Archive for the ‘Testing’ Category

Rapid Lyme Disease Tests Could Soon Be Heading to a Doctor’s Office Near You

https://www.globallymealliance.org/news/rapid-lyme-disease-tests-could-soon-be-heading-to-a-doctors-office-near-you

Rapid Lyme Disease Tests Could Soon Be Heading to A Doctor’s Office Near You

by Admin at Global Lyme Alliance on January 13, 2022

<span id="hs_cos_wrapper_name" class="hs_cos_wrapper hs_cos_wrapper_meta_field hs_cos_wrapper_type_text" style="" data-hs-cos-general-type="meta_field" data-hs-cos-type="text" >Rapid Lyme Disease Tests Could Soon Be Heading to A Doctor’s Office Near You</span>

Photo credit: University of Central Florida

Global Lyme Alliance is funding researchers at The University of Central Florida to create a Lyme disease rapid test.

By Suhtling Wong-Vienneau for UCF.edu

Mollie Jewett, associate professor and head of the Immunity and Pathogenesis Division at the College of Medicine, and Brian Kim, associate professor in the College of Engineering and Computer Science, will split a $325,000 grant over two years from the Global Lyme Alliance to create a rapid test that can detect the disease weeks earlier than current tests allow. The new test would eliminate the need to visit diagnostic labs and wait for the results.

Lyme disease is carried by deer ticks and infects people when they are bitten by ticks carrying the bacteria borrelia burgdorferi.  Deer ticks are especially common in the northeastern United States and people are exposed to the ticks usually during outdoor activities. Warming temperatures have helped tick populations explode and infiltrate more areas of the country increasing the chance of getting the disease.

The Centers for Disease Control and Prevention estimate that 476,000 people are infected with Lyme disease every year.

Early symptoms of Lyme disease are fever, headache, fatigue and the possibility of a telltale bullseye rash at the site of the bite. If left untreated, the infection can spread to the joints, heart, and nervous system and cause debilitating long-term conditions.

“Testing is a real obstacle for patients, the longer the patient goes without treatment the higher the potential for significant persistent symptoms,” says Jewett.  “Lyme disease antibodies takes up to 14 days to become detectable. By directly detecting the bacteria that causes Lyme disease, the test will fill the current blind spot in the time from infection to diagnosis.”

When the infection is caught early and treated with antibiotics in the preliminary stages, patients can recover quickly without long-term effects. Patients who are treated in later stages of the disease tend to respond well to antibiotics, however, some continue to suffer from ongoing symptoms, termed Post-treatment Lyme disease Syndrome.

Jewett is creating a molecular test that can not only test for antibodies in the blood specific for the infection, but also directly detect the bacteria that causes Lyme disease. The hand-held diagnostic device which the researchers call the Lyme iDS, combines Jewett’s molecular test with Kim’s detection device.

Click here to read the rest of the article.

_________________

**Comment**

One of the hardest things to accept is that testing for Lyme/MSIDS is imperfect at best and abysmal at worst.  The pathogens depress the immune system and some of the sickest NEVER test positive.  It doesn’t help that testing has been rigged for vaccine development but there are so many issues with testing it’s really a bust.  For far too long patients have had a literal laundry list of severe symptoms but are told they don’t have Lyme/MSIDS because they test negative.

Lyme literate doctors understand this and embrace clinical diagnosis based upon symptoms and exposure.  Mainstream medicine, on the other hand, misdiagnoses patients every single day of the year.  Patients have endured decades of abuse and gas-lighting.

Category:

Lyme, Testing

Problematic Lyme Testing Shortchanges Patients, Especially Children

https://www.lymedisease.org/greenberg-lyme-testing-problems/

Problematic Lyme testing shortchanges patients, especially children

by Rosalie Greenberg, MD

Many scientists and physicians agree that there are important issues concerning present Lyme disease (LD) testing.

In this post, I will address how the commercial testing cleared by the Food and Drug Administration (FDA) and approved by the Centers for Disease Control and Prevention (CDC) results in under-identification of the number of individuals, especially children, suffering from LD.

Two-tier testing

First, let’s review the recommended testing to confirm exposure to Borrelia burgdorferi (Bb), the bacteria that causes LD. Testing consists of two parts or “tiers.” Results of these two tests depend upon the ability to detect the antibodies that our bodies make when exposed to the Bb bacteria.

The first is an enzyme-linked immunosorbent assay (ELISA). The ELISA is considered a screening test. According to CDC recommendations, if the ELISA result is negative, the search is over and no further testing is needed.

Looking for antibodies

If the result is equivocal or positive, the second part of the test, or second tier called a Western Blot (WB), should be done. The WB looks for the presence of antibodies to certain proteins (each numbered according their different weights) associated with Bb.

These proteins are depicted on special testing strips as lines called bands. The bands are numbered 18, 22, 23-25, 28, 30, 31, 34, 39, 41, 45, 58, 66, 73, 88, and 93, reflecting their weight in units called kilodaltons.

Testing consists of exposing the patient’s serum (blood without the clotting factors or blood cells) to the antigen bands to see if a reaction occurs. A positive band is supposed to represent an antibody response to a protein found on the Lyme spirochete. I say “supposed to” because there is the potential that some of the bands can become positive from other infections.

The initial goal of this two-tiered approach, using the ELISA as an initial screen followed by the more specific WB, was to create a test that was highly sensitive and specific in identifying the studied infection.

By eliminating the unlikely cases during the first part of the testing and then using more specific identifiers in the second part, the test should be very good, or specific, in identifying most real or true cases of LD. This, in a nutshell, is the rationale for using the two-tiered testing.

Lyme suppresses the immune system

The problems with this type of testing are many. One major difficulty in using the ELISA and WB is that the bacterial organism responsible for Lyme disease, Bb, is in itself immunosuppressive.

So how could a test that depends upon the person’s immune response (the production of antibodies) be much good if we know the organism suppresses the immune system? In other words, if what you are measuring (antibodies) can be affected by the cause of the illness itself (Bb), then depending on this test to make the LD diagnosis is questionable.

This major flaw in the recommended testing diminishes the value of the test. Unfortunately, relying on a test that is so subject to error is the weak foundation that has provided support for much of LD research. This testing is additionally problematic in many ways.

The ELISA is a poor screening test

The concept of two-tier testing is not unique to LD and has been used effectively in diagnosing other illnesses such as Acquired Immunodeficiency Syndrome (AIDS).

But in LD, the first step, the ELISA, is very limited, on average detecting only 56% of cases. It is so very insensitive, it actually misses 44% of cases of people who do have LD. This is in stark contrast to the 99.5% effective rate found when used in testing for AIDS.1

Compounding this insult, the rule that only those whose results are either indeterminate or positive on the initial ELISA test should go on to the second part of the test.

Basically, present recommended use of the ELISA to screen for LD actually eliminates close to half the LD cases from further testing. According to the official guidelines, testing is halted with a negative ELISA and the individual is told that he/she does not have LD.

Clearly, this easily leads to an underdiagnosis of LD infections. Going on to use the WB in those who were indeterminate or positive on the ELISA, results in a 99% specificity (accuracy). But if you’ve already missed half the infected group, then the testing is quite problematic.

The Western Blot has its own issues

The WB looks for the presence of an immune response to Bb proteins, focusing on two types of antibodies: immunoglobulin M (IgM) and immunoglobulin G (IgG).

When a person comes in contact with an infectious agent, the body makes IgM antibodies as its first line of defense. In general, it takes two to four weeks to be at a consistently detectable level, with production peaking at around four weeks and becoming undetectable after six months.

Persistent ongoing detectable IgM levels beyond the one-month period are subject to controversy in their meaning. Some scientists consider these false positives, while others view them as evidence of persistent infection and associated with chronic illness.

The second antibody produced in the body is IgG. It develops over four to eight weeks after exposure to Bb, peaks at approximately six weeks and is gone in less than one year.

IgG antibodies are produced to target specific threats like viruses, bacteria and other potentially harmful microorganisms, and forms the basis of long-term protection against microorganisms.

Difference between IgM and IgG? Not so clear cut

Typically, with infectious illness exposure, the IgM antibody response decreases after a while and one is left only with the IgG response. But this transition is not so clear with exposure to the Lyme bacteria.

In the WB test, the laboratory compares the patient’s blood with blots representing a pattern of numbered bands to those seen in previously well documented CDC LD cases. To be considered a positive WB, the tested blot must show a match by having the required minimum number of reactive bands.

As noted, the bands are numbered by weight, with the following bands previously identified as: 18, 22, 23-25, 28, 30, 31, 34, 39, 41,45, 58, 66, 73, 88, and 93. All of the bands written in black are specific indicators that are seen only in Bb infections.

Three of these bands have been considered highly specific for LD and are given names based on their outer surface proteins (OSP). These bands are known as OSP A (Band 31), OSP B (Band 34) and OSP C (Band 23).

Some doctors believe that a positive result on even only one of these highly specific bands is good evidence of exposure to the Bb bacteria. It’s important to keep in mind that one can be exposed to an infectious agent (e.g. virus, bacteria, fungus, etc.) but not necessarily become ill. Therefore exposure and actual illness are different.

In the listing, the color blue has been used for bands 28, 45, 58, 66 which are considered nonspecific to LD. This means they can appear positive because the person can have other infections, not only LD . Band 41 is somewhat controversial regarding specificity and that is why I colored it green.

A positive WB assay is based on having two of the following three bands 23, 39, 41 being positive to be considered an IgM (Immunoglobulin M) antibody positive test. A positive WB IgG (Immunoglobulin G) antibody test requires the presence of 5 of 10 bands: 18, 23-25, 28, 30, 39, 41, 45, 58, 66, or 93.

“Positive” vs. “false positive”

According to present CDC guidelines, an IgM antibody test can be considered a positive indicator of early exposure to the infection only during the first 30 days after onset of illness.

A positive IgM antibody test is generally considered a marker of an acute (recent onset) illness. The official recommendation is that positive IgM antibody results should be disregarded if the patient has been sick for more than 30 days (i.e. 30 days after the bite.)

After that time, the “gospel” according to the CDC and Infectious Disease Society of America (IDSA) proclaims that a positive IgM antibody test is a false positive. A false positive means that the test is read as positive but isn’t due to LD but caused by another infection or problem.

As noted previously, the typical immunologic progression with infections is a transition from initial production of IgM antibodies to the subsequent production of IgG antibodies. But the situation in LD isn’t typical.

As previously discussed, Bb bacteria are capable of immunosuppression. This means that the organism itself can interfere with the immune system’s response to infections. The normal transition from making IgM antibodies to IgG antibodies can be hindered.

In part, this is because of problems that occur in what’s called germinal centers, the part of the lymphoid tissue where the antibodies are made.2

“The rule” that all IgM antibodies present after 30 days from the initial infection must be considered false positives, effectively serves to dismiss and minimize the number of real cases of LD.

A negative IgM WB test with a positive IgG WB are considered to indicate either late-stage LD or are a residual result left over from a past infection that is no longer present.

The result of this two-tiered testing system is meant to be 99% specific – meaning these are real cases of LD and not false positives.

This present testing approach is so flawed that a statistical analysis by Cook and Puri found that the LD two-tiered testing resulted in 500 times more false-negative (read as non-Bb but really is) outcomes than similar two-tiered tests used in the diagnosis of AIDS.3

Dearborn conference

The 1994 Second National Conference on Serologic Diagnosis of Lyme Disease was held in Dearborn, Michigan. It was attended by representatives of the Association of State and Territorial Public Health Laboratory Directors, CDC, the FDA, the National Institutes of Health (NIH), the Council of State and Territorial Epidemiologists, and the National Committee for Clinical Laboratory Standards.

The goal was to establish a set of nationwide standards for LD testing for the purpose of creating consistency in reporting WB results. Unfortunately, the standards selected at that meeting are still in use. In addition to selecting the two-tier testing, the decision was made to eliminate two of the highly specific bands, 31, and 34, from the required testing.

​These bands were removed because a vaccine against LD using these proteins was in the planning stage. Investigators knew that the use of these two specific proteins in the vaccine could create false positives for these bands in vaccinated individuals. Put another way, because these proteins were to be used in the vaccine, the vaccinated individuals could test positive for these bands but not have LD.

Participants at the Dearborn meeting seemed to doubt the ability of doctors to remember to ask if the individual had already received the vaccine when the person was getting new testing for LD. Could it be that such a simple step, of asking a question, was all that would have been needed to retain these two highly specific bands as possibilities for optimal testing?

LYMErix

In 1998, the FDA approved a Lyme vaccine, LYMErix™, which absolutely did have the potential to make these two very specific bands become positive in vaccinated individuals. Although for a variety of reasons that are complicated and will not be addressed here, by February 26, 2002, SmithKline Beecham withdrew the vaccine from the market.

What was accomplished by removing these two highly specific bands? It’s important to keep in mind that these bands were so significant that they were used to make the vaccine. Eliminating them from the diagnostic testing detracted from the WB test’s diagnostic sensitivity.

Band 31 is also special because it is not seen until at least months after initial infection. Its presence could potentially serve as an indication of an ongoing infection (chronic rather than acute infection at time of testing.)

In addition, bands 31 and 34 have been associated with the presence of neuropsychiatric illness in LD, which could have a crucial impact in the approach to treatment in similarly affected patients. Eliminating these bands removed potentially critical information.

Continuing to omit these bands from the tests defies logic.

Dr. Paul Fawcett and colleagues reported results of an important study at a Rheumatology Symposia Conference in Texas in 1995. The research was designed to look at the effect of eliminating the two specific bands from the WB criteria.4

The authors compared the diagnostic utility of applying the older criteria (including bands 31 and 34) vs. the newer WB criteria (as decided at the Dearborn meeting) to 66 child patients with known histories of a tick bite, an erythema migrans rash and symptoms of the illness.

Inclusion of bands 31 and 34 resulted in the identification of 100% of the youth as positive for LD. Using the newer criteria where OSP A and OSP B were omitted resulted in only 31% of the youth being identified as positive for LD.

Grossly inadequate

From their analysis, the investigators concluded:

“The proposed Western Blot Reporting Criteria are grossly inadequate, because it excluded 69% of the infected children.”

Basically by eliminating these bands from the WB, kids became discriminated against and undercounted in the statistics.

It’s unconscionable that these bands were never put back nor to my knowledge has there been significant discussion to reinstate them. This leaves doctors in the position of missing more people who really have LD.

There is more to consider in how the official change in testing criteria has shortchanged children, adolescents and even adults. Common sense dictates that testing for bands 31 and 34 in anyone born after 2002 (when the vaccine was taken off the market) would result in higher sensitivity and specificity. The more bands available for identifying the illness, the more likely you’ll identify positive individuals. Why would any medical professional argue against this?

The omission of bands 31 and 34 presents yet another problem for kids. Evidence in the medical literature indicates that positivity for these bands is associated with the presence of neuropsychiatric issues such as autism. Wouldn’t one want to include in the testing, markers that might alert one to these issues, especially in children?

Continuing to omit these bands for more than two decades has only served to deny the real number of people who have in the past, and perhaps still continue, to suffer from LD. By removing these two bands, we may be removing years of optimum health, as well as impairing social and cognitive development for some children for their lifetime.

Current two-tiered testing is indirect

Since the bacteria is difficult to isolate, much of the current testing is designed to look for reactions indicating that the bacteria is present, further complicating the diagnostic process.

Let me explain. Present approved testing looks for the presence of and intensity level of an individual’s immune response to the LD bacterial proteins. Testing would be much less controversial if the organism could be directly cultured or identification of the bacterial DNA occurred. Most scientists would agree that the indirect approach of looking at antibody response with an illness that can cause immunosuppression is inherently fraught with problems and limitations.

Interestingly, at present some research laboratories are focused on developing better and more direct methods of testing for Bb. This is sorely needed. Consider that in 2020, the National Institute of Health allotted only 13% ($5.3 million) of its total LD budget to advance diagnostic Lyme testing.5

Given that testing is the foundation of much research on the diagnosis and treatment, and present recommendations are problematic, 13% is a small amount. It is disturbing to realize that 30% of this allotted money went toward more antibody testing research (i.e. more indirect testing). This only serves to perpetuate the present problem of using an indirect method to identify an immunosuppressive bacterium.

Current tests only identify a few species of Bb

There are multiple strains or types of Borrelia bacteria that can cause Lyme as well as other diseases (e.g. Borrelia miyamotoi causes tick-borne relapsing fever.) Most labs use the strain B 31 for LD testing. IGeneX laboratory uses two strains: B 31 and Bb 297. The more strains used as possibilities, the increased likelihood of getting a positive test result.

This is part of why IGeneX gets more positive testing for LD than bigger labs like Quest and Labcorp. How many types of Borrelia that cause illness are we missing because of the limitations of our tests?

As you can see, there are multiple problems inherent in the recommended testing. It is crucial to acknowledge that the present faulty testing, which serves as the foundation for many studies, creates bias in all the research that is dependent upon it.

This major flaw has affected and colored too many aspects of our knowledge about LD. The present system of testing results in a significant underestimation of the number of individuals who suffer from LD. Our people, and especially our children, deserve much better from American medicine.

Dr. Rosalie Greenberg is a Board-Certified Adult, Child and Adolescent Psychiatrist, known for her expertise in the diagnosis and management of complex psychiatric problems in children, and pediatric psychopharmacology. Her website is rosaliegreenbergmd.com.

References

1 Stricker RB and Johnson L. Lyme disease diagnosis and treatment: lessons from the AIDS epidemic. Minerva Med 2010 Dec;101(6):419-25. PMID: 21196901.

2 Hasley CJ, Eisner RA, Barthold SW and Baumgarth N. Delays and Diversions Mark the Development of B Cell Responses to Borrelia burgdorferi Infection. J Immunol June 1, 2012, 188 (11) 5612-5622;

3 https://doi.org/10.4049/jimmunol.1103735. Cook MJ and Puri BK. Application of Bayesian decision-making to laboratory testing for Lyme disease and comparison with testing for HIV. Int J Gen Med. 2017; 10: 113–123. Published online 2017 Apr 10. doi: 10.2147/IJGM.S131909 PMCID: PMC5391870.

4 Paul Fawcett et al. Rheumatology Symposia Abstract # 1254. 1995 Rheumatology Conference in Texas.

5 https://www.documentcloud.org/projects/nih-lyme-research-funding-2

________________

For more:

“Setting arbitrary level of antibodies to diagnose a disease that has not been amenable to Koch’s postulates seems open to question.  By the same token, ignoring antibody results unless they meet arbitrary levels seems suspect.  The vast majority of patients in this series showed some WB antibody exposure, but many did not meet the arbitrary limits set….in our present state of knowledge, the diagnosis of chronic Lyme disease is a clinical one.  Many of the patients in this series have suffered serious ‘hurts’ when they have been told that they could not have LD because their WB did not meet arbitrary limits.”   ~ Dr. Burton Waisbren

Category:

Lyme, Testing

What We Know & Don’t Know About Lyme Disease

https://www.frontiersin.org/articles/10.3389/fpubh.2021.819541

MINI REVIEW article

Front. Public Health, 21 January 2022 | https://doi.org/10.3389/fpubh.2021.819541

What We Know and Don’t Know About Lyme Disease

Sam T. Donta*

Consultant, Infectious Diseases, Falmouth Hospital, Falmouth, MA, United States

We know the cause of Lyme disease. We know that the bacteria can be found in the initial rash, and occasionally in the blood in the subsequent 2–3 months, but after then, its subsequent location is unknown. Whereas diagnosis and treatment of early Lyme disease is generally straightforward, the etiology of relapsing or persisting symptoms is yet to be defined, and presents clinical challenges. There are no current tests to determine if the infection is still present or absent, thus complicating diagnosis and treatment. Presented here are approaches to the diagnosis and treatment of persisting Lyme disease, based on available published information, and the experience of the author.

Introduction

It has been more than 40 years since the discovery of the causative agent of Lyme disease. Much has been learned, but several key questions remain:

  1. how do we know if the infection has been eradicated
  2. can it become dormant
  3. can it reactivate in patients with persistent symptoms, are these due to continuing infection or to non-infectious sequelae, and 4-are there treatments that can resolve the infection

Pathogenesis

We know that Lyme disease is caused by the bacterium Borrelia burgdorferi, transmitted by the bite of an Ixodes tick. We know that the bacteria may be isolated from the typical erythema migrans rash, and can be occasionally recovered from the circulating blood in the subsequent 2–3 months (1). After that time, it has not been possible to consistently isolate the bacteria from any body fluids or tissues.

So, where are they? Under the skin, as demonstrated in studies with macaque primates (2), and similarly in preliminary studies in humans (3)? Intracellularly, as is the case of most, if not all pathogens that can become latent, then recur? Or both? Hence, the central question at the heart of the controversy surrounding the diagnosis and treatment of Lyme disease; i.e., whether persisting or relapsing symptoms are due to continuing infection or due to post-infectious phenomena.

Accumulating evidence regarding the persistence of biologically active, albeit non-replicating bacteria derives from several studies in various animal models. Hodzic et al. demonstrated that B. burgdorferi can persist in mice following antibiotic treatment but were non-cultivatable (4). Casselli et al. demonstrated that B. burgdorferi can colonize the dura mater in mice, are biologically active, and induce host gene inflammatory responses (5). Embers et al. demonstrated post-antibiotic treatment persistence in a non-human primate naturally tick infected model (6) and recovery of the spirochete by xenodiagnosis (2). Similarly, there was recovery of non-cultivatable B. burgdorferi by xenodiagnosis in a few human patients who had had an erythema migrans rash and had had prior antibiotic treatment (3). These results, plus observations by us and others that retreatment of patients with recurring or persisting symptoms following initial antibiotic treatment using specific antibiotic regimens (7), lend strong support to the hypothesis that it is persistent infection by B. burgdorferi that is the likely cause of persisting symptomatology. In contrast, attribution of post-infectious symptoms to some post-infectious phenomena has only been speculative without any supporting evidence.

Diagnostic Issues

Currently, in the absence of any currently available means to directly detect the bacteria or its products, the diagnosis is dependent on the clinical history and any associated manifestations, along with the results of serologic studies. A major clinical problem is, that with the exception of patients with Lyme arthritis, most patients with continuing symptoms have no objective signs for Lyme disease, making the diagnosis dependent on the clinical picture that overlaps with that of chronic fatigue syndrome and fibromyalgia. Making it more difficult is the fact that many such patients do not have robust serologic responses to the causative organisms (8). And, despite claims that once one is treated with 4 weeks of antibiotics, one no longer has Lyme disease, or, if Lyme test results revert to negative, it means one no longer has Lyme disease, these claims being unsupportable in the absence of any means to prove the bacteria’s absence (9).

It also appears illogical, when patients have persisting or relapsing symptoms identical to those at the initial presentation, to opine that the infection is no longer present and that the remaining symptoms are post-Lyme disease of yet to be defined cause. It would seem more logical to assume that the infection has not been eradicated. It may be that ongoing symptoms are due to post-infectious factors, e.g., autoimmunity without provocation from persistent infection, but that has yet to be demonstrated as an obvious cause of the ongoing clinical picture. It seems much more likely that the cause of symptoms are due to some bacterial product, be it an exotoxin or endotoxin, similar to that that is at the root of most, if not all other bacterial infections, accompanied with host-responses to that virulence product or products, including inflammatory and autoimmune responses (10).

Serologic Issues

A similar lack of logic is present in analyzing the results of Lyme Western blot reactions, specifically IgM responses. How logical is it to use positive IgM responses to support the diagnosis of early Lyme disease, but deem that those same responses in patients with ongoing or relapsing symptoms are false-positive responses? Is it not more logical to assume that continued IgM reactivity, in the presence of ongoing symptoms, might be an indicator of unresolved infection in the absence of any available test to determine the continuing presence or absence of the causative organisms? In support of that conjecture, the results of several studies in various animal models, indicate that the causative borrelia are able to modulate humoral antibody responses such that the normal conversion of IgM to IgG antibody responses is abrogated (11).

Treatment Issues

As if confirming the diagnosis isn’t sufficiently difficult, the treatment of relapsing or persisting symptoms has presented its own challenges. There are many antibiotics that are active in vitro against the Lyme bacteria, but have not been clinically very effective. In early Lyme disease, treatment with doxycycline, amoxicillin, or cefuroxime over a period of a few weeks is generally effective. It is in patients with relapsing or persisting symptoms, including those previously treated, inadequately treated, or untreated, that the question arises as to whether any further antibiotic treatment is effective. The answer appears to be yes, if one looks at the pharmacology of specific antibiotics.

Doxycycline appears to have limited efficacy in patients with persisting or relapsing symptoms, especially in patients with symptoms present for greater than a few months. Doxycycline is highly protein-bound in the circulation, and it is unlikely that sufficient antibiotic can diffuse into tissues and cells to affect the borrelia. In contrast, tetracycline, which is not highly protein bound, appears to be clinically effective (10). Our observational results in several thousands of patients since our initial publication attests to both the greater efficacy of tetracycline vs. doxycycline in terms of both dosing and duration of treatment (12).

Beta-lactam antibiotics, including intravenous ceftriaxone, appear to be of limited clinical efficacy, perhaps because (a) that class of antibiotic has its effects on multiplying organisms, and there is no evidence that the Lyme borrelia are multiplying in persistent or relapsing disease, and (b) they are incapable of intracellular penetration. These antibiotics may offer temporary symptom relief, which might be due to their effects on glutamate accumulation during neurotransmission (13), without resolving the underlying infection.

Of particular interest are the effects of macrolide antibiotics (e.g., erythromycin, clarithromycin, azithromycin) on Lyme disease. They are highly active in vitro, and are capable of intracellular penetration, but appear to be of limited clinical value in patients with persistent symptoms. In analyzing the possible reasons, if the borrelia reside intracellularly in an acidic endosome, as is the case for numerous other microbes capable of intracellular persistence, macrolide antibiotics are not very active at an acidic pH. The use of a lysosomotropic agent (e.g., hydroxychloroquine, amantadine) to alkalinize the acidic endosome appears to result in clinical efficacy (14).

There have been two clinical trials using differing antibiotic regimens over a 3 month period of time in patients with persisting symptoms of Lyme disease. In the first trial, patients were given a month of ceftriaxone followed by 2 months of doxycycline vs. placebo treatment, and positive PCR reactivity to Borrelia burgdorferi was an exclusionary criterim for this study (15). In the other trial, patients with persisting symptoms were given an initial week of IV ceftriaxone, then randomized to being given the combination of clarithromycin and hydroxychloroquine vs. placebo for 3 months (16). In neither trial was there any reported greater improvement between the antibiotic treatment arms and placebo arms. The results of these studies have been reviewed with several reservations being expressed about study design, the instruments used to measure changes in symptoms, and interpretation of the results (17). In the former trial, neither ceftriaxone nor doxycycline were given for 3 months, and the assumption that both antibiotics are of equal efficacy is not supportable according to differing mechanisms of action. In the case of ceftriaxone, its antibiotic activity is based on its interference with replicating organisms, and given that there is no evidence to indicate that, once B. burgdorferi has established itself, there is any multiplication of note, it would not be expected to be effective in patients with persistent symptoms. And in the author’s observational experience, even the use of ceftriaxone over periods of time up to 6 months or more was without much if any benefit, with any possible benefit in a few patients due to ceftriaxone’s interference with the glutamate receptor system. In the case of doxycycline, whether a longer duration of treatment or increased dosing would have been effective remains unanswered. Observations by numerous clinicians suggest that higher doses of doxycycline, i.e., 300–400 mg/day might be more effective than the commonly used dosing of 200 mg/day.

In the trial utilizing the combination of clarithromycin and hydroxychloroquine, based on our initial published report, the trial was contaminated by the use of ceftriaxone in all patients prior to randomization to the active or placebo groups. Of greater importance is the failure to consider both the duration of prior symptomatology and the duration of treatment itself. As indicated in our published observations (12, 14), patients with persistent or relapsing symptoms for less than a year appeared to be cured, ie no recurring symptoms for greater than a year, by a treatment course of 3–6 months. In patients with persisting symptoms for >2 or more years, however, treatment success required a treatment duration of 6 or more months, and up to 18 months in patients with persisting symptoms for >5 or more years. Another likely flaw in that trial was not controlling for the use of adjunctive vitamin C. Supplemental vitamin C can be a strong acidifying agent, counteracting the effects of hydroxychloroquine (7, 14), and thus possibly accounting for some of the trial’s failure to show any benefit of this treatment.

Future Directions

The key remaining questions are whether there can be found a better, more direct detection test to indicate the presence or absence of active B. burgdorferi, and whether additional controlled treatment trials using longer durations of treatment with the tetracycline or clarithromycin/hydroxychloroquine regimen, or regimens utilizing different antibiotics or combination of certain antibiotics that might prove effective. The results of recent in vitro and early animal model experiments by Zhang (18) and by Lewis (19) might hold promise of other potentially effective approaches to the management of patients with persistent symptoms of Lyme disease.

Of additional likely importance is the potential role of antibiotic tolerance as a mechanism of persistence and “resistance” of B.burgdoferi to treatment in patients with persisting symptoms. Recent results of experiments with other bacterial organisms that can persist demonstrate the likely role of antibiotic-tolerance as the mechanism by which they persist (20). This mechanism apparently relies on a ribonuclease produced by the organisms. If our preliminary results with BB0755, an annotated ribonuclease, that demonstrated cytotoxic activity with tissue-cultured cells of neural origin (21), is due to its ribonuclease activity, then this possibility might offer an explanation to B.burgdorferi’s antibiotic tolerance.

There are additional questions that a better understanding of the pathophysiology of Lyme disease might lead to better approaches to the diagnosis and treatment of Lyme disease, especially in its persistent form. These include the possible role of antibiotic-tolerant persisters.

Author Contributions

The author confirms being the sole contributor of this work and has approved it for publication.

Conflict of Interest

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

Publisher’s Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

References

1. Nowakowski J, McKenna D, Nadelman RB, Bittker S, Cooper D, Pavia C, et al. Blood cultures for patients with extracutaneous manifestations of Lyme disease in the United States. Clin Infect Dis. (2009) 49:1733–5. doi: 10.1086/648076

PubMed Abstract | CrossRef Full Text | Google Scholar

2. Embers ME, Hasenkampf NR, Jacobs MB, Tardo AC, Doyle-Meyers LA, Philipp MT, et al. Variable manifestations, diverse seroreactivity and post-treatment persistence in non-human primates exposed to Borrelia burgdorferi by tick feeding. PLoS ONE. (2017) 12:e0189071. doi: 10.1371/journal.pone.0189071

PubMed Abstract | CrossRef Full Text | Google Scholar

3. Marques A, Telford SR III, Turk SP, Chung E, Williams C, Dardick K, et al. Xenodiagnosis to detect Borrelia burgdorferi infection; a first-in-human study. Clin Infect Dis. (2014) 58:937–45. doi: 10.1093/cid/cit939

PubMed Abstract | CrossRef Full Text | Google Scholar

4. Hodzic E, Imai D, Feng S, Barthold SW. Resurgence of persisting noncultivable Borrelia burgdorferi following antibiotic treatment in mice. PLoS ONE. (2014) 9:e86907. doi: 10.1371/journal.pone.0086907

PubMed Abstract | CrossRef Full Text | Google Scholar

5. Casselli T, Divan A, Vomhof-DeKrey EE, Tourand Y, Pecoraro HL, Brissette CA. A murine model of Lyme disease demonstrates that Borrelia burgdorferi colonizes the dura mater and induces inflammation in the central nervous system. PLoS Pathog. (2021) 17:e1009256. doi: 10.1371/journal.ppat.1009256

PubMed Abstract | CrossRef Full Text | Google Scholar

6. Embers ME, Barthold SW, Borda JT, Bowers L, Doyle L, Hodzic E, et al. Persistence of Borrelia burgdorferi in rhesus macaques following antibiotic treatment of disseminated infection. PLoS ONE. (2012) 7:e29914. doi: 10.1371/annotation/4cafed66-fb84-4589-a001-131d9c50aea6

PubMed Abstract | CrossRef Full Text | Google Scholar

7. Donta ST. Issues in the diagnosis and treatment of Lyme disease. Open Neurol J. (2012) 6:140–5. doi: 10.2174/1874205X01206010140

PubMed Abstract | CrossRef Full Text | Google Scholar

8. Donta ST. Chronic late lyme disease. Med Clin N Am. (2002) 86:341–9. doi: 10.1016/S0025-7125(03)00090-7

PubMed Abstract | CrossRef Full Text | Google Scholar

9. Lantos PM. Chronic lyme disease. Infect Dis Clin North Am. (2015) 29:325–40. doi: 10.1016/j.idc.2015.02.006

PubMed Abstract | CrossRef Full Text | Google Scholar

10. Lebrun I, Marques-Porto A, Pereira AS, Pereira A, Perpetuo EA. Bacterial toxins: an overview on bacterial proteases and their action as virulence factors. Mini Rev Med Chem. (2009) 7:820–8. doi: 10.2174/138955709788452603

PubMed Abstract | CrossRef Full Text | Google Scholar

11. Elsner RA, Hastey CJ, Baumgarth N. CD4 cells promote antibody production but not sustained affinity maturation during Borrelia burgdorferi Infection. Infect Immun. (2015) 83:48–56.

PubMed Abstract | Google Scholar

12. Donta ST. Tetracycline therapy of chronic Lyme disease. Clin Infect Dis. (1997) 25:S52–6. doi: 10.1086/516171

PubMed Abstract | CrossRef Full Text | Google Scholar

13. Rothstein JD, Patel S, Regan MR, Haenggeli C, Huang YH, Bergles DE, et al. Beta-lactam antibiotics offer neuroprotection by increasing glutamate transporter expression. Nature. (2005) 433:73–7. doi: 10.1038/nature03180

PubMed Abstract | CrossRef Full Text | Google Scholar

14. Donta ST. Macrolide therapy of chronic Lyme disease. Med Sci Monit. (2003) 9:136–42.

PubMed Abstract | Google Scholar

15. Klempner MS, Hu LT, Evans J, Schmid CH, Johnson GM, Trevino RP, et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. disease. N Engl J Med. (2001) 345:85–92. doi: 10.1056/NEJM200107123450202

PubMed Abstract | CrossRef Full Text | Google Scholar

16. Berende A, ter Hofstede HJ, Vos FJ, van Middendorp H, Vogelaar ML, Tromp M, et al. Randomized trial of longer-term therapy for symptoms attributed to Lyme disease. N Engl J Med. (2016) 374:1209–20. doi: 10.1056/NEJMoa1505425

PubMed Abstract | CrossRef Full Text | Google Scholar

17. Delong AK, Blossom B, Maloney EL, Phillips SE. Antibiotic retreatment of Lyme disease in patients with persistent symptoms: a biostatistical review of randomized, placebo-controlled, clinical trials. Contemp Clin Trials. (2012) 33:1132–42. doi: 10.1016/j.cct.2012.08.009

PubMed Abstract | CrossRef Full Text | Google Scholar

18. Feng J, Auwaerter PG, Zhang Y. Drug combinations against Borrelia burgdorferi persisters in vitro: eradication achieved by using daptomycin, cefoperazone and doxycycline. PLoS ONE. (2015) 10:e0117207. doi: 10.1371/journal.pone.0117207

PubMed Abstract | CrossRef Full Text | Google Scholar

19. Sharma B, Brown AV, Matluck NE, Hu LT, Lewis K. Borrelia burgdorferi, the causative agent of lyme disease, forms drug-tolerant persister cells. Antimicrob Agents Chemother. (2015) 59:4616–24. doi: 10.1128/AAC.00864-15

PubMed Abstract | CrossRef Full Text | Google Scholar

20. Holden DW. Persisters unmasked. Science. (2015) 347:30–2. doi: 10.1126/science.1262033

PubMed Abstract | CrossRef Full Text | Google Scholar

21. Donta ST, Martin SE, Cartwright MJ. A novel ADP-ribosylating toxin of Borrelia Burgdorferi.In: Abstracts of the IDSA 36th Annual meeting. Denver, CO (1998). 922 p.

Keywords: Lyme disease, Lyme diagnosis, Lyme pathogenesis, Lyme treatment, Lyme serology

Citation: Donta ST (2022) What We Know and Don’t Know About Lyme Disease. Front. Public Health 9:819541. doi: 10.3389/fpubh.2021.819541

Received: 21 November 2021; Accepted: 20 December 2021;
Published: 21 January 2022.

Edited by:  Christian Perronne, Assistance Publique Hopitaux De Paris, France

Reviewed by:  Robert Carroll Bransfield, Rutgers, The State University of New Jersey, United States

Copyright © 2022 Donta. 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.

Category:

Lyme, research, Testing, Treatment

Bannwarth Syndrome in Early Disseminated Lyme Disease

https://danielcameronmd.com/bannwarth-syndrome-lyme-disease/  Video Here

Bannwarth syndrome in early disseminated Lyme disease

Man with Bannwarth syndrome and lyme disease huntched over and holding his lower back.

Welcome to another Inside Lyme Podcast with your host Dr. Daniel Cameron. In this episode, Dr. Cameron will be discussing the case of a 66-year-old man with Bannwarth syndrome with urinary retention in early Lyme disease.

By

Omotosho and colleagues described this case in an article entitled “A Unique Case of Bannwarth Syndrome in Early Disseminated Lyme Disease.”¹

The man presented to the emergency room with generalized myalgia, fatigue, and severe neck pain. The symptoms had been occurring for two weeks and began shortly after he was bitten by two ticks while performing yard work.

The patient reported having dull mid-back pain, intermittent headaches, and neck stiffness. His doctor initially suspected he had pneumonia and prescribed an antibiotic. But his symptoms worsened.

“His pain then radiated down his entire spine into his upper and lower extremities, leading to right arm weakness and new urine retention onset,” the authors wrote.

“His paraspinal tenderness and diminished deep tendon reflexes bilaterally.” His pain score was 8 out of 10. The ESR rate was 100 and C-reactive protein of 8.8 mg/L.

“Physicians need to be aware of the rare neurological manifestations of [Lyme neuroborreliosis] … Prompt diagnosis and treatment with antibiotics can reduce unnecessary imaging, patient anxiety, and, most importantly, avert debilitating complications.”

Test results indicated a white blood cell count of 12 k/uL, C-reactive protein of 8.8 mg/L, sedimentation rate of 100 mm/h, and creatinine kinase of 27 units/L.

Western blot and ELISA Lyme disease tests were positive and confirmed an early stage infection with Borrelia burgdorferi. In addition, a spinal tap showed lymphocytic pleocytosis and a positive Lyme disease titer.

The man was diagnosed with Bannwarth syndrome (BWS) based on his severe radiculopathy, upper extremity weakness, and urinary dysfunction. “All of these findings are pathognomonic for [Bannwarth syndrome],” wrote the authors.

Typically, Bannwarth syndrome affects a person’s limbs. In this case, Lyme disease induced sacral radiculitis leading to neurogenic urinary dysfunction.

The authors were not sure why the patient’s urinary tract was affected. They suggested, “the influence of the radiculitis on innervating fibers” and “direct invasion of the spirochetes into the bladder wall” might have played a role.

“Early recognition of this rare presentation associated with Lyme disease and treatment with antibiotics can prevent disease progression and detrimental neurological sequelae.”

The man was treated with a 21-day course of IV ceftriaxone and “his symptoms improved with complete resolution of his urinary retention,” the authors wrote.

About Bannwarth syndrome

Bannwarth syndrome has been reported most often in Europe. And despite disputes over its incidence in the United States, “the condition does occur but is often misdiagnosed.”

BWS is characterized by a wide range of symptoms including:

  • radicular pain (100%)
  • sleep disturbances (75.3%)
  • headache (46.8%)
  • fatigue (44.2%)
  • malaise (39%)
  • paresthesia (32.5%)
  • peripheral nerve palsy (36.4%)
  • meningeal signs (19.5%)
  • paresis (7.8%)

The syndrome can cause severe pain. “BWS typically manifests itself with severe zoster-like segmental pain that is worse at night,” the authors wrote. “The pain has a burning, stabbing, biting, or tearing character and usually responds poorly to all common analgesics.”

Author’s Conclusion:

“The constellation of neurological symptoms, particularly when associated with a recent or suspected tick bite in an endemic region, should prompt thorough evaluation for [Lyme neuroborreliosis] and assessment for BWS,” the authors wrote.

The following questions are addressed in this Podcast episode:

  1. What is Bannwarth syndrome?
  2. How is BWS diagnosed and treated?
  3. What is radicular pain?
  4. What is the significance of the spinal tap findings?
  5. What is the significance of an elevated sedimentation rate and c-reactive protein?
  6. Why is BWS rarely diagnosed in the USA?
  7. What can we learn from this case?

Thanks for listening to another Inside Lyme Podcast. Please remember that the advice given is general and not intended as specific advice to any particular patient. If you require specific advice, please seek that advice from an experienced professional.

Inside Lyme Podcast Series

This Inside Lyme case series will be discussed on my Facebook page and made available on podcast and YouTube.  As always, it is your likes, comments, and shares that help spread the word about this series and our work. If you can, please leave a review on iTunes or wherever else you get your podcasts.

References:
  1. Omotosho YB, Sherchan R, Ying GW, Shayuk M. A Unique Case of Bannwarth Syndrome in Early Disseminated Lyme Disease. Cureus. Apr 25 2021;13(4):e14680. doi:10.7759/cureus.14680

For more:

Category:

Lyme, Pain Management, research, Testing, Ticks, Treatment

Science (Again) Says Natural Immunity is Best, Majority of COVID Deaths have Comorbidities, & Testing Will Not Save Us

**UPDATE**

https://kdvr.com/news/coronavirus/covid-19-vaccine/cdc-report-natural-immunity-stronger-than-vaccines-alone-during-delta-wave/

CDC: Natural immunity stronger than vaccines alone during delta wave

by:

Updated:

DENVER (KDVR) — Natural immunity was six times stronger during the delta wave than vaccination, according to a new report from the U.S. Centers for Disease Control and Prevention.

The report, published Jan. 19, analyzed COVID outcome data from New York and California, which make up about one in six of the nation’s total COVID deaths. (See link for article)

What the article doesn’t mention are the overwhelming amount of adverse reactions and deaths recorded in VAERS after the COVID shots.

https://popularrationalism.substack.com/p/science-says-natural-immunity-following

Science Says… Natural Immunity Following Severe COVID-19 is Superior

Survivors of Severe COVID-19 Take Heart. More data needed on Mild Cases Due to Likelihood of PCR False Positives.
“We found that NAb against the WT virus persisted in 89% and S-IgG in 97% of subjects for at least 13 months after infection.”
As measured by neutralizing antibody assays, immunity to SARS-CoV-2 from vaccination wanes after 3-4 months.

This study in the European Journal of Immunology has some good news: Survivors of severe COVID-19 from had very high immunity against Delta 13 months after their initial infection with earlier variants.

The study was conducted on 2586 subjects ≥18 years of age whose native language was Finnish or Swedish who lived within five selected hospital districts in Finland and with a “PCR-confirmed COVID-19 diagnosis”.

The authors examined neutralizing antibody levels (Nab) against Wild-Type (Wuhan), Alpha, Beta and Delta proteins, studying both the Spike glycoprotein (S-protein)) and the viral nucleoprotein (N-protein)) at 8 and 13 months following infection.

The Spike protein Nab measured as antibodies against two epitopes) was higher at 13 months than against the nucleoprotein (N-protein), as would be expected given the easier access of the spike protein to our immune system. That said, N-protein NAb production was still very high.

The greatest result, which is very, very welcome, came when the authors examined the Nab in subgroups. They looked at NAbs in people who had mild infections and those who had severe COVID-19.

Those who had severe COVID-19 have the highest Nabs against both proteins. And that’s excellent news for people who had to suffer severe COVID-19.  (See link for full article)

__________________

**Comment**

Despite the well known scientific fact that natural immunity is always far-superior to vaccines, which Fauci even admitted pre-2019, our corrupt government and any organization that follows in lock-step has misrepresented and denied this plain, simple fact.  People have lost their jobs.  Soldiers have been kicked out of the military. Children have lost out on educations due to this injustice.

But Fauci states his pre-2019 comment about natural immunity was taken out of context, and then erroneously stated:

“The issue of vaccines actually, at least with regard to SARS-CoV-2, can do better than nature,” Fauci said at the time.

This, has been proven to be completely untrue.  We now have a pandemic of the “vaccinated.”

The collateral damage due to ignoring natural immunity can not be overstated.

All of a sudden mainstream is talking about natural immunity and an opinion piece in the WSJ, Dr. Makary states that Omicon provides “superimmunity” which will be stronger against new variants & future coronaviruses, making “normal” life possible even as the virus continues to spread and mutate – just like the flu bug does every single year.  Ironically, experts have been saying this the whole time but it’s finally making mainstream news. They remain mum on the fact these injections, which aren’t vaccines, actually reprogram innate immune responses, as well as on results of autopsies on the “vaccinated“, which show horrific findings, revealing they will only go so far with transparency, and pointing to a predetermined, agreed upon outcome.

Facts and data are getting harder and harder to deny.

https://thehighwire.com/videos/who-is-dying-from-covid/ Video Here (Approx. 11 Min)

75% of COVID Deaths Had Four Comorbidities

Hear what CDC Director, Rochelle Walensky had to say.

Del BigTree was “fact-checked” by Snopes stating he took this out of context and that the deaths were among the fully “vaccinated” patients, and that somehow this supports the idea that the “vaccines” are effective.

BigTree than went back and showed the Aug. 2020 report, before the mass “vaccination” campaign, that showed that 94% of COVID deaths had over two comorbidities.

The clear point is the majority of COVID deaths are among the already ill, whether you are “vaccinated” or not.  This is important to understand for public policy.  As BigTree points out, we should not be masking healthy people, stopping children’s education, firing people, stopping the world, blaming the unvaccinated, and mandating a shot that is non-sterilizing, ineffective, and dangerous.

_________________

https://thevaccinereaction.org/2022/01/testing-will-not-save-us/

Testing Will Not Save Us

by Vinay Prasad, MD | Guest Writer
Published January 16, 2022 | Opinion

Testing Will Not Save Us

I have heard many people say that at this moment—January 2022—testing will save us. They cite success stories like the National Basketball Association’s bubble (of 2020) to show what testing can accomplish.  Unfortunately, here are nine considerations that they are missing when it comes to mass testing.

1. No one has any tests.

2. Many tests have limited sensitivity.

3. Low pre-test probability.

4. The distribution of testing.

5. Testing is only helpful if you have the resources to make salutatory choices as a result of the information.

6. Risk reduction vs delaying infection.

7. Harms of testing.

8. Contact tracing is impossible in most circumstances.

9. Testing creates anxiety and anchors our mind.

(See link for full article)

_________________

https://thevaccinereaction.org/2022/01/treatment-protocols-for-covid-19-an-overview/

Overview of COVID Treatment Protocols

by Barbara Cáceres
Published January 11, 2022
Excerpts:
Two years into the global pandemic of the novel coronavirus SARS-CoV-2, there is scant guidance from government agencies, universities, or professional medical organizations to help individuals recover from the SARS-CoV-2 infection that causes COVID-19 without the need for hospitalization.
Although the recovery rate for SARS-COV-2 infections is between 97 and 99.5 percent,4 and most people recover without hospitalization, there are currently 125,922 people hospitalized with COVID in the U.S., and numbers are on an upward trend.5 Recent estimates of costs associated with inpatient treatment for COVID average from $31,339 to $472,213 per person, depending upon the severity of the case.6

The article then highlights the following treatments:

Monoclonal antibodies

While a number of doctors have successfully treated COVID with monoclonal antibodies, there have been reported infusion-related reactions to activation of the immune system by the monoclonal antibodies, such as flushing, itching, shortness of breath and low blood pressure,14 and there is a possibility of immediate or delayed serious adverse events, including cytokine release syndrome, acute anaphylaxis, serum sickness, infections, cancer, autoimmune disease and cardiotoxicity.15 16 There is uncertainty about whether the currently available monoclonal antibodies are effective in treating the Omicron variant of SARS-CoV-2.17

Further, Dr. Ruby states the experimental monoclonal antibodies are like renting an army for a day, vs your own immune system which sticks around in case they are needed.

FLCCC Critical Care Alliance Protocols

https://covid19criticalcare.com/covid-19-protocols/  protocols and the science behind them for every stage of illness in twelve languages

Truth for Health Protocol

https://www.truthforhealth.org/patientguide/patient-treatment-guide/

Protocol of World Council for Health

https://worldcouncilforhealth.org/resources/early-covid-19-treatment-guidelines-a-practical-approach-to-home-based-care-for-healthy-families/

The Role of Zinc Ionophores

Controversy has surrounded the use of the drug ivermectin29 and other zinc ionophores.  A meta-analysis published in August 202133 concluded that there was moderate-certainty evidence for large reductions in COVID deaths using ivermectin. A June 2020 systematic review published in the medical journal Antibiotics34 identified ivermectin as having “antimicrobial, antiviral and anti-cancer properties.” The authors stated that the drug “is highly effective against many microorganisms including some viruses.”

Metabolic Syndrome Ignored As Risk Factor In COVID-19 Response

Despite the contribution of obesity and metabolic disorders to the disease burden of COVID, weight loss and prevention of metabolic disorders are not currently part of any published COVID public health policy.

Vaccination Under Emergency Use Authorization Not Allowed If Adequate Treatments Are Available

(See link for article)

Category:

research, Testing, Treatment, vaccines, Viruses