Archive for the ‘Lyme’ Category

Potential Patient-Reported Toxicities With Disulfiram Treatment in Late Disseminated Lyme Disease

Potential Patient-Reported Toxicities With Disulfiram Treatment in Late Disseminated Lyme Disease

Alain Trautmann1*, Hugues Gascan2 and Raouf Ghozzi3*
  • 1Université de Paris, Institut Cochin, INSERM U1016, CNRS UMR8104, Paris, France
  • 2Institut de Génétique et Développement de Rennes (IGDR), Rennes, France
  • 3Centre Hospitalier de Lannemezan, Lannemezan, France

Recently, disulfiram has been proposed as a promising treatment for people suffering from persistent symptoms of Lyme Disease. Disulfiram has several distinct molecular targets. The most well-known is alcohol dehydrogenase, a key enzyme for detoxifying the organism after alcohol ingestion. Other targets and modes of action of disulfiram, that may present problematic side effects, are less commonly mentioned. The French Federation against Tick Borne Diseases (French acronym, FFMVT), which associates three main Lyme patient organizations, MDs and PhDs, has recently been alerted to severe and persistent toxic events in a patient suffering from a late disseminated form of Lyme Disease following disulfiram intake. FFMVT reacted by launching a national call to examine whether other patients in France following a similar treatment could be identified, and what benefits, or side effects could be reported. The statements of 16 patients taking disulfiram have been collected and are presented here. Thirteen out of 16 patients reported toxic events, and seven out of 16 reported benefits for at least part of their symptoms. Based on the collected observations, it seems too early to promote disulfiram as a promising new treatment until the reasons underlying the reported toxicities have been explored, and the results of a well-conducted double blind clinical trial published. The importance of taking into account patient-reported outcomes in Lyme Disease is underlined by the present study.


Each year, in the USA, about one person out of 1,000 develops Lyme Disease as declared by the general practitioners, which leads to a total of around 300,000 annual cases (1). Similar frequencies have been reported in Europe, in particular in France (2) and in Germany (3). The patients usually take antibiotics for a few weeks, and in most of cases they recover. However, after several months or even years, a fraction of these properly treated patients, will develop a post-treatment Lyme Disease syndrome (PTLDS) linked to pathogens injected by the tick, usually Borrelia bacteria, often associated with other bacteria like Bartonella, parasites like Babesia, or even viruses. Another group of patients develops a late disseminated form of the disease without having noticed any initial event, like the pathognomonic cutaneous erythema migrans, rendering more difficult the Lyme Disease diagnosis.

There is no consensus for the optimal treatment of these late forms of disease. The major difficulties in their diagnosis and in their treatment are reflected in the number of different names they have been given: late Lyme Disease, persistent Lyme Disease, chronic Lyme Disease, PTLDS, and in France SPPT for “sémiologie persistante polymorphe après morsure de tique” according to the new French government guidelines.

In such a context, there is a desperate need for many people to receive the optimal treatment. Recently, a new treatment has been reported, and many patients are currently trying it despite the fact that the main active compound, disulfiram (DSF), has never been clinically evaluated in the context of a chronic infection, either alone or in combination with antibiotics. In the present work, to try to answer this pressing issue, we have analyzed the scientific literature on DSF and collected patient-reported results in order to inform patients suffering from late forms of Lyme Disease of the potential risks or benefits of DSF treatment.


After an alert in October 2019 from a patient presenting severe and persistent symptoms after taking DSF, the FFMVT (French Federation against Tick Borne Diseases) decided to launch two actions. One was a thorough analysis of the scientific literature, in order to try to understand the possible causes of such an apparent toxicity. The other one was to collect reported-outcomes from Lyme Disease patients having taken DSF. Three associations of patients, France Lyme, Lympact, Relais de Lyme, sent a standardized questionnaire, prepared by the authors, to their members suffering from PTLDS as described, among others, by J. Aucott (4), or from SPPT, the term used in France by Haute Autorité de Santé (High Health Authority) ( and in a case law of the French Council of State (

Concerned patients who were willing to contribute to this enquiry sent back the appropriate information on their clinical status and disease. Information requested included age, sex, health state, dosage and duration of the DSF treatment, concomitant medications, self-reported health improvements and potential toxicities. The answers were collected over a 2-weeks period, and anonymously transferred from patient associations to the authors of the present paper, before being tabulated and analyzed, as presented in Table 1. Note that the Research Integrity Specialist of Frontiers asked us to omit the gender information, and not to indicate the precise age, to reduce the risk for the patients to be indirectly identifiable.


www.frontiersin.orgTable 1. Responses of 16 patients to DSF treatment (France, July–November 2019).

This enquiry allowed us to rapidly collect the appropriate information for evaluating whether or not reported severe adverse events in a first patient were exceptional or not. However, no definite conclusion can be drawn under such conditions, taking into account the sample size, the different doses of DSF used, and different combinations of concomitant medications used.


The first part of this section will present potential reasons why toxicity is expected in patients taking DSF, and not exclusively following alcohol ingestion. The second part will concern the analysis of 16 patient-reported outcomes collected in November 2019 in France.

DSF, an ALDH Inhibitor

DSF has been clinically used for nearly 70 years, essentially for treating alcohol dependence. DSF inhibits an enzyme that is required for full alcohol degradation, preventing the detoxification that should follow alcohol drinking. This leads to severe nausea and discomfort in DSF-treated patients when they drink alcohol. This induced association between alcohol and severe discomfort is the basis of DSF use for the treatment of alcohol-dependent patients. More than 3,000 scientific publications mention DSF in their title, and most of them are related to alcohol consumption.

After ingestion, alcohol (ethanol) is degraded in two steps:

                                         ADH                                            ALDHEthanol(CH3.CH2.OH)Acetaldehyde(CH3.CHO)Acetate(CH3.COO)

The first reaction is catalyzed by alcohol dehydrogenase (ADH), the second one by aldehyde dehydrogenase (ALDH). The final product, acetate, has no toxicity. By contrast, acetaldehyde (AcH), also known as ethanal, is much more toxic than ethanol. Ethanal is quite volatile, and at low concentration gives off a pleasant smell of green apple, whereas at higher concentrations, its smell becomes pungent. Acute AcH toxicity may involve in particular the nervous system (5). In long term exposure, AcH is also a carcinogen (6). Note that ALDH is only weakly expressed in 30–40% of Asian, individuals, preventing them from properly eliminating alcohol, which explains why many of them have a low tolerance to alcohol.

The potent DSF-induced ALDH inhibition is copper-dependent (7). In vivo, DSF is cleaved, giving rise to diethyldithiocarbamate, an efficient copper chelator (8). Through this mechanism, DSF inhibits copper-dependent enzymes, such as ALDH, abundant in the liver (9), or dopamine β-hydroxylase in the brain (10). The best described effect of DSF, but not the only one, is its toxicity in the presence of alcohol, and sometimes even in its absence, as discussed below.

There are two main places in the organism where the enzymes ADH and ALDH allow the degradation of alcohol to acetate. The first is the ALDH-rich liver, which plays a key role after alcohol drinking. The second, which is seldom mentioned but nevertheless quite important, is the microbiota of the digestive tract, with its billions of bacteria and fungi particularly abundant in the mouth and the large intestine. In some bacteria, the ADH enzymatic activity is significantly stronger than the ALDH one. As a result, in the presence of alcohol, such bacteria, including the commensal ones, trigger an increase in the concentration of toxic AcH (11). This might contribute to a higher frequency of mouth and throat cancers in alcohol-dependent patients (12).

In addition, some anaerobic bacteria and yeasts are able to convert glucose into ethanol (this “alcoholic fermentation” is the basis for the manufacturing of alcoholic beverages). Under certain culture conditions, it is possible, when supplying some of these microorganisms only with glucose, to generate alcohol and then AcH. Thus, the yeast Candida albicans is capable of producing high levels of toxic AcH, after glucose fermentation (11). It can thus be predicted that the toxicity of DSF should be particularly marked in people suffering from candidiasis.

Finally, other bacterial families, such as Lactobacillus, have an ALDH activity larger than that of ADH, which makes them good detoxifiers, by preventing the accumulation of AcH (6).

Other Modes of Action of DSF

Although the DSF toxic effects occurring in the treatment of alcohol-dependent patients have been known for a long time, additional effects have been described more recently. It has been shown in particular that, in vitro, DSF can be cytotoxic for cancer cells (13). These results prompted the launch of three clinical trials including DSF in the treatment in prostate, pancreas and glioblastoma cancers ( None of these trials, started in 2016 and 2017, has yet given rise to publication.

It was initially thought that these newly discovered effects were also due to the inhibition of ALDH, but this is not always true, and several other DSF targets have been identified. Thus, the protein NLP4, which is necessary for the cellular response to various stresses, is inhibited by DSF-copper complexes (13, 14). In addition, DSF can block an intracellular detoxifying pathway. It can inhibit the proteasome (15), a multi-protein complex required for the elimination of improperly folded proteins. DSF can also block the activation of NF-κB (15, 16), a key molecule in inflammatory stresses, known for inhibiting apoptosis.

In vitro, DSF can neutralize a DNA methyltransferase involved in DNA repair (17). It may also inhibit P-gp, a multidrug pump responsible for the extrusion of toxic molecules, which contributes to cellular resistance to many cytotoxic molecules (18). The effect of DSF on NF-kB, DNA repair, and P-gp may all contribute to the in vitroeffects of DSF against tumor cell lines. The effect of DSF on P-gp has been more particularly studied in fungi and yeasts, offering a possible explanation for the antifungal effect of DSF (19). However, some authors have attributed DSF anti-fungal properties to its capacity to elicit oxidative stress in yeasts (20). Still in vitro, DSF also displayed toxic effect against Plasmodium falciparum, the causative agent of malaria (21), and also against some bacteria (22).

As mentioned previously, DSF can act as a copper chelator, thus inhibiting copper-dependent enzymes. Some bacteria express such enzymes, rendering them sensitive to DSF. However, it is unclear whether the anti-bacterial effect of DSF is due to copper depletion or to direct effects of copper complexation inside bacteria (8, 23).

Most demonstrations of an antibacterial effect of DSF were performed in vitro (24, 25), at concentrations not always compatible with its in vivo use. For instance, one study claims that DSF is toxic to Mycobacterium tuberculosis, including the dormant form, both in vitro and in vivo (24). In fact, the experimental protocol allowed the evaluation of the effect of DSF on the global bacterial load, but showed nothing on in vivo bacterial dormancy. In this study, the efficient dose of DSF would have been equivalent to 1,100 mg of DSF / day for a human of 70 kg, well above the dose tolerated by Lyme Disease patients (see below). Thus, the conclusions of this study still remain to be validated.

In summary, DSF is a pleiotropic drug with multiple targets, without specificity for one molecule or a single pathogen. Most of the reported anti-bacterial effects of DSF have been obtained in vitro, making it difficult to extrapolate for its in vivo use, especially when used in combination with antibiotics.

A Clinical Trial With DSF for Treating Lyme Disease

In March 2019, Pr. Brian Fallon started a clinical trial using DSF and including 24 Lyme Disease patients ( The results of Professor Fallon’s study should provide important information in the near future. On the website, the Study Description indicates that DSF is active against Borrelia’s dormant form. However, evidence to support this claim is not provided. The clinical trial document refers to three previous articles (22, 26, 27). In 2016, Pothineni et al. published an in vitrohigh-throughput screening of more than 4,300 drug candidates, against Borrelia burgdorferi grown to its stationary-phase (26). DSF appeared to be a very efficient bactericidal molecule for Borrelia in vitro, but no in vivo results have been reported yet. In 2017, Dr. Long has shown that, in vitro, DSF is cytostatic for Gram-positive bacteria, such as Staphylococcus or Streptococcus, but not for Gram-negative species (22). Finally, in 2019, Dr. Liegner reported three cases of patients who had been treated with DSF after a Lyme Disease that had lasted for several years with heavy treatments (27). For instance, at one point, one patient simultaneously took amoxicillin, clarithromycin, hydroxychloroquine, metronidazole, atovaquone / proguanil, and amitriptyline. After 9 years of illness he took DSF for 3 months: the symptoms of the Lyme Disease seem to have disappeared but the patient had a temporary psychiatric hospitalization. The second patient was on DSF for 6 weeks. The symptoms of the Lyme Disease improved but the treatment was stopped following a syncope, which resulted in a concussion and required hospitalization. In summary, the Liegner study reports three cases in which DSF seems to have been effective against late Lyme Disease, but in two of them neurological problems occurred during the treatment. These three cases have attracted considerable attention and raised great hopes in the Lyme Disease patient communities. However, in a recent talk at the 2019 ILADS Symposium, Dr. Liegner presented data on 30 Lyme Disease patients that he had treated with DSF. In 18 of them, DSF provoked either peripheral neuropathies or psychiatric problems, or both.

DSF Neuronal Toxicity ?

For tens of years, it has been known that DSF can cause occasional and sometimes severe neuropathies (28). In optic neuropathies, with a partial loss of vision, recovery took about 6 months after stopping DSF (29). When DSF is used to treat alcohol dependence, the incidence of undesirable neuropathies has been estimated as 1/15,000 (30). As for the totality of the undesirable effects caused by the DSF, their frequency has been evaluated at 1 per 200–2,000 patients (9).

Are DSF associated neurological disorders (neuropathies or psychiatric problems) related to DSF anti-ALDH activity leading to AcH synthesis? It has been demonstrated that, in vitro, AcH can have an acute toxicity on neurons due to an increase of reactive oxygen species, but this observation has not been extended in vivo (5).

An AcH increased toxicity could theoretically occur even in the absence of alcohol intake, for example in patients with Candida infections, or harboring a high load of microorganisms capable of alcoholic fermentation. Alcoholic fermentation, typically performed by yeasts, should be distinguished from lactic fermentation, more common in anaerobic bacteria. A few cases have been reported of people suffering from Gut Fermentation Syndrome (31, 32). Such patients had up to 2 g/L of alcohol in their blood, without any alcohol intake. This alcohol was produced by fermentation by large colonies of the yeast Saccharomyces cerevisiae in their intestine.

Another DSF target is dopamine β-hydroxylase, a copper-dependent enzyme, responsible for converting dopamine (DA) to norepinephrine (NE) in noradrenergic neurons. This enzyme is mostly expressed in the brain, adrenal gland and liver ( By inhibiting dopamine β-hydroxylase, DSF simultaneously reduces NE and elevates DA in these tissues. A link has been established between psychosis and DSF-induced increase of DA in the mesolimbic system (10, 33). Dopamine β-hydroxylase is also expressed in some peripheral sensory neurons and it has been suggested that neurotoxic products of catecholamines metabolism in nociceptors can cause neuronal dysfunction underlying neuropathic pain (34).

Patient-Reported Outcomes

We have recently received from French associations of Lyme patients the results of an enquiry sent to their members suffering from persistent Lyme Disease. The main questions were: have you taken DSF as a treatment for your disease? Which benefits or side effects did you experience? 16 patients have answered.

The clinical features most frequently reported were major fatigue, articular pain and cognition complaints mainly involving memory, whether or not patients were seropositive for Borrelia. The results are presented in Table 1. The conclusions are: 13 out of 16 patients experienced DSF-induced toxic or side effects, mainly concerning the nervous system (neuropathies, headaches, dizziness, difficulty of concentration and expression, sleep disturbance, general pain increase, increase in general fatigue). Several patients reported a more specific increase in their osteo-articular pains, nausea or intestinal disorders.

When taking DSF, some patients simultaneously experienced both negative effects on some symptoms and improvement of others. All in all, 7 out of 16 patients perceived benefits mainly on fatigue and pain, especially after stopping DSF. Others could not differentiate whether partial improvements were due to DSF or to the antibiotics taken during the same period.

Some of DSF toxic effects observed in Lyme patients could be due in part to high initial DSF doses, similar to those used for alcohol-dependent patients. On the other hand, some of these effects could have been due to Jarisch Herxheimer reactions triggered by DSF-induced death of Borrelia. However, some patients, who had already experienced Jarisch Herxheimer reactions before, reported that some of the reactions encountered with DSF treatment were clearly of a different nature. Collectively, these observations suggest that patients with persistent Lyme Disease are more sensitive to the toxicity of DSF than people who have been treated for alcohol dependence, and that in these patients, DSF-induced toxicities are not all related to Jarish Herxeimer reactions.


Published scientific articles allow us to draw the conclusion that, in vitro, DSF can undoubtedly kill certain bacteria strains, and that in vivo, DSF can be toxic to both bacteria and the human body. These toxicities can be both acute and long-term.

One can propose different hypotheses to explain these toxicities. They might be mediated by the inhibition of copper-dependent enzymes, such as ALDH or dopamine β-hydroxylase, or the blocking of the NLP4 molecule, or through an oxidative molecule increase, and possibly through yet unidentified mechanisms. Part of these toxicities may also depend on the microbiota, in which some bacterial or yeasts species have a propensity to produce fermentation-derived toxic AcH. It would be worth testing if any intake of bacteria such as Lactobacillus, which have a high ALDH activity, could be used to counter the DSF-induced toxicities.

On the other hand, many studies have reported that patients with PTLDS have an increased sensitivity to pain, which can affect vision, hearing, touch, and even smell, as reviewed by Batheja et al. (35). These chronic pains can be related multiple to chemical sensitivity and chronic fatigue syndrome, in which the pain sensitivity is modified as well, as reported in Gulf war veterans (36). There is increasing evidence for abnormal sensory processing in these syndromes, with a low “unpleasantness threshold” for multiple types of sensory stimuli (37).

The differences observed for effective concentrations of DSF between alcohol-dependent patients and those suffering from PTDLS or SPPT could also be linked to a such central sensitization often observed in patients suffering from borreliosis (35).

It is necessary to understand why DSF toxicity appears particularly severe and frequent in patients with Lyme Disease, and to rapidly explore the reasons for such DSF toxicity in Lyme Disease animal models. Until we have the first answers to this question, it would be premature to consider DSF as the new miracle molecule for patients suffering from late disseminated Lyme Disease.

Basic Science vs. Social Networks

Case reports are a very useful approach for drawing attention to the possible effectiveness of a new treatment. Undoubtedly, the case report published by Liegner (27) has played such a role. However, the next logical step should have been to examine the potential toxicity of DSF for Lyme patients. This could have been achieved first by using animal models, and then within a standardized clinical trial. These steps were rapidly short-circuited, due to the strong social demand for Lyme Disease treatments. This pressure is exerted largely by social networks, emphasizing their speed and efficiency, but at the same time a lack of analysis and scientific rigor.

Importance of Patient-Reported Outcomes

Following the rapid spread of the idea that DSF could be a major improvement for the treatment of late Lyme Disease, hundreds of patients began using DSF in the hope of treating their disease. At this point, it is important to require, as we do here, on rapid feedback from the patients themselves. No one knows better than patients the severity and importance of secondary toxicities from treatment. They know themselves better than physicians, who sometimes tend to overestimate the benefit/risk ratios (38, 39).

The limitation of the present study is linked to the small number of included patients. This highlights the need for follow-up studies with a larger number of patients to specify the risk/benefit of DSF in late Lyme Disease. The results and experiences reported by the patients should be included in these studies to determine how many of them have truly benefited from DSF treatment. Aiming at distinguishing Jarish Herxheimer reactions due to bacterial die-off and toxic side effects of the drug will be an important issue. More generally, a patient survey will have to be designed to evaluate how many patients have benefited of DSF and how many have not. A long term follow up of the DSF treated patients using an online patient feedback tool will be necessary to determine if they have any relapse or stable remission. All this information is necessary to determine the risk/benefit ratio of DSF for Lyme Disease. This will require a close collaboration between patients, doctors and researchers.

Data Availability Statement

All datasets generated for this study are included in the article/supplementary material.

Ethics Statement

An ethical review process was not required according to national legislation and institutional requirements for the present study. Patient treatment was decided by their physician independently of the study. Patients associations were asked by the authors to collect patient-reported outcomes, which have been transferred anonymously to the authors. All patients that participated to this enquiry were volunteers and have given a written agreement to participate in this study.

21 patients had initially sent a patient-reported outcome. Following your recommendation, they were all asked to give their agreement to participate to this study. No one refused, but five of them did not answer. Therefore, the revised manuscript only presents the 16 cases of patients who sent their written consent.

Author’s Note

AT and HG are members of the scientific council of Fédération Française contre les Maladies Vectorielles à Tiques (FFMVT), and RG is president of FFMVT.

Author Contributions

AT: analysis of the literature. HG, RG, and AT: synthesis and analysis of the patient-reported outcomes. RG: medical advice. AT and HG: writing the manuscript.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


We thank Nathalie Torres, Anne Colin, and Pierre Hecker, and the three associations of patients (France Lyme, Lympact, and Relais de Lyme) federated in FFMVT for their invaluable contribution in the collection of patient-reported outcomes. We thank the members of the scientific council of FFMVT for discussion on DSF treatment in late Lyme Disease, and Philippe Ascher, and Boris Barbour for improving the English of the manuscript.


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Citation: Trautmann A, Gascan H and Ghozzi R (2020) Potential Patient-Reported Toxicities With Disulfiram Treatment in Late Disseminated Lyme Disease. Front. Med. 7:133. doi: 10.3389/fmed.2020.00133

Received: 10 December 2019; Accepted: 27 March 2020;
Published: 20 April 2020.

Edited by:

Ying Zhang, Johns Hopkins University, United States

Reviewed by:

Monica E. Embers, Tulane University, United States
John Lambert, University College Dublin, Ireland

Copyright © 2020 Trautmann, Gascan and Ghozzi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Alain Trautmann,; Raouf Ghozzi,


For more:

FREE: The Lyme Times for Lyme Awareness For the Month of May

FREE: The Lyme Times For Lyme Awareness Month in May

In honor of Lyme Disease Awareness Month, the COVID-19 Issue is open access – freely available to all. The hope is you will enjoy and share these issues with your family and friends. Without you, Lyme Disease Organization would not be where they are today, and they’re so thankful for all of your support.  (Click on link for access)


Lyme Carditis Symptoms May Go Undiagnosed in Mexico


man having heart problem from Lyme carditis symptoms

Lyme carditis symptoms can be a serious complication of Lyme disease. While the condition is well-recognized in the United States, officials in Mexico are reluctant to acknowledge Lyme disease in their country. In a letter entitled “Advanced AV-block: Is it time to consider Lyme carditis as a differential diagnosis in Mexico?” physicians describe the challenges of proving that a patient has Lyme carditis. [1]

The authors highlight the case of a 23-year-old woman who presented to their hospital “with a chief complaint of dyspnea and chest pain and was found to have a third degree AV-block on the electrocardiogram (ECG).”
A temporary pacemaker was implanted. And after an exhaustive work-up for other causes, the woman was eventually tested for Lyme disease. While Lyme carditis symptoms can be difficult to recognized, test results were positive by the Centers for Disease Control and Prevention (CDC) two-tier Western blot criteria.
Unfortunately, despite a three-week course of intravenous ceftriaxone, the woman required a permanent pacemaker. “At 3-month follow-up, she was still dependent on pacing,” writes Carrizales-Sepulveda and colleagues.
They argue that the woman lived in an endemic region and had visited the hospital with complaints consistent with Lyme carditis symptoms four weeks earlier. The authors cite the CDC, pointing out that “a region can be considered as endemic for [Lyme disease] if: at least two confirmed cases have been previously acquired or in which established populations of a known tick vector are infected with B. burgdorferi.”

Officials reluctant to acknowledge Lyme disease exists in Mexico. CLICK TO TWEET

However, the medical community in Mexico has been reluctant to acknowledge Lyme disease as a possible cause of the woman’s heart block. Officials argue “there is no convincing evidence that Borrelia burgdorferi is present in Mexico.”READ MORE: Which treatment guidelines should you follow for Lyme carditis?

Despite such resistance, Carrizales-Sepulveda and colleagues report “a seroprevalence of 6.2% for the Northeast region of Mexico and 3.4% for Mexico City, using a two-tier approach with enzyme-linked immunosorbent assay (ELISA) and western blot (WB) as recommended.”

Unfortunately, these results were dismissed as false positives, the authors write.

Furthermore, their Lyme carditis diagnosis was questioned with officials suggesting “the advanced AV-block that our patient presented had another cause that was not thoroughly investigated,” Carrizales-Sepulveda explains.

The authors recommend that Lyme carditis be considered as a possible diagnosis for patients living in Mexico.

“We agree that in our country other causes should be ruled-out first, however, there is no reason to leave out [Lyme carditis] as a diagnosis,” they write.

“[Lyme disease] in our country might be under looked, underdiagnosed, and underreported.”

  1. Carrizales-Sepulveda EF, Jimenez-Castillo RA, Vera-Pineda R. Advanced AV-block: Is it time to consider Lyme carditis as a differential diagnosis in Mexico? J Electrocardiol. 2020.



We are indebted to Dr. Lapenta, a South American doctor, who has written on Lyme in the Southern Hemisphere and numerous other issues with tick-borne illness.

Thankfully, there is doctor training going on for tick-borne illness going on in South America.

It’s up to us to tell others that Lyme disease is everywhere. 

For more:

Chronic Lyme Disease – Does It Exist?

Chronic Lyme disease – does it exist?

Lyme disease patients hold a rally outside the Irish Parliament. Artur Widak/NurPhoto via Getty Images

Her symptoms started quickly: neck pain, extreme fatigue and intermittent fever and chills. The woman had been healthy until then, and since she enjoyed gardening and landscaping at her rural Maryland home, she wondered if a tick bite might have given her Lyme disease although she had not noticed the telltale bull’s-eye skin lesion.

Her doctor told her it was likely just a virus. The next day, she felt worse and went to the emergency room, where she was diagnosed with mononucleosis.

The woman, a nurse in her 40s, returned to the emergency room a few weeks later with breathing trouble and low blood pressure. Doctors tested her for Lyme disease and found it had spread to her heart, a rare manifestation of Lyme disease that can be fatal.

Antibiotics resolved her heart and respiratory symptoms, but the fatigue, as well as joint pain and trouble concentrating, continued. Doctors told her it was just the recovery process, but the symptoms were debilitating and didn’t go away. It wasn’t until several months later, when she got a second opinion, that she was diagnosed with post-treatment Lyme disease, a known complication of Lyme disease.

“I felt dismissed and abandoned,” she later told me. “No one stopped to listen to my story and advocate for me.”

Her experience gives insight into a highly controversial medical term: chronic Lyme disease.

Because there are no definitive tests or treatments for this condition, patients who have symptoms can be dismissed by the medical establishment. Many are denied medications such as antibiotics they believe can control the chronic infections they suspect they have.

I am the former chair of the tick-borne diseases working groupat the U.S. Department of Health and Human Services and a medical researcher who has studied chronic Lyme disease for 20 years. It has become obvious to me that the problem is deeper and more complex than the polarized debate over the controversy would make one believe.

My colleagues and I have closely followed the health of Lyme disease patients as they recover, and what we have discovered runs counter to the mainstream teaching about Lyme disease. Doctors still often don’t know how to accurately diagnose patients with Lyme disease, and patients don’t always get better, even when they are diagnosed and treated. Physicians lack the diagnostic tools for early diagnosis or for documenting cure of the disease.

Studying this subgroup of post-treatment Lyme disease patients who are treated for Lyme disease but don’t get better is a clue on my way to find to understand chronic Lyme disease. While it may not provide definitive answers yet, we hope it will add to the body of knowledge about this perplexing set of conditions that are likely diverse in origin.

Don’t joke they should just “suck it up,” because I can pretty reliably guarantee you they already are. 

Yes, I Can Function With Chronic Illness. No, You Can’t Judge My Pain Off That.

A woman with chronic illness and pain describes the decades of struggle and fighting it took for her to be functional, and why we can’t judge someone’s pain off their ability to function or not.

The chronic Lyme controversy

Lyme disease, first identified in the United States in the 1970s, has grown into a health epidemic as the ticks that transmit it to humans expand their range. The Centers for Disease Control and Prevention now estimates that about 300,000 people in the U.S. become newly infected every year now. The symptoms can be debilitating, including neurological symptoms, extreme fatigue and muscle and joint pain.

When symptoms linger long after a diagnosed patient receives the standard antibiotic treatment, like the nurse in Maryland experienced, the patient may have a condition called post-treatment Lyme disease syndrome, a subset of chronic Lyme disease. Many experts in the field estimate about 10% to 20% of patients diagnosed with Lyme disease get this syndrome.

The controversy around chronic Lyme disease emerged when patient advocacy groups and some doctors began to use the term to describe patients who had nonspecific symptoms such as fatigue and pain, and testing did not always show that they had been exposed to Lyme disease.

At the heart of the controversy is the question: Can a person have a chronic bacterial infection that may not show up on tests?

These patients are frustrated with a medical establishment whose focus is on evidence-based treatment in a field where evidence is often lacking. Without a diagnosis by the establishment, these sick patients are often dismissed and can’t get treated, leading to a sometimes toxic environment as they fight for treatment.

Symptoms without evidence

My training in infectious diseases didn’t prepare me for the patients I started seeing after moving to a Lyme-endemic region in 1996. Patients that I had treated for well-documented Lyme disease were experiencing chronic joint pain, neurological symptoms and extreme fatigue, yet most lacked “objective measurable manifestations” of Lyme disease, like abnormalities in blood tests or radiologic imaging evidence of tissue damage.

Can Lyme disease be a chronic infection? Artur Widak/NurPhoto via Getty Images

It was, and still is, uncomfortable telling patients that we don’t know exactly what is going on or how to best treat their illness. My chronic Lyme patients were sicker and had less hope than the AIDS patients I worked with, but the underlying mechanism of illness remained elusive.

Part of the challenge is the lack of definitive tests for chronic Lyme disease. After treatment with antibiotics, the bacteria that causes Lyme disease – Borrelia burgdorferi – is rarely detected, yet symptoms often continue.

There are several theories about why symptoms might continue for months if not years. Some of the bacteria might be able to evade the immune system, bacterial residue might remain that trigger ongoing inflammation or a severe initial infection, delayed treatment or coinfections from the tick bite, such as babesiosis, might lead to an uncontrolled and ongoing overreaction by the patient’s immune system.

Without laboratory findings, however, most doctors are uncomfortable with diagnosis and treatment of chronic Lyme disease.

This may be because Lyme disease symptoms can be mistaken for those of other illnesses, such as chronic fatigue, fibromyalgia and depression. Doctors also recognize the public health risks of antibiotic overuse and the potential risk to patients from long-term antibiotic treatments.

A group of doctors has championed the care of patients with chronic Lyme disease and developed guidelines for their care. Some of their practices have been criticized, especially long-term intravenous antibiotics which have the potential for serious side effects. Yet it is not uncommon for patient anecdotes and experience to report that long-term antibiotic therapy and other complementary care interventions have helped despite the lack of FDA approval or randomized trials to support their use.

Diagnosing the syndrome

Our research has shown that post-treatment Lyme disease syndrome can be meticulously identified in patients with previously treated Lyme disease by a constellation of quality-of-life symptoms, including fatigue, sleep disturbance, musculoskeletal pain and cognitive problems, and by the severity of those symptoms.

However, the holy grail for diagnosing post-treatment Lyme disease syndrome – and sorting out chronic Lyme – would be a blood biomarker to identify the biology of the disease in patients. Molecular markers are rapidly being discovered that provide insights into the mechanisms of disease that show the potential interplay of both microbial and host inflammatory responses that may cause ongoing symptoms in previouslytreated Lyme disease patients.

Once molecular markers are established, this will set the stage for new treatment trials.

The true extent of this insidious epidemic is still unknown, but it is clear, based on my experience and work, that it no longer accurate to simply argue that chronic Lyme disease doesn’t exist.



One of the fairest pieces I’ve read in a long time.

My only correction:

  • Researchers keep saying it’s only 10-20% that go on to have persistent symptoms. This percentage is based upon those who are diagnosed and treated early. There’s a much larger group (nearly everyone I work with) that is diagnosed and treated late.  According to Microbiologist Holly Ahern, this larger group constitutes 40-60% of patients. For an accurate percentage, you need to add both groups together to get a full picture of who remains with symptoms.  According to Ahern, up to 60% of ALL patients go onto have persistent, sometimes life-long symptoms:

The reason this distinction needs to be made is 1) patients will be taken more seriously when authorities know many people are affected by this. 2) it is much more likely research monies will be directed toward an issue involving more people 3) it’s important to be accurate in science.

I would like to highlight a few thoughts in the article that hit a cord with me:

My colleagues and I have closely followed the health of Lyme disease patients as they recover, and what we have discovered runs counter to the mainstream teaching about Lyme disease.

My chronic Lyme patients were sicker and had less hope than the AIDS patients I worked with.

The true extent of this insidious epidemic is still unknown, but it is clear, based on my experience and work, that it no longer accurate to simply argue that chronic Lyme disease doesn’t exist.

For more:

Peer-Reviewed Evidence of Persistence of Lyme:MSIDS copy




Morgellons NOT Associated With Fungus

  Approx. 1 Hour 15 Min.

Morgellons NOT Associated With Fungus

May 17, 2020

Interview with microbiologist Marianne Middleveen.

For more:

What a Difference a Year Makes

by Jennifer Crystal

When I was little, my grandmother used to sing the Dinah Washington song, “What a difference a day makes, twenty-four little hours…” Later, memories of her singing those lyrics carried me through some of my toughest days of tick-borne illness. They remind me even today that I just need to get through the next hour, the next minute, because things could be better tomorrow.

Sometimes they were better. A Herxheimer reaction might settle, a solid night’s sleep might lower my emotional temperature, or my actual fever might go down. And sometimes, the tomorrows weren’t much better. When I first started intravenous antibiotics, I felt horrible for six weeks before noticing any improvement. Often the next day was worse than the last. I learned that while I could coach myself to survive each minute or second, I had to wait longer to really live again and even longer to thrive, which was my desire. For that type of progress, it was better to chart my improvement over months, if not years. Check here for an overview of some of my long-term recovery strategies.

Birthdays are always a nice time to reflect on the year passed, and this has been especially true since I’ve been sick with chronic Lyme, two tick-borne co-infections—babesia, ehrlichia—and Epstein-Barr virus. A lot can happen in a year, both good and bad. We never know what joys or sorrows await us. Lyme patients don’t know how they’ll respond to treatment or how long it will take them to feel better. For many, though, they can see real progress—with dips and valleys—over a year or more.

I was thinking back to my 29th birthday recently, when I was in the midst of a relapse. Sick and exhausted, I wondered if I could endure further treatment. I struggled with my self-esteem. Frankly, there didn’t seem to be much to celebrate.

But flash forward a year to my 30th birthday party. I worea pretty pink dress. I was surrounded by friends and family. I was smiling, my cheeks glowing, with much to celebrate: a return to remission, to independent living and the resumption of freelance work. However, improvement over that year was by no means linear. I had many bad days, sometimes weeks. But when I considered the headway I made between my 29th and 30th birthdays, all I could think was, “What a difference a year makes.”

When I blew out the candles that year, I wished for continued health, for my life to keep blossoming—and it did. A couple years later, I moved to Boston and started graduate school. In the decade since, I’ve written two books and forged a teaching career. I have gotten back on my skis. I have also wrestled brief flare-ups of my illnesses, grieved the death of loved ones and mourned the loss of love. Those have been my low points, but when I see how many gains I’ve made over the last decade—and how much my stamina has improved—I want to pinch myself. I can hardly believe it.

As I blew out my candles last year, I never could have imagined the world would be in the midst of a global pandemic by my next birthday. But I also couldn’t have imagined all of the good things that have happened to me this year, including landing a literary agent, surviving COVID-19 despite my underlying health conditions. And thus, I hold onto hope—for me, for you, for the Lyme community, for our world.

When I blow out my birthday candles this week I’ll wish for a healthier year for all of us. I hope that by this time next year, I’ll be able to celebrate that wish coming true.

jennifer crystal_2

Opinions expressed by contributors are their own.

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



Well, that made my day!  I love to see patients improve. If you are having a rough day, month, or year – hang tight.  It will get better in time.  

More Ticks, Risk of Lyme Disease in Wisconsin (News Video Here)

More ticks, risk of Lyme disease in Wisconsin

WAUSAU, Wis. (WAOW) — A mild winter combined with a larger population of deer in Wisconsin this year could mean more ticks to look out for.

Experts at the Tick-Borne Illness Center of Excellence in Woodruff treat people from across the country, but they say Northern Wisconsin stands out.

“It is a highly prevalent area for wood tick diseases and deer tick diseases,” said center manager Kathy McCaughan.

This year, experts say they’re seeing the impact of a mild winter.

“The ticks really don’t go away in the winter they just go underneath the leaves and the snow kind of insulates them and the first tick that we had reported here was the beginning of March already,” said Clinic Program Director Connie Campbell.

Combine that with a higher deer population and more people outside, there could be a higher risk of spreading lyme disease.

“Now with COVID, everyone is out and about a little bit trying to get fresh air, just kinda be vigilant,” said Campbell. “You wear light-colored clothing so that you can spot them really easily, deet helps but you don’t spray it on your skin you spray it on your clothes.”

The Centers for Disease Control and Prevention also says to tuck your pants into your socks when you’re going out and perform a tick check when you get back home.

You can learn more about Lyme disease on the State’s Health Department Website.

You can also download an app from UW-Madison to track ticks and learn about removal/prevention.



We really have no idea why there are more ticks. Blaming the weather isn’t prudent considering ticks are ecoadaptive and survive about anything but fire. Research shows it’s migrating birds and photoperiod (light required for ticks to molt) that propagates ticks and the diseases they carry: (research conducted by an independent researcher)

But this doesn’t fit the climate change narrative that keeps being pushed upon us. Right now, climate change is a popular topic so if researchers want grant money they put that moniker in their work so they obtain money.  Even if it’s untrue.

Please see:

This is just another example of how finances dictate the science being done.  Sad but true.

“For blacklegged ticks, climate change is an apocryphal issue.” -John Scott