Archive for the ‘Lyme’ Category

Antibiotic Resistance: Researchers Have Directly Proven That Bacteria Can Change Shape Inside Humans To Avoid Antibiotics

https://theconversation.com/antibiotic-resistance-researchers-have-directly-proven-that-bacteria-can-change-shape-inside-humans-to-avoid-antibiotics-124296

Antibiotic resistance: researchers have directly proven that bacteria can change shape inside humans to avoid antibiotics

Newcastle University Research Fellow, Newcastle University

Disclosure statement

Katarzyna Mickiewicz receives funding from European Research Council. This work was funded by a European Research Council (grant number 670980) to J.E. The contribution of L.D., R.P., J.H. and P.D.A. to this work was supported by the NIHR Newcastle Biomedical Research Centre awarded to the Newcastle upon Tyne Hospitals NHS Foundation Trust and Newcastle University. We thank Agata Starosta and Andreas Weiser for providing pMCL200 yfp plasmid. Zebrafish work was carried out with Prof. Serge Mostowy (London School of Hygielne and Tropical Medicine)
Researchers have evidence of another method that bacteria use to avoid antibiotics. Sirirat/Shutterstock

Widespread antibiotic use is largely to blame for the emergence of antibiotic resistant bacteria, which is currently one of the biggest threats to global health. Not only does antibiotic resistance already cause an estimated 700,000 deaths a year, it’s also made numerous infections, including pneumonia, tuberculosis, and gonorrhoea, harder to treat. Without knowing how to stop bacteria from developing antibiotic resistance, it’s predicted that preventable diseases could cause 10m deaths a year by 2050.

Some of the ways that bacteria become resistant to antibiotics is through changes in the bacteria’s genome. For example, bacteria can pump the antibiotics out, or they can break the antibiotics down. They can also stop growing and divide, which makes them difficult to spot for the immune system.

However, our research has focused on another little known method that bacteria use to become antibiotic resistant. We have directly shown that bacteria can “change shape” in the human body to avoid being targeted by antibiotics – a process that requires no genetic changes for the bacteria to continue growing.

Virtually all bacteria are surrounded by a structure called the cell wall. The wall is like a thick jacket which protects against environmental stresses and prevents the cell from bursting. It gives bacteria a regular shape (for example, a rod or a sphere), and helps them divide efficiently.

Human cells don’t possess a cell wall (or “jacket”). Because of this, it’s easy for the human immune system to recognise bacteria as an enemy because its cell wall is noticeably different. And, because the cell wall exists in bacteria but not in humans, it’s an excellent target for some of our best and most commonly used antibiotics, such as penicillin. In other words, antibiotics targeting the wall can kill bacteria without harming us.

However, bacteria can occasionally survive without their cell wall. If the surrounding conditions are able to protect the bacteria from bursting, they can turn into so-called “L-forms”, which are bacteria that don’t have a cell wall. These bacteria were discovered in 1935 by Emmy Klieneberger-Nobel, who named them after the Lister Institute where she was working at the time.

In a lab, we often use sugar to create a suitably protective environment. In the human body, this change in form is typically triggered by antibiotics that target the bacteria’s cell wall, or certain immune molecules – such as lysozyme, a molecule that’s present in our tears which helps protect us from bacterial infections.

Bacteria without a cell wall often become fragile and lose their regular shape. However, they also become partially invisible to our immune system, and completely resistant to all types of antibiotics that specifically target the cell wall.

Scientists long suspected that L-form switching might contribute to recurrent infections by helping bacteria hide from the immune system and resist the antibiotics. However, it was difficult to find evidence for this theory due to the elusive nature of L-forms and lack of appropriate methods to detect them.

Watching bacteria change shape

Our study, published in Nature Communications, looked specifically at bacterial species associated with recurrent urinary tracts infections (UTIs). It found that many different bacterial species – including E. coli and Enterococcus – can indeed survive as L-forms in the human body. This is something that has never been directly proven before. We were able to detect these sneaky bacteria using fluorescent probes that recognise bacterial DNA.

We tested urine samples from elderly patients with recurrent UTIs by growing them in a petri dish high in sugars. Not only did this environment help protect bacteria from bursting, it also isolated the L-form bacteria that were present in these samples. In a separate experiment, we were able to see the whole process take place in living zebrafish embryos in the presence of antibiotics.

After the antibiotic was removed, the bacteria transformed back from L-forms to their regular form with cell walls. (Credit to Newcastle University, UK)

Importantly, our study shows that antibiotics need to be tested in conditions more reflective of the human body. The ones that are currently used in the medical laboratory don’t provide enough protection for delicate L-forms to survive.

Before we can fully understand how important L-form switching is compared to other forms of antibiotic resistance, further research using more patients will be needed. It will also be important to investigate what role L-forms may play in other recurrent infections, such as sepsis or pulmonary infections.

Until now, research into L-forms has been a controversial field, but our hope is that these findings will motivate more research into L-forms in disease situations. Our hope is that these findings will help find a way to clear these sneaky bacteria from our body. Combining cell wall active antibiotics with ones that would kill L-forms might be one solution of fighting antibiotic resistant infections.

Our battle with bacteria is ongoing. As we come up with new strategies to fight them, they come up with ways to fight back. Our study highlights yet another way that bacteria adapt that we’ll need to take into account in our continuing battle with infectious disease.

_________________

**Comment**

Dr. Lida Mattman wrote an important book on cell wall deficient forms which are thought to play a role in the resistance of the Lyme disease bacterium to antibiotics:  https://madisonarealymesupportgroup.com/2019/05/24/microbiology-professor-im-convinced-lyme-disease-is-transmittable-from-person-to-person/

Mattman and her colleague, Dr. Joanne Whitaker, a victim of Lyme disease since childhood, developed a direct test for Bb and were the first to identify the cell wall deficient form of the spirochete.  Interestingly, the CDC has made 2-tier blood serology testing for Lyme a literal mandate, purposely avoiding direct detection:  https://madisonarealymesupportgroup.com/2018/04/03/cdc-deliberately-avoids-direct-detection-testing-methods-for-ld/

Mattman, an expert on spirochetes and the cell wall deficient form, isolated living Borrelia spirochetes in mosquitoes, fleas, mites, semen, urine, blood, plasma and Cerebral Spinal Fluid. She discovered that this bacteria is dangerous because it can survive and spread without cell wall (L shape). Because L-forms do not possess cell wall, they are resistant to antibiotics that act upon the cell wall.  https://madisonarealymesupportgroup.com/2019/04/02/transmission-of-lyme-disease-lida-mattman-phd/

Dr. Horowitz is having success with two mycobacterium drugs: https://madisonarealymesupportgroup.com/2016/10/09/mycobacterium-drugs-for-ld/

And of course the latest find is disulfiram/Antabuse: https://madisonarealymesupportgroup.com/2019/06/03/disulfiram-in-the-treatment-of-lyme-babesiosis-3-case-reports/

https://madisonarealymesupportgroup.com/2019/07/14/disulfiram-breakthrough-drug-for-lyme-other-tick-borne-diseases/

Just beware that disulfiram toxicity has caused some patients to have psychosis: https://madisonarealymesupportgroup.com/2019/10/15/disulfiram-psychosis-update/

Regarding antibiotic resistance, I would make a case that using antibiotics in agriculture is really the problem: https://www.nhs.uk/news/medication/antibiotic-use-in-farm-animals-threatens-human-health/

What does the report say?

The report made a range of observations:

  • The evidence suggests the amount of antimicrobials used in food production internationally is at least the same as that in humans, and in some places is higher. For example, in the US more than 70% of antibiotics that are medically important for humans are used in animals.

  • This form of antimicrobial usage is likely to rise because of the economic growth, increasing wealth and food consumption in the emerging world.

  • When properly used, antibiotics are essential for treating infections in animals, but excessive and inappropriate use of the drugs is a problem.

  • A considerable amount of antibiotics are used in healthy animals to prevent infection or speed up their growth. This is particularly the case in intensive farming, where animals are kept in confined conditions.

  • Some suggest that stopping the use of antibiotics for growth promotion would be significant, particularly in lower-income settings, and would be unjustified without clearer evidence of the extent of the threat to human health.

  • In a literature review of published peer-reviewed research articles carried out as part of the report, only 5% of the 139 academic papers identified argued there was not a link between antibiotic consumption in animals and resistance in humans, while 72% found evidence of a link. The report’s authors suggest this supports a link and provides enough justification for policy makers to aim to reduce the global use of antibiotics in food production to a more appropriate level.

  • Some last-resort antibiotics for humans are being used extensively in animals, and there are no replacements currently on the way. This was illustrated by a recent study from China, which identified a gene responsible for colistin resistance in bacteria from livestock, also covered by Behind the Headlines.

  • There is concern over the potential for pollution from antimicrobial manufacture – for example, if untreated waste products containing high levels of end-products or active ingredients are discharged into water courses.

 

Category:

Lyme, Treatment

Seroprevalence of Lyme in Northwest Spain – It’s High

https://www.ncbi.nlm.nih.gov/pubmed/31488336

Seroprevalence of Lyme disease in southwest Asturias.

[Article in English, Spanish]
Barreiro-Hurlé L1, Melón-García S2, Seco-Bernal C3, Muñoz-Turrillas C3, Rodríguez-Pérez M2.

Abstract

INTRODUCTION:

To correctly interpret the serological markers of Lyme disease, it is very important to determine the region’s infection rate. The aim of this study was to ascertain the prevalence of specific antibodies against Borrelia burgdorferi in a rural district in northern Spain.

METHODS:

The presence of IgG antibodies against B. burgdorferi was determined by qualitative enzyme immunoassay in the serum of 1,432 people divided into 3groups: 316 blood donors, 432 individuals who attended the hospital without infection and 684 for whom Lyme serology testing was specifically requested as part of a differential diagnosis. In the latter group, the presence or absence of an occupational risk factor was recorded.

RESULTS:

Antibodies against B. burgdorferi were detected in 189 individuals (13.2%): 16 (5.1%) in the blood donors group, 62 (14.4%) in subjects who attended hospital without infection and 111 (16.2%) in subjects in whom a differential diagnosis of Lyme disease was requested (p < 0.0001). In subjects with an occupational risk factor, the prevalence was 23.5%, peaking at 45.8% in men over 65 years.

CONCLUSION:

Our study showed a high prevalence of antibodies against B. burgdorferi and higher than that seen in other areas with similar characteristics in Spain. However, our results are similar to those published from other European regions. The prevalence in the blood donors group was lower than that observed in the other groups. Older age, the male gender and occupational risks were associated with a higher prevalence of Lyme disease.

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**Comment**

Please remember that tests which look for antibodies are insensitive – missing many who actually are infected.  I was told by the most experienced practitioner in Wisconsin that some of the sickest patients NEVER test positive.

The organism doesn’t hang out in the blood but sequesters in tissues.

More on testing: https://madisonarealymesupportgroup.com/2018/09/12/lyme-testing-problems-solutions/

According to Dr. Sin Lee faulty serology tests for Lyme disease missed 85.7% of the walk-in patients in the Emergency Room of Milford Hospital:

https://madisonarealymesupportgroup.com/2018/01/16/2-tier-lyme-testing-missed-85-7-of-patients-milford-hospital/

 

 

 

 

Category:

Lyme, research, Testing

Study Links Eating Disorders to Childhood Infections (Lyme/MSIDS Can Do This)

https://giving.massgeneral.org/eating-disorders/

Study Links Eating Disorders to Childhood Infections

New data from a Mass General researcher highlights a link between the immune system and the onset of eating disorders.

Published by

The question of what causes eating disorders has puzzled the medical community since “wasting disease” was first described in the 17th century. Today, researchers and clinicians agree that, in addition to psychosocial and environmental risk factors, there is a strong biological basis to these disorders. Now, new data from a Massachusetts General Hospital researcher suggests that exposure to common childhood infections, such as strep throat or bronchitis, may significantly raise a person’s risk of developing anorexia nervosa, bulimia nervosa and other eating disorders.

“Infections, by and large, have typical behaviors associated with them, and among those most commonly reported is loss of appetite.”

Results of the population-based study, published in JAMA Psychiatry, found that infections that required hospitalization or treatment with anti-infective medications, such as antibiotics, antifungals or antivirals, increased the risk of developing an eating disorder by as much as 39%. The multi-institutional study, which analyzed the health histories of more than 500,000 adolescent girls in Denmark, also found that recurrent infections and repeated treatment increased the risk.

Infections and Behavior

“Infections and inflammation more broadly have been recognized to play a role in psychiatric diseases like schizophrenia, but this has been less explored in eating disorders,” says Lauren Breithaupt, PhD, a clinical psychologist in the Mass General Eating Disorder Clinical and Research Program, and lead author of the study. “We’re hoping that a better understanding of the relationship between the immune system and disordered eating will help identify a mechanism behind the increased risk and biochemical changes we see happening.”

Lauren Breithaupt, PhD
Lauren Breithaupt, PhD

As an observational study, the findings don’t point to a single cause or effect, but one possible explanation, according to Dr. Breithaupt, is that the infection or treatment of the infection disrupts the gut microbiome, which in turn alters the brain’s neurobiological reward system. Another possibility is the body’s own inflammatory response. Inflammatory proteins have been shown to cause changes in behavior, such as loss of appetite.

“Infections, by and large, have typical behaviors associated with them, and among those most commonly reported is loss of appetite,” Dr. Breithaupt says. “If you’re already at risk for an eating disorder, this period of no appetite could have a priming effect.” Although more research is needed, Dr. Breithaupt is encouraged the findings further enforce the biological nature of the disease.

Eating Disorder Stereotype

“Eating disorders have long been seen as social constructs — think of the stereotype of the wealthy white girl who isn’t eating because she wants to look a certain way,” says Dr. Breithaupt. “It’s taken a lot of evidence — more than most other mental illnesses — to blow that stereotype out of the water. We now know that the rates are similar across the world and across cultures. We’re even seeing that there may not be as big a gender discrepancy as we previously thought.”

Despite mounting biological evidence, there is still a great deal of confusion in the medical community about how to diagnose and treat eating disorders. Dr. Breithaupt is hopeful that the team’s findings can lead to increased awareness of the signs and symptoms and that more hospitals and treatment centers adopt a more scientific approach to treating these diseases.

The Role of Philanthropy

“The Eating Disorders Clinical and Research Program at Mass General offers gold standard evidence-based treatment for eating disorders, but we receive so many referrals per year that unfortunately we can’t treat every patient who seeks services,” she says. “That’s why philanthropy is so important to the growth of our program. The work that we do is often funded by individuals and families who have been touched by these diseases.”

The other key to advancing the understanding and treatment of eating disorders, Dr. Breithaupt says, is education.

“In order to identify biological markers, we need larger sample sizes and data sets, which requires individuals with the disorder to come forward and to participate in research,” she says. “By educating the public about the biology underlying eating disorders, we can break down barriers and overcome the stigma.”

To learn more about how you can support eating disorder programs and research at Mass General, please contact us.

________________

**Comment**

Great read and a fantastic reminder that eating disorders often have a biological basis.

If a wild animal is sick with an infection it stops eating. This begins to make sense when we understand that nearly 5-15% of our body’s energy goes into digestion:  http://discovermagazine.com/2009/dec/20-things-you-didnt-know-about-digestion

According to Dr. Bransfield eating disorders are common with Lyme/MSIDS:  https://madisonarealymesupportgroup.com/2015/10/18/psychiatric-lymemsids/

In addition, Lyme can trigger a condition known as pediatric acute-onset neuropsychiatric syndrome (PANS) which in turn can also cause eating disorders. http://www.childrenslymenetwork.org/children-pans-pandas/  PANS, similarly to Lyme, still has not been accepted by mainstream medicine despite thousands upon thousands suffering from both.

For more on PANS:  https://madisonarealymesupportgroup.com/2017/12/01/guidelines-for-treating-pans-its-real/ In short, treat the infection(s), inflammation, and deal with the psychiatric issues.

Hypoglycemia can also be a player. And according to this article, insulin resistance “causes the body to have problems metabolizing carbohydrates into biological energy called ATP. This energy is essential in the production of feel good neurotransmitters such as serotonin. Thus without that energy the person may tend to feel depressed. The unabsorbed carbohydrates are converted to, first, glycogen and then into fat cells. Thus we find that depressed people may be overweight AND depressed. They are not depressed because of obesity, but because of insulin resistance!! (MedicalNewsToday 8 Oct 2009) See also Hemat.”  http://www.hypoglycemia.asn.au/2011/eating-disorders-anorexia-and-bulimia/

The article has great advice if you suspect hypoglycemia is your issue:

“If you suspect that an eating disorder is related to insulin resistance (a pre-diabetic condition called hypoglycemia) then have this tested by a doctor. See How to test for hypoglycemia. If found to be positive, encourage your client to adopt the Hypoglycemic Diet.

For most people sticking to a regime of frequent snacks of high proteins (every 2 ½ hours), plus various vitamins and mineral – so as never to feel hungry – should supply sufficient energy from proteins to produce feel good neurotransmitters such as serotonin. This together with regular – but not excessive –  exercises should prevent unabsorbed carbohydrates from being converted to fat cells! But keep in mind possible allergies and food sensitivities that may affect the digestive system.”

I knew a patient who was not over weight at all but due to severe hypoglycemia and hypothyroidism they developed eating disorders. When they adopted the hypoglycemic diet and began supplementing with natural thyroid hormone the eating disorders disappeared.
Please spread the word as many doctors will only continue to look at this as a psychiatric problem when there are often biological causes.

Category:

Lyme, PANS, Psychological Aspects, research

Lyme Disease – Chris Newton Refutes BBC Report Stating Most Patients Just Have Chronic Fatigue

https://www.linkedin.com/pulse/lyme-disease-bbc-reports-experts-who-have-answers-chris-newton/?

Lyme disease: the BBC reports on experts who have the answers!

Chris Newton
Chris Newton
Research Director CIMMBER (Center forImmuno-Metabolism, Microbiome… See More
64 articles

Those familiar with this site will note several previous articles on the roll-out of the 5G communications system. In one of these (‘The BBC: arbiter of reality!’) I commented on a BBC article entitled, ‘Does 5G pose health risks?’. This article was posted on their website by their ‘Reality Check Team’. Now I respond as Dr Chris Newton, Scientific Lead for Fight Lyme Now (a science-based lobby group for Lyme disease), to a recent BBC article on Lyme disease where again opinionated experts are quoted.

The strapline to the BBC article posted on the 10th of this month was ……The majority of people who believe they have a chronic form of Lyme disease are more likely to have chronic fatigue syndrome, experts suggest.

The article apparently uses sources within PHE and the NHS and quotes Dr Sarah Logan from London’s Hospital for Tropical Diseases, who suggested that:

“Most people who now think they may have had Lyme disease, in fact have a syndrome that is more in keeping with chronic fatigue syndrome.”

The article appears to target individuals who believe they have contracted Lyme disease and seek help outside the NHS. As someone familiar with the medical condition of individuals who apparently have Lyme disease, I will now present a counter argument in support of these patients.

When an individual first presents to a health professional, such as a GP (under the current UK system), information has to be gleaned within the short allotted time for the appointment. Bearing in mind that Lyme disease is a complex condition, where the symptom complex crosses-over with other conditions (including, chronic fatigue syndrome; see Schwarzbach, 2016), it is not easy to to give a definitive diagnosis on first interviewing the patient. The exception to this, is where the patient presents with the erythema migrans or bullseye rash, as presented in the caption of the BBC article.

So I have reason to believe that I have contracted Lyme disease and I present my condition to the NHS health professional. What is the most likely diagnosis?

To derive data on this, in late 2015, my colleagues and I established a survey to look at diagnosis, treatment and cost of Lyme disease in the UK. One of the first questions asked of individuals who suspected they had Lyme disease was, ‘When you first reported and/or presented your symptoms to the NHS, what INITIAL diagnosis were you given?‘ In response, the top 10 diagnoses were;

  1. 1) CFS
  2. Fibromyalgia (Fmy)
  3. Psychiatric disorder (Psy)
  4. ME
  5. Post Viral Infection Syndrome (PVIS)
  6. Irritable Bowel Syndrome (IBS)
  7. LYME DISEASE
  8. Sleep disorder
  9. Autoimmune condition (Au)
  10. Gastroesophageal Reflux Disease
The number of conditions diagnosed on initial presentation extended to 40 or more and these included rheumatoid arthritis, thyroid disorders, Alzheimer’s disease and multiple sclerosis.

From the survey data we next considered individuals who managed to convince their health professional to run a ‘Lyme disease test’. The NHS considers their Lyme test ‘highly accurate‘ (see BBC article), so how many individuals responding to the survey tested positive. At the time of presenting these data (Newton, 2017), 790 of 1120 survey respondents, were tested. Of these, blood from 220 individuals tested positive for antibodies to Borrelia. Further analysis revealed that only around 25% of these 220 individuals received a clinical diagnosis of Lyme disease at first presentation.

In total 93 individuals from the group of around 790 who were tested for antibodies to Borrelia, received an initial NHS clinical diagnosis of Lyme disease. By considering the number of test positive samples as a proportion of the 93 or so individuals who received a clinical diagnosis of Lyme disease (at first interview), the clinical sensitivity for the laboratory confirmation of Lyme disease in Scotland, England and Wales was around 63%. From the group of individuals who were given Lyme disease as an initial diagnosis, 12 were diagnosed in Scotland and of these, 11 tested positive (in Scotland). So the laboratory test sensitivity for Scotland was just over 90%. Subtracting these cases from the total (Scotland, England and Wales) gave a sensitivity for laboratory confirmation of Lyme disease in England and Wales of around 60%.

Drilling down a little further into the survey data, of the remaining individuals (around 75%) from the group who had a positive laboratory test (220), a range of diagnoses were given on initial presentation of their symptoms to an NHS health care professional (usually GP). For this group the most prevalent diagnoses were CFS followed by a Psychiatric disorder (Psy), PVIS, autoimmunity (Aut), Fibromyalgia (Fmy) and IBS. When test positive results were considered for each category of diagnosis for all individuals in the group of 790 (those who managed to get their blood tested for Borrelia antibodies), percentage positivity for each diagnostic group was; 19% (CFS, 45/233), 32% (Psy, 12/38), 38% (PVIS, 9/24), 15% (Aut, 7/47), 16% (Fmy, 7/45) and 41% (IBS, 5/12). Where no diagnosis was given, the sensitivity was 54% (27/50).

How do these data address the assertion that….. ‘Most people who now think they may have had Lyme disease, in fact have a syndrome that is more in keeping with chronic fatigue syndrome’.

Although not a scientific study, our survey represents the very population that Dr Sarah Logan is addressing, i.e. self diagnosed individuals who believe they have Lyme disease. It would appear from the survey that when first diagnosed, ‘most’ individuals have a condition other than Lyme disease but it is not true to say that most have CFS, as more than half were diagnosed with a condition other than CFS. Surprisingly or not, for those individuals where no diagnosis was given, the sensitivity approached that of the Lyme disease group (54% no diagnosis v. 63% Lyme).

Notwithstanding the lack of scientific rigour, these survey data agree with other studies for non-selected patients (non-clinically selected by health care professional or biomedical scientist) in that the sensitivity (quoted as accuracy in BBC article) of the NHS laboratory testing system was around 60% in England and Wales. This could mean that out of the 790 samples tested for Borrelia antibodies, as opposed to 220 positives, around 316 blood samples should have tested positive, this is a positivity rate of 40% (from a self-selected group) (see below for sensitivity with at least two tests).

In the context of our survey, the use of the word ‘most’ by Dr Logan is not appropriate. It undermines the high proportion of individuals with a positive NHS test result, (especially if you are one of the 96 (316-220), out of the 790 tested, who are told to ‘go and see a psychiatrist‘ as your result was negative (or indeed, even if it was positive-see survey statistics above). Also, what about the 330 out of 1100 respondents (29%) to the survey who ‘didn’t make the cut’ (no lab. test performed). Perhaps their powers of persuasion or their conviction was not up to muster (with respect to getting a test done)!

As the reader will note, this short article hasn’t begun to address the issue of tests performed by the NHS versus tests performed by the private sector. In my experience, individuals do not initially consider the NHS tests as ‘rubbish‘. Private testing is expensive and so the first approach (and I would advise) is to get testing done by the NHS. Often in desperation (many of these people are extremely unwell and have been this way for some time) individuals go to private clinics in the UK, Germany and sometimes the US. Often multiple tests are performed and overall test positivity is high.

Our survey shows that for around 500 individuals who could not get tested or for whom the test came back negative, 90% received a positive result from a private lab.

In terms of multiple tests or a combination of at least two tests, the paper by (Callister et al., 2016) is most important. Although it is not entirely clear what test is performed for Lyme disease (Borrelia antibody detection) in all the regional hospital laboratories (not all samples are sent to the PHE reference laboratory), the reference laboratory runs the C6 Elisa. The Callister paper shows that by combining the C6 Elisa with a test that measured IFNgamma secreted from activated T lymphocytes (those exposed to Borrelia antigens), sensitivity was increased from 59% for the C6 alone, to 83% for the C6 in combination with the T-cell test. This is a relatively large increase in sensitivity.

If the same protocol was applied to our group of self-reporting ‘Lyme patients’, the result could be that the overall picture changed to most individuals having a laboratory diagnosis of Lyme disease.

Most branches of science concern data. Words alone are not enough and articles on Lyme disease, where hypotheses (or even thoughts) are discussed, without presenting data (as in the case of the recent article on the BBC website), serve only to further the divide (antagonism) between the professional and the informed individual.

Long-term Lyme disease ‘actually chronic fatigue syndrome’ https://www.bbc.co.uk/news/health-49998344?fbclid=IwAR2_pdpHycbTEqMDK5pm2892RpC2E_6MomS1LJo3o2kRMhgoPeblRdLZBZY

Schwazbach A (2016) Personal communication

Callister SM, Jobe DA, Stuparic-StancicA, Miyamasu M, Boyle J, Dattwyler RJ, Paul M. Arnaboldi PM (2016). Detection of IFN-γ Secretion by T Cells Collected Before and After Successful Treatment of Early Lyme Disease. Clinical Infectious Diseases 62(10):1235–41

Note about the author: In 2015, Dr Chris Newton joined Dr Armin Schwazbach and Mr Demetrios Loukas to form the Lyme disease lobby group, Fight Lyme Now. Chris is an experienced biomedical scientist with academic interests in infection, inflammation and chronic disease. As will be apparent from some of his recent posts, he is not only passionate about biomedical science, he is interested in all areas of science, particularly those that impinge on the wellbeing of our global population (of all species).

Category:

Activism, Lyme, research

Study Showing Mitochondrial Disease Symptoms Hastened by Lyme Infection & Possibly Worsened by Treatment (Patient Had Genetic POLG Mutation)

https://www.ncbi.nlm.nih.gov/pubmed/31655921

Neurogenetics. 2019 Oct 26. doi: 10.1007/s10048-019-00593-2. [Epub ahead of print]

Infectious stress triggers a POLG-related mitochondrial disease.

Gaudó P1, Emperador S1,2, Garrido-Pérez N1,2, Ruiz-Pesini E1,2,3, Yubero D2,4, García-Cazorla A2,4, Artuch R2,4, Montoya J1,2, Bayona-Bafaluy MP5,6.

Abstract

A 3-year-old girl presented with severe epilepsy in the context of Borrelia infection. After ceftriaxone/lidocaine administration, she showed secondarily generalized focal crises that led to neurological and motor sequelae. Genetic studies identified in the patient two heterozygous POLG mutations (c.2591A>G; p.Asn864Ser and c.3649G>C; p.Ala1217Pro). Through analysis of POLG activity in cultured fibroblasts, we confirmed that the mutations altered the mtDNA turnover. Moreover, patient fibroblasts were more sensitive than controls in the presence of a mitochondrial replication-affecting drug, the antiretroviral azidothymidine. To test if ceftriaxone treatment could worsen the deleterious effect of the patient mutations, toxicity assays were performed. Cell toxicity, without direct effect on mitochondrial respiratory function, was detected at different antibiotic concentrations.

The clinical outcome, together with the different in vitro sensitivity to ceftriaxone among patient and control cells, suggested that the mitochondrial disease symptoms were hastened by the infection and were possibly worsened by the pharmacological treatment.

This study underscores the benefit of early genetic diagnosis of the patients with mitochondrial diseases, since they may be a target group of patients especially vulnerable to environmental factors.

________________

**Comment**

Great work hailing from Spain demonstrating that some patients have a genetic predisposition setting them up for treatment failure. This is not a “21 days of doxycycline” treatment and the sooner mainstream medicine wakes up from its coma the better!  Until it does, patients will not improve.

I found I had a genetic predisposition which caused disulfiram psychosis:  https://madisonarealymesupportgroup.com/2019/10/15/disulfiram-psychosis-update/

https://madisonarealymesupportgroup.com/2019/10/27/disulfiram-psychosis-update-2/

Reports are coming in that I’m not alone.  For research regarding this:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290718/

Abstract

Disulfiram is the commonly prescribed drug for the treatment of alcohol dependence. It’s major metabolite (diethyldithiocarbamate) is an inhibitor of dopamine-betahydroxylase, an enzyme that catalyzes the metabolism of dopamine to norepinephrine resulting in psychosis. We recommend that disulfiram should be used at the lowest effective dose, possibly 250 mg daily and caution should be taken while prescribing disulfiram for patients with personal and familial antecedents of psychosis.…..Disulfiram-related psychiatric complications are reported to be more prevalent in eastern countries,3) which suggests that genetic factors may play a role in disulfiram induced psychosis.
________________________________________________________________________________________

In this paper, a hypothesis of vulnerability to disulfiram psychosis is proposed, based on the current lines of evidence for the biological mechanisms involved in the psychoses.

Disulfiram Is a DA Agonist

Disulfiram is an inhibitor of dopamine-beta- hydroxylase (DBH), an enzyme that catalyzes the metabolism of DA to norepinephrine (NE).3 By inhibiting the metabolic pathway from DA to NE in the central nervous system, disulfiram results in an increase of DA concentrations. Therefore, disulfiram is a DA agonist, and is likely to exacerbate preexisting or latent psychosis, similar to amphetamine, methylphenidate and L-dopa.

DA and Affective Psychosis

Increased brain DA is highly correlated with psychomotor activity in animals, and L-dopa has been shown to produce episodes of hypo mania and mania in most patients with bipolar affective psychosis.4 It is possible, therefore, that disulfiram can uncover a preexisting or latent hypomania or mania.

 

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Genetic Mutations, Lyme, research, Treatment