Methylene Blue and Lyme

 

Is there a magic bullet and is it methylene blue?  Methylene has been shown to have activity against malaria/Babesia, Bartonella and Lyme.  It has activity against persister forms of Bartonella and Lyme (borrelia) as well as biofilms.  It is active against coronavirus (Covid).  It has neuroprotective effects, inhibits tau proteins in the brain and therefore may help fight Alzheimer’s disease and other neurodegenerative brain disorders. It has been used with photodynamic therapy to treat cancer, including lung and breast malignancies. The drug is also known to strong psychoactive properties and has been shown to benefit patients with psychiatric illness, including bipolar disorders.

It has serotonergic effects and cannot be taken by patients on antidepressants.

The drug was developed in the late 1800s.  No patents, no money, and no research--may be a problem.  It is not commercially available (orally), but capsules are prepared by some compounding pharmacies.

The most common use in the past century has been the treatment of methemoglobinemia, a relatively rare condition in which oxygen carrying hemoglobin is converted to a non-active form, generally a genetic disorder trigged by an outside agent.

It sounds like the MacGyver of drugs – or Swiss army knife of drugs. 

Lyme patients are not infrequently desperate, suffering despite much standard and experimental therapy, looking for the next thing.

The question is: Is methylene blue (MB) safe and effective for chronic Lyme patients? Is it finally the Holy Grail?

First off, MB has been shown to be safe and effective in humans (malaria).  It was the first synthetic anti-malaria drug, preceding commercial penicillin by about 50 years.  Recent studies employ high doses of the drug administered over 3 days. Malaria has become more resistant to a wide array of therapies and MB has been resurrected and dusted off as if it is something new.  Short term use does not provide cover for long-term usage, the hallmark of Lyme and associated diseases therapy. 

Effectiveness for Lyme patients is inferred from in vitro (test tube) studies (Lyme, Bartonella, Babesia).

Methylene blue has broad spectrum antimicrobial activity against protozoans, bacteria and virus.  Generally I prefer narrow spectrum drugs.  A scorched earth drug may be problematic. I don't think we know anything about its effect on the microbiome, especially with prolonged use. 

MB is undergoing clinical in vivo trials for the treatment of Covid. This adds a log to the evidential fire of drug safety.  The Covid trials employ low doses, MB 100 mg twice daily but for only 5 days. Malaria trials have used higher doses but only for 3 days--10 mg/kg for 2 days followed by of 5 mg/kg for one day.  For example, a typical 70 kg man receives 700 mg for 2 days followed by 350 mg on the third day.

It should be clear that long-term clinical use for non-studied infections is entirely experimental. But at this point there are numerous anecdotal reports which praise MBs efficacy and appear to support safety when used this way.  

I spoke at length with a patient today who is a big fan. He has tried various doses and found 200-400 mg per day to be an effective dose. He has found it works well only as part of cocktail therapy.  One therapy, Zithromax, Rifampin and MB worked well for Bartonella.  For Babesia it has been effective when combined with artemisinin (or Coartem) and primaquine (or tafenoquine).

MB is now part of the Lyme disease armamentarium. It has been in common use, in some corners for more than 2 years. Treatments must always be individualized.  

If the drug is used, I recommend starting with a low dose like 50 mg twice daily and gradually increasing as tolerated.

All drugs have numerous side effects and drug interactions. Please do not purchase MB on the internet and treat yourself. The consequences could be disastrous. Don't have a fool for a doctor and a fool for a patient. 

Methylene blue plays an increasingly important role in the management of tickborne disease and may ultimately have other important clinical applications.  

 

 

Old drug, new drug: nimodipine

Mary, a 35 years old woman was extremely healthy – until she wasn’t.  The culprit was Lyme disease, an ancient, thin, spiraled bacterium called a spirochete – one that is insidious and opportunistic.  But Lyme disease is more often than not so much more.

Our ability to stave of infection frequently depends on a healthy immune system.

Many factors can adversely impact normal immune function.  Stress is a huge factor.

Lyme and Mary’s immune system had been locked in mortal combat with Lyme for some time. Life stressors mounted and a tipping point was reached. Lyme won the battle and spread throughout her body attacking many organ systems.

These were some of the stressors. Her father died of a sudden heart attack, a child was diagnosed with autism, her husband was emotionally abusive and this led to an ugly divorce.

Mary managed stress by gardening – more and more. Ironic.

The fatigue was overwhelming. It felt like she had been run over by a Mack truck. Mary was diagnosed with chronic fatigue syndrome/CFS, myalgia encephalitis or systemic exertional intolerance disorder – three names for the same thing. She simply could not function. Sleep was miserable, too much or too little. She struggled to get out of bed. She needed help with simple household chores. She rarely got dressed; she no longer put on makeup and she took few showers. Sadly, Mary blamed herself for her poor health. She lost all self-esteem.

Headaches diagnosed as migraine came out of the blue. Pounding, throbbing, ice pick, with temporary loss of vision nausea. The pain was unbearable.  Several doctors were of no help and she seriously considered suicide.  


Symptoms mounted. Doctors said it was psychosomatic. Family members believed the doctors. Mary was abandoned by both family and friends.

Mary had so many symptoms, symptoms which inexplicably came and went.

She frequently felt like she had the flu. She had night sweats, drenching at times.

Her whole body hurt at times. Sometimes the pain was localized to a particular joint or body part.

She experienced frightening cognitive impairments, poor memory, trouble thinking clearly, difficulty finding words. She frequently felt disoriented and depersonalized. She experienced depression, air hunger, sudden bouts of crying, intermittent joint swelling, weakness, numbness and tingling and trouble sitting up and standing.  


With changes in posture, from lying to sitting and then to standing symptoms her heart raced, brain fog increased, she became dizzy, felt she would black out and had to immediately sit down or lie down.

We know Mary has Lyme and Babesia. But she is not going to get better if we treat her only with antibiotics and anti-Babesia drugs.

Migraines:  There are a variety of new ways of treating migraines including those that antagonize calcitonin gene related peptide, a relatively new and sometimes successful therapy. Migraine therapy will be reviewed in detail in the future.

POTS:  With further questioning Mary had problems with her bowels, bladder, vision and temperature regulation.  POTS is a piece of the larger disease, dysautonomia or broken autonomic nervous system. A patient history, exam with measurement of vital signs in different positions can confirm the diagnosis. A tilt table test is unnecessary. There is a close connection between dysautonomia and CFS. Mary’s heart rate only increased by 20 points with standing not the requisite 30. Of course she was too dizzy to stand for long.

There are many effective therapies which usually work when prescribed properly. Described elsewhere.

Even when tests for POTS are negative, patients with chronic fatigue syndrome may benefit from POTS’ therapies including salt tablets and fludrocortisone.

Lyme patients, patients with chronic fatigue syndrome and patients with POTS all complain of brain fog. An old/new drug may be incredibly effective.

The calcium channel blocker nimodipine, which must be prescribed carefully dilates cerebral blood vessels and increases blood flow in the brain treating chronic encephalopathy. Patients with Lyme, POTS and CFS may all suffer with dysregulated blood flow to the brain.

Nimodipine may work well with other neurotropic drugs including Adderall and Namenda.

I have treated Mary for less than a year and she has done very well.

She is back at work, part time, telecommuting and even smiling at times.

Summer flu, Lyme or Covid?

Lyme patients, those suffering with chronic illness must be considered immune suppressed and at higher risk for serious Covid related illness.

There are dangers at the edge of the woods and dangers from neighbors and family.  The world is surreal.  But it is the real world, the one we have to live in.

The Covid nightmare, is in some ways like 911, a watershed event that will forever change our prior naivety regarding person to person transmission of deadly germs.

I am optimistic that meds given early in the course of illness will prove effective. Current candidates include

The summer flu. It has long been acute stage Lyme misdiagnosed by the doc-in-a-box. Now we have another bigger worry.

The presentation of the two illnesses can in some cases be identical:  fever, malaise and achiness. 

Testing should be done, although deficient for both.

Do not get the Covid antibody test. 100 non-vetted companies, tests.  Get the nasal swab sent for PCR which directly identifies the RNA virus. There are still false negatives and you may want to repeat the test.

Lyme testing. Many of us are operating remotely doing telemedicine. That obviates the ability to send specimens to more reliable Lyme labs:  Stony Brook, MDL, IgeneX etc. We have to manage with LabCorp or Quest.  Get the Western Blot test, not the reflex to WB.  Also get C6 peptide.  Coinfection testing must include Babesia duncani, WA1, IFA IGG.

Do not worry too much about poor Lyme blood tests.  Patient history is the most reliable test.

If there is any doubt treat both.   Doxycycline and (ivermectin which many Lyme patient feels has been effective) is a good starting place. If you are worried about sun induced toxic skin reaction, I recommend you stay in the shade and tough it out for at least 3 weeks. This is the only drug that has widespread effectiveness against many coinfections.  Amoxicillin, Ceftin and Minocycline are not adequate substitutes.


Search my blog for more about ivermectin.


Despite what you may have heard or red otherwise, Covid cases and deaths are very underreported.  Same as Lyme.  With Lyme some elected officials have helped promote the cause.  With Coivd, unfortunately, it is the other way around.

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Telemedicine vist

Telemedicine visit

Your doctor does not want to see you in his/her office. At least your doctor should not want to see you in his/her office. Not now.

We are in the middle of a pandemic – goes without saying. Covid-19 stands for coronavirus disease 2019. Its novel because it is new and something the human immune system has not previously encountered.  We have experience with other deadly coronavirus infections. SARS had a mortality rate of around 15% and MERS was scary deadly with a mortality rate in the smallpox range, 30+ percent. Covid-19 is less deadly but much more contagious. The true numbers of those infected and the mortality rate are to date unknown.

Covid-19 is the dreaded pandemic, more than an epidemic.

An epidemic occurs with rapid dissemination of an infectious illness through a susceptible population. It may be worldwide as occurs yearly with influenza.

A pandemic is worldwide dissemination of a new deadly infectious disease. This is the stuff of sci-fi movies.

A friend’s parents live in a Maryland Assisted Living facility and tested positive for Covid.  Both presented with diarrhea and without fever or cough. Unusual presentations may not be unusual.

A typical physician’s medical examination room is an 8X10 or somewhat larger rectangle with relatively poor circulation. It is a perfect incubation chamber for coronavirus. Infectious particles may persist in air – droplets and aerosols and on incompletely sterilized surfaces. I am more concerned about transmission to patients from asymptomatic medical staff.

Covid is present in at least two thirds of our state’s nursing homes. Family members are barred. The virus is invariably introduced by unwitting staff members.

When possible, and it mostly is, stay at home and stay safe.

Telemedicine in Maryland is defined as a medical encounter with the use of an audiovisual aid such as a computer using a HIPPA approved platform. Telephone calls are excluded from the definition of telemedicine.

State licensure rules regulate the use of this technology for out of state patients. Most states have loosened the rules. But changes in regulations vary tremendously from state to state.

Telemedicine is more personal than phone medicine and feels more like a normal doctor-patient visit. I can get a sense of the patient’s general overall health based on his/her appearance. Objective data is missing but patients can help fill in some of the blanks.  Patients have easy access to home BP devices, oximeters, scales and thermometers. I can look at a throat, rash or swelling. I can see where pain is without having to guess. I can get a general sense of breathing based on observation. And many patients can get an EKG with a wristwatch or other portable device and show me the tracing on the screen. Prescriptions are electronic.

If a patient needs more advanced care, at an ER for example, the platform is extremely helpful vs a phone call. 

Please use the doxy.me or another similar platform. It’s easy to use and does not require an app. And I can hear much better as well.

Mold toxins in perspective, a science based approach

Mycotoxins – the noxious chemical defense of these ancient and troublesome microorganisms.  Recently a  patient showed me a urine test. Mycotoxins were present in high concentrations. The patient was prescribed cholestyramine and the next test was almost clear. He said “his mold level” had improved. He fundamentally misunderstands the problem.

First, we want to know if he is right about his “mold level.” Are there a significant number of pathogenic mold organisms living in our body actively secretin caustic toxins?  Mold is not generally found in our bodies, at least at high or clinically significant levels.

Sure, we are all a waking zoo of microorganisms: bacteria, yeast viruses, perhaps some protozoa but no mold. Although yeasts and mold are cousins and frequently killed by the same drugs they act very differently.

I ask again: why are the toxins found in our urine at measurable concentrations.

Most readers likely believe that the primary source is largely aerosolized spores emanating from hiding places – wet basements and the like.

In actuality the biggest source of mold/mold toxin is food.  Many foods we eat all the time may have high levels of mold. We have all found moldy bread in the fridge at one time or another (I certainly have). Before the putrid green and blue areas appear mold long present. Just not in numbers easily observable to the naked eye. Our berries are covered in mold before the white exudate appears. Mold is present in many foods: cereals, grains, corn, fruit, peanuts and peanut butter, eggs, milk, meat, coffee beans, coffee – especially from our Keurig with its inaccessible wet, warm environs, a perfect culture media, etc.

The more serious, life threatening mold infections, for example aspergillosis of the lung or brain generally occur in those seriously immunosuppressed.  Ordinarily, aspergillus is a common food mold, a good source of aflatoxin and ochratoxins. Another common food mold, penicillin is a good source of ochratoxin. There are many other food molds and food toxins.

Black mold, Stachybotry lives in our homes. It eats cellulose, things like ceiling tiles, tiles and fiberboards. Its spores are aerosolized, along with very noxious trichothecene toxins.

Many mold toxins are xenobiotics recycled from liver produced bile to the intestines and back again endlessly (or perhaps 20 times). Enterohepatic recirculation may be beneficial in some circumstances. In this scenario the liver is assaulted by the same destructive toxins over and over again.

I have written about this system in a few posts. The bottom line is that this process explains why bile acid sequestrants (BAS) like cholestyramine and Wellchol work. Activated charcoal also works because at high concentrations it performs like a BAS. In fact, like the BASs, activated charcoal (24 gm daily) lowered cholesterol by 25%. These drugs grab bile acids and biliary toxins causing excretion through the colon – and the liver makes new bile acids, primarily from cholesterol.

The drugs  lower the overall level of toxins in the blood and therefore spare the liver and kidneys by a second mechanism.

 But we have not fixed or addressed the underlying problem.

Dietary sources of mold and mold toxins are significant.  We may need to seriously change our diets.

We may need to remediate our homes, especially wet basement areas if black mold spores are in the air.

But these molds do not really or should not really take up residence in our bodies.  They are not part of our normal microbiota.  But this in not always the case, especially with deep, chronic infection and immunosuppression.

 Where is the mold then hiding?  Sinuses, lungs and skin are possibilities. Specific antimicrobial therapy is indicated, either intranasally or with systemic agents.  The mold may be eliminated, or numbers significantly reduced. Retreatment may be par for the course.

A lot is made about epigenetics, especially MTHFR variants Genetic variations may interfere with “methylation.” DNA methylation is part of a switching -- turning genes on and off, with far reaching consequences. This is a real phenomenon. Complex and poorly understood.

Eliminating exposure to toxins is the most important part of therapy. You cannot get better if the fundamental problems is ignored.  BASs and vitamins for MTHFR can be given simultaneously- icing on the cake -- not the cake.  MTHFR for another day.

Detoxing and science and doctors

I talked to a patient today who is mad. Mad at doctors who are unprofessional, disrespectful and who disparage other doctors. This is what I recommend.  Calmly call out the doctor's misbehavior. Be the grownup. Rise above the petulant, entitled child who never grew up.  This describes many doctors.  My patient wants to be proactive, respond to ill=treatment form doctors.  Something about ratings in Apps. No comment.

If you are like me you sometimes grab an orange from the basket, hold it under the faucet for a few seconds, peel and eat it.  Perhaps you grab a waxed apple and do the same. You should scrub the fruit with a natural detergent. Your produce is likely grown in an invisible stew of things like the widely used pesticide 1,3 dichlorpropene banned in the European Union, Roundup, Organophosphates, Arsenic related and others to name a few.  Big agra-business makes the oranges and apples shine – with more chemicals.  The FDA assures us the levels of toxins and carcinogens are safe. Organic produce has less of the same but is exposed to the same contaminated water table and soil, our toxic biosphere.  The FDA tells us the levels of these entirely safe.  The Mayo Clinic suggests natural products used by organics farmers are not proven safer than unpronounceable chemicals known to quickly kill white mice.  Who told them that?

Weeds, like unwanted bacteria are becoming increasingly resistant to the usual pesticides calling for more drastic measures. Nice. 

This is not my usual topic and I know little about the subject and have much to learn.  But I hear a lot about detoxing. This what it might mean to me. 

Enter the word Xenobiotic.

You already know about probiotics and antibiotics. 

Xenobiotics are foreign, non-biological substances which may be toxic to tissues including liver and kidneys. Very bad toxic substances we ingest daily. 

Likely the doctor has never heard the word.  Give them scientific source material. 

Xenobiotics can be difficult to eliminate and cycle endlessly through enterohepatic re-circulation.
This is where activated charcoal comes in.  It waits in the intestines for the toxin laden bile, grabs the xenobiotics and eliminates them through the colon. Charcoal and cholestyramine eliminate mold toxins (mycotoxins) the same way. They may also eliminate your expensive medicines. Follow directions. 

Frequently sage allopathic doctors, especially infectious disease experts, jump down the gullets of Lyme patients who say they are “detoxing.” The word detoxing is foreign to mainstream medicine and practitioners. It raises the antennae of doctors who are quick to denounce such talk as voodo pseudoscience.  

Lyme bacteria do not have toxins they will opine. 

It’s true Lyme bacteria lack the endotoxins of pathogenic gram-negative bacteria. That’s not at issue. 

I always try to teach patients how to talk to doctors. The answer is, “Of course not. The chronically ill patients may have difficulty with toxic xenobiotics (look up the word doctor). General inflammation challenges the ability of the overworked liver and kidneys to remove the toxic chems.  And doctor, if you are content with paraquat and roundup in your diet it doesn’t apply to you.” (Less snarky -- unless the doctor is a narcisistic, arrogant piece of excement).

The doctor may come away realizing there is something here to learn. Nah. 

In general, don't mention detoxing. Its not worth it. 

Charcoal helps with Herxeimer reactions because it binds cytokines. This can be further explained if the doctor if she/he is still standing in the exam room. This straightforward, unassailable science. 


A lot of doctors don't like science. Ironically they are quick to lable those with whom they disagree anti-science. Old news. 

Don't be angry with doctors. Set realistic expectations. Unless they attack me. Then go for the jugular. JK.

Organic foods  are better.  GMOs are not the problem. They are the bright, shiny object which distracts. A discussion for another day.

DSF, dose, activated charcoal managing the Herxheimer reaction

My patient is feeling optimistic. The best she has felt in years.  Disulfiram/Antabuse, AKA DSF is the game changer.  She takes a tiny amount.  I prescribed 10 mg compounded capsules, a very low dose. She started with one capsule every 4 days and has increased the dose to 2 caps, 20 mg daily. She reacts to this small dose, significantly.

She feels OK the first day of disulfiram pulse. The second day she is assaulted with a variety of symptoms: fatigue, brain fog, muscle/joint pain, shooting pains, muscle twitching, head pressure, etc. She feels increasingly better over the next 4 days and the cycle repeats.
She is happy. No longer depressed. Really happy.

She tells me she manages the second day Herxheimer reaction with doses of activated charcoal.
I’m naturally skeptical.  Everything has to make sense. Scientifically and logically.

Herxheimer reactions are modulated by the immune system, something like a cytokine storm. This is all very complicated so let’s not get lost in the weeds. These cytokines are a complex set of proteins which regulate activity of the immune system (traffic the immune system). When Lyme is killed cytokines and the immune system are kicked into high gear. This leads to inflammation, too much inflammation, a bad thing. We need to reduce cytokine activity and/or cytokines themselves.

It’s exciting to learn that activated charcoal is incredibly effective at binding cytokines. When blood is filtered through activated charcoal cytokines are removed.

How does that help us? Blood has to be removed from your body and filtered. Not likely. Activated charcoal is the “universal antidote” and good for reducing bloating and gas. It stays in the gut. It does not get into the blood where cytokines live.

Ah ha. Like cholestyramine, it interferes with the natural recycling of bile (from the liver) to the intestines and back to the liver. OK. And..

A published study looked at oral charcoal in mice loaded with malaria and treated with an intravenous antimalarial drug.  Charcoal reduced brain swelling and reduced key cytokines. Gut only charcoal did all this. 

Cytokines may be cycled through enterohepatic pathway and processed through the intestines.  Charcoal may be there waiting to gobble them up. (Conjecture on my part).
I finally have an idea why Wellchol/cholestyramine lowers C-reactive protein. CRP is cytokine driven.

Normal functioning of the enterohepatic pathway impacts the concentration of medicines, toxins and other substances present in serum. I discussed this in another post. Messing with the enterohepatic re-circulation of bile can do good and bad things. This is a very complex and vital part of our physiology.

The best treatment for Herxheimer reactions may be antioxidants (oxidative stress) and activated charcoal.

I do listen to my patients and believe what they say. I worry that many desperate patients are taken advantage of by various scams. I worry about overpromoted nostrums, a mass placebo effect.  Think-- The Emperor’s New Clothes.

My patient today snickered at my skepticism.  I am humbled.  She was right and I was wrong.

I still want people to stop think Herxheimer reactions are caused by toxins and cholestyramine/Wellchol and charcoal remove toxins. Speaking of  toxins specific to the Herxheimer reaction. This does not make scientific sense. (I am not saying other toxins are not removed, I am speaking of the mechanism of the Herxheimer response).

Yes, the best starting dose (and ending up dose) of disulfiram is variable.  Starting low is a good idea. 10 mg seems to be a good starting place, for sensitive patients. Options include 25 mg, 62.5 mg and others generally are well tolerated.  Gradually increasing the dose likely mitigates damage caused by an overly eager immune system.

Take home points:  DSF, start low.  Herxheimer reactions -- antioxidants and charcoal.
Also, if you had a bad reaction with a higher dose of DSF you may do well with a small starting dose.

CFS, SEID, (a little POTS?)

If you treat Lyme you see boatloads of patients with chronic fatigue syndrome and many with POTS. CFS, myalgia and encephalitis has been renamed SEID, systemic exertional intolerance disorder. Many patients with SEID have orthostatic intolerance.  When they stand up for any period of time they feel the need to sit down or lie down. Is there a connection we are missing?

POTS, postural orthostatic tachycardia syndrome is a manifestation of dysautonomia, a broken autonomic nervous system. This important part of the nervous system does many things. With POTS with focus on a cardiac manifestation.

A lot of disorders are diagnosed based on cutoffs. The numbers are somewhat arbitrary. For example, POTS is diagnosed when supine pulse goes up 30 points with standing.  Perhaps a lying down heart rate goes from 60 to 90 when a patient stands, and stays there and may increase.

A patient may need to stand for 15-20 minutes before the change occurs.  Some patients are tortured with a tilt table test (not originally designed to diagnosed POTS).

Today I saw a 54 year old male I have been following for a number of years.  His main problem has been crippling fatigue.  Maybe he has Lyme, not clear.  Antibiotics were a little helpful (or placebo effect). With high viral titers, EBV and HHV6 the antiviral Valcyte helped, for a while. Maybe. Always looking for the next thing he asked me to prescribe rituximab (kills EBV?). NO WAY. He is always looking for a new cure. He tends to overdo exercise when he feels better and relapses.. Treatment for mast cell activation disorder has been somewhat helpful. 

Today he is feeling the best he has felt in 10 years -- normal.  How did we get there?

When he changed position lying to standing his pulse only increased about 12 points. No POTS by standard criteria.

I wondered what would happen if I treated him for POTS.

I didn't make many changes.  He has high blood pressure.  I changed his BP med, an ARB, Cozaar, a standard go to BP med to Coreg.  Coreg is an alpha/beta blocker and has been shown to help POTS. Normal B blockers should not be used.  I started him on salt (only started  one gm NaCl) and he added more to food. ( crazy in a patient with HTN, right?)

The change in pulse corrected.  His blood pressure did not go up.  Only a small subset of blood pressure patients are salt sensitive, especially blacks and the elderly.

Will it work for others? I don't know. I don't  know if it will continue to work for him.

The experience of one patient may be a fluke and mean nothing.

Both POTS and CFS are poorly understood.  They share certain features.

Mast cell activation syndrome may overlap as well in many cases. The diagnosis is usually clinical.

This therapy must be done slowly with careful patient monitoring.

A  little dysautonomia, a little POTS, a spectrum, continuum? Maybe. Medicine is frequently gray. Black and white cut off points should be looked at critically.

A thought.

Lyme update 2020: Key points

Eradication

We go back to the three legged monster I described so many years ago. The tickborne monster has legs of Lyme, Babesia and Bartonella.

For the first time Lyme has been eradicated in an animal model (murine/mice).  Dr. Zang of Hopkins was successful with a daptomycin based 3 drug cocktail: daptomycin, ceftriaxone and doxycycline. These 3 FDA approved drugs are well known and well used. Short of human studies, considered repurposing of vetted drugs may be considered. 

IV therapy is preferred and/or the standard of care in specific cases: sometimes indications are gray.  The risks of IV therapy include infection and venous access line and possible sepsis, thrombosis/blood clots and pulmonary embolism.  The use of intravenous antibiotic does not decrease the likelihood of C. difficile infection. The mainstay of intravenous antibiotic therapy has been Rocephin for many years.  Other antibiotics frequently employed include Flagyl, azithromycin and doxycycline.  Treatment incorporating daptomycin is new and has been well tolerated.  The drug itself is actually quite old.  It has been reserved for serious, resistant infections in many institutions and infectious disease experts have cautioned against first line therapy or other inappropriate use.

The primary indications for intravenous therapy include: Acute/subacute neurological disease ranging from encephalitis, meningitis to peripheral neuropathies including Bell’s palsy and others; acute inflammatory arthritis nonresponsive to oral therapy; Lyme carditis.  Patients with chronic Lyme encephalitis, /neuroborreliosis with cognitive problems are frequent candidates.  Patients who fail aggressive oral therapy, suffering with a multisystem disorder and poor quality of life are candidates.  The choices available for oral therapy are evolving.  As a general rule, IV antibiotics and oral antibiotics should be started and added one ag a time. The anticipated duration of therapy is always completely unknown. Every case is different.

Antabuse

Antabuse/disulfiram may be a game changer. In Vitro studies (Stanford University) demonstrated efficacy against Lyme spirochetes, round forms and biofilm forms. Antabuse has been used for more than a century as an antiparasitic, a commercial agent used for rubber manufacturing and for treating alcoholism.  Antabuse inhibits degradation of acetaldehyde, a toxic intermediary of alcohol metabolism.  Alcohol with disulfiram is a miserable experience one will never forget.  There are better ways to treat alcohol abuse. Antabuse has new life as a Lyme killer.  Antabuse has been effective against resistant forms of bacteria, including Staphylococcus (including biofilms) in-vitro. It seems to have a narrow spectrum against gram positive bacteria and should be easier on the gut. 

Side effects and tolerability described in older literature regarding aplicability for alcoholism does not to apply to our experience with Lyme patients.  For example, rare neuropathy described in alcoholics is not rare for Lyme patients. Herxheimer reactions are common and frequently severe; lower doses of the drug is required.

One option is to cut a 250 mg tabs into quarters enabling initial treatment with 62.5 mg. Compounding allows for more flexibility. Disulfiram can be compounded to any dose you like, for example, 10 mg or 25 mg. A target dose of 250 mg is frequently effective. Some patients claim that the 500 mg dose is more effective. I still combine disulfiram with traditional antibiotics for an optimal response. 

In my experience disulfiram does not eradicate Babesia. In many cases Lyme and Babesia are mysteriously linked. When Lyme clears and remits Babesia too may recede into remission. This may give the appearance the drug kills Babesia. 

Babesia

The malaria like red blood cell parasite is very problematic.   B. duncani and other unidentified organisms are very troublesome. Full eradication should be the goal.  Recurrences can be very difficult since the parasite often returns resistant to an arsenal of anti-Babesia drugs. Most “virgin” Babesia cases respond to Mepron. It is important to start with 10 cc or 2 tsp twice daily with fat. The 5 cc dose frequently recommend is inadequate. Mepron must be used with Zithromax.  Zithromax has the unique ability to concentrate inside cells at an incredibly high level. Other drugs like Biaxin, doxycycline, Bactrim and clindamycin are not effective.   I recommend more than one anti-Babesia drug even when Mepron appears effective. Bellwether symptoms:  night sweats, air hunger, random tearfulness are important but Babesia may cause many other symptoms as well. Coartem is my next favorite agent. It includes a much more bioavailable and effective artemisinin derived component, artemether. 

My third preferred agent is tafenoquine (well tolerated excluding G6PD deficiency). It comes in 2 forms.  Krintafel comes in 150 mg tabs and is used as a single dose for Malaria, repeated at intervals, e.g. weekly and  Arakoda, approved for malaria prevention.  The 100 mg tab is approved for daily use for malaria prevention. 

How long is Babesia treated? We say until symptoms are gone.  I have seen many cases of hoped for cure relapsee. I currently treat for 4 months beyond the point of complete remission if possible.  . 

Bartonella

This small bacteria lives in the cells that cover the inside of blood vessels. The bacteria may occupy red blood cells after infection until they "Uber" into blood vessel lining cells (endothelial cells).  Bartonella persistern forms have been observed.  Complex antibiotic cocktails with multiple bacteriostatic antibiotic, including tetracyclines, macrolides, rifamycins and sulfa drugs do not eliminate the bacteria. Bactericidal drugs, including gentamicin and daptomycin have proved effective. (only by injection, IV or IM). Quinolones should be avoided for safety reasons. 

Chronic nocardiosis, Morgellons?

My lab is certified by CLIA and the College of American Pathologists for blood parasitology.  I examine blood for bloodborne parasites: Plasmodium (malaria), Babesia, Trypanosomes – flagellates, microfilaria. Today I became aware of a bacterium which may appear in the blood but is not bloodborne. Nocardia. I have a patient with this infection. I have been treating her for a long time.  We think Nocardia infection it is chronic along with tickborne pathogens. The bacterium is found in soil and water and is ubiquitous, there are numerous species, some not yet speciated/characterized. We (the patient and me) have thought she suffers with chronic nocardiosis.  She has a clear, documented history of Nocardia: positive pulmonary infiltrate and positive blood culture. This is a slow growing organism. Texts say this rarely seen organism cultures slowly, 3-5 days. Her culture was positive only after 28 days. Nocardia infections is thought to primarily occur in patients with impaired immunity. She lacked clear evidence of immune dysfunction. The bacteria forms lesions in the skin, lungs and brain. Generally, IV antibiotics are recommended initially followed by oral therapy. Standard sources say skin infection is always curable, lung infection is usually curable and brain infection is curable half the time. Texts don’t address chronic nocardiosis, but I haven’t done a literature search.

This bacterium takes on an unusual appearance.  We are accustomed to rods, cocci and spirochetes.  Microscopically these appear as fungal-like filamentous structures.  The filaments vary in length.  Over the years I seen similar things I thought they were contaminants or artifacts and most likely were (not using the same stain).  Perhaps I missed something.  Of course, this was not on my radar.  Images are startling. Images of clumped filamentous structures, looking not like bacteria at all but rather the dense threads seen with Morgellons appear. The images, if correct (I have not validated them) can be found on google images. I know for a fact that some images on google images are incorrect.

Then there are patient images of skin lesions of the cutaneous form of the disease. Some look horrible.  Some clearly resemble lesions seen with Morgellons.

The chest X rays and brain MRIs are distinct from those seen with tickborne disease.

Again, this organism is found on skin and in the lungs and brains. In severe cases it may also appear in blood, gram stains. I don’t know if it also appears in Giemsa stains I perform.

I wonder if some cases of Morgellons are misdiagnosed nocardiosis. I wonder if Lyme immunosuppression plays a role in the pathogenesis of the disease.  Antibiotics recommended are some of the same ones used for Lyme but not exactly the same ones. The initial early treatment recommended is IV Bactrim.

Lyme and biliary disease

Most readers have some familiarity with the liver and gallbladder.  The biliary (bile duct) system includes the gallbladder and a collection of ducts coming from the liver which join to enter the first part of the small intestines, the duodenum, the first part of the small intestines (bowel) just below the stomach. 


The liver is best known as our body’s detoxification organ (along with kidneys). The liver “metabolizes,” alters and excretes medicines and other substances. 


The liver makes bile, a yellow viscous fluid stored in the gallbladder, located directed under the liver. The gallbladder contracts with meals. Bile made of bile acids, from cholesterol, aid in the digestion of fat (an emulsifier) but has many other functions.  


The liver detoxifies medications and toxins through a system of enzymes with names like cytokine P450. Toxins and medications may end up in bile. 

Adsorption of medications may be dependent on something called the enterohepatic recirculation of bile.

Most bile is recycled from the gut which is considered 95% efficient. A particular bile acid molecule may be used 20 times before it is replaced. This is not necessarily a bad thing. The process of repeated cycling may enhance the function of therapeutic drugs and delay their excretion. For liver toxins this works the other way.  Proper functioning of the enterohepatic system depends in part on a healthy gut flora and specific bacterial enzymes.  Higher doses of antibiotics may be required because disruption of normal flora and necessary enzymes caused by the antibiotic(s). 

The use of bile acid sequestrants to remove unknown toxins like cholestyramine is not supported by scientific evidence. 

Some antibiotics promote the production of biliary cholesterol sludge and gall stones, primarily Rocephin, the popular intravenous drug used to treat Lyme disease.  Cholecystitis (gall bladder attacks) with or without the presence of gall stones is a common occurrence. 

Lyme anecdotally can attack the biliary system. Cases of positive Lyme PCR/DNA from gallbladder tissues are known to me but there are no published reports to date. 

Published reports have established Lyme liver disease in the form of granulomatous hepatitis. 
Tests like sonogram, HIDA/CCK scan and others may be used diagnostically for problems with gallbladder and bile ducts.  Negative test results do not rule out gallbladder/biliary disease. 

I am treating a patient with primary biliary cholangitis (PBC). Generally, the disorder is considered autoimmune, “idiopathic,” which of course means the patient is pathological and the doctor is an idiot. Some European literature (this patient is European) connects Lyme with this enigmatic illness. The patient has a clear history of Lyme. No such connection is made in the U.S. PBC is now a treatable disease. 

Bile via an array of ducts ultimately empties into the common bile duct. Bile the empties into the duodenum into a structure called the Ampulla of Vater. The flow of bile is regulated by a muscle called the sphincter of Oddi. 

After cholecystectomy, (surgical removal of the gallbladder), prior gallbladder pain may seem to recur. The bile ducts may become dilated. When a medical workup excludes a left-over stone stuck in bile duct, liver disease, pancreatic disease and other rare diseases, the diagnosis may be post-cholecystectomy syndrome or sphincter of Oddi dysfunction.

These syndromes are more common in Lyme patients, many of whom suffer with gallbladder disease and biliary tract disease and have had their gallbladders removed. 

The diagnosis is commonly missed or not taken seriously. The disorder can be disabling. Effective medical therapy, in my recent experience, is available but overlooked.

PANDAS: diagnosed 15 years after the fact

A young adult is struggling with PANDAS/PANS and much more.   He is 33 years old, I diagnosed him at age 29. I treated him briefly. We arranged a single dose of IVIG. The plan was long term therapy. He was directed to another physician who treated him with a single dose of IV rituximab. He got better – for a while but quickly regressed. 


He had a normal childhood – until he didn’t, excelling academically and in sports. But that changed overnight. One day normal the next the beginning of a nightmare that has never ended. Mom and dad wanted to know what happened to their son. He had become a different person, for no good reason, out of the blue. He became withdrawn, irritable and rageful. He developed tics, anxiety and OCD. Mom took him to his pediatrician who referred him to a psychiatrist. 


He was dosed with psychotropic meds which never made a difference. He refused to go to school.

Finding no alternative, his parents sent him off to boarding school for 2 years. He returned sullen, paranoid and angry.  He dropped out of school and worked odd jobs, never for more a few months. He wandered around, from on place to the next, from one relationship to the next. 


There were numerous suicide attempts and hospitalizations. He was given every psychiatric diagnosis in the book, schizoaffective to borderline personality to bipolar. He was prescribed every psychotropic: atypical antipsychotics, SSRIs, SNRIs, mood stabilizers, anticonvulsants and lithium. The diagnoses were wrong, and the medications never worked. 


He lives on the other side of the country and I have not seen him in years. I care for a family member who referred him to me because he suffers with Lyme disease and thought the patient might have the same. 


Our patient is a little better than he was the day I met him, but he is not a functional human being.  

He is uncontrollably enraged constantly mourning the life he has lost. He is so angry at his parents. Unfairly he blames them for the delayed diagnosis of PANDAS (15 years), and there is so much other water under the bridge.

He in fact has Strep related PANDAS and also tickborne disease picked up later which stoked the fire. 


The medical literature offers nothing in this case and other like it stating PANDAS is a pediatric illness. An NIH paper admits some young adults may be afflicted but it stops there.

Unfortunately, I suspect there are a lot of patients who have a similar story. PANS was not diagnosed in childhood. In adulthood they are diagnosed. What is there to do about it. And I do have other similar patients in my practice. 

Do doctors imagine that undiagnosed pediatric PANDAS cures itself in adulthood?  The problem is doctors who write papers are academics and don't see a lot of patients. They only see cohorts of carefully culled patients who meet study criteria. And they usually don't see those patients for long term follow up.


Patients are frequently diagnosed with Strep, Lyme, Bartonella and others.

Treatment, the right treatment can be prohibitively expensive. Tonsillectomy is recommended and may help.  Antibiotics are part of the treatment.  There may be psychiatric Herxheimer reactions. Steroids are “the poor man’s IVIG.” A therapeutic response to steroids is predictive of a positive response to IVIG.  IVIG is dosed high, 1.5-2 gm/kg every 3 weeks may be effective. Rituximab is a third line treatment. Some patients are managed with a combination of IVIG, Rituximab, steroids and antibiotics. Whatever works. 


These patients need a lot of supportive services and therapies. 


All of this new, largely opinion driven, because there is little research or science. The waters are uncharted because PANDAS wasn’t recognized until the late 1990s and tickborne PANS much later. There may be countless young adults suffering in much the same way. 

Naturally I think my approach is the most logical and effective given what we currently know. 


Treatment: tonsillectomy, antibiotics, steroids, IVIG, rituximab. Rituximab is not a substitute for IVIG, it is third tier therapy.  

Intensive therapy and psychotropic meds are going to be part of the picture. Psych drugs are not bad. It fact, they are incredibly helpful. It must be understood these meds are adjunctive, supportive and do not target the underlying cause of the illness. 

Disulfiram resistant strains of Lyme!

No. I don't know if there are disulfiram resistant strains of Lyme. However, the emergence of such strains seems inevitable but may be preventable.

How does disulfiram kill bacteria?  Biochemistry.  Disulfides or thiols bind to critical metabolites in the bacteria. Medical literature claims it has a narrow spectrum of action killing specific gram-positive organisms, like Staph aureus and several others. The construction of the cell wall of susceptible bacteria determines the entre of the drug.  Spirochetes like Borrelia burgdorferi, are neither gram positive nor negative. The out surface of the spirochete is comprised of double membrane, one that is lipophilic (loves fat). The disulfiram molecule is also lipophilic (loves fat). This shared biochemistry dooms the Lyme spirochetes.  The disulfiram molecule carrying its poisonous chemicals is a trojan horse and quickly puts the spirochetes out of commission.

A narrow spectrum may be a good thing. This is the ideal scenario. The drug kills the target and only a few bystanders (collateral damage). Most antibiotics essentially nuke, or carpet bomb our bodies, carrying around their 2-8 pounds of normal flora – bacteria, indiscriminately killing huge numbers of good guys.

Disulfiram represents an entirely new class of antibiotic with a novel way of killing bacteria.

Traditional antibiotics work by inhibiting cell wall synthesis, inhibiting protein synthesis by disrupting ribosomes, interfering with DNA or RNA function – and that’s about it.

We don’t know if antibiotic resistance will emerge against disulfiram. The best predictor of what might happen is history.

There currently exist bacteria resistant to antibiotics from each of the known classes.

It may be wise to listen to Alexander Fleming, the Nobel laureate who discovered Penicillin. Over the course of his career he watched susceptible strains of Staphylococcus become resistant to the the wonder drug, penicillin, in a few short years.

He cautioned that one must make sure the antibiotic is necessary, then make sure the dose is high enough and the drug is given long enough to prevent the emergence of resistant strains of bacteria.

Popular pulsing and prescription of low, subtherapeutic doses of antibiotics/disulfiram are practices which needed to be avoided lest we kill the goose who lays the golden eggs

The emergence of resistance is nearly universal.  It has happened with every bad infectious disease you can think of, ranging from malaria and tuberculosis to HIV. It is the rule, not the exception.

The Lyme buggers are very, very smart. Expect no less.

ID doctors and the IDSA frequently talk about stewardship of antibiotics. I think they are frequently wrong about the details, but the concept is sound.

The thousands of patients suddenly taking disulfiram are a Facebook ragtag army with no sense of the history of antibiotics and germs and the decades long battles, lost and won.

My suggestion is simple but probably hard to implement.

Hit Lyme hard and long (disulfiram, and as I think about, a cocktail of other antibiotics makes a lot of sense). Treat for months after the disappearance of symptoms.

Using disulfiram as monotherapy, the only drug, may accelerate the evolution of disulfiram resistant Lyme strains.


In the words of the immortal Bob Marley “you have to kill it before it grows.”

Disulfiram, disulfiram and Monurol?

Perhaps, when the  history of Lyme disease is told at some future date, it will be divided into the pre-and post-worlds of disulfiram.  Maybe since Antabuse is not classified as an antibiotic, the IDSA will back off, who knows.  


The drug seems to be amazingly effective for so many patients. Still, it’s not for everyone.  Some patients tolerate relatively high doses of the drug out of the gate; for the most part, is better start low and gradually increase the dose as many patients do not tolerate high doses.  The effective dose is unknown.  250 mg may be effective for  many patients (not 500 mg).


Patients have had a hard time finding the drug, scouring pharmacies across the continent.  A patient I saw today did incredibly well after 6 weeks of therapy.  Then, she could not find any more drug and symptoms returned with a vengeance.  She is now well stocked from an overseas pharmacy. With nearly 30 years of disease, the majority of her life, she suffers with POTS, EDS and MCAS – and chronic pain.  Antabuse is not going to fix everything.  I continue to enjoy excellent success managing pain without opioids. 


Antabuse for most patients may not be a quick fix.  But it’s effectiveness is undeniable and it is quickly changing the game.


Elevated liver function tests are common.  Frequently the drug can be stopped for several days until labs normalize and tolerated at a lower dose without budging liver numbers. Liver function tests in excess of 3 times the upper limit of normal (120ish) should be of immediate concern.  
Another novel therapy been very effective for 1 of my patients.  Fosfomycin, Monurol is a 3 g powder is typically used for urinary tract infections.  It also works very well against Lyme persister.  With a typical UTI the dose is a single 3 gm packet. The drug has a prolonged duration of effects, about 48 hours, despite a short half-life:  it continues to work because of its PAE (post antibiotic effect). A current patient is responding beautifully to twice weekly dosing along with doxycycline and Zithromax – Zithromax combined with Mepron for Babesiosis. 


There are more great and effective options than ever before, including IV daptomycin. 


I am accepting new patients with Lyme (and coinfections) and a host of other conditions: PANS, POTS, CVID, CIDP, EDS, MCAS, CFS, FMS, neuropathic and central pain syndromes, headaches and chronic, mysterious difficult to diagnose ailments. 


I offer blood Giemsa staining screening for active Babesia infection:  Lab CLIA approved and certified by College of American Pathologists.

Blogging about Lyme and related topics since 2008.

Disulfirm/Antabuse

Its true: Antabuse/disulfiram is the most exciting new therapy for Lyme since daptomycin.

We are getting a lot more experience with disulfiram/Antabuse.  In some cases, it seems to be very effective.  I don’t think it is clear which microbes it is active against. It is an old drug repurposed as an antibiotic.  Its antimicrobial spectrum may remain unknown for the foreseeable future (there is no money researching it).  One thing worse than dreaded MRSA is VRSA – vancomycin resistant Staph aureus.  In vitro it was shown that the addition of disulfiram to vancomycin conferred the ability to kill this dreaded superbug. This should be catching some eyes, even outside the Lyme world.

Disulfiram clearly has potent antibiotic effects. It also has side effects. Twenty five percent of users have some rise in liver function tests –markers of liver inflammation. The rise is usually modest, and therapy can continue if AST/ALT numbers don’t exceed 2-3 twice the normal limit, with close monitoring. Three times makes me nervous. My comfort zone limits closer to 2.  Waiting for numbers to normalize and restarting with a lower dose may work. Severe liver disease may occur 1-2% of the time, not a trivial number.

ONLY YOUR DOCTOR CAN MAKE CLINICAL DECISIONS REGARDING ANTABUSE AND LIVER TEST.  THIS IS WRITTEN FOR GENERAL INFORMATIONAL PURPOSES ONLY; FULMINANT LIVER DISEASE CAN BE FATAL.

You should never treat yourself. The man who has himself as his doctor has a fool for a patient.

Side effects may include, dizziness, brain fog, fatigue, GI intolerance and others – in my patients. Many patients have had to discontinue because of side effects. Monotherapy may be fine. It runs counter to my experience, so I tend to prescribe it with doxycycline.

A word for the wise. We don't really know how safe the drug is.  Sometimes problems only become known when an occasional drug becomes one in common use. We have seen it over and over, for example, fenfluramine off fen-fen fame caused unexpected heart and lung disease and Vioxx the great new anti-inflammatory caused heart disease. Drug companies who have studied drugs extensively and had FDA approval call this "post-marketing" side effects.

Yes, Antabuse is an old drug used by hundreds of recovering alcoholics. When this old drug, largely disregarded from decades, it is suddenly used by thousands of lyme sufferers it many ways acquires characteristics of a new drug. In this case one that has not been tested. Quality control of generics is increasingly becoming an issue, e.g. Zantac.

I am prescribing the drug, just not throwing caution to the wind.

There is the issue of dose.  For alcoholics the loading dose is 500 mg and maintenance dose is 125-250 mg. This suggests that lower doses have efficacy.

There is some confusion about Lyme Herxheimer reactions.  From experience, Lyme, Babesia and Bartonella have separate and distinct Herxheimer responses.  Herxheimer reactions occur when mass killing of chronic, entrenched infection leads to an over-reaching immune response, a cytokine storm. The average, non-Lyme doctor, is unaware of the phenomenon treating mostly acute infections. These same doctors no doubt encounter a fair number of Herxheimer reactions which are misdiagnosed, e.g. drug allergy. Some patients have an “allergy” to every antibiotic. No, they don’t. Other patients say, “every time I take an antibiotic it hits me hard.”

Babesia and Bartonella Herxheimer reactions are very vexing, chronic and sometimes difficult to manage. They are qualitatively different from Lyme Herx reactions.

Lyme “Herxes” tend to be easier and follow a specific pattern.  An antibiotic is introduced, with days severe symptoms ensue, like fatigue (inability to get out of bed fatigue) low grade fevers, brain fog, achiness etc. After a period of days, weeks, usually no more than 3 weeks, symptoms begin to improve and go away and the patient improves. The Herxheimer reaction (Lyme only) should not return in cycles. Such cycles, apparent recurring Herxes, may be the result of normal ups and downs of the disease or due to killing something else other than Lyme. If we add one or more drugs, which gain access to a previously off-limits group of bacteria (round forms, biofilms etc.) a Herx may return, maybe even a more difficult Herx.

Dr. Zhang has dichotomized Lyme bacteria for us: active forms (free spirochetes) and stationary/persister forms (round bodies, biofilms).

After a reasonable amount of treatment with antibiotics targeting both populations, e.g. doxycycline, rifampin and Flagyl we would like to think there are few Lyme bacteria left. We are incorrect.

Add in disulfiram and an intense Herxheimer reaction may ensue (in some cases, not all).  Patient tolerance to  varying doses of the drug is all over the map.  Some handle 500 mg out of the gate, others struggle with 125 every other day.

It makes sense to start with a low dose and gradually increase over time.  I am more aggressive apparently than many others.  Most patients can increase from 250 mg daily ramped to 500 mg over a week or two. For sensitive patients much lower doses and more gradual ramping is required.

I have seen patients on the border of needing IV antibiotics  get better with Disulfiram.

It doesn’t always work. There is still no one drug that works for every patient.  And symptoms still relapse quickly with discontinuation after a few months.  Some patients are still going to need IV antibiotics, (Rocephin, daptomycin, doxycycline) if possible.

In my experience disulfiram doesn't appear to kill Babesia. My experience. Babesia is an opportunistic infection riding on Lyme’s coat tail.  Lyme has inherent immune suppressing properties. If Lyme is largely gone, Babesia symptoms may abate as well. In a normal host the body's immune system can eradicate Babesia, or reduce it to a mild parasite causing no symptoms. Just a thought.

So far, we only know that Antabuse kills Lyme spirochetes and Staphylococcus. Hopefully research will be funded so we can learn more about the drug. We really don't know what it does or doesn't kill.

Bottom line: Go for it! Monitor labs, watch for side effects (no alcohol including herbal tinctures): disulfiram –is  not an overnight miracle cure -- but it is quickly rising to the top of the list of  go-to Lyme drugs.  

Unecessary suffering and beating a dead horse

My new 40 year old patient is besides herself.  She has struggled with a tickborne illness for 5 years.  She has managed to keep her job, but barely. She cries uncontrollably.  She is very irritable and angry. She complains of anxiety and panic attacks.  Mostly, she is depressed. She admits to night sweats.  She denies air hunger.  Ongoing symptoms include exhaustion, chills, poor sleep, tinnitus, painful lymph nodes, abdominal pain and nausea, GERD, irregular menses, joint pain, headache, dizziness and vertigo and feeling off balance, dysesthesias and crawling sensations, panic attacks, suicidal ideation (no plan or intent), brain fog, trouble with with focus and concentration and thinking clearly. She has had a lot of unexplained abdominal pain over the years.

She has seen 2 "Lyme"  doctors off and on over the last 5 years. She has also seen many "regular" doctors.  The first Lyme doctor diagnosed Bartonella and treated her extensively with minocycline, azithromycin and rifampin.She didn't get better.   A second Lyme doctor confirmed the diagnosis of Bartonella.  Laboratory tests were negative but the physician was certain on clinical grounds the diagnosis was correct.   After all, what else causes severe GI symptoms and abdominal pain?  Anxiety and irritability are typical symptoms, almost diagnostic - she heard somewhere.

The "regular" doctors diagnosed depression, fibromyalgia, chronic fatigue syndrome and hypochondriasis.

One Lyme doctor treated her with ivermectin for one year.   She states she thinks she had a Herxheimer reaction but does not know why this drug was prescribed. The treatment did not help.

The same doctor prescribed Biaxin and rifampin.  The dose of rifampin was increased to 1200 mg daily.  After 9 months of this therapy she has gotten worse.  The doctor told her she has not been treated long enough. She decided she has waited long enough.  She thinks she had Herxheimer reactions but never got better.

She has never been treated for Babesia or even Lyme. A course of doxycycline with other Lyme drugs was never prescribed -- or anti-Babesia therapy.

A LymeWestern Blot was equivocal by MDL standards, IgG only.
Serologial tests demonstrated a low positier titer for Rickettsia species.
All other serological tests, inclusive of  Bartonella and Babesia were negative.
CRP was elevateed at 10.

I am able to offer another test in my CLIA certified blood parasitology lab.

Her an image taken from her Giemsa smear:

If a patient doesn't respond to a therapy the clinician is obligated to go back to the blackboard and take another look.

The slide shows marked infection with the malaria-like red blood cell parasite: Babesia. Few things are black and white in Lyme's orbit. This is an exception.

This CDC endorsed standard malaria/Babesia smear is a gold standard.    Many tests circulating in the Lyme-osphere are questionable.

Even without this piece of dramatic evidence, the patient should have been treated for Lyme, e.g. Doxycycline/Ceftin (Tindamax, Flagyl, disulfiram and others) and also treated for Babesia.

This poor long-suffering patient went  5 years, with night sweats and profuse tearfulness (depression) and Babesia was never considered or treated.

Hundreds of things can cause abdominal pain other than Bartonella, etc, etc. The symptoms of Lyme and common coinfections overlap. No one symptom should be attributed to  a particular tickborne pathogen.

Babesia treatment includes Zithromax and high doses of Mepron plus Coartem plus Krintafel. It is important to completely knock out Babesia when first encountered.  Otherwise, the parasites relapse and return mean and drug resistant.  *Please don't use Malarone because Mepron, the yellow paint is hard to stomach. Two malarone twice daily provides a daily Atovaquone dose of 1000 mg.  Two tsp of Mepron twice daily provides 3000 mgs of atovaquone, three times the dose. This dose falls within FDA approved, manufacturer guidelines. This high initial dose must be used to avoid drug resistance and years of misery. If its virgin Babesia you have one change to hit it hard and fast. Don't miss.

I am optimistic. We will get her better and sooner rather than later.

Lyme germ warfare?

Complex subjects, like the provenance of Lyme, are oversimplified into a soundbite and the truth is lost in the noise. The Washington Post does us a disservice.

Sam Telford, in the Washington Post told us that Lyme is not an escaped military bioweapon. The headline is  an implicit smirk at the alternative Lyme community said to be steeped in unfounded conspiracy theories. Ant-science. Fits right into the IDSA narrative.

Dr. Telford is a smart guy, a professor of Biowarfare at Tufts University, who has researched the topic for decades. Largely, he is telling the truth. Largely.

Let's listen to his truth. It speaks volumes.

Lyme is an old disease, even ancient.   Lyme was found in the 5300-year-old ice man dug up from the permafrost in the Alps – previously published in National Geographic.  Lyme infected ticks were found from 1945 and 1896 in the northeast US. Facts.

Ticks (Lyme carrying ticks) were studied during the cold war as a means of transmitting germ warfare.  Fact.

Deadly agents, including Tularemia and Q fever – transmitted by the same Ixodes ticks were studied (and continue to be an area of research -- other source).

The double helix of DNA was discovered in 1953.  Scientists during the cold war (1950s - 1980ish) lacked technology to modify germs and make them more deadly. Now it can be done.

Germ warfare research was done at Fort Dietrich and Plum Island. Modern Biocontainment procedures were unknown. (Animals and Ixodes ticks were allowed to roam free on the Island, with the belief they could not leave the island -- other sources). It was unknown that seabirds could ferry ticks to the mainland.

Lyme and the coming epidemic was something military researches could not have imagined.  The Lyme Bacteria was not discovered until 1981.

The Lyme epidemic cannot be entirely sourced to Plum Island since the epidemic broke out in the Midwest and West Coast at around the same time as Lyme Connecticut. The author does not say that Plum Island didn't contribute to the epidemic. 

Willie Burgdorfer participated in tickborne biowarfare research for the US Department of Defense.

Dr. Telford says a few dumb and obviously incorrect things: Willie was just joking with the interviewer about his role in germ warfare research.  Plum Island was repurposed for agriculture research in 1954 -- during the height of the cold war. (not a cover story).
And -- the US stopped bioweapon research in 1969 because Nixon said so. 

These are the clearly established facts.

In summary:  Our government was involved in germ warfare research for years. Some of the research involved ticks and tickborne disease (Q fever, Tularemia). Willie Burgdorfer, whose names is attached to the Lyme agent, B. burgdorferi worked for the government and  some of this research was with the same ticks that transmit Lyme disease. Biocontainment procedures were unknown and government scientist did not know the ticks and the unknown pathogen (Lyme) could easily jump across the Long Island Sound to Lyme Connecticut. 

It is easy to conjecture the Government unwittingly helped spread the epidemic of Lyme disease to New England as an unexpected consequence of secret germ warfare research. And, it is widely known the Government has a habit of not admitting wrong doing and covering its tracks. 

When we say Lyme was not an escaped bioweapon the statement is both true and false. There was no conspiracy to infect Americans with a horrible disease. But is seems likely that an unexpected consequence of tickborne disease bioweapon research on Plum Island was the spread of some Lyme infected ticks to the mainland. 

The law of unintended consequences applies and there is much we will never know.

Congress can investigate and it will be a waste of time.

Novel drugs for Lyme

The dry spell is over. We have some promising new therapies.

Investigators have been used a method to screen large numbers of drugs which might treat Lyme. Dr. Lewis has apparently found that disulfiram, Antabuse, used to treat alcoholics and makes them vomit if they drink alcohol seems to kill Lyme. Apparently, he has discussed his findings at lectures. Practicing doctors don’t get the low down until findings are published in a journal. A recent case report of 3 patients showed efficacy of the drug.  Antabuse is something I have used throughout a 37-year career in medicine. It is generally safe, but liver tests need to be monitored. Repurposing the drug empirically seems quite reasonable. Dr. Fallon, Columbia University, is doing a clinical study. 

The fact that Antabuse is not an antibiotic is exciting.

The combination of Rocephin, doxycycline and daptomycin may be effective in humans. A clinical question is how long do the drugs need to be given?  Will we see durable benefits in 30 days, 60 days etc.?  Can an intensive IV therapy circumvent months, even years of other complex and perhaps less effective therapies? Let’s find out.

Controlled clinical trials are important. Placebos are incredibly effective. Personal interactions influence outcomes as do other confounding variables.  Studying a complex disease like Lyme is challenging; coinfections are not accounted for and a million other variables are not and perhaps cannot be taken into account.. Study results must be interpreted with care, nuance and ample discussion. The limitations of the study must be addressed. And I hope investigators will not be strong armed by politically motivated institutions to parse words when stating conclusions.  These few words have been misinterpreted, willfully with far reaching ramifications. The IDSA drew incorrect and absurd conclusions from Fallon's last Lyme study. And here we go with another set of IDSA recommendations.

Tafenoquine in the form of Krintafel is being used for treatment resistant Babesia. Looks good so far.

Bartonella persisters and daptomycin: two for the price of one?

While Lyme persistence I denied for political reasons the persistence of other human zoonotic pathogens is recognized. 

I have seen two cases of brucellosis recently and Brucella is recognized as a persistent bacterium, perhaps impossible to eradicate, at least with currently used and/or recommended therapy.

B. abortus is one of several well-known human pathogens of the genus, the one which may be acquired via tick bites.

Brucellosis can be acquired by consumption of uncooked meat and raw milk. I don’t understand the fad of drinking unpasteurized milk, a potentially deadly fad.

Brucellosis may cause numerous untoward clinical syndromes many of which similar to those seen with chronic Lyme.

Bartonella, especially B. henselae is a well known tickborne pathogen also known to exhibit persistence. The bacteria, a fastidious (difficult to culture) gram negative rod is an obligate (facultative) intracellular gram-negative bacteria associated with well described clinical syndromes, discussed elsewhere. Spotty medical literature supports the notion that Bartonella infection is clinically persistent.

Biologically, Bartonella are the only bacteria which may reside in red blood cells. The only other RBC pathogens are malaria and babesia species. Specific biological features, a protected niche and the discovery of stationary forms provide an ample narrative of fact and biological plausibility for persistence. 

The primary home for these bacteria is not RBCs but the endothelial cells that line blood vessels. This is why bartonellosis causes well known vasculitis syndromes. 

Zhang, a prolific publisher, should now be a star at JHH published about Bartonella persisters in antibiotics April. Again, daptomycin is the star.   Daptomycin has the best activity against stationary (persister) forms. Only aminoglycosides, e.g gentamycin are competitive.  In my experience, gentamycin may eradicate clinical infection, but not consistently. Complex multidrug regimens are frequently recommended for Bartonellosis, perhaps this is unnecessary.

This study added to others vis-à-vis Lyme raises the clinical (preclinical) question. Should patients with chronic illness caused by Lyme and Bartonella be treated with combination IV therapy, Rocephin, Doxycycline and Daptomycin earlier rather than later in the course of treatment?

From an Evidenced Based Medicine approach this is anathema,  such therapies can only be recommended after randomized clinical trials, peer reviewed and published.

Such studies are perhaps decades away.  Currently the political divide make diagnosis of Lyme nearly impossible, let alone coinfections.

The preclinical approach allows for empiric use of the therapy without waiting for IDSA approval, which may or may not ever come.

This concept of applying preclinical data (translational medicine) is well developed and well used in the field of oncology. Of course, cancer is considered a serious disease (and Lyme isn’t?).

Those of us in the alternative universe of Lyme disease are accustomed to very long-term antibiotics, including IV ones.  In this world, the use of these 3 IV drugs sounds reasonable. In the other world we are no strangers to cocktail therapy and IV therapy.  In the IDSA/CDC world of doxy for 3 weeks even discussion of this idea is heresy or treasonous, if such things apply in medicine (apparently, they do).

Treating chronic Lyme through the other world approach is very complicated, lengthy and expensive. This sort of preclinical information should be considered in lengthy, informed consent discussions with patients.  

Lyme arthritis, peptidoglycans and political correctness

Medical science and other branches of science are biased and political.  A researcher, an investigator(s) has to walk on eggshells when their findings bump up against beliefs of mainstream beliefs espoused by the experts. They have to fall in line with political correctness if they hope to see their research published, and if they want to keep their jobs as academic researchers. .  

The research findings published in the PNAS, Proceedings of the National Academy of Science this month entitled Borrelia burgdorferi peptidoglycan is a persistent antigen in patients with Lyme arthritis appears to be excellent science.

The research moves the ball forward in our understanding of chronic inflammation associated with Lyme disease. Political correctness and conformity with mainstream thinking corrupts the paper from the start seriously damaging the credibility of the authors.  Immediately the terms postinfectious Lyme arthritis and posttreatment Lyme disease are used and they poison the broth.

The preponderance of scientific evidence, overwhelming and mounting evidence supports the understanding that Lyme bacteria persist in the face of the standard antibiotic therapies discussed.

The finding that peptidoglycan (PPG), the crosslinking molecules which comprise cell walls in gram-negative and gram-positive bacteria are a major determinant of persistent Lyme arthritis is new information that moves the ball forward.

Borrelia spirochetes have a double outer membrane and lack PG cell walls. However, PG molecules are present internally, inside the outer membrane (cell envelope) providing support to the spirochetes.

The fragments of PG are call muropeptides.

We learn Bb, Lyme processes a unique PG structure. And we learn these fragments are highly immunogenic – incite an excessive immune response or cytokine response likely responsible for clinical manifestations of Lyme arthritis.

Perhaps the peptide fragments do cause an autoimmune response. Although the theory is discussed at length this is not what the research shows. Lyme related joint inflammation is directly caused by unique Lyme PGs.  


A variety of experiments, controlled experiments using a variety of bacteria with different PGs, a variety of clinical diagnoses, mice, humans, joint fluid and serum support the findings. The findings are based on a great deal of animal and human research.

Antibodies were developed against Lyme specific PGs. These antibodies could be the basis for a new, more accurate diagnostic test.

From recent research we know that Lyme biofilms and planktonic round forms cause more inflammation than spirochete forms. We know these are the most antibiotic tolerant forms or resistant forms.

The article at length discusses issues related to diminished bacterial recycling of PGs compared with gram negative bacteria.

Two theories are proffered as to how Lyme PG persists after “curative therapy” with a short course of doxycycline or Rocephin. The authors suggest that these mechanisms account for the persistence of symptoms lasting weeks or months.

But Lyme arthritis lasts for years. Biofilm forms are impervious to standard antibiotic therapies.

Somehow the authors suggest that immune suppressive therapy should be considered rather than additional antibiotics.

We have heard catchy phrases like “persistence of evidence or evidence of persistence." The issue has prevsiously be settled.

Good science can easily self-destruct with the unforced errors all for the sake of political correctness.

To bad.