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.