Newborn dried blood spot screening is performed within the first few days of life. A few drops of blood are collected from the baby’s heel onto a filter paper card and analyzed to identify infants with certain genetic, metabolic, and endocrine disorders.

The first thing to note is that the specificity of the newborn screening test is low. As a result, many healthy infants initially receive abnormal (positive) results but are later found, after confirmatory testing, not to have the suspected disorder. There may be as many as 100 unaffected infants with false-positive results for every affected infant identified, as reported in a 2001 publication.

“For NBS, most of those with an initial positive screening test are found to be healthy after additional testing, a false-positive screen. The positive predictive values for many newborn screening tests is generally between 1% and 10%, so there may be 10–100 unaffected infants with false-positive results for every affected infant identified.”

Overdiagnosis occurs when a medical test identifies an abnormality that does not provide benefit to the patient. Unlike misdiagnosis, overdiagnosis involves an accurate finding—a true-positive result—but one that does not improve the patient’s health outcomes. This is discussed in the 2014 article Overdiagnosis: How Our Compulsion for Diagnosis May Be Harming Children in the journal Pediatrics.

“Overdiagnosis is defined as the identification of an abnormality where detection will not benefit the patient. Unlike misdiagnosis, the finding is accurate; the condition detected may be precisely the condition that was meant to be detected (a true-positive). The notion that an accurate diagnosis could be anything but beneficial runs counter to the conventional wisdom that the more that is known about a patient, the better. Unfortunately, not only do overdiagnosed patients fail to benefit from their diagnosis, they may also be harmed.”

As the authors note, conversations between patients and healthcare providers often emphasize potential benefits, while potential harms receive less attention. Yet a single test can give rise to a cascade of follow-up procedures and interventions, many of which have the potential to harm.

“Medical tests are more accessible, rapid, and frequently consumed than ever before. Discussions between patients and providers tend to focus on the potential benefits of testing, with less regard for potential harms. Yet a single test can give rise to a cascade of events, many of which have the potential to harm.”

Physically, unnecessary tests and interventions can cause direct harm.

“The physical effects of testing and interventions motivated by overdiagnoses are the most visible harms of unnecessary detection of an abnormality.”

Psychological effects are common consequences of overdiagnosis.

“Subtle but potentially common byproducts of overdiagnosis are psychological effects, because all diagnoses, whether beneficial to the patient or not, change the perception of the child for the child, his or her caregivers, and society.”

An example of overdiagnosis can be seen in newborn screening for an enzyme deficiency termed MCADD, which can identify infants who may never develop symptoms. Many of these infants have biochemical abnormalities that may never cause harm, yet they can undergo repeated testing, dietary changes, and medical monitoring without any clinical benefit. As the authors note:

“A portion of newborns identified by newborn screening may never experience symptoms of their enzymatic defect. Studies have identified affected but completely asymptomatic older siblings of screening-identified newborns, and some mutations identified by newborn screening have acylcarnitine profiles that normalize over time.”

When newborns began to be screened for this enzyme deficiency in Denmark, screening detected approximately four times more cases than expected based on clinical presentations. A substantial portion of these newly identified infants may remain asymptomatic. This was reported in the article MCAD Deficiency in Denmark.

“In Denmark we have screened 519,350 newborns for MCADD by MS/MS and identified 58 affected babies. The diagnosis of MCADD was confirmed in all 58 newborns by mutation analysis. This gives an incidence of MCADD detected by newborn screening in Denmark of 1/8954. In sharp contrast to this we found that the incidence of clinically presenting MCADD in Denmark in the 10 year period preceding introduction of MS/MS-based screening was only 1 in 39,691. This means that four times more newborns with MCADD are detected by screening than what is expected based on the number of children presenting clinically in an unscreened population … We conclude that MCADD is much more frequent than expected, has a reduced penetrance.”

This example illustrates how newborn screening can label infants who are unlikely to become sick, yet still subject them to medical follow-up, dietary changes, and monitoring. Although the test is purportedly accurate, many of these infants gain no benefit from the diagnosis, highlighting how screening can contribute to overdiagnosis.

A 2016 publication in the Maternal and Child Health Journal evaluated the harms associated with newborn screening.

Positive Laboratory Results Associated with Unaffected Infants (Clinical “False Positives”)

Positive screening results for an unaffected infant (“false positive”) or screening for condition with a long interval between a positive screening result and confirmatory diagnostic testing may induce considerable short-term parental anxiety [32– 36]. Potential psychosocial or nonphysical harms include “the possibility for stigmatization, unnecessary anxiety, adverse impacts on parent and family relationships, and other ethical, legal, and social implications” [2]. Newborn hearing screening and other point-of-care testing paradigms may be especially prone to false positive results [37]. To date, falsely identifying unaffected infants due to positive screening results may have been the most commonly identified harm to families from newborn screening. The etiology of falsely identifying unaffected infants is inherent in the trade-off between laboratory cutoffs for screening sensitivity (needing to approach 100 %) and specificity. The impact of false identification unfolds with the need to verify laboratory results from newborns who are later determined to be trait carriers, born to affected mothers, or have clinical factors such as acute illness, prematurity, hyperalimentation, or transfusion. Although there is anecdotal evidence of parental concerns following positive screening results from unaffected infants, evidence of long-term harm is generally lacking [32]. Harms to the newborn screening system from frequent false identification may also arise, such as provider laxity about prompt re-testing and referral for infants, inclusive of those later determined to have true positive results [38], and burdens on public health and clinical staff [39].

Potential Harms Associated with Diagnostic or Prognostic Procedures

Physical Pain or Medical Risk Associated with Diagnostic Evaluation

Harm may arise from diagnostic processes that require invasive medical procedures (e.g. skin biopsies), or risky procedures such as anesthesia or radiation exposure due to diagnostic procedures (e.g. CT scans). Diagnostic processes that are performed on an affected infant or child prior to treatment would not generally be included as an incremental harm because the affected infant would be expected to be subjected to these (and other) tests with clinical presentation. The differential harm from screening would arise for infants with false positive screens who would not normally have undergone the testing, or for whom clinically indicated diagnostic testing would be at an older age when, in some cases, testing would be less onerous or risky.

Psychosocial Harm from Diagnostic or Prognostic Uncertainty

Newborn screening identifies infants at risk for a particular condition, with the expectation that diagnostic evaluation will be confirmed or ruled out. However, family anxiety may arise through diagnostic uncertainty when a standard clinical evaluation requires signs or symptoms typically observed in an infant or child who has had more disease progression (e.g. Krabbe disease) [40]. Uncertainty can arise due to broad phenotypic expression, poor genotype–phenotype correlation with a spectrum of disease manifestations, or delayed age of onset. Harms associated with uncertainty also include the possibility of abandoning the true diagnosis to follow other disorders, in addition to psychological harm to the child as well as to their family. Such harms could stem from requirement for monitoring for disease manifestations (e.g. Krabbe disease) [40], anxiety, reproductive issues for parents, and decisions pertaining to treatment, health care utilization, insurance, location, and infant– parent bonding [41–44]. Family anxiety may also arise from diagnostic or prognostic uncertainty when a decision needs to be made about particularly risky treatment (e.g. hematopoietic stem cell transplantation). These uncertainties may be short-lived or may persist and require long-term monitoring. A similar range of harms may arise from the medical futility of disorders for which no treatment currently exists if diagnosis were derived from incidental findings of screening [45].

Potential Harms Associated with Treatment

Physical Pain or Medical Risk Associated with Treatment

Standard care for an affected infant would not generally be included as differential harm associated with screening because treatment of an affected infant would be expected. Treatment of infants diagnosed by screening could occur earlier than for children diagnosed clinically. Although earlier treatment may be more effective, younger children may be more vulnerable to treatment-associated harms. The potential adverse events or complications associated with a standard treatment should be included as a potential harm within our framework if the treatment is also likely to be offered to (1) test positive but clinically unaffected infants; (2) affected infants whose disease phenotype renders treatment as less effective or who might not require treatment; (3) younger children who may have greater vulnerability to adverse effects of treatment; or (4) children for whom risks from treatment would otherwise be substantially delayed due to later onset disease manifestation. In these scenarios, treatment harms could result if screening leads to medically risky treatment for children who would otherwise not have undergone those treatments, which is more likely for conditions with a broad spectrum of disease intensity, poor genotype–phenotype correlation, or variable age of onset. Substantial harms may occur if treatment is painful, medically risky or even life-threatening, such as hematopoietic stem cell transplantation or other major biologic therapy, or medications with narrow therapeutic windows or serious adverse effects.

Psychosocial Harm from Treatment Decisions

Harm may include family distress related to adverse disease outcomes if declining treatment (e.g., family refuses presymptomatic therapy because of their perceived risk of treatment), or if treatment is delayed or is not available despite disease progression (e.g., no matched donor for stem cell transplantation, expensive or complex treatment is not available in the local community).

Over the past two centuries, mortality rates have declined substantially in many societies. These changes are frequently attributed to advances in medical science. Although such advances have played an important role in reducing suffering and preventing death in specific contexts, their overall contribution to mortality decline has often been overstated. Historical and epidemiological evidence reveals that the most significant reductions in mortality occurred prior to the introduction of medical measures.

A 2016 publication entitled Explanations for 20th Century Tuberculosis Decline: How the Public Gets It Wrong highlights a striking gap between public perception and historical reality. While most people believed that medical treatments were the main cause of the decline in tuberculosis mortality, the historical record shows that most of the reduction occurred before medical interventions were available, driven instead by improved living conditions. In the early 1900s, tuberculosis was the second leading cause of death in the United States.

“The public’s perception that medical procedures played the predominant role in reducing tuberculosis mortality is strongly contradicted by the historical record (see Figure 1). The decline in tuberculosis mortality in the developed world has resulted mostly from improved living conditions and not because of modern medicine.”

Thomas McKeown was a British physician, epidemiologist, and historian of medicine. Drawing largely on demographic data from England and Wales, he argued that medical measures played a limited role in the historical decline of mortality rates, as noted by a 2002 publication.

“The McKeown Thesis states that the enormous increase in population and dramatic improvements in health that humans have experienced over the past 2 centuries owe more to changes in broad economic and social conditions than to specific medical advances or public health initiatives.”

In his 1979 book The Role of Medicine, McKeown contends that medical interventions were not a significant contributor to the dramatic improvements in health and longevity over the past three centuries, which he attributes primarily to improvements in nutrition, environment and behavior. The introduction of the book reads as follows:

“In analyzing the factors that have improved health and increased longevity over the last three centuries, Thomas McKeown contends that nutritional, environmental, and behavioral changes have been and will continue to be more important than specific medical measures, particularly clinical or “curative” interventions.”

Building on Thomas McKeown’s earlier research, epidemiologists John McKinlay and Sonja McKinlay concluded in their 1977 study, The Questionable Contribution of Medical Measures to the Decline of Mortality in the United States in the Twentieth Century, that medical treatments and preventive measures played only a minor role in the substantial decline in mortality since 1900.

“In general, medical measures (both chemotherapeutic and prophylactic) appear to have contributed little to the overall decline in mortality in the United States since about 1900—having in many instances been introduced several decades after a marked decline had already set in and having no detectable influence in most instances.”

Within the 20th century, average life expectancy in industrial countries increased from approximately 45 to 75 years, an improvement often assumed to be largely the result of advances in the content and distribution of medical care. However, by relying on the purported efficacy and harm of medical interventions, a 1994 publication entitled Improving Health: Measuring Effects of Medical Care concluded that only about five of the 30 years gained in life expectancy since 1900 can be attributed to medicine.

“Within this century, average life expectancy has increased from approximately 45 to 75 years for citizens of industrial countries, an improvement assumed by many to be largely the result of advances in the content and distribution of medical care. This assumption has been called into question by a number of observers. … In order to identify the separate contribution of medical care, we have chosen to estimate the contributions of individual medical interventions to life expectancy … All told, then, Tables 1 and 2 illustrate an estimated current gain in life expectancy of about five years.”

Most of the increase in life expectancy during the 19th and 20th centuries resulted from reductions in infant mortality. While mortality fell across all age groups, the greatest gains were among children under one year, who were increasingly spared from poverty-related illnesses such as diarrhea. A 2000 study published in Pediatrics concluded that nearly 90% of the decline in childhood infectious disease mortality in the United States occurred before 1940, when few antibiotics and vaccines were available. This evidence underscores that improvements in living conditions—not medical interventions—were the primary drivers of the pronounced rise in life expectancy.

“Once again, nearly 90% of the decline in infectious disease mortality among US children occurred before 1940, when few antibiotics or vaccines were available.”

Jordan’s Substack

Gallery of Graphs

For easy reference I have gathered together, and presented on this page all the graphs that I created for the essay series Vaccine Evangelists, Apostates, and Apologists…

Read more

3 years ago · 114 likes · 27 comments · Jordan Henderson

The gay nightlife of the early 1980s was characterized by heavy use of carcinogenic nitrate inhalers, among other drugs. These volatile chemicals had a pronounced effect on blood vessels. Unsurprisingly, this scene soon saw clusters of men developing cancer of the blood vessels (Kaposi sarcoma), pneumonia, and other conditions.

Although these diseases were not new, virologists began hunting for a novel “virus.”

These virologists (Montagnier [1] and Gallo [1, 2, 3, 4]) took tissue from sick patients, saw a handful of chemical reactions in their test tubes, and thus proclaimed that they had discovered a causative virus.

However, these proxy markers purporting to have established the existence of HIV—particle detection, enzyme activity, and protein reaction—are in fact decidedly non-specific.

A 1993 Nature article raised fundamental doubts about the electron microscopy images that had been presented as evidence of the virus’s physical presence—the particles said to represent HIV. The authors highlighted that structures identical to those labeled as HIV had been observed long before the AIDS era, in completely unrelated biological contexts.

“In the 1970s, such particles were frequently observed in human leukaemic tissues, cultures of embryonic tissues, and “in the majority, if not all, of human placentas.”

The Nature authors cited an electron microscopy study in which particles indistinguishable from those claimed to be HIV were observed in uninfected tissues. The researchers of that study emphasized that particle detection does not constitute proof of the presence of a virus, because such particles cannot be distinguished from naturally occurring structures.

“In the only EM study, either in vivo or in vitro, in which suitable controls were used and in which extensive blind examination of controls and test material was performed, virus particles indistinguishable from HIV were found in a variety of non-HIV associated reactive lymphadenopathies leading the authors to conclude: “The presence of such particles do not, by themselves indicate infection with HIV.”

In light of the non-specificity of the protein reactions (antibody-antigen) relied upon as evidence for HIV, a 1997 medical journal article argued that the evidence for the existence of HIV should be critically reevaluated.

“The demonstration of specific antibody/protein reactions is the fundamental assumption underlying proof of HIV isolation, proof of HIV infection, and the claim that HIV causes AIDS. However, because antibodies that react with the supposed ‘HIV’ proteins also arise in non‑HIV–infected animals and humans after allogeneic stimuli, and in mice and humans with autoimmune disorders … the evidence for HIV’s existence and its alleged causal role in AIDS must be reappraised.”

In 1990, for example, researchers reported that normal, healthy dogs—an animal considered to be incapable of being infected with HIV—exhibited reactions to “HIV proteins.”

“In a serological survey, using the immunoblotting technique, we found that substantial numbers of dog sera from both normal and diseased dogs, including dogs with neoplasia, reacted with one or more human immunodeficiency virus (HIV) recombinant proteins. A total of 144 dog sera were tested, and 72 (50%) of them reacted with one or more HIV recombinant structural proteins … Six dog sera reacted with at least the major core protein of HIV.”

Research over several decades has shown that the enzyme (reverse transcriptase) relied upon as evidence for HIV is widespread and is found in normal, uninfected cells. As virologist Harold Varmus noted in 1988:

“Although reverse transcription was first encountered in the retrovirus life cycle, it is hardly unique to retroviruses; it is now recognized as a widespread phenomenon in eukaryotic cells and viruses. Indeed, as much as 10% of the eukaryotic genome may be composed of products of reverse transcription.”

As early as 1971, Howard Temin, the discoverer of this enzyme, reported the detection in uninfected rat cells and remarked that the enzyme does not “necessarily represent oncogenic [retro] viruses.”

A year later, Temin detected it in “uninfected chicken embryos and cells in culture” and noted; “it is tempting to assume that this activity is related to normal cell function.”

The non-specific nature of this enzyme was clearly underscored by Varmus in 1987, who described it occuring “even in the uninfected cells of yeast, insects and mammals.”

Medical authorities expanded the definition of AIDS beyond the first so-called “AIDS-defining” diseases.

In 1986, for instance, the World Health Organization introduced a diagnostic criterion for developing countries that classified anyone with a handful of common, non-specific symptoms—such as weight loss and diarrhea—as an AIDS patient.

A 1995 publication in the World Journal of Microbiology & Biotechnology argued that the diseases attributed to AIDS in Africa have long been present, affect both men and women equally, and result from factors unrelated to HIV.

“Both acquired immune deficiency (AID) and the symptoms and diseases which constitute the clinical syndrome (S) are of long standing in Africa, affect both sexes equally and are caused directly and indirectly by factors other than human immunodeficiency virus (HIV).”

Another widely used definition of AIDS relies upon a decline in a specific cell type (CD4). However, such a decrease is a non-specific phenomenon occurring in a wide range of unrelated conditions, as noted by a 2024 medical journal publication.

“Others have documented CD4 reduction in cases of malaria, viral, bacterial, and parasitic infections, psychological stress, burns, malnutrition, corticosteroid use, overexercising, pregnancy, and normal variation.”

The study that “represents the largest assessment of the relationship between surrogate outcomes and clinical events to date” reported that they “were unable to demonstrate a relationship between change in CD4 cell count or viral load and clinical events.”

In short, AIDS surrogate markers do not reflect actual health outcomes.

A 2004 publication argued that the scientific literature has consistently failed to show that AIDS is a contagious disease.

“The HIV theory predicted that HIV was sexually transmitted and therefore AIDS would spread throughout the heterosexual population. This has not occured. In fact data from the largest, longest, best designed and executed studies available conducted in the USA and Africa show that HIV is not heterosexually transmitted.”

For instance, a 1996 study followed 176 couples over several years in which one partner was HIV positive, and despite regularly sleeping together and engaging in unprotected intercourse, no instances of transmission occurred.

“No transmission occurred among the 25 percent of couples who did not use condoms consistently at their last follow-up nor among the 47 couples who intermittently practiced unsafe sex during the entire duration of follow-up.”

The influenza pandemic at the end of World War 1 is claimed to have been a highly contagious disease.

“This flu was highly contagious and spread through cough, sneezes, talks, respiratory droplets, and transmitted through the air.”

However, during the outbreak, the government of the United States conducted a number of experiments on volunteers to determine the cause and mode of spread of influenza, all of which yielded negative results. The outcomes of these experiments were summarized in a 2010 article published in the journal Public Health Reports.

“It seemed that what was acknowledged to be one of the most contagious of communicable diseases could not be transferred under experimental conditions.”

In Epidemic Influenza (1927), bacteriologist Edwin Jordan reflected that the repeated failure of transmission experiments during the Spanish flu exposed a profound contradiction between the widespread assumption of contagion and the actual experimental evidence, which failed to demonstrate it.

“The outcome of all these experiments is to show that the requirements for the transmission of influenza from man to man, such as apparently exist commonly under natural conditions, are not readily imitated experimentally.”

Although the contagion theory dominated medical thought in the early twentieth century, the transmission experiments conducted during the 1918 influenza pandemic repeatedly failed to confirm it. In fact, as noted in a 2008 article published in the Virology Journal:

“Jordan reports that all five studies failed to support sick-to-well transmission, in spite of having numerous acutely ill influenza patients, in various stages of their illness, carefully cough, spit, and breathe on a combined total of >150 well patients.”

His analysis in Epidemic Influenza thus highlighted a critical tension of the period: while public-health authorities and physicians assumed contagion as fact, the available experimental evidence could not substantiate it.

In 1920, at the end of the Spanish flu, Paul Fildes and James McIntosh reviewed the research on influenza and exposed a deep uncertainty at the core of early virology. They observed that scientists across many countries had come to accept the idea of an invisible viral cause, even though clear, physical evidence for such an agent was lacking. The concept of a “virus” allowed researchers to claim discovery without demonstrating any discrete physical entity.

“With remarkable unanimity investigators in nearly every country have described an ultramicroscopic virus as the cause of influenza. This unanimity alone carries with it considerable weight, but it must be confessed that the trivial nature of most of the papers and the obvious lack of experience in some of the investigators, compels caution in accepting the claims. This caution will be understood to be all the more desirable when it is realised that the introduction of the invisible virus concept absolves the discoverers from the necessity of producing evidence of a morphologically characteristic microbe.”

Microbiologists failed to isolate a pathogen or reproduce the disease through direct experimentation, but the assumption of a contagious etiology persisted nonetheless.

A 1919 newspaper article pointedly questioned the validity of the germ theory in light of ongoing failures to prove its role in the Spanish flu. Despite widespread belief in pathogenic microbes, experiments conducted by Dr. John Fraser and government researchers showed unsuccessful results in their attempts to transmit alleged infectious material through voluntary exposure. The article underscored a key point; more conclusive proof of the germ theory is required than has yet been produced.

“It would seem that more conclusive proof of the germ theory is required than has yet been produced. For the benefit of humanity as well as in the interest of science the medical profession should perform experiments similar to Dr. Fraser’s and those made by the government last winter, when unsuccessful attempts were made to cause the “flu” by inoculation and voluntary exposure to contagion. If the germ theory is right, the results of such experiments will prove it. And if it is wrong, the sooner the world knows it the better.”

On November 26, 1918, a significant experiment was conducted to test the transmissibility of influenza by replicating natural conditions.

“This experiment was designed to test the transmissibility of influenza by what is assumed to be the natural means, viz, by the expired breath and cough.”

Ten volunteers without a record of influenza during the outbreak were chosen. Nine of the volunteers had no history of an attack of influenza at any time.

“Of these 10 men none had a record of influenza during the recent epidemic; 1 (No. 43), however, had a doubtful history of a previous influenza-like attack.”

These men were taken to a hospital were 30 cases of influenza were being treated, and were exposed to 10 especially selected acute cases.

“They were taken to the naval hospital at Chelsea and in a ward in which 30 cases of influenza were being treated, were exposed to infection from 10 especially selected acute cases”

The volunteers engaged in close personal contact with the acutely ill influenza patients, speaking with them at the bedside and having the patients breathe and cough directly into their faces for several minutes each. The total exposure time for each volunteer ranged from 30 and 50 minutes. None of the volunteers developed any indication of illness following the exposure.

“Each volunteer took a position close to the bedside of one of the selected patients and conversed with him for two or three minutes, then the patient was directed to breathe five times and then cough five times directly into the face of the volunteer. After this was done the volunteer proceeded to the bedside of a second patient. In this manner each of the volunteers was exposed in succession to each of the 10 selected cases, the exposure to each being between three and five minutes. The total exposure for each volunteer, therefore, was between 30 and 50 minutes. Results.—None of these volunteers developed any indications of illness following this exposure.”

The full details of the experiments conducted during the Spanish influenza can be found at the link below:

https://www.govinfo.gov/app/details/SERIALSET-07803_00_00-002-0854-0000

A peculiar fact is that the so-called Spanish flu was inextricably linked to the soldiers of the First World War, as noted by a 2009 publication entitled Origins of the Spanish Influenza pandemic (1918–1920) and its relation to the First World War.

“The main conclusion of the present research into the origins and beginning of the Spanish Influenza pandemic is that it appears to be inextricably linked to the soldiers who fought during the First World War.”

The disease disproportionately affected young, healthy soldiers, a pattern that directly defies the expectations of an infectious outbreak, which would predict a more random or vulnerable distribution of cases.

This strikingly unique soldier connection raises serious doubts about the prevailing germ theory explanation. Instead, the evidence points toward a toxicological and environmental phenomenon, relating to the Great War, as discussed in Origins of the Spanish Influenza pandemic (1918–1920) and its relation to the First World War

“The causal factors included the poor quality living conditions of the soldiers, the agglomeration, stress, fear, war gasses used for the first time in history in a massive and indiscriminate manner, life exposed to the elements, the harsh cold with especially harsh winters, such as that of 1916; rain, snow”

Central to the extraordinary impact on troops was the large-scale introduction of numerous toxic war gasses. In a 1919 publication entitled Climate and Its Relation to Acute Respiratory Conditions, a writer postulated that the battlefield environment, saturated with chemical agents and noxious gases, was largely responsible for the influenza pandemic. He argued that influenza was not a contagious disease, but rather a consequence of exposure to environmental conditions.

“The numerous gases used on the battlefields of Europe with their highly poisonous properties, the liberation of large quantities of ground air high in carbon dioxide content due to trench digging and shell holes, the gases from decomposing bodies of men and lower animals, and those set free by the destruction of cities and munition dumps during the last four years may have combined to form a gaseous compound with highly toxic properties probably due to rearrangement of molecules by the tremendous concussion produced by high explosives.” With this idea in mind he states: “I am going to advance the theory that the condition termed influenza is in reality a non-bacterial, non-contagious disease caused by the inhalation of small amounts of depressing, highly irritating high density gas present in the atmosphere, especially at night when the air is surcharged with moisture, more particularly near the surface of the earth.” He also states: “The mode of transmission is undoubtedly through the agency of the atmosphere.”

The 1918 influenza pandemic starkly reveals that the widely accepted “contagion” narrative does not withstand scrutiny. Experiments deliberately exposing healthy volunteers to the sick failed to produce illness, yet authorities clung to the idea of an invisible, unproven pathogen. The so-called pandemic’s disproportionate impact on young soldiers points decisively toward toxicological and environmental factors.

Jerm's Substack

Michael Bryant on the Spanish flu myth

The Spanish flu was a global pandemic that occurred in 1918-1919, caused by an H1N1 influenza virus. It spread quickly and infected about a third of the world’s population, leading to millions of deaths. The virus was especially deadly because it affected healthy young adults, not just the elderly or sick…

Listen now

2 years ago · 33 likes · 8 comments

The Virology Controls Studies Project

The Spanish Flu Hoax

All of the content that is put out on this Substack is going to be for free. If you feel so inclined to donate or Sign up for a Paid Subscription that is very much appreciated. It will keep me writing, putting out content and continuing the largest Control Studies Project falsifying Virology…

Read more

2 years ago · 402 likes · 175 comments · Jamie Andrews

Dr Sam Bailey

Exploding the Spanish Flu Myth

This is the video version of "Exploding the Spanish Flu Myth", first published by the Health Freedom Defense Fund (HFDF) Team on the 20th of June, 2024. It asks why millions of reported deaths starting in 1918 were blamed on a "virus" when there were numerous other environmental factors involved, including the mass deployment of deadly chemicals during …

Listen now

2 years ago · 545 likes · 181 comments · Dr Sam Bailey

In the early 1880s, Louis Pasteur released a vaccine for anthrax, a disease which primarily afflicts livestock.

However, evidence soon began to mount concerning the inefficacy and dangers of the inoculations.

In 1882, the Turin Veterinary School of Italy performed an experiment to test Pasteurs alleged prophylactic. But the experiment was an “extraordinary fiasco”, as described in Pasteur’s biography, The Life of Pasteur. All the sheep, vaccinated and unvaccinated, had died due to the inoculation of the blood of a sheep which had died of anthrax—thus disproving the claims of immunity from vaccination.

“A year before this (Peter had not failed to report the fact) an experiment of anthrax vaccination had completely failed at the Turin Veterinary School. All the sheep, vaccinated and non-vaccinated, had succumbed subsequently to the inoculation of the blood of a sheep which had died of charbon [anthrax]. This took place in March, 1882.”

Dr. Michel Peter, French physician and member of the Académie de Médecine, was a fierce critic. He accused Pasteur of creating diseases like anthrax and rabies through the very vaccines meant to prevent them. In the book Pasteur and Rabies, he outlines a notable example; in 1888, 4,564 sheep were vaccinated against anthrax in Southern Russia, of which 3,696 died—a percentage of 81.

“Inoculation as preventive of charbon [anthrax] was practised upon 4,564 sheep at Kachowka, in Southern Russia, of which 3,696 died. M. Bardach, in August, 1888, inoculated 4,564, of which only nineteen per cent. survived. This is called protective inoculation! The promotor of this gigantic holocaust was M. Meczikow, a doctor of philosophy, director of the Bacteriological Institute of Odessa.”

As such, the fiasco in Italy was not an isolated example, as noted by E. Douglas Hume in her book Bechamp or Pasteur?

“Thus the Turin disaster is shown to have been by no means an isolated example.”

Numerous examples of the failure of vaccination were provided in a 1891 issue of The Times and Register. These instances were translated from the work of Auguste Lutaud, one of the most virulent opponents of Louis Pasteur, in his work Studies on Rabies and the Pasteur Method (Études sur la rage et la méthode Pasteur).

“With regard to the vaccine of splenic fever (charbon) [anthrax] … they have gone out of vogue, and are not practised to-day, the majority of veterinary surgeons having recognized their inefficacy. The following facts borrowed from Lutaud will seem startling to those who have read only one side of this question:

• On a farm in the suburbs of Laon, the proprietors caused to be vaccinated three times, with a fortnight of interval, a flock of sheep affected with charbon, but the disease went on unchecked.

• On a neighboring farm, the veterinary vaccinated the horses which were not sick, and three perished from the operation; M. Magnier, the proprietor, demanded reimbursement for the price of the horses, and obtained it.

• In the suburbs of Meaux, a veterinary physician having killed four cows with the famous vaccine, M. Pasteur paid the price of the cows to stop a law suit.

• In 1882, M. Franchamp, a farmer of Chateauneuf, lost in consequence of the anthracoid vaccinatious, horses, cattle and sheep to the value of five thousand francs.

• In 1882, M. Fournier, a veterinary of Augerville (Loiret), vaccinated a flock of four hundred sheep; a few days after the application of the first vaccine ninety sheep succumbed to splenic fever.

• In 1884, Henri Thirouin, Mayor of St. Germain-le-Gaillard, and Marcel Lebrun, a farmer in the same commune, had their sheep vaccinated by Pasteur’s method; a considerable part of their flocks died as the result of the vaccination.

• A similar fatality occurred in 1888 in a Russian commune from the Pasteurian vaccinations, as reported in the Semaine Medicale of that year; the proprietors of several large estates caused their cattle, sheep and horses to be vaccinated to protect them against an epidemic which was raging in the surrounding country, and lost a large part of their flocks from the inoculated disease.

The Sanitary Commission of the Hungarian Government in 1881 thus terminated its report on the inoculation of cattle according to Pasteur’s method:

“The most grave diseases, pneumonia, catarrhal fevers, etc., have smitten exclusively the animals subjected to vaccination. It follows from this that the Pasteurian inoculation tends to accelerate the action of certain latent diseases, and to hasten the mortal issue of other grave affections.”’

The Hungarian government then and thereafter prohibited these inoculations.”

The Hungarian government was not alone in denouncing Pasteur’s anthrax vaccine; the Fourth Annual Report of the American Anti-Vivisection Society stated that the German and British governments also condemned the vaccine.

“But Dr. Hughes errs in supposing that his researches as to anthrax or splenic fever have ever been of any value ; the Hungarian, German, and English Government Commissions appointed to enquire into this subject have unanimously condemned his system of inoculation for these diseases.”

Even Robert Koch, renowned bacteriologist, criticized Pasteur’s vaccine on account of its inefficacy and danger.

“The preventive inoculation of Pasteur against splenic fever [anthrax] cannot be considered as practically utilizable on account of the insufficient protection that it gives to animals against natural infection, on account of the short duration of that protection, and on account of the great danger to which it subjects men and other non-inoculated animals.”

In a publication presented at the Sixty-second Annual Meeting of the American Veterinary Medical Association in 1925, A. Eichhorn describes how Pasteur’s anthrax vaccine frequently failed to protect animals from the disease.

“A closer analysis reveals that in certain notorious anthrax districts, the vaccination frequently failed to produce in the animals a sufficient resistance against the natural exposure.”

ViroLIEgy Newsletter

The Germ Hypothesis Part 1

According to the Encyclopaedia Britannica, the germ “theory” of disease, which states that certain diseases are caused by the invasion of the body by microorganisms too small to be seen, has “long been considered proved.” Harvard University says that the “theory” was “developed, proved, and popularized in Europe and North America between about 1850 and 1920…

Read more

2 years ago · 100 likes · 7 comments · Mike Stone

Anthrax, Arsenic and Old Lace

https://www.westonaprice.org/health-topics/anthrax-arsenic-and-old-lace

After his tuberculin disaster in the early 1890s, Robert Koch looked for new fields of research. To make up for his failures in Europe and restore his prestige as a renowned scientist, Koch took to the study of tropical disease in Africa.

“His fame in public had been established through uncovering aetiologies, and an attempt to transform this into a therapeutic research program on common infections failed spectacularly in 1891 when Koch’s tuberculin failed as a cure for tuberculosis. As a consequence, he gave his studies some new directions during the 1890s and took to the study of tropical infectious disease.”

Sleeping sickness was afflicting native populations. Koch believed the disease was caused by parasites, and thus, he established concentration camps for the sick individuals. Inside these camps the patients were to be isolated and treated, if necessary against their will. Koch’s team carried out tests using injections of arsenic to treat the disease.

“Based on this understanding Koch planned serial examinations and the establishment of what he called “Konzentrationslager” (concentration camps) for those infected with sleeping sickness on German colonial territory. Inside these camps the patients were to be isolated and treated, if necessary against their will.”

He viewed the indigenous patients in Africa like economic commodities or livestock. As Koch spelled it out, the value of the campaign would not be the healing of individuals, but the maintenance of the population’s workforce as a whole.

“By giving priority to the fight against the epidemic instead of a therapy of individual patients, Koch brought his veterinary experience to bear, which moreover combined swiftly with the racist ideological background of ‘koloniale Menschenökonomie’, of treating indigenous patients in Africa like economic commodities or livestock and having double ethical standards for them and patients in Germany. As Koch spelled it out, the value of the campaign would not be the healing of individuals, but the maintenance of the population’s workforce as a whole.”

The colonised became the field of experimentation, reduced to their social and economic value. The arsenical drug Atoxyl was used in full dose, despite knowing that it caused poisoning, blindness, and even death. In order to continue experimenting, Koch sent out a colonical police to arrest and bring people to the concentration camps.

“His biopolitical interventions through science engendered othering, deprived human beings of their agency, as the body of the colonised became the field of experimentation, reduced to its social and economic value. As he was there, his team carried out tests using Atoxyl to treat sleeping sickness among the native population. Atoxyl, however, was used in its full dose, despite knowing that it caused poisoning, blindness, and even death. As the indigenous people returned to the villages in light of the health improvements, colonial police was sent out to arrest and bring them back to concentration camps to continue the medical experiments. His idea was to isolate them from the villages to lower infection rates – but also to continue experimenting, with all the necessary force to sustain the workforce.”

Thousands of Africans became the objects of dangerous therapeutical and pharmacological research. Koch accepted the pain and agony of countless of patients, even to the point of death.

“Koch accepted the pain and agony of thousands of patients, even to the point of death, say his critics, including the Haitian-American historian of science Edna Bonhomme.”

Patients suffered pain, blindness, and death.

“Conditions in this camp were bad, and Koch began injecting patients with an arsenic-containing drug, called Atoxyl. When it didn’t work, Koch raised the dose. Patients suffered intense pain, blindness — and every 10th person died.”

Robert Koch’s campaign in Africa was a fiasco. He was not able to find an cure for sleeping sickness—instead the unwanted side effects of the painful injections were clearly proven.

“Koch’s sleeping sickness expedition can hardly be called a success. A chemotherapy with lasting effectivity was not found; instead the toxicity of the ‘tested’ substances, in other words of the unwanted side effects of the painful injections were clearly proven.”

In 1890, Robert Koch presented a paper entitled On Bacteriological Research to the International Medical Congress, in which he declared that he had developed a substance that hindered the growth of tubercle bacilli.

The announcement was hailed with great enthusiasm, and tuberculosis patients began to converge on Berlin.

“Europe witnessed a strange but not unprecedented spectacle last month. In the Middle Ages the discovery of a new wonder-working shrine, or the establishment of the repute of the grave of a saint as a fount of miracles, often led to the same rush which has taken place last month to Berlin ... The consumptive patients of the Continent have been stampeding for dear life to the capital of Germany. The dying have hurried thither, sometimes to expire in the railway train, but buoyed up for a time by a new potent hope.”

An editorial in the Journal of the American Medical Association mocked the response to the news of Koch’s new “cure.”

“Think of it! Thousands of physicians—Germans, Austrians, Italians, Russians, English and Americans (and possibly those of other nations), flocking to Berlin to see Prof. Koch’s treatment, scrambling for places, and offering fabulous prices for a few drops of the liquid whose composition they do not know and cannot find out! And when asked why they want it, reply, “Because Koch thinks it will cure tuberculosis!” When has the practice of medicine witnessed such a spectacle?”

According to Koch, tuberculin was ineffective when administered orally and had to be injected subcutaneously.

In his 1890 presentation, Robert Koch describes how bacteriologists had only produced such insignificant practical results, in spite intense efforts.

“Up till now I have purposely left one question untouched, although it is precisely the one which is most frequently, and not without a certain amount of reproach, addressed to bacteriologists. I mean the question of what profit all the weary labour which has up to the present been expended on the investigation of bacteria has been? … We have hardly any directly acting, that is, therapeutical, agents to place beside the indirect ones … Although in these directions, in spite of endless toil, bacteriological research has only such insignificant results to show.”

With Koch’s sensational announcement of a cure for tuberculosis, bacteriology and germ theory was on trial, as stated by an article in The Lancet.

“Indeed, apart from the fact that we may be on the verge of a revolution in therapeutics, it may be said that bacteriology itself is on its trial in this momentous investigation.”

Koch had based his conception of a cure on a previously acquired understanding that germs were the cause of tuberculosis.

The excitement of Koch’s remedy was short-lived. Tuberculin was not only declared to be of no value, but decidedly dangerous, as outlined by the Glasgow Medical Journal.

“Its fame was short-lived. Robert Koch had made an announcement which could not be backed up by results. In the spring of 1891, but a few months after its introduction, at the annual meeting of the British Medical Association, tuberculin was declared to be not only of no value, but decidedly dangerous. It exhausted the strength of the patient; it led to the extension of the disease; it favoured the production of cavities; it not infrequently caused the death of the patient.”

The introduction of tuberculin as a “cure” for tuberculosis was a fiasco—Dr. E. A. Duncan reported in 1924 that many patients died as a consequence of the poisonous injections.

“On Koch’s recommendation tuberculin was hailed with enthusiasm as a cure for tuberculosis and its use begun. It was administered in what we would regard today as massive dosage and the results were disastrous. All over Germany the poor patients were “‘todespritzt’’—injected to death—as this doctor put it. This fiasco resulted in prompt abandonment of tuberculin.”

Koch’s scandal caused a severe setback in public optimism toward bacteriological innovation, as maintaned by a 2002 publication.

“The repercussions had both adverse and effective consequences. The widespread public disappointment caused a severe setback in public optimism toward bacteriological innovation.”

A publication in Medical History (2001) recounts that with the failure of tuberculin, the whole conception of tuberculosis centred on the pathogen started to slip. Bacterial reductionism was criticized for its non-scientific conception of disease.

“It seems that with the failure of that cure the whole conception of tuberculosis centred on the pathogen started to slip. This can be shown in minor details, such as when Koch’s critics from Pettenkofer’s school in Munich managed to produce his tuberculin reaction by the means of extracts of entirely different bacteria. In addition to this, we find, immediately after the tuberculin scandal, a whole set of fundamental critiques of Koch’s bacteriology. Some critics, such as Heinrich Lahmann, criticized it as illustrating the hypocrisies of scientific medicine. Others, more surprisingly, accused Koch’s bacteriology of mysticism. Bacterial reductionism, which had been regarded as the peak of scientific medicine in the early 1880s, was now censured for its ontological conception of disease, which appeared to be non-scientific … Although the tuberculin disaster probably did a lot to discredit the concept of infectious diseases as bacterial invasion, there is no indication that Koch himself realized this erosion of his work.”

Some contemporaries and historians have postulated that Koch was a deceiver with ulterior motives.

“The issue of Koch’s ideas about tuberculin includes a question I have not yet posed: namely, whether he thought he had a remedy at all. The notion of a “tuberculin fraud” has been put forward by contemporaries and historians and some features of his conduct are indeed hard to comprehend, if one entirely excludes the notion of Koch being a deceiver. He supplied scarce and misleading information about his cure, for example, by linking it rhetorically to the well-established and successful disinfection. When criticized, he was unable to show the guinea pigs he had cured with tuberculin. Further, the manner in which Koch pursued his commercial plans ended up in mutually attempted blackmail by himself and Prussian government officials.”

ViroLIEgy Newsletter

The Germ Hypothesis Part 2

In the first part of this investigation into the germ hypothesis, we established what exactly a hypothesis is supposed to be in regard to natural science, which is a proposed explanation for an observed natural phenomenon. We briefly touched on what led to Louis Pasteur conjuring up his explanation of disease through germs with his plagiarized work on fermentation that he lifted from Antoine Bechamp. We also examined the experimental evidence that he produced for both chicken cholera and rabies in order to see if his germ hypothesis was ever scientifically proven and validated. What became clear upon investigating was that Pasteur’s experiments did not reflect his hypotheses for how the germs were supposed to invade a host in order to cause disease as “seen” in nature, thus invalidating his results. On top of that, Pasteur also misinterpreted what he was working with in regard to chicken cholera, and he was unsuccessful in isolating any microbe as the causative agent for rabies, further invalidating those experiments as he had no valid independent variable (assumed causative agent) that he was working with. There were also issues with the vaccines that were produced by Pasteur, with his chicken cholera vaccine determined to be ineffective while his rabies vaccine was linked to causing the very disease it was supposed to prevent…

Read more

2 years ago · 86 likes · 21 comments · Mike Stone

ViroLIEgy Newsletter

Koch's Cholera Catastrophe

In 1877, German bacteriologist Robert Koch formulated a series of logical criteria that he felt were the necessary requirements that must be satisfied in order to establish a microorganism as the causative agent of disease. These steps were formally published in 1890, and are as follows…

Read more

3 years ago · 43 likes · 5 comments · Mike Stone

The linked resources below each disease are listed with the best and most informative resources first.

Please let me know if you would like to see any changes or additions in the list.

Press Ctrl + F to search.

Adenovirus:

Article: https://viroliegy.com/category/adenovirus/

Alpha-gal Syndrome:

Article: https://odysee.com/@drsambailey:c/War-on-Meat-Alpha-gal-Syndrome

Anthrax:

Articles: https://viroliegy.com/category/anthrax/

Video: https://drsambailey.com/resources/videos/germ-theory/bioweapons-101-the-story-of-anthrax/

Article: Pasteur’s Anthrax Disaster

Book (page 184): What Really Makes You Ill?

Article: https://www.westonaprice.org/health-topics/anthrax-arsenic-and-old-lace

Article: Woolsorters’ Disease: Arsenic, Not Anthrax

Autoimmune Diseases:

Book (page 386): What Really Makes You Ill?

Video: https://drsambailey.com/resources/videos/germ-theory/is-immunity-a-scientific-concept/

Article: Autoimmunity: The Diagnostic Fiction

Video: https://www.bitchute.com/video/BScnJiQlpSve/

Article: A closer look at ‘autoimmune diseases’

Bacteriophage:

Article: The “Virus” Model

Bird Flu / H5N1 / Avian Flu:

Books (page 213): Virus Mania

Articles: https://viroliegy.com/category/avian-flu/

Video: https://odysee.com/@drsambailey:c/Taking-Away-Your-Chickens

Article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7173052/

Black Death / Plague:

Video: https://odysee.com/@drsambailey:c/What-We-Weren't-Taught-About-The-Plague

Book (page 142): What Really Makes You Ill?

Article: The Infectious Myth Busted: Is Plague Contagious?

Book: New Light on the Black Death: The Cosmic Connection

Article (page 11): https://archive.org/details/epidemicsofmiddl00unse/page/10/mode/2up

Article: https://web.archive.org/web/20160827132415/https://www.history.com/news/can-we-stop-blaming-rats-for-the-black-death

Article: https://archive.org/details/black-death-and-abrupt-earth-changes-in-the-14th-century

Article: https://web.archive.org/web/20230124193356/https://www.sott.net/article/145683-New-Light-on-the-Black-Death-The-Cosmic-Connection

Video: What Really Happened During The Dark Age's Global Climate Catastrophe?

Video: How Mike Baillie was right: links between volcanoes, ice cores, tree-rings and societal responses

Video: Peter Mungo Jupp: The Black Death & Cosmic Chaos | Thunderbolts

Book: https://academic.oup.com/ahr/article

Bovine Tuberculosis:

Video: https://odysee.com/@drsambailey:c/TB-Cows-Lies-And-Koch-Ups

Book (page 172): What Really Makes You Ill?

Video (at 14:50): https://odysee.com/@drsambailey:c/Why-Pathogens-Don%27t-Exist:d?t=890

Chestnut Blight:

Video (at 34:00): https://odysee.com/@Dr.TomCowan:8/qa112923:1?r=C1UswANJowFUp5gVqrn3CRoyobEsJN32&t=2040

Chicken Cholera:

Article: https://viroliegy.com/2024/05/23/the-germ-hypothesis-part-1-pasteurs-problems/

Chickenpox:

Video: Chickenpox Parties and Varicella Zoster Virus?

Articles: https://viroliegy.com/category/chickenpox/

Article: Chickenpox Contagion: Fact or Fiction?

Video (at 4:35): https://odysee.com/@drsambailey:c/5-Spectacular-Fails-From-Germ-Theory:c?t=275

Video: https://rumble.com/v3zrcod-two-chickens-with-one-stone-mike-stone-and-alec-zeck-respond-to-chris-sky.html

Chlamydia:

Article (scroll down to “Chlamydia”): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

Cholera:

Articles: https://viroliegy.com/category/cholera/

Article: https://viroliegy.com/2024/06/07/the-germ-hypothesis-part-2-kochs-crisis/

Article (scroll down to “cholera”): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

Video (at 8:39): https://odysee.com/@drsambailey:c/5-Spectacular-Fails-From-Germ-Theory:c?t=519

Article: https://archive.org/details/b24976714

Common Cold:

Book: Can You Catch A Cold?: Untold History & Human Experiments

Article: https://whatreallymakesyouill.com/why-modern-medicine-cannot-cure-the-common-cold/

Coronaviruses:

Articles: https://viroliegy.com/category/coronaviruses/

Covid-19:

Article: https://drsambailey.com/wp-content/uploads/2024/12/Unmasking-the-Viral-Paradigm-30-June-2024.pdf

Article: https://drsambailey.com/wp-content/uploads/2021/11/THE-COVID-19-FRAUD-WAR-ON-HUMANITY-2.pdf

Article: https://drsambailey.com/wp-content/uploads/2022/10/A-FAREWELL-TO-VIROLOGY-Expert-Edition.pdf

Articles: https://viroliegy.com/category/sars-cov-2/

Article: https://www.fluoridefreepeel.ca/fois-reveal-that-health-science-institutions-around-the-world-have-no-record-of-sars-cov-2-isolation-purification/

Articles: https://www.denisrancourt.ca/categories.php?id=1&name=covid

Videos: Part One, Part Two, Part Three

Books (page 367): Virus Mania

Dengue:

Video: https://odysee.com/@drsambailey:c/The-Dengue-Drop-Shot

Diphtheria:

Article: Unveiling the Germ Theory of Diphtheria

Video: Diphtheria Disinformation

Article: https://archive.org/details/the-schick-inoculation-for-immunisation-against-diptheria/mode/1up

Article: https://viroliegy.com/2022/04/28/emil-von-behrings-diphtheria-tetanus-papers-1890-precursor-to-antibodies/

Images (press Ctrl + F + diphtheria): https://dissolvingillusions.com/graphs-images/

Ebola:

Articles: https://viroliegy.com/category/ebola/

Video: The Truth About Ebola

Video (at 04:50): https://odysee.com/@drsambailey:c/Bioweapon-BS:b?t=290

Article: https://blog.nomorefakenews.com/2022/01/12/ebola-shattering-the-lies-and-the-fakery/

Video (at 35:55): https://odysee.com/@Dr.TomCowan:8/April52023Webinar:e?r=CmfbLuoZhUGfSqfYhxkfRtbeShr98Z7g&t=2155

Escherichia Coli (E. Coli):

Video (at 11:12): https://odysee.com/@drsambailey:c/Health-Risks-Of-Using-Your-Cell-Phone-On-The-Toilet:1?t=673

Article (scroll down to E. Coli): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

Epstein-Barr Virus / Glandular Fever:

Video: https://odysee.com/@drsambailey:c/Glandular-Fever-and-the-Fable-of-EBV

Fever:

Video: https://odysee.com/@drsambailey:c/The-Truth-About-Fever

Foot-and-Mouth Disease:

Video: The Dark Side of Foot-and-Mouth Disease

Article (scroll down to FMD): The “Virus” Concept

Fungi:

Book (page 106): What Really Makes You Ill?

Video: https://odysee.com/@niodagar:b/Mold-Fungi-Parasites

Gangrene:

Video (at 5:57): https://odysee.com/@drsambailey:c/The-Truth-About-Antibiotics:7?r=C1UswANJowFUp5gVqrn3CRoyobEsJN32&t=357

Gonorrhea:

Video: What We Weren’t Taught About Gonorrhea

Article (scroll down to “gonorrhea”): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

Hantavirus:

Video: https://drsambailey.com/resources/videos/viruses-unplugged/hollywoods-hantavirus/

Video: Welcome Aboard the Hantavirus Cruise

Helicobacter Pylori:

Video: https://drsambailey.com/resources/videos/germ-theory/can-you-catch-stomach-ulcers/

Article: H. pylori and the Ulcer Myth

Article (scroll down to H. Pylori): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

Hepatitis:

Video: https://odysee.com/@drsambailey:c/What-We-Weren%27t-Taught-About-Hepatitis

Books (page 169): Virus Mania

Book (page 491): What Really Makes You Ill?

Herpes:

Video: https://odysee.com/@drsambailey:c/What-We-Weren%27t-Taught-About-Herpes

HIV / AIDS:

Articles: https://www.theperthgroup.com/

Article: The Aids Hoax

Article: https://www.theperthgroup.com/HIV/TPGVirusLikeNoOther.pdf

Article: https://www.theperthgroup.com/POPPAPERS/Yin&Yang1999.pdf

Videos: Part One, Part Two, Part Three

Documentary: House of Numbers

Documentary: The Emperors New Virus? - An Analysis of the Evidence for the Existence of HIV

Books (page 101): Virus Mania

Book (pages 152 & 500): What Really Makes You Ill?

Articles: https://viroliegy.com/category/hiv-aids/

Video: https://www.bitchute.com/video/sng4VgccakOP/

Human Papillomavirus (HPV):

Video: https://odysee.com/@drsambailey:c/HPV-Pointless-Tests-and-Toxic-Shots

Articles: https://viroliegy.com/category/hpv/

Video: https://odysee.com/@Dr.TomCowan:8/Does-HPV-Cause-Cervical-Cancer-Webinar-from-January-15th2025:6

Books (page 261): Virus Mania

Article: The HPV Lie: Pap Smears, Gardasil, and a Cancer Caused by Something Else

Book (page 56): What Really Makes You Ill?

Ignaz Semmelweis:

Video (at 12:48): https://odysee.com/@drsambailey:c/5-Spectacular-Fails-From-Germ-Theory:c?t=768

Influenza:

Book: Can You Catch A Cold?: Untold History & Human Experiments

Video: Secrets of Influenza

Articles: https://viroliegy.com/category/influenza/

Article: Did Vaccines Reduce Flu and Pneumonia Deaths?

Kuru:

Video: Papua New Guinea Pigs

Books (page 89): Virus Mania

Book (PDF pages 16 & 76): Inventing the AIDS Virus

Leprosy:

Book (page 126): What Really Makes You Ill?

Article: https://t.me/theundercovervirologist/4

Listeria:

Video: https://drsambailey.com/resources/videos/germ-theory/the-listeria-hysteria/

Long Covid:

Article: So Long “Covid”

Lyme:

Video: https://odysee.com/@drsambailey:c/The-Lyme-Disease-Lie

Video: https://odysee.com/@niodagar:b/What-About-Lyme

Article: https://drsambailey.com/the-lyme-disease-lie/

Video: https://drsambailey.com/resources/videos/germ-theory/how-lyme-disease-was-weaponized/

Video (at 31:40): https://www.bitchute.com/video/uGbIzsEwmMue/

Article: https://www.westonaprice.org/health-topics/lyme-disease-symptoms-causes

Mad Cow Disease / Bovine Spongiform Encephalopathy (BSE):

Book (PDF): Animal Pharm

Books (page 170): Virus Mania

Book (page 175): What Really Makes You Ill?

Article: ANIMAL PHARM

Video: https://www.bitchute.com/video/beYnrEqcC9eQ/

Article: https://www.beyondpesticides.org/assets/media/documents/infoservices/pesticidesandyou/Summer%2003/mad_cow.pdf

Malaria:

Article: The Malaria Malady

Video: https://odysee.com/@Dr.TomCowan:8/webinarwithdanielroytas91124

Video: https://odysee.com/@Dr.TomCowan:8/malaria:b

Book (page 510): What Really Makes You Ill?

Article: Malaria or mal'aria?

Article (scroll down to “malaria”): https://www.fluoridefreepeel.ca/do-health-authorities-have-studies-proving-that-bacteria-cause-disease-lets-find-out-via-freedom-of-information

Marburg Virus:

Article: https://viroliegy.com/2022/08/29/the-marburg-virus-precursor-to-ebola/

Measles:

Article: The Measles Hoax

Articles: https://viroliegy.com/category/measles/

Video: https://odysee.com/@drsambailey:c/themeaslesmyth

Images (press Ctrl + F + measles): https://dissolvingillusions.com/graphs-images/

Article: Has the Measles (MMR) vaccine scientifically been shown to reduce measles cases or deaths?

Video: Dr Stefan Lanka Measles Virus On Trial

Meningitis:

Video: https://odysee.com/@drsambailey:c/The-Meningitis-Mystery

MERS:

Article: https://viroliegy.com/category/mers/

Mold:

Video: https://odysee.com/@niodagar:b/Mold-Fungi-Parasites

Podcast: https://www.buzzsprout.com/1766625/11589868

Video: https://www.bitchute.com/video/bFkIOVJpPIQ6/

Video: Is Mould The Cause Of Disease?

Monkeypox:

Video: https://odysee.com/@drsambailey:c/Monkeypox-Mania-Summit:2

Articles: https://viroliegy.com/category/monkeypox/

Article: https://drsambailey.com/monkeypox-mythology/

Mumps:

Article: Mumps: Infectious and Contagious?

Article: What is Mumps?

Myxomatosis:

Book (page 178): What Really Makes You Ill?

Article: https://nourishingtraditions.com/myxomatosis/

Native Populations:

Video: https://drsambailey.com/resources/videos/germ-theory/what-killed-the-native-populations/

Book (page 119): What Really Makes You Ill?

Article: https://whatreallymakesyouill.com/smallpox-dispelling-a-popular-myth/

Nipah Virus:

Article: https://viroliegy.com/category/nipah/

Norovirus:

Article: https://viroliegy.com/category/norovirus/

Parasites:

Video: The Parasite Panic

Video: https://odysee.com/@Dr.TomCowan:8/webinarwithdanielroytas91124

Video: https://odysee.com/@niodagar:b/Mold-Fungi-Parasites

Article: Parasites: friend or foe?

Parvo:

Video: https://drsambailey.com/resources/videos/viruses-unplugged/the-truth-about-parvovirus/

Article: The Parvo Papers: How Two Flawed Studies Became “Proof” of a Disease

Article: https://rotationalmonofeeding.com/the-truth-about-parvo/

Plague of Justinian:

Video: What Really Happened During The Dark Age’s Global Climate Catastrophe?

Rabies:

Article: The Rabies Hoax

Articles: https://viroliegy.com/category/rabies/

Video: https://odysee.com/@drsambailey:c/What-About-Rabies

Article: Rabies: The Ignored Facts

Article: THE RABIES HOAX

Article: https://www.vaccinationinformationnetwork.com/rabies-pasteur-and-the-rabies-vaccine/

Article: Rabies

Article: Pasteur and Rabies (1890)

Article: The Rabies Delusion Revealed

Rhinovirus:

Articles: https://viroliegy.com/category/rhinovirus/

Rotavirus:

Video: https://odysee.com/@drsambailey:c/Pharmaceutical-Fraud-and-the-Discovery-of-Rotavirus

RSV:

Article: https://viroliegy.com/category/rsv/

Video: https://odysee.com/@drsambailey:c/The-RSV-Vaccine-Up-sell

Russian Flu:

Book (page 130): Can You Catch A Cold?: Untold History & Human Experiments

Polio:

Article: The Polio Hoax

Article: The Case Against Polio Contagion

Articles: https://viroliegy.com/category/polio/

Book (Chapter 10: The Mysteries of Polio): Turtles All The Way Down: Vaccine Science and Myth

Book: The Moth in the Iron Lung: A Biography of Polio

Book (page 51): What Really Makes You Ill?

Article (page 172): https://archive.org/details/sim_archives-of-pediatrics_1952-04_69_4/page/172/mode/2up

Video: https://odysee.com/@drsambailey:c/Toxicology-vs-Virology-Rockefeller-Institute-and-the-Criminal-Polio-Fraud

Article: Polio: Rethinking the Origins of Paralysis

Pneumonia:

Article: Did Vaccines Reduce Flu and Pneumonia Deaths?

Rubella:

Video: Rubella Vaccines: What You NEED To Know

Salmonella:

Article (scroll down to “salmonella”): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

Scarlet Fever:

Article: The Infectious Myth Busted: Is Scarlet Fever Contagious?

Images (press Ctrl + F + scarlet fever): https://dissolvingillusions.com/graphs-images/

Sepsis:

Video: Sepsis - Are Antibiotics Life Saving?

Sexually Transmitted Diseases:

Article: https://whatreallymakesyouill.com/theres-no-such-thing-as-a-sexually-transmitted-disease-2-2/

Shingles:

Articles: https://viroliegy.com/category/shingles/

Article: What Is Shingles?

Smallpox:

Book: Dissolving Illusions: Disease, Vaccines, and the Forgotten History 10th Anniversary Edition

Documentary: https://odysee.com/@katie.su:7/thetruthaboutsmallpox

Articles: https://viroliegy.com/category/smallpox/

Article: Dispelling the Myth of Smallpox Contagion

Article: Smallpox and the Sanitary Revolution

Article: The Story of Smallpox and Vaccination

Article: Smallpox and the First Vaccine

Book (page 49): What Really Makes You Ill?

Article: https://whatreallymakesyouill.com/smallpox-dispelling-a-popular-myth/

Article: https://www.westonaprice.org/health-topics/smallpox-myths-and-the-birth-of-the-vaccine-awareness-movement

Spanish Flu / 1918 flu:

Article: The Spanish Flu Hoax

Podcast: Michael Bryant on the Spanish flu myth

Article: https://healthfreedomdefense.org/exploding-the-spanish-flu-myth/

Video: https://drsambailey.com/resources/videos/viruses-unplugged/exploding-the-spanish-flu-myth/

Book (page 149: Can You Catch A Cold?: Untold History & Human Experiments

Article: The Spanish Flu Hoax

Book (page 133): What Really Makes You Ill?

Article: https://www.govinfo.gov/app/details/SERIALSET-07803_00_00-002-0854-0000

Article: https://pmc.ncbi.nlm.nih.gov/articles/PMC2805838/

Video: https://odysee.com/@niodagar:b/Contagion-Spanish-Flu

Streptococcus:

Video: Part 1: Does Strep Actually CAUSE Illness?

Video: Part 2: How to Cure Strep without Antibiotics

Video: Part 3: Strep & Rheumatic Fever

Strep A:

Video: https://drsambailey.com/resources/videos/germ-theory/strep-a-superbug/

Article: Strep A-symptomatic

Article: A new bacterial disease? No, it's just more fearmongering

Article: https://whatreallymakesyouill.com/more-about-strep-a-what-is-going-on/

Syphilis:

Articles: https://viroliegy.com/category/syphilis/

Video: https://odysee.com/@drsambailey:c/The-Shame-of-Syphilis

Book (page 129): What Really Makes You Ill?

Article: https://whatreallymakesyouill.com/the-real-tragedy-of-tuskegee/

Article: What Is Syphilis?

Article: From the Syphilic Man to present day

Article (scroll down to “syphilis”): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

SV40:

Video: https://drsambailey.com/resources/videos/viruses-unplugged/shh-dont-mention-sv40/

Swine Flu:

Books (page 289): Virus Mania

Articles: https://viroliegy.com/category/swine-flu/

Tetanus:

Article: https://x.com/sanjay_world/status/1736030687646355773

Article: Tetanus - Lockjaw

Video: https://drsambailey.com/resources/videos/exclusive-content/do-i-need-a-tetanus-shot/

Article: https://viroliegy.com/2022/04/28/emil-von-behrings-diphtheria-tetanus-papers-1890-precursor-to-antibodies/

Tobacco Mosaic Virus:

Article: TMV: The First “Virus”

Video: https://odysee.com/@drsambailey:c/tobacco-mosaic-virus-the-beginning-and-end-of-virology

Video: https://odysee.com/@niodagar:b/TMV

Video (at 01:13:03): https://odysee.com/@spacebusters:c9/A-Farewell-to-Virology-pt-1-Final:3?t=4383

Article (scroll down to “TMV”): The “Virus” Concept

Tuberculosis:

Article: The Tuberculosis Hoax

Book (page 140): Dissolving Illusions

Articles: https://viroliegy.com/category/tuberculosis/

Article: Tuberculosis

Book (pages 146 & 505): What Really Makes You Ill?

Article: What Is Tuberculosis?

Article (scroll down to “tuberculosis”): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

Video: https://odysee.com/@drsambailey:c/TB-Cows-Lies-And-Koch-Ups:a

Urine Infections:

Video: Urine Infections

West Nile Virus:

Video: https://drsambailey.com/resources/videos/viruses-unplugged/dr-faucis-west-nile-virus/

Article: https://web.archive.org/web/20200716063805/http://davidcrowe.ca/SciHealthEnv/alive-wnv.html

Whooping Cough / Pertussis:

Video: https://drsambailey.com/resources/videos/germ-theory/whooping-cough-and-the-vaccine-myth/

Book (page 432): Dissolving Illusions

Article: Whooping Cough and Vaccines

Article: Whooping Cough and Vaccination

Article: Whooping Cough: Of Course They Were Coughing

Article (scroll down to “pertussis”): https://viroliegy.com/2022/10/10/kochs-postulates-and-the-great-asymptomatic-escape/

Images (press Ctrl + F + whooping cough): https://dissolvingillusions.com/graphs-images/

Yellow Fever:

Video: https://odysee.com/@drsambailey:c/What-You-Need-To-Know-About-Yellow-Fever

Zika:

Article: Zika: Covering for Pesticides and Vaccines

Article: ZIKA: Crazy Rabbit Hole Exposing a Scheme That Has NOTHING to do with VACCINES, "VIRUSES" or Big Pharma!

Article: https://theecologist.org/2016/feb/10/argentine-and-brazilian-doctors-suspect-mosquito-insecticide-cause-microcephaly

Book (page 429): What Really Makes You Ill?

In the late 1800s, German bacteriologist Robert Koch developed four postulates, which outline a set of logical criteria necessary to establish that a microbe causes a specific disease.

They emphasize association, isolation, causation, and re-isolation. While phrased slightly differently in various sources, the postulates are most commonly stated as follows:

1. The microorganism must be found in abundance in all cases of those suffering from the disease, but should not be found in healthy subjects.

2. The microorganism must be isolated from a diseased subject and grown in pure culture.

3. The cultured microorganism should cause the same disease when introduced into a healthy subject.

4. The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.

Even though these logical principles were popularized by Robert Koch in the late 1800s, they remain timeless. The four postulates are rooted in pure logic, providing a framework for falsifiability and aligning seamlessly with the scientific method.

Postulate 1: The microorganism must be found in abundance in all cases of those suffering from the disease, but should not be found in healthy subjects.

During 1958, the state of Michigan experienced its largest epidemic of poliomyelitis in many years, with more than 1,200 cases reported to the state department of health.

The greatest percentage of victims of a large polio epidemic subjected to laboratory investigation was carried out.

“Virological laboratory tests were carried out on 1,060 persons, probably the greatest percentage of victims of a large epidemic of poliomyelitis ever to be subjected to laboratory investigation.”

An in-depth analysis of the diagnosed cases revealed no polio “virus” could be detected in the majority of cases.

“During an epidemic of poliomyelitis in Michigan in 1958, virological and serologic studies were carried out with specimens from 1,060 patients. Fecal specimens from 869 patients yielded no virus in 401 cases, poliovirus in 292, ECHO (enteric cytopathogenic human orphan) virus in 100, Coxsackie virus in 73, and unidentified virus in 3 cases. Serums from 191 patients from whom no fecal specimens were obtainable showed no antibody changes in 123 cases but did show changes diagnostic for poliovirus in 48, ECHO viruses in 14, and Coxsackie virus in 6. In a large number of paralytic as well as nonparalytic patients poliovirus was not the cause. Frequency studies showed that there were no obvious clinical differences among infections with Coxsackie, ECHO, and poliomyelitis viruses. Coxsackie and ECHO viruses were responsible for more cases of “nonparalytic poliomyelitis” and “aseptic meningitis” than was poliovirus itself.”

“Antibody” changes were also absent in the majority of polio victims.

In a 1953 publication, Dr. Ralph Scobey describes how “virus” recovery was often negative in cases diagnosed with certainty, including fatal cases.

“Inconclusive evidence of a virus etiology in all cases of poliomyelitis is demonstrated by other facts. For example, in many cases where the diagnosis is made with certainty, virus recovery tests have proved to be negative. Even in fatal cases, it has not been possible in some cases to demonstrate a virus in the feces or in the spinal cord.”

Such was also reported by Dr. J. F. Edwards in 1956.

“Postmortem material derived from the C.N.S. of polio victims frequently fails to produce polio virus.”

The vast majority of patients claimed to have been infected with the polio virus are asymptomatic, as described by a 2015 publication.

“More than 99% of poliomyelitis cases are asymptomatic”

The medical authorities diagnostic procedure does admittedly not have a statistical relationship to the disease for which it is employed. Their test clearly does not establish an association between the claimed causative agent and the disease.

Robert Korns, N. Y. State Public Health Officer, acknowledged that the alleged detection of a polio virus did not have any real practical value, given that the claimed etiologic agent supposedly only causes the disease in a small fraction of people.

“Korns (1953), N. Y. State Public Health Officer, states that the isolation of the poliomyelitis virus for diagnostic purposes is almost never done and is of little practical value … He points out further that isolation of the poliomyelitis virus from the patient by no means establishes the diagnosis since the virus is widely prevalent in the population during epidemic periods without producing disease.”

2. The microorganism must be isolated from a diseased subject and grown in pure culture.

In 1949, a man named John Enders developed a technique for allegedly cultivating the polio “virus” in vitro. He observed some chemical reactions in a cell culture, and proclaimed that a virus was present.

However, such a procedure does not represent the isolation of a pathogen in a pure culture, as acknowledged by virologist Joseph L. Melnick in 1951.

“There is as yet no clear evidence that the [polio] virus has been obtained in pure form”

Ender’s later admitted that these lab-created effects could not be “considered as necessarily the result of viral activity.”

The cell culture method has long been used as the gold standard for polio “virus” cultivation, and the WHO still rely upon it for “virus” detection.

“The World Health Organization’s Global Polio Eradication Initiative continues to rely upon cell culture to isolate poliovirus”

No published scientific paper has ever shown that particles fulfilling the definition of polio viruses have been directly isolated and purified from any tissues or bodily fluids of any sick human or animal.

In her 1993 article published in Nature, biophysicist Eleni Papadopulos-Eleopulos describes how the detection of an indirect phenomena can not be considered virus isolation.

“Isolation, however, is defined as separating the virus from everything else and not detection of some phenomena attributed to, or similar to it. Such phenomena can only be used for viral detection, and even then, if and only if, they have been proved to be specific for the virus.”

3. The cultured microorganism should cause the same disease when introduced into a healthy subject.

4. The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.

The fact that scientists could induce paralytic disease in experimental animals by inoculating sterile biological material raises serious concerns about the uncontrolled nature of virologists transmission attempts.

Despite decades of artificial inoculations in monkeys, virologists were unable to demonstrate the phenomenon they hypothesized to occur: host-to-host transmission—suggesting that the artificially induced disease was not caused by a pathogenic agent.

• S. Flexner, 1910 - “No instance of the spontaneous transfer of the virus from a paralyzed to a normal monkey arose, although many opportunities for contagion in the course of our many experiments occurred.”

• I. Strauss, 1911 - “No observer has ever seen a monkey acquire poliomyelitis spontaneously … Leiner and v. Wiesner kept a monkey in the cage with paralyzed monkeys for fifty-two days without his acquiring the disease.”

• R. W. Lowett & M. W Richardson, 1911 - “No instances as yet have been reported in which one monkey has taken the disease [polio] from another, although long continued and intimate contact has been maintained.”

• Scientific American Supplement, 1912 - “Poliomyelitis artificially induced in monkeys has never been spontaneously transmitted to animals confined in the same cage or room.”

• J. J. Moren, 1912 - “Monkeys suffering from polio in the same cage with healthy monkeys, do not infect others.

• E. M. Mason, 1912 - “Healthy monkeys have been kept in cages with others in various stages of the disease, yet no infection has been reported.”

• R. Farrar, 1912 - “Attempts to convey the disease [polio] to non-infected monkeys by exposure to contagion from infected monkeys in the same cage have hitherto failed.”

• H. W. Frauenthal & J. VV. Manning, 1914 - “Advocates of the contagion theory were at a loss to account for the fact that spontaneous [polio] transmission among laboratory monkeys was never known to occur.”

• M. J. Rosenau, 1918 - “Monkeys have so far never been known to contract the disease [polio] spontaneously, even though they are kept in intimate association with infected monkeys.”

• International Committee for the Study of Infantile Paralysis, 1932 - “The natural insusceptibility of monkeys is also evidenced by the fact that [polio] contagion from one animal to another has never been demonstrated … Natural contagion from monkey to monkey has never been noted, although well monkeys have been caged with poliomyelitic monkeys at all stages of the disease.”

• K. F. Meyer, 1934 - “Well monkeys caged with poliomyelitic animals, or laboratory workers exposed to these apes, do not contract the disease.”

• K. F. Meyer, 1939 - “There is no record of one monkey catching the infection [polio] from another monkey by exposure.”

• J. A. Toomey, 1941 - “No animal gets the disease [polio] from another, no matter how intimately exposed.”

• R. R. Scobey, 1952 - “It is extremely difficult to understand how a human can contract poliomyelitis from another individual through dissemination of a virus by contact, carriers, excrement, unclean hands, unwashed fruits and vegetables, flies, etc. when a healthy animal in the same cage with an ‘infected’ animal, exposed to all of these natural factors, remains unaffected.”

Furthermore, epidemiological evidence demonstrates that the “virus” and the disease are not transmitted from the sick to the healthy in the hypothesized manner.

“The epidemiological facts are strongly against the theory that infantile paralysis is spread from person to person by direct or indirect contact.”

— Dr. Mark Richardsson, 1918

The measles virus began as an imagined construct to explain why people get sick. A particle was not observed first and subsequently a virus theory was developed.

As described by a 1924 article, researchers were unable to consistently observe any microbe in the bodily fluids of people with measles. Despite this, they presupposed that a minute pathogen existed that could explain sickness—what came thereafter arose to fulfil the presuppositional premise.

“Nevertheless, the search for the parasitic invaders by microscopic examination has failed to demonstrate constantly or consistently present forms in the Koplik spots or skin lesions of measles. Microscopy of the blood has likewise afforded only negative results; yet there are evidences of the presence of the virus in the blood stream, if one may trust the reports of experimental inoculation of measles in man with the blood of measles patients. The tests on animals have proved somewhat unsatisfactory because of the difficulty of identifying the exanthems. The "experimental measles" produced in monkeys by various sorts of inoculation are suggestive, though they by no means offer exact proof of the susceptibility of these animals to the human disease. The conclusion that the virus of measles is filtrable rests primarily on such animal tests. Sellards prefers to consider the filtrability an entirely open question.”

The measles “virus” was nothing more than an unseen, imagined entity—brought about by uncontrolled and artificial animal experiments.

However, the results were often irregular or entirely negative, according to a publication from 1962.

“Reproduction in monkeys of signs of mild measles after inoculation of bacteria-free materials from patients was reported subsequently by a number of investigators, although the results were often irregular or entirely negative.”

In 1924, Dr. Andrew Sellards published A Review of the Investigations Concerning the Etiology of Measles. He describes how the symptoms of the monkeys experimented upon were “rather vague”, and that the scientists were plagued by “conflicting results” and “marked variation”.

These inconsistent results are further weakened by the fact that comparable results could be produced in humans by the injection of a mixture of normal blood from healthy individuals.

One person developed “a fairly extensive maculopapular eruption appearing first over the chest and then over the arms.”

Another subject exhibited “a well-marked erythema which was widely distributed over the chest, back, abdomen and extremities.”

Virologists did not have a laboratory method to detect the presence of an alleged measles virus, as acknowledged by an article published in 1950.

“Further difficulties in the study of measles have been the inability to obtain experimental measles in any host less inconvenient and expensive than the monkey, and the absence of a laboratory method for detecting the presence or quantity of virus.”

Instead, they based their belief on fallacy loop of circular reasoning. In 1948, virologist Wendell Stanley stated that evidence for the existence of a virus was provided by the manifestation of disease.

“The sole means of recognizing the existence of a virus is provided by the manifestations of disease”

This is because the “virus” was nothing more than a concept—an idea rather than a concrete entity.

It wasn’t until 1954 that the measles virus was first claimed to have been propagated in the laboratory.

“A possible lead towards developing a preteventive vaccine against measles has been reported by Dr. John F. Enders, of Harvard Medical School, who won a Nobel prize for his polio research.

He announced Wednesday "very suggestive" evidence of the long-sought isolation of the elusive measles virus—and of possible means for its laboratory growth. The method described uses a "tissue culture" method like that which paved the way for development of the Salk vaccine for polio.

Enders told an audience of scientists at the National Institutes of Health that he and assistants had found in washings and blood of measles patients "an agent" which has passed certain tests indicating it may be the actual causative organism of measles.

It remains to be proved, he said, that it actually is the measles virus”

In a 1954 experiment, John Enders postulated that signs of deterioration in organ tissue in vitro would indicate the presence of a measles virus, despite the fact he didn’t observe any virus particles.

However, several researchers subsequently reported that the same lab-created effects occurred without the addition of a presumably infected specimen.

In 1956 for example, virologist Gisela Ruckle observed the same degenerating changes attributed to measles virus in uninoculated cultures, and in cultures inoculated with clinical material other than from measles patients.

“The examination of the stained preparations of one batch prepared on June 23, 1955, revealed the presence of cytopathic changes identical with those induced by measles virus in the control, as well as in the cultures inoculated with clinical material other than from measles patients … A greater number of uninoculated cultures derived from cell batches prepared on June 29, 30 and July 8, were examined and also showed changes, in a number of cultures, which had been associated until this time only with measles virus.”

These spontaneously degenerating cultures were also shown to be “immunologically indistinguishable from human measles virus”.

In light of these problems, virologists admitted in 1959 that their laboratory tools could not establish the existence of a measles virus.

“Agents that are identical to measles virus in terms of their serological relationships, cytopathological effects and range of tissue culture susceptibility have been found in uninoculated cultures (Ruckle, 1956; Brown, 1957). In view of these complications, cultures of monkey kidney cannot be considered a suitable tool for the isolation or propagation of measles virus. Even if, by careful serological and cytological tests, one identifies an agent grown in monkey kidney as measles virus, there can be no certainty that it did not derive from the cultures themselves.”

Moreover, these virologists acknowledged that no virus particles could be identified in tissue assumed to be infected with measles virus.

“Electron microscopic observations of amnion cells in cultures infected with measles virus have been reported (Baker et al., 1957), and similar studies are in progress in our laboratory (Reissig, 1958). Many abnormal structures are present in the infected cells, but none of them has yet been identified with the virus particle.”

Virology had refuted itself. Despite access to electron microscopy, virologists could not locate any physical entity that could be identified as a measles virus, and their indirect laboratory tools turned out to be non-specific.

It was not until 1961 that Anthony Waterson et al. claimed to have imaged the elusive measles virus.

“Although it has been possible for many years to grow the virus of measles in experimental animals and, more recently, in tissue culture, information about the nature of the particle has been scanty.”

They located some dots in tissue claimed to have been infected with measles virus. These particles were declared to represent measles virus, despite that the biological function of these structures remained unestablished.

Furthermore, it is known that a myriad of minute vesicular particles can be found in normal tissue, as seen on the image below.

The symptom complex termed ‘measles’ does not require the existence of a virus. The same set of symptoms can be caused by various non-microbial factors, such as drug eruptions, and metal toxicity, as noted by a 1912 publication.

“The stimulating effect of salvarsan [arsenic compound] on the skin is seen in the way it causes eruptions such as urticaria, and erythemas that may simulate the rashes of measles or of scarlet fever.”

In 2020, a 9-year-old female patient was initially misdiagnosed as having measles, subsequently a diagnosis of mercury intoxication was established.

The polio fraud began in the early 1900s with Simon Flexner of the Rockefeller Institute.

He is said to have established the etiologic agent of polio by a number of experiments, as described by a 1911 publication.

“All doubt as to the infectious character of the disease has been removed by the experimental investigation of Flexner and others.”

Ground up nervous tissue was injected into the brains of monkeys. Signs of paralysis in the monkeys was proclaimed by Flexner as evidence for the presence of an unseen pathogen in the biological material inoculated.

Medical men were perplexed by the absence of contagion during the experiments.

“Monkeys did not spontaneously take the disease, and the question naturally arose why a disease which was so fatal in this species should not occur naturally or spontaneously in that species.”

Answers to that question could have been provided if control experiments weren’t neglected. Could it be that the sickness observed in the monkeys were not caused by an imagined pathogen?

Simon Flexner disregarded the fact that any injection into the brain is invariably attended with consequences to the creature operated on, with paralysis as a frequent complication, as noted by a 1886 publication.

“Every physiologist or pathologist knows that intradural inoculation [into the brain].. even of the simplest septic or aseptic product, is almost invariably attended with consequences most grave to the creature so operated upon. Naturally, paralysis most frequently follows.”

[…]

“If an opening be made in the cranium of the dog, or the rabbit, directly over the nerve-centres,—and the nervous system of either is much more impressible than that of man, and a drop of pus, blood, or bouillon introduced in the submeningeal space, the miracle would be if the creature did not speedily develop a paralysis of facial muscles and posterior extremities!”

In 1886 for example, Dr. Edward Spitzka injected into the brains of dogs a variety of innocuous substances, such as normal calf tissue and soap. Paralysis and death followed.

Simon Flexner jumped to conclusions based on erroneous evidence, because the inflammation of the nervous system set up by the placement of a foreign substance in contact with the brain was sufficient to account for all the symptoms displayed by the monkeys experimented on—no imagined virus required.

Despite decades of artificial inoculations in monkeys, virologists were unable to demonstrate the phenomenon they hypothesized to occur: host-to-host transmission. In 1932, the International Committee for the Study of Infantile Paralysis reported that all attempts to demonstrate experimental contagion had been futile.

“The natural insusceptibility of monkeys is also evidenced by the fact that contagion from one animal to another has never been demonstrated.”

The complete failure to experimentally demonstrate contagion made Dr. Ralph Scobey question the purported transmissibility of the disease in an article published in 1952.

“It is extremely difficult to understand how a human can contract poliomyelitis from another individual through dissemination of a virus by contact, carriers, excrement, unclean hands, unwashed fruits and vegetables, flies, etc. when a healthy animal in the same cage with an “infected” animal, exposed to all of these natural factors, remains unaffected.”

Due to the inability to isolate and image the alleged polio virus, Dr. Oliver Dahl questioned the existence of a polio virus in an article published in The Times News in 1935.

“How is any thinking person to believe that there is a virus that in some way causes inflammation in the gray matter of the spinal cord of infants when this supposed to be virus has never been isolated? It is but a hypothetical something. A reasoning mind could better believe that the moon is made of cheese, for the moon at least has the shape and color of cheese. No one has ever seen, smelt nor felt, nor in any other way isolated this supposed to be poliomyelitis virus.”

In fact, epidemiologist and public health administrator Leslie Lumsden admitted that they didn’t actually know with certainty whether polio was infectious.

“We do not know the main source or sources of the infection nor, with certainty, whether the disease is infectious.”

Virologists were baffled by the simple question: “What is the disease agent in infantile paralysis?”

“Before we begin to discuss the disease itself in humans, I feel we should have a clearer understanding of the laboratory side. Doctor Meyer, will you summarize the present status of poliomyelitis in the field of experimental research? Dr. Meyer: That is a difficult question to answer directly, since we are still baffled by the simple question, “What is the disease agent in infantile paralysis?” … We do not know whether it is a living germ or something else growing in the cells of the brain. We cannot isolate it like a germ in a test tube, and it is too small to be seen with a microscope.”

The polio “virus” was nothing more than an unseen, imagined entity—brought about by uncontrolled and artificial animal experiments. Until the 1950s, the only way to isolate a polio “virus” was through the inoculation of a monkey.

“Until recently, inoculation of monkeys has remained the only means of isolating these viruses, and the production in the monkey of the characteristic myelitis with anterior-horn-cell degeneration has been the criterion for the identification of this group of agents.”

However, the belief in the existence of this hypothetical pathogen was based on faulty evidence, because the injection of uninfected tissue into laboratory animals could likewise produce paralytic disturbances, as described by a 1986 article published in Journal of the American Medical Association.

“It would be demonstrated that injection of uninfected nervous tissue into laboratory animals could produce paralytic disturbances with central nervous system inflammation and demyelination.”

The fact that researchers could induce paralysis in experimental animals by the injection of normal tissue brought the field of virology into question in an article published in the journal Archives of Pediatrics in 1950.

“Although Landsteiner and others have been able to inject emulsions of spinal cord material into experimental animals to cause a paralytic disease, a number of workers have also caused paralysis in experimental animals simply by injecting normal nervous tissues. This fact would indicate that some of our modern studies relating to the so-called virus of poliomyelitis require careful reappraisal.”

For example, in a study entitled The Effects of the Injection of Normal Brain Emulsion into Rabbits published in 1932, Dr. Edward Hurst demonstrated that the injection of sterile brain tissue into rabbits can cause severe toxic manifestations, including paralysis and death.

“The introduction parenterally in rabbits of emulsions of normal brain tissue is followed by severe toxic manifestations leading to wasting and death. In a few cases paralyses occur.”

In the 1940s, when the electron microscope was developed for biological material and commercial use, virologists finally had access to a powerful microscope to view their imagined polio virus.

However, virologists could not find anything different in hosts supposedly infected with a polio virus from what could be imaged in healthy subjects.

In 1949, a group of virologists perfomed control experiments and found particles indistinguishable from what was believed to be polio “viruses” in normal uninfected tissue.

“Rhian et al. (1949) concluded that none of the occurrences in electron micrographs of preparations of poliomyelitis virus published up to that time showed any conclusive evidence that they really corresponded to poliomyelitis virus. These authors obtained particles of essentially the same size, shape, and nitrogen content from both normal and Lansing poliomyelitis virus-infected tissue.”

These virologists concluded that the imaged particles purporting to depict polio “viruses” were simply non-specific debris.

“From a critical examination of our work, and that of others, we conclude that there is no evidence that a virus of the poliomyelitis group has ever been unequivocally identified on electron micrographs thus far published.”

In agreement, virologist Joseph L. Melnick stated in 1951 that there was no clear evidence that the polio virus had been isolated and imaged, because when experiments were adequately controlled by subjecting normal tissues to the same procedures, no difference was found in normal tissue compared to the presumably infected tissue.

“In spite of many attempts, there is as yet no clear evidence that the virus has been obtained in pure form or that it has been visualized in the electron microscope. When such experiments are adequately controlled by subjecting normal tissues to the same procedures of differential sedimentation or fractional precipitation, then similar "purified" material has been obtained (43, 82, 83).”

In the early 1950s, the alleged polio virus began to be study in vitro. Polio researchers would inoculate harvested organs of monkeys, instead of injecting living monkeys.

It was postulated that signs of deterioration in the organ tissue would indicate the presence of a virus.

However, researchers soon discovered that these lab-created effects were not dependent on the addition of a (presumable infected) host sample, as described by a 1973 article.

“It has been recognized for a long time that uninoculated cell cultures may show spontaneously the cytopathological effects (CPE)”

It has since been established that these tissue changes are artifacts resulting from the artificial conditions of the experiment.

The Virology Controls Studies Project

CELL CULTURE ISOLATION CONTROL EXPERIMENT

All of the content that is put out on this Substack is going to be for free. If you feel so inclined to donate or Sign up for a Paid Subscription that is very much appreciated. It will keep me writing, putting out content and continuing the largest Control Studies Project falsifying Virology…

Read more

2 years ago · 105 likes · 30 comments · Jamie Andrews

This faulty method was used to produce a polio vaccine—and when the polio vaccine was launched, the diagnostic criteria of polio changed, thus artificially reducing case numbers which brought about favourable results of vaccination.

Polio as a disease does not necessitate the existence of a virus, as described by polio researcher Dr. Ralph Scobey in 1953.

“It is generally believed at the present time that poliomyelitis is a communicable disease caused by a virus. However, this broad definition excludes other conditions to which the term "poliomyelitis" can also be applied. The meaning of the Greek words from which "poliomyelitis" is derived implies inflammation of the gray matter of the central nervous system regardless of the etiology.”

In his 1952 article entitled The Poison Cause of Poliomyelitis and Obstructions to Its Investigation, he describes how polio, resulting from poisons, has been demonstrated clinically in humans and produced artificially in experimental animals. The marked seasonality of polio could be explained by the use of poisonous insecticides, Scobey suggests.

“The poison cause of paralysis has been known for many years. Poliomyelitis, resulting from poisons, has been demonstrated clinically in humans and produced artificially in experimental animals. A relationship between harvest and poliomyelitis has been suggested repeatedly. At such times, corresponding with epidemics of poliomyelitis, some foods of harvest may be poisonous as a result of fertilizers, insect sprays and intrinsic chemical changes.”

Arsenic, once a common insecticide, has been shown to cause pathological alterations typical of polio, as described by a 1905 publication.

“We know that such poisons as lead, arsenic, etc., are able to produce distinct changes in the cells of the central nervous system. Pathological alterations, typical of anterior poliomyelitis, have been demonstrated in poisoning of various kinds, more especially by lead.”

In 1882 for example, Edward C. Sequin established that arsenic can cause poliomyelitis, in his publication Myelitis Following Acute Arsenical Poisoning.

“Arsenical paralysis is the expression of a myelitis. This myelitis approximates the type known as poliomyelitis.”

Dr. Robert Lovett outlines a few examples of polio resulting from the exposure to metallic poisons in an article published in 1907.

“Vulpian produced, experimentally, paralysis of the extensors and lesions resembling those of poliomyelitis in a dog by lead poisoning, and in a case of lead poisoning found pronounced poliomyelitis with colloid degeneration and cell atrophy. Phillippe and Gauthard report a case of anterior poliomyelitis from lead poisoning, and Obrastoff one from arsenical poisoning. Onuf reported the case of a painter with flaccid paralysis of both legs, in whom autopsy showed lesions characteristic of the disease.”

Louis Pasteur’s rabies investigation began in the late 1800s. However, his initial attempts to establish the etiology of rabies were unsuccessful, as described by the Pasteur Institute.

“Louis Pasteur’s initial efforts to isolate the rabies virus proved unsuccessful as the virus remained invisible.”

Pasteur did not give up. In his book The Private Science of Louis Pasteur, historian Gerald Geison describes how Pasteur utilized a hit-or-miss approach—inject a variety of animals with a wide range of substances and then watched what happened.

“Pasteur’s frustration becomes most evident in the notebook pages devoted specifically to efforts to find a vaccine against rabies … Charting through the Byzantine maze of Pasteur’s early laboratory notes on rabies, one eventually realizes that his basic procedure was simply to inject a variety of experimental animals—though mainly rabbits—with a wide range of cultures or substances and then watch what happened.”

Eventually, he discovered a successful method. Pasteur would use the nervous tissue from a diseased animal and inject it directly into the brain of a healthy animal through a hole drilled into its skull.

“But as rabies is a disease of the nervous system, together with Emile Roux, Louis Pasteur then had the idea of inoculating part of a rabid dog’s brain directly into another dog’s brain. The inoculated dog subsequently died.

The experiment was then conducted on rabbits as the risk for the experimentalists was less than with rabid dogs.”

This highly invasive methodology did not reflect how an animal would presumably acquire the disease in the natural world.

According to Dr. G. Archie Stockwell in 1886, it was not surprising that the animals became diseased, because such an inoculation is invariably attended with consequences to the creature operated on, with paralysis as a frequent complication—no hypothetical pathogen required.

“Every physiologist or pathologist knows that intradural inoculation,—the means employed by Pasteur to secure “infected” (?) spinal cords,—even of the simplest septic or aseptic product, is almost invariably attended with consequences most grave to the creature so operated upon. Naturally, paralysis most frequently follows, yet it is the evidences of paralysis upon which Pasteur so confidently relies for his diagnosis of rabies. If an opening be made in the cranium of the dog, or the rabbit, directly over the nerve-centres,—and the nervous system of either is much more impressible than that of man, and a drop of pus, blood, or bouillon introduced in the submeningeal space, the miracle would be if the creature did not speedily develop a paralysis of facial muscles and posterior extremities!”

Louis Pasteur was never able to purify and isolate a rabies microbe. Despite his failure to identify the causative agent he expected to find, he never wavered in his belief. His invisible white whale remained just that—a belief.

“The microbe of rabies has not been isolated as yet, but, judging by analogy, we must believe in its existence.

Pasteur clung to his belief in an invisible enemy, adjusting his approach to fit his narrative rather than letting evidence guide him. He mastered the art of manipulating fear and fantasy, convincing people to line up for his toxic treatments.

Pasteur’s neglect of controls in his animal experiments was noted by Dr. Thomas M. Dolan in his 1886 article entitled M. Pasteur’s Prophylactic.

“Control experiments were neglected.”

Dr. Edward Charles Spitzka was an eminent late-19th century psychiatrist, neurologist, and anatomist.

Dr. Spitzka was particularly critical of Louis Pasteur. In order to disprove Pasteur, Spitzka conducted experiments to show that foreign substances injected into the brain would cause inflammatory disturbances, the symptoms of which would be identical to those of “rabies.” He injected into the brains of dogs varied substances such as calf tissue and even soap.

“The experiments that Dr. Edward C. Spitzka has been conducting at the Veterinary Infirmary in East Fourteenth street, in support of his theory that rabies or hydrophobia can be produced in dogs by the insertion into their brains of any foreign substance, have satisfied him, so he says, of its truth.

Of six healthy dogs inoculated, five have died. Some portions of the spinal cord of a healthy calf and other substances were introduced into their brains.”

By establishing that symptoms of nervous system disturbance and paralysis could be produced by introducing non-rabic foreign substances into the brain of dogs, Spitzka demontrated that Pasteur’s rabies method was invalid. He published his results in The Journal of Comparative Medicine and Surgery (an alternative link can be found here).

As previously stated, Pasteur preferred to inoculate rabbits, due to the convenience.

However, Dr. N. E. Brill reported in his 1887 publication that the symptoms of “rabies” in the rabbit were vague and indefinite.

“The symptoms of hydrophobia in the rabbit are vague and indefinite. No two authors and experimenters have found them to be the same.”

Together with Dr. Edward Spitzka, he was able to produce paralysis in rabbits by the inoculation with spinal cords from healthy animals.

“We have been able to produce paralysis in a rabbit by inoculation with healthy spinal cord which had been treated in the manner described by Pasteur.”

They utilized the spinal cords of these paralytic rabbits and inoculated them into dogs, and produced in the dogs the symptoms which have been ascribed to as rabies.

“In a series of experiments made a little over a year ago, in connection with Dr. E. C. Spitzka, we found that we could produce the symptom-complex assigned to hydrophobia in rabbits by inoculating with septic material, or with the healthy spinal material of another rabbit; but the symptoms varied, with the exception of paralysis, which was constant in each, almost as often as the number of experiments … We utilized the spinal cords of these paralytic rabbits prepared in strict accordance with Pasteur’s directions and inoculated them into dogs, and produced in the dogs those symptoms which have been ascribed to dumb rabies in the dog.”

Dr. G. Archie Stockwell reported in an 1888 issue of the Therapeutic Gazette, that he was able to induce the symptoms alleged to mark rabies in rabbits by the inoculation of saliva from various healthy creatures.

“The writer, during a series of experiments, developed all the symptoms alleged to mark hydrophobia, or rabies, in rabbits by the intradural inoculation of healthy saliva taken from various creatures, man included; also by tartar from human and canine teeth!”

Thus, the symptom complex Pasteur observed in rabbits following the intracerebral injections was simply a result of the experimental procedure itelf.

In a study entitled The Effects of the Injection of Normal Brain Emulsion into Rabbits published in 1932, Dr. Edward Hurst established that the injection of normal brain emulsions into rabbits leads to severe toxic manifestations, including paralysis and death.

“The introduction parenterally in rabbits of emulsions of normal brain tissue is followed by severe toxic manifestations leading to wasting and death. In a few cases paralyses occur.”

The results of these control experiments made physicians doubt the validity of Pasteur’s inoculation practice. In a paper published in The Lancet by surgeon-general Charles A. Gordon, the diagnostic method of intercranial inoculation was brought into question—due to the fact that animals likewise took sick when innocuous matter from healthy animals were injected in the same manner.

“The reliability as a crucial test of intercranial inoculation as practised in Paris is by no means generally accepted; on the contrary, effects identical in character have followed similar inoculation from healthy dogs with innocuous matters and from the preliminary operation in the absence of any inoculation.”

In fact, the existence of rabies as a disease was questioned by many, Dr. Gordon describes.

“Opinions differ as to the existence of rabies as a definite and specific disease due to one particular cause, and to it only, or as an attendant condition in the course of various maladies.”

As early as 1826, a surgeon named Robert White doubted that rabies (hydrophobia) was a specific disease spread by the bite of a dog. In his book entitled Doubts of Hydrophobia as a Specific Disease to Be Communicated by the Bite of a Dog, he describes how he inoculated himself with the fluids of a presumably rabid animal without becoming sick.

“I have also inserted a portion of the supposed poison on the point of a lancet in my own arm, an experiment I would at any time repeat, but without any effect, not even the slightest irritation succeeding the wound.”

According to Dr. Charles Gordon, the symptom complex termed ‘rabies’ or ‘hydrophobia’ was looked upon by many physicians as a non-specific condition resulting from various causes.

“By a considerable number of capable observers hydrophobia is looked upon as not being itself a specific disease due to one cause alone, but as a “condition” resulting in different cases from various causes, including traumatic injuries and nervous “shocks,” as a complication in the course of various diseases, and as occurring in the absence of apparent cause. In these respects the disorder is referred to the class of maladies which includes also tetanus, epilepsy, chorea, &c.”

In agreement, Dr. G. Archie Stockell concluded that the disorder termed hydrophobia, or rabies, is merely a development of irritated nerves arising from numerous and variable causes.

“The conclusion is rapidly being forced upon thinking and observant minds that so-called hydrophobia is merely a development of irritated nerves arising from numerous and variable causes, wholly devoid of elements of specificity.”

In an article entitled Dr. Pasteur a Fraud - There Is No Such Thing as Hydrophobia, Dr. J. M. Crawford states that rabies is an old established superstition.

“I do not believe that there is such a disease. And furthermore, I don’t think you will find many reputable physicians who do believe in it. This feeling has been a growth of recent years, and has come with the improvement in the art of diagnosis. It is an old established superstition, a tradition, that the saliva of a mad dog is a deadly poison, and people won’t get it out of their heads for a long time yet. But physicians shake their heads now and look dubious at the mention of hydrophobia.”

Dr. Joseph W. Hearn, professor of clinical surgery, claims that the bite of a dog is no more dangerous than the scratch of a pin, in a 1896 article entitled Is Hydrophobia a Myth?

“It is encouraging to be informed by distinguished professors of medicine and surgery that hydrophobia is, at best, a theory and has no actual existence. It belongs, according to a pamphlet recently published in Philadelphia, to the class of simulated diseases. “I am of the opinion,” says Dr. Joseph W. Hearn, professor of clinical surgery in Jefferson Medical college, “that the bite of a dog is no more dangerous than the scratch of a pin”

Dr. Matthew Woods published an article in 1896 in which he provided evidence of the non-existence of rabies. In Philadelphia, 150,000 vagrant dogs were handled without a single case of rabies. In London, of the 2,668 patients that had been bitten by angry dogs, not one had developed rabies, and in another hospital in London, no case of rabies developed in 4,000 patients bitten by supposed rabid dogs. After sixteen years of investigation, Dr. Charles W. Dulles failed to find a single case on record that could be conclusively proved to have resulted from the bite of a dog.

“At the Philadelphia Dog Pound, where, on an average, over six. thousand vagrant dogs are taken up annually, and where the catchers and keepers are frequently bitten while handling them, not one case of hydrophobia has occurred during its entire history of twenty-five years, in which time about 150,000 dogs were handled.

The record of the London Hospital a few years ago showed 2,668 persons bitten by angry dogs. None of them developed hydrophobia. St. George’s Hospital, London, records 4,000 patients bitten by dogs supposed to have been mad. No case of hydrophobia.

Finally, Dr. Charles W. Dulles, lecturer on the History of Medicine at the University of Pennsylvania, who has had the honor of being repeatedly appointed by the medical societies of the State to investigate rabies, and has read various papers on the subject before the American Medical Association, the College of Physicians of Philadelphia, the Philadelphia County Medical Society, the Medical Society of Pennsylvania, the Medico-Legal Society of New York, and has corresponded on the subject with most of the distinguished medical men of Europe, a physician familiar both with the literature of rabies, the history of Pasteur and the institutions called by his name, and who in addition has performed the almost incredible task of investigating, either personally or by correspondence with the physician or others in attendance, every case reported in the newspapers of the United States for the past sixteen years, shows that hydrophobia is extremely rare, so much so that he inclines to the view that “there is no such specific malady,” having “after sixteen years of investigation failed to find a single case on record that can be conclusively proved to have resulted from the bite of a dog”

A 1897 newspaper reported that over 100.000 dogs were handled by agents without protection, many of the dogs were supposedly rabid — yet no one ever got rabies, despite frequent bites and scratches.

“Dogs are shot or clubbed to death daily for rabies when they are simply ill, just as a man might be, and not mad. A dog may tumble down in a fit, but he isn’t mad. He may have trouble with his stomach and sulk, but he isn’t mad. He may have epilepsy and froth at the mouth, and not be mad. Within the last four years our agents have handled over 100,000 dogs and over 150,000 cats. They have been called upon to shoot so-called mad dogs, and instead of doing so have picked them up in their arms and put them into the ambulance. They have been scratched and bitten again and again at our shelters. Sometimes they have had an arm or a hand crushed by a savage bite, and have had to stay a week in hospital; but no one of them ever had hydrophobia”

The Daily Pioneer wrote in 1903 about a dog warden that had been bitten or scratched over 300 times. Many of the dogs were mad and frothed at the mouth — yet he didn’t develop rabies.

“Scientists and veterinarians of this day are pretty generally agreed that hydrophobia is largely superstition; that the people of this country are needlessly worrying themselves about “mad” dogs, very much to the benefit of “institutes” that “cure” dog bites.

During the past twenty years the Society for the Prevention of Cruelty to Animals of Hudson, N. J., has employed about twenty different dog wardens, who are constantly handling dogs of all degrees and of all ailments, but hydrophobia is unknown to any of these experts.

One of these wardens, employed continuously for the last seven years by that society and the Jersey City board of health, has handled in that time nearly 10,000 dogs, always catching even the most vicious with bare hands and without the aid of gloves, nets or accessories.

He was bitten or scrached over 300 times, and bears eighty marks from these mutilations—bitten by alleged mad dogs many times, in some instances where they frothed at the mouth.”

A number of other diseases besides “rabies” have the common features of dread and inability to swallow water, as maintained by Dr. Irving C. Rosse.

“The chief reason then for skepticism in regard to this badly elucidated disease seems to be the faulty nature of the evidence. Many of the so-called cases, when thoroughly sifted, resolve themselves into some distinct, recognizable disease, generally hysterical or nervous, in which terror and expectant attention are the main factors. In fact a number of other diseases besides hydrophobia have the common features of dread and inability to swallow water, associated with convulsive movements and psychic manifestations.”

The hallmark symptom of rabies is considered to be dysphagia (hydrophobia). However, as stated by Dr. Matthew Woods, this condition is non-specific and can be featured in atleast 30 other diseases besides rabies.

“We are aware that dread and inability to swallow water, associated with convulsive movements, and striking manifestations are common features of at least 30 other diseases besides rabies.”

Such was outlined in Dr. Charles Dulles publication entitled Disorders Mistaken for Hydrophobia, in which he noted that the symptoms of hydrophobia appeared in no fewer than thirty disorders—and likely many more.

“Meningitis, whether cerebral or spinal, may give rise to all the symptoms of excitement and dread of drinking which are commonly attributed to hydrophobia.”

In a case report of polio for example, the non-specific symptoms of rabies were present.

“On attempting to drink some of the fluid, swallowing was evidently difficult and accompanied by much pain. There was considerable mucous flowing from the nose and mouth, the mucous being thick and ropy.”

In the dog, the symptoms ascribed to as rabies may be induced by various causes, as outlined by Dr. Stockwell.

“Excessive saliva in the canine is induced by all forms of fatigue, by affections of the ear and throat, mouth and teeth,—especially dental caries,—eating of “dog” or “quitch” grass (Triticum repens), distemper, choking, inflamed wounds, fear, paralysis, etc.; and paralysis, independent of rabic condition, is a concomitant of many local, sympathetic, brain, and nerve disorders. The same is also true of twitching of eyes, eyelids, jaws, muscles, etc.; of lolling tongue, indrawn tail, updrawn flanks, drooping head, slinking gait, and wandering habit (the last is much more likely to be due to a taste for mutton than any disease); one and all, save as indications of misery and suffering, are not of the least value alone, and nearly all are present in mastoiditis, anæmias, fevers, and the lesser forms of illness.”

Rabies has also been shown to arise idiopathically (spontaneously), according to Dr. Charles Gordon.

“That the condition so described has in particular instances arisen idiopathically is attested by observers whose statements are beyond question.”

In 1931 for example, Dr. E. Weston Hurst documented an outbreak of rabies without a history of bites.

Louis Pasteur gained fame and recognition, despite the problematic nature of his rabies research. But this was largely a consequence of the popular press, wrote Dr. Elmer Lee, Vice President of the American Academy of Medicine.

“So great is the influence of the modern press that a scientific proposition, while still in the germinative state, is heralded throughout the civilized world, and is quickly transformed into a perfected science by writers of the press. There were a few who were able to doubt the truth of the allegation as to the curative influence of the Pasteur lymph. Long before cool and scientific inquiry could be made by physicians away from this center of discovery, the die had been cast that hydrophobia was curable by Pasteur lymph. At this present moment there are unmistakable proofs that error in judgment and in practice is the largest element in the hydrophobia cure.”

Pasteur became alarmed at his own work due to the many deaths among the patients, according to Dr. Lee.

“During the first few years of the experimental inoculations for rabies, many deaths occurred among the patients; so many, in fact, that Pasteur himself became alarmed at his own work.”

Dr. Charles Bell Taylor of England strongly condemned Pasteur’s treatment for rabies.

“Pasteur’s treatment for hydrophobia is the most extraordinary delusion which has afflicted men of science for centuries.”

Pasteur was accused of cruelly decieving the world in a 1895 article entitled The Remedies of the Celebrated French Physician Pronounced Useless Always and Dangerous Often.

“Pasteur’s best known act was the declaration in 1884 that he had discovered a certain remedy for hydrophobia. He declared what was not true, and cruelly deceived the world … I hold in my hand a list of 270 people who have died after undergoing Pasteur’s ‘sure cure’ for hydrophobia.”

Agent131711’s Substack

Foot Soldiers of Scientism: Vaccines are Satanic Rituals (Untold History of Louis Pasteur)

“More than ridiculous - it is irrational - to say that corrupt matter taken from the boils and blisters of an organic creature could affect the human body other-wise than injure it” - Dr. Stowell, MRCS of London when speaking of his experience of thirty years of being a vaccine practitioner…

Read more

2 years ago · 230 likes · 155 comments · Agent131711

Diphtheria is said to be a contagious disease which is characterized by an inflamed throat. In severe cases, a grey coating develops in the throat, called a pseudomembrane.

The disease is purported to be caused by a toxin produced by the bacterium Corynebacterium diphtheriae, also known as the Klebs–Löffler bacillus, because the German bacteriologists Edwin Klebs and Friedrich Löffler (also called Loeffler) is said to have discovered the bacterium that allegedly causes diphtheria, in the late 1800s.

Edwin Klebs (1883) did not perform any experiments, he simply discovered the presence of the bacterium in people with diphtheria, and assumed a causal association.

Under the section Etiology in the 1895 book entitled Diphtheria and Its Associates, it is declared that Klebs did not establish a causal relationship between the bacterium and diphtheria.

“To Klebs, therefore, the credit of having discovered this organism is undoubtedly due. But since he never definitely announced that he had been able to obtain pure cultures of it, it must be said that he failed in establishing its causal relationship to the disease.”

A mere association between a microorganism and a disease does not establish causation, as stated by Dr. Herbert Snow in 1913.

“Hence a natural temptation, whenever a micro-organism is found in connection with a malady, to assume that the latter is directly due to the former, and to overlook necessary links in the chain of scientific proof.”

Further, the Dr. Snow describes how there is ample evidence contradicting the causal association between microorganisms and disease.

“There has never been anything approaching scientific proof of the causal association of micro-organisms with disease; and in most instances wherein such an association has been pretended, there is abundant evidence emphatically contradicting that view.”

This fact became evident to Friedrich Loeffler, who could not detect the presence the Klebs-Loeffler bacterium in all cases of diphtheria.

Rather than admitting to be wrong, Loeffler made up excuses as to why his belief could still be true despite evidence to the contrary, known as the ad hoc rescue.

Robert Koch and Friedrich Loeffler formulated Koch’s postulates, which are four criteria designed to establish a causal relationship between a microbe and a disease. The first postulate states that the microorganism must be found in abundance in all organisms suffering from the disease.

In his 1895 publication entitled Ueber die Beziehungen des Löffler’schen Bacillus zur Diphtherie, Dr. David Hansemann critically examines the germ theory of diphtheria. On page 364, he quotes Friedrich Loeffler’s admission how he falsely corroborated Koch’s first postulate in diphtheria by labeling the cases where the bacterium was absent as something different.

“The pathogen of diphtheria is the diphtheria bacillus. However, since there are illnesses that appear clinically as diphtheria, but in which the bacillus is missing, all of these illnesses must henceforth be separated from diphtheria as something completely heterogeneous. Only where the bacillus is present is there genuine diphtheria.”

[Translated using an online translator.]

The term “pseudo-diphtheria” was thus born. Cases of diphtheria where the Klebs-Loeffler bacterium was missing was diagnosed as such, as described by a 1891 article.

“Pseudo-diphtheria. This term is employed through want of a better one. It is proper to state in this connection that clinical observations and experiments, carefully made, have demonstrated the fact that certain other microbes besides the Klebs-Lœffler bacillus, sometimes produce a pseudo membranous inflammation upon the faucial or other surface, which as regards its anatomical characters, appears to be identical with that in true diphtheria. The only differerence thus far discovered has been the absence of the Klebs-Lœffler bacillus.”

Loeffler could therefore claim that the bacterium was present in all cases of the diphtheria, because the presence of the microbe was a necessary prerequisite for the diagnosis of diphtheria.

Friedrich Loeffler (1884) is claimed to have established a causal relationship between the bacterium and diphtheria by inoculating animals with cultured bacteria.

However, the use of highly invasive methodologies does not reflect the hypothesized mode of transmission; his results can thus not be extrapolated to external conditions.

This non sequitur fallacy was outlined by Dr. John Fraser in 1939.

“If you ask the germ theorist to point out the relation between injecting germs into small animals and giving humans the same germs in food or drink, they have to admit that these are two distinct procedures with practically no relationship.”

The problem with invasive routes of exposure such as injections is that the administered substances bypass all natural protective mechanisms of the body. Oral exposure is a completly different toxicokinetics than exposure through injection. Toxicokinetics describes how the body handles a substance, in terms of the concept of ADME (Absorption, Distribution, Metabolism, and Elimination).

What occurs in the body after the injection of a substance can not be positively compared to what would occur in the body by a different route of exposure.

Bacteriologists attempts to induce diphtheria in animals by means of natural pathways were unsuccessful according to Dr. Hansemann, on page 374.

“It has never been possible to make animals sick with diphtheria naturally. All attempts, by adding it to food or by inhalation, have been futile and have had entirely negative results.”

Loeffler’s diphtheria experiments were not accompanied by any control experiments, which is a considerable weakness.

In his 1895 on diphtheria, Dr. John Macintyre describes how Dr. David Hansemann opposed the animal experiments purporting to demonstrate transmission. Hansemann, criticized the invasive methodologies used, and that the injury afflicted was ignored. He stated that chemicals and other microorganisms could likewise induce diphtheria by the same routes of exposure.

“He next criticised the animal experiments, and maintained that subcutaneous injections might set up serious infiltrations and hyperæmia of the kidneys; that on uninjured mucous membranes the bacillus often produced no effect. It might of course produce fibrous exudation on an injured mucous membrane, but the same results could be produced by chemicals and other micro-organisms ... The guinea-pig was susceptible to Loeffler’s bacillus, but never to spontaneous diphtheria.”

Animals experiments concerning diphtheria was likewise brought into question by Drs. Horatio Wood and Henry Formad in their 1882 publication entitled Memoir on the Nature of Diphtheria, originally published in the National Board of Health Bulletin.

Wood and Formad injected animals with material from people with diphtheria into rabbits. However, the rabbits developed tuberculosis, rarely diphtheria.

“These experiments seem to warrant the deduction that inoculation with materials taken from patients suffering from the endemic mild diphtheria of Philadelphia frequently produces a secondary or indirect tuberculosis in the rabbit, but very rarely, if ever, causes any disease in the rabbits comparable to diphtheria in man.”

Wood and Formad performed experiments to determine if organic irritants other than diphtheric material may induce diphtheria in animals.

“To see whether organic irritants other than diphtheritic exudations will produce a pseudo-membranous trachitis, the following experiments were performed:”

They inoculated rabbits with normal pus and various foreign bodies. The animals developed symptoms of diphtheria by the inoculation of normal pus, which succeeded in a larger proportion than with diphtheritic material from a previous experiment.

“In looking over the last table, it will be seen that in two of the ten experiments pseudo-membranous trachitis was caused by the introduction of organic matter into the trachea. In both of the cases in which false membrane was produced the injected material was pus; and it will be noticed that only four such experiments were made, so that the proportion of successful result is very large; larger, indeed, than with true diphtheritic exudation in our experiments.”

Inoculations with material from gangrene also induced diphtheria.

“We have also made several inoculations with material taken from a case of what might be termed hospital gangrene … These experiments seem to show that this so-called spreading or hospital gangrene is capable of producing in the rabbit symptoms and lesions similar to those caused by diphtheritic exudation.”

Drs. Edward Curtis and Thomas E. Satterthwaite also came to the same conclusions in their experiments.

“It would seem therefore that the disease produced in the rabbit by inoculations of diphtheritic matter, is not only not specifically diphtheritic in character, but not even peculiar to the diphtheritic infection; since a disease essentially similar, if it be not pathologically identical, is produceable, though in variable intensity, by inoculations of material at once non-diphtheritic and non-infectious to human mucous-membrane.”

Drs. Wood and Formad referenced another researcher who demonstrated that various chemicals irritants are capable of causing diphtheria. Wood and Formad acknowledged that diphtheria is a non-specific manifestation which can be induced by any irritant of sufficient intensity.

“Trendelenburg found that not only ammonia, but also various other chemical irritants are capable of causing the formation of false membrane in the trachea. Many years since it was proven that tincture of cantharides will do the same thing. It would seem, therefore, that in the trachea the formation of a pseudo-membrane is not the result of any peculiar or specific process, but simply of an intense inflammation which may be produced by any irritant of sufficient power.”

The following conclusions were drawn:

“It is difficult to produce in the rabbit a rapid septic disorder with the matter taken from ordinary cases of so-called diphtheria … Both septic animal matter and non-organic irritants placed in the trachea cause pseudo-membranous trachitis which cannot be distinguished from diphtheritic trachitis … The occurrence of a false membrane in the trachea is the result not of the specific character but of the intensity of the inflammation.”

Their conclusions align with the results of other researchers; who only succeeded in a small proportion of the attempts to produce diphtheria in animals, as outlined by the 1889 book entitled Diphtheria: Its Nature and Treatment.

“In the recorded experiments for the communication of diphtheria to the lower animals by inoculation it is to be observed that the operation is attended with great uncertainty, succeeding in only a small proportion of all cases; that it has usually failed when attempted in the mucous membrane of the mouth and fauces, but has much more often succeeded in the trachea.”

Although some researchers have induced paralysis in animals by the inoculation of Klebs-Loeffler bacteria and its derivatives, they are undermined by the fact that “a number of workers have also caused paralysis in experimental animals simply by injecting normal nervous tissues.”

No hypothetical pathogen is required in diphtheria, since the signs and symptoms have been shown to be caused by various non-microbial substances.

Such was reported a 1896 publication entitled Is Membranous Croup Always Due to the Microbe of Diphtheria?.

“It is established, both experimentally and clinically, that pseudo-membranous inflammations of the throat may be produced by a variety of causes, such as inhalations of hot vapour, the swallowing of corrosive poisons, etc.”

In his 1891 article entitled The Etiology of Diphtheria, Dr. J. Lewis Smith describes how diphtheria can be caused by various irritating agents and poisons.

“M. Talamon states that not only other microbes, a besides the Klebs-Lœffler bacillus, but also certain irritating medicinal and chemical agents, have the power to excite an inflammation with fibrinous exudation upon the faucial, or other surface, to which they are applied, which cannot be distinguished by its appearance and anatomical characters from that of true diphtheria except by the absence of the cause of the latter disease, to-wit, the Klebs-Lœffler bacillus. The inflammation produced by non-microbic irritating agents, as steam, boiling water, chlorine, cantharides, and ammonia.”

A similar statement can be found in the 1895 book Diphtheria and Its Associates.

“False membranes of essentially the same macroscopic and microscopic character as those of truly diphtherial origin have been reported as produced on the mucous lining of the buccal cavity and air-passages by every kind of traumatism, as, for example, irritant poisons, solid, fluid, or gaseous, scalding water, scorching heat, chemical or galvano-caustics, or even strong Eau-de-Cologne. Oertel performed the experiment of dropping a few minims of liquor ammoniæ into the trachea of seventeen animals, and succeeded, in every instance, in generating an artificial croup.”

This should not be a surprise even to bacteriologists, given that their designated pathogen is frequently absent in cases of diphtheria.

In a 1926 publication, it was reported that “bacterial examination is not infrequently negative in just those cases of diphtheria which are most serious.”

Careful investigations from various hospitals over the world showed that the Klebs-Loeffler bacilli was only detected in 50-80% of diphtheria cases.

“The results from these hospitals are all the more valuable because the cases came from all parts of the various cities in which the respective hospitals were located, and hence special local conditions were not likely to greatly influence the general results obtained. Thus Baginsky, in Berlin, found the diphtheria bacilli in 120 out of 154 cases; Martin, in Paris, in 126 out of 200; Janson, in Switzerland, in 63 out of 100; Morse, in Boston, in 239 out of 400; and Park, in New York, in 127 out of 244. Thus from 20 to 50 per cent. of the cases sent to diphtheria hospitals did not have diphtheria.”

In an analysis of 5611 cases of suspected diphtheria, the bacterium could only be found in 60% of the cases.

The Results of the Bacteriological Examination of 1,000 Cases of Suspected Diphtheria showed that “in 40.9 per cent., or about two-fifths, of the cases, the diphtheria bacillus was not found.”

In the 1912 Report of Royal Commission on Vivisection, it was found that the bacterium was absent in 20% of cases.

The Klebs-Loeffler bacterium was not found in 28% of diphtheria cases, as reported in The Principles and Practice of Medicine, published in 1915.

In a 1898 article from The Lancet, it was stated that the bacterium was not present in 14% of diphtheria cases.

The purported causal relationship between the microbe and diphtheria is further weakened by the fact that the bacterium is frequently found in healthy people.

“Humans are the usual reservoirs, and carriers are usually asymptomatic.”

The WHO states that most “infections” are asymptomatic.

“Most infections with C. diphtheriae are asymptomatic”

The ubiquitous nature of the diphtheria bacilli was affirmed by professor Ulrich Friedemann in 1928, who stated that in one year about one-third of the population are “infected” with the Klebs-Loeffler bacterium without contracting the disease.

“We come to the conclusion that in one year about one-third of the population is infected with diphtheria bacilli without contracting the disease.”

The higher proportion of bacterial presence in symptomatic individuals is not surprising, considering the saprophytic role of bacteria in nature; breaking down devitalized organic material. This was understood as early as 1896 by Dr. Elmer Lee.

“It is undoubtedly true, that suitable nourishment for the growth of germs is found in the throats of children whose general system is impaired with diphtheritic sepsis. The so-called specific germ is found upon the tonsil both in health as well as in disease. Is it, therefore, a reliable means of determining the diagnosis of diphtheria?

Is the explanation of the false membrane which forms upon the throat, thus interfering with respiration, to be found by bacteriologic inquiry? When the system is impaired, and a determination of the weakened vital forces results in an inflammation of the fauces, there is thrown out upon the mucous membrane a thick, tenacious, glairy fluid, which dries and thickens into a membrane. The inflammatory state of the mucous membrane keeps adding fresh serous discharges, thus augmenting the deposit and ultimately filling the free space of the throat. In this serum the colonies of a variety of germs find normal food for nourishment and growth.”

The belief in the germ theory of diphtheria was in odds with clinical experience, which meant that new diagnoses such as “pseudo-diphtheria” had to be used.

“The differential diagnosis between diphtheria and so-called pseudo-diphtheria is of great importance. The latter condition may be defined as an inflammation of the mucous membrane of the throat, accompanied by the formation of pseudo-membrane which resembles that of true diphtheria, in which the Klebs-Löffler bacilli are absent.”

In the 1915 book The Principles and Practice of Medicine, it is stated that there was a great discrepancy between the clinical and bacteriological diagnosis.

“The diagnosis of the Klebs-Loeffler bacillus is regarded by bacteriologists as the sole criterion of true diphtheria, and as this organism is associated with all grades of throat affections, from a simple catarrh to a sloughing, gangrenous process, it is evident that in many instances, there will be a striking discrepancy between the clinical and bacteriological diagnosis.”

The use of unsubstantiated bacteriological tests that were in odds with clinical signs was condemned by Dr. Herbert Snow in 1913.

“A very important misuse of the Germ Theory lies in the substitution, sometimes enforced officially, of artificial and unreliable diagnostic methods for the previous reliance upon clinical signs. This is in the highest degree prejudicial to medical education, tending to develop an academic race of practitioners devoid of practical acquaintance with their calling as healers of men, relying upon book-knowledge and artificial tests for disease, bigoted and narrow in an extreme degree. The fallacy of a microscopic test founded on the presence or absence of a particular germ, for any special malady whatever, is conspicuous in every single instance already stated. No microbe can invariably be detected in cases indisputably of the malady with which its name has been associated. Every such micro-organism has been over and over again detected when there could be no suspicion of the malady it was supposed to bring.”

Friedreich Loeffler failed to fulfill the postulates he himself helped to formulate.

That Kleb-Loeffler bacteria are innocuous when experimentally introduced into the body through normal pathways was demonstrated by Dr. John Fraser, who published his results in a 1916 issue of The Canada Lancet. Fraser and six volunteers swallowed millions of active Klebs-Loeffler bacilli in milk, bread, fish and alone, without any subsequent ill-effects.

“The first test was whether the Klebs-Loffler bacilli would cause diphtheria, and about 50,000 were swallowed without any result; later 100,000, 500,000 and a million and more were swallowed, and in no case did they cause any ill-effect.”

[…]

“The investigations covered about two years and forty-five (45) different tests were made giving an average of fifteen tests each. I personally tested each germ (culture) before allowing the others to do so; and six persons (3 male, 3 female) knowingly took part in the tests and in no case did any symptom of the disease follow.

The germs were swallowed in each case, and were given in milk, water, bread, cheese, meat, head-cheese, fish, and apples also tested on the tongue.

Most of the cultures were grown by myself some from stock tubes furnished by Parke, Davis & Co., and one tube furnished by the Toronto Board of Health through one of their bacteriologists.”

The same negative results were obtained by Dr. Matthew Rodermund, who “sprayed the poisons of diphtheria … into the throat, nose [of his patients], or had them breathe into the lungs, repeating the experiments in most cases every one or two weeks for months with the result that no disease could be developed.”

Exposure to the sick was likewise not accompanied by danger.

Dr. Walter Scott reported in a 1937 publication published in The Lancet, the results of a careful investigation into the problem of “The Contact in Industry.” With regard to diphtheria he found that, over a period of ten years, out of 7697 contacts with the disease, only 0.36% subsequently developed the disease.

“Diphtheria contacts amounted to 7697, and of these only 1 contact in every 274 cases (0.36 per cent.) subsequently developed the disease.”

It has to be remembered that cases coinciding with contact is inevitable.

The Schick test was developed for determining susceptibility to diphtheria. The Schick test consists in injecting a small quantity of the toxin of the Klebs-Loeffler bacilli into the skin, and is therefore based on the belief that the germ is the cause of the disease.

A positive reaction, it is claimed, indicates susceptibility; a negative reaction, immunity from diphtheria.

“By the use of a simple test (Schick test), it is possible to find out those children who are liable to take the disease and those who are not.”

A diphtheria vaccine was developed as well. It consisted of diphtheria “antitoxin” combined with a neutralized form of the Klebs-Loeffler toxin.

The theory of immunity is based on the assumption that exposure to the purported bacterial toxin will provoke a condition of “immunity” in the body which will protect it from further attack. It is believed that in both the naturally acquired and the artificially induced disease, protection is brought about by the development of “antitoxin” in the blood of the individual.

However, repeated attacks of diphtheria were not unusual, which is a fact that is difficult to reconcile with the theory of immunity.

In a book published in 1902 entitled Quain’s Dictionary of Medicine, it is stated that one attack of diphtheria does not confer immunity.

“One attack of diphtheria confers no prolonged immunity upon its subject. Even during convalescence the patient has been known to develop the disease afresh, and this may be repeated more than once.”

Dr. Claude Buchanan Ker wrote in his 1922 publication A Manual of Fevers, that it was quite common to suffer from diphtheria more than once.

“Second attacks are quite common, many persons suffering twice, or even more frequently, from diphtheria.”

It is difficult to imagine that the immunity which natural diphtheria cannot give to the child may be produced by vaccination.

A closer scrutiny reveals that the theory of immunity did not correspond to clinical experience.

In his 1939 publication entitled The “Schick” Inoculation for Immunisation Against Diptheria, Dr. Maurice Beddow Bayly’s thorough examination disclosed that “many authorities have reported undoubted cases of diphtheria in patients giving a Schick-negative reaction.”

In an article entitled Should the Schick Test be Abandoned? in the American Journal of Public Health, 1925, Dr. Wilfred H. Kellogg, Director of the Bureau of Communicable Diseases, California State Board of Health, asserted that the Schick test should be abandoned on account of its unreliability.

“In this paper evidence is presented to support the contention that the Schick test for diphtheria susceptibility should be abandoned absolutely, not only in private but also in public health practice.

An extensive and accumulating experience in the Schick testing of large groups of persons, both children and adults, and the retesting of them after toxin-antitoxin immunization, has brought to light a number of sources of error that constitute a danger both from a public health standpoint and as regards the welfare of the individuals concerned.”

Using statistics from numerous countries, Dr. Bayly uncovered ample “positive evidence of the failure of inoculation to immunise.”

In Ireland for example, a vaccination campaign “was greatly hampered by the continual occurrence of reported cases of diphtheria among treated or partially-treated children.”

In Germany, opinions about the value of immunization against diphtheria were conflicted. Several writers had reported cases of diphtheria in which the Schick test were negative.

“Though wholesale immunization against diphtheria has been undertaken in Germany during the past few years, opinions are yet divided about its value. It would seem that there is at present no criterion by which the degree of protection against diphtheria afforded by active immunization can be gauged. Schick himself was of the opinion in 1922 that a negative Schick test put diphtheria out of court; but several writers have reported cases of diphtheria in which the Schick test was negative.”

Several statistical fallacies were brought about that contributed to favourable results of vaccination, according to Dr. Maurice Bayly.

“There remain to be considered the fallacies which afford an explanation of apparently favourable statistics.”

These mainly relate to a hesitation in diagnosing diphtheria in patients with a presumed immunity, as outlined in Dr. Bayly’s publication.

“But in addition to this fundamental change of front there has to be mentioned another alteration in diagnosis. This consists in the refusal to classify cases as diphtheria among the immunised, on the ground that they only present mild symptoms. According to the Medical Officer of Health for Ipswich (see East Anglian Times, February 22nd, 1934), it has become the practice not to regard as diphtheria persons who, after immunisation, develop sore throats even though the presence of the Klebs-Loeffler bacilli (hitherto considered to be diagnostic of the disease) can be demonstrated in them.

Such a manoeuvre is not only bound to falsify all subsequent vital statistics, but can be shown to be unjustifiable on grounds of medical pathology, for the assumption that mild cases are not likely to be diphtheria is not borne out by historical records.”

Conclusion

The claim of the Klebs-Loeffler bacterium to be considered the causal agent in the production of diphtheria is unsupported by scientific evidence; with abundant evidence emphatically contradicting that view.

The “Schick” Inoculation for Immunisation Against Diptheria by Dr. Maurice Beddow Bayly is a comprehensive document about the danger and fallacies of diphtheria immunization. Kindly provided by John Wantling.

In his article entitled Emil Von Behring’s Diphtheria/Tetanus Papers (1890): Precursor to Antibodies, Mike Stone details the history and discovery of the so-called diphtheria antitoxin.

The Fallacy of Antitoxin Treatment as a Cure for Diphtheria by Dr. Elmer Lee is self-explanatory.

If you know German, Dr. David Hansemann’s publication Ueber die Beziehungen des Löffler’schen Bacillus zur Diphtherie is a refutation of the germ theory of diphtheria.

A reverse transcriptase is said to be an enzyme used to convert RNA to DNA, a process termed reverse transcription. Enzymes are proteins.

This in vitro phenomenon, amongst others, was claimed to prove the isolation and existence of HIV (a retrovirus) by Luc Montagnier [1] and Robert Gallo [1, 2, 3, 4] in the 1980s.

The experiments of Montagnier and Gallo were essentially the same.

The detection of reverse transcriptase activity in presumable infected tissue stimulated with a lectin called PHA was used as evidence for the existence of a virus (HIV).

However, in 1973, Gallo himself demonstrated that reverse transcriptase can be found in “PHA stimulated (but not in unstimulated) normal human blood lymphocytes.”

Reverse transcriptase was discovered in the early 1970s associated with alleged retroviruses.

But subsequent research discovered that this phenomenon was widespread, as described by virologist Harold Varmus in 1988.

“Although reverse transcription was first encountered in the retrovirus life cycle, it is hardly unique to retroviruses; it is now recognized as a widespread phenomenon in eukaryotic cells and viruses. Indeed, as much as 10% of the eukaryotic genome may be composed of products of reverse transcription.”

As early as 1971, Howard Temin, the discoverer of reverse transcriptase, reported the detection of a reverse transcriptase from uninfected rat cells and concluded that reverse transcriptase activity does not “necessarily represent oncogenic [retro] viruses.”

A year later, Temin detected a reverse transcriptase from “uninfected chicken embryos and cells in culture” and concluded; “it is tempting to assume that this activity is related to normal cell function.”

The non-specific nature of reverse trancription was plainly described by Harold Varmus in 1987, who stated that it occurs “even in the uninfected cells of yeast, insects and mammals.”

In the documentary The Emperor’s New Virus? - An Analysis of the Evidence for the Existence of HIV, Nobel laureate David Baltimore states that “reverse transcription is very widespread.”

In light of the non-specifity of reverse transcriptase, how can this phenomenon be evidence of a virus?

The original polio vaccine was developed by Jonas Salk and was introduced in 1955.

In the mid-1950s, the National Foundation for Infantile Paralysis released a film order to promote the Salk vaccine.

The film shows the questionable production of the vaccine.

1. Monkeys imported.

A 1957 article entitled Production of formalinized poliomyelitis vaccine (Salk-type) on a semi-industrial scale describes how rhesus monkeys were imported from India.

“The monkeys were Macaca mulatta imported from India, and weighed on the average 2-4 kg.”

2. The glassware were placed inside a hot steam bath in order to be sterile.

3. A mixture called "medium 199" was prepared.

A mixture containing about 68 ingredients was prepared. This included amino acids, vitamins, inorganic salts, as well as other chemicals such as phenol red.

According to the previously cited article entitled Production of formalinized poliomyelitis vaccine (Salk-type) on a semi-industrial scale, the mixture also contained antibiotics, antifungals and calf serum.

“…medium Mixture No. 199 containing 2% calf serum, 200 units/ml penicillin, 200 µg/ml dihydrostreptomycin and 50 units/ml Mycostatin.”

4. Monkeys were slaughtered and their kidneys harvested.

To create his polio vaccine, Salk had to slaughter monkeys and harvest their kidneys. The kidneys were placed into a tube and hand minced with scissors into small bits.

In his 1956 publication The story of the Salk anti-poliomyelitis vaccine, Dr. Maurice Beddow Bayly describes how countless of monkeys were slaughtered in the name of “science.”

By 1954, Jonas Salk had killed more than 15,000 monkeys.

“Some idea of the quantities of monkeys that are required in polio research can be gained from the statement, made by Dr. Salk when addressing an International Conference in Rome on the subject of poliomyelitis in 1954, that he had already at that time made use of 15,000 of them.”

5. Monkey kidneys were centrifuged with trypsin.

According to the 1957 article, the kidney tissue were washed with phosphate buffered saline, mixed with trypsin, and centrifuged.

6. Monkey kidneys were mixed with medium 199 and put on the bench.

The monkey kidney tissue were mixed with the medium 199 mixture and were placed on the bench for about a week.

7. More medium 199 is added.

Half of the culture medium were siphoned off to be replaced by fresh medium.

8. "Virus" added.

Three different “strains” of the polio “virus” were added, as outlined by an article entitled History of polio vaccination.

“The strains of virus used in the vaccine were Mahoney (type l), MEF-I (type 2) and Saukett (type 3).”

The Saukett Strain

The ‘Saukett’ polio strain was obtained by Jonas Salk himself in the 1950s by inoculating a monkey with cultured poo from a paralyzed boy. Very scientific.

“The Saukett strain was isolated in this laboratory by direct inoculation of tissue culture with a fecal specimen from a patient paralyzed in 1950.”

The Mahoney Strain

As described by Albert Sabin in 1973, the ‘Mahoney’ polio strain was “discovered” in 1941 from the feces of three healthy children.

“The Mahoney virus was isolated in 1941 by Drs Fancis and Mack from the pooled faeces of three healthy children in Cleveland.”

In Drs. Francis and Mack’s original publication, they don’t even claim to have identified a polio ‘strain.’

They took the poo of three healthy children, blended the feces with chemicals, and then injected this gruesome mixture into monkeys. Not surprisingly, some of the monkeys became ill.

The MEF1 Strain

Lastly, the MEF1 ‘strain’ was “discovered” in the early 1940s by inoculating monkeys directly into the brain with material from paralyzed military personnel, combined with material from sick monkeys.

This ‘strain’ was then “maintained” by repeatedly inoculating mice into the brain.

“The MEF1 strain of Lansing-type poliomyelitis virus was the one mainly used in this work, and finally chosen for the adaptation. This strain has been maintained by intracerebral mouse passage since its isolation in 1943 (14). The number of passages in mice is unknown, probably not more than 40.”

9. Cultures decayed.

The cultures were put on the bench for a few days to decay.

10. Microscopic examination.

The decayed solution was visually examined under a microscope to do a ‘titration test’ in order to discern how much “virus” is in the solution; hand counting particles that could have been anything.

11. Filtration using asbestos.

The solution was filtered through porcelain and then through multiple sheets of asbestos.

12. Chemicals added.

The 1957 article entitled Production of formalinized poliomyelitis vaccine (Salk-type) on a semi-industrial scale describes how additional additives such as sodium bisulfate and parabens (a known carcinogen and endocrine disruptor) were added.

“Sodium bisulfite and parabens were added…”

13. Animals inoculated.

Rabbits, monkeys, guinea pigs, and chickens were injected with the “live virus” vaccine solutions to ensure it was free of other “pathogens.”

14. Formaldehyde added to vaccine solution.

In order to “inactivate” the “virus” in the vaccine solution, formaldehyde was added, and the solution was then put on the bench for 60+ hours in a warm incubator room.

15. Additional chemicals and preservatives added.

More chemicals and preservatives were mixed into the vaccine solution.

16. Testing.

A couple tests and animal experiments were performed.

Children were then injected with this toxic concoction derived from decades of human and animal suffering.

Vaccines are witchcraft, rooted in pseudoscience predicated on insane barbarism, rife with fraud and immense hubris.

The field of virology was invented before establishing if viruses actually existed. There was no understanding how these hypothesized entities actually looked and functioned.

The existence of viruses were postulated on theoretical grounds, based on pathological changes in laboratory animals, induced by uncontrolled inoculations of filtered biological material. This was as noted by virologist Charles E. Simons in 1926.

“…he is inclined to look upon these smallest forms, which may properly be termed ultraviruses, as representing living matter of such intermediate type, the existence of which we have postulated on theoretical grounds.”

Virologist Karl F. Meyer expressed the uncertainty of the virus theory in a 1939 radio discussion.

“Doctor Meyer, will you summarize the present status of poliomyelitis in the field of experimental research? Dr. Meyer: That is a difficult question to answer directly, since we are still baffled by the simple question, “What is the disease agent in infantile paralysis?” … We do not know whether it is a living germ or something else growing in the cells of the brain. We cannot isolate it like a germ in a test tube, and it is too small to be seen with a microscope. There is only one species of animal—the Old World monkey—in which we can induce the same disease as seen in children. Yet these monkeys are not as susceptible as man, since there is no record of one monkey catching the infection from another monkey by exposure.”

In the 1940s, when the electron microscope was developed for biological material and commercial use, virologists finally had access to a powerful microscope to view their invisible entities.

However, virologists could not find anything different in hosts supposedly infected with a virus from what could be imaged in healthy subjects, as described by a 1942 publication entitled Studies on the Nature of the Virus of Influenza.

“While certain properties of the influenza virus have been inferred from numerous immunological and epidemiological studies published in recent years, little definite information as to its physical nature has been obtained.”

[…]

“No differences between the infectious and non-infectious preparations could be demonstrated.”

[…]

“Since the only source of active influenza virus has, until recently, been infected tissue, the identification, isolation, and chemical characterization of the active agent has been complicated by the presence of cellular debris and intact cytological components. The difficulties introduced by the presence of these adventitious elements in close association with the infectious material are, to a considerable extent, encountered in studies of most other virus diseases, particularly those affecting animals. Several investigations within the past 2 or 3 years have called attention to the presence in normal cells, of particulate material separable from tissue emulsions by the identical procedures adopted for isolation of the infective agents.”

Virologist learned that particles of the same morphology are found in both healthy and diseased tissue, as outlined by a 1945 article entitled Some Biophysical Problems of Viruses.

“Viruses have been especially easy to recognize through the diseases they produce, but we are now learning that other substances of similar particle size exist. These substances frequently complicate and even render impossible the purification of viruses … Cases are being found where viruses have much the same size and stability as components of the healthy tissues involved. Mouse lungs infected with influenza provide an example. Ultrafiltration or centrifugation of normal lungs yields a suspension of particles about 100 mµ in diameter. Infectiousness is found associated with particles of this size when infected lungs are similarly treated.”

The same was described in a 1946 publication.

“The isolation of some animal viruses is complicated by the presence of normal materials which are indistinguishable chemically and physically from the infectious material.”

Virologists discovered that the particles imagined to be viruses were found both in ‘infected’ and ‘uninfected’ material.

Such was reported in a 1950 study entitled Artifacts, with other nonspecific appearances resembling virus particles.

“Round and oblong particles resembling many virus particles that are depicted in the literature were noticed in the background of several fields.”

[…]

“Particles resembling those of influenza, poliomyelitis, and pox group viruses are seen in several fields. Evidence is presented that many of these appearances are artifacts originating from erythrocyte stromatolysis, whereas others are either crystals with rounded corners or what may be protein particles.”

The authors described the work of a group of virologists who perfomed control experiments and found particles indistinguishable from polio “viruses” in normal uninfected tissue.

“Rhian et al. (1949) concluded that none of the occurrences in electron micrographs of preparations of poliomyelitis virus published up to that time showed any conclusive evidence that they really corresponded to poliomyelitis virus. These authors obtained particles of essentially the same size, shape, and nitrogen content from both normal and Lansing poliomyelitis virus-infected tissue.”

These virologists concluded that the imaged particles purporting to depict polio “viruses” were simply non-specific cellular debris, as described in their 1949 publication entitled An Electron Microscope Study of Material from Tissue of the Central Nervous System of Poliomyelitic and Normal Mice and Cotton Rats.

An Electron Microscope Study Of Material From Tissue Of The Central Nervous System Of Poliomyelitic And Normal Mice And Cotton Rats

17.5MB ∙ PDF file

Download

Download

“Our knowledge of the physical and chemical characteristics of the virus of poliomyelitis is attended by a considerable degree of uncertainty and contradiction, despite the great amount of work that has been done to describe these characteristics with precision. Ultrafiltration studies have indicated that the viruses of the poliomyelitis group have a size between 8 and 17 mµ (1, 2). Several workers in the field of electron microscopy have described what they believe to be the virus of poliomyelitis, but, in our opinion, there is no convincing evidence to date that the virus has been identified on electron micrographs. It is the purpose of this paper to present evidence to show why there is reasonable doubt that the virus of poliomyelitis has been identified by electron microscopy.”

[…]

“During the past three years we have examined by electron microscopy suspensions of material obtained by differential centrifugation from tissues of the central nervous system of mice and cotton rats. Wholly comparable material from both normal (noninfected) and poliomyelitic animals has been subjected to the same treatments and examined at the same time throughout this work. The suspensions were derived from 22 independent sets of source material of both normal and infected tissue which were carried through the purification procedures, were tested for biological activity, and were examined in the electron microscope.”

[…]

“Electron-microscopic study of purified preparations, derived from central nervous system tissue of mice and cotton rats by differential centrifugation, has shown that particles alike as to size and shape are obtained from both normal and poliomyelitic tissue. The total yield of nitrogenous material has been essentially the same from both normal and infected tissues.”

[…]

“From a critical examination of our work, and that of others, we conclude that there is no evidence that a virus of the poliomyelitis group has ever been unequivocally identified on electron micrographs thus far published.”

In agreement, virologist Joseph L. Melnick stated in 1951 that there was no clear evidence that the polio virus had been isolated and imaged, because when experiments were adequately controlled by subjecting normal tissues to the same procedures, no difference was found in normal tissue compared to the ‘infected’ tissue.

“In spite of many attempts, there is as yet no clear evidence that the [polio] virus has been obtained in pure form or that it has been visualized in the electron microscope. When such experiments are adequately controlled by subjecting normal tissues to the same procedures of differential sedimentation or fractional precipitation, then similar "purified" material has been obtained (43, 82, 83).”

An electron micrograph from a 1954 publication depicted particles from uninoculated tissue, indistinguishable from “viruses”, allegedly destroying a cell.

Virologist Sven Gard admitted in 1955 that viruses were artifacts.

“Electron microscopy has sometimes been called the science of artefacts. Even if this is a slight exaggeration, production of artefacts is one of the great problems facing the student in this field. As an illustration, it may be sufficient to mention that the virus of Newcastle disease assumes on the electron-microscope screen the shape of spheres, dumb-bells, tailed tadpoles, or short rods, depending upon the salt concentration of the medium from which the specimen is prepared for microscopy. The virus seems to be insoluble in the absence of electrolytes, flocculating in the shape of spherical particles, while in the presence of salts it is soluble, assuming a rod shape.”

In 1957, virologist Robley C. Williams admitted that there was no certainty that the particles purporting to depict ‘viruses’ actually were viruses.

“The identification of a particle, seen in sections, as a virus particle will always be presumptive … Eventually, also, we may hope for techniques that will allow us to put our finger on an image of a tiny particle and say with some confidence that in all ways, save infectivity, it has been demonstrated that this is a virus particle.”

That the biological role of the particles said to be viruses remained undetermined was acknowledged in a 1959 publication entitled Some Problems of Electron Microscopy in the Study of Virus-Infected Cells. The authors recognized that particles may be mistaken for ‘viruses.’

“In the electron microscopy of virus-infected cells... the infectivity of particles visualized in cells cannot be tested.”

[…]

“In the absence of direct tests of infectivity, attempts at visualization of viral particles in cells have utilized comparisons of infected with uninfected cells. Under these conditions, however, it is possible that particles other than those of virus may appear as the result of viral action and may be mistaken for viral particles. For these reasons, we prefer to speak of viruslike particles, although it seems fairly sure in some instances that viral particles have been identified in cells.”

[…]

“Present methods do not permit direct infectivity tests of particles in sectioned cells so that the true viral nature of intracellular particles cannot be tested.”

A 1960 study named Virus Particles in "Normal" Chick Embryos identified particles morphologically indistinguishable from chicken tumor “viruses” in normal healthy chicken tissue.

“However, several studies also revealed that particles similar to those associated with tumors can be found in a rather high percentage of tissues obtained from "normal" fowls, chicks, and chick embryos (3, 5, 6, 15). It was concluded that these were viruses of an unknown variety, but most likely tumor viruses, which were carried within the tissues of apparently "normal" birds. The biological significance of these virus particles found within "normal" tissues is as yet poorly understood. The present report deals with such virus particles in "normal" chick tissues. Particles which morphologically are indistinguishable from chicken tumor viruses were found incidentally in the course of cytologic studies of chick embryo aorta and liver.”

[…]

“The work of a group of investigators in Paris has shown that virus-like particles morphologically indistinguishable from the known chicken tumor viruses can also be found in thin sections of tissues obtained from "normal" chickens, chicks, or chick embryos (3, 5). Similar particles were seen in sections of tissue cultures originating from "normal" chick tissues (15). The present report confirms this previous information.”

[…]

“Of major interest is, we believe, the fact that the cells of the "infected" tissues as described here looked entirely "normal".”

Even under strict aseptic conditions, virologists saw particles identical to viruses arise in cell cultures themselves. If these structures appear without external infection, how solid is the assumption that such particles represent viruses?

“Virus-like particles identical in morphology to the RNA tumor viruses have been observed by electron microscopy in six lines of marine L cells and one line of marine liver cells.”

During the 1980s, particles identified as HIV were observed in tissue of AIDS patients. However, identical particles were also observed with the same frequency in tissue of patients who did not have AIDS and were not at risk of AIDS.

Such was outlined in an extensive, detailed and blinded electron microscopic study from Harvard. ‘HIV particles’ were found in 18/20 (90%) of patients with ‘AIDS’ whereas identical particles were found in 13/15 (87%) of patients without ‘AIDS.’

In a 1993 publication in Journal of Medical Virology, particles budding for cells were found in uninfected cells.

As electron microscopy has improved, microbiologists still find indistinguishable particles in uninfected tissue. A 2020 paper found particles identical to “SARS-CoV-2” in tissues from patients negative for covid as well as in biopsies from the pre-covid era.

“Since the discovery of the causative agent for the novel severe acute respiratory syndrome (SARS)–like pneumonia syndrome pandemic that started in China in 2019 (1,2), a coronavirus named SARS coronavirus 2 (SARS-CoV-2), electron microscopy images have populated the medical literature (2) and media outlets alike displaying the characteristic 60–140 nm round particles surrounded by a “corona” of 9–12 nm distinctive spikes (2). Although many of these images were obtained after “in vitro” infection of cultured cells with SARS-CoV-2 (2) and are thus likely a true representation of viral particles, we have observed morphologically indistinguishable inclusions within podocytes and tubular epithelial cells both in patients negative for coronavirus disease 2019 (COVID-19) as well as in renal biopsies from the pre–COVID-19 era.”

Additional information about this topic can be found on Category: Electron Microscope Images at viroliegy.com.

Futher reading on the concept and history of viruses can be found in the article below.

ViroLIEgy Newsletter

The "Virus" Concept

“You go through narrow-pored clay filters, which hold back all bacteria, easily pass through and you have they are not yet visible with the best microscopes, including the ultramicroscope can do. We must infer their existence because they represent various human, animal and plant diseases. It's a very special strange fact that we are dealing with these…

Read more

3 years ago · 64 likes · 13 comments · Mike Stone

The disease now called tuberculosis was formerly known as consumption, phthisis, the white plague, and scrofula. Keep this in mind when reading through the historical texts in this article.

These older names capture the dreadful symptoms of the disease. The victims were slowly wasting away and being “consumed” by the illness; which is in odds with the idea that tuberculosis is a disease that you “catch” from someone, as described by Chester Levere in 1923.

“Tuberculosis and consumption, like all other diseases are caused by an excess cell and tissue degeneration. These conditions are not caused by germs. Their very nature makes it impossible. The fact that they are of slow growth, requiring months and sometimes years to develop, is sufficient to oppose all thought of contagion. Germs, as stated before, are only scavengers, feeding upon septic matter. They are present in dead and dying tissue to aid in liquefying it so that it may be eliminated from the system. While germs destroy dead tissue in the lungs, they take no part in producing the long train of conditions that bring on the disease, and which may take several years to develop.”

In agreement, Dr. Simon Louis Kratzoff disputed the germ theory of tuberculosis in his 1921 publication entitled Timely Truths on Human Health.

“Some claim that the cause of tuberculosis is a little germ called Bacillus Tuberculosis … We agree with those members of the profession who hold that no germ causes tuberculosis. Germs do not cause any disease.”

With Robert Koch’s discovery of the bacterium claimed to cause tuberculosis in the late 1800s, medical men began to embrace the alleged contagious nature of the disease.

The contagiousness of tuberculosis is now fully embeded in the medical world, as indicated by the Mayo Clinic.

“Tuberculosis can spread when a person with the illness coughs, sneezes or sings. This can put tiny droplets with the germs into the air. Another person can then breathe in the droplets, and the germs enter the lungs. Tuberculosis spreads easily where people gather in crowds or where people live in crowded conditions.”

But did the discoverers of the TB bacterium really prove the contagiousness of the disease?

Paul Clemens von Baumgarten is credited as being the co-discover of Mycobacterium tuberculosis, yet he did not know of a single well-established case of person-to-person transmission. Baumgarten also performed experiments keeping inoculated animals in the same cage as non-inoculated animals; yet no instance of transmission occurred.

“Baumgarten, to whom belongs the credit of being a co-discoverer of the bacillus tuberculosis, and who implicitly believes that this organism is the causative agent of pulmonary phthisis, says that he never knew of a single well-established case of phthisis which was acquired through respiring an atmosphere vitiated by the exhalation of consumptive people. And he further says that during the last ten years he made and had made in the Pathological Institute at Köningsberg a large number of inoculation experiments on rabbits with tuberculous material, constantly keeping inoculated animals in the same cage with the non-inoculated, the latter thus being exposed to an atmosphere infected with bacilli; yet in no single instance was the tubercular poison conveyed from the inoculated to the non-inoculated animal.”

Robert Koch’s experiments involved the inoculation of cultured bacteria into animals. Koch utilized invasive methodologies that did not reflect natural conditions, his results were therefore of low external validity, as noted by Dr. Charles Winslow Dulles in 1897.

“Almost all believers in the infectiousness of consumption have founded their arguments upon experiments that do not seem so conclusive when we reflect that the results of inoculation experiments conducted upon animals of a weak and unresisting constitution, and under circumstances most favorable to the destruction of their health and life, ought not to be compared without reserve to the dissimilar conditions of human beings who usually have the supposed materies morbi brought into contact with their unbroken cutaneous or mucous surfaces and, in the case of the lungs, only after sifting through the nasal passages.”

In his 1884 paper on tuberculosis, Dr. Henry F. Formad describes how Koch ignored the injury afflicted on the animals.

“Koch has not proved that his bacillus is the only agency at work in the production of tuberculosis. Although he undoubtedly inoculated the pure bacillus, he ignored the specific reaction of the soil; and it is the latter which I hold plays. The most important role in determining the formation of tubercle. In introducing the bacillus into the animal organism, another factor—the injury inflicted, and its effects upon the living cells of the body—must be taken into consideration.”

Dr. Formad outlined numerous studies which demonstrated that tuberculosis could be induced by substances other than tubercular, administered by inoculation.

This fact became evident to Dr. Burdon Sanderson, which made him come to the conclusion that “infectious” material was not a necessary prerequisite in the causation of disease by inoculation.

“From these facts it is evident that these lesions can no longer be regarded as dependent on any property or action possessed by the inoculated material in virtue of its having been taken from the diseased organs of a phthisical patient.”

According to Dr. Sanderson, any irritation of the requisite intensity may induce pathological changes indistinguishable from those produced by insertion of tuberculous material.

“In rodent animals the tuberculous process may originate not merely by the inoculation of tubercle, but by any irritation of the requisite intensity applied to the subcutaneous tissue, and that any external injury, provided that the animal survives its immediate effects, is capable of becoming the first link in a chain of pathological changes which cannot be distinguished from those produced by insertion of tuberculous material.”

Such was also confirmed by Dr. Orlando C. Robinson in 1881, who outlined numerous facts refuting the infectious etiology of tuberculosis.

“1. Tuberculosis artificially produced in animals is not due to a specific virus [noxious/infective agent].

2. To produce tuberculosis in animals the inoculation with tubercular matter is not necessary.

3. Failures to produce tuberculosis by inoculation with substances other than tubercular are in the same proportion as failures with true tubercular matter.

4. The introduction under the skin of any foreign substance capable of exciting an inflammation or any traumatic injury can produce tuberculosis, provided the animal is of scrofulous habitus.”

Isaac Burney Yeo published a book about tuberculosis in 1882 entitled The Contagiousness of Pulmonary Consumption and Its Antiseptic Treatment. He describes how numerous researchers opposed the animal experiments purporting to demonstrate infectious transmission. They performed experiments showing that tuberculosis could be produced by the inoculation of various substances, indicating that the affliction was an inflammatory reaction; not an infectious pathology.

“Other experimenters (including Drs Burdon Sanderson and Wilson Fox, in this country) soon opposed other views to those of Villemin and Chauveau. They stated that, in order to produce tuberculosis in rabbits and guinea-pigs, it was not at all necessary to inoculate these animals with tuberculous matter; that they might be rendered tuberculous by other means. They stated that, in the guinea-pig and some other animals, tuberculosis might be produced by inoculations with pus, or with caseous matter of inflammatory origin, or with sarcoma, just as well as with tubercle; that, in the guinea-pig, tuberculosis had been produced by the application of a simple seton; and that, in the rabbit, deep wounds, without inoculations of any sort, would produce pulmonary tuberculosis. Wilson Fox, in his experiments on guinea-pigs, introduced under the skin various substances—portions of putrefied muscle, fatty liver, and even vaccine virus, with the same result; and it was maintained by others that such substances as aniline blue, cinnabar, caoutchouc, cottou, &c., caused similar effects.”

A final nail in the coffin for the doctrine of contagion was provide by Dr. Max Schottelius, who induced pathological changes suggestive of tuberculosis by having dogs inhale aerosolized calf’s brain, cheese, and sputa from patients who did not have tuberculosis.

“[Schottelius] arranged a cage and atomizer after the manner of Tappeiner, and had four dogs inhale daily for several weeks (1) the sputa of phthisical persons (2) sputa from patients who were not tuberculous, (3) finely rubbed up Limburger cheese, and (4) fresh calf’s brain. In all of these there were found similar miliary granulations in the lungs, which, whether they were to be considered as tubercles or not, prove to him that the conclusions of the former experimenters, Lippl and Tappeiner, in assigning a specific character to tuberculosis, were not justified in this regard, since a similar state of affairs could be produced by such different means.”

Knauff and Inis obtained the same results with coal and stone dust.

“Yet Knauff (quoted after Spina, p. 57) obtained the same results by having the animals inhale coal-dust; Inis (quoted after Spina, p. 57), by using stone-dust and lamp-black.”

Robert Koch himself acknowledged that his attempts to prove the contagious nature of tuberculosis had been a failure.

“Attempts have been made repeatedly to prove the contagious nature of phthisis, but they must be looked upon as failures, as such views have never found acceptance among scientists. Some clinical authorities, to be sure, have not lost view of the possibility of contagion, but on the whole physicians consider phthisis a non-contagious disease.”

Koch introduced a cure for tuberculosis with disastrous results. Many patients died as a consequence of his poisonous drug.

“On Koch’s recommendation tuberculin was hailed with enthusiasm as a cure for tuberculosis and its use begun. It was administered in what we would regard today as massive dosage and the results were disastrous. All over Germany the poor patients were “‘todespritzt’’—injected to death—as this doctor put it. This fiasco resulted in prompt abandonment of tuberculin.”

According to Duncan Turner, a member of the Royal College of Physicians, before Koch’s discovery of the TB bacterium, the prevailing understanding among the medical practitioners was that tuberculosis was non-contagious. The section of the medical profession who subsequently accepted the contagion doctrine were people who gathered their information from the laboratory, not from clinical experience.

“But it was not until the discovery of the tubercle bacillus by Koch in 1882 that the doctrine became general, and although it has never been accepted by the bulk of medical practitioners in Great Britain and Ireland or in the Australian colonies, still it is largely acquiesced in on the continent of Europe and America, and invariably so by that section of the medical profession, found in all countries, which writes but does not practise, and which gathers its information from the laboratory of the physiologist and bacteriologist and not from clinical experience.”

In his 1890 article, Dr. Thomas J. Mays, professor of diseases of the chest, contemplated whether clinical experience could throw any light on the truth or falsity of the contagion doctrine. If tuberculosis was contagious, those who were most exposed to the sick would be more likely to contract it, Dr. Mays postulated.

“Let us see, then, whether clinical medicine is able to throw any light on the truth or falsity of the contagion doctrine. In discussing this side of the question I will start out with the fundamental and self-evident proposition that, if other things are the same, those who are most exposed to a contagious disease are most liable to contract it. It is inevitable, therefore, that physicians, nurses and attendants of consumption hospitals, and intimate relatives of consumptive patients are more subject to the disease than those who are but seldom exposed. What are the facts?”

The facts were in odds with the contagion theory, which Robert Koch conceeded in his 1905 Nobel Lecture; stating that it was very common for tuberculosis patients to live with their families for years without spreading the disease to the family members.

“It can indeed very often be observed that such [tuberculosis] patients live for years with their families, without infecting any of them.”

This matter was outlined by Dr. Thomas Mays, who provided statistics showing that in 1626 married couples where tuberculosis existed in one of the partners, only 2.73% of the consorting partners subsequently became afflicted with tuberculosis.

“When direct statistical evidence, such as that submitted in this paper, shows that among one thousand six hundred and twenty-six married persons, where consumption existed either in the wife or in the husband, only the same disease occurred in the other partner in only forty-four instances, the certainty of non-contagiousness is placed beyond the shadow of a doubt. Here we have the picture of more than 1,600 people who were subjected to a much closer intimacy than that which obtains in any other condition of social life, occupying for years the same bed at night and the same room by day, and yet only forty-four or 2.73 per cent. of the consorting partners became fellow-sufferers.”

The lack of transmission within families made Dr. W. Peyre Porcher question the theory of contagion. He was doubtful if there had ever been a clearly proven instance of infection from a sick to a healthy individual.

“If there were any truth in the theory of the extreme contagiousness of consumption, how many devoted wives who have nursed their husbands through prolonged illnesses would themselves be doomed to a lingering death! How many instances do we see where one death occurs in a family and when no other cases follow at all. Of course we all know of instances where amid unhealthy surroundings, damp, water-soaked buildings, where whole families either become infected or succumb to the disease, but here again we cannot prove that the bacillus tuberculosis was not a product rather than a cause of the disease. It is doubtful if there ever has been a clearly proven instance of infection from a unhealthy to a healthy individual.”

In her 1916 book about tuberculosis, Dr. Maurice Fishberg negates the idea that contact was causally related to the disease which afflicted a minority of consorting partners. He describes how partners to the sick were at no greater risk to develop the disease, and that a German writer found cancer more common than tuberculosis to occur in both partners. The rate of tuberculosis in consorting partners was not more common than the normal occurence of tuberculosis in the population.

“For many years the writer was physician to a charitable society, having under his care annually 800 to 1000 consumptives who lived in poverty and in want, in overcrowded tenements, having all opportunities to infect their consorts; in fact most of the consumptives shared their bed with their healthy consorts. Still, very few cases were met in which tuberculosis was found in both the husband and the wife. Widows, whose husbands died from phthisis, were only rarely seen to develop the disease. This experience is not unique … Pope, Pearson, Elderton, and Goring have made careful statistical studies of this problem in England and arrive at the conclusion that the chances of tuberculosis occurring in both consorts are about the same as insanity, and a German writer has shown that cancer in both consorts is more apt to occur than phthisis … Haupt found among 1553 tuberculous couples that 106, or 7 percent were both affected. This being the highest percentage recorded, it is essential to remember that it is exactly the proportion in which humanity suffers from the disease.”

Dr. Fishberg noted that hospital staff in institutions harboring tuberculosis patients did not suffer from tuberculosis more than others.

“The safety of adults from tubercular infection is shown by the fact that the hospital staffs in institutions harboring tuberculosis patients do not suffer from tuberculosis more than others. Even laryngologists, who are often coughed at while examining patients, are safe, as has been proved by carefully collected statistics.”

This fact was reinforced by Dr. Robert Hunter, a physician with over 50 years of experience and having examined over 50,000 patients. He stated that there was no evidence of any sick-to-well transmission over 60 years in the largest lung-disease hospital in the world.

“The great Hospital for Consumption at Brompton, London, in existence for over sixty years, is the largest hospital for lung diseases in the world. It has a large staff of physicians, with scores of nurses and other hospital attendants. If consumption was infectious it certainly would show itself among those in such close and constant contact with it, in all its worst and most advanced stages; and yet Dr. Williams, the senior physician, says: ‘Infection in the wards of the hospital between consumptives and non-consumptives is unknown.’ ”

[…]

“My own personal experience for more than 50 years of active professional life, the chief part of which has been given to the study and treatment of lung diseases as a specialty—each day being spent in the examination of their chests, analyzing their sputa, exposed at all times to their breath and to emanations from their bodies, with the expectorations always in my cuspidors [spitting bowl]—show conclusively that it is not infectious and cannot be communicated by association. I have never in my fifty years of practice met with an instance of infection, or seen anything to make me believe it could be communicated from the sick to the well.

With the records of over 50,000 cases so examined and treated by me, I am able to speak with all confidence and assured judgment in saying that there is no warrant or foundation for any belief consumption is infectious or communicable in any degree or under any circumstances whatever. The assumption that it can be communicated is disproved by the statistics of consumption in all civilized lands, by the reports of consumption hospitals and all institutions for the treatment of lung diseases, and by the united clinical experience of scientific specialists throughout the civilized worlds who have made lung diseases a life study.

No physician can believe consumption is infectious without discrediting the annals of his own profession, the teachings of its leading authorities, and the overwhelming judgment of the great body of medical practitioners. In the face of these facts, the setting up of this bogy and fake infection was an outrage and crime against truth, science and humanity ... Consumption is not infectious—It is not communicated from sick to the well.—And it can neither be prevented nor cured by segregation in pest hospitals.”

Medical men were not suffering from tuberculosis more than other professions, despite their frequent exposure to the exhalation and bodily fluids of tuberculosis patients, as noted by Dr. E. Markham Skerritt.

“Next to nurses and attendants on the sick, there are none who by their occupation are more exposed to the risk of infection than are medical men. During the examination of a phthisical patient, the physician must frequently breathe his bacillus-carrying exhalations, together with chance particles of sputum expelled by cough. In spite of this, however, medical men do not suffer from phthisis in an unusual degree, and enjoy a greater immunity from the disease than do editors, dentists, architects, and public officers.”

The statistics from hospitals were in odds with the contagion theory, according to Dr. Charles Theodore Williams.

“The statistics of the Brompton Hospital, established now forty years, which have been published by Dr. Cotton and Mr. Virtue Edwards and myself, and those of the Victoria Park Hospital, published by Dr. Andrew, directly negative the idea of infection, either to the resident staff or to patients admitted into the wards for other diseases than consumption.”

This became evident to Dr. R. Douglas Powell, who describes how exposure to tuberculosis patients in crowded waiting rooms did not result in any transmission.

“The out-patient rooms of the old building at Brompton were, however, far from being efficiently ventilated; yet I have watched cases of emphysema, of chronic bronchitis, of asthma, of chest-rickets, of cardiac disease, of anaemia with spurious haemoptysis, and the like, for months, some of them, at intervals, for years, and they have not become phthisical. Now, these people have been, for two or three hours at a stretch, exposed to the ”virulent” atmosphere of a crowded waiting-room, nine-tenths of the occupants of which have been phthisical. With a courage, perhaps begotten of ignorance, I have myself sat for three or four hours twice a week, for eight years, practically in the midst of these people; taking my luncheon in the same room, and washing down the bacilli with my coffee. I have more than once observed in the breath of a colleague, after such a long out-patient day, the very peculiar odour of cavity stage phthisis, showing how thoroughly he must have taken in any poisonous emanation; yet he is well, and so am I.”

Sharing similar experience, Dr. James Edward Pollock stated that he had seen many instances of close contact between sick and healthy individuals, with an absence of contagion.

“I have seen many instances in which the most assiduous personal nursing of the sick, living in the same room, sleeping in the same bed, and undergoing the same influences of air and lodging, of anxiety and harass as the sick, has failed to produce it [tuberculosis]. There have been waste of flesh and strength, loss of sleep and appetite, and all the evidence of depressed vital powers in numerous cases, but no phthisis.”

Dr. Henry Bennet noted that contact with sick patients was not attended with danger. Despite living in close quarters with tuberculosis patients, no transmission occurred.

“I may say that I have lived with numbers of these consumptives in the large hotel which I have always inhabited, and have attended shoals [many] of them living in other hotels, or in small boarding-houses, or in villas. Often these consumptives passed their lives, especially the Continental ones, notwithstanding my persistent advice, in badly ventilated rooms, surrounded by relations and servants, who lived with them for many months consecutively for half the year, and yet I cannot recollect a single case of evident contagion occurring at Mentone amongst them.”

Based on decades of experience, Dr. Duncan Turner firmly asserted that tuberculosis was non-contagious.

“After thirty years of professional experience, the greater part of which I spent in general practice where a medical attendant has opportunities of observing patients and families for many years, I can safely say that thousands of consumptive patients have passed through my hands, and that I have treated and observed patients in all classes of society, under all sorts of conditions, viz., in hospitals, at private homes, on board ship, at seaside and mountain health resorts. This enables me to affirm that not a single case of consumption, which I could positively say had arisen from contagion and no other cause, ever came under my notice.

[…]

I have seen devoted wives and husbands nurse each other through years of illness and suffering, occupying the same room and in many instances the same bed, and yet remaining in perfect health... I could quote scores of cases where persons, living in immediate contact with consumptive invalids for years, and moreover, much worn by sorrow and suffering, when one would think that if contagion were possible they could not escape, have nevertheless come out of the ordeal unscathed.

[…]

That the experiences of London Consumption Hospitals, European Health Resorts for Consumptives, and the observations of unbiased observers in private practice, are entirely opposed to the contagion theory.”

The confident assurance in the non-contagiousness of tuberculosis was shared by Dr. Henry F. Formad, who opposed the contagion theory in his 1884 article on tuberculosis.

“There is no proof whatever that tuberculosis is conveyed from person to person by contagion … daily observations and statistics show that there are thousands of instances which disprove the hypothesis of the contagiousness of phthisis.”

These epidemiological observations, statistics and experiments pose a significant challenge to the medical establishment’s dogmatic notion of tuberculosis contagion. If tuberculosis is contagious, why was the experience of numerous doctors with decades of clinical experience in odds with the alleged contagious nature of the disease?

For more information on tuberculosis, have a look at Mike Stone’s article The Germ Hypothesis Part 2: Koch’s Crisis.

ViroLIEgy Newsletter

The Germ Hypothesis Part 2

In the first part of this investigation into the germ hypothesis, we established what exactly a hypothesis is supposed to be in regard to natural science, which is a proposed explanation for an observed natural phenomenon. We briefly touched on what led to Louis Pasteur conjuring up his explanation of disease through germs with his plagiarized work on fermentation that he lifted from Antoine Bechamp. We also examined the experimental evidence that he produced for both chicken cholera and rabies in order to see if his germ hypothesis was ever scientifically proven and validated. What became clear upon investigating was that Pasteur’s experiments did not reflect his hypotheses for how the germs were supposed to invade a host in order to cause disease as “seen” in nature, thus invalidating his results. On top of that, Pasteur also misinterpreted what he was working with in regard to chicken cholera, and he was unsuccessful in isolating any microbe as the causative agent for rabies, further invalidating those experiments as he had no valid independent variable (assumed causative agent) that he was working with. There were also issues with the vaccines that were produced by Pasteur, with his chicken cholera vaccine determined to be ineffective while his rabies vaccine was linked to causing the very disease it was supposed to prevent…

Read more

2 years ago · 77 likes · 21 comments · Mike Stone

A 2004 publication entitled Smallpox: An ancient disease enters the modern era of virogenomics outlined some difficulties in the attempts to transmit smallpox to laboratory animals; stating that researchers had to restort to invasive methodologies to induce sickness in monkeys due to the failure of more natural exposure routes.

In the 1880s, Dr. Lorinser was one of the leading physicians in Vienna, Austria. He voiced his opinion concerning the idea of smallpox contagion; stating that thousands of people have been living in daily contact with people afflicted with smallpox, yet have not caught the disease. He also asserted that hospital attendants who were most exposed to contagion were not at a risk of developing smallpox (also called variola).

“But when we ask whether there is a single fact that could prove the existence of such a contagion, and its power of conveying the disease, we are bound to reply in the negative. We know, as a matter of fact, that thousands of persons, though living in daily contact with variolous [smallpox] patients, have not caught the disease; but that one single person has ever caught it by inhaling the ‘volatile contagion’ can never be proved, considering that variola, like all other diseases, can also break out spontaneously. Nevertheless, both doctors and patients cling fondly to this belief in a volatile contagion”

“… if such a thing as volatile contagion really existed, it would be found in its greatest concentration and virulence in small-pox hospitals, and nothing would be more natural than that the attending doctors and nurses should be those most frequently affected by it. Yet such is not the case. Neither in the terrible epidemic of 1871, nor in any subsequent epidemic, have I heard of a single case of a doctor or a nurse catching the disease in the Vienna smallpox hospital … And this being so, the question arises. What is it we want to disinfect? What is it we dread? In truth we do not know. That is the only answer we can give or we ought to give. The belief in infection has no scientific basis”

The non-contagiousness of smallpox is reinforced by Dr. Henry Littlejohn, who worked as a sanitary inspector. For 25 years he engaged in active sanitary work and had to deal with serious outbreaks of smallpox, and yet he never communicated the disease to his children or dependents. He did not know of any sanitary inspector who had contracted or communicated smallpox while in service.

“For twenty-five years I have been engaged in active sanitary work, and have had, with very limited staff, to cope with serious outbreaks of Cholera, Small-pox, Fever, Scarlatina, Measles, and Hooping-cough, and although I have during that period brought up a large family, I have never communicated any of these diseases to my children or dependents, nor am I aware that any of the numerous sanitary inspectors who have acted under me have ever contracted or communicated these diseases while in the public service.”

In 1849, Dr. John Evans claimed that the difficulty of tracing disease transmission provides evidence for the non-contagious nature of nearly all diseases, including smallpox. He quotes a doctor who attended 40 patients attacked with smallpox, not one of whom had been in contact with a previous case of smallpox, or consciously visited an infected neighborhood.

“But the difficulty of tracing the communication, would, if admitted as valid argument, prove the non-contagious nature of nearly all diseases. Prof. Dickson says he attended in the winter of 1847-8, forty patients attacked with small-pox, “not one of whom had ever seen a case, or consciously visited an infected neighborhood.”

In the World Health’s Organizations book entitled Smallpox and its eradication, one can read that smallpox developed in such a small proportion of people known to be in contact with smallpox patients. Careful laboratory studies showed that only 1% of household contacts to cases of smallpox developed the disease.

“However, careful laboratory studies by Sarkar et al. (1973b, 1974) showed that about 10% of household contacts of cases of smallpox harboured detectable amounts of variola virus in their oropharyngeal secretions. Only about 10% of such carriers subsequently developed smallpox.”

Of course, there is no evidence that the contact was the cause of disease; because cases coinciding with contact is inevitable.

In his 1905 book entitled Health and Disease, Dr. C. G. R. Moutoux describes how many unvaccinated people who were in contact with smallpox patients escaped the disease.

“It is a fact that persons who never had been vaccinated have acted as nurses of smallpox patients, yet did not contract the disease; while others who had been successfully vaccinated did contract it, in such a malignant form as to lose their lives. Many persons not vaccinated at all have escaped the disease, although belonging to the same family as those afflicted, and attending them while sick; which proves that those persons were not susceptible to smallpox.”

Dr. W. L. Scott, reported in a 1937 publication in The Lancet, the results of a careful investigation into the problem of “The Contact in Industry.” With regard to smallpox he found that, over a period of ten years, out of 511 contacts with the disease, only 2.1% subsequently developed the disease.

The following paragraph is an excerpt from Daniel Roytas book Can You Catch A Cold? about Dr. Rodermund’s smallpox experiment.

Dr. Matthew Joseph Rodermund, an American ophthalmologist, was a particularly outspoken critic of germ theory. He was so assured in his belief that germs were not the cause of disease, he conducted a rather questionable experiment with smallpox, that would ultimately lead to his imprisonment.

On Monday, the 21st of January 1901, Dr. Rodermund visited a young female patient with smallpox. Upon entering her room, he asked the girl’s mother if she feared contracting the disease. When the mother replied she was not afraid, Dr. Rodermund proceeded to burst open several smallpox pustules located on the girl’s face and arms to remove the fetid pus from them. He then proceeded to smear his face, hands, beard, and clothes, with the infected fluid. Rodermund was convinced smallpox was not contagious because he had performed this experiment dozens of times over the course of 15 years, each time with a negative result.

After covering himself in the pus, Rodermund returned home, ate dinner with his family, consulted with patients in his medical practice, and played cards at the local Businessmen’s Club. By his own account, Rodermund touched the faces and hands of at least 10 different people that evening. The next day, Dr Rodermund travelled by train to a nearby town, without washing his hands, face, or clothes from the night before, and mingled with those he encountered. Throughout the course of the day, he consulted with a further 27 patients, again touching their faces and hands. For almost 48 hours, Dr. Rodermund had been covered in the pus of smallpox which, according to his estimates, he rubbed onto the faces and hands of at least 37 unsuspecting individuals.

When news broke of Dr Rodermund’s actions, he was held under police guard in a quarantine facility. He somehow managed to escape this facility the evening of his arrest and travelled to a nearby town to visit an acquaintance. Shortly after meeting with his acquaintance, he was arrested for the second time in 24 hours. After four days in quarantine, he was released when the police could find nothing to charge him with. Despite directly exposing himself and dozens of people to the bodily fluids of a smallpox patient, not a single case of the disease occurred. This is odd considering smallpox is thought to be highly contagious. Dr. Rodermund’s exploits were so daring, they made headlines across the United States, and his deeds continue to be reported by media outlets to this very day.

A few years later, Dr. Rodermund performed an experiment upon 17 people in which he attempted to transmit smallpox by spraying and having them inhale diseased fluids. None of the people became sick.

“I made the experiments upon seventeen people between the ages of fifteen and thirty years, but in no instance could a case of consumption, scarlet fever, smallpox or diphtheria be produced.

These experiments were made in the following manner: I sprayed the poisons of diphtheria, small-pox, scarlet fever, or consumption into the throat, nose, or had them breathe them into the lungs, repeating the experiment in most cases every one or two weeks for months, with the result that no disease could be developed. Of course, I could not let the patients know what I was doing. I was supposed to be treating them for catarrh of the nose or throat.”

Note: varicella = chickenpox.

Chickenpox & Shingles: No Transmission is a great article on the failure to experimentally demonstrate chickenpox transmission.

In this article I will provide further evidence for the non-contagious nature of chickenpox using two publications (1, 2) unearthed by Daniel Roytas of Humanley.com, as well as some other studies I found.

Between 1912-14, Dr Frederick Thomson & Dr Clifford Price conducted human experiments in a hospital setting to assess the contagious nature of chickenpox. They conducted 54 experiments which involved putting children with chickenpox into wards with ‘healthy’ children. They were not allowed any direct contact with each other. Of the 521 ‘healthy’ children, 210 were considered ‘immune’ (40.3%) because they had contracted the disease previously, and 311 were considered non-immune (59.6%).

In just seven of the 54 experiments (12.9%) did a child become sick. Across these seven experiments, just 15 of the 521 children (2.8%) developed chickenpox. Of these, six were ‘non-immune’ (40%), one was ‘immune’ (6.6%), and the immune status of the remaining eight cases was not reported (53.3%).

Cases of disease after the encounter with chickenpox patients did occur; but it by no means follows that the contact was the cause, given that such a small percentage (2.8%) of children became ill, and no control was performed to establish the normal occurrence of chickenpox among children in the population.

In a second series of seven experiments, children with chickenpox were put into wards with healthy children. They were allowed direct contact with each other. Of the 130 healthy children, 61 were ‘immune’ (46.9%) and 69 were ‘non-immune’ (53%). None of the children (0%) developed chickenpox.