Archive for the ‘Mycoplasma’ Category

Role of Myofascial Therapy in Interstitial Cystitis

Many Lyme/MSIDS patients deal with Interstitial Cystitis (IC).  Recently, Dr. Rawls wrote a great article on the topic found here:  Dr. Rawls believes that IC could be triggered by Lyme or Mycoplasma and that herbs could be of great benefit as it hasn’t responded well to antibiotics.

The following article supports the use of myofascial therapy, a manipulation technique that is both internal and external to the pelvic floor (focusing specifically on abdominal, pelvic, and hip girdle muscles and other tissue).”


February 11, 2016 In Women’s Health 
Rosia Parrish, Jennifer Pilon, Daeyon JooRi Jun, Kris Somol, ND

The American Urological Association defines Interstitial Cystitis (IC)/Pelvic Bladder Syndrome as an unpleasant sensation perceived to be related to the urinary bladder that is associated with lower urinary tract symptoms greater than 6 weeks’ duration, in the absence of infection or other identifiable causes.1 The condition is 5 to 10 times more common in women than in men. In the absence of clear diagnostic criteria, this condition is underdiagnosed, with an estimated prevalence of 3 to 8 million women in the United States.2

The treatment of IC is a clinical challenge. As a diagnosis of exclusion without a clear etiology, first-line treatment strategies for IC are varied and tend to focus on food-trigger avoidance, stress reduction, and bladder retraining. However, these therapies remain ineffective for some patients, warranting implementation of second-line therapies. These include pelvic floor physical therapy, amitriptyline, antihistamines, and intravesical drug combinations.3

The question of whether myofascial physical therapy (MPT) is an effective treatment for IC is a particularly relevant question for naturopathic doctors, many of whom are trained in and practice a variety of hands-on myofascial therapies. When choosing from among these second-line treatments, naturopathic philosophy would suggest that manual physical therapy would be more effective than conventional treatments in treating the cause of the condition, particularly in cases where somatic abnormalities of the pelvic floor are contributing to the syndrome. The goal of this literature review is to investigate the following clinical question: In female patients with a diagnosis of interstitial cystitis, does the use of myofascial physical therapy decrease symptoms of urinary urgency, urinary frequency, and pelvic pain when compared with conventional treatments?

A search of PubMed and Embase was performed, including combinations of the following terms (designated medical subject headings and other relevant terms): physiotherapy, interstitial cystitis, therapeutics, complementary therapies, physical therapy modalities, alternative medicine, massage, pelvic floor rehabilitation, electrostimulation, and physiatrics. The original searches were done without limiting them to randomized controlled trials (RCTs), in order to accurately assess the current state of the research and identify possible directions for other searches. Combinations of the terms interstitial cystitis, physical therapy modalities, therapeutics, and massage revealed studies that were the most relevant to our clinical question. In the final analysis, only English language RCTs conducted within the last 10 years that were available as free, full-text articles through Bastyr University were considered for review. Complete detail of searches and results is shown in Table 1 (Please see link above for Table 1).

There were 3 English-language RCTs that fulfilled our final search criteria. Of note, there were no studies that directly compared MPT with conventional drug treatments for IC. One particular study was ultimately chosen for review because it was most relevant to the clinical question being asked and to the scenarios which we would be likely to encounter in naturopathic practice.4 This study was performed solely on women (as opposed to other studies which included both women and men with painful bladder syndrome), who had not experienced relief with at least 1 course of conventional first-line management for IC. This is relevant to the fact that almost all patients experiencing IC symptoms are female. Additionally, it is consistent with how many patients seek out naturopathic medicine after experiencing a lack of success with conventional treatments. In a primary care practice, adult women may present with IC within a wide range of ages. This clinical reality is reflected in the study, which included women aged 18-77. Finally, the outcomes measured in this study not only included specific frequency of symptoms, but also a global, subjective measure of improvement as determined by the patient. This contributed to our choice of study, since including this outcome may better reflect changes in quality of life post-treatment than symptom-based questionnaires alone.

The study chosen for review4 sought to answer whether females aged 18-77 with a clinical diagnosis of IC or painful bladder syndrome (PBS), using a standardized myofascial physical therapy protocol (MPT) as compared to a standardized Western global therapeutic massage (GTM) program, show improvement of overall symptom picture and/or specific symptoms of pain, frequency, urgency, and sexual function. Participants were recruited from July of 2008 through May of 2009 across 11 academic clinical centers across North America, and the study lasted 12 weeks. Physical therapists (PTs) providing the MPT were trained in a standardized protocol to minimize variability between therapists. The protocol was not described in the paper chosen, but has been described in detail in a feasibility study conducted by the same authors.5

There were 2 arms of the study: MPT and GTM. MPT is a manipulation technique that is both internal and external to the pelvic floor (focusing specifically on abdominal, pelvic, and hip girdle muscles and other tissue). GTM, in contrast, is a full-body therapeutic massage. Those patients in the GTM treatment group had a series of 10 one-hour massages.

The inclusion criteria included clinical diagnosis of IC/PBS, average recorded ratings for bladder pain, frequency, and urgency of at least 3/10, and present for a minimum of 3 months and a maximum of 3 years. Furthermore, pelvic floor tenderness on vaginal examination, identified by the study’s physician and confirmed by a PT, was required for study inclusion. There were no significant differences in demographics between the MPT and the GTM groups at baseline. Demographic factors assessed were age, ethnicity, education level, employment status, and annual family income; demographic factors were listed in the feasibility study cited in this article.5 Of note, no other specific prognostic factors relating to their clinical diagnosis were assessed, including smoking. Most of the patients were Caucasian, and the exclusion of women without pelvic pain on vaginal examination eliminated a significant number of IC sufferers for whom this treatment might be beneficial. For this reason, the results are difficult to generalize to the population at large.

Patient assignment to treatment groups was randomized. Physical examiners and nurses collecting data were blinded to treatment assignment, but there was no indication of whether investigators were blinded from the process of randomization. Outcome assessors and all study coordinators were also blinded to the group allocation. Randomization process occurred via a pre-specified sequence distributed in a series of sealed envelopes to receive MPT or GTM. Patients were analyzed in the groups to which they were randomized; there was no crossover between the groups. Even though the patients were not told outright what group they were assigned to, given the differences between MPT and GTM, it is likely that they were aware of the group to which they were assigned.

Outcomes were measured with the 7-point Global Response Assessment (GRA) scale, the O’Leary Sant IC Symptom and Problem Index, a 24-hour urinary voiding diary, the 2000 Female Sexual Functioning Index, and the 12-Item Short-Form Health Survey.

Of the 81 patients recruited, 78 (96%) were able to complete the full 12-week duration of the study (including initial follow-up at the completion of treatment phase at 12 weeks, and additional follow-up for 3 months after the 12-week follow-up). Of these 78 participants, 72 (92%) completed at least 7 of the 10 treatments that were assigned to them during the 12 weeks: In the MPT group 55% completed all 10 treatments, and in the GTM group 38% of the GTM group finished 100% of their 10 treatments. The 3 who withdrew from the study had received <5 treatments. During the follow-up phase of the study, the retention rate was smaller, with 77% of the MPT, and 67% of the GTM, participating. Because many of the study’s subjects did not participate in the final follow-up session, it is difficult to draw conclusions about durability of treatment.

The primary outcome of this study was that 59% of the MPT group, compared to 26% in the GTM group, reported moderate or marked improvement (p=0.0012) on the GRA scale. Within the GTM group, 43% reported no change in symptoms, compared to only 18% of the MPT group reporting no change. Both treatment groups reported improved symptoms via the O’Leary Sant IC Symptom and Problem Index of pain, urgency, frequency; there were also reported improvements in quality of life as well. No statistical significance was noted among these secondary symptom outcomes of the study. The Mantel-Haenszel test was employed to take into account the need to control variability at the 11 sites. The Number-Needed-to-Treat to determine 30% effect was 88, and only 81 were recruited; however, this study was still significantly powered.

Adverse events (AE) were also reported. Bladder or pelvic pain was the most commonly reported AE, reported in 14% of the participants. There was no statistical significance in the number of AEs reported by each treatment group. The authors conjectured that the AEs reported, especially that of pain, in part had to do with the intermittent nature of the disorder and was not necessarily related to treatment intervention. Other AEs reported were infection (reported by 12% of the patients), constitutional symptoms like fever (11%), and digestive symptoms (10%).

The age range of subjects in the study (18-77) and the duration of their symptoms (3 months to 3 years) are similar to patients who would potentially be seen in naturopathic medical clinics. It is feasible for naturopathic physicians to determine pelvic floor tenderness during a vaginal exam and to discern suitable candidates for this treatment option. It would also be feasible to refer patients to physical therapists for co-management. However, determining the optimal elements of an effective MPT regimen and finding PTs who can deliver effective pelvic floor MPT might be an obstacle.

The study reviewed here answered the question of whether the use of MPT can improve symptoms associated with IC, including but not limited to urinary urgency, urinary frequency, and pelvic pain. However, the paper did not compare the effects of MPT to conventional treatments, such as food-trigger avoidance, bladder retraining methods, or pain medications. In fact, the study did not disclose whether subjects were concurrently using any other treatment modalities while participating in the study, potentially biasing the results.

Further questions raised by the literature review process and the results of this paper include whether the results of the study can be generalized to the IC patient population at large. For example, it is questionable whether MPT would also be beneficial to patients who do not demonstrate pelvic tenderness on examination. This also points to the currently inadequate understanding we have about the relationship between somatic abnormalities and IC. Another aspect of whether the study could be generalizable centers around the fact that study participants were primarily Caucasian.

A future study examining the durability of subjects’ improvement with this therapy would make the results more clinically meaningful. Due to the loss to follow-up at 3 months post-treatment, the question of how long the beneficial effects of MPT last, remains. It would be very exciting, indeed, to investigate whether the effects are long-lasting and could potentially be a cure of sorts to the unending suffering experienced by patients with interstitial cystitis.

Finally, developing an effective training program for physical therapists and other providers would be critical so that this therapy would become accessible to a large number of patients.

The evidence from the study reveals that MTP is indeed beneficial for improving symptoms of IC, suggesting that physical therapy is an important modality to consider in a treatment plan for a patient suffering from the disease. It adds credibility to the idea that there are specific pelvic somatic abnormalities involved with IC, as the study showed the treatment effect was not merely due to general therapeutic touch.

The process of finding a robust paper to review to answer our question yielded only 1 study that fit the aforementioned criteria. This points to the lack of research available on myofascial physical therapies to treat IC.

However, even with the limited evidence, considering the strength of the paper reviewed and the fact that no serious adverse events were reported, MPT can be considered a safe and potentially effective therapy for IC that could be recommended and provided to patients. The question as to whether it is more effective than other first- and second-line treatments still remains and requires further research.


Interstitial Cystitis and Lyme Disease

by Dr. Bill Rawls
Posted 8/25/17

Things often come around.

Early in my career practicing Ob/Gyn, I became aware of a subset of patients who suffered from a condition called interstitial cystitis (IC), sometimes referred to as painful bladder syndrome.

People with interstitial cystitis feel like they have a bladder infection that never goes away. It doesn’t respond to antibiotics, and urine cultures are typically negative. Because these patients are often treated repeatedly with antibiotics, however, they frequently end up having chronic urinary tract infections with antibiotic-resistant bacteria induced by taking antibiotics. The condition occurs more often in women than men at a 5:1 ratio.

Interstitial cystitis is considered idiopathic — cause unknown. It is notoriously difficult to treat. I developed a special compassion for these people because no other physicians wanted to see them. For years, I searched for solutions, but my efforts were focused primarily on relieving symptoms — gains were minimal and short-lasting.

Symptoms of Interstitial Cystitis

  • Urinary frequency & urgency
  • Bladder pain with full bladder
  • Pain in perineum & urethra
  • Chronic pelvic pain
  • Vulvar/vaginal pain (female)
  • Pain in testicles (male)
  • Painful sex

The Lyme Connection

Interestingly, with my professional interests now focused on chronic Lyme disease, I’m starting to hear from chronic Lyme patients who suffer from bladder pain and symptoms consistent with IC. I’m also hearing from men with chronic Lyme who have bladder symptoms and chronic prostatitis (chronic infection of the prostate gland).

And, interestingly, remembering back to patients from the past, sufferers of IC frequently had chronic pain in other areas of the body. Many of them also had fatigue and symptoms common to fibromyalgia and chronic Lyme disease.

This makes me believe there has to be a microbial connection. 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. Twenty-five years ago, when I first started practicing medicine, routine testing for mycoplasma and ureaplasma was not available. That’s starting to change — DNA testing has become more reliable, and providers are testing for these microbes more routinely.

And they are finding them — not just in symptomatic patients, but also commonly in people with no symptoms.

That makes things complicated — mycoplasma and ureaplasma are commonly found in the urinary tracts of people who don’t have symptoms. It turns out that it’s actually a very common microbe. Some experts have even defined it as a normal flora. This is why many experts discount the connection between mycoplasma/ureaplasma and bladder problems.

It presents the same kind of conundrum found in chronic Lyme disease — why do some people with these microbes develop symptoms and others do not?

What I didn’t know 25 years ago that I learned from understanding chronic Lyme disease is that the immune system is the key. If people have robust immune function, they can harbor these microbes and not have symptoms. People become chronically ill only when a perfect storm of factors comes together to disrupt immune function, which allows the microbes to flourish.

Therefore the solution must go beyond killing or suppressing microbes — you must restore immune system functions to optimal levels to overcome this illness.

Overcoming Mycoplasma and Ureaplasma

Mycoplasma and ureaplasma respond poorly to synthetic antibiotics for the same reason that other microbes associated with chronic Lyme disease respond poorly to antibiotics — they live inside cells, grow very slowly, and occur in low concentrations in tissues. In addition, mycoplasma and ureaplasma do not have a typical cell wall and other characteristics common to bacteria.

To control them, you must suppress them for a very long time and boost immune function at the same time. If you try to do it with synthetic antibiotics, normal flora are disrupted long before the targeted microbes are eradicated.

Herbs provide a more practical solution. Herbs suppress these types of microbes, but do not disrupt normal flora, so they can be used for extended periods of time (months to years) without concern. Herbs also reduce inflammation and boost immune functions — especially natural killer cells important for eliminating cells infected with microbes.

My favorite herb for mycoplasma and ureaplasma in the urinary tract is anamu (Physalis angulata) because it is concentrated in the intestines and urinary tract. The dose I recommend is 1200 mg (2 – 600 mg capsules) twice daily. It is well tolerated with only noticeable side effect being a mild odor to urine and stool. The herb comes from South America, but is readily available from many manufacturers online.

Mullaca (Physalis angulata), another South American herb, is also good for mycoplasma species. It can be taken as a complement to amamu. It can be found online as a loose powder (add to smoothies or make your own capsules) or tincture, as well.

Stephen Buhner, in his book defining therapy for mycoplasma, recommends Chinese skullcap, Isatis, Houttuynia, Sida acuta, and Cordyceps for a primary herbal protocol. I consider Cordyceps and Chinese skullcap to be part of a core protocol for chronic Lyme in general.

Individuals are reporting symptomatic relief of IC symptoms with use of essential oils rubbed into the pubic area several times a day. I have been recommending a formula of tea tree oil and frankincense oil mixed 1:4 in a carrier oil, such as jojoba or grapeseed oil. Recently, I’ve also been recommending adding cannabidiol oil (CBD) from hemp (get a product with 1500 mg CBD per fluid oz.). So far, people are reporting positive benefits.

The recovery protocol for overcoming mycoplasma and ureaplasma in the urinary tract mirrors recovery from chronic Lyme disease or any other condition associated with chronic immune dysfunction. Focusing on a specific microbe alone is not enough; immune system function must be restored. Primary antimicrobial herbs and immune modulating herbs, complemented by cultivation of a healing environment within the body, are your best allies in the fight against interstitial cystitis and Lyme disease.

Dr. Rawls is a physician who overcame Lyme disease through natural herbal therapy. You can learn more about Lyme disease and recovery in Dr. Rawls’ new best selling book, Unlocking Lyme. You can also learn about Dr. Rawls’ personal journey in overcoming Lyme disease and fibromyalgia in his popular blog post, My Chronic Lyme Journey.


Wonderful article.  Thank you Dr. Rawls for explaining a particularly troubling issue that Lyme/MSIDS patients can suffer from.

More on Mycoplasma:

“….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 incognitus.
*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 can be supposedly cleared for years only to reappear when conditions are right.”

For more:

The evidence from the study reveals that MTP (Myofascial Therapy) is indeed beneficial for improving symptoms of IC, suggesting that physical therapy is an important modality to consider in a treatment plan for a patient suffering from the disease. It adds credibility to the idea that there are specific pelvic somatic abnormalities involved with IC, as the study showed the treatment effect was not merely due to general therapeutic touch.

Of Birds and Ticks

In the Battle Against Ticks and Lyme Disease, Scientists Look to the Skies

  JUL 3, 2017

As we head into the Maine outdoors this summer, the all-too-familiar warnings about how to avoid ticks reverberate in many of our heads.

Stay on the trail. Steer clear of wooded and brushy areas where ticks congregate.

But while most of us take pains to dodge the eight-legged pests, Chuck Lubelczyk heads straight for them.

As a field biologist at the Maine Medical Center Research Institute’s Lyme and Vector-Borne Disease Laboratory, he studies the spread of diseases carried by ticks, as well as by mosquitoes. That means venturing out into the fields, forests and coastlines of Maine to collect the bugs and evaluate where they pose the most risk to humans.

On a recent June day, Lubelczyk trudged into the greenery of the Wells Reserve, a 2,250-acre spread in York County headquartered at a restored saltwater farm. He partnered with researchers from the Biodiversity Research Institute in Portland to collect ticks from creatures less often associated with them: birds.

The team, assisted by several interns, set up wide nets to ensnare the birds as they flew through the area. They then delicately extricated them, tucked the birds into breathable collection bags, and toted them to a shady picnic table for easier handling. Using tweezers, the team plucked off each tick — typically feasting around the birds’ eyes, bills, and throats — and preserved the bugs for later testing at the lab.

Lubelczyk held up a vial containing at least 50 tiny nymphal deer ticks swirling in a preservative solution. They’d been tweezed off a single bird, a towhee, that morning.

Once free of ticks, the birds were then safely released to continue on their way. (Video here)

While mice, chipmunks and deer get most of the attention as hosts for ticks, “Not a lot of people talk about the bird issue,” he said. “They’re understudied in a big way, I think. They do have a real role to play.”

Ticks are an annoyance to birds, but they don’t transmit disease to them or slowly and lethally drain them of blood, as researchers have seen among moose calves in Maine. But birds facilitate the spread of ticks, picking them up in Maryland, Connecticut and other eastern states as they fly north in the spring, Lubelczyk explained.

“As they’re migrating, they’re either dropping the ticks off as they fly or when they land. They’re kind of seeding them along migration patterns.”

Emerging diseases

By tracking the birds and the ticks they carry, researchers hope to predict where Lyme and other tick-borne diseases are most likely to accelerate. Lyme is now present in every county in the state, after hitting a record of 1,488 cases in 2016, but ticks are just getting established in areas such as Aroostook and Washington counties, Lubelczyk said.

Along with Lyme, Lubelczyk tested the ticks for other two other emerging diseases, anaplasmosis and the rare but potentially devastating Powassan virus. Powassan, carried by both the deer tick and the groundhog or woodchuck tick, recently sickened two people in midcoast Maine, following the death in 2013 of a Rockland-area woman.

A recent survey Lubelczyk led found the virus in ticks crawling around southern Maine, Augusta and on Swan’s Island in Hancock County.

In the modest Scarborough lab, medical entomologist Rebecca Robich furthered the findings of that survey. Clad in a white coat and blue gloves, she cloned a tiny band of the Powassan virus’ inactivated RNA, using a sample derived from the ticks that tested positive in the survey. Robich began the work, designed to confirm the earlier test results, last winter.

She expects to know conclusively within the next month what percentage of the sampled ticks were infected with Powassan, she said.

“We’re this close to finishing,” Robich said.

Growing exposure

Ticks have become so prevalent in Maine that Lubelcyzk and his colleagues are increasingly called upon to educate the public about the health risks the arachnids pose. That includes speaking at community forums, town meetings, garden clubs and even to groups of employees.

“They’re widespread enough now that DOT, CMP, people like that are bumping into them on a regular basis,” he said. “Even people like law enforcement. The warden service, regular police with police dogs, they’re exposed.”

Their outreach also includes plenty of phone calls to the lab, fielded by its small staff of four, not counting summer interns.

“If somebody calls, we never really turn them down,” he said.

Many people don’t realize that the lab no longer identifies ticks for the public, Lubelczyk said. Now located in Scarborough along with MMC’s medical and psychiatric research centers, the lab formerly operated in South Portland, where it identified a tick’s species for anyone who walked in the door or mailed a sample. The University of Maine Cooperative Extension in Orono has since taken over that service (it does not test ticks for disease).

“It’s very hard to say no to someone when they’re really frantic because they found a tick on themselves, or their child, or even their pet,” he said. “And they’re sitting out in the parking lot.”

So far this season, the lab has fielded numerous calls from worried residents only to discover after viewing a photograph that the tick in question is a dog tick, not a deer tick. Maine is home to 15 species of ticks, and the dog tick is not among those that transmit disease to humans, at least in this region.

Through its outreach work, the lab has also found itself at the center of debates about how to manage ticks. Lubelczyk recalled a town forum on Long Island a couple of years ago that grew tense as residents discussed the use of pesticides.

“As soon as the topic of any kind of spray was brought up, not even by us, by somebody else, the fishing community was dead set against it,” he said. “Understandably, they’re worried about the stock. It really makes that difficult because you start to have divisions in how to control the ticks.”

The lab’s research on the role of birds in spreading tick-borne disease is similarly delicate, because many birds are under threat ecologically, Lubelczyk said.

“No one really cares if you try to target mice. Birds are federally protected in a lot of cases,” he said.

That other biting pest

Educating the public represents a large part of the lab’s mission but only a small part of its budget. Its outreach work is funded largely through small grants from foundations, Lubelczyk said.

Most of its research funding is targeted toward mosquitoes rather than ticks, boosted by the federal government’s initiative to combat the Zika virus, he said. While Zika hasn’t appeared in Maine, warming temperatures due to future climate change could make the state habitable for one of the mosquito species that carries it.

Lubelczyk explained this as he stood in the lab’s testing area, next to a large freezer storing petri dishes packed with frozen mosquitoes. A piece of yellow tape affixed to the door warned, “Not for food.”

While Lyme is far more prevalent, diseases carried by mosquitoes, such as West Nile virus and Eastern Equine Encephalitis, can lead to more acute illness. Both can cause inflammation of the brain and other serious complications.

Funding for tick research is generally less reliable, Lubelczyk said. The recent Powassan survey, for example, was funded by the Maine Outdoor Heritage Fund, which collects money through the sale of instant scratch lottery tickets.

A continuing threat

The lab’s role in helping to prevent tick-borne diseases has only grown as the tick population and the diseases they carry spread. The incidence of Lyme in Maine is among the highest rates in the country, averaging 82.5 cases per 100,000 people between 2013 and 2015.

Anaplasmosis and babesiosis are less common but becoming increasingly worrisome.

Lubelczyk understands the illnesses on both a professional and personal level. He contracted Lyme several years ago, after a deer tick latched onto him while he made a pitstop on the way home from work one steamy July day, he said. He had just changed into shorts and sandals and jumped out of his car for 30 seconds to hang a mosquito trap in Wells, he recalled.

A day and a half later, he spotted the tick bite. After a round of antibiotics, he recovered, Lubelczyk said.

His usual garb for field work includes long sleeves and pants treated with permethrin, along with gaiters over his boots.

“It’s embarrassing,” he said, wincing. “We always talk about wearing appropriate clothing.”



I’m thankful someone is dealing with the bird issue in relation to tick propagation as I believe it will be found to be much more of an issue than previously thought.  It would help explain why folks insist they’ve been infected while near trees as birds would drop them onto trees (as well as various rodents).  Like deer, birds serve primarily as transits that can spread ticks far and wide.

While Lubelczyk doesn’t feel dog ticks are important carriers (at least in his area) – he’s mistaken.  Every tick should be suspect until proven otherwise.  Think about it:  they all exchange bodily fluids with their hosts.  Dog ticks are known to carry Tularemia, Rocky Mountain Spotted Fever, Ehrlichia, Mediterranean Spotted Fever, Babesia in dogs (which should also make it suspect for humans), and potentially Bartonella.  No, it would not be wise to think of the Dog Tick in friendly terms.  Remember that ticks are moving all over the place defying commonly held beliefs about geography.  And while folks fighting for research grants want to promote and blame the supposed “global warming” mentioned in this article, there are many who disagree for good reasons:  John explains, “The climate change range expansion model is what the authorities have been using to rationalize how they have done nothing for more than thirty years. It’s a huge cover-up scheme that goes back to the 1980’s. The grandiose scheme was a nefarious plot to let doctors off the hook from having to deal with this debilitating disease. I caught onto it very quickly. Most people have been victims of it ever since.”
“This climate change ‘theory’ is all part of a well-planned scheme. Even the ticks are smarter than the people who’ve concocted this thing,” he says.
“Climate change has nothing to do with tick movement. Blacklegged ticks are ecoadaptive, and tolerate wide temperature fluctuations. On hot summer days, these ticks descend into the cool, moist leaf litter and rehydrate. In winter, they descend into the leaf litter, and are comfortable under an insulating blanket of snow. Ticks have antifreeze-like compounds in their bodies, and can tolerate a wide range of temperatures. For instance, at Kenora, Ontario, the air temperature peaks at 36°C and dips to –44°C, and blacklegged ticks survive successfully.

Also, please note that although there has only been one Zika death in an elderly man with a preexisting health condition the continental U.S., all the funding is going to it and mosquito research.  This is causing untold harm here where Lyme is causing around 400,000 new cases per year.  There is no official tally on all the other coinfections they often come with Lyme as they aren’t even reportable in many states but are a crucial detail in understanding the complexity of Lyme/MSIDS.  People are often infected with numerous pathogens.

To treat this complex as a one organism/one disease would be folly.  

Also, he claims that West Nile virus and Eastern Equine Encephalitis, can lead to more acute illness, I would disagree again.  Lyme (borrelia), Babesia, Bartonella, Mycoplasma, and numerous other viruses, and funguses have killed people outright.  Heart block, encephalitis, meningitis, and other serious illnesses are caused by TBI’s. Powassan can be transmitted in under 15 minutes and can kill. Rocky Mountain Spotted Fever is another killer.  There is much to show that if the non-cell wall and biofilm formation of borrelia isn’t successfully dealt with, it could lead to dementia or Alzheimer’s in the future:

And of course, while many cases of Lyme (borrelia) don’t kill immediately, it can make you want to die and disrupt life in such a way people commit suicide.

If that isn’t serious, I don’t know what is.




Mycoplasma and Other Intracellular Bacterial Infections in Rheumatic Diseases: Comorbid Condition or Cause?  by Garth Nicolson, May, 2017  Open Journal of Tropical Medicine

Letter to the Editor

Although the causes of rheumatic diseases have remained relatively unknown, systemic intracellular bacterial infections are commonly found in rheumatic disease patients [1-4]. Because of this, certain infections have been confused with comorbid conditions.

Often patients with rheumatic diseases have co-morbidities, and some authors have concluded that this can include chronic infections. “Infections continue to be a significant cause of morbidity and mortality in patients with rheumatic diseases, and, consequently, early diagnosis and treatment of infection is critical to the successful medical management of these patients” [5].

A link between certain types of infections and rheumatic diseases has been seen by a number of authors. For example, infections with Mycoplasma species, Borrelia species and other intracellular bacteria have been linked to various forms of rheumatic disease [1-4, 6-13]. In addition, animal models of rheumatic disease have been established by infection with Mycoplasma species [13-15]. In one of these contributions experimental arthritis was induced by a clinical isolate from M. fermentans injected into the joints of rabbits [15]. Outbreaks of rheumatic disease, such as polyarthritis, have been traced to infections by Mycoplasma species [16]. Arthritis in animals caused by Mycoplasma species infections closely resemble the signs and symptoms found in patients with rheumatoid arthritis [17]. In addition, reactive arthritis following M. pneumonia infection has been seen in patients [18]. Mycoplasma infections have also been found in the joints of patients with rheumatic disease [19-21]. In a case-control study the presence of antibodies against Mycoplasma pneumoniae have been statistically correlated to the clinical features of rheumatoid arthritis (p<0.001) [21]. Furthermore, genetic analyses and transmission in animals indicate that arthritis is not directly linked to genetic abnormalities [22]. The pathogenesis of rheumatoid arthritis appears to be linked to immunological features of infection(s) involving host recognition of foreign antigens that mimic host antigens or host antigens that are incorporated into microorganism structures and the presence of localized immune complexes and the influences of environmental conditions [22].

Standard treatments of chronic infections like mycoplasma often employ long-term antibiotics, such as but not limited to tetracyclines and other antibiotics [23-26]. The U.S. National Institutes of Health sponsored a double-blind, placebocontrolled, long-term clinical trial that showed that the antibiotic minocycline was safe and effective for the treatment of rheumatoid arthritis. The antibiotic-treated patients showed greater improvements in joint swelling and tenderness (p<0.02), and the treatment group also had better improvements in hematocrit, SED rate, platelet counts and rheumatoid factor with no serious toxicity [27, 28]. A 4-year follow-up indicated that the minocycline-treated patients had fewer relapses and less frequent need for immune-suppressive drugs to control their RA (p<0.02) [29]. Although treatment of arthritis with antibiotics was effective and safe, treatment failures can, just as in any treatment for arthritis, be due to therapeutic failures, resistance and/or mutation of the microorganism [30].

Part of the reason that most rheumatic disease patients do not receive antibiotic treatment may have more to do with the enormous pressure from the marketing and sales of various drugs that do little to address the underlying causes of rheumatic diseases than the effectiveness of various treatments.

In summary, intracellular bacteria are commonly linked to rheumatic diseases, especially rheumatoid arthritis and similar conditions, and these infections can be successfully treated with antibiotics. Treatment often but not always resulted in significant reductions in rheumatic signs and symptoms. Thus chronic infections, such as intracellular bacterial infections, do not appear to be simply co-morbid conditions in rheumatic disease patients. Although there is circumstantial evidence, such as the animal transmission experiments discussed above, that infections like Mycoplasma species may be the cause of rheumatic diseases like rheumatoid arthritis, this has still not been conclusively proven in clinical cases.


1. Ford D (1991) The microbial causes of rheumatoid arthritis. J Rheumatol 18: 1441-1442. Link:

2. Krause A, Kamradt T, Burnmester GR (1996) Potential infectious agents in the induction of arthritides. Curr Opin Rheumatol 8: 203-209. Link:

3. Hyrich KL, Inman RD (2001) Infectious agents in chronic rheumatic diseases. Curr Opin Rheumatol 13: 300-304. Link:

4. Horowitz S, Evinson B, Borer H, Horowitz J (2000) Mycoplasma fermentans in rheumatoid arthritis and other inflammatory arthritides. J Rheumatol 27: 2747-2753. Link:

5. Segal BH, Sneller, MC (1997) Infectious complications of immunosuppressive therapy in patients with rheumatic diseases. Rheum Dis Clin North Amer 23: 219-237. Link:

6. Ponka A (1979) Arthritis associated with Mycoplasma pneumoniae infection. Scand J Rheumato 8: 27-32. Link:

7. Schaeverbeke T, Vernhes JP, Lequen L, Bannwarth B, Bébéar C, et al. (1997) Mycoplasmas and arthritides. Rev Rheumatol Engl 64: 120-128. Link:

8. Schaeverbeke T, Gilroy CB, Bebear C, Dehais J, Taylor-Robinson D, et al. (1996) Mycoplasma fermentans but not M. penetrans detected by PCR in synovium from patients rheumatoid arthritis and other rheumatic disorders. J Clin Pathol 49: 824-828. Link:

9. Hoffman RW, O’Sullivan FX, Schafermeyer KR, Moore TL, Roussell D, et al. (1997) Mycoplasma infection and rheumatoid arthritis analysis of their relationship using immunoblotting and an ultra-sensitive polymerase chain reaction detection method. Arthritis Rheumatol 40: 1219-1228. Link:

10. Haier J, Nasralla M, Franco AR, Nicolson GL (1999) Detection of mycoplasmal infections in blood of patients with rheumatoid arthritis. Rheumatol 1999; 38: 504-509. Link:

11. Lünemann JD, Zarmas S, Priem S, Franz, J, Zschenderlein R, et al. (2001) Rapid typing of Borrelia burgdorferr sensu lato species in specimens from patients with different manifestations of Lyme Borreliosis. J Clin Microbiol 39: 1130-1133. Link:

12. Ford DK (1979) Yersinia-induced arthritis and Reiter’s syndrome. Ann Rheum Dis 38: 127-128. Link:

13. Cole BC, Griffi th MM (1993) Triggering and exacerbation of autoimmune arthritis by the Mycoplasma arthritidis super-antigen MAM. Arthritis Rheumatol 36: 994-1002. Link:

14. Mu HH, Nourian MM, Jiang HH, Justin WT, barry CC, et al. (2014) Mycoplasma super-antigen initiates a TLR4-dependent Th17 cascade that enhances arthritis after blocking B7-1 in Mycoplasma arthritidis-infected mice. Cell Microbiol 16: 896-911. Link:

15. Rivera A, Yanez A, Leon TG, Silvia G, Eduardo B, et al. (2002) Experimental arthritis induced by a clinical Mycoplasma fermentans isolate. BMC Musculoskelet Disord. Link:

16. Agnello S, Chetta M, Vicari Mancuso R, Manno C, Console A, et al. (2012) Severe outbreaks of polyarthritis in kids caused by Mycoplasma mycoides subspecies. Vet Rec. Link:

17. Jansson E, Backman A, Kakkarainen K, Miettinen A, Seniusová B (1983) Mycoplasmas and arthritis. Zeit Rheumatol 42: 315-319. Link:

18. Alvarez LB, Ceballos, BI, Alonso JL (2002) Reactive arthritis following a Mycoplasma infection. Med Clin (Barc).

19. Gilroy CB, Keat A, Taylor-Robinson D (2001) The prevalence of Mycoplasma fermentans in patients with infl ammatory arthritides. Rheumatol 40: 1355- 1358. Link:

20. Ataee RA, Golmohammadi R, Alishiri GH, Esmaeili D, JonaidiJ, et al. (2015) Simultaneous detection of M. pneumoniae, M. hominis and M. arthritidis in snovial fl uid of patients with rheumatoid arthritis by multiplex PCR. Arch Iran Med 18: 345-350. Link:

21. Ramirez AS, Rosas A, Hernandez-Rerain JA, orengo JC, Saavedra P, et al. (2005) Relationship between rheumatoid arthritis and Mycoplasma pneumonia: a case-control study. Rheumatol 44: 912-914. Link:

22. Ford DK (1969) Current views on the pathogenesis and etiology of rheumatoid arthritis. Canad Med Assoc 101: 147-151. Link:

23. Nicolson GL, Nasralla M, Nicolson NL (1999) The pathogenesis and treatment of mycoplasma infections. Antimicrob Infect Dis Newsl 17: 81-88. Link:

24. Nicolson GL, Nasralla M, Franco AR, A. Robert F, Nancy LN, et al. (2000) Diagnosis and integrative treatment of intracellular bacterial infections in chronic fatigue and fi bromyalgia syndrome, Gulf War illness, rheumatoid arthritis and other chronic illnesses. Clin Pract Alt Med 1: 92-102. Link:

25. Baseman JB, Tully JG (1997) Mycoplasmas: sophisticated, reemerging and burdened by their notoriety. Emerg Infect Dis 3: 21-32. Link:

26. Couldwell DL, Lewis DA (2015) Mycoplasma genitalium infection: current treatment options, therapeutic failure and resistance-associated mutations. Infect Drug Resist 8: 147-161. Link:

27. Tilley BC, Alarcon GS, Heyse SP, David ET, Rosemarie N, et al. (1995) Minocycline in rheumatoid arthritis. A 48-week, double-blind, placebocontrolled trial. MIRA Trial Group. Ann Intern Med 122: 81-89. Link:

28. Pillemer SR, Fowler SE, Tilley BC, Graciela SA, Stephen P, et al. (1997) Meaningful improvement criteria sets in a rheumatoid arthritis clinical trial. MRIA Trial Group. Minocycline in rheumatoid arthritis. Arthritis Rheumatol 40: 419-425. Link:

29. O’Dell JR, Paulsen G, Haire CE, Kent B, William P, et al. (1999) Treatment of early sero-positive rheumatoid arthritis with minocycline: four year follow-up of a double-blind, placebo-controlled trial. Arthritis Rheumatol 42: 1691-1695. Link:

30. Razin S, Yogev D, Naot Y (1998) Molecular biology and pathogenicity of mycoplasmas. Microbiol Mol Biol Rev 62: 1094-1136. Link:

For more on Mycoplasma see:

More on Minocycline:

Clinical Association: Lyme Disease and Guillain-Barre

According to this abstract in The American Journal of Emergency Medicine,  the authors state an association between GBS and Lyme is rare; however, the following article states that Epstein-Barr, also known as Mono, is an infection that triggers Guillain-Barre as well as mycoplasma and cytomegalovirus.

Dr. Garth Nicolson states that Mycoplasma is the most common co-infection with Lyme (borrelia).  Cytomegalovirus (herpes virus family) is also a coinfection to LD.

Which leaves EBV.

In Dr. Waisbren’s book, Treatment of Chronic Lyme Disease, the majority of his 51 cases of chronic Lyme had high EBV titers.  He also states,

“As will be seen in other cases, the Epstein-Barr virus may be a candidate for a co-infection associated with LD.”  

Waisbren often treated this co-infected patients that had EBV with 1000mg of Valtrex three times a day with good success.  He also used gamma globulin (4cc twice a week).

I think this is another great example of proclaiming something is rare when little research has been done.  Until Lyme patients are routinely tested for GB, I think it unwise to assume a connection is rare.  Researchers need to tread carefully in all things related to TBI’s, understanding that their words have been used against patients for decades.

Time to admit there’s a lot we frankly just don’t know.


Wolbachia – The Next Frankenstein?

Transmission electron micrograph of Wolachia within an insect cell

Credit:  Public Library of Science/Scott O’Neill

The latest in the effort for world domination over bugs and the diseases they carry is Wolbachia, a Gram-negative bacterium of the family Rickettsiales first found in 1924 and in 60% of all the insects, including some mosquitoes, crustaceans, and nematodes (worms). For those that like numbers, that’s over 1 million species of insects and other invertebrates. It is one of the most infectious bacterial genera on earth and was largely unknown until the 90’s due to its evasion tactics. It’s favorite hosts are filarial nematodes and arthropods.

Wolachia obtains nutrients through symbiotic relationships with its host. In arthropods it affects reproductive abilities by male killing, parthenogenesis, cytoplasmic incompatibility and feminization. However, if Wolbachia is removed from nematodes, the worms become infertile or die. These abilities are what make it so appealing for insect controlcytoplasmic incompatibility, which essentially means it results in sperm and eggs being unable to form viable offering.  (Nifty slide show here)

It also makes it appealing for use in human diseases such as elephantiasis and River Blindness caused by filarial nematodes, which are treated with antibiotics (doxycycline) targeting Wolbachia which in turn negatively impacts the worms. Traditional treatment for lymphatic Filariasis is Ivermectin but they also use chemotherapy to disrupt the interactions between Wolbachia and nematodes. This anti-Wolbachia strategy is a game-changer for treating onchocerciasis and lymphatic filariasis.

Lyme/MSIDS patients often have nematode involvement.  Both Willy Burgdorfer, the discoverer of the Lyme bacterium, as well as Richard Ostfeld, an animal ecologist found nematode worms in ticks. Since then, some provocative research involving nematodes, Lyme/MSIDS, dementia, and Alzheimer’s has been done.  Yet, according to many, Wolbachia is the next eradicator of Dengue Fever and possibly Malaria, chikungunya, and yellow fever because it stops the virus from replicating inside mosquitoes that transmit the diseases. The approach is also believed to have potential for other vector-borne diseases like sleeping sickness transmitted by the tsetse fly.  Evidently, Wolbachia does not infect the Aedes aegypti mosquito naturally, so researchers have been infecting mosquitoes in the lab and releasing them into the wild since 2011. The article states it hopes that the method works and expects infection rates in people to drop and hopes that the mosquitoes will pass the bacterium to their offspring, despite it disappearing after a generation or two of breeding and needing to “condition” the microbes to get them used to living in mosquitoes before injecting them. They also state Wolbachia is “largely benign for mosquitoes and the environment,” and “To humans, Wolbachia poses no apparent threat.” Their work has shown that the bacterium resides only within the cells of insects and other arthropods. They also state that tests on spiders and geckos that have eaten Wolbachia mosquitoes are just fine and show no symptoms. An independent risk assessment by the Commonwealth Scientific and Industrial Research Organizatioin (CSIRO), Australia’s national science agency, concluded that, “Release of Wolbachia mosquitoes would have negligible risk to people and the environment.”

Interestingly, trials are underway in Vietnam, Indonesia, and now Brazil.

They state that scaling up operations to rear enough Wolbachia mosquitoes is too labor-intensive and in Cairns they are going to put Wolbachia mosquito eggs right into the environment. Evidently, other researchers are wanting to release genetically modified (GMO) mosquitoes that carry a lethal gene, and they’ve done it, and it’s causing an uproar:  As of July 14, 2017, Google’s bio-lab, Verily Life Sciences,  started releasing Wolbachia laced mosquitoes in California as part of project, Debug Fresno to reduce the mosquito population.  Numerous studies show unexpected insertions and deletions which can translate into possible toxins, allergens, carcinogens, and other changes.  Science can not predict the real-life consequences on global pattens of gene function.

So, why question the use of Wolbachia as a bio-control?

For Lyme/MSIDS patients, 3 words: worms and inflammation.

Dogs treated for heart worm (D. immitis) have trouble due to the heart worm medication causing Wolbachia to be released into the blood and tissues causing severe Inflammation in pulmonary artery endothelium which may form thrombi and interstitial inflammation. Wolbachia also activates pro inflammatory cytokines. Pets treated with tetracycline a month prior to heart worm treatment will kill some D. immitis as well as suppress worm production. When given after heart worm medication, it may decrease the inflammation from Wolbachia kill off.

The words worms and inflammation should cause every Lyme/MSIDS patient to pause. Many of us are put on expensive anthelmintics like albendazole, ivermectin, Pin X, and praziquantel to get rid of worms and are told to avoid anything causing inflammation due to the fact we have enough of it already. We go on special anti-inflammatory diets and take systemic enzymes and herbs to try and lower inflammation.

Seems to me, many MSIDS/LYME patients when treated with anthelmintics, will have Wolbachia released into their blood and tissues causing wide spread inflammation, similarly to dogs.

And that’s not all.

According to a study by Penn State, mosquitoes infected with Wolbachia are more likely to become infected with West Nile – which will then be transmitted to humans.“This is the first study to demonstrate that Wolbachia can enhance a human pathogen in a mosquito, one researcher said. “The results suggest that caution should be used when releasing Wolbachia-infected mosquitoes into nature to control vector-borne diseases of humans.” “Multiple studies suggest that Wolbachia may enhance some Plasmodium parasites in mosquitoes, thus increasing the frequency of malaria transmission to rodents and birds,” he said.  The study states that caution should be used when releasing Wolbachia-infected mosquitoes into nature.

So besides very probable wide spread inflammation, and that other diseases may become more prevalent due to Wolbachia laced mosquitoes, studies show Wolbachia enhances Malaria in mosquitos. Lyme/MSIDS patients are often co-infected with Babesia, a malarial-like parasite that requires similar treatment and has been found to make Lyme (borrelia) much worse. It is my contention that the reason many are not getting well is they are not being treated for the numerous co-infections.  Some Lyme/MSIDS patients have Malaria and Lyme.

Regardless of what the CDC states, all the doxycycline in the world is not going to cure this complicated and complex illness.

Lastly, with Brazil’s recent explosion of microcephaly, the introduction of yet another man-made intervention (Wolbachia laced mosquitos) should be considered in evaluating potential causes and cofactors. And while the CDC is bound and determined to blame the benign virus, Zika, there are numerous other factors that few are considering – as well as the synergistic effect of all the variables combined. Microcephaly could very well be a perfect storm of events.

I hate bugs as much as the next person, but careful long-term studies of Wolbachia are required here.  “Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.

In short, borrelia (as well as numerous pathogens associated with Lyme/MSIDS), is a smart survivor.

While borrelia have been around forever with 300 strains and counting worldwide, epidemics, such as what happened with Lyme Disease in Connecticut are not caused by genetics but by environmental toxins – in this case, bacteria, viruses, funguses, and stuff not even named yet.

Circling back to Wolbachia.

Hopefully it is evident that many man-made interventions have been introduced into the environment causing important health ramifications: Wolbachia laced mosquitoes and eggs, GMO mosquitoes including CRISPR, and in the case of Zika in Brazil, whole-cell pertussis vaccinations (DTap) for pregnant women up to 20 days prior to expected date of birth, a pyriproxyfen based pesticide applied by the State in Brazil on drinking water, as well as aerial sprays of the insect growth regulators Altosid and VectoBac (Aquabac, Teknar, and LarvX, along with 25 other Bti products registered for use in the U.S.) in New York (Brooklyn, Queens, Staten Island, and The Bronx) to combat Zika. “We feel it’s critical that the scientific community consider the potential hazards of all off-target mutations caused by CRISPR, including single nucleotide mutations and mutations in non-coding regions of the genome … Researchers who aren’t using whole genome sequencing to find off-target effects may be missing potentially important mutations. Even a single nucleotide change can have a huge impact.”

All of this is big, BIG business.

Is the introduction of Wolbachia another puzzle piece in the perfect storm of events causing or exacerbating human health issues?

The jury’s still out, but it’s not looking good – particularly for the chronically ill.

One Tick Bite Could Put You at Risk For at Least 6 Different Diseases by Kevin Loria, June 28,2017

The deer tick, also known as the blacklegged tick, is a fascinating but nasty little creature, and it’s spreading.

The tiny arthropods carry Lyme disease — the serious illness that we most associate them with — but that’s not the only pathogen they spread.

“One thing that people really need to be aware of is that Lyme disease is not the only pathogen that’s out there — there’s quite a few of them, [including] probably quite a few that we haven’t discovered yet,” says Rafal Tokarz, an associate research scientist at Columbia University’s Mailman School of Public Health.

And the deer tick, which as far as we know carries more illnesses than any other tick, “has been expanding its range enormously in the last 30 years,” says Durland Fish, professor emeritus of epidemiology at the Yale School of Public Health. Before the early 70s, it was largely unknown outside the Northeast, but now it has spread north, south, and west.

The diseases that we know deer ticks spread are all serious:

1. Lyme disease, which is transmitted by ticks infected with the bacterium Borrelia burgdorferi, infects roughly 300,000 Americans every year. It can be treated with antibiotics if caught early, but can cause severe inflammation, nerve, and joint pain, among other symptoms, if left untreated.

2. When people are infected with babesiosis, parasites infect and destroy red blood cells. Not everyone shows symptoms but it can be life-threatening for some at-risk patients. It’s “like tick-borne malaria,” says Fish, and is the most important contaminant of the blood bank right now, he says.

3. Anaplasmosis is spread by another bacteria carried by deer ticks. It usually shows up a week or two after a bite and can cause fever, headaches, nausea, and general malaise, among other symptoms. If untreated it can be severe, leading to hemorrhage, renal failure, and for a small fraction of even healthy patients, potentially can be fatal.

4. Deer ticks can also spread the Borrelia miyamotoi bacteria, which Fish says is similar to the one that causes Lyme. Symptoms include joint pain, fatigue, fever, chills, and headache.

5. A relatively recently discovered disease that’s spread by deer ticks as well as dog and Lone Star ticks is ehrlichiosis, caused by a bacteria in the same family as the one responsible for Rocky Mountain spotted fever. Symptoms often present like the flu.

6. Powassan virus has been around for a while but has received more attention recently, especially since the deer tick (which frequently bites humans) started spreading it — the ticks that transmitted the first reported cases in the 1950s rarely bite people. Unlike Lyme, which often takes many hours or even a couple days before it’s transmitted, Powassan infection can occur in as little as 15 minutes. Not everyone who gets bitten by an infected tick gets sick, but if they do, it’s a serious problem since there’s no treatment. In those (still rare) cases, Fish says that there’s about a 50% chance of permanent neurological damage and a 10% chance of death.

The broad range of potential conditions means that doctors don’t even necessarily know what to look for. Even worse, “ticks can frequently be co-infected with more than one pathogen,” says Tokarz. That’s especially true in certain locations, like on Long Island. One bite could transmit both Lyme disease and babesiosis, conditions that would normally be treated quite differently.

It’s also possible that having two or more illnesses could change the way the disease manifests. “We still don’t know whether co-infection exacerbates a disease or doesn’t make a difference,” says Tokarz.”Studies have shown both.”

Unfortunately, we don’t have any good way to control ticks and to stop the ongoing expansion, which will lead to more people getting sick.

In the places where people are at risk of picking up a tick “it is a very important, very severe problem, but the only thing that can be done is to educate people on the dangers of coming into contact with ticks,” says Tokarz.

If you get one on you, pull it off right away — don’t bother with urban legends about needing to burn it off. And protect yourself if you are going to be hiking or spending time in a place where ticks are common. Use permethrin-treated clothing for outdoors work and use insect repellent that contains DEET.


**My letter to the author**

Dear Mr. Loria,

Thank you for your piece on ticks and the pathogens they carry. I just wanted to add to your list; however, as there are many more pathogens carried by ticks. Also, they are discovering a variety of ticks carry pathogens, and if you think about it logically for a moment, ticks have similar habits and mouth parts, and require blood meals to survive, which technically makes every tick suspect. Unfortunately, geographical maps and entomology information (which ticks spread what) have been used to deny patients diagnosis and treatment. A doctor will look at the CDC map and claim, unequivocally, that since such and such isn’t supposed to be in that state, it isn’t TBI’s (tick borne infections). and then eventually they have to admit they are wrong:

How many went undiagnosed through the years?

Borrelia miyamotoi
Bourbon Virus
Colorado Tick Fever
Heartland Virus
Meat Allergy/Alpha Gal
Pacific Coast Tick Fever: Richettsia philipii
Powassan Encephalitis
Q Fever
Rickettsia parkeri Richettsiosis
Rocky Mountain Spotted Fever
STARI: Southern Tick-Associated Rash Illness
Rick Paralysis

I run a physical support group here in Wisconsin, 6th in the nation for TBI’s, and nearly all of us are co-infected, and while Tokarz states he doesn’t know whether coinfection exacerbates a disease, we all do.

Babesia can increase the severity of Lyme disease. Coinfected patients were more likely to have experienced fatigue, headache, sweats, chills, anorexia, emotional lability, nausea, conjunctivitis, and splenomegaly more frequently than those with Lyme disease alone. [7]
Babesia can also increase the duration of illness with Lyme disease. Babesia patients can remain symptomatic for years with constitutional, musculoskeletal, or neurological symptoms. One study found that 50% of coinfected patients were symptomatic for 3 months or longer, compared to only 4% of patients who had Lyme disease alone. [7] Meanwhile, one-third of patients with a history of both Babesia and Lyme disease remained symptomatic an average of 6 years. [2]

“The clinical pictures for 3 out of our 4 coinfected patients included a large number of symptoms, and 1 coinfected patient had persistent fatigue after treatment,” according to a study by Steere and colleagues. [8]”

For a fantastic book on all of this and more, read science journalist and past Executive Editor of Discover Magazine, Pam Weintraub’s work, Cure Unknown: Inside the Lyme Epidemic.

Alicia Cashman
Madison Lyme Support Group