Published on Feb 14, 2018
Suncoast News Network – Living with Lyme – A 4-year search for 1 diagnosis
Published on Feb 15, 2018
SNN: Living with Lyme – What is Lyme?
Published on Feb 14, 2018
Suncoast News Network – Living with Lyme – A 4-year search for 1 diagnosis
Published on Feb 15, 2018
SNN: Living with Lyme – What is Lyme?
The following article explains that Borrelia Miyamotoi is not new to California. First considered nonpathogenic, it wasn’t even reported until 2011 in Russia. http://www.nejm.org/doi/full/10.1056/NEJMc1215469 Diagnosis relies on PCR testing during acute infection and two-tiered testing for Lyme will not pick it up. It is not a reportable illness so prevalence is pure conjecture. Dr. Horowitz states clinicians should be vigilant for clinical pictures that look like viral infections such as high fever, headache, and muscle and joint pain. In publications, only 16% of patients presenting with BMD were seropositive for IgG and/or IgM antibody to B. miyamotoi rGlpQ, so PCR should also be considered in patients with a history of tick bites and appropriate clinical manifestations.
This is also an important reminder that new strains and species are being discovered continually, so nothing about Tick Borne Illness should be set in stone and open minds are a must.
Like forensic detectives, using a bank of frozen blood serum from the 1980s, tick researchers from both the west and east coasts set out to determine how prevalent Borrelia miyamotoi infection is in California. What they discovered should set off more than a few alarms.
B. miyamotoi is a spiral-shaped bacterium in the same genus as Borrelia burgdorferi, the agent of Lyme disease. But it is most closely related to the group of relapsing fever Borrelia spirochetes. It has recently been recognized as causing a form of borreliosis that is similar to Lyme disease—Borrelia miyamotoi disease (BMD).
B. miyamotoi is transmitted by the same hard-bodied ticks that carry Lyme disease—the blacklegged or deer tick (Ixodes scapularis) and the western blacklegged tick (Ixodes pacificus).
The symptoms of BMD are similar to Lyme disease but generally more severe, with the addition of a relapsing fever, and the absence of a typical bull’s-eye rash. Because BMD is not a reportable disease in the US, there is very little information about its symptoms or prevalence.
For this study, the researchers were given access to a biobank of 101 blood samples collected from a rural community in Mendocino County, California, after an outbreak of Lyme disease in the late 1980s. The area has since been the focus of many tick studies and is known for high prevalence of ticks that carry both BMD and Lyme disease.
Three quarters of the people in the study reported frequent tick bites in the one to two years prior to the blood draw. Later, a confirmatory blood test showed that 79% had antibodies to tick saliva—a rate nearly three times that of residents of Block Island, Rhode Island (29%), where Lyme disease is highly endemic.
For the BMD screening, researchers used two different methods to look for evidence of prior exposure to B. miyamotoi—a two-step glycerophosphodiester phosphodiesterase enzyme-linked immunosorbent (rGlpQ) assay and a whole-cell lysate (WCL) assay.
Twenty-six of the 101 samples were reactive for BMD. [Note: the B. miyamotoi GlpQ assay is not affected by Lyme disease infection because B. burgdorferi does not produce GlpQ antigen.]
The samples were also tested for Borrelia hermsii and Borrelia burgdorferi, to examine the possibility of cross-reactivity and/or dual infection.
The researchers feel there is probable cause of BMD infection for several reasons:
Studies showing 0.5% to 15% of Ixodes pacificus ticks carry B. miyamotoi infection in Northern California, B. miyamotoi is passed from parent to offspring (transovarial transmission), increasing risk of infection from nymphal ticks, and mild climates allow for nearly year-round activity of ticks in California.
“No human cases of B. miyamotoi previously have been reported from the western United States even though I. pacificus ticks in northern California have a spirochete-infection prevalence similar to or exceeding that of I. scapularis ticks in the Northeast and upper Midwest,” according to the authors.
The authors go on to warn, “Healthcare professionals in the far-western United States should be aware that B. miyamotoi disease may occur throughout the geographic distribution of I. pacificus and that improved relapsing fever group spirochete antibody assays are urgently needed.”
In summary, while B. miyamotoi is considered an “emerging” infectious disease, it is not new to California. The fact that there are no previously reported cases is because 1) until recently there have been no commercially available tests and 2) since BMD is not a reportable disease, nobody collects such information.
This study highlights the pressing need to develop better diagnostic tests capable of detecting all tick-borne diseases–and to collect the results of those tests in a way that’s accessible to the public.
Interestingly, the CDC states that PCR and antibody-based testing for Bm are under development and not widely available but can be ordered from a few CLIA-approved labs.
Now that’s sweet isn’t it? Up until now the CDC has vilified all CLIA approved labs – especially for Lyme testing.
Dr. Cameron points out the hypocrisy marvelously here: http://danielcameronmd.com/fda-test-borrelia-miyamotoi/ Researchers have had to diagnose B. miyamotoi based on blood smear, direct detection of spirochetes in cerebrospinal fluid and follow-up polymerase chain reaction (PCR) and molecular detection of B. miyamotoi DNA in acute whole blood from patients. These are all non FDA-approved tests. So, where would these patients be if the FDA insisted on only its tests being utilized?
You gotta love fate.
Buchholz MJ, Davis C, Rowland NS, Dick CW.
Parasitology Research, online first 2018 Feb 7.
The incidence of tick-borne zoonoses such as Lyme disease has steadily increased in the southeastern United States. Southeastern states accounted for 1500 of over 28,000 confirmed cases of Lyme disease reported in the United States during 2015. Borrelia burgdorferi, the etiologic agent of Lyme disease, is maintained in small mammal reservoirs and vectored to new hosts by ixodid ticks.
This study examined ecological relationships of the B. burgdorferi/vector/reservoir system in order to understand the dynamics of Lyme disease risk in Kentucky. Small mammals were captured using live traps from November 2014 to October 2015. Ticks were removed and blood and tissue collected from small mammals were screened for B. burgdorferi DNA by PCR with primers specific to the OspA gene.
Prevalence of B. burgdorferi (21.8%) in Kentucky small mammals was comparable to the lowest recorded prevalence in regions where Lyme disease is endemic. Moreover, infestation of small mammals by Ixodes scapularis, the primary vector of B. burgdorferi, was rare, while Dermacentor variabilis comprised the majority of ticks collected.
These findings provide ecological insight into the relative paucity of Lyme disease in Kentucky.
The conclusion of this study is all wrong. Bb was found Kentucky mammals. That in itself is important. Also, the fact the preponderance of ticks were dermacentor variabilis (wood tick or American dog tick) which supposedly has not been proven to be a competent vector of Bb as supposedly it doesn’t efficiently pass Bb from inside the tick to humans or other hosts), it does transmit Tularemia and Rocky Mountain Spotted Fever.
BTW: these transmission studies given as references for this fact were done from 1997-2006. It’s now 2018. http://labs.russell.wisc.edu/wisconsin-ticks/wisconsin-ticks/dermacentor-variabilis/ Notice it states, “It doesn’t efficiently pass Bb.” What if it passes it inefficiently? It still passes!
Regardless of whether the wood tick can transmit Bb or not, they do transmit pathogens. The fact that nearly 22% of small Kentucky mammals have Bb due to the black legged deer tick and most of the ticks they picked up were wood ticks, those deer ticks were particularly infected.
Hear ye, hear ye, the South has Lyme.
https://madisonarealymesupportgroup.com/2016/09/24/arkansas-kids-denied-lyme-treatment/ According to Dr. Naveen Patil, Director of the Infectious Disease Program, ADH,
“We don’t have Lyme Disease in Arkansas, we have the ticks that transmit Lyme Disease but we don’t have any recorded cases of Lyme Disease.”
https://madisonarealymesupportgroup.com/2017/03/02/hold-the-press-arkansas-has-lyme/ A news report emphasizing the CDC’s belief Arkansas is a “low incident” state in regards to Lyme Disease, is countered by the Arkansas Lyme Foundation that claims at least 150 cases, and they just started counting. http://www.thv11.com/news/local/arkansas-lyme-foundation-claims-over-150-lyme-disease-cases-in-state/414489522 (Video here)
“People are dying and I’m not exaggerating, people are calling us every week in desperate situations,” said Sikes.
https://madisonarealymesupportgroup.com/2017/10/24/no-lyme-in-oklahoma-yeah-right/ Last summer, a friend who lives in Oklahoma found a classic bullseye rash on her seven-year-old daughter.
“That’s a spider bite,” a local pediatrician told her. “We don’t have Lyme in Oklahoma.”
The doctor was wrong. Had my friend taken his advice, her daughter would not have been diagnosed in a timely fashion and she would likely have developed symptoms over the next few months or years. She probably would have become severely debilitated, and the infections might have crossed the blood-brain barrier and become chronic.
Get the picture yet? Lyme/MSIDS is everywhere.
Quit saying it’s rare!
Krause PJ, Carroll M, Fedorova N, Brancato J, Dumouchel C, Akosa F, Narasimhan S, Fikrig E, Lane RS.
PLoS One. 2018 Feb 8;13(2):e0191725. eCollection 2018.
To determine whether human Borrelia miyamotoi infection occurs in the far-western United States, we tested archived sera from northwestern California residents for antibodies to this emerging relapsing fever spirochete. These residents frequently were exposed to I. pacificus ticks in a region where B. miyamotoi tick infection has been reported.
We used a two-step B. miyamotoi rGlpQ assay and a B. miyamotoi whole-cell lysate (WCL) assay to detect B. miyamotoi antibody. We also employed Borrelia hermsii and Borrelia burgdorferi WCL assays to examine if these Borrelia induce cross reacting antibody to B. miyamotoi. Sera were collected from 101 residents in each of two consecutive years.
The sera of 12 and 14 residents in years one and two, respectively, were B. miyamotoirGlpQ seroreactive. Sufficient sera were available to test 15 of the 26 seropositive samples using B. miyamotoi and B. hermsii WCL assays. Two residents in year one and seven residents in year two were seroreactive to both Borrelia antigens.
Although discernible differences in seroreactivity were evident between the B. miyamotoi and B. hermsii WCL assays, infection with one or the other could not be determined with certainty. Sera from two Borrelia burgdorferi /B. miyamotoi seropositive subjects reacted strongly against B. miyamotoi and B. hermsii WCL antigens. Ecological, epidemiological, and clinical data implicated B. miyamotoi as the probable cause of infection among those whose sera reacted against both antigens.
Our findings suggest that human B. miyamotoi infection occurs in northern California and that B. hermsii and B. burgdorferi infections produce antibodies that cross-react with B. miyamotoi antigens. Health care professionals in the far-western United States should be aware that B. miyamotoi disease may occur throughout the geographic distribution of I.pacificus and that improved relapsing fever group spirochete antibody assays are urgently needed.
This study points out one the biggest reasons we are in this quagmire: poor testing and cross reactivity of antigens. Remember, testing for miyamotoi is new so folks could have been infected with this pathogen for a long time and it flew under the radar. They got tested for borrelia burgdorferi (Lyme) with a test that misses over half of all cases, and are sent home and told, “Go home and be well.”
There very probably are other strains and pathogens we don’t have testing for yet.
It also demonstrates Tick borne illness is everywhere, despite Speilman’s maps: https://madisonarealymesupportgroup.com/2018/01/19/how-ticks-find-you/ (Scroll down to comment section after article)
Looking through history with knowledgable eyes, historian M.M. Drymon underscores how tick-borne illness has been with us since the beginning of time, and that many prominent historical figures showed signs of it in her latest book, The Persistent Spiral – The Ancient History of Lyme Disease and Tick-borne Infections.
First, she gives details of Ozti, the ancient man discovered in 1991 who represents the earliest documented case of Lyme Disease. Evidently, Ozti was carrying mushrooms with antibiotic qualities. He walked the forested area now located between Italy and Austria – one of the highest rates of modern LD in Europe. They even know he died in the Spring due to the intact pollen cells in his stomach.
Interestingly, from many standpoints, he had 57 tattoos – many in places that coincide with acupuncture points used to treat Lyme and pain relief – some 2,000 years before their documented use in China. https://www.huffingtonpost.com/2015/01/26/otzi-iceman-new-tattoo_n_6546884.html
And while all these intimate details of a fellow sufferer are intriguing, the recent discovery of what Drymon calls the pot smoking, dispersed living, individualistic Bronze Age Cowboys, enlightens for sure. The discovery of the Yamnaya helps explain old Chinese books describing people of great height, deep-set blue or green eyes, long noses, full beards,and red or blonde hair. These nomadic horse breeding and cattle and sheep herding people contributed to many ancestries and very well may relate to how modern patients handle Lyme Disease (LD). For more on the Yamnaya: https://dna-explained.com/2015/06/15/yamnaya-light-skinned-brown-eyed-ancestors/
Drymon and many others believe genetics to be one reason some become so ill with tick-borne illnesses.
The Yamnaya were grassland inhabiters who eventually migrated into Northern Europe and may be the reason most of us can tolerate lactose, which was rare previously. They also might be a reason we don’t handle tick illness well. Since they lived outside tick infested areas, they most probably had immune systems inexperienced with Tick borne illness (TBI’s) and when exposed suffered with autoimmune illness.
Drymon states the Chinese had more experience treating LD due to historically inhabiting temperate forests which harbor ticks. Traditional Chinese medicine indicates this fact by having treatments for spirochetal diseases and specific herbs for Bell’s palsy, joint pain, inflammation, heart problems, fever and skin diseases, and convulsions – all of which are TBI symptoms.
Fast forward to the Crusades and the fact both King Richard I and Philippe Augustus II became ill and nearly succumbed to Trench Mouth which is caused by Bacillus fasiformis & Borrelia vincenti (a strain of borrelia, and also a spirochete). Richard apparently became ill again later with Autumnal Fever which has a relapsing nature and is proposed to be tick-borne.
Then there’s Catherine of Aragon, lover of the hunt, who after staying at a hunting lodge, survived The Sweat and was periodically ill from that point on. A physician of the time described The Sweat as a pestilence with copious sweating, stinking, redness of face and body, continual thirst, with a great headache. Symptoms followed a pattern – sudden flu-like symptoms, apprehension, headaches, shivering, with muscle aches, and fatigue. Then came gut pain, vomiting, a hot and sweaty stage followed by headaches and delirium. There were also chest pains and difficulty breathing with great fatigue. (Sound familiar?) If patients didn’t die, they were repeatedly afflicted. It seemed to be a summer illness found in rural families. It also made many chronically affected for life.
There is no record of The Sweat until the landing of Henry Tudor’s soldiers in Wales after camping in forest edge environments. After that there were periodic outbreaks and two hundred and fifty years later an identical illness appeared in the exact same region. Another physician noted that black marks were sometimes on the skin.
Drymon lists the symptoms of numerous tick borne infections and how they look precisely like The Sweat. Symptoms of Borrelia miyamotoi cause high relapsing fevers, vomiting, nausea, diarrhea, heart problems, shortness of breath, and a whole slew of neurological symptoms. Babesia is known to cause drenching sweats, anxiety, fatigue, headache, muscle, chest, and hip pain, and the ever lovely shortness of breath.
Poor Catherine struggled through seven pregnancies and her confessor reported that one knee pained her. If the babies weren’t still-born, they all died young except one daughter who became Queen Mary I. After Catherine was put to death by Henry, his next wife, Anne Boleyn battled The Sweat as well, and after marrying Henry also had a series of miscarriages with the only surviving heir being a daughter who became Queen Elizabeth I. Catherine and Anne had a lot in common, including the same husband, and while Drymon didn’t go over the probability of sexual transmission, there is evidence: https://madisonarealymesupportgroup.com/2017/02/24/pcos-lyme-my-story/ and https://madisonarealymesupportgroup.com/2018/02/06/lyme-in-the-southern-hemisphere-sexual-transmission/
Regarding pregnancy and TBI’s, fertility problems, miscarriages, birth defects and still births, are all possibilities. https://madisonarealymesupportgroup.com/2017/10/15/pregnancy-in-lyme-dr-ann-corson/ Autopsy’s have revealed borrelia in the placenta, spleen, fetal myocardium, kidneys, liver, arachnoid space of fetal mid brain, and bone marrow. https://durayresearch.wordpress.com/about-2/seven-provocative-p2/
After Anne was put to death by Henry, and all likenesses of her were ordered to be destroyed, one of the few surviving pictures show a protruding lymph node below her jaw – another common TBI symptom.
Drymon goes through the various theories of what caused The Sweat, and logically refutes them all except for tick-borne illness. One telling quote by John Josselyn in the early seventeenth century states,
“there be infinite numbers of tikes hanging upon the bushes in summer time that will cleave to a man’s garments and creep into his breeches eating themselves in a short time into the very flesh of a man. I have seen the stockins of those that have gone through the woods covered with them.”
Evidently ticks were a problem then too.
Dr. John Caius who treated patients with The Sweat recommended regular burnings of fields and forest understory, as well as insect repellents and herbal treatments such as enula root and wormwood, herbs that are known even today to have action against borrelia and Babesia.
Drymon also discusses burnings in her other book, Disguised as the Devil,
https://madisonarealymesupportgroup.com/2016/10/08/did-lyme-create-witches/, another fascinating read about TBI’s and the witchcraft hysteria. She draws a connection between the fact that burnings were often abandoned in times of war due to upheaval and the absence of men to do the job. This in turn allowed ticks to propagate which in turn probably meant more people got infected – particularly women of that era who wore long dresses that essentially became tick drags.
Unfortunately, this effective method of reducing the tick population is frowned upon today due to the fear of pollution. Drymon states the ramifications of burning should quantified to determine its seriousness and if accommodations could be made.
While the entire book is fascinating, and frankly a lot of fun to read, one of the most important take-aways for me is the ever present issue of reducing ticks safely, effectively, and economically.
Burning is such a simple yet brilliant method that it begs to be used.
Being a Lyme patient and advocate, I’ve read about burning before. In fact, when I asked an older Wisconsin Representative who has lived here his whole life why this practice was abandoned, he repeated precisely what Drymon said about folks being concerned about pollution. He also said burnings worked and he wished they were still being done.
When I asked well known and respected entomologists in Integrated Pest Management, they assured me that burnings weren’t successful and gave me a 1998 study conducted in Connecticut using a single controlled burn on two different days with varying burn intensities. The results state that in both burns ticks were reduced substantially (74% and 97%). What the authors felt made it unsuccessful was an abundance of ticks in the fall – meaning, they felt it was temporary.
I detect much more excitement from those in the field when you mention releasing GMO mice, lacing pellets with pesticides for rodents to eat, and high powered acaricides. All things that cost a lot of money and have significant blow-back to the environment and humans. https://madisonarealymesupportgroup.com/2016/06/21/first-frankenbugs-now-frankinmice/ and https://madisonarealymesupportgroup.com/2017/07/10/wolbachia-the-next-frankenstein/
I was thankful for Drymon’s usage of a 2014 burn study performed in Georgia and Florida over a two year time period that indicates regular prescribed burning is an effective tool for reducing ticks and probably reduces disease as well.
I think we need to seriously revisit burning.
Drymon’s book reminds us that tick borne illness is as old as time and if we are going to get well it would behoove us to learn from the past.
http://www.courant.com/news/connecticut/hc-tick-bite-verdict-stands-20180209-story.html by Edmund H. Mahony, Contact Reporter
A federal appeals court has upheld a $41.7 million jury verdict for a Connecticut private school student who was severely and permanently disabled after developing encephalitis from a tick bite while on a class trip to China.
The case, which has been litigated for nine years, established that schools in Connecticut are obligated to protect children in their care, a conclusion that insurers, schools and other groups have warned could reduce educational travel opportunities for students.
The suit was brought in federal court in Bridgeport in 2009 by the parents of Cara Munn of New York, who at age 15 and at the conclusion of her freshman year at the private Hotchkiss School in Salisbury, was bitten by a tick and developed encephalitis while hiking in a remote, mountainous area of China during a school study program.
“She is gratified that the justice system worked,” her lawyer, Antonio Ponvert said Friday. “She is also happy and proud that her case might encourage custodians of minor children to be more careful.”
As a result of the insect bite, Munn suffered permanent brain damage and became seriously disabled. She has lost control over some movement, has lost problem-solving ability and is unable to speak. Her condition is expected to worsen with age.
She and her family sued the school for negligence and her jury returned the staggering verdict in 2013, ordering the school to pay her and her family $10.25 million in economic damages and $31.5 million for pain and suffering.
Lawyers for Hotchkiss argued that the school had no duty to warn Munn and her parents against contracting tick-borne encephalitis on 2007 trip because such an event could not have been foreseen.
The U.S. Court of appeals for the Second Circuit, which took the appeal, sent the case the the state Supreme Court for the resolution of two, central questions: Are Connecticut schools obligated by state policy and law to warn of the danger of contracting an insect-borne illness on field trips? And was a $41.7 million verdict excessive?
The state’s high court said last summer there is an “affirmative duty” to warn and upheld the verdict.
The case returned to the second circuit, where a panel of three judges published an unsigned summary order Tuesday dismissing the school’s remaining appellate claims and affirming the verdict.
The Hotchkiss lawyers were not immediately available Friday. If the school chooses to press its appeal further, it could ask the entire second circuit bench to hear the case or petition the U.S. Supreme Court.
A strain of bacteria commonly found in milk and beef may be a trigger for developing rheumatoid arthritis in people who are genetically at risk, according to a new study from the University of Central Florida.
A team of UCF College of Medicine researchers has discovered a link between rheumatoid arthritis and Mycobacterium avium subspecies paratuberculosis, known as MAP, a bacteria found in about half the cows in the United States. The bacteria can be spread to humans through the consumption of infected milk, beef and produce fertilized by cow manure.
The UCF researchers are the first to report this connection between MAP and rheumatoid arthritis in a study published in the Frontiers in Cellular and Infection Microbiology journal this week. The study, funded in part by a $500,000 grant from the Florida Legislative, was a collaboration between Saleh Naser, UCF infectious disease specialist, Dr. Shazia Bég, rheumatologist at UCF’s physician practice, and Robert Sharp, a biomedical sciences doctoral candidate at the medical school.
Naser had previously discovered a connection between MAP and Crohn’s disease and is involved in the first ever phase III-FDA approved clinical trial to treat Crohn’s patients with antibiotics. Crohn’s and rheumatoid arthritis share the same genetic predispositions and both are often treated using the same types of immunosuppressive drugs. Those similarities led the team to investigate whether MAP could also be linked to rheumatoid arthritis.
“Here you have two inflammatory diseases, one affects the intestine and the other affects the joints, and both share the same genetic defect and treated with the same drugs. Do they have a common trigger? That was the question we raised and set out to investigate,” Naser said.
For the study, Bég recruited 100 of her patients who volunteered clinical samples for testing. Seventy-eight percent of the patients with rheumatoid arthritis were found to have a mutation in the PTPN2/22 gene, the same genetic mutation found in Crohn’s patients, and 40 percent of that number tested positive for MAP.
“We believe that individuals born with this genetic mutation and who are later exposed to MAP through consuming contaminated milk or meat from infected cattle are at a higher risk of developing rheumatoid arthritis,” Naser said.
About 1.3 million adults in the U.S. have rheumatoid arthritis – an autoimmune and inflammatory disease that causes the immune system to attack a person’s joints, muscles, bones and organs. Patients suffer from pain and deformities mostly in the hands and feet. It can occur at any age but the most common onset is between 40 and 60 years old and is three times more prevalent in women.
Although case studies have reported that some RA patients suffer from Crohn’s disease and vice versa, the researchers say a national study needs to investigate the incidence of the two diseases in the same patients.
“We don’t know the cause of rheumatoid arthritis, so we’re excited that we have found this association,” Bég said. “But there is still a long way to go. We need to find out why MAP is more predominant in these patients – whether it’s present because they have RA, or whether it caused RA in these patients. If we find that out, then we can target treatment toward the MAP bacteria.”
The team is conducting further studies to confirm findings and plan to study patients from different geographical and ethnic backgrounds.
“Understanding the role of MAP in rheumatoid arthritis means the disease could be treated more effectively,” Naser said. “Ultimately, we may be able to administer a combined treatment to target both inflammation and bacterial infection.”
Naser holds a Ph.D in Medical Microbiology from New Mexico State University. He joined UCF in 1995. He has been investigating Crohn’s disease and other auto-immune diseases for more than 30 years. He has published more than 100 peer-reviewed articles and has presented his work at numerous conferences. He has several patents including a licensed DNA technology for detecting MAP.
Bég, a board-certified rheumatologist, has been with UCF since 2011 after completing her fellowship in rheumatology at Baylor College of Medicine in Houston. In addition to practicing medicine at UCF Health, she is a full-time faculty member at the college. Her research and clinical interests include conditions such as rheumatoid arthritis, psoriatic arthritis, lupus and osteoporosis.
Lyme/MSIDS patients need to take note of this study as RA is often undiagnosed tick-borne infections – including Mycoplasma. The genetic issue as well as consuming infected animal products should be a concern to us all; however, being infected with TBI’s is right up there on the list.
BTW: Garth Nicholson has been sleuthing on the role of Mycoplasma and Lyme/MSIDS for years: https://madisonarealymesupportgroup.com/2017/07/16/mycoplasma-and-other-intracellular-bacterial-infections-in-rheumatic-diseases-comorbid-condition-or-cause/
And previously to that, Dr. Brown way back in the 40’s and 50’s believed that RA was caused by mycoplasmas and used tetracycline rather than prednisone, the drug of choice. He eventually modified his treatment which included Minocycline and brought over 10,000 patients into remission. (This demonstrates the importance of dealing with the infection)
I find it interesting that Minocycline was probably the drug that helped me the most: https://madisonarealymesupportgroup.com/2017/06/04/minocycline-for-ms-and-much-more/
https://madisonarealymesupportgroup.com/2015/08/12/connecting-dots-mycoplasma/ This link also shows Nicholson’s discovery that 90% of evaluated ALS patients had Mycoplasma. 100% of ALS patients with Gulf War Syndrome had Mycoplasma and nearly all of those were specifically the weaponized M. fermentans incognitos. One of the hallmark symptoms of Mycoplasma is fatigue.
And the bad news for us is that Nicholson’s experience has found Mycoplasma to be the number one Lyme coinfection, and similar to other coinfections in that it can be supposedly cleared for years only to reappear when conditions are right.
One other note is that immunosuppressive drugs for folks that have TBI’s are going to worsen their condition, so TBI’s must be ruled out before the administration of them, which is going to be tricky business as the tests for all of these pathogens is abysmal. I highly recommend having patients fill out the Horowitz questionnaire along with testing and for doctors to make a clinical diagnosis not based on testing only: https://madisonarealymesupportgroup.files.wordpress.com/2016/01/symptomlist.pdf
This study also shows the dire need for medical professionals to be properly trained regarding TBI’s or they run the risk of putting patients on immunosuppressive drugs to their demise. So far the education in med school on Tick borne infections is antiquated and brief, considering Lyme is the #1 vector borne disease in the U.S. No one has accurate numbers on coinfections. If you know of doctors who are willing to be trained in this area, please send them this: https://madisonarealymesupportgroup.com/2017/06/20/help-doctors-get-educated-on-lyme-and-tick-borne-illness/Dr. Betty Maloney, President, Partnership for Tick-borne Diseases Education created LymeCME.info a website built specifically for the purpose of offering accredited, evidence-based continuing medical education (CME) modules on Lyme and other tick-borne diseases (TBD) for doctors and other healthcare professionals. Doctors will like the convenience of on-demand learning that’s available on PC and mobile devices. The modules I developed for LymeCME provide a concise review of the evidence, highlighting points that are especially relevant to patient care. And, they’re free!
https://madisonarealymesupportgroup.com/2017/08/26/interstitial-cystitis-and-lyme-disease/ Dr. Rawls states: “Borrelia, the microbe commonly associated with Lyme disease, could be a culprit. However, I would lay odds on mycoplasma and a closely related bacterium called ureaplasma. About 75% of chronic Lyme disease sufferers have been found to harbor at least one species of mycoplasma.
It fits. Mycoplasma and ureaplasma are the smallest of all bacteria. They are obligate intracellular microbes — which means they must live inside cells of a host to survive. They typically infect linings of the body — linings of lungs, intestines, joints, and the urinary tract.
Different species of mycoplasma and ureaplasma prefer certain areas of the body, but any species of these microbes can be found in different places the body. The most common species found in the urinary and reproductive tract are Ureaplasma urealyticum and Mycoplasma hominis. These microbes typically spread sexually, but they can be acquired by other routes. Mycoplasma pneumoniae, a frequent cause of respiratory infections, can also be found in the urinary tract. Mycoplasma and ureaplasma are notoriously difficult to culture.”
But back to Mycobacterium…..Dr. Horowitz is finding that Mycobacterium drugs are working for his treatment resistant patients: https://madisonarealymesupportgroup.com/2016/10/09/mycobacterium-drugs-for-ld/ The case study has based on a woman with Borrelia burgdorferi, Borrelia hermsii, possible prior exposure to tularemia, exposure to Mycoplasma pneumonia, multiple viruses, fibromyalgia, and rheumatoid arthritis.
Under Dr. Horowitz’s care she improved from 30% to 50%, but with the addition of Dapsone had a sudden fourfold increase in tularemia titers as well as Bartonella titers turning positive. While making continuous progress the patient had ongoing joint pain which interfered with sleep as well as ongoing severe blood-filled blisters, oral/genital ulcerations, and increased granulomas.
While a rheumatologist wanted to put her on an immunosuppressive, she and Dr. Horowitz chose to try 500mg (based on body weight) of PZA twice a day combined with rifampin and minocycline. Her liver was monitored every two weeks and was helped with alpha lipoid acid 600mg and milk thistle 250mg. Two months later she reported up to 80% of normal functioning…
The fact that the addition of a mycobacterium drug that gave this woman 80% of normal functioning is something that needs to be noted. It also leads to the conclusion that her prior diagnosis of RA is probably infectious in nature and improved with microbials.
Now if that isn’t a success story, I don’t know what is. So something is going on here with Mycobacterium or a mycobacterium-like pathogen. This needs to be hunted to ground.