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why is lyme so hard to treat_gla blog

Why Is Lyme Disease So Hard to Treat?

For many Lyme disease patients, the bacteria seem to outsmart antibiotic treatment. Why?

 

It’s a hotly debated topic, and one that is still not completely understood – what causes the persistent symptoms in many Lyme disease patients?  Why is it that 10-20% of patients, after early diagnosis and treatment with antibiotics, continue to face long-term, chronic, even debilitating, symptoms including joint or muscular pain, fatigue, and/or neurocognitive problems? And why do patients diagnosed later in their disease often have a more difficult time finding an effective treatment? Key possible culprits, persister bacteria, are under investigation, and researchers are uncovering their fascinating and diverse array of adaptive abilities, with the goal of one day eradicating them and more effectively helping patients.

Lying in Wait

Borrelia burgdorferi, the spirochete bacteria that cause Lyme disease, have an elaborate lifecycle, critical for their own day-to-day survival. They have evolved adaptations to multiple, sometimes harsh, environments – moving from bloodmeal-source host animals to ticks, repeating the cycle back into host animals, and sometimes into humans. Persistence is an essential and multi-faceted strategy that B. burgdorferi and other bacteria use to survive and adapt to their highly varied environments.

Unfortunately, these same adaptive abilities may also provide B. burgdorferi the ability to survive an onslaught of antibiotics. In vitro (in culture), treatment with antibiotics kills off most cells, but a small number survive because they adapt to have a new superpower – they are tolerant (although not resistant) to an aggressive antibiotic challenge. Their strategy is to lie dormant during an onslaught of antibiotics, changing their protein composition and shape. When the conditions are just right, and the antibiotics are cleared from the host’s system, they can then transform back into mobile spirochete form (thus giving them the freedom to resurge and multiply). GLA-funded research by Kim Lewis and his team at Northeastern University as well as research by GLA-funded Ying Zhang and his group at Johns Hopkins University revealed this amazing strategy. Their teams independently confirmed the existence in culture of dormant, persister B. burgdorferi, providing evidence that these persisters arise during antibiotic treatment and transform back into mobile spirochetes post-treatment. Whether this phenomenon occurs in patients remains to be shown, but it suggests a way to explain why antibiotic treatment is inadequate in a sizeable proportion of patients.

Interestingly, persistence is not unique to B. burgdorferi. The bacteria that cause other chronic diseases (e.g., tuberculosis, syphilis and leprosy) also form persisters.

A Master of Disguise

How do persisters survive harsh conditions such as antibiotic treatment? For one, they have an altered gene expression profile, producing key proteins which allow them to live in the presence of antibiotics. Throughout its life cycle, B. burgdorferi is a master chameleon, transforming itself from its corkscrew-shaped spirochete form into a variety of shapes, such as round (metacyclic), L-form bacteria, spore-like granules or cysts, and then back again into spirochetes. These different forms can impact diagnosis. For example, there is some limited evidence that B. burgdorferi takes on L-forms in spinal fluid, which could impact methods used for screening when a case of neuroborreliosis (a neurological manifestation of Lyme disease) is suspected, for example.

Borrelia bacteria in the blood
Borrelia bacteria in the blood

B. burgdorferi, similarly to other bacteria, may also transform itself into biofilms, which are a complex aggregate of bacteria with a protective slimy mucus layer surrounding it. Studies by Kim Lewis provided evidence of biofilms contributing to persistence in other diseases, such as Cystic Fibrosis and oral thrush. However, there is only minimal in vitro evidence in the case of B. burgdorferi, which is limited in usefulness until more research is done, and further studies will illuminate whether biofilm forms of B. burgdorferi exist in patients.

Yet another strategy used by the wily B. burgdorferi and other bacteria is to invade host cells. For example, the bacterium that causes tuberculosis (TB), Mycobacterium tuberculosis, can exist in a dormant persister state in TB lesions, which necessitates much longer antibiotic treatment in patients than is seen in vitro. Some preliminary findings suggested that in cultured neurons, glial cells, macrophages, and skin keratinocytes, atypical and cystic B. burgdorferi have been found.

Promising Research

Researchers have had very limited success in cultivating replicating B. burgdorferi directly from animals or humans post-antibiotic treatment, which is part of the difficulty in doing experiments on persisters. There is some indirect evidence of persisters from multiple studies in animals (mice, dogs, monkeys) infected with B. burgdorferi and treated with antibiotics. For example, using a mouse model of Lyme disease, after one month of antibiotic treatment, researchers isolated B. burgdorferi DNA and detected non-dividing but infectious spirochetes.

Researchers have also been able to isolate live B. burgdorferi from animals using xenodiagnostic ticks’, in which uninfected ticks feed from an infected animal or human and become infected after feeding. This offers proof that the host was infected with B. burgdorferi. In a study with infected animals who exhibited a clear resurgence of bacteria following antibiotic treatment, B. burgdorferi was then isolated using xenodiagnostic ticks, a strong indication that these are persisters.

When B. burgdorferi-infected nonhuman primates were treated with antibiotics, bacteria were also recovered from multiple tissues, suggesting that bacteria could survive. Signs of inflammation in and around these tissues were also observed.

In an exciting 2019 study, Ying Zhang and team isolated slow-growth forms of B. burgdorferi (including biofilm-like, round body and spirochetes) from culture and compared mice inoculated with these slow-growing forms versus mice inoculated with fast-growing spirochetal B. burgdorferi. The slow-growth persister B. burgdorferi were not only more tolerant to the standard Lyme disease antibiotic treatment with doxycycline or ceftriaxone but they were also associated with more severe arthritis in mice than the fast-growing spirochete form. However, a cocktail of antibiotics – Daptomycin, Doxycycline and Ceftriaxone – did successfully eradicate the infection in the mice infected with slow-growing persisters. Human studies modeled after these would be helpful in understanding the disease course, especially the response to antibiotics.

In other studies, different cocktails of antibiotics, as well as essential oils, have been successful in eradicating B. burgdorferi in vitro. Disulfiram, a drug used for treating alcoholism, has been shown to be extremely effective in eradicating many forms of B. burgdorferi in vitro and in mice, and in a small study in humans.

Despite all these promising results in culture and in animals, trials in humans have not advanced well. Based on research done to date, researchers cannot confirm or exclude that live persisters are present in antibiotic-treated patients who have persistent symptoms (i.e., patients with post-treatment Lyme disease symptoms). One large part of the problem is the shortage of confirmed Lyme disease patients for clinical trials, as many patients lack concrete clinical (serological) evidence of having Lyme disease. In three separate clinical trials, only 4% of 5457 patients made it through the screening process to enter a trial.

Altogether, some critical groundwork has been established in the study of persisters.  However, studies surrounding persisters are still in early stages, and their connection to ongoing symptoms of post-treatment Lyme and chronic Lyme still warrant more confirmation and extended studies. There is a great need for evidence-based research conducted at all levels of research involving persisters, from in vitro studies through clinical trials. Supporting these efforts calls for improved diagnostics and detection methods for persisters, and an incremental move into larger-scale human studies which confirm the presence of live persisters and explore treatment options. GLA is optimistic that with future studies, there will be new breakthroughs in this very important area.


By Global Lyme Alliance and Dana Barberio, M.S., Scientific/Medical Writer and Principal, Edge Bioscience Communications

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Learn more about GLA’s research initiatives and accomplishments:

Research Report
Published Research Findings
Current Grantees 
First Observational Study for Lyme Disease Treatment
Post-treatment Lyme: Two Million by 2020
Blog: Why Good Science is Crucial

No Set Protocol

by Jennifer Crystal

WHY ISN’T THERE A SET TREATMENT PROTOCOL FOR LYME DISEASE?

Patients often write asking how I fought off Lyme and two other tick-borne diseases. I understand why they ask. When you read that someone is doing well, you want to know how they got there. Im always curious about the techniques others patients have used, too, and am eager to learn about the latest treatment options. I love connecting with other Lyme warriors. But I cant give them my medical protocol.

Its not because I dont want to. It’s not because Im not a doctor and cant give medical advice. Its because doing so truly wouldnt really help them. Over 427,000 people are diagnosed with Lyme disease each year, and every single one of those cases is different. Not even two of them are alike. Medication protocols must be individually tailored for each individual patient by a Lyme Literate Medical Doctor (LLMD).

Why is this the case? There are set protocols, or at least variations on a theme, for other illnesses like bronchitis and certain cancers. It would seem reasonable to assume that the same would hold true for Lyme, but it doesn’t. For starters, spirochetes (Lyme bacteria) attack people in any number of ways. A few examples: some people may have multi-system symptoms, while others may have mostly joint aches and pains; still another may have mainly psychiatric manifestations. And I’m barely scratching the surface when it comes to how variable Lyme’s effects can be.

Different symptoms are best treated with different families of antibiotics or combinations thereof. Some people do well with an anti-inflammatory that works in conjunction with antibiotics, and some do not. Some people tolerate oral antibiotics just fine, while others develop gastro-intestinal problems and do better on intravenous or intramuscular antibiotics. Again, the family of antibiotics that combats one patients symptoms might not work for another at all.

Some people react quickly to treatment; for others it takes a long time and several Herxheimer reactions before they start to notice improvement. Response time can depend on a variety of factors such as whether you have other illnesses unrelated to Lyme (for example, I also have chronic Epstein-Barr virus) and one’s individual immune function. In addition to response time, other factors come into play such as: how long did the patient go undiagnosed, does he or she have tick-borne co-infections (as I do) that can complicate treatment, and has infection crossed the blood-brain barrier. Once an LLMD gets a full picture of a patients medical history, they often must try alternating combinations of drugs before they land on what works.

And heres another wrinkle: what works well for one week or one month might not work so well the next. 

That’s another reason I can’t talk about my protocol. It’s because I haven’t had just one but many. If there were a single magic cocktail that gave me steady improvement, Id gladly share it. But there isn’t. I started on oral antibiotics for six weeks. Then I switched to intravenous antibiotics for a year. Then I went back on different oral antibiotics for another few months before getting well enough to go off medication entirely. And then, three months after that period of remission, I relapsed entirely, and had to start over with another combination of meds altogether. 

In addition to antibiotics, Ive also taken different anti-malarial medications at times to combat one of my co-infections, babesia. Ive switched up sleep medications, anti-depressants, and nutritional supplements. Ive tried various homeopathic remedies. Ive done adjunct therapies like integrative manual therapy (which involves neurofascial processing and cranial sacral therapy), neurofeedback (a non-invasive technique that helps with sleep), and traditional physical therapy. Ive done talk therapy for different periods of time at different points in my journey.

The only thing that has stayed exactly the same for over a decade is my diet: no gluten, sugar, alcohol, or caffeine. But even that has gotten slightly more lax at times. I now eat small amounts of dark chocolate, when for many years I didnt touch the stuff at all.

So yes, as Ive got better and better over the course of more than a decade, I have settled into a certain combination of treatments and therapies that have worked well for me, but that was built on the foundation of treatments I did in the past. Why, even my current protocol isnt foolproof. Just this past spring, I had a flare-up that required me to tweak my medications and supplements. Even a patient in long-term remission must change her protocol based on waxing and waning symptoms. I will continue to need to do so as needed, likely for the rest of my life or until a cure is found.

But that doesnt mean you will need to be on medication for the rest of your life or until a cure is found. Depending on the severity of your case, you may only need a short course of treatment. Let my story of eventual remission inspire you, but dont let it scare you. As long as youre in the hands of a LLMD, youll eventually figure out the treatment plan that works for you. In the meantime, please know that I understand your frustrations, fears, and physical pain, and I am cheering you on!


jennifer crystal_2

Opinions expressed by contributors are their own.

Jennifer Crystal is a writer and educator in Boston. Her memoir about her medical journey is forthcoming. Contact her at [email protected].

image of the word risk

Risk-Benefit Analysis of Tick-Borne Disease Treatments

by Jennifer Crystal

Asking important questions when it comes to Lyme treatment. Do the benefits outweigh the risks?

At the 2019 International Lyme and Associated Diseases Society (ILADS) conference in Boston, there was a lot of buzz about two up-and-coming Lyme treatments: Disulfiram and Dapsone. Both medications have shown powerful efficacy against Lyme, and Disulfiram may also treat babesia. Learning of the success stories of late-stage Lyme patients who have taken these medications—subsequently enjoying remissions of six months or more—makes many people want to run out and try them. I am among them.

However, like most medications, these drugs also come with risks. Both can cause strong Herxheimer reactions, especially if taken at too high a dose too quickly. Disulfiram, more commonly known as Antabuse, a drug used to treat alcoholism, causes a severe reaction if the patient comes in contact with alcohol. And not just from having taken a sip of a drink; the slightest contact with alcohol-based lotions, hand sanitizers, mouthwashes, shampoos, or other products can make the patient vomit and feel extremely hungover. More rarely, the drug may cause psychosis.

If I were bedridden with tick-borne illnesses, as I once was, I would be eager to try one of these medications. At that time I was so sick I would have tried anything. My head throbbed with migraines; I was plagued with insomnia, and when I did sleep, I had hallucinogenic nightmares. I felt tied to my bed as if by the world’s worst case of flu. This went on for years. Eventually, antibiotic and antimalarial treatments, combined with nutritional supplements and adjunct therapies like neurofeedback and integrative manual therapy, helped me into remission. After one serious relapse, I have stayed in remission for over a decade, seeing steady improvements.

At 80% of restored health, I am living a good life. I can work part-time, write, socialize, and exercise. However, I also still have to stick to a strict sleep schedule; I still have to take low-dose antibiotics and other medications, and I still have to take a nap every afternoon. As I listened to doctors talk about  Disulfiram and Dapsone at the ILADS conference, I wondered, “Could one of those medicines help me get even better? Could it eliminate my afternoon nap, or reduce my reliance on antibiotics?” 

I asked one of the panelists, a Lyme Literate Medical Doctor (LLMD), this very question. Lets say a patient was at 80% restored health after years of battling tick-borne disease,I said, explaining all the things this hypothetical patient could and could not do. Is that a case in which you would prescribe Disulfiram or Dapsone, or are those medications better for someone in the acute stages of the illness?

Thats up to the patient,the doctor replied. Are they satisfied with their 80% lifestyle? Are they willing to feel terrible when theyre on the medication in order to feel better afterward? Its really a question of risk-benefit analysis.

This was a term Id heard in my early days of Lyme treatment, and one I wrestled with many times as I tried new protocols. At each juncture, I had to consider, do the risks of taking this medication outweigh the benefits or vice-versa? For example, when I started taking sleep medication, I worried that I would become addicted. My doctor reasoned, But you aren’t sleeping. You cant get well without sleep. So the benefit of the medication outweighs the risk.

I also did a cost-benefit analysis years ago when I was trying to decide if I should continue with oral antibiotics or try intravenous antibiotics through a Peripherally Inserted Central Catheter (PICC). My doctor said that intravenous antibiotics would get at the infection faster, and would take the pressure off my gut, since oral antibiotics come with their own adverse side effects, intestinal yeast overgrowth among them. I was managing that risk with a specialized diet and probiotics, but intravenous antibiotics would help.

However, intravenous antibiotics also came with risks. Herxheimer reactions could be more severe. The PICC line could clot. I had to be very careful not to get it wet, or water could go in the line, to my heart. Moreover, the specific intravenous antibiotic my doctor recommended could, in rare cases, cause gallstones.

At that point in my journey, I was so sick that I wanted to try the strongest, fastest course of action possible. To me, the possible benefits of intravenous antibiotics outweighed the risks, so I made the choice to get a PICC line.

My Herxheimer reactions were indeed severe. My line did clot once, and a nurse had to make an emergency visit to my home to fix it. As if that weren’t enough downside, I also developed gallstones and had to have my gallbladder removed (Note: Not all intravenous antibiotics have this side effect, and there are now medications to help counter it). Despite these complications, the PICC line helped move me towards remission within a year, so I feel the treatment was worth it.

Now that Im doing well, my view of the risks and benefits of new medications is different. If I were still as sick as I once was, I absolutely would try Disulfiram or Dapsone. But in my current life, I cant take time off to battle severe Herxheimer reactions, nor do I want to. I dont want to run the risk of losing the gains Ive earned. Id love to give up my afternoon nap, but Im not currently willing to feel worse in order to possibly make that happen, especially with no guarantee. I certainly dont want to get to a point where I say, Remember when I was doing so well that all I had to do was take an afternoon nap?

For now, Im content making smaller tweaks to my treatment protocol such as adding supplements and lowering antibiotic doses that might improve my energy. The risks of these moves are relatively low. At some point, I may want to take a larger leap. After more research is done on Disulfiram and Dapsone, I may decide their benefits do indeed outweigh their risks and try one of them.

Another patient in my shoes might feel differently. They might be willing to possibly go back to 50% if that meant they could get 100% wellness eventually. I respect that. The bottom line is that you have to do whats right for your body, and you and your LLMD need to weigh the risks and benefits of choices for your specific case. At the end of the day, youre the one living with Lyme disease and possibly other tick-borne infections, so you get to decide what risks you do and dont want to take.


jennifer crystal_2

Opinions expressed by contributors are their own.

Jennifer Crystal is a writer and educator in Boston. Her memoir about her medical journey is forthcoming. Contact her at [email protected].

What to Do When You Hit a Plateau in Treatment

By Kerry Heckman

My numbers won’t budge. Every month I go in for a blood test and every month I get an email from my doctor stating that my inflammatory markers are the same. The numbers are not so high to cause a panic, but they’re not low enough to signal any real improvement either. I’ve tried everything from meditation to medication, but nothing seems to work. Each month I pray the numbers will drop and I’m devastated when month after month they stay the same.

I’ve put in all the work; there’s been no stinting. I’ve been in treatment for three years. I’ve changed my lifestyle, my diet, and most difficult of all, my mindset. But I keep coming up short. There’s no doubt I’m better. My bedridden days are mostly in the past, and the pain that keeps me up at night (painsomnia, I call it) happens once or twice week instead of every day. Another marker of my improvement is after treatment my herxheimer reactions are greatly diminished. These are positive trends, but still I am not where I want to be. I want clinical proof that my recovery is real. I want to know unequivocally that I’m heading toward remission. I’ve  been at this dreaded plateau for months waiting to break free. I anxiously await the day when my inflammatory markers take a dramatic drop.

Your plateau may be different than mine. Maybe you, too, made big improvements in the beginning and now it’s tapering off, or maybe you’re stuck waiting for any minuscule improvement at all. Either way the lack of progress may be the hardest thing to bear.

All this was weighing heavily on me. Then one day I started thinking about actual plateaus in nature. Consider for a moment you are climbing up a mountain and reach a plateau. You’ve done the grueling work of going up the mountain and now you are walking on level ground. You are still moving forward, that hasn’t changed, but you’re not increasing your elevation. Maybe that’s what plateaus are in treatment—a leveling off that doesn’t feel like progress, because you aren’t climbing anymore. But you have achieved an incremental improvement in your recovery.

This bit of visualization changed the way I thought about my lack of headway, though  there were still some questions I needed to ask myself— questions you may need to  ask yourself as well:

Q: Have I really plateaued or is my progress just going slowly?

A: With Lyme disease the improvement can be slow . . . very slow. As they say, any progress is good progress. If you feel comfortable with your treatment protocol, you may need to practice patience and remember you are getting better. However, sometimes the progress is too slow and even if there is incremental improvement you may want talk to your doctor about exploring ways to speed up your treatment plan.

Q: Have you hit a plateau before? What helped jumpstart my healing?

A: If this has happened before, what was it that made the difference? Maybe it’s a new supplement or an increased dose of medication. Maybe your thyroid or adrenals are out of balance and need attention. Try to remember back to what helped you before and try it again. It may help to keep a journal about what you think is and isn’t working for you.

Q: Do I need to change my treatment or ride it out?

A: As I said, with Lyme getting better takes time. Ask yourself if you think your current treatment plan is sufficient to to get you better. This is a good place to use your intuition. If you feel skeptical every time you meet with your doctor that might be your body telling you something.

Q: If I plan to stay the course when will I know it’s time to adjust?

A: Give yourself a timeline—six months, nine months—for when you want to reevaluate. Verbalize your timeline to your doctor, so she or he knows what you’re thinking. Ask if there is a test that can be run at that time to compare where you were before to where you are now.

Q: Am I testing too often?

A: If you’re like me and your numbers aren’t budging, maybe it’s time to put more space between tests. This depends naturally on what is medically advisable. But I I did realize that the constant testing was causing me frequent disappointments, which weren’t good for my healing. I have since decided to go from once a month to once every other month for my bloodwork and focus on other things in the meantime.

Q: Is there something else I could do to move forward?

A: A plateau is the perfect time to reevaluate your habits. Perhaps it’s time to add more nutrients to your diet or increase detox. Have you always wanted to try a complementary therapy? Now may be the time. Or are there other options?

Q: Is this a good time for a healing pause?

A: Have no doubts, recovery from Lyme treatment is a full-time job. It seems like there’s always something else you can try, but is that the best thing for your body? This could be an indication that it’s time to take a break from all the intensity and let your body rest at the top of the mountain.

Take some time and ask yourself these questions. Get quiet and let your intuition speak. There are few doctors, medications, or therapies that can give us as much insight as our own common sense. Remember the image of the mountain and keep walking forward on the level ground of the plateau—the uphill slope may be only a few steps ahead.


kerry heckman

Opinions expressed by contributors are their own.

Kerry J. Heckman is a licensed therapist and author of the healing and wellness blog Words Heal. She was diagnosed with chronic Lyme disease in 2016.

essential oils_lyme disease research

GLA POV: Essential Oils as Treatment Against Lyme Disease

by Mayla Hsu, Ph.D., Director of Research and Science, GLA

Global Lyme Alliance’s Director of Research and Science offers perspective on newly published research on using essential oils to treat Lyme disease

 

Global Lyme Alliance (GLA)-funded investigator Ying Zhang, Ph.D. (Professor at Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health) details new findings on the effectiveness of certain essential oils to treat Lyme disease; “Identification of Essential Oils with Strong Activity against Stationary Phase Borrelia burgdorferi.”

Persister forms of B. burgdorferi, the bacterium that causes Lyme disease, are dormant or slow-growing, and tolerant of antibiotic treatment. It’s not clear yet whether persister bacteria, immune dysfunction, or some combination of the two is responsible for post-treatment Lyme disease syndrome (PTLDS), in which patients treated with antibiotics continue to suffer symptoms.

The search for novel compounds to kill persister bacteria has led to the discovery that essential oils (EOs), aromatic compounds produced by plants, may be promising. In an article published in Antibiotics, a peer-reviewed journal, scientists led by Dr. Ying Zhang identified 10 EOs that have strong activity against stationary phase B. burgdorferi at a low concentration of 0.1%. The study, underwritten by GLA, found that of the 10 EOs, those of garlic, allspice, and Palmarosa were active at even at 0.05% concentration. In addition, cinnamaldehyde, a major ingredient isolated from cinnamon bark, was active against both stationary phase bacteria as well as replicating B. burgdorferi at a 0.02% concentration.

A stringent test of antimicrobial activity against stationary phase bacteria is the capacity to block subcultured bacteria from growing. This means that after killing bacteria in culture with the inhibitor, a small amount of that culture is transferred to fresh growth media that lacks the inhibitor. Any regrowth indicates that the inhibitor did not completely kill all bacteria from the original culture. Under these conditions, only garlic and cinnamaldehyde were effective against the regrowth of B. burgdorferi spirochetes subcultured for 21 days.

These results indicate that certain EOs or their ingredients are potent in eliminating persister B. burgdorferi, and should be studied in greater depth to analyze their utility as potential treatments.

Is Lyme Disease Treatable?

Dr. Harriet Kotsoris, chief scientific officer with Global Lyme Alliance, discusses Lyme disease treatment, prevention, and transmission.

 

Below is an excerpt from, “Lyme Disease: An Overview”, a podcast with Dr. Kotsoris and Dr. Mayla Hsu, science officer with GLA. Listen to the entire podcast below.


 

Host: Is Lyme disease treatable? What are some of the common treatments?

Dr. Kotsoris: Lyme disease is what we’d call treatable, the question in everybody’s mind is “Is it completely curable?” In the acute stages, the school of thought is that it is curable with prompt adequate treatment with 3-4 weeks of Doxycycline or Amoxicillin. The longer a person walks around with the disease undetected and untreated the more difficult it is to eradicate. That’s because the Borrelia burgdorferi organism is fleeting in the bloodstream and quickly hides and travels to other organs of the body including the muscles, joints, heart, brain, mostly connective tissue.

It is felt that even in the face of antibiotics these Borrelia burgdorferi bacteria may actually become tolerant, not resistant, but tolerant. That means that they go dormant and hide in the tissues only to reactivate at a later date when the body is put under some type of stress. Again, these issues are quite controversial and this is because many feel that although the bacteria may be viable in the body they’re not culturable. In other words, we cannot prove that there are still living bacteria in these patients with post-treatment Lyme disease syndrome. We’re just hopeful that one day we’ll have better detection methods, both early and late to distinguish acute cases in a prompt fashion, which will then lead to a higher success rate of treatment. Also markers for chronic phase of the illness or post-treatment, or post-infectious Lyme disease, to show whether or not there still are viable bacteria left in this patients body.

Host: How is Lyme disease transmitted?

Dr. Kotsoris: Lyme disease is transmitted by a vector, that is an agent that will a pathogen or disease-producing organism from itself to a host. In the instance of Lyme disease, the human is an accidental dead-end host. In the United States as I mentioned before, the disease is transmitted by the blacklegged tick. The tick crawls around, attaches to a nice warm moist area of the human body and then bites the host, and in doing so transmits the bacterium from the tick belly into the bloodstream of the human being. Dr. Hsu will elaborate more as to the adaptations that are required for this to be a successful event.

Host: What are some adaptations that ticks have that allow them to so successfully transmit Lyme disease?

Dr. Hsu: The tick genome was actually just sequenced this past year, 2016. It revealed all sorts of interesting information about why ticks have evolved to be so successful at transmitting Lyme disease. It turns out that ticks have very efficient olfaction, or smell detectors on their sensory organs. They are able to, as Harriet said, crawl around and look for parts of our body that are damp and hidden, and that they can hide. They attach once they’ve found this good spot, like your belly button or between your toes. They have barbed mouth parts, so they efficiently saw through the skin and they and they attach.

Once they’re attached they can’t detach very easily owing to this barbed penetrating mouth part. Once they start feeding, their saliva is like this very incredible chemical soup that has all kinds of components in it that facilitate disease transmission, but it also where’s it’s supposed to facilitate feeding by the ticks. It has an anesthesia so you cannot feel it. They have also in their saliva a blood thinner, so your blood flows better, blood vessel dilators so you bleed better. The tick itself stays attached for up to 36 hours while it’s feeding on you, and its body size can actually increase by 100 times.

Host: How could you protect yourself from Lyme disease?

Dr. Hsu: I think there are, as Harriet said, it all hinges on that tick bite. There are low-tech protection that you can have, which is just simply to avoid tick bite in the first place, tucking your pants into your boots, wearing bug sprays that contain DEET, which repel ticks, checking yourself for ticks and removing them immediately. Another strategy is to wash our clothes in Picaridin or Permethrin, and these are chemicals that will repel ticks and other mites, bugs from biting us. It’s interesting to note that the Armed Forces are now doing this with their clothes to protect our military.

Host: What are some adaptations that have made the Lyme disease bacterium so successful?

Dr. Kotsoris: Borrelia burgdorferi is quite an intelligent bacterium. Initially, when it first enters the bloodstream it … Actually, because of its shape, the corkscrew shape can penetrate into tissues like a roto-rooter machine. Likewise, the outer surface of Borrelia burgdorferi has a whole host of fatty substances and proteinaceous substances. These proteinaceous substances vary from strain to strain, and so it’s incredibly difficult for the immune system to be able to combat Borrelia burgdorferi effectively. In fact, Borrelia burgdorferi has adapted many mechanisms and actually hijack the immune system that cause certain antibody-producing cells not to operate effectively, so that the bacterium cannot be coated by antibodies and then can’t be mopped up by other immune-related cells in your body.


 

Listen to entire podcast below: