Fluorescent Image of Borrelia, the Causative Agent of Lyme Disease.
Click on link for picture. Permission granted by Dr. Benjamin L. Clark, University of Minnesota Medical School, Director, Bridges to the Baccalaureate Degree Program, Director, Pathways to Advance Degrees in the Life Sciences, 218-726-6587
Green is the intracellular Borrelia, blue-purple is the nucleus of the macrophage, a type of white blood cell of the immune system that is supposed to engulf and digest pathogens and anything else considered a foreign invader.
The red is a cell surface marker (CD86) known as Cluster of Differentiation 86, a protein expressed on antigen-presenting cells that provides costimulatory signals necessary for T cell activation and survival. It is the ligand for two different proteins on the T cell surface: CD28 and CTLA-4. CD86 works in tandem with CD80 to prime T cells. Co-stimulation is an essential step in the induction of adaptive immune responses.
There are probably 4 or more spirochetes in the phagosome (a vacuolewithin a phagocytethatcontainsbacteria or otheringestedparticlesthatbecomesfusedwith a lysosome which functions as the digestive system of the cell).
Dr. Clarke’s future work will be to study that internal chamber and how the spirochete potentially thrives.
When it is proven & accepted that Bb infects white blood cells, it will give a potential answer to some late-disseminated Lyme cases as an immune-deficiency syndrome demonstrating why some patients have frequent and prolonged infections and may acquire new allergies as well as Mast Cell issues.
Kelly Oggenfuss is walking into the woods. Leading her team of four young researchers through a thicket of slender oak trees, she doles out assignments by letters corresponding to a grid. As early morning light filters through the canopy, Oggenfuss and her colleagues pull on latex gloves then disperse to gather surveillance data.
For 20 years, this has been a post-dawn ritual for Oggenfuss, a senior research specialist at the Cary Institute of Ecosystem Studies in Millbrook, New York, a bucolic town in the state’s Hudson Valley region. Four times a week from April to November — traditionally the most active tick season in the Northeast — she leads a platoon of field researchers as they don white coveralls, drive a pair of old Chevy Tracker SUVs down an overgrown dirt road, and hike to a five-acre tract designated “Henry Control” on the grounds of the institute. Their mission is to seek out and study ticks in one of the most tick-infested areas in America.
Oggenfuss and the others work methodically across a grid of 242 spring-loaded box traps, checking for rodents lured overnight by whole-oat seeds. Sharing updates via walkie-talkie, the team gathers after a squirrel is found in one of the traps. The new researchers transfer the animal to a plastic mesh sleeve and take turns examining it. A similar process unfolds with chipmunks.
Most often, the traps capture mice, which Oggenfuss and her team carry with them, still in the trap, until the grid check is complete. Then the group convenes around a collapsible table. As one researcher records data (grid location, gender, tag number, etc.), the others apply tags to the mice and collect blood, urine, and stool samples. Finally, Oggenfuss and her team meticulously comb the mice with tweezers and blow on their fur, pushing it aside in search of ticks.
“Look there’s a nymph,” says Oggenfuss. “And I’ve got one, two, three larvae. Can you see them?” She pulls a patch of the mouse’s fur back to reveal a blacklegged tick no bigger than a poppy seed burrowed into its head. The larvae are barely perceptible.
A researcher named Agi holds up another mouse. “Look,” she announces. “That’s a larva on top of that nymph. We have a co-feeding situation here.” The theory is that their feeding sites are so close that pathogens move between them easily, Oggenfuss explains. The potential result is one tick sharing infectious material directly with another through the host mouse as if it were a straw, speeding the spread of disease. “That could have an effect on infection prevalence,” Oggenfuss adds. “It’s one of the things we’re studying.”
Since 1992, the Cary Institute has been compiling a record of tick ecology that they believe to be the longest continuous study of this kind in the U.S. and possibly the world. Mostly its researchers encounter the blacklegged, or deer, tick (Ixodes scapularis), but in recent years, they’ve also been seeing increasing numbers of lone star ticks (Amblyomma americanum), which are native to the American Southeast but now range from northern Mexico to Canada. Over the years, an alarming number of ticks in the surrounding area have been revealed to carry Borrelia burgdorferi, the bacteria that causes Lyme disease, while others have tested positive for the pathogens that cause other tick-borne illnesses, including the potentially fatal Powassan virus.
Because ticks acquire pathogens from hosts, understanding tick-borne diseases means understanding ticks’ so-called disease reservoir, especially mice. If the urban rat was the primary carrier of bubonic plague, the country mouse is it for Lyme disease. And just as the fleas that fed on infected rats spread the plague, ticks that feed on infected mice transmit Lyme.
On this early May morning, the team’s trap yield is relatively modest — four mice, two squirrels, and a chipmunk. “It’s early days still,” says Oggenfuss. In August, during the so-called larval peak, the researchers sometimes catch as many as 220 mice and can find 150 or even 200 tick larvae crawling on a single mouse. It can be an unnerving moment. “When the ticks are looking for a feeding site,” Oggenfuss says, “the mouse fur just seems to move on its own.”
The process for counting ticks not affixed to hosts is called a drag — the researchers pull a one-square-meter sheet of fabric along the ground for 30 meters then tally the number of ticks affixed to it. Oggenfuss holds the Cary Institute record for ticks collected in a single drag: 1,700. As horrifying as that haul was — and it would, by extrapolation, put the tick population on the Cary Institute’s 2,000-acre campus at 2 billion — Oggenfuss is quick to note it was exceptional, and tick density is irregular. Her more conservative calculations of average tick populations, based on drags done during the same time of year (August, the larval peak), are only reassuring by comparison: upward of 20,000 ticks per acre, more than 100,000 on the Henry Control grid, and more than 40 million on the Cary Institute grounds.
The scary thing is, that’s nothing. Experts say the worldwide tick population is exploding,triggering a dramatic spike in the incidence of Lyme disease and a rise in other tick-borne illnesses, some of which, like Powassan, are far more dangerous than Lyme.
First identified in 1975 in the leafy New England town of Old Lyme, Connecticut, Lyme disease has now reached what experts consider pandemic proportions. According to the Centers for Disease Control and Prevention (CDC), the number of confirmed cases of Lyme disease in the U.S. has more than doubled in the two decades leading up to 2017 (the most recent year for which final figures are available) and increased 17% from 2016 to 2017 alone. More than half the counties in the U.S. are considered high-risk areas for Lyme, according to the CDC, and in some areas, as many as six out of 10 ticks carry the infection.
“It’s been a relentless expansion since the 1980s,” says John Aucott, director of the Lyme Disease Clinical Research Center at Johns Hopkins University School of Medicine. “There may be down years and up years, but the trends are in place, and there’s no indication that they’re going to reverse.”
We now live in a frightening new normal: It’s estimated that 300,000 people contract Lyme every year in the U.S., with victims found not just in traditionally tick-heavy areas like upstate New York and Maine, but also in all 50 states and Washington, D.C. While most people are cured quickly with antibiotics, some go on to experience lingering symptoms characteristic of Lyme, like headaches, fatigue, and joint and muscle pain, for months or longer after they’ve been treated, a condition known as post-treatment Lyme disease syndrome (PTLDS). According to a recent study led by experts at the Brown University School of Public Health, the number of people in the U.S. with PTLDS was estimated to be 1.5 million in 2016 and is predicted to rise to nearly 2 million by 2020.
“There is little doubt that [Lyme disease] is pandemic. It calls for a huge national and concerted international effort to bring it under control.”
Tick populations now exist on every continent, even Antarctica, and Lyme disease can be found throughout most of Europe, where it ranks as the most common vector-borne disease, and beyond. “To me, there is little doubt that it is pandemic,” says Mary Beth Pfeiffer, author of Lyme: The First Epidemic of Climate Change. “It’s in China, Russia, Japan, Australia. It’s moving fast into Canada. It is all across the U.S. It calls for a huge national and concerted international effort to bring it under control.”
The incidence of other tick-borne illnesses is also sharply rising. According to the CDC, the occurrence of those diseases in the U.S. has nearly tripled since 2004 and increased more than 22% from 2016 to 2017. In addition to Lyme, ticks transmit a slew of pathogens, including those that cause babesiosis, ehrlichiosis, anaplasmosis, southern tick-associated rash illness, tick-borne relapsing fever, tularemia, Colorado tick fever, Q fever, Rocky Mountain spotted fever, and Powassan encephalitis. Most of the bacterial diseases are treatable if diagnosed early. Others, like Rocky Mountain spotted fever, are potentially fatal, particularly in children, if not treated quickly. Incidences of spotted fever rickettsiosis, which includes Rocky Mountain spotted fever, increased more than 12-fold from 2000 to 2017 (up from 495 to 6,248). And while more rare still, cases of Powassan virus, which can kill one in 10 people who are infected and for which there is no treatment, are rising as well. In 2008, only two cases were reported. In 2016, that number jumped to 22 and again in 2017 to 33.
“Ticks account for more diseases than all other biting insects and arthropods in the United States,” says Ben Beard, deputy director for the Division of Vector-Borne Diseases at the CDC. “It’s hard to know what the maximum or the ceiling might be. All we can say is that the number of cases is growing every year.”
Alarms are going off all over the globe. South Africa, where tick-bite fever (a form of rickettsias) is common, has seen an increase in incidences of Crimean-Congo hemorrhagic fever (CCHF), which is deadly in 30% to 40% of cases. The tick that carries CCHF, a native of sub-Saharan Africa and eastern Europe, has been found in Spain, Portugal, Germany, and the United Kingdom, where it is believed to have been brought from Africa by migratory birds. Bites from the lone star tick have been shown to cause alpha-gal syndrome, which manifests in rapid-onset allergies to meat, typically beef and pork, that can result in unexplained anaphylactic reactions. There is no treatment, other than eschewing the consumption of red meat.
In North America, news reports in Maine and southern Canada this spring featured a shocking number of sightings of what are called ghost moose — skeletal-looking, malnourished, denuded animals that have rubbed off their fur in response to tick irritation after hosting up to 75,000 feeding ticks through the winter. Many emerged anemic after being the source of so many blood meals, and a number of calves died after losing too much blood to ticks — a vampire-like end to life known as exsanguination.
If Lyme disease has reached pandemic proportions, why haven’t we heard more about it? Because, experts say, Lyme doesn’t strike fear into people’s hearts the way some other illnesses, like Ebola or Zika, do. People respond to dramatic pictures or dramatic mortality, says Aucott.
“It’s hard for them to have a perspective on the real impact of Lyme disease because it doesn’t cause visible changes. People with Lyme disease don’t look sick.”
ORONO, Maine (WABI) – “Through our lab we’re kind of trying to provide surveillance on tick populations as well as the pathogens that they spread,” says Griffin Dill.
Griffin Dill is doing critical research on ticks at the University of Maine Cooperative Extension. He says reported cases of disease from ticks is increasing and so is the population here in Maine.
“It’s a more forested state with the human element mixed in so it’s kind of created the perfect habitat for ticks as well as their wild life hosts.”
He says people don’t have to change their lifestyle, but it is important to take some simple precautions, like treating clothing and gear with repellents, like permethrin which is a highly effective repellent for ticks.
“We want people to be aware of ticks but not afraid. We want people to go outside.”
“I got sick after two tick bites.”
Constance “Happy” Dickey is a founding director of Maine Lyme. Happy and the others behind the organization have made education, support and prevention their mission because they know isolating and costly it can be.
“Everything after the tick bite is more complicated than preventing the tick bite. We need to make prevention second-nature to us.”
There are multiple resources on the Maine Lyme website for prevention and education including what to do if you find a tick attached to your skin. It’s important not to put any soaps, ointments, alcohol or heat on the tick and do not squeeze the body of it. Take note of when the tick was found and mark the bite area. Report any illness or rashes to your doctor. You can even send the tick to the UMaine Tick Lab for testing.
Your pets are susceptible, too.
“”For the most part of if your animal gets sick with it they have a fever. That’s one of the first signs. So same with a human if you feel tired, lethargic, you don’t really feel like moving around, so if you see that, it’s one of the things we start to think of,” says Dr. David Cloutier at the Veazie Veterinary Clinic.,
They can also test and treat for Lyme at the Veazie Veterinary Clinic. Care that comprehensive for people is what those in this fight are hoping for.
“I’ve heard from so many of my constituents.”
Including Senator Susan Collins who has recently introduced the TICK Act.
“It’s evident from the exploding numbers of these illnesses that are borne by ticks that we need to do much more.”
Dill says he meets with a group run by the Maine CDC ona regular basis for a statewide strategy. He says he wants people to know work in being done in the fight against Lyme.
“Hopefully, we make some breakthroughs on potential management strategies for controlling tick population’s as well as the medical side with the potential for new treatments even vaccination.”
After watching both of these news reports and being in a few of my own, one thing sticks out to me: there’s never reporting on effective treatments.
Because it’s sticky and the way this is being treated by mainstream medicine, the CDC, and other authorities isn’t working. Period.
It’s easier to do a 2-4 minute sound bite and interview a tick researcher than it is to get to the bottom of this plague which is riddled with conflicts of interest and frankly patient abuse.
Babesiosis is a tick-transmitted intraerythrocytic zoonosis. In Korea, the first mortalities were reported in 2005 due to Babesia sp. detection in sheep; herein we report epidemiological and genetic characteristics of a second case of babesiosis. Microscopic analysis of patient blood revealed polymorphic merozoites. To detect Babesia spp., PCR was performed using Babesia specific primers for β-tubulin, 18S rDNA, COB, and COX3 gene fragments. 18S rDNA analysis for Babesia sp., showed 98% homology with ovine Babesia sp. and with Babesia infections in Korea in 2005. Moreover, phylogenetic analysis of 18S rDNA, COB, and COX3 revealed close associations with B. motasi. For identifying the infectious agent, Haemaphysalis longicornis (296) and Haemaphysalis flava (301) were collected around the previous residence of the babesiosis patient.Babesia genes were identified in three H. longicornis: one sample was identified as B. microti and two samples were 98% homologous to B. motasi.
Our study is the first direct confirmation of the infectious agent for human babesiosis.This case most likely resulted from tick bites from ticks near the patient house of the babesiosis patient. H. longicornis has been implicated as a vector of B. microti and other Babesia sp. infections.
The full-length article tells the unfortunate story of an elderly men’s death 36 hours after hospitalization due to an emerging type of Babesia due to a tick bite.
A blood sample was obtained from the jugular vein in the patient that presented with dizziness and general weakness.
No microorganisms were isolated from the blood culture.
Microscopy revealed the following:
Upon light microscopic examination, variable intraerythrocytic parasites as ring forms, pear-shaped forms, paired pyriforms, pleomorphic ring forms, and multiple-infected parasites and clusters of extracellular rings were detected in Giemsa-stained blood smears. The percentage of parasitaemia was 1.8% (Figure 1). Maltese cross forms comprising four masses in an erythrocyte that are often described as a characteristic of B. microti infection were not detected in most blood smears (Figure 1).
Please note that the patient would have failed a simple blood test and even microscopy revealed atypical findings as well as the fact parasitemia was less than 2%.
Yet, 2% was enough to kill a man.
Tick collections were performed by dividing the area around the patient’s residence and the findings were:
A total of 597 ticks were collected around the patient’s residence, including 296 H. longicornis(186 adult, 41 nymphs, and 68 larvae) and 301 Haemaphysalis flava (1 adult and 300 larvae) (Table 2). Among these, 94% of the ticks were collected in both the front yard of patient’s residence (442 ticks) and associated hill III (124 ticks). Based on the results of the amplification of Babesia genes in each tick, 2 (0.3%) were positive for 18S rDNA of Babesia species, 1 (0.2%) for COB and COX3, and 1 (0.2%) for β-tubulin gene of B. microti. While the nymph of H. longicornis yielded a positive result for only 18S rDNA, one female tick of H. longicornis yielded positive results for 18S rDNA, COB, and COX3 gene fragments. Also, one female tick of H. longicornis only yielded positive results for β-tubulin gene of B. microti (Table 3).
Please note two things: the high amount of ticks found right in his yard and the low incidence of infected ticks – yet, it only took one to kill him.
The Discussion section reveals some interesting things:
Previously, seven different Babesia spp., B. microti, B. divergens, B. bovis, B. canis, B. duncani, B. venatorium, and a novel Babesia sp. similar to ovine babesias were reported to cause human babesiosis...Human babesiosis (KCDC-1) in 2017 was the second case identified in Korea and the sequence of Babesia sp. was very closely related to that of KO1 and Liaoning, China. These large Babesia are clearly distinct from other agents of human babesiosis based on their shape and phylogeny. These results suggest that the causative agent in their case of babesiosis is a novel large Babesia parasite infecting humans and may be highly fatal….
the identified Babesia parasites (in the patient) might be B. motasi, and this is the first study to detect B. motasi in human babesiosis and H. longicornis in Korea.
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.
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).1 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.
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.
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.
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] [Google Scholar]
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.
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.
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
Treatment failures were found in Lyme arthritic patients who were treated with intramuscular (IM) benzathine penicillin following steroids. 
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.” 
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
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.
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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.