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.