Was Smallpox Really Eradicated?

On May 8th, 1980, the World Health Organization (WHO) announced the complete global eradication of the smallpox “virus.” This moment in time is considered one of the greatest success stories in all of modern medicine. Humanity had come together in a worldwide effort and finally conquered a deadly foe by utilizing the medical “miracle” of vaccination. This triumphant achievement has been used as justification for every vaccination drive ever since. The death of smallpox by way of lethal injection has been heavily promoted to sell the public on the current rushed experimental mRNA vaccines being forced upon us during the “SARS-COV-2” campaign of terror.

However, what if the eradication of smallpox does not hold up under scrutiny? What if the same symptoms of disease known as smallpox still exist today? What if these symptoms never disappeared and were given new names and identities in the pharmaceutical Witness Protection Program? What if the very vaccines used to eradicate this “virus” actually caused the same symptoms as smallpox, or worse? What would this tell us about the very organizations that claimed success and took a victory lap?

Let’s see what we can uncover about this supposed eradication of one of the “deadliest diseases of all time.”

The 1958 Call for the Global Eradication of Smallpox

Propaganda from 2010.

In 1958, even though a vaccine for smallpox had been in use for well over a century and prevalence of the disease had already declined, the WHO decided it was finally time to push for the eradication of the “virus.” The goal was to create a vaccination infrastructure around the world in order to stamp out this disease once and for all. Fortunately for major countries like the US, smallpox had already disappeared. It was the smaller countries which needed the US and the Soviet Union to step in and supply 150 million doses of vaccines to establish defeat and secure victory:

Smallpox Vaccine: The Good, the Bad, and the Ugly

The first large smallpox eradication effort was launched in 1950 with the goal of eliminating smallpox in the Americas. In 1958, the World Health Assembly passed a resolution calling for the global eradication of smallpox. Although some countries established smallpox eradication programs, there was no coordinated infrastructure. Many programs faltered due to insufficient vaccine supplies and limited resources. The more virulent form of smallpox, variola major, was widespread in the United States during the 19th century, but only two major outbreaks occurred from 1900 to 1925. In contrast, the milder form of smallpox (variola minor) was common until the 1930s. After 1949, there were no endemic cases of smallpox in the United States, but the disease continued to be a serious problem in less developed countries. By 1966, smallpox remained endemic in 33 countries. After extensive debate, the World Health Assembly approved $2.4 million to initiate a global eradication program over the next 10 years. Early in the campaign the Soviet Union and the United States donated more than 150 million doses of vaccine. Around the same time, the bifurcated needle was developed, which simplified delivery and reduced the volume of vaccine required.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1069029/#__ffn_sectitle

The intended goals of the campaign were listed in this 1958 release by the WHO:

  1. REQUESTS the Director-General to study and report to the Executive Board at its twenty-third session on the financial, administrative and technical implications of a programme having as its objective the eradication of smallpox, the study to include the various problems involved in carrying out the following activities:
    (a) investigation of the means of ensuring the world-wide eradication of smallpox, taking into account the fact that smallpox persists in certain areas despite repeated vaccination campaigns;
    (b) encouragement of the preparation during 1958-1960 of the necessary amount of smallpox vaccine in national laboratories and institutes;
    (c) training of vaccinators among the local population in countries in which mass immunization campaigns will be conducted;
    (d) the pooling of experience and the formulation of recommendations for the production of a sufficient amount of thermostable smallpox vaccine suitable for prolonged storage and use in tropical
    and subtropical regions of the world, and
    (e) study of the measures to be taken in order to avoid complications which might result from smallpox vaccination;
  2. RECOMMENDS to all governments:
    (a) that during 1959-1960 the population be vaccinated in countries in which principal endemic foci of smallpox exist; and
    (b) that during 1961-1962 additional vaccination of the population should be carried out in foci where the disease persists, and that subsequently revaccinations be given to the extent it becomes necessary in accordance with the experience acquired in each country;
  3. RECOMMENDS that all countries in which smallpox vaccination is compulsory continue to give smallpox
    vaccinations during the eradication of this disease throughout the world;
  4. CALLS upon medical scientists and scientific institutions active in the field of microbiology and epidemiology to stimulate their efforts towards improving the quality and the technology of the production of satisfactory smallpox vaccine resistant to the influence of temperature; and
  5. REQUESTS the Director-General to report to the Twelfth World Health Assembly on the progress made and the results obtained.

https://apps.who.int/iris/handle/10665/88784

As can be seen from the WHO in 1958, there was an increased push to vaccinate the population for smallpox, especially in poorer countries. This effort was being enacted despite the fact that repeated vaccination campaigns in certain areas had failed and also despite the fact that there were known dangers involved with the use of the vaccine. The WHO called for additional vaccination and the revaccination of certain populations. In other words, the WHO pushed for a mass vaccination campaign with boosters while simultaneously calling for safety studies on the vaccines themselves. Does this sound familiar?

The Most Dangerous Vaccine Known to Man

When the vaccine is deadlier than the threat of an “eradicated virus.”

While it appeared the safety of the vaccines were still in question in 1958, we have the fortune of hindsight to see what kinds of devastating effects that were ultimately discovered in the long run:

ADVERSE EFFECTS OF VACCINATION

Frequency and Clinical Features

“Smallpox vaccine is less safe than other vaccines routinely used today. The vaccine is associated with known adverse effects that range from mild to severe. Mild vaccine reactions include formation of satellite lesions, fever, muscle aches, regional lymphadenopathy, fatigue, headache, nausea, rashes, and soreness at the vaccination site.13,18,19 A recent clinical trial reported that more than one-third of vaccine recipients missed days of work or school because of these mild vaccine-related symptoms.18

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1069029/#__ffn_sectitle

According to the CDC:

“In contrast, most people who get the smallpox or monkeypox vaccine have only minor reactions, like mild fever, tiredness, swollen glands, and redness and itching at the place where the vaccine is given. However, these vaccines do have more serious risks, too.

Based on past experience, it is estimated that between 1 and 2 people out of every 1 million people vaccinated will die as a result of life-threatening complications from the vaccine.”

https://www.cdc.gov/poxvirus/monkeypox/clinicians/smallpox-vaccine.html

It would seem that the symptoms alone for the mild reactions to the smallpox vaccine is the smallpox disease itself. On top of that, there is the likely underestimation by the CDC of the deaths associated with the vaccine. This raises the question: is it better to get the symptoms of smallpox from vaccination or through “natural” means? If you are President of the US at a time when the “virus” is globally eradicated, the obvious answer would seem to be to give the symptoms of smallpox to the populace through vaccination.

In 2003, President Bush made the decision to make smallpox vaccination mandatory to all military personnel as well as to recommend the vaccine for half-a-million healthcare workers. Even though smallpox was declared globally eradicated a good 23 years prior to Bush Jr.’s decision and the disease itself was considered non-endemic in the US since 1949, the threat of the eradicated “virus” being used as a bioweapon was used as justification for this decision. Reporting by CBS at the time paints a very dark picture of the vaccine:

The Most Dangerous Vaccine

“Smallpox may be the worst disease ever known to man. It killed about half a billion people from 1880 to 1980, before it was eradicated.

And the smallpox vaccine is deadly, too. Scientists call it the most dangerous vaccine known to man.”

“That’s according to administration sources who say the shots will be mandatory for about 500,000 military personnel and recommended for another half-million who work in hospital emergency rooms and on special smallpox response teams.

The general public will be offered the vaccine on a voluntary basis as soon as large stockpiles are licensed, probably early in 2004, though the government will not encourage people to get them.

60 Minutes II Correspondent Dan Rather reports that in evaluating the potential danger of smallpox, the Bush administration has faced a deadly dilemma: Do not vaccinate the population against small pox and leave millions of people vulnerable to one of the worst scourges known to man. Or treat people with a vaccine that is extremely effective at blocking the disease but can cause dangerous, sometimes fatal, reactions.”

“The vaccine was created in 1796. The vaccine used today is essentially the same, Offit says. “We tend to think of vaccines as being very safe and every effective, which they are. But all the vaccines that we use today are the result of modern technology. That’s not true of the smallpox vaccine. It has a side effect profile that we, we would not accept for vaccines today,” he says.

The smallpox vaccine is made from a weak biological cousin of the smallpox virus. When you get vaccinated with the weaker virus, you become immune to the smallpox virus.”

https://www.cbsnews.com/news/the-most-dangerous-vaccine/#app

The decision to mandate vaccination for those willing to give their lives to defend our country with the most dangerous vaccine in history boiled down to a theoretical “What if…?” Even after the supposed eradication of smallpox, the pharmaceutically-controlled Government found a way to continue to sell fear and push its poison onto a scared population using fictional propaganda. It is clear just from these few sources that the vaccine was creating the very disease it was supposed to have eliminated.

The Arrival of the Monkeypox

While the WHO set off a global call to eradicate smallpox in 1958, the “poxviruses” apparently did not get the memo as another curious thing happened that year: the discovery of the monkeypox. This was a new disease eerily reminiscent of smallpox that supposedly only affected monkeys in captivity that were used for experimentation. However, twelve years after its discovery and a decade before the declaration of the defeat of smallpox, the monkeypox conveniently decided to jump from animal to man. Of course, the fact that this identical-to-smallpox-in-every-way “virus” jumped ship to infect humans at the height of the smallpox vaccination campaign is just a “coincidence.” Or could it be that the same symptoms of disease associated with smallpox were rebranded, relabeled, and sold as a new disease in order to give the appearance of a successful eradication campaign? They did it before with the chickenpox as I detailed here:

https://viroliegy.com/2022/01/03/did-william-heberden-distinguish-chickenpox-from-smallpox-in-1767/

It’s not too difficult to see that this same trick was played out here with monkeypox. Two sources help to show the amazing similarities between these supposedly distinct “viruses:” The first is straight from the WHO:

“The clinical presentation of monkeypox resembles that of smallpox, a related orthopoxvirus infection which was declared eradicated worldwide in 1980.”

“Monkeypox is a viral zoonosis (a virus transmitted to humans from animals) with symptoms similar to those seen in the past in smallpox patients, although it is clinically less severe. With the eradication of smallpox in 1980 and subsequent cessation of smallpox vaccination, it has emerged as the most important orthopoxvirus. Monkeypox occurs in Central and West Africa, often in proximity to tropical rainforests.”

“Human monkeypox was first identified in humans in 1970 in the Democratic Republic of the Congo (then known as Zaire) in a 9-year-old boy in a region where smallpox had been eliminated in 1968. Since then, most cases have been reported from rural, rainforest regions of the Congo Basin, particularly in the Democratic Republic of the Congo, where it is considered to be endemic.”

Transmission

“Infection of index cases results from direct contact with the blood, bodily fluids, or cutaneous or mucosal lesions of infected animals. In Africa, evidence of monkeypox virus infection has been found in many animals including rope squirrels, tree squirrels, Gambian poached rats, dormice, different species of monkeys and others. The natural reservoir of monkeypox has not yet been identified, though rodents are the most likely. Eating inadequately cooked meat and other animal products of infected animals is a possible risk factor.”

Diagnosis

“The clinical differential diagnosis that must be considered includes other rash illnesses, such as chickenpox, measles, bacterial skin infections, scabies, syphilis and medication-associated allergies. Lymphadenopathy during the prodromal stage of illness can be a clinical feature to distinguish monkeypox from chickenpox or smallpox. If monkeypox is suspected, health workers should collect an appropriate sample and transport it safely to a laboratory with appropriate capability. Confirmation of monkeypox depends on the type and quality of the specimen and the type of laboratory test. Thus, specimens should be packaged and shipped in accordance with national and international requirements. Polymerase chain reaction (PCR) is the preferred laboratory test given its accuracy and sensitivity. For this, optimal diagnostic samples for monkeypox are from skin lesions – the roof or fluid from vesicles and pustules, and dry crusts. Where feasible, biopsy is an option. Lesion samples must be stored in a dry, sterile tube (no viral transport media) and kept cold. PCR blood tests are usually inconclusive because of the short duration of viremia relative to the timing of specimen collection after symptoms begin and should not be routinely collected from patients.

As orthopoxviruses are serologically cross-reactive, antigen and antibody detection methods do not provide monkeypox-specific confirmation. Serology and antigen detection methods are therefore not recommended for diagnosis or case investigation where resources are limited. Additionally, recent or remote vaccination with vaccinia vaccine (e.g. anyone vaccinated before smallpox eradication, or more recently vaccinated due to higher risk such as orthopoxvirus laboratory personnel) might lead to false positive results.

In order to interpret test results, it is critical that patient information be provided with the specimens including: a) date of onset of fever, b) date of onset of rash, c) date of specimen collection, d) current status of the individual (stage of rash), and e) age.

How monkeypox relates to smallpox

“The clinical presentation of monkeypox resembles that of smallpox, a related orthopoxvirus infection which has been eradicated worldwide. Smallpox was more easily transmitted and more often fatal as about 30% of patients died. The last case of naturally acquired smallpox was detected in 1977, and in 1980, smallpox was declared to have been eradicated worldwide after a global vaccination campaign. It has been 40 years or more since all countries ceased routine smallpox vaccination with vaccinia-based vaccine. As vaccinia vaccine also protected against monkeypox in West and Central Africa, unvaccinated populations are now also more susceptible to monkeypox virus infection.

Whereas smallpox no longer occurs naturally, the global health sector remains vigilant in the event it could reappear through natural mechanisms, laboratory accident or deliberate release. To ensure global preparedness in the event of reemergence of smallpox, newer vaccines, diagnostics and antiviral agents are being developed. A new third generation vaccinia vaccine has now been approved for prevention of smallpox and monkeypox. Antiviral agents are also being developed. These may also now prove useful for prevention and control of monkeypox.”

https://www.who.int/news-room/fact-sheets/detail/monkeypox

As can be gleaned from the information supplied by the WHO, monkeypox and smallpox are the exact same disease. They share the same symptoms, the same mode of transmission, the same vaccine, and the same theoretical antibody response. The only difference claimed by the WHO is that monkeypox is estimated to be less fatal than smallpox and it comes from an animal of unknown source whereas smallpox is only found in humans. Both of those claimed differences are theoretical by the way.

If the WHO was not convincing enough about the identical nature of these two diseases, excerpts from the highly detailed 1988 fictional classic Smallpox and its Eradication by Frank Fenner may sell this point. From Chapter 29 of this nearly 1800 page masterpiece of creative writing:

HUMAN MONKEYPOX AND OTHER POXVIRUS INFECTIONS OF MAN

“Human monkeypox was first recognized in 1970; it is a severe systemic disease with a generalized pustular rash, clinically indistinguishable from smallpox. In addition to variola and monkeypox viruses, 7 other species of poxvirus, of 4 genera, can cause lesions in man (Table 29 .1). Although infection with each of these viruses produces at the most mild symptoms and usually only a localized skin lesion, the diseases in question presented a potential diagnostic problem during the global eradication of smallpox, since virus particles found in lesions by electron microscopic examination could be confused with those of variola virus.”

MONKEYPOX IN CAPTIVE PRIMATES

“Monkeypox virus was discovered in 1958, when it was isolated from the lesions of a generalized vesiculo-pustular disease among captive monkeys at the State Serum Institute, Copenhagen (Magnus et al ., 1959). It was apparent that if an animal reservoir of variola virus existed the eradication of smallpox would be impossible (see Chapter 10). The close resemblance between smallpox and monkeypox in captive primates focused attention on monkeypox virus as a potential threat to smallpox eradication (Arita & Henderson, 1968). WHO therefore contacted laboratories in Europe and North America which used monkeys (27 in 1968 and 51 in 1970; Arita et al., 1972), inquiring about the occurrence of monkeypox and asking specifically whether any infections had occurred among laboratory workers or animal handlers. The ensuing investigations revealed 4 other reported outbreaks and 4 hitherto unreported outbreaks in primates (Table 29.2), but there were no reports of infection in humans. Monkeypox virus was recovered in 6 of these episodes. All except episode 3 occurred in Asian monkeys, although in some outbreaks African primates (and, in episode 2, New World monkeys) were also infected.

The circumstances of these outbreaks have been summarized by Arita et al. (1972). One episode described in their paper, but omitted from Table 29.2, calls for special comment namely, the observation made by Gispen & Kapsenberg (1966) of the National Institute of Public Health in Bilthoven, Netherlands, that monkeypox virus had been recovered from normal cynomolgus kidney cell cultures. Subsequent examination of the laboratory records led Dr J. G. Kapsenberg (personal communications, 1980, 1983) to decide that this isolation was probably due to inadvertent laboratory contamination of the culture with monkeypox virus, which had been isolated in the same laboratory at about this time from animals infected in the Blijdorp Zoo outbreak (episode 2).

Seven of the 9 outbreaks of monkeypox in captive monkey colonies between 1958 and 1968 occurred in monkeys shipped from Asia, leading to the suspicion that the reservoir of monkeypox virus was probably located in that continent. However, collaborative serological surveys organized by WHO failed to detect orthopoxvirus antibodies in over 1000 monkey sera collected in India, Indonesia, Japan and Malaysia (Arita et al., 1972). After the discovery of human monkeypox in Africa in 1970 (see later in this chapter), sera were collected from monkeys and other animals in Zaire and several countries of western Africa. Monkeypox-virus-specific antibodies were demonstrated in sera from 8 species of monkey and 2 species of squirrel, and monkeypox virus was recovered from the organs of a squirrel (see below).

Although primates from Asia, Africa and South America (and an anteater from the last-mentioned area) experienced infections with monkeypox virus in captivity, there is no evidence that the virus occurs naturally anywhere except in Africa. During the period 1958-1968 large numbers of primates were being imported into Europe and North America from Asia, and smaller numbers from western Africa, mainly for the manufacture and safety testing of poliomyelitis vaccines. At that time the conditions under which monkeys were moved from their place of capture in Asia or Africa to the recipient laboratory in Europe or North America presented many opportunities for them to be infected with agents carried by other wild animals or by man while in transit (Kalter & Heberling, 1971). The cessation of outbreaks after 1968 can be ascribed to improved conditions in the shipment of primates at about that time and the much more extensive use by laboratories of monkeys bred in captivity in Europe and North America.”

“Subsequently it was reported that variants called “whitepox” viruses, which resembled variola virus by all biological tests, could be recovered from certain laboratory stocks of monkeypox virus, either by passage in hamsters (Marennikova & Shelukhina, 1978) or by inoculation on the chorioallantoic membrane (Marennikova et al. 1979). This initially raised important questions about a possible animal reservoir of variola virus, but these were subsequently discounted. By about 1982 accumulating evidence had convinced most laboratory workers that the “whitepox” viruses were in fact strains of variola virus inadvertently introduced as laboratory contaminants (see Chapter 30).”

“An understanding of the ecology of monkeypox virus depends either on the isolation of virus from animals captured in the field or on serological surveys for monkeypox-virus-specific antibodies. The isolation of virus from animals captured in the field is likely to be a rare event in orthopoxvirus infections, in which persistent infection does not occur, and in fact only one such isolation has been made (see below).”

HUMAN MONKEYPOX

Discovery of Human Infections

“The first case of human monkeypox was found in the Basankusu Hospital, Equateur Province, Zaire (Ladnyj et al ., 1972). The Basankusu Zone covers an area of about 20,000 square kilometres and in 1970 had an estimated population of 62,000, mostly primitive farmers and hunter-gatherers living in small villages in dense tropical rain forest. The last known outbreak of smallpox in Basankusu Zone occurred in 1968 and comprised 70 cases with 18 deaths. Several suspected cases of smallpox were treated at the hospital in 1969, but none was confirmed. Two suspected cases were reported in 1970; one of these turned out to be chickenpox, and the other was the first case of human monkey-pox to be detected. The patient, a 9-month old boy, became ill with fever on 22 August 1970 and a rash developed 2 days later. He was admitted to hospital on 1 September, the 9th day of the rash, which had the characteristic centrifugal distribution of smallpox. Crusts were collected for laboratory examination and sent through WHO in Geneva to the WHO collaborating centre in the Moscow Research Institute for Viral Preparations, USSR. The patient recovered and was about to be discharged, but on 23 October he developed measles (acquired while in hospital) and died 6 days later.”

“The discovery of human monkeypox in central Africa in September 1970 was followed by the demonstration that 4 cases of suspected smallpox in Liberia and 1 case in Sierra Leone in 1970, and 1 each in Nigeria and Cote d’Ivoire in 1971 (Foster et al ., 1972) were cases of human monkeypox (Lourie et al ., 1972). A series of coordinated laboratory and field studies was organized to determine the incidence of the disease, to study its clinical features and epidemiology and to search for the animal reservoir or reservoirs of the virus.”

Recognition of Human Monkeypox in Central and Western Africa

Virologists interested in the poxviruses had known since 1959 that monkeypox virus could cause a generalized disease resembling smallpox in cynomolgus monkeys, and in the 1960s similar cases were recognized among other species of monkeys and in anthropoid apes. Although animal handlers had been exposed to risk during the several outbreaks among laboratory and zoo primates during the 1960s, there was at this time no indication that monkeypox virus would infect humans.

At the first meeting of the WHO Informal Group on Monkeypox and Related Viruses, in Moscow in March 1969, the experts agreed that the first indication that virus recovered from a skin lesion might be monkeypox virus would be the haemorrhagic appearance of the pocks produced on the chorioallantoic membrane after 3 days’ incubation at 35 ° C.

On 23 September 1970 Dr S. S. Marennikova, Dr E. M. Shelukhina and Dr N. N. Maltseva, of the WHO collaborating centre in Moscow, recovered a virus on the chorioallantoic membrane from material sent from a patient in Zaire. When examined after incubation for 2 days, the pocks were “perfectly typical” of variola virus. However, after another day’s incubation at 35 ° C, there was some haemorrhage around the pocks, a feature never seen with variola virus and characteristic of monkeypox virus. Further tests showed that, like monkeypox virus and unlike variola virus, the Zaire isolate produced large lesions in the rabbit skin.

Meanwhile, a diagnosis of variola virus had been made in the WHO collaborating centre in Atlanta with material obtained from 2 cases of smallpox-like disease discovered in different parts of Liberia in mid-September. This diagnosis caused great concern, since Liberia was thought to have been free of smallpox since 1969. Having learned of the occurrence of human monkeypox in Zaire, Henderson suggested to the WHO collaborating centre in Atlanta that the Liberian isolates should be carefully examined by appropriate tests to see whether they might be monkeypox virus. The Liberian isolates, and subsequent isolates from Sierra Leone and Nigeria, were then found to have the characteristics of monkeypox virus (Lourie et al., 1972).

Arrangements were made for further examination of both the Zaire and the Liberian isolates by Dr Keith Dumbell in London and Dr Rijk Gispen in Bilthoven, as well as in the WHO collaborating centres in Atlanta and Moscow. Work on these isolates formed the main topic of discussion at the second meeting of the Informal Group on Monkeypox and Related Viruses in February 1971. The experts attending that meeting agreed that these isolates were indeed monkeypox virus. This conclusion was a source of considerable relief, since it excluded the possibility that smallpox had been recurring in the most unlikely epidemiological situations; yet it also caused some concern, in that a new generalized orthopoxvirus disease of man had been discovered, the public health importance of which was unknown.”

Clinical Features

“A description of the clinical features of human monkeypox based on 47 cases diagnosed up to the end of 1979 (Breman et al.,1980) needs little revision in the light of experience since then (Arita et al. 1985). Clinically, human monkeypox closely resembles discrete ordinary-type or, occasionally, modified-type smallpox, as described in Chapter 1. No case has yet been seen, among the cases diagnosed in the years 1970-1984, with confluent lesions on the face, nor has any case comparable to flat-type or haemorrhagic-type smallpox been diagnosed. The obvious clinical feature that differentiates human monkeypox from smallpox is the pronounced lymph-node enlargement seen in most cases of monkeypox (Plates 29.4 and 29.5), sometimes only in the neck or inguinal region, but more often generalized. Lymph-node enlargement occurs early, and has often been observed at the time of onset of fever, usually 1-3 days before the rash appears. Lymph-node enlargement was observed in 90% of 98 cases in which its presence or absence was recorded and was a presenting sign, preceding the rash, in 65% of these cases.

The eruption begins after a prodromal illness lasting 1-3 days, with fever, prostration and usually lymph-node enlargement. As with smallpox, the lesions develop more or less simultaneously and evolve together at the same rate, through papules, vesicles and pustules, before umbilicating, drying and desquamating. This process usually takes about 2-3 weeks, depending on the severity of the disease.”

Sequelae

“As in smallpox, pitting scars may develop, most frequently on the face, but they tend to diminish in prominence with time. Secondary infection of the lesions is common and this may play a role in scarring.”

Laboratory confirmation

“Throughout the investigations, great importance was attached to obtaining laboratory confirmation of the clinico-epidemiological diagnoses, initially because of the possible occurrence of smallpox and later because of the suspicion that “whitepox” virus (see Chapter 30) might infect humans. All laboratory diagnoses were made in the WHO collaborating centres, with the results shown in Table 29.4. The methods of laboratory diagnosis were those used for smallpox, supplemented by serology in cases in which viral isolation was not possible. This combination allowed positive diagnoses to be made in the great majority of cases. In spite of unavoidable delays in the collection and transmission of specimens, the percentage of recoveries of virus from samples taken from cases eventually diagnosed as human monkeypox was high. Virtually all the cases found positive by electron microscopy were also found positive by culture, and vice versa, but 60 (22%) of the cases were seen too late to obtain lesion material and could only be confirmed serologically. Retrospective diagnosis by serology was unequivocal in unvaccinated subjects but sometimes less clear in vaccinated persons, although with the experience gained over the past few years diagnoses are now possible in these cases also.”

Investigations by the WHO collaborating centre, Moscow.

Between 1971 and 1975 serological and virological investigations concerning a wild-animal reservoir of monkeypox virus were carried out at the WHO collaborating centre in Moscow. Some 200 sera from areas distant from what is now recognized as the monkeypox enzootic area (see Fig . 29.2) were virtually all negative, whereas monkey sera from Zaire collected in 1971 and 1973 showed 14 out of 81 positive by the HI test and 11 out of 65 by the neutralization test (Marennikova et al., 1975). Subsequently another collection of sera from Zaire yielded 24 HI-positive monkey sera out of 117 tested and 26 HI-positive rodent sera out of 245 tested.

Attempts were made to isolate virus on the chorioallantoic membrane from the kidneys of primates, rats, and squirrels collected in Zaire. None yielded monkeypox virus, but “whitepox” virus was said to have been obtained from 4 specimens and vaccinia virus from 1 specimen (see Chapter 30, Table 30.2).

Investigations by the WHO collaborating centre, Atlanta.

In July 1979 a large-scale ecological survey in Zaire was organized by Dr Joel Breman, of the WHO Smallpox Eradication unit. Sera and organs were obtained from a wide variety of wild animals. The animal species were identified by expert zoologists and the sera and organs were tested at the WHO collaborating centre in Atlanta. In all, 1331 sera from 45 species of wild animals were tested by the HI test as a screening test for orthopoxvirus antibodies; 227 sera (17%), from a wide range of animals, gave positive results (J . H. Nakano, personal communications, 1983, 1986). All 50 sera from Rattus spp. were negative.

The subsequent testing of certain sera by radioimmunoassay adsorption tests cast doubt on the significance of the positive results obtained by the HI test, since none of 25 HI-positive sera of the squirrel Heliosciurus rufobrachium gave positive results by radioimmunoassay (Table 29 .11). On the other hand, additional radioimmunoassay adsorption tests on monkey and squirrel sera from this collection revealed positive results in 5 species of monkey and in squirrels of the genus Funisciurus (J. H . Nakano, personal communication, 1986).

Kidneys and spleens from 930 of the animals from the 1979 Zaire study, including all the monkeys, were passaged in Vero cells, and the monkey material was also tested on the chorioallantoic membrane, with negative results (J . H. Nakano, personal communication, 1983).”

MONKEYPOX: THE OVERALL PICTURE

“Laboratory studies show that monkeypox virus is a distinct species of Orthopoxvirus. First reported as the cause of epizootics among captive monkeys in laboratory colonies in Europe and the USA and in an epizootic in a zoological garden in the Netherlands, it was found in 1970 to be the causative agent of a generalized human infection that clinically resembled smallpox.”

https://www.google.com/url?sa=t&source=web&rct=j&url=https://biotech.law.lsu.edu/blaw/bt/smallpox/who/red-book/Chp%252029.pdf&ved=2ahUKEwiJi_G355X1AhWKZM0KHd9IAA8QFnoECDEQAQ&usg=AOvVaw0o1ZKfIZFos-R50YesS-Wp

Link to download the full monstrosity of WHO sponsored propaganda:

https://apps.who.int/iris/handle/10665/39485

Smallpox or monkeypox? Which is which?

It should be clear by now that monkeypox and smallpox are the exact same symptoms of disease. Monkeypox is said to be clinically indistinguishable from smallpox. They can not be differentiated under EM as the particles are exactly the same. It was admitted that if an animal reservoir of smallpox was found, it could not be eradicated. Thus, instead of claiming that the smallpox “virus” was infecting animals as well as humans which would destroy the story of eradication, a new “virus” was created in order to say that an identical “virus” had jumped ship from animal to man. This is how they can get away with saying smallpox is eradicated while simultaneously saying that the same disease exists yet is caused by a different “virus.” This way, virologists can have their cake and eat it too.

Is Lymphadenopathy Specific to Monkeypox?

Virologists do, however, attempt to create the illusion that these are separate diseases caused by different “viruses” by claiming lymphadenopathy is a defining characteristic of monkeypox. They state that the enlargement of the lymph nodes is specific to monkeypox and was not seen in smallpox. However, this story falls apart if lymphadenopathy is also found in cases of smallpox and is not present in all cases of monkeypox. Let’s take a look and see if their fiction holds up:

This first source from November 2020 states that enlarged lymph nodes is not always present in monkeypox:

“Human monkeypox resembles smallpox, with a rash and constitutional signs, but the symptoms are generally milder and, unlike smallpox, the lymph nodes are usually (though not always) enlarged. Most often, the illness begins with nonspecific, flu–like symptoms that may include malaise, fever, chills, headache, sore throat, myalgia, backache, fatigue, nausea, vomiting and a nonproductive cough. Lymphadenopathy can be regional or generalized, and most often affects the submandibular, postauricular, cervical and/or inguinal lymph nodes.”

https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.cfsph.iastate.edu/Factsheets/pdfs/monkeypox.pdf&ved=2ahUKEwjbisbW55b1AhWMVs0KHWnpCIEQFnoECA8QAQ&usg=AOvVaw2PW5tjGW6hoy4kjQRZpktS

While this second source from 2018 states that swollen lymph nodes are not usually seen with smallpox, and thus we can infer that there are cases where swollen lymph nodes have occurred:

What are the symptoms of monkeypox?

“In humans, the signs and symptoms of monkeypox are similar to those of smallpox, but they are usually milder. Monkeypox causes fever, headache, backache, swollen lymph nodes (not usually seen in smallpox), sore throat, and cough.”

https://www.vdh.virginia.gov/epidemiology/epidemiology-fact-sheets/monkeypox/

Virologists needed a new specific symptom in order to sell the idea that monkeypox is somehow different from smallpox. However, it would appear from these sources that swollen lymph nodes are not always a symptom of monkeypox and can be a symptom that accompanies smallpox as well. Thus, this symptom can hardly be considered specific to monkeypox nor a way of differentiating the two.

How is it then that they can claim that swollen lymph nodes is not a characteristic of smallpox? Was it really a symptom that was not found in cases of the disease or could it be that lymphadenopathy was not looked for during examination? A third source from 2012 backs up the latter by stating that lymph swelling was not well described for smallpox as very little attention was paid to this symptom upon examination. However, hypertrophy (enlargement) and hyperameia (excess blood) of the lymph glands were noted in cases of smallpox. It was said that this enlargement occurred due to fluid retention. It is also claimed in this source that monkeypox cases were most likely diagnosed as smallpox (or logically vice versa) and that monkeypox was not even recognized as a separate disease until 1970, meaning they were the same disease until then:

“Lymph node pathology in naturally occurring smallpox is poorly described. Councilman et al. (1904) note that in the pre-20th century literature ‘very little attention has been paid to the condition of the lymph nodes in variola’. In his case series, Bras (1952) reports that the lymph nodes were not examined regularly, and his description of them is limited to three sentences. Of the data available, the most commonly reported gross nodal changes are hypertrophy and hyperaemia; however, in many cases the lymph nodes are reportedly normal. Histologically, the enlargement, if present, appears to be due primarily to oedema and congestion. Councilman et al. (1904) specifically state that the ‘enlargement of the node is due more to oedema than cellular hyperplasia’. Sinus histiocytosis and multifocal haemorrhage with erythrophagocytosis and abundant fibrin and are also reported. As with the spleen, many authors also describe multiple foci of necrosis and lymphocytolysis, with or without bacteria; however, an association with a specific disease type is not always made. In a few reports, necrosis with intralesional bacteria is said to be more common with haemorrhagic disease.”

“Prior to the eradication of smallpox, human MPXV infections were likely misdiagnosed as VARV infections due to the prevalence of smallpox and the similarity of cutaneous disease presentation and progression. Monkeypox was not recognized as a disease distinct from smallpox until 1970 when the elimination of smallpox from the Democratic Republic of Congo revealed the continued occurrence of a smallpox-like disease (Fenner et al., 1988b).”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498598/

Clearly, lymphadenopathy is not specific to monkeypox however there may be a reason for an increase in this symptom if that truly is the case. In the earlier section on the side-effects of smallpox vaccination, lymphadenopathy and swollen glands were highlighted as known reactions to vaccination. This was documented by a study on the adverse reaction from 1968:

“Postvaccinal lymphandentitus is the expression designating the reactive changes that occur in lymph nodes in response to a smallpox vaccination.”

https://www.google.com/url?sa=t&source=web&rct=j&url=https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142(196804)21:4%253C632::AID-CNCR2820210415%253E3.0.CO%3B2-O&ved=2ahUKEwjt1ZOq3pr1AhXTHM0KHXTRBzEQFnoECCcQAQ&usg=AOvVaw04F0k-07_e4UnQUW7NRqmJ

Lymphadenopathy is also mentioned in Meyler’s Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions (Fifteenth Edition) in 2006:

“From 1983 to 1991, 4649 doses of smallpox vaccine were administered, of which 57% were given in 1989–91. The proportion of primary vaccinations increased from 4% in 1983–88 to 14% in 1989–91. Of vaccinees 93% reported no signs or symptoms after vaccination. Reported adverse reactions were mild: lymphadenopathy, fever or chills, and tenderness at the site of vaccination. No severe adverse effects were reported. However, one vaccinee reported a spontaneous abortion 5 months after primary vaccination (16).”

https://www.sciencedirect.com/science/article/pii/B0444510052005490

Even the CDC knew of this reaction to Smallpox vaccination and considered it normal:

“A range of reactions, from mild to life-threatening, can occur after vaccination (see accompanying table). Some are similar to those caused by other vaccines (e.g., high fever, anaphylaxis, erythema multiforme). Reactions specific to smallpox vaccine include inadvertent inoculation, ocular vaccinia, generalized vaccinia, progressive vaccinia, eczema vaccinatum, postvaccinial encephalopathy (PVE), postvaccinial encephalomyelitis (PVEM), and fetal vaccinia. Normal reactions that do not require specific treatment include fatigue, headache, myalgia, regional lymphadenopathy, lymphangitis, pruritus, and edema at the inoculation site, as well as satellite lesions, which are benign, secondary lesions proximal to the central vaccination lesions. In a recent trial, about one third of vaccinees became ill enough to have trouble sleeping or to miss work, school, or recreational activities.”

https://www.aafp.org/afp/2003/0415/p1827.html

If we are keeping track, the smallpox vaccine was known to cause lymphadenopathy as well as every other symptom associated with both monkeypox and smallpox. A mass vaccination campaign began in the 1950’s with a call by the WHO for the global eradication of smallpox in 1958. Coincidentally, monkeypox was also discovered in 1958 in captive monkeys used for polio vaccination experiments. In 1970, a boy in Zaire, a region said to be free of smallpox since 1968, was said to be the first human case of monkeypox, a disease said to be clinically indistinguishable from smallpox except for the symptom of lymphadenopathy, a known reaction to smallpox vaccination and an overlooked symptom of smallpox. If one examines this situation critically and logically, it is easy to see that the sudden appearance of monkeypox was the perfect cover story for the WHO to use in order to keep the myth of the eradication of smallpox alive and to cover-up adverse reactions to vaccination.

In Summary:

  • The first large smallpox eradication effort was launched in 1950 with the goal of eliminating smallpox in the Americas
  • In 1958, the World Health Assembly passed a resolution calling for the global eradication of smallpox
  • After 1949, there were no endemic cases of smallpox in the United States, but the disease continued to be a serious problem in less developed countries
  • Early in the campaign the Soviet Union and the United States donated more than 150 million doses of vaccine
  • Around the same time, the bifurcated needle was developed, which simplified delivery and reduced the volume of vaccine required
  • In their 1958 notes, the WHO admits to the fact that smallpox persists in certain areas despite repeated vaccination campaigns
  • While the WHO pushed for an increase in the production of vaccines, it also called for study of the measures to be taken in order to avoid complications which might result from smallpox vaccination
  • They called on all governments during 1959-1960 to vaccinate the population in countries in which principal endemic foci of smallpox exist
  • They also stated that during 1961-1962, additional vaccination of the population should be carried out in foci where the disease persists, and that subsequently revaccinations be given to the extent it becomes necessary in accordance with the experience acquired in each country
  • The final call was upon medical scientists and scientific institutions active in the field of microbiology and epidemiology to stimulate their efforts towards improving the quality and the technology of the production of satisfactory smallpox vaccine resistant to the influence of temperature
  • In other words, the WHO pushed for a mass vaccination campaign with boosters while simultaneously calling for safety studies on the vaccines themselves
  • Smallpox vaccine is “less safe” than other vaccines routinely used today
  • Mild vaccine reactions include:
    1. formation of satellite lesions
    2. fever
    3. muscle aches
    4. regional lymphadenopathy
    5. fatigue
    6. headache
    7. nausea
    8. rashes
    9. soreness at the vaccination site
  • According to the CDC’s always “accurate” estimates, it is estimated that between 1 and 2 people out of every 1 million people vaccinated will die as a result of life-threatening complications from the vaccine
  • The smallpox vaccine is deadly and scientists call it the most dangerous vaccine known to man
  • In 2003, the Bush administration made it mandatory for all military personnel to get vaccinated against smallpox and recommended healthcare workers receive the vaccine
  • This was predicated on the threat of an eradicated “virus” being used as a bioweapon
  • The dilemma was described as such:
    1. Do not vaccinate the population against smallpox and leave millions of people vulnerable to one of the worst scourges known to man.
    2. Or treat people with a vaccine that is extremely effective at blocking the disease but can cause dangerous, sometimes fatal, reactions.
  • The vaccine was created in 1796 and the vaccine used today is essentially the same
  • The side effect profile of the smallpox vaccine would not accepted for vaccines today
  • The smallpox vaccine is made from a weak biological cousin of the smallpox “virus”
CDC Propaganda
  • In 1958, the monkeypox “virus” was discovered in caged primates used for scientific experiments and eventually jumped ship into humans in 1970
  • According to the WHO, the clinical presentation of monkeypox resembles that of smallpox
  • Monkeypox is a “viral” zoonosis (a “virus” transmitted to humans from animals) with symptoms similar to those seen in the past in smallpox patients
  • Human monkeypox was first identified in humans in 1970 in the Democratic Republic of the Congo (then known as Zaire) in a 9-year-old boy in a region where smallpox had (conveniently) been eliminated in 1968
  • Despite the name, the natural reservoir of monkeypox has not yet been identified, though they claim rodents are the most likely
  • The clinical differential diagnosis that must be considered includes other rash illnesses, such as chickenpox, measles, bacterial skin infections, scabies, syphilis and medication-associated allergies
  • Lymphadenopathy (we’ll touch more on this later) during the prodromal stage of illness can be a clinical feature to distinguish monkeypox from chickenpox or smallpox
  • Polymerase chain reaction (PCR) is the preferred laboratory test given its accuracy and sensitivity
  • For this, optimal diagnostic samples for monkeypox are from skin lesions – the roof or fluid from vesicles and pustules, and dry crusts
  • PCR blood tests are usually inconclusive because of the short duration of viremia relative to the timing of specimen collection after symptoms begin and should not be routinely collected from patients
  • In other words, “virus” is somehow present in skin lesions but not the blood…
  • As “orthopoxviruses” are serologically cross-reactive, antigen and antibody detection methods do not provide monkeypox-specific confirmation (i.e. they would test positive for smallpox or any other “poxvirus”) and are not recommended
  • Additionally, recent or remote vaccination with vaccinia vaccine (e.g. anyone vaccinated before smallpox “eradication,” or more recently vaccinated due to higher risk such as “orthopoxvirus” laboratory personnel) might lead to false positive results
  • In other words, antibodies are a useless measure as they will say one is positive for smallpox
  • In order to interpret test results, it is critical that patient information be provided with the specimens including:
    1. Date of onset of fever
    2. Date of onset of rash
    3. Date of specimen collection
    4. Current status of the individual (stage of rash)
    5. Age
  • This obviously shows PCR results are meaningless without patient information
  • The WHO admits again that the clinical presentation of monkeypox resembles that of smallpox, a related orthopoxvirus infection which has been eradicated worldwide
  • They also state that whereas smallpox no longer occurs naturally, the global health sector remains vigilant in the event it could reappear through natural mechanisms, laboratory accident or deliberate release
  • From the 1988 book Smallpox and its Eradication, it is stated that monkeypox is a severe systemic disease with a generalized pustular rash, and that it is clinically indistinguishable from smallpox
  • In addition to variola and monkeypox “viruses,” 7 other species of “poxvirus,” of 4 genera, can cause lesions in man
  • Monkeypox presented a potential diagnostic problem during the global eradication of smallpox, since “virus” particles found in lesions by electron microscopic examination could be confused with those of variola “virus”
  • In other words, they found the exact same unpurified/non-isolated particles in cultures yet claimed they are different “viruses”
  • It was apparent that if an animal reservoir of variola “virus” existed, the eradication of smallpox would be impossible (and lo and behold, an animal reservoir exists…)
  • After the discovery of monkeypox in 1958, the WHO investigated other outbreaks
  • The ensuing investigations revealed 4 other reported outbreaks and 4 hitherto unreported outbreaks in primates, but there were no reports of infection in humans
  • In one of these instances, monkeypox “virus” had been recovered from normal cynomolgus kidney cell cultures
  • After the discovery of human monkeypox in Africa in 1970, sera were collected from monkeys and other animals in Zaire and several countries of western Africa
  • “Monkeypox-virus-specific antibodies” were demonstrated in sera from 8 species of monkey and 2 species of squirrel (which goes against the more current information from the WHO that specific antibodies for monkeypox do not exist)
  • Although primates from Asia, Africa and South America (and an anteater from the last-mentioned area) experienced infections with monkeypox “virus” in captivity, there is no evidence that the “virus” occurs naturally anywhere except in Africa
  • During the period 1958-1968 large numbers of primates were being imported into Europe and North America from Asia, and smaller numbers from western Africa, mainly for the manufacture and safety testing of poliomyelitis vaccines
  • In other words, the animals used for the testing of experimental vaccines became ill between experiments during shipping in horrific conditions
  • It was reported that variants called “whitepox viruses,” which resembled variola “virus” by all biological tests, could be recovered from certain laboratory stocks of monkeypox “virus,” either by passage in hamsters or by inoculation on the chorioallantoic membrane
  • This initially raised important questions about a possible animal reservoir of variola “virus,” but these were subsequently discounted (remember, they admitted smallpox could not be eradicated if an animal reservoir was found)
  • By about 1982 accumulating evidence had convinced most laboratory workers that the “whitepox viruses” were in fact strains of variola “virus” inadvertently introduced as laboratory contaminants (how convenient…)
  • The “isolation” of “virus” from animals captured in the field is likely to be a rare event in “orthopoxvirus” infections, in which persistent infection does not occur, and in fact only one such “isolation” has been made
  • The last known outbreak of smallpox in Basankusu Zone occurred in 1968 and comprised 70 cases with 18 deaths
  • Several suspected cases of smallpox were treated at the hospital in 1969, but none was confirmed
  • Two suspected cases were reported in 1970; one of these turned out to be chickenpox, and the other was the first case of human monkey-pox to be detected
  • The first monkeypox case had a rash on the 9th day which had the characteristic centrifugal distribution of smallpox
  • The patient recovered and was about to be discharged, but on 23 October he developed measles (acquired while in hospital) and died 6 days later (measles was also regularly confused with smallpox)
  • The discovery of human monkeypox in central Africa in September 1970 was followed by the demonstration that 4 cases of suspected smallpox in Liberia and 1 case in Sierra Leone in 1970, and 1 each in Nigeria and Cote d’Ivoire in 1971 were all cases of human monkeypox (can’t have cases of smallpox popping up while it’s being “eradicated…”)
  • Virologists interested in the “poxviruses” had known since 1959 that monkeypox “virus” could cause a generalized disease resembling smallpox in cynomolgus monkeys, and in the 1960s similar cases were recognized among other species of monkeys and in anthropoid apes
  • At the first meeting of the WHO Informal Group on Monkeypox and Related Viruses, in Moscow in March 1969, the experts agreed that the first indication that “virus” recovered from a skin lesion might be monkeypox “virus” would be the haemorrhagic appearance of the pocks produced on the chorioallantoic membrane after 3 days’ incubation at 35° C
  • On 23 September 1970 Dr S. S. Marennikova, Dr E. M. Shelukhina and Dr N. N. Maltseva, of the WHO collaborating centre in Moscow, recovered a “virus” on the chorioallantoic membrane from material sent from a patient in Zaire
  • When examined after incubation for 2 days, the pocks were “perfectly typical” of variola “virus”
  • However, after another day’s incubation at 35 ° C, there was some haemorrhage around the pocks, a feature never seen with variola “virus” and characteristic of monkeypox “virus”
  • In other words, they determined that the haemorrhagic appearance of chorioallantoic membrane after an extra day of incubation was monkeypox
  • Meanwhile, a diagnosis of variola “virus” had been made in the WHO collaborating centre in Atlanta with material obtained from 2 cases of smallpox-like disease discovered in different parts of Liberia in mid-September
  • This diagnosis caused great concern, since Liberia was thought to have been free of smallpox since 1969
  • They decided the isolates should be carefully examined by appropriate tests to see whether they might be monkeypox “virus”
  • The Liberian isolates, and subsequent isolates from Sierra Leone and Nigeria, were then found to have the characteristics of monkeypox “virus” (the magic of viroLIEgy…)
  • Arrangements were made for further examination of both the Zaire and the Liberian isolates and work on these isolates formed the main topic of discussion at the second meeting of the Informal Group on Monkeypox and Related Viruses in February 1971
  • The “experts” attending that meeting agreed that these isolates were indeed monkeypox “virus”
  • This conclusion was a source of considerable relief, since it excluded the possibility that smallpox had been recurring in the most unlikely epidemiological situations (whew…)
  • Clinically, human monkeypox closely resembles discrete ordinary-type or, occasionally, modified-type smallpox
  • The obvious clinical feature that differentiates human monkeypox from smallpox is the pronounced lymph-node enlargement seen in most (i.e. not all) cases of monkeypox
  • Lymph-node enlargement was observed in 90% of 98 cases in which its presence or absence was recorded and was a presenting sign, preceding the rash, in 65% of these cases
  • The eruption begins after a prodromal illness lasting 1-3 days, with fever, prostration and usually lymph-node enlargement
  • As with smallpox, the lesions develop more or less simultaneously and evolve together at the same rate, through papules, vesicles and pustules, before umbilicating, drying and desquamating
  • As in smallpox, pitting scars may develop, most frequently on the face, but they tend to diminish in prominence with time
  • Throughout the investigations, great importance was attached to obtaining laboratory confirmation of the clinico-epidemiological diagnoses, initially because of the possible occurrence of smallpox and later because of the suspicion that “whitepox virus” might infect humans
  • The methods of laboratory diagnosis were those used for smallpox, supplemented by (non-specific) serology in cases in which “viral” isolation was not possible
  • This combination allowed positive diagnoses to be made in the great majority of cases (what about those where diagnosis could not be made…?)
  • Virtually all the cases found positive by electron microscopy were also found positive by culture, and vice versa, (why should this is not be the case as the EM material comes from culture…?) but 60 (22%) of the cases were seen too late to obtain lesion material and could only be confirmed serologically (which, again, is non-specific due to cross-reactions to smallpox and other “viruses”)
  • The WHO undertook serology testing from some 200 sera from areas distant from what is now recognized as the monkeypox enzootic area and all were virtually negative, whereas monkey sera from Zaire collected in 1971 and 1973 showed 14 out of 81 positive by the HI test and 11 out of 65 by the neutralization test
  • Subsequently another collection of sera from Zaire yielded 24 HI-positive monkey sera out of 117 tested and 26 HI-positive rodent sera out of 245 tested
  • Attempts were made to isolate “virus” on the chorioallantoic membrane from the kidneys of primates, rats, and squirrels collected in Zaire
  • None yielded monkeypox “virus,” but “whitepox “virus” was said to have been obtained from 4 specimens and vaccinia “virus” from 1 specimen
  • In another WHO serology study, 1331 sera from 45 species of wild animals were tested by the HI test as a screening test for “orthopoxvirus” antibodies; 227 sera (17%), from a wide range of animals, gave positive results 
  • All 50 sera from Rattus spp. were negative
  • The subsequent testing of certain sera by radioimmunoassay adsorption tests cast doubt on the significance of the positive results obtained by the HI test, since none of 25 HI-positive sera of the squirrel Heliosciurus rufobrachium gave positive results by radioimmunoassay
  • Kidneys and spleens from 930 of the animals from the 1979 Zaire study, including all the monkeys, were passaged in Vero cells, and the monkey material was also tested on the chorioallantoic membrane, with negative results
  • What this all means is that the antibody results are absolutely meaningless
  • The chapter concludes monkeypox was found in 1970 to be the causative agent of a generalized human infection that clinically resembled smallpox
Smallpox by way of injection.
  • It has been claimed that lymphadenopathy is a defining characteristic of monkeypox, however, it is not always present
  • Most often, the illness begins with nonspecific, flu–like symptoms
  • Lymph node pathology in naturally occurring smallpox is poorly described
  • Councilman et al. (1904) note that in the pre-20th century literature ‘very little attention has been paid to the condition of the lymph nodes in variola’
  • In his case series, Bras (1952) reports that the lymph nodes were not examined regularly, and his description of them is limited to three sentences
  • Of the data available, the most commonly reported gross nodal changes are hypertrophy and hyperaemia
  • Histologically, the enlargement, if present, appears to be due primarily to oedema and congestion
  • Councilman specifically stated that the ‘enlargement of the node is due more to oedema than cellular hyperplasia’
  • Prior to the eradication of smallpox, human MPXV infections were likely misdiagnosed as VARV infections due to the prevalence of smallpox and the similarity of cutaneous disease presentation and progression
  • Monkeypox was not recognized as a disease distinct from smallpox until 1970 when the elimination of smallpox from the Democratic Republic of Congo revealed the continued occurrence of a smallpox-like disease
  • Lymphadenopathy and swollen lymph nodes are a known reaction to smallpox vaccination
  • Postvaccinal lymphandentitus is the expression designating the reactive changes that occur in lymph nodes in response to a smallpox vaccination
  • Reported adverse reactions in smallpox vaccination in the 1980’s included lymphadenopathy, fever or chills, and tenderness at the site of vaccination
Smallpox or…?

Was smallpox actually eradicated as claimed by the WHO way back in 1980? That depends on what the definition of “eradicate” means. If it is referring to the elimination of the name “smallpox” as used to describe a set of recognizable symptoms of disease, then the answer is an absolute YES as the name was retired and replaced by monkeypox (or chickenpox, measles, rubella, etc.). If one is referring to the complete removal of the symptoms associated with the name, then the answer is an emphatic NO as the exact same symptoms of disease appear in various illnesses under different names and are even aquired through routine vaccinations. The “eradication” of smallpox was nothing more than a smokescreen used to sell the world on the “miracle” of vaccination. It is a claim that does not hold up under scrutiny.

49 comments

  1. Great collation of research, will keep this link. I always wondered if it ever disappeared, obviously not. Other factors that I include are arsenic poisoning as the symptoms are similar and historically arsenic was used in soaps and skin creams until the 20th century. Also bed bugs were a possible factor if Dr. Charles Campbell’s odd experiments had any truth to them. This in my opinion shows that the invention of cheap washing powder had more effect in stopping smallpox along with removal of arsenic from drinking water. The fact the ‘last case’ of smallpox was in Bangladesh where arsenic is still poisoning water adds to arsenic being a factor.
    ‘Based on an investigation of the present incident and a review of the literature, skin lesions associated with acute arsenic poisoning can be characterized as follows. Within a few days of the poisoning, transient flushing of the skin on the face, trunk or extremities and facial oedema may be seen, particularly on the eyelids, and also conjunctival haemorrhage. At 4-6 days after the ingestion of arsenic, when hepatic dysfunction starts to develop, peculiar erythematous papules suggestive of malaria develop symmetrically in the intertriginous areas. Because the same clinical picture was found regardless of whether prior treatment with sodium thiosulphate had been carried out, we believe that this eruption is characteristic for acute arsenic poisoning. In some cases, these papules may be confluent and form diffuse erythema, spreading over the entire body over several days to develop into exfoliative dermatitis accompanied by numerous small blisters or pustules. At 6-20 days after the ingestion of arsenic, hyperkeratosis and lamellar desquamation of the hands and feet develop, that may last for more than 3 months. Starting at 2-4 weeks after ingesting arsenic, Mee’s or Beau’s lines begin to appear on the nails. Periungual or labial pigmentation is also observed. During or after acute arsenic poisoning, some patients exhibit herpesvirus infection. Histopathologically, abnormalities of the dermal capillaries are found in the erythematous papules which appear 4-6 days after the ingestion of arsenic. The endothelial cells are swollen, and the vascular walls are occasionally destroyed. Around these capillaries, moderate to marked inflammatory cell infiltration, consisting mainly of lymphocytes and histiocytes, and occasional neutrophils and eosinophils, is observed. Numerous pigment granules, which are positive for Masson-Fontana stain, are sometimes seen in histiocytes around the capillaries or among the collagen fibres in the papillary dermis. When the eruption becomes more intense, the perivascular cellular infiltration is more pronounced, and apoptosis of the basal cells of the epidermis becomes apparent.’
    Skin Manifestations in Acute Arsenic Poisoning: Discussion

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    1. Some have suggested arsenic poisoning. I have not yet looked into that angle. Others have said bed bugs but I think that is far-fetched. The symptoms can also be brought out by the vaccine as well. The best bet is environmental toxins that the body is responding to by attempting to eliminate them from the skin.

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      1. The first nations people were afflicted by smallpox some time after Europeans settled in North America. There were no environmental toxins around at that time, at least as we understand toxins that what we are exposed today. It is in that context that I am looking for plausible explanations (e.g. nutritional deficiencies?) as to the cause of smallpox, that is, other than a virus.

        In my discussions with friends, family and strangers, those that unconditionally accept the premise of viruses routinely bring up polio and smallpox as examples in support of viruses. There is a substantial amount of data/evidence to support the position that polio is a man-made disease. But I am having little success finding data to support the position that smallpox is also a man-made disease.

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      2. It’s hard to say as we don’t really know what they were exposed to back then. We do know that as sanitation improved and food/water became cleaner, diseases such as smallpox declined consistently well before vaccination. Smallpox belongs to a group of diseases that all share similar/same symptoms (chickenpox, measles, shingles, etc.). At one point in time, they were all considered to be the same disease until they were separated by name. The symptoms remain the same. The only difference is the name. This is why monkeypox just happened to arrive on the scene as smallpox was being “eradicated.” They shifted the blame for anyone with the same symptoms to monkeypox. In other words, smallpox still exists just under a new identity.

        Malnutrition, toxic environment, vaccination, etc. can all lead to these same symptoms as they are all part of the same detoxification process. There can be many causes so we can honestly not factor it down to just one.

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      3. British ship “doctors” took poisons with them on exploratory voyages, e.g. strychnine. These were very frequently used to poison hostile natives (I know of multiple instances where this was done during the colonial era here in Australia, especially the poisoning of flour, biscuits or other rations distributed to ‘unwelcome’ native tribes).

        I think the chemical cause of smallpox is most likely, but am unsure exactly what kind of secret chemical formula is being used, but it’s probably an arsenic compound (not pure arsenic). Pure arsenic eruption legions on the hands, feet and face do not look quite the same as smallpox.

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      4. @JP – You wrote, “British ship “doctors” took poisons with them…” Do you have any references I could read to know more about this?

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      5. Thanks for the question, Ian Bell.

        One only has to look at the standard contents of a ship pharmacy or medicine chests in the 18th and 19th centuries, although these varied widely and changed over time with increasing legal regulation and standardisation.

        The 1904 edition of the Handbook for the Ship’s Medicine Chest, pp.8-9, shows some toxic substances in the inventory:
        – Mercurial iodide
        – Mercury bichloride
        – Castor oil (ricin)
        – Strychnine phosphate
        https://archive.org/details/handbookforships00unitrich/page/8/mode/2up

        Unfortunately I couldn’t get my hands on the original 1881 edition which may have shown substances like arsenious acid which was in the inventory of earlier ship pharmacies/medicine chests. Joseph Bonds’ 1847 “The Master-Mariners Guide in the Management of His Ship’s Company, with Respect to Their Health, being Designed to Accompany a Ship’s Medicine Chest” may also have valuable information in regards to this, but this book was also inaccessible to me at this time.

        Another very interesting recent article suggested that some 18th-19th century ship medicine boxes contained secret compartments for storing the most lethal or dangerous medicines, toxins and poisons (section 4.9.1 in https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8385731/ ). Unfortunately the original citation goes to an article in Croatian, so I could not verify exactly what kind of medicines were kept in that particular example (and in any case, only 10 of the glass vials in that preserved ancient medicine chest have survived). However, the point remains that certain high-level individuals with agendas outside public knowledge could have willfully transported dangerous and lethal poisons for use at any time on their ships. This was not necessarily limited to the ship doctor/surgeon, but that individual would typically have received the most pharmacological training of all the crew.

        The Pharmacopoeia has been a book published since the 17th century, first in Latin and later standardised in the 19th century. http://www.gp.org.au/London_Pharmacopoeia_1791.html
        This book lists a great variety of homeopathic remedies, mostly based on plant material. A ship version tailored for ship medicine chests, the Pharmacopoeia Maritima, was also known to have existed and was widely used, especially on merchant ships lacking a specialist surgeon or doctor. Obviously, like encyclopaedias, pharmacopoeias were updated over time as knowledge of substances and their effects on human physiology/biology improved, as well as new substances were discovered. It remains to be said, however, that many substances now regarded as highly poisonous were once in regular use in ship medicine chests, as these old pharmacopoeias attest.

        A well known case of ship poisoning was Captain Charles Francis Hall, who perished of arsenic poisoning on the ill-fated U.S.S. Polaris expedition to the North Pole in 1871. Arsenious acid was a known component of ship medicine kits at the time. Ship surgeon Emil Bessels was chief suspect but never charged; most ship medicine chests at the time were under lock and key at the captain’s control in any case. https://siarchives.si.edu/blog/wait-did-really-happen-potential-poison-polaris

        It is generally unattested that illnesses like measles, smallpox, scarlet fever and other similar conditions “followed” exploratory crews wherever they encountered natives. We have always been told that lack of immunity in the native populations was the major reason for the devastation caused by these illnesses. But it is also known that, at times, native populations were deliberately poisoned in order to remove violent or nuisance natives from interfering with various colonial objectives (Timothy Bottoms, Conspiracy of Silence, 2012).

        I think the presence of secret medicine compartments in ship pharmacies of the 18th-19th centuries, in addition to known toxic chemicals being used in those chests, e.g. mercurial compounds, arsenious acid, strychnine etc., when combined with pharmacopoeias directing use, and the possibility of secret-society style advanced knowledge of poisoning by select upper echelon members of exploratory crews, the result is accidental or deliberate poisoning with substances that may be proven to cause symptoms similar to many of the “diseases” that Europeans were alleged to have spread across exotic places the world over. Perhaps the truth is far more insidious than that, but it requires more detailed research than what I have undertaken above.

        Cheers,
        JP.

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      6. There are always so many factors, the well poisoning was as common as shooting in Australia so it should be expected elsewhere with colonisation. I often wondered if the practice of letting pigs loose in South America led to garden destruction and disease arriving even before conquistadors came. These diseases listed such as measles and scarlet fever can simply be strep infections as well, add in a population hiding from invaders and starving and health quickly can go downhill. ‘It is generally unattested that illnesses like measles, smallpox, scarlet fever and other similar conditions “followed” exploratory crews wherever they encountered natives.’ Arsenic is only one of the possible poisons and it seemed to be common practice to add these poisons to make up products which would explain wealthy people suffering ‘smallpox’. There were events like beer poisoning in the UK in 1900 that caused chickenpox outbreaks so I often wonder what widespread use of things like arsenic and lead in make ups and soaps did in populations often devoid of sunlight and suffering scurvy. 1900 study here.. ‘Another observation made by several medical men is the increase. in recent months in the number of cases of herpes zoster.’ The Epidemic of Peripheral Neuritis Traced to Arsenical Contamination of Beer-Making Materials
        The question ‘was Smallpox really eradicated’ is well answered in this Viroliegy article though.

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      7. One of the things that puzzles me about the idea that westerners infected new worlders with our diseases is that the new worlders seem not to have infect us with theirs. Shouldn’t we have wiped each other out?

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      8. That is a really good point. Yes, how come? Some say it’s the domestication of farm animals that causes disease to fester and jump to humans, which westerners were doing more of and had developed ‘resistance’ to. But you’d think there would be some other viruses and diseases that they hadn’t encountered before. When Spanish forces arrived in Veracruz in Mexico in 1520 they devastated the town with viruses, smallpox and pustules (and blamed an African slave). However this is centuries before vaccination. How come sailors and Westerners had immunity? Or rather how come they stopped having immunity by the time the vaccine was being marketed? https://georgiedonny.substack.com/p/disease-and-colonialism
        Jo

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      9. One curious thing was historical mention of people dying with empty towns even before the invaders came. I did wonder if the pigs they released brought new bacteria or simply wiped out their crops

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      10. (I can reply no deeper in the thread than this, but this is a reply to Cal and Georgie.)

        “Some say it’s the domestication of farm animals that causes disease to fester and jump to humans, which westerners were doing more of and had developed ‘resistance’ to.”

        I thought this would be an assertion out there. And I asked myself, why might farming do that? What evidence is there to support that assertion? Animals living close together and with humans? Pigs live close together in the wild; all pack/social animals do. They do roam far in the wild, but that helps prevent things like fleas, not viruses I’d think. Furthermore, farming was not unique to westerners at that time, it seems. I’m reading “The Dawn of Everything” by Graeber and Wengrow, in which we learn that our ancestors were highly varied in the sorts of social modes they experimented with, including fixed settlements going waaaay back, and, of course, pastoral shepherding of herd animals that managed massive herds. Were the differences between western ways of life and those of the natives in America sufficiently marked, I wonder?

        And there’s the problem of how pox illnesses are said to spread; skin contact or contact with the pocks’ excretions. The invaders would need not only to have symptoms of whichever pox, i.e., be sick, but come into close contact with the natives while sick, right? So I don’t see that set of requirements as compatible with a viral-vector explanation for genocidal wipeout of native populations via smallpox at that time. Poisons in wells, starvation, war, slavery, etc., seem better explanations to me, as a whole. Cal’s point about pigs introduced to that environment destroying crops adds to the list of highly disruptive variables causing terrible damage. Weirdly, all this is in fact virus-like; the ‘pathogenic’ nature of one culture imposing itself on another, where one has a sociopathic/fanatical sense of its right to own, to take, and to kill everything in its way.

        More deeply, and somewhat at a tangent, there’s how viruses evolved in the first place, the theories on offer seem weak to me, and I’ve been meaning to voice my early thoughts. A couple of quotes from https://www.profolus.com/topics/origins-of-viruses-hypotheses-and-theories/

        “One of the hypotheses on the origins of viruses is the virus-first hypothesis, which asserts that they arose from complex molecules of proteins and nucleic acids before cells appeared on earth. Essentially, it argues that viruses predated primitive forms of life, and they contributed to the emergence of cellular life.”

        How long did these viruses lie around before there was any life to use for replication? Millions of years of being accidentally created until the things they ‘need’ for replication accidentally emerged alongside them? And those things are then destroyed by that replication procedure? It doesn’t pass the sniff test, in my opinion.

        “The food source also gave rise to lipid-like molecules that could self-assemble into vesicles that, in turn, could enclose or envelope replicons. Replicons close to the food source thrive, but those farther away, they depended on resources inside the vesicles.”

        This version sounds a little more plausible as a chemical process but nevertheless would, I think, have a hard time explaining how defenceless cells could survive their drifting ‘predators’ being all around them. One virus in, millions out are not odds that favour cellular survival. And no ‘immune system’ on the horizon for further millions of years…

        To my mind, all this (desperate?) extrapolation sounds nonsensical. The language used imputes to dead chemistry things suggestive of survival instinct. I suspect this is primarily a weakness of language, but it reveals, I think, the deeper problem of how chemistry becomes biology becomes felt experience, instinct, desire … a sequence that bedevils materialism generally.

        In terms of mechanics and probability, how do non-motile bits of chemistry get from a to b other than drift or float? They are at the mercy of circumstance. They lack anything approaching a sense of the world out there, have no way of detecting anything at all, are as passive as air. How then do they dock onto anything – surely a very precise procedure –, accidentally, to perform their replication? And all this before life really got underway, somehow as assistive to life’s flourishing!

        That said, such docking must still be, surely, just as tricky in vivo (and in vitro) today. (Mechanically, how DOES docking of virus to cell happen accidentally? Does anyone know the odds of a successful docking of virus to cell receptor? Things like weight of virus, number of viruses relative to number of target cells, viscosity of medium travelled through, speed of approach, impact pressure, angle of approach, etc., would all have to be calculated. Could such be modelled as a 3D animation??)

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      11. I can’t find the piece but I remember reading about Conquistadors releasing pigs to have something to hunt and eat when they went further in travels.
        This is from 2013, the new parasites are also a problem.
        Lack of food and starvation causes scurvy regardless which makes the same skin symptoms as smallpox, especially with new bacteria.
        ‘Wild pigs stick to one area until all food sources are tapped out. Their method of “rooting up” buried treasures (roots, acorns and the like) creates large swaths of cratered, barren terrain. The scorched earth is then abandoned in the hunt for another food source.

        This voraciousness is problematic for many reasons – destruction of natural ecosystems, choking out native species – but none is more prevalent than decimated crops. Harvests of corn, rice, soybeans, and even cotton have been wiped out by roving boars.’
        Who Can Stop These Adorable Pigs?
        https://modernfarmer.com/2013/04/who-can-stop-these-adorable-pigs/

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      12. Checked your blog which mentioned the plague, the rat theory was definitely totally improbable.
        I think everything is multifactorial and had some other causes here. I suspect radiation from the sun or cosmos as other factors we always miss.
        Did Arsenic or other poisonous gases cause the Plague?
        https://calcrilly.com/?p=462

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      13. Here is an example of the thought they could wipe out gardens and cause starvation well before the conquistadors came along. ‘Pigs were so easy to transport that a few were generally carried along and deposited on islands, left to reproduce prolifically until a later voyage might hungrily come across them, as this message to the incoming governor of Río de la Plata attests:

        ‘There remain on one of the islands of San Gabryel a pig and a sow for breeding; do not kill them, and if there are too many, take what they need and leave them always for casting, and also on the way throw a pig and a sow on the island of Martyn Garcia, and in the others that you see fit, so that they do caste’.[11]

        We witnessed this same logic when Columbus defended his decision not to let his eight puercas be slaughtered for the one-time benefit of a tasty pork barbecue. Pigs were “seeded” on many islands that explorers would often only much later come back to, including Barbados, Bermuda, and the Channel Islands near California.[12]

        Another of the pig’s key selling points was undoubtedly that it, unlike other livestock, could be herded through difficult and varied terrain. Pigs did not rely on large pastures of grass as did sheep and cows; these animals might have subjected the horses to unfavorable competition during long expeditions over rugged terrain. Instead, the pigs pretty much fended for themselves, eating whatever they could find en route, freeing the Spanish soldiers from a large investment in food or herders. Pigs adapted both to the tropical humidity as well as the mountains and dry land. They were also resistant to hunger and even lack of water because they do not perspire through the skin. Through varying American terrain, the pigs continued commendably, keeping up with the soldiers and finding novel food sources as they went.[13]

        While herding pigs was relatively easy, and the Spanish had millennia of experience in this matter, keeping control of hundreds or even thousands of these self-reliant animals was not an exact science. An untold number of pigs escaped and went on to populate the regions through which they were being led. These pigs turned wild, just as they had in the Antilles, and reverted to a form similar to wild boars. Given their remarkable fecundity and resourcefulness, descendents of these hogs were destined to outpace the Spaniards in their conquest of the Americas. Coronado in his exploration of the American West would encounter Indians who had been hunting and exploiting wild boars well before his arrival.[14] Later expeditions would benefit from this wild game, which could be hunted.’
        El Puerco Conquistador: The pig as a tool for Spanish explorers
        https://www.bzhumdrum.com/pig/chapter3.html

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      1. Have you got Alfred Wallace’s 1898 article on smallpox vaccination? Wallace was the guy who also came up with the ‘theory of natural selection’ and discussed it with Darwin.
        VACCINATION A DELUSION. Its Penal Enforcement a Crime:
        PROVED BY THE OFFICIAL EVIDENCE IN THE REPORTS OF THE ROYAL COMMISSION. Alfred Russel Wallace 1898
        http://people.wku.edu/charles.smith/wallace/S536.htm

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      2. Hi Cal Crilly, thank you, I’m going to look this up. I was also interested in your comments on arsenic, as toxins seem to be involved in the poxes (and many things!) I used to work in histopath so have done a very few Masson Fontanas in my time- not as many as the the reticulin silver stain- which I must have done 100’s! thanks again, Jo

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      3. Thank you, yes I will! Great interview with Jerm BTW. He seemed to still be clinging on to ivermectin- I guess we all have blind spots. We’ve all had such a radical change in our view of disease and the medical profession over the past 2 years, we can have some lee way of adjusting.
        It’s also been incredibly empowering – I will never trust an expert again- I’m really confident now in my own research and discernment abilities.
        Jo

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