synovial fluids may explain why some people experience symptoms of late stage Lyme disease in the absence of an obvious infection. In this case, the usual antibiotic treatments for Lyme disease would no longer be helpful, but this discovery might provide avenues for new treatments, the press release said.

Members of the Jacobs-Wagner lab purified the peptidoglycan and removed all other bacterial components and asked: is peptidoglycan all on its own capable of causing arthritis in a mouse model?

According to the release, within 24 hours post-injection, mice presented with dramatic joint inflammation, indicating that peptidoglycan can cause arthritis.

Jutras is continuing his research at Virginia Tech on peptidoglycan by more thoroughly studying its chemical composition to determine how it is able to persist in the human body. This will also help further the understanding of how this bacterial product contributes to other manifestations of Lyme disease.

“We are interested in understanding everything associated with how patients respond, how we can prevent that response, and how we could possibly intervene with blocking therapies or therapies that eliminate the molecule entirely,” Jutras said.

**Comment**
This article brings up more questions than answers.
1) Were these patients used for this study truly treated appropriately to begin with?  For example, was the mono-therapy of doxycycline only used for a short period of time?  This treatment has been shown again and again to have treatment failures from the beginning of time. For examples of effective treatment:  https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/  In a nutshell, effective treatment takes into account pleomorphism, polymmcrobialism, and biofilm. Doxy alone will not do these things.
2) Would an anti-peptidoglycan treatment only be a bandaid covering up a systemic infection? Everything I know about borrelia would answer a resounding “yes,” to this question.  While that may not be a bad thing, we must be honest about what the treatment’s really doing as well as the fact borrelia can persist in the human body, something The Cabal isn’t admitting at this point. Again, we truly need to end this Lyme War and according to microbiologist Tom Grier, that isn’t going to happen until post mortem studies are completed:  https://madisonarealymesupportgroup.com/2018/04/13/chronic-lyme-post-mortem-study-needed-to-end-the-lyme-wars/ Isn’t it a bit ironic that The Cabal is just fine with creating a patentable drug but NOT fine with doing the proper science that would put all of this to rest?
3) Bandaids on symptoms are used all the time to lesson pain and other symptoms; however, they shouldn’t be used at the expense of true, effective treatment for a systemic infection that’s relapsing in nature. In the case of Lyme disease, that would simply mean long-term antimicrobials. While I do not know the study parameters used here my guess would be the treatment that “didn’t work” was the mono-therapy of doxycycline which certainly doesn’t work for many coinfections such as Babesia, as well as the fact Eva Sapi has shown it to push the spirochete into the noncell wall form invitro:  https://www.dovepress.com/evaluation-of-in-vitro-antibiotic-susceptibility-of-different-morpholo-peer-reviewed-article-IDR
Just this year another study was done about it by Caskey et al.:  https://www.ncbi.nlm.nih.gov/pubmed/31057493

Treatment failures were found in Lyme arthritic patients who were treated with intramuscular (IM) benzathine penicillin following steroids. [3]

In another study, two patients were ill for 3 years and one patient for 6 years despite receiving intravenous (IV) ceftriaxone. The authors explained, “Patients unresponsive to ceftriaxone were more likely to have received corticosteroid treatment.” Dattwyler et al. from Stony Brook Medical Center found an “association of steroid use with an increased failure rate or worsening of disease is understandable in view of the well-known effects of these agents on the inflammatory and immune responses.”

Dattwyler advised against the use of steroids in Lyme disease patients based on these two studies. “In view of the strong association between the use of steroids and the lack of response to antibiotic therapy, we believe that glucocorticoids should not be used in the treatment of Lyme borreliosis.” [2]

This article highlights yet again the importance of needing the right research to be done. The Cabal continues full-steam ahead doing research built upon false premises that could hurt patients in the end.

 

SPbU Scientists Have Discovered the First Family of Extracellular Rickettsia-Like Bacteria

https://www.eurekalert.org/pub_releases/2019-06/spsu-ssh061419.php

NEWS RELEASE 

SPbU scientists have discovered the first family of extracellular Rickettsia-like bacteria

Microbiologists have discovered a new family of bacteria belonging to the order Rickettsiales — Deianiraeaceae; this is the first report of the Rickettsia-like bacteria that display a unique extracellular lifestyle and are in fact predators

ST. PETERSBURG STATE UNIVERSITY

Like Heracles’ wife

The Deianiraeaceae, which has become the fourth family in the order Rickettsiales, currently contains one genus, Deianiraea. All previously investigated Rickettsiales are obligate intracellular specialised parasites. By contrast, Deianiraea not only attacks the victim from the outside, but also it never enters the host cell throughout its entire life cycle. Deianiraea colonises the extracellular surface of the ciliate Paramecium: the predatory bacterium attacks the ciliate and replicates on its surface, taking the victim’s resources, and eventually its life.

The name for the newly discovered bacterium – Deianiraea – refers to the myth of Deianira, the wife of Heracles. According to legend, the centaur Nessus attempted to kidnap Deianira, but she was rescued by Heracles. Heracles shot the centaur with an arrow dipped in the Lernaean Hydra’s venomous blood. The dying Nessus, seeking vengeance, persuaded Deianira to take some of his blood, as it would allegedly make a powerful love potion. When Deianira heard that Heracles had fallen in love with another woman, she feared that he would leave her. Deianira sent him a tunic smeared with the centaur’s blood. The tunic poisoned with the Hydra’s venom in the centaur’s blood killed Heracles. ‘Similarly, the Deianiraea bacterium kills the ciliates, covering the host cell like a poisoned tunic,’ notes Alexey Potekhin, Professor at the Department of Microbiology of St Petersburg University and a member of the international research team.

Predator of the microworld

The novel bacterium was discovered by chance. Natalia Lebedeva is one of the co-authors of the study and a leading expert of the Centre for Culture Collection of Microorganisms at the St Petersburg University Research Park. She took a sample of water from a waste water stream in Larnaca, Cyprus. Microbiological analysis of the water sample revealed that it contained a large number of ciliates. Laboratory observation showed massive loss of cilia, which are employed for locomotion and feeding. This resulted in the death of the affected ciliate. Other paramecia, which were added into the same culture, also soon died. Upon closer inspection of the affected ciliates it became evident that the deciliated areas of the cell surface were covered by tightly packed bacteria – unknown to science at that moment.

‘New bacterial families are rarely discovered these days. It is always an important finding, no matter what order this family may belong to. In our case, a new family has been found in a very well-studied order – the Rickettsiales. Previously, only DNA of related bacteria were detected in the samples. Therefore, the bacteria were classified as Rickettsia-like, as the scientists were not able to place them into the existing system of families of the order. It was the first time that we had found these bacteria alive. The molecular phylogenetic analysis enabled us to reassemble all the data fragments and, consequently, to establish a new bacterial family – Deianiraeaceae. One may say we were lucky,’ says Alexey Potekhin.

Strong and almost independent

Unlike other Rickettsia-like bacteria, Deianiraea is not only able to replicate – to reproduce outside the cell – but also to sustain itself with less dependence on the host. ‘Deianiraea possesses a higher capability to synthesise amino acids, compared to all other Rickettsiales. It can synthesise 16 amino acids, including the 8 that other representatives of the order cannot produce. 16 out of the 20 main amino acids is almost a full set. The rest it is most likely to acquire from its victims, but we do not know that for certain. Moreover, Deianiraea can synthesise nucleotides: other Rickettsiales do not do this because they receive them from the host,’ Alexey Potekhin explains.

Another feature of Deianiraea is that it has several secretion systems. In bacteria, this enables protein secretion that can be employed for interaction with other cells as well. Deianiraea does have a specialised secretion system for interacting with other bacteria. It also has a specialised type IV secretion system which putatively enables it to establish contact with the ciliate. At present, the researchers have not yet established the exact mechanism of the parasite-host cell interaction, and what the bacterium may acquire from the ciliate or other host organisms.

Related to mitochondria

The order Rickettsiales encompasses three previously known families of highly diverse representatives of intracellular symbionts and parasites associated with eukaryotes, including animal and human pathogens (e.g., typhus). It has been suggested that all Rickettsia-like may have shared a common ancestor with mitochondria. Mitochondria are responsible for ATP synthesis in all eukaryotic cells, i.e. for energy metabolism. The discovery of a novel — extracellular — Rickettsiales bacterium suggests that the evolutionary path of mitochondria may have been different, contrary to what has been previously assumed.

‘Evolution, whenever possible, tends to choose the path of least effort, reducing the number of redundant functions: all that is unnecessary is eliminated. It has been assumed that the common ancestor of all Rickettsia-like bacteria was a specialised intracellular parasite with a low biosynthetic potential. In other words, it was unable to synthesise many of the essential substances, acquiring them from the host. It could sustain itself and reproduce only inside host cells. The results of our research allow us to assert with confidence that the last common ancestor of all Rickettsia-like bacteria led an extracellular lifestyle, lived in water, had a flagellum and was metabolically independent. It also must have had cellular systems that enabled parasite-host interactions. Adaptation to the lifestyle of intracellular parasites of the modern families of the Rickettsiales order would have evolved later in parallel and independently in different sub-lineages. The discovery of Deianiraea impels us to reopen the debate about the time when the ancestor of mitochondria would have established itself inside a proto-eukaryote, and the particular traits this mitochondrial ancestor would have possessed,’ the scientist concludes.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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For more on Rickettsia:  https://madisonarealymesupportgroup.com/2016/10/12/willy-speaks-from-the-grave-rickettsia-helvetica/

https://madisonarealymesupportgroup.com/2019/05/06/rickettsiales-in-ticks-removed-from-outdoor-workers-from-georgia-florida/

https://madisonarealymesupportgroup.com/2019/03/22/1st-report-of-anaplasma-found-in-thai-bartonella-rickettsia-leptospira-scrub-typhus-in-humans-as-well-even-more-found-in-ticks/

https://madisonarealymesupportgroup.com/2019/01/11/rickettsia-found-in-ticks-on-brazilian-snakes/

https://madisonarealymesupportgroup.com/2019/01/03/tick-bite-in-ear-gave-uk-teacher-rickettsial-typhus-infection/

Lastly, I’ll never forget what Dr. Hoffman, RIP, told me years ago when he was a medical resident in Illinois treating people with tick-borne illness before it had a name (Lyme).  He called it a “Rickettsial-like” disease.  He may have been closer to the truth than he knew.

Scientists Figured Out How to Make a Better Antibiotic With Electricity

https://www.thedailybeast.com/scientists-figured-out-how-to-make-a-better-antibioticwith-electricity?

Scientists Figured Out How to Make a Better Antibiotic—With Electricity

Every year in the U.S., 1.1 million people suffer from burns that need to be medically treated. Surgeries cause more than 100 million wounds. And countless others suffer from various cuts, lacerations, and traumas that land them in the hospital.

Every single one of these is an injury that needs to be protected from infection, but unfortunately a hospital isn’t a great place to do that. Hospital-acquired infection is extremely prevalent (so much so that the Centers for Disease Control has a program aimed at fighting it).

At the moment the best method of treatment is antibiotics—but those come with their own problems.

So Chandan Sen, a physiologist and vice chair of research at the Indiana University School of Medicine, and his team decided to re-invent the antibiotic—using electricity to help stop bacteria from evolving immunity.

“There’s a lot of people developing new antibiotics, let’s not do that,” Sen told The Daily Beast. “Let’s ask a broader question: are there ways of defeating these types of infection that are not pharmacology-based because we know drug resistance is easy to acquire for bugs,” he said.

Defeat meant Sen had to look at how the bacteria attach themselves together.

One of the reasons why infection is difficult to treat is because of the way bacteria congregate to create it. They form what’s called a biofilm—groups of different types of bacteria that join together and secrete a sticky mesh that holds them in place inside a wound. The mesh also helps protect the bacteria from attempts at treatment, making biofilms more resistant to antibiotics then individual bacteria. According to the CDC and the National Institutes of Health, it’s estimated that between 65 and 80 percent of all infections are caused by these difficult-to-treat biofilms.

“When bacteria chooses to become a biofilm there is quorum sensing; they talk to each other and say, ‘We have a quorum let’s form a biofilm,’” Sen said. “They have electrical communication.”

They do this either by connecting to each other using microscopic nanowires or through sending electrical signals in the form of current. But that led Sen and his team to wonder: “If we disrupt this electrical micro-environment can we disrupt them?”

Turns out, yes.

If a small external electrical current passes through a biofilm, the matrix that holds the bacteria together falls apart and the bacteria die, essentially confusing the signal. The bacteria start sending their messages in the wrong direction because their ions and electrons are attracted incorrectly.

“With this system you disintegrate the biofilm and it allows the immune system to come in fight it. It’s a cooperation,” he said.

The amount of electricity needed is minuscule. In fact, according to Sen, it is well below the amount that the FDA says is safe for human exposure. Their ultimate solution is a wound dressing—a piece of fabric—printed with a pattern of silver and zinc dots. When the fabric comes into contact with any type of body fluid, the combination produces enough energy to disrupt the bacteria.

“We have lit up an LED thermometer with that current.,” Sen said. “If you touch the fabric you can’t tell there’s any metal. Visually it looks like polka dots.”

In one of the experiments done with the fabric, the team tested it on an infection that had been allowed to spread untreated for seven days. “Once the biofilms formed we intervened with textiles,” he said. “The data was so convincing the Department of Defense has just started a clinical trial.”

The current version of the fabric creates an electrical field that can treat wounds a few millimeters deep. They have also developed a second version still in testing that uses a hearing aid battery, which provides a larger amount of electricity to silver circuitry on the dressing. This can create a bigger field, allowing for treatment of larger areas.

Sen says he’s excited about how this principle could be developed beyond his wound dressings, noting that they have research they are about to publish that shows its effects on other infections, such as those that come from fungus.

Overall, Sen believes it’s possible after more research this might be able to one day reduce the medical community’s need to rely on antibiotics. “We have not done research on that but I can see a clear path,” he said.

The first generation of the product is already on the market, sold as a wound dressing, but is going through FDA approval to be used as an infection treatment.

Ontario Public Health Officials Called Out on Shoddy, Biased Research Utilizing An Erroneous ‘Climate Change’ Model to Program a Futuristic Tick Problem

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Ontario Public Health Officials Called Out on Shoddy, Biased Research Utilizing An Erroneous ‘Climate Change’ Model To Program a Futuristic Tick Problem

The following comment by independent Canadian tick researcher John Scott on the article by Schillberg, E., et al; “Distribution of Ixodes scapularis in Northwestern Ontario: Results From Active and Passive Surveillance Activities in the Northwestern Health Unit Catchment Area,” is a fantastic example of why we as patients should care about where and how research dollars are being spent.

Research article found here:  https://www.ncbi.nlm.nih.gov/pubmed/30314334.  Comment  here: Scott, 2019, 3 errata, comments on Schillberg et al., 2018

Scott outlines three important corrections (errata) on the research article on various ticks in northwestern Ontario.  Please refer to the Scott link above for the full details, but I highlight the major issues below:

1.  Correction #1 has to do with shoddy research. Scott points out that important details are completely omitted from the study about the proper identification of ticks making one wonder if it’s even true. There are no details on history of travel, collection data, life stage, identification method, and who identified it. There was no molecular analysis (i.e. DNA barcoding) which is important on a foreign tick found in a place it shouldn’t be situated. For example, the Amblyomma cajennense tick has been divided into 6 separate tick species. Then there’s the issue of five years lapsing between tick collection until publication.

2.  Correction #2 has to do with research bias. Researchers always cite previous research that pertains to their work and either correct or build upon it. Schillberg, et al. purposely left out previous published work outlining important history on tick movement, infection rate, ecology, and epidemiology. Then, they go on to state more research is needed when it’s’ already been done, making the reader seriously wonder if they are just looking for further research funding. They underplay the problem by only citing five tick species, when there are nine, eight of which are positive for Lyme disease, and five of which  bite humans. Of particular note and importance to patients, Scott provided key information on the pathological and neurological manifestations of Lyme disease for health care providers. By not citing this work, Schillberg, et al., which are all public officials, are clearly using research bias by flat out ignoring previous work that doesn’t fit their paradigm. It just simply doesn’t fit with what they want people to believe.

3.  Correction #3 has to do with creating an erroneous climate change model to fit their bias. Schillberg, et al., cited references that were hypothetical computer models that had erroneous baseline maps. They completely ignore and dismiss previous published work and instead create their own reality to show a gradual tick expansion northward due to supposed climate change.  The problem is tick populations already existed in those locations. Scott’s most telling statement for patients to be aware of regarding research on climate change and ticks is this theory would,

“explain to the public a reason for not tackling this serious health care issue earlier. The tick problem was programmed for the future. Thus, ill-founded statistical analyses culminated in fabricated erroneous data and, ultimately, resulted in a series of maps that turned out to be flawed science.”

Scott also states the authors’ hypothesis on temperature increase is based on the United Nations International Panel on Climate Change Computer forecasts that have been consistently wrong. And yet, articles & books continue to be pumped out stating that warmer winters mean more ticks, when in fact, Scott has shown that overwinter survival of ticks dropped to 33% when the snow melted in late winter exposing black legged ticks to sudden drops in overnight temperature. This has been substantiated by other researchers as well.  https://madisonarealymesupportgroup.com/2018/11/07/ticks-on-the-move-due-to-migrating-birds-and-photoperiod-not-climate-change/

4.  Lastly, if I had a dollar for every article and book that came across my desk pushing this “warmer winters mean more ticks” mantra due to ‘climate change’, I’d be a millionaire. More research under this false pretense is being done by the minute.

How much does that cost? How many research dollars are being diverted from important issues patients and the doctors treating them really need answers to?

Even well-meaning Lyme advocates/journalists write books on Lyme being a disease driven by climate change.

Meanwhile, in the real world, thousands upon thousands of patients continue to be misdiagnosed with everything from medically unexplained symptoms (MUS), to depression, to MS and fibromyalgia. They are flat-out denied treatment and are told, “It’s all in your head.” The subset of patients (30%-40% of us) that are undiagnosed and untreated for months to years continue to be ignored by research and mainstream medicine. We have no new research on potential modes of transmission, good diagnostics, and effective treatments.

There were 53 troubling points noted throughout this research article.

Schillberg et al., 2018 was created by public officials so desperate to keep their jobs that they will literally fabricate a paradigm and create an alternate reality.

Speak up in your sphere of influence, and insist that your tax dollars go towards research that will help sick people – not line the pockets of dishonest researchers and public officials.

For more: https://madisonarealymesupportgroup.com/2018/08/13/study-shows-lyme-not-propelled-by-climate-change/

https://madisonarealymesupportgroup.com/2018/11/17/uw-madison-phd-in-ecological-climatology-climate-change-computer-models-fudged-except-russian-model/  Dr. Patrick Michaels, director of the Center for the Study of Science at the Cato Institute, provides insight into the debate over climate change and the political games played to create policy.

Political games surrounding Lyme/MSIDS have gone on long enough. Do research on important issues that will help patients.