Archive for the ‘Treatment’ Category

Case of Cerebral Vasculitis Due to Neurobartonellosis

A case of cerebral vasculitis due to neurobartonellosis

Meryim Poursheykhi, Farhan Mithani, Tanu Garg, Christian Cajavilca, Siraya Jaijakul, Steve Fung, Richard Klucznik, Rajan Gadhia

We report a case of a 60-year-old right-handed woman with hypertension, hyperlipidemia, and hypothyroidism who presented with a three-week history of:

  • recurrent thunderclap headaches 
  • photophobia (aversion to light)
  • phonophobi (aversion to sound)
  • nausea
  • vomiting

She reported one brief episode of:

  • slurred speech
  • expressive aphasia (inability to understand and formulate language)
  • right facial droop
  • right hemiparesis suggestive of a TIA

Family history was remarkable for primary angiitis of the CNS (PACNS) in the mother. Neurologic examination was unremarkable. CT of the head was negative; CT angiography (CTA) of the head and neck suggested fibromuscular dysplasia in bilateral cervical internal carotid arteries and distal right vertebral artery. MRI of the brain showed no correlating abnormalities. A digital subtraction angiography (DSA) revealed multivessel intracranial medium and large vessel narrowing and fusiform dilatations, suggestive of reversible cerebral vasoconstriction syndrome (RCVS) vs vasculitis. Subsequent MR intracranial vessel wall imaging (IVWI) showed multifocal concentric vessel wall thickening and enhancement consistent with vasculitis (figure). Transcranial Doppler showed no evidence of elevated intracranial velocities. CSF studies were unremarkable with an opening pressure of 10 cm H2O, 2 white blood cells (normal 0–5/mm3), 2 red blood cells (normal 0–1/mm3), 58 mg/dL glucose (normal 40–70, serum glucose 87), 41 mg/dL protein (normal 15–45), normal Q-albumin ratio, normal IgG synthetic rate, and IgG index. Serum inflammatory and infectious studies had been negative thus far. Empiric high-dose IV steroids lead to complete symptom resolution.

Final infectious workup revealed strongly positive serum Bartonella IgM titer of 1:256 and negative IgG, consistent with her reported cat exposure.

She was started on an outpatient two-week course of doxycycline, rifampin, and oral steroids. Four weeks later, repeat vessel wall MRI and Bartonella serologies (IgM titer 1:80) showed improvement.

FigureVessel imaging

(A) Angiogram of the left internal carotid artery showing multifocal narrowing and fusiform dilatations (arrows) pretreatment. (B) Intracranial vessel wall MRI showing multifocal concentric vessel wall thickening and enhancement (arrows) pretreatment. (C) Intracranial vessel wall MRI showing reduction in vessel wall enhancement (arrows) posttreatment. (D) Magnetic resonance angiography (MRA) head showing multifocal stenoses (arrows) pretreatment. (E) MRA head showing improvement of stenoses (arrows) posttreatment.


We present an individual with symptoms initially concerning for RCVS vs vasculitis who was subsequently found to have secondary CNS vasculitis due to cat-scratch disease (CSD). To our knowledge, this is the first adult case of Bartonella henselae-associated CNS vasculitis, particularly without encephalopathy as the presenting symptom.

CSD typically presents with self-limited regional lymphadenopathy and fever.1 Neurologic complications are rare, occurring in 2% of cases with encephalopathy as the most common manifestation.2 Neuroretinitis, seizures, coma, myelopathies, and cranial and peripheral nerve involvement have also been reported. CNS vasculitis associated with CSD, however, has only been reported in 2 pediatric cases which presented with strokes.3,4

Diagnostically, identifying primary and secondary CNS vasculitis can be challenging both clinically and radiographically. No specific studies in serum or CSF are available for the diagnosis of CNS vasculitis. As in neurobartonellosis, CSF may be unremarkable or reveal nonspecific mild lymphocytic pleocytosis. Cerebral vasculopathies can present with similar luminal patterns, and therefore, imaging modalities such as DSA, magnetic resonance angiography (MRA), and CTA provide nonspecific results leading to difficulties identifying and differentiating between common etiologies of intracranial disease including vasospasm, atherosclerosis, and inflammation. Although DSA remains the gold standard for vessel imaging, it is an invasive study that provides information limited to the vessel lumen. Conversely, IVWI allows direct visualization of the vessel wall by subtracting the signal of blood in the vessel lumen and has shown to improve diagnostic specificity.5 In CNS vasculitis, IVWI shows multifocal concentric vessel wall enhancement and thickening as seen in our patient. In RCVS, vessel wall thickening may be present but with minimal or no enhancement.5

At this time, there is no clear evidence-based treatment regimen or duration for neurologic manifestations of CSD including CNS vasculitis.1 We recommend concomitant treatment of the infection with antibiotics and secondary vasculitis with high-dose steroids. Our patient received a 2-week combination of doxycycline 100 mg and rifampin 300 mg twice daily per current expert opinion.6 In addition, we initiated 5 days of high-dose IV steroids, followed by a 1-week oral steroid taper. To avoid recurrent invasive testing, we repeated IVWI 4 weeks later for treatment monitoring and found significant reduction in vessel wall enhancement (figure).

Our case reiterates the importance of ruling out rare causes of CNS vasculitis including assessing animal exposure before diagnosing PACNS. Detection of the etiology of vasculitis is essential to guide treatment and for prognostication. Noninvasive imaging such as an IVWI provides valuable diagnostic information and can be useful in assessing the treatment response over time by minimizing the need for repeat invasive DSA.

Study funding

No targeted funding reported.


M. Poursheykhi, F. Mithani, T. Garg, C. Cajavilca, S. Jaijakul, S. Fung, R. Klucznik, and R. Gadhia report no disclosures. Go to for full disclosures.


The authors thank Dr. Gadhia for his mentorship.



Since Bartonella is a vascular disease, it follows that it will cause vasculitis pretty much anywhere in the body.

It also creates tumors, many neurological manifestations including PANS and other mental health issues.

The concern with their treatment is it wasn’t long enough and she could relapse, which is common.  Bartonella, in my opinion, is as bad if not worse than Lyme disease and together it’s a one, two punch – you are out.

Marna Ericson’s work has demonstrated it to survive right along side a PICC line with antibiotics being pumped directly into the body:  The subject is her son who has chronic bartonellosis.




Remdesivir For COVID-19 – Not Backed By Results

The New COVID-19 Medication Isn’t Backed by Results

The HighWire does a deep dive into Anthony Fauci’s NIH-Funded study of Remdesivir, the new Covid treatment darling approved by the FDA today, and uncovered some shocking discoveries.

Analysis by Dr. Joseph MercolaFact Checked


  • Results from trials for the newest COVID-19 drug have disappointed. The first was stopped because of an adverse event; with the second, the WHO reported that more people died on the drug than off it; and the third investigation has significant problems with how the study was conducted
  • Gilead appears unfazed, insisting the drug is effective. The drug company is giving 940,000 vials of the drug to the U.S. government; the combination of scarcity and “generosity” will help set the price
  • Potential price gouging doesn’t upset scientists as much as the idea that a noneffective drug will be used; results from another study showed that using a combination of other drugs was effective

Big Pharma companies have worked hard to portray themselves as benevolent corporations that pour billions of dollars into the creation of drugs and vaccines. Biotech giant Gilead Sciences is no different. They manufacture remdesivir, the newest drug being hyped to treat SARS-CoV-2, which is discussed above in The High Wire video by Del Bigtree from Informed Consent Action Network.

The director of the National Institute of Allergy and Infectious Disease (NIAID), Anthony Fauci, along with the media, has been making public statements that cannot be scientifically supported.

In a press conference April 29, 2020, Fauci discussed the preliminary results of a remdesivir trial, and claimed the drug has a “clear-cut positive effect in diminishing the time to recovery. This is really quite important for a number of reasons.”1

Yet, the data from scientific studies do not support his claims. He went on to say that while a “31% improvement doesn’t seem like a knock-out 100%, it is a very important proof of concept, because what it has proven is that a drug can block this virus.”

Remdesivir Trial Stopped Early for ‘Benefit’

The most recent data on remdesivir were published in The New England Journal of Medicine (NEJM).2 Researchers concluded that the drug worked better than a placebo in reducing the amount of time it took adults to recover from COVID-19 while hospitalized. The study was stopped early for benefit.

However, as Peter Gøtzsche from the Institute for Scientific Freedom wrote, the benefit was not a reduction in mortality but, rather, in shortened hospital days — from 15 to 11 days.3 Bigtree and Gøtzsche (in the video) also pointed out there were several problems with the research design and, consequently, the data.4

The release of the study generated enthusiasm and triggered immediate action across many countries, including the U.S. The U.S. Food and Drug Administration issued an emergency use authorization May 1, 2020, for remdesivir, as the drug had not been approved for use. They said:5

“While there is limited information known about the safety and effectiveness of using remdesivir to treat people in the hospital with COVID-19, the investigational drug was shown in a clinical trial to shorten the time to recovery in some patients.”

Health and Human Services Secretary Alex Azar praised the speed at which the FDA approved the drug for emergency use, calling it “seamless cooperation between government and private industry” and an uncommon approval “two days after the National Institutes of Health’s clinical trial showed promising results …”6

Gøtzsche7 began his written commentary by comparing the expense of remdesivir to Tamiflu, both of which have been touted for treating their respective illnesses. Swiss drug maker Roche claimed Tamiflu, used for influenza, could shorten hospital admissions by 61% and reduce the use of antibiotics to treat respiratory tract infections by 55%.

When the data were finally available for review, however, it turned out that the claims could not be supported. When Tamiflu is used at the first sign of symptoms, it only shortens the length of the illness by 17 hours. In a seemingly parallel journey, the data from the study published in the NEJM appears to have been manipulated to generate statistically significant results, as detailed by Bigtree.

Bigtree points out that Bill Gates said we need a “miracle” treatment that is 95% effective:8 Yet, as Bigtree says, and as has been documented by the CDC,9 the Centre for Evidence-Based Medicine at the University of Oxford10 and corresponding studies,11 the majority of healthy people will recover from SARS-CoV-2 without any secondary effects.

The Results Don’t Live Up to the Promise

So, is Gates referring to the need for a 95% cure of the 5% who experience severe disease, since the majority don’t experience significant illness? This must happen to stop the production of a vaccine that will not have the time to undergo placebo-controlled, double-blind randomized studies to prove safety, which Fauci clearly believed was needed in February 2020:12

“We urgently need a safe and effective treatment for COVID-19. Although remdesivir has been administered to some patients with COVID-19, we do not have solid data to indicate it can improve clinical outcomes. A randomized, placebo-controlled trial is the gold standard for determining if an experimental treatment can benefit patients.”

In the video, Bigtree outlines the progress of the study, which includes several challenges:

  • The study evaluating the efficacy of remdesivir was designed as an “adaptive, randomized, double-blind, placebo-controlled study” performed by the NIAID, headed by Anthony Fauci.13 An adaptive study can be changed to protect patients when the results are obvious. This happens, for instance, if the participants receiving the intervention are doing so well that those on the placebo are moved to the intervention.
  • Although Bigtree mentions a seve-point scale, the researchers wrote the initial measurement was an eight-point scale to evaluate the participant results, one of which was death.
  • While Fauci has been claiming this study is a double-blind, placebo-controlled design, the placebo that was used was a lyophilized formulation containing hydrochloric acid or sodium hydroxide. The placebo group, in Bigtree’s words, is receiving a known poison — not saline.
  • One month after the study began, they increased the participants from 197 to 220 and then to 286 in each arm of the study: One received remdesivir and the other got the “placebo.” At this point, there were 572 participants. By the end of the study they had increased the total group to 1063.14
  • It was also noted that with the rising number of participants, if the group ran out of the hydrochloric acid placebo, they could substitute normal saline. As Bigtree pointed out, if the trial ran out of the substance being used as a placebo, they could use what should have been used in the first place, a substance without a known effect.

In the middle of the study (April 20, 2020), the researchers changed the primary outcome measures from eight15 to just three, none of which included measurement of mortality. The idea for the drug was to keep people from dying, but the researchers stopped measuring that important outcome. The final criteria were:16

  • Hospitalized, not requiring supplemental oxygen — no longer requires ongoing medical care
  • Not hospitalized, limitation on activities and/or requiring home oxygen
  • Not hospitalized, no limitations on activities

Gøtzsche Believes the Results of the Study Are Suspect

The increasing number of participants, the “placebo” and the reduction in primary outcome measurements resulted in the conclusion that: “Remdesivir was superior to placebo in shortening the time to recovery in adults hospitalized with Covid-19 and evidence of lower respiratory tract infection.”17

However, as Gøtzsche pointed out, physicians use highly subjective data to determine when their patient can be discharged home. He also reports that viral load was not measured by the research team and he questions how an antiviral can be successful if it doesn’t decrease viral load.

Gøtzsche believes the researchers violated “good scientific practice to fish for subgroup results that tell a better story. But this is what the two Danish professors did.”18 He went on to describe the difference between what the Danish researchers were proclaiming and what’s evident from the statistical analysis, writing:

“What is important is that the trial statisticians tested if the primary outcome was different in the various patient categories, those who did not need oxygen, those who needed oxygen, those who needed noninvasive ventilation, and those who needed invasive mechanical ventilation or extracorporeal membrane oxygenation (the most severely ill patients).

There was no difference, which makes it even worse that the two Danish professors embarked on a fishing expedition in the data focusing on only 23 deaths in subgroup 5 out of a total of 86 deaths …”

Other Remdesivir Studies Don’t Yield Positive Results

During the same time period, another team evaluated the use of remdesivir in patients with severe COVID-19. They conducted a randomized, double-blind, placebo-controlled, multicenter trial and enrolled patients who were 18 years and older with lab-confirmed infection in 10 hospitals in China.19

The patients had an oxygen saturation of 94% or less and radiologically confirmed pneumonia. The primary endpoint measurement was how long it took for clinical improvement, measured up to 28 days. Adverse events were reported in 66% of those receiving remdesivir versus 50% of those getting the placebo.

The drug was stopped early in 12% of the patients for adverse effects after researchers found there was no statistically significant clinical benefit to receiving it.

Before the release of the remdesivir study published in The New England Journal of Medicine and the second study in The Lancet, Bloomberg20 reported that the World Health Organization accidentally posted results of a third study.

While the summary was removed, details were published that showed “the drug wasn’t associated with patients getting better more quickly; and 13.9% of patients getting the drug died, versus 12.8% getting standard care.”

Gilead Sciences quickly took action. Infectious disease expert Frederick Hayden, who was involved with the study, told a reporter, “That is not correct. My interpretation of them is not consistent with that headline.”21

Gilead said the study was stopped because of low enrollment, adding that the “trends in the data suggest a potential benefit for remdesivir, particularly among patients treated early,” and it was expected that the following two studies would “add to a growing but still inconclusive body of evidence for remdesivir.”

Gilead appeared to be referring to the study published in The Lancet, whose authors concluded that the drug was not effective, as well as the subsequent study published in The New England Journal of Medicine, which had several problems with the data.

Remdesivir Hype Lining Gilead’s Pockets

On the same day The Lancet study was published — the one whose authors concluded the drug was not effective — Gilead announced “positive data emerging from the National Institute of Allergy and Infectious Disease (NIAID) study.”22 This implies the company may be relying on the court of public opinion, which is swayed by public relations, as opposed to scientific data.

The Alliance for Human Research Protection23 reports that Fauci has a vested interest in the development of remdesivir, and it was he who declared the results to be “highly significant.” When he was asked about the results of the study published in The Lancet, he dismissed it as “not adequate.”

Between the public relations campaign and the excitement Gilead has generated in investors and the public, they may reap a significant financial reward. The company has set up distribution in 127 countries and is expecting to begin commercial sales in June. The drug was initially developed as a potential treatment against Ebola using $79 million in U.S. funding.24

The company donated 940,000 vials to the U.S. federal government, which is in turn sending them to state health departments. However, it is not enough to treat all patients.

The state of Virginia is holding a lottery for the most severely ill patients, while doctors in Alabama have set up a task force to identify those who should receive it. The initial scarcity and apparent “generosity” will likely help Gilead set its price on the medication.

Yet it’s not the potential for price gouging that upsets most scientists. William Haseltine, a scientist whose life’s work is studying viruses and who helped lead the government’s response against HIV/AIDS, explains:

“Remdesivir doesn’t work at all, as far as I can tell, or has only a minor effect. It is comparable to Tamiflu and maybe not even as good.”25

You Have At-Home Choices

Buried in the hype of remdesivir was another recently released published study in The Lancet,26which showed that a combination of interferon beta-1b, lopinavir–ritonavir, and ribavirin was a safe and effective method of reducing viral shedding and lowering hospital admissions in those who had confirmed mild-to-moderate COVID-19.

You have options to protect your health and potentially lessen the severity of the infection if you do get sick. On my Coronavirus Resource Page you’ll find some of the latest news stories and my top tips to help combat the virus. These include ensuring adequate serum levels of vitamin D, getting enough sleep, protecting your gut microbiome and using micronutrients that have demonstrated antiviral effects.

+ Sources and References



Remdesivir isn’t cheap.  In fact, this article states it costs $320 per vial and will be sold for $3,120 per 6 vial treatment: That’s a lot of money for a drug that hasn’t even been shown to lower viral load.

Hydroxychloroquine in the other hand costs $1 per treatment, while chloroquine costs a measly 30 cents!

The article also points out an ugly conflict of interest web between Gilead, the manufacturer of Remdesivir and UNITAID which Soros, Gates, and the Clinton Health Access Initiative, are large investors – with Drs. Fauci and Birx associated with the Clinton Health Access initiative.  And of course, Dr. Fauci has worked with Gilead for a long, long time. Government employees should not be allowed to have financial ties to manufacturing companies and then turn around and make public health policy.


Approximately $70 million in U.S. taxpayer funding began Gilead’s partnership with the U.S. Army, Centers for Disease Control and Prevention (CDC) and National Institutes of Health (NIH) to develop remdesivir. Initially for treating Ebola, it failed to show benefit and was shelved. If remdesivir is used to treat COVID-19, Gilead shareholders, not the taxpayers, will profit.

Early results of the first clinical trial of remdesivir against placebo in coronavirus showed modest benefits, according to The New York Times. Surviving patients given remdesivir were discharged four days sooner than patients given placebo, though no criteria were given for determining improvement. Death rates were not significantly different. About 25% of patients receiving remdesivir had potentially severe side effects, including multiple organ dysfunction, septic shock, acute kidney injury and low blood pressure. Another 23% showed evidence on lab tests of liver damage.

Gilead’s own press release revealed the side effect of acute respiratory failure in 6% of patients in the remdesivir five-day treatment group, and 10.7% of patients in the 10-day treatment group, clearly ominous findings with a drug designed to treat respiratory failure caused by COVID-19.

Dr. Steven Nissen, a Cleveland Clinic cardiologist who has conducted dozens of clinical trials, explained to The New York Times:

The disclosure of trial results in a political setting, before peer review or publication, is very unusual. Scientists will need to see figures on harms associated with the drug in order to assess its benefits. … This is too important to be handled in such a sloppy fashion.”

Going back to 1997, Donald Rumsfeld chaired the Board of Directors at Gilead and after 2001 he held share packages valued at $5-25 Million. Gilead originally developed Tamiflu. George P Shultz, US Secretary of State also was on the board. He sold stocks at a value of more than $7 million. CA governor’s Pete Wilson’s wife also sat on the board.

‘I don’t know of any biotech company that’s’ so politically well-connected [as Gilead],‘ Andrew McDonald, of the analyst firm Think Equity Partners, told Fortune.” (Source: “Virus Mania, How the Medical Industry Continually Invents Epidemics Making Billion Dollar Profits At Our Expense”)

Disseminated Lyme Disease More Likely In Those With Weakened Immune System


Sick woman sitting on couch with disseminated Lyme disease

Individuals with a weakened immune system are more susceptible to developing infections, such as COVID-19. A review study has also found that people with compromised immune systems are at a greater risk of developing disseminated Lyme disease. The authors of “Erythema Migrans: Course and Outcome in Patients Treated With Rituximab” investigated patients diagnosed with Lyme disease, who were also taking Rituximab, a medication known to impair immunity. [1]

The small study examined the risk of developing disseminated Lyme disease for people with weakened immune systems. Researchers enrolled 7 patients with an EM (erythema migrans) rash who were diagnosed with Lyme disease. All of the patients were receiving Rituximab for another underlying medical condition. Out of the 7 patients, 4 were also being treated with additional immunosuppressant drugs (e.g., corticosteroids, methotrexate, and bortezomid).

“Rituximab is the anti-CD20 monoclonal antibody that influences B cells and consequently impairs secretion of antibodies, antigen presentation, and secretion of cytokines,” writes Maraspin and colleagues.

Rituximab is used for non-Hodgkin lymphoma, rheumatoid arthritis, chronic lymphocytic leukemia, and granulomatosis with polyangiitis (Wegener granulomatosis).

Signs of disseminated Lyme disease

According to the authors, 43% of the patients treated with Rituximab showed unusually high signs of disseminated Lyme disease, compared to 8% of immunocompetent individuals.

The isolation rates of Borrelia from the blood before antibiotic treatment were also unusually high (40%) when compared with immunocompetent patients (<2%).

“Impaired immunity might be an explanation for the complicated course of LB (signs of disseminated LB or unfavorable outcome after antibiotic treatment) present in 57% of our patients, but rarely seen in immunocompetent adult patients with EM, of whom only about 8% have disseminated disease and approximately 10% have treatment failure, most often the presence of LB-associated symptoms,” the authors write.

In their study, 3 of the patients with multiple EM rashes were treated with intravenous antibiotics. The remaining individuals received oral antibiotics.

READ MORE: Lyme disease manifests as autoimmune disorder

One patient, a 65-year-old woman, failed initial treatment. “Her skin lesion persisted for >2 months after the start of treatment with doxycycline,” explains Maraspin. “However, it disappeared after retreatment with amoxicillin and the subsequent clinical course was uneventful.”

At their 1-year follow-up, none of the patients had any objective (or physical) signs of Lyme disease. However, the authors did not mention the presence of other symptoms, such as fatigue, pain, and cognitive problems.

Retreatment for immunocompromised patients 

Meanwhile, a study by Maraspin and colleagues reports that 25% of Lyme disease patients who had received immunosuppressive drugs, such as adalimumab, infliximab, etanercept, golimumab, failed treatment for Lyme disease. Three of the four patients required retreatment.

Patients with weakened immune systems were also more likely (18.8%) to develop signs of disseminated Lyme disease when compared to Lyme disease patients who were immunocompetent.

Editors note: The increased chance of disseminated Lyme disease in patients with impaired immunity needs further study. I would also address the risk of treatment failures on other outcomes including fatigue, pain, and cognitive problems.

  1. Maraspin, V., et al. (2019). “Erythema Migrans: Course and Outcome in Patients Treated With Rituximab.” Open Forum Infect Dis 6(7): ofz292.



The one question that hasn’t been answered fully is what exactly is causing this impaired immunity?  While many would love to solely blame the patient’s immune system, many have yet to consider the interplay between how over time these pathogens directly impact the immune system negatively.  From experience I can state that most Lyme/MSIDS patients, prior to becoming infected, are some of the healthiest people I know.  They eat right, exercise, love the outdoors, and take their health seriously.

Until the answer to impaired immunity is determined (and it may vary from patient to patient), patients will not be treated appropriately.

For more:

Rocky Mountain Spotted Fever Can Be Deadly: How to Prevent, Diagnose, & Treat it

Rocky Mountain Spotted Fever Can Be Deadly: How to Prevent, Diagnose, and Treat the Tick-Borne Disease

Rocky Mountain Spotted Fever Can Be Deadly: How to Prevent, Diagnose, and Treat the Tick-Borne Disease

by Jenny Lelwica Buttaccio
Posted 6/11/20

When it comes to tick-borne diseases (TBD), there are several other infections with the potential to make you sick beyond the best-known Borrelia burgdorferi, the bacteria that causes Lyme disease.

For starters, there are well-known Lyme disease coinfections like Bartonella and Babesia that may compound Lyme symptoms and add insult to injury for many people. Cases of these are on the rise as environmental and climate patterns continue to shift in such a way that supports tick populations, and as housing developments expand into wooded areas, bringing people, animals, and ticks in increasingly close proximity to one another.

Additionally, there’s an emerging threat of lesser-known pathogens that seem to garner media attention each year. One such infectious agent is Rickettsia rickettsii, a bacteria that causes Rocky Mountain spotted fever (RMSF).

Rickettsia has a preference for infecting cells lining blood vessels, specifically endothelial cells — this makes for a much more virulent bacteria,” says Dr. Bill Rawls, MD, Medical Director of RawlsMD and Vital Plan.

Dermacentor Reticulatus On Green Leaf. Also Known As The Ornate Cow Tick, Ornate Dog Tick, Meadow Tick, And Marsh Tick. Family Ixodidae. Ticks Are Carriers Of Dangerous Diseases.

RMSF is spread through the bite of an infected tick. Whereas black-legged ticks are the arachnids responsible for Lyme disease, the Rocky Mountain wood tick, the brown dog tick, and the American dog tick are the chief transmitters of RMSF.

Prompt medical intervention is crucial for a successful recovery from RMSF — the consequence of delaying treatment can be life-threatening. Here, we’ll discuss the broad strokes of RMSF, including signs, symptoms, testing, and treatment.

An Overview of Rocky Mountain Spotted Fever

RMSF is a gram-negative obligate intracellular bacteria — in other words, it’s a parasitic-like microorganism that grows and reproduces inside a host’s cells. As a pathogenic disease, it was first reported in the 1920s.

The disease is part of a larger category called Spotted Fever Rickettsiosis (SFR). In 2010, the name was given to signify a group of related conditions caused by the Rickettsia bacteria for which the available serologic testing can’t discriminate between the different species of the disease-causing bacteria.

Each year, there are approximately 2,000 new cases in the United States, as reported by the Centers for Disease Control and Prevention (CDC). However, in 2017 RMSF cases jumped to 6,248, with marginally fewer cases reported in 2018.

To better understand RMSF, it helps to know some facts about testing methods, times of the year when ticks are most active, and the profile of people who are most at risk of contracting the illness.

1. The Annual Incidences of RMSF Aren’t Precise.

Because the testing doesn’t identify which species of Rickettsia is the culprit, there’s no way to tell how many cases are specific to RMSF versus other Rickettsial diseases that may cause less serious types of spotted fevers. However, the mortality rate for RMSF may be between 5% and 10%, according to a review in The New England Journal of Medicine. By comparison, related Rickettsial bacteria like Ehrlichia and Anaplasmosis have fatality rates of 3% and 1%, respectively.

2. The Transmission of RMSF Varies Depending on Geography and Time of Year.

Ticks carrying RMSF tend to be most active in May through August, but there’s some variability due to geographic location in the U.S. and the type of tick that’s carrying the pathogen. Like Lyme disease, ticks carrying RMSF may be active year-round in parts of the country where temperatures stay above freezing.

Although RMSF can be found throughout the United States, the majority of cases come from these five states:

  1. Arkansas
  2. Missouri
  3. North Carolina
  4. Tennessee
  5. Virginia

3. Certain Individuals May Be More At Risk of Acquiring RMSF.

People who live near wooded areas or in an area of the country known to be hospitable to ticks are at risk of acquiring the infection. Additional information from the CDC indicates:

  • Reported cases of RMSF occur more often in men than women.
  • Most cases occur in individuals over the age of 40. However, the mortality rate of RMSF is highest among children in the 10 and under age group.
  • People with glucose-6-phosphate dehydrogenase (G6PD) deficiency, a genetic disorder affecting red blood cells, show a higher propensity for the infection.
  • Immunocompromised individuals are more likely to require hospitalization from RMSF.

Symptoms of Rocky Mountain Spotted Fever

Because RMSF attacks the vascular system, one of the most vulnerable places in your body, severe illness is much more likely than you might encounter with other TBDs. On average, symptoms of RMSF generally start 12 days after a tick bite, but it can range from 5 to 21 days.

black woman with a fever, husband holding hand to her forehead

The telltale signs of infection include high fever, chills, muscle aches, and a rash. “Certainly, a history of a tick bite is a tipoff to infection,” says Dr. Rawls. “But because tick bites are painless and people often are not aware of being bitten, that history is not always helpful.”

Let’s take a closer look at the signs and symptoms of RMSF:

  • Fever
  • Chills
  • Headache
  • Muscle aches
  • Joint pain
  • Rash
  • Confusion
  • Sensitivity to light
  • Feeling unwell (malaise)
  • Thirst
  • Abdominal pain
  • Nausea
  • Vomiting
  • Diarrhea
  • Changes in appetite

An important note about the rash: Typically, the rash associated with RMSF develops two to five days after the onset of fever. However, it can occur later in the course of the illness, even after treatment is started, says Dr. Rawls.

Small, pink, non-itchy spots, with a diameter of 1 to 5 millimeters, first show up on wrists, forearms, and ankles. The spots may spread to the trunk of the body and the soles of the feet as well. As the disease progresses, the spots may become red or purple, which is known as petechiae (puh-TEE-kee-uh).

However, just as some people don’t develop a rash when they contract Lyme disease, not everyone gets a rash with RMSF either.

Diagnosis of Rocky Mountain Spotted Fever

“Diagnosis is a real challenge because Rocky Mountain spotted fever resembles other, more common infectious diseases,” says Dr. Rawls. “But it’s critical to initiate therapy early in the course of the disease, especially if you live in an endemic area.”

Test tube full of blood in lab employees hand

Because time is of the essence, your healthcare provider will likely initiate treatment first, and then test to confirm the diagnosis of RMSF. Testing methods that may be used include:

  1. General labs: Complete blood count (CBC), complete metabolic panel (CMP), liver panel, etc.
  2. Indirect Immunofluorescent Assay (IFA): An antibody test that measures IgG and IgM antibodies for R. rickettsii
  3. Polymerase chain reaction (PCR): This is a DNA test that may be most helpful when used to test a biopsy of the rash or lesion. Concentrations of R. rickettsii in the blood may be low, so a negative PCR doesn’t eliminate the diagnosis of RMSF.
  4. Urinalyses: A test that may be useful to detect blood or protein in the urine

Treatment of Rocky Mountain Spotted Fever

“There are a lot of variables that play into why a person becomes sick with Rocky Mountain spotted fever, but if they become ill, they become very ill,” says Dr. Rawls. “It’s a microbe where, if you develop symptoms, you need antibiotics to try to knock down the infection as quickly as possible.”

Serious complications, like the loss of extremities (fingers, toes, or limbs), can occur due to a decrease in circulation, especially if treatment is delayed. For acute RMSF, the standard of care is doxycycline. “Herbal therapy shouldn’t be used as the primary therapy, but it can be used as a supportive measure,” advises Dr. Rawls.

The following are treatment recommendations, according to the CDC:

  • Doxycycline dose in an adult: 100 mg twice daily
  • Doxycycline dose in children < 45 kg (100 lbs): 2.2 mg / kg twice daily

Antibiotic therapy should be administered for 30 days, suggests Dr. Rawls, or until three days after the fever subsides. At a minimum, treatment with antibiotics should be no shorter than five to seven days as per CDC guidelines. If a patient doesn’t respond to doxycycline, that’s an indication that acute tick-borne infection isn’t present, and other infections such as a virus or Babesia may be causing symptoms.

If an individual doesn’t tolerate doxycycline, a broad-spectrum antibiotic called chloramphenicol may be used. However, this drug carries with it a high potential for side effects. The dosage for chloramphenicol is12.5 mg per kg of body weight orally every 6 hours. In certain cases, IV antibiotics may be required in some people with acute RMSF.

Incorporating Herbal Therapy

Although treatment for RMSF requires antibiotic therapy, herbs can be used to protect vascular cells, promote healing, and act as a complement to drug therapy. However, remember to consult with your doctor before adding natural remedies to your existing treatment protocol.

Essential oil of hawthorn, selective focus

Here are some of Dr. Rawls’ preferred herbs and natural ingredients of choice:

1. To improve circulation and to enhance blood flow:

  • Hawthorne
  • French maritime pine bark
  • Lutein and zeaxanthin (antioxidants called carotenoids found in brightly-colored vegetables like carrots, squash, kale, and spinach)

2. To increase oxygenation of the tissues in the body and bolster the immune system:

3. To help decrease your microbial load and provide antioxidant support:

Final Thoughts

Ultimately, tick prevention is the key to avoiding RMSF. “We all should be vigilant about ticks,” urges Dr. Rawl. “Pay attention. If you get a tick bite, if you end up with symptoms of fever or a rash, you need to see a healthcare provider for that immediately. The quicker you get treatment, the less likely you are to have long-term ramifications.”

Dr. Rawls is a physician who overcame Lyme disease through natural herbal therapy. You can learn more about Lyme disease in Dr. Rawls’ new best selling book, Unlocking Lyme.
You can also learn about Dr. Rawls’ personal journey in overcoming Lyme disease and fibromyalgia in his popular blog post, My Chronic Lyme Journey.

1. Dumler JS, Walker DH. Rocky Mountain spotted fever–changing ecology and persisting virulence. N Engl J Med. 2005;353(6):551‐553. doi: 10.1056/NEJMp058138
2. Lyme and Other Tickborne Disease Increasing. Centers for Disease Control and Prevention website.
3. Rocky Mountain Spotted Fever Epidemiology and Statistics. Centers for Disease Control and Prevention website.
4. Rocky Mountain Spotted Fever Treatment. Centers for Disease Control and Prevention website.
5. Rocky Mountain Spotted Fever. MedlinePlus website.
RMSF, normally transmitted by the American dog tick and the closely related Rocky Mountain wood tick, has also been spread by the brown dog tick — a completely different species.  And here, we discover it’s been found in the Asian Longhorned tick and is capable of being transmitted within ticks through ova.
This is a great example of how ticks are spreading things they are not known to spread, as well as the fact they are now being found in new places and it has nothing to do with the weather:

Dr. Meryl Nass Discovers Hydroxychloroquine Experiments Were Designed to Kill COVID Patients- How Many Were Murdered?

This is quite a damning article and is a ‘must read.’ In brief, Dr. Nass exposes that the doses used in the HCQ trials were high enough to kill a horse.  Again, “the dose makes the poison.”

Dr. Meryl Nass Discovers Hydroxychloroquine Experiments Were Designed to Kill COVID Patients – How Many Were Murdered?

June 25, 2020

Covid-19 Has Turned Public Health Into a Lethal, Patient-Killing Experimental Endeavor

by Vera Sharav
Alliance for Human Research Protection

Dr. Meryl Nass has uncovered a hornet’s nest of government sponsored Hydroxychloroquine experiments that were designed to kill severely ill, Covid-19 hospitalized patients. On June 14th Dr. Nass first identified two Covid-19 experiments in which massive, high toxic doses – four times higher than safe of hydroxychloroquine were being given to severely ill hospitalized patients in intensive care units.

  • Solidarity was being conducted by the World Health Organization, on 3500 Covid-19 patients at 400 hospitals, across 35 countries. The trial was suspended following the fraudulent Surgisphere report in The Lancet that claimed 35% higher death rates in patients receiving Hydroxychloroquine. But when The Lancet retracted the report, the WHO resumed the Solidarity trial. More than 100 countries expressed interest in participating in the trial.
  • Recovery experiment used very similar doses. It was sponsored by the Wellcome Trust (GlaxoSmithKline) and the Bill and Melinda Gates Foundation and the UK government. The experiment was conducted at Oxford University, on 1,542 patients of these 396 patients (25.7%) who were in the high dose Hydroxychloroquine arm, died.
Update: After Dr. Nass’ discovery was publicly disseminated, the WHO suspended the trial on Wednesday June 17th.

On Friday, June 19th, Dr. Nass uncovered a third, “Even Worse” hydroxychloroquine experiment. REMAP targets patients who are on a ventilator, or in shock – i.e., near death. Such patients are hardly capable of giving consent. Rather than attempting to save their lives, they are being used given multiple high doses of hydroxychloroquine and other drugs whose combination is contraindicated.

Of note: All the online protocols have been stamped “Not for IRB (Institutional Review Board) submission.

This is an ongoing medical atrocity being perpetrated by medical doctors at 200 sites in 14 countries: include: Australia, Belgium, Canada, Croatia, Germany, Hungary, Ireland, Netherlands, New Zealand, Portugal, Romania, Spain, United Kingdom, and the United States of America.

Since all medicines are potential poison at high doses, why one wonders, are influential academic physicians and international public health institutions designing and conducting experiments that expose extremely vulnerable patients to poisonous levels of the drug Hydroxychloroquin?

As recognized by the Swiss physician Paracelsus, “the Hippocrates of the Renaissance”:

“What is there that is not poison? All things are poison and nothing is without poison. Solely the dose determines that a thing is not a poison.”

His insight is as relevant today as it was in the 16th century.

Dr. Meryl Nass is a physician practicing individualized medicine in Maine, in accordance with the Hippocratic Oath. She is a longtime member of the board of the Alliance for Human Research Protection.


Friday, June 19, 2020
Even worse than ‘Recovery,’ potentially lethal hydroxychloroquine study in patients near death

What could be worse than giving potentially lethal doses of hydroxychloroquine to Hospitalized Covid-19 patients?

The REMAP-Covid study is using the same HCQ dose as the Recovery trial for 6 days.  But it is even worse for the following reasons:

  1. You have to be close to death, either on a ventilator or in shock, on pressor medications, to be included in the trial, according to the trial documents.  However, in a talk by Professor Anthony Gordon, HFNO, CPAP and NIV are additionally said to be inclusion criteria.
  2. You may receive HCQ alone, or HCQ in combination with 2 more drugs, lopinavir/ritonavir.  Yet lopinavir/ritonavir predisposes to QT prolongation, as does HCQ, and the drug label states, “Avoid use in combination with QTc- or PR-interval prolonging drugs.”
  3. Patients who are in shock or on a ventilator may be unable to give their consent to enroll in a clinical trial. But the trial investigators have deemed that consent may not be required“For patients who are not competent to consent, either prospective agreement or entry via waiver of consent or some form of deferred consent can be applied, as required by an appropriate ethical review body.”
  4. For patients too sick to swallow a pill, the drug will be administered via a feeding tube. This could entail an extra procedure for patients.

From the Covid protocol page 23:

“Dosing will be hydroxychloroquine administered by the enteral route. A loading dose is important because of the large volume of distribution. The loading dose will be 800 mg, administered 6-hourly, until 2 doses have been administered. Subsequently, starting 12 hours after the first loading dose, the dose will be 400 mg administered 12-hourly for 12 doses. The preferred method of administration is tablets swallowed whole but, if a patient is unable to swallow, crushed tablets dispersed in water can be administered via an enteral tube (a large bore gastric tube is preferred). No dose adjustment is required when hydroxychloroquine is administered via a gastric tube. No dose adjustment is necessary for renal dysfunction or concomitant use of renal replacement therapy. Clinicians should consider a dose adjustment in the presence of liver failure, however no dose adjustment is necessary for abnormal liver function tests in the absence of liver failure.

This is 2400 mg hydroxychloroquine in the first 24 hrs, over 1.86 g of the “base,” then 800 mg/day for 5 more days or until discharge from the ICU, or 6.4 g total. Dosing fails to take into account weight, renal and hepatic function.

The ignorant doctors who justified toxic doses by invoking ‘volume of distribution’ (which is 40,000 liters) failed to notice that the high ‘volume of distribution’ is an artifact related to the drug accumulating in tissue as opposed to plasma.  Drug levels in lung are 200-700 times higher than in plasma. Furthermore,

renal and hepatic insufficiency lead to higher plasma concentrations for a given daily dose and raise the risk of toxicity.

WHO’s consultant Weniger reported in 1979 that a single dose of 1.5-2 g of chloroquine “base” “may be fatal.” A detailed discussion of therapeutic and toxic doses of chloroquine and hydroxychloroquine can be found in my article of June 14. I acknowledge that hydroxychloroquine is a bit less toxic than chloroquine.  But this trial studies the most fragile human beings, and if the trial investigators were unsure of the right dose, they should have “started low and gone slow” as clinicians are advised to do.

The REMAP study protocol acknowledges that the combination of lopinavir/ritonavir and hydroxychloroquine increases the risk of ventricular arrhythmia, but states that the risk is mitigated because patients this sick will be on cardiac monitors, with QTc monitoring.  However, it fails to say that the most likely arrhythmia in this setting is torsade de points, which is very difficult to treat.  Patients who are already critically ill are unlikely to survive if it occurs.  So why use such an excessive hydroxychloroquine dose on these, or any, patients, and risk it?  That is not explained.

The REMAP clinical trial is ongoing in 200 sites in 14 countries. They include: Australia, Belgium, Canada, Croatia, Germany, Hungary, Ireland, Netherlands, New Zealand, Portugal, Romania, Spain, United Kingdom, USA.

All their online protocols have been stamped “Not for IRB (Institutional Review Board) submission,” which makes one wonder what was changed when the trial arms were put before IRBs for approval.

Five UK chief medical officers wrote a “Dear Colleague” letter, begging physicians to enroll their Covid patients in clinical trials, including ‘Recovery’ and REMAP, and discouraging “off-label” treatments for Covid outside of trials.  Did they know they were asking treating physicians to significantly up the risk of death for their patients?  Are they aware that as of today, June 19, the UK has had more deaths from Covid-19 than any country in the world outside the US and Brazil, with 5 and 3 times the UK population, respectively.

Why is public health being turned on its head?  This is the third major, multicenter clinical trial of hydroxychloroquine testing toxic doses on Covid patients.  The Recovery and Solidarity trials (with almost identical toxic HCQ doses as REMAP) abruptly ended their hydroxychloroquine studies in the past two weeks, coincidentally as people began noticing the excessive doses, especially on Twitter.

Who or what is willing to maim and kill patients in order to to kill hydroxychloroquine’s use in Covid-19?


WHO and UK trials using potentially lethal hydroxychloroquine dose–according to WHO consultant, posted June 14, 2020

The Solidarity Trial is a WHO-led conglomeration of many national trials of treatments for Covid-19. Per the WHO:

As of 3 June 2020, more than 3500 patients have been recruited in 35 countries, with over 400 hospitals actively recruiting patients. Overall, over 100 countries have joined or expressed an interest in joining the trial, and WHO is actively supporting 60 of them…

The hydroxychloroquine arm of the Solidarity trials restarted enrolling patients June 3, after being halted  May 25 by WHO Director-General Dr. Tedros Ghebreyesus and the Executive Group of the Solidarity Trial. (The hydroxychloroquine (HCQ) arm of the trials was stopped after publication of the Lancet Surgisphere study, which claimed 35% higher death rates in patients who received hydroxychloroquine, but the study was retracted when no one could verify that the Surgisphere database existed).

Below are the drugs being tested in Solidarity:

  • Remdesivir
  • Hydroxychloroquine
  • Lopinavir with Ritonavir
  • Lopinavir with Ritonavir plus Interferon beta-1a.

However, the doses were not specified on WHO’s list of the drugs to be trialed, nor were the actual doses specified, surprisingly, in WHO’s consultation on chloroquine (CQ) dosing, dated April 8. Instead, the introduction of the report of that meeting notes,

“The chloroquine or hydroxychloroquine schedule selected for the trial includes two oral loading doses (250 mg per tablet CQ or 200 mg per tablet HCQ), then oral twice-daily maintenance doses for ten days. This meeting convened to discuss the appropriateness of the selected doses for the trial.”

Last week, I was alerted to the fact that India’s ICMR, its official medical research agency, had written to the WHO, telling WHO that the hydroxychloroquine doses being used in the Solidarity trial were 4 times higher than the doses being used in India.  Then I learned that Singapore has been hesitant to participate in the WHO trial, due to the hydroxychloroquine dose.

The UK “Recovery” trial was one part of the international Solidarity conglomeration of clinical trials.  The trial ended its HCQ arm on June 4, reporting no benefit. In-hospital mortality of the 1542 patients receiving hydroxychloroquine was 25.7%, or 396 people.

The Recovery trial Study Protocol notes it is funded in part by the Wellcome Trust and the Bill and Melinda Gates Foundation, and by UK government agencies.  The Protocol provides the doses of hydroxychloroquine used, on page 22.  Twitter users began to notice a dosing issue, with hashtag #Recoverygate.

The quote from the WHO report on dosing, 4 paragraphs ago, seems to be deliberately vague or even misleading, as the actual dose used in the Solidarity and Recovery trials is

  • 12 tablets during the first 24 hours (800mg initial dose, 800 mg six hours later, 400 mg 6 hrs later, 400 mg 6 hours later),
  • then 400 mg every 12 hours for 9 more days.
  • This is 2,400 mg during the first 24 hours, and a cumulative dose of 9.2 grams over 10 days.

While I could not find the WHO HCQ dosing on the WHO website, co-Principal Investigators of the Recovery trial, Drs. Peter Horby and Martin Landray, claimed they followed the WHO dosing.  Landray also told the periodical Paris Soir he was using the same hydroxychloroquine dose used for amebiasis.  However, the accepted use for HCQ in amebiasis is only for a liver abscess and only then in pregnancy, when other drugs cannot be used.  That dose is 600 mg per day for 2 days, then 300 mg per day, less than half the Recovery dose.  Professor Horby said that Paris Soir misinterpreted Landray’s comments, but Paris Soir said Landray had confirmed what he told them in an email.

We also know, from an official Belgian guideline document issued June 8, that high doses were used not only by Recovery in the UK, but also by the Discovery trial in the EU and by the WHO.

We also know that in Brazil, both a high dose and a low dose were trialed, and by April 17 the high dose arm was stopped prematurely due to an excess of deaths.  The low dose trial continues in Brazil.

How is the drug hydroxychloroquine normally used?  For chronic daily use in systemic lupus erythematosus or rheumatoid arthritis, patients usually receive between 200 and 400 mg daily.  In acute Q fever, 600 mg daily may be given at the start of treatment.

We also know from WHO’s March 13 Informal consultation on the potential role of chloroquine that the Gates Foundation had been studying the drug’s pharmacokinetics, and of the 25 participants at this meeting, 5 were from the Gates Foundation.

The only treatment dose mentioned in their report was in a paragraph about preventive doses.  It said,

“Higher doses would be considered for treatment, i.e., 10mg/kg base, followed by 5mg/kg twice daily for seven days.”

What is the “base”?  A 200 mg dose of chloroquine or hydroxychloroquine contains 155 mg “base” drug.

The typical 70 kg person would, if this suggestion had been followed, receive 700 mg base, or  900 mg of hydroxychloroquine, as a loading dose. Generally, a loading dose refers only to a first dose, not to several additional doses within 24 hours, but it can potentially refer to more.

What is a toxic dose?  All experts agree. “… chloroquine has a small toxic to therapeutic margin,” according to Goldfrank’s Toxicologic Emergencies It is very safe when used correctly in the right patients, but a bit more can potentially kill.  Prof. Nicholas White, who attended both WHO consultations on the chloroquines, has mentioned this.

The WHO hired a consultant to explore the toxicity of hydroxychloroquine in 1979. The consultant, H. Weniger, looked at 335 episodes of adult poisoning by chloroquine drugs.  Weniger on page 5 notes that a single dose of 1.5-2 grams of hydroxychloroquine base “may be fatal.

The Recovery trial used 1.860 grams hydroxychloroquine base (equal to 2400 mg of hydroxychloroquine) in the first 24 hours for treatment of already very ill, hospitalized Covid-19 patients, a potentially lethal dose.

The dose used in the Recovery trial is not recommended for therapy of any medical condition, which I confirmed with Goodman and Gilman’s Pharmacology textbook, the drug’s label, and the online medical encyclopedia UptoDate.

This excessive dose apparently continues to be used in WHO Solidarity trials in countries around the world.

It appears that the Solidarity trials are not testing the benefits of HCQ on Covid-19, but rather testing whether patients tolerate toxic, nontherapeutic doses.

The WHO Solidarity trials, in order to rapidly enroll patients and spare clinicians a lot of paperwork, collect only limited information on side effects.  No information has yet been provided regarding causes of death in the completed hydroxychloroquine arm of the Recovery trial, in which 396 patients died.

The Solidarity trial design being employed by WHO may help obscure whether mortality is due to drug toxicity (in which case, one would expect cause of death to be arrhythmias such as torsade de points, neuropsychiatric effects, or hypoglycemia) versus Covid-19.

The WHO report of its meeting on chloroquine dosing states,

“Although the preponderance of opinion tilted towards a reasonable benefit risk profile for the intervention, there was some scepticism about what was considered a ‘minimalistic safety data collection’ currently included in the protocol.”

The high dose regimen being used in the Solidarity trials has no medical justification.  The trial design, with its limited collection of safety data, may make it more difficult to identify toxic drug effects, compared to standard drug trials.  This is entirely unethical.

Excessive dosing makes it impossible to assess therapeutic benefit, if any, of HCQ.

Giving the drug only to hospitalized patients means that the window of time during which HCQ would be expected to provide the most benefit, when viral titers are rising, has passed.

To sum up:

  1. HCQ is being given in non-therapeutic, toxic dose
  2. HCQ is being given too late in the disease course to determine its value against SAR-CoV-2.
  3. Limited safety data in the Solidarity trials serves to protect trial investigators and sponsors from disclosure of adverse drug effects, including death
  4. I suspect WHO has been deliberately misleading regarding the doses chosen.
  5. The conclusions to be drawn are frightening:
    a)  WHO and other national health agencies, and charities, have designed huge clinical trials to assure that hydroxychloroquine will fail to show benefit, presumably to advantage its much more expensive competitor(s) and vaccines in development.
    b)  In so doing, these agencies and charities have conspired to increase the number of deaths in these trials.
    c)   In so doing, they have conspired to deprive billions of people from potentially benefiting from a safe and inexpensive drug during a major pandemic.  This could lead to prolongation of the pandemic and many increased cases and deaths.

My recommendation is for WHO to immediately stop using this dosing schedule, give trial subjects clinically appropriate doses, and collect more complete safety data.  I would remind WHO that if the consent forms fail to inform patients that the dose of HCQ they may receive is much higher than for any other indication, that WHO may be subject to legal action for injuries incurred in its sham of a clinical trial.


Read the full article at



Excellent article pointing out the flaws in government sponsored HCQ research.  It’s definitely looking like they really didn’t want to help COVID patients – but discover HCQ toxicity.  Notice once again, that these unethical researchers didn’t change their ways until people pointed this out and started spreading the world.

Is this the end of science? Will we only get the truth if every single study is watch-dogged by unaffiliated 3rd parties?

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