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Chickenpox, shingles, smallpox, monkeypox and friends
'Chickenpox', 'shingles', 'smallpox' and 'monkeypox' are all said to be different 'diseases' caused by different 'viruses'. But are they?
Disclaimer: nothing in this article is to be taken as medical advice. The information provided here is to be used purely for informational and educational purposes.
‘Chickenpox’, also known as ‘varicella’, is defined by Brittanica as: “a contagious viral disease, characterized by an eruption of vesicles (small blisters) on the skin”. The causative agent is said to be the ‘varicella-zoster virus’. It stands somewhat apart from other ‘viruses’, in that it is also said to cause a different ‘disease’, known as ‘shingles’ or ‘herpes zoster’.
According to the WHO, transmission occurs “via droplets, aerosols, or direct contact with respiratory secretions, and almost always produces clinical disease in susceptible individuals”. Note the use of the word ‘susceptible’, which as discussed here, suggests that the individual in question may not be in the best of health. And most of the time, this is said to be the result of ‘secondary immunodeficiency’, which is attributed to so-called ‘environmental factors’. The WHO go on to state that: “while mostly a mild disorder in childhood, varicella tends to be more severe in adults. It may be fatal, especially in neonates and in immunocompromised persons”. This is confirmed by the Mayo Clinic, who list various complications, including encephalitis, pneumonia, toxic shock syndrome and death. The Mayo Clinic also state that: “most people who have had chickenpox or have been vaccinated against chickenpox are immune to chickenpox. A few people can get chickenpox more than once, but this is rare”. We are not told what ‘rare’ in this case, means.
‘Chickenpox’ is primarily thought of as a childhood disease – although adults can ‘catch it’ too, as seen in the recent example of musician George Ezra (age 28 at the time of writing). It is said that the ‘disease’ is more dangerous in adults: “in the United States, adults with chickenpox are over four times more likely to die from the disease than children who have it, according to an article in the journal BMJ. An estimated 31 out of 100,000 adults with chickenpox die from the condition”. Thus, ‘pox parties’ were (and still are) organised in order to ‘immunise’ children, although scientists have been calling for an end to this practice in favour of ‘vaccination’. The latter, according to them, offers a ‘lower risk’ approach.
According to the Oxford Vaccine Knowledge Project, the ‘vaccine’ confers immunity. However, some may still ‘catch it’, but their symptoms will be “generally milder”. We are not told how frequent an occurence this is. The Mayo Clinic state that the disease is “generally mild in healthy children”, which of course begs the question; if it’s already “mild”, then how much “milder” does the ‘vaccine’ make it? And, once again, it is children who are ‘immunocompromised’ who stand to benefit the most from this treatment.
One could therefore argue that the ‘vaccine’ may benefit those who meet this criteria. But we are then told by the Oxford Vaccine Knowledge Project that “the vaccine should not be given to people who are clinically immunosuppressed (either due to drug treatment or underlying illness)”. An individual could, of course, become ‘immunocompromised’ later in life – so if they have the opportunity to have the ‘vaccine’ when they’re healthy, there is an argument to say they ought to. But if they become ‘immunocompromised’ later in life, this suggests that it is the result of ‘environmental factors’ (so-called ‘secondary immunodeficiency’) which raises the all-important question; what caused said ‘immunodeficiency’? And are the symptoms of the ‘disease’ therefore the end-result of the ‘infection’ – or of whatever caused the ‘immunodeficiency’?
According to the Mayo Clinic, ‘shingles’ is a ‘complication’ of ‘chickenpox’: “it is caused by the varicella-zoster virus — the same virus that causes chickenpox. After you've had chickenpox, the virus lies inactive in nerve tissue near your spinal cord and brain. Years later, the virus may reactivate as shingles”. They go on to state that: “eventually, it may reactivate and travel along nerve pathways to your skin — producing shingles. But, not everyone who's had chickenpox will develop shingles”.
Why and how this happens, is apparently “unclear”, but it “may be due to lowered immunity to infections as you grow older. Shingles is more common in older adults and in people who have weakened immune systems”. So once again we find that it is people who are ‘immunodeficient’, who are at risk. And once again, the ailment itself appears to have nothing to do with whatever caused the ‘immunodeficiency’ – it’s all down to the ‘re-activation’ of this ‘dormant virus’, which somehow is able to ‘survive’ for years in a ‘hostile environment’, in much the same way that the bacteria that allegedly causes ‘tuberculosis’ does, for reasons that to this day, scientists are unable to explain.
According to the CDC, ‘shingles’ was originally thought to have no relation to ‘chickenpox’: “the association between chickenpox and shingles was first noticed by von Bokay in 1888. He noted that chickenpox sometimes developed in susceptible children after exposure to persons with acute shingles”. They also state that “chickenpox was not reliably distinguished from smallpox until the end of the 19th century”. Indeed, we are told here that “the name ‘chickenpox’ was used by Richard Morton (1637-1698) who characterized it as a mild form of smallpox”. Unlike other pox-viruses that allegedly trace their origins back to specific animals (‘camelpox’, ‘racoonpox’, ‘gerbilpox’ etc), ‘chickenpox’ apparently has nothing to do with chickens; “the exact origin of the name ‘chickenpox’ remains unclear. Samuel Johnson suggested that since the disease was ‘of no great danger,’ it was a ‘chicken’ form of smallpox”.
Despite the same ‘virus’ being involved in both diseases, if a person has ‘shingles’, then transmission is said to usually occur “through direct contact with the open sores of the shingles rash”, rather than ‘aerosol’. If a person with ‘shingles’ then ‘infects’ someone else, that person will “develop chickenpox ... not shingles”. In other words, ‘shingles’ requires a prior ‘chickenpox’ infection. However, there appear to be exceptions to this rule, as we find that there are also recorded cases of individuals who develop shingles, but have no history of chickenpox. It is of course, entirely possible that these individuals weren’t diagnosed at the time; perhaps they were ‘asymptomatic’ but then the question is; on what basis is the assertion made that ‘shingles’ requires a prior ‘chickenpox’ infection?
‘Shingles’ is also said to be the more serious of the two conditions, but curiously, ‘death’ is not listed by the Mayo Clinic as one of the possible ‘complications’ – unlike ‘chickenpox’. The risk factors for ‘shingles’ are said to include “being older then 50”, “having certain diseases”, and “undergoing cancer treatments” or “taking certain medications” – which once again, suggests that it is people who are ‘immunosuppressed’, who risk developing this condition.
Although it is usually said to be an adult disease (as one must first have ‘caught’ ‘chickenpox’ – which is said usually occur in childhood), ‘shingles’ can also develop in children – although it is said that if and when this happens, the symptoms are generally “mild”. It is interesting to note that there doesn’t appear to be any reliable statistics available for estimates of what % of the human population harbours the ‘varicella virus’. Is it 50%? 80%? 100%? If this figure is not known, then on what basis do scientists make the claim that this particle is ‘contagious’ and responsible for the ‘disease’?
To summarise; ‘chickenpox’ can spread through ‘aerosol’. It is usually ‘mild’, but in some cases can cause death. Children usually ‘catch’ it, but sometimes adults do too. ‘Shingles’ is thought to be the more serious condition, and usually adults get it, but sometimes children get it. And although it is said to be more serious that ‘chickenpox’, the actual complications listed are less severe than those of ‘chickenpox’ (doesn't include death, for instance).
The same ‘virus’ is responsible for both diseases, but someone with ‘shingles’ cannot easily spread ‘it’ through ‘aerosol’ – it mainly happens through skin contact. If they do ‘transmit it’ to someone else, the person ‘catching it’ would get ‘chickenpox’, not ‘shingles’ – unless of course they’ve had ‘chickenpox’ before, in which case they are essentially, ‘immune’ – except (of course), in ‘rare’ cases where they could get ‘chickenpox’ a second time.
‘Chickenpox’ and ‘smallpox’ were thought to be the same ‘diseases’, whereas ‘shingles’ was thought to be a separate ‘disease’. Now, ‘smallpox’ is a separate ‘disease’, caused by a different ‘virus’, whereas ‘shingles’ and ‘chickenpox’ are different ‘diseases’ caused by the same ‘virus’.
Does this absurd merry-go-round make any sense to you? Are these two ‘diseases’ really completely separate entities? Is a ‘virus’ even involved?
Studies on Varicella
In 1923, Rockefeller Foundation virologist Thomas Rivers, wrote a paper titled Studies on Varicella, in which he makes, as he habitually does, a number of startling revelations; “Salmon, Tyzzer, and Teissier, Gastinel, and Reilly were unable to obtain a specific reaction on rabbits' corneas inoculated with fresh fluid from varicella vesicles”. In other words, they were unable to ‘transmit’ the ‘virus’ by injecting the fluid from chickenpox lesions, into the cornea (eyes) of rabbits. Then: “Park, Martin, and Tyzzer were unable to transmit chicken-pox to monkeys” and “Hess and Unger failed to produce varicella in normal children by inoculating them upon the mucous membranes of the nose and throat with vesicle lymph and material collected from the nose and throat of patients with chicken-pox, or by inoculating them intracutaneously”. In other words, they took secretions from the nose and throat of ‘chickenpox’ patients, and then attempted to ‘transmit’ the 'virus' to them, using a variety of methods, including injection. They were unable to achieve the desired effect.
“Kling stated that to obtain positive results at least six inoculations should be made, and that even then only one may be successful. These reports seem to indicate that the virus in the vesicles either is very dilute or has lost its virulence”. Six injections were needed to achieve the desired results – but only in some cases. And apparently, this is because the ‘virus’ had lost its ‘virulence’ in the vesicles (pustules) – even though they are said to be one of the routes of transmission.
“From reports in the literature it was found that the eruption of many of the exanthemata can be made to localize by irritation, provided the irritant is applied before or shortly after the appearance of the eruption. Von Pirquet and Schick have demonstrated this phenomenon in measles, Heim and John in scarlet fever, Swoboda in chicken-pox, and Hebra, Tische and many others in smallpox … Calmette and Guerin, Gins, Camus, and Levaditi and Nicolau have shown that vaccine virus injected intravenously into rabbits can be made to localize in the skin if certain areas be injured immediately after the injection by shaving or pulling out the hair”. So for various ‘diseases’, we are told here that researchers have been able to get the reaction they’re after by applying some form or other of trauma to the inoculation site.
According to Rivers, these observations indicate that “the virus of chicken-pox probably is present in the blood”, and therefore, “that it might be possible to demonstrate the disease in animals by injecting them with patients’ blood”. He then proceeds to perform various experiments on rabbits, using the blood of ‘infected’ patients; “blood was drawn from patients with chicken-pox usually during the first 24 hours after the appearance of the eruption. The blood was not citrated and before clotting occurred was injected in 2 cc. amounts into each testicle of normal rabbits”. Rivers also informs us that “these large quantities of blood were used intentionally”. We are not told why these “large quantities” were necessary, but one could imagine that injecting any fluid into the testicles of any creature, will lead to unpleasant effects. He goes on to describe the following: “at the time of inoculation the needle was moved about in the tissues to produce a certain amount of trauma ... 4 days later the testicles were removed, ground up thoroughly with sterile, chemically clean sand, and mixed with 10 cc. of physiological salt solution … Then 1 cc. of the emulsion was injected into each testicle of normal rabbits. Two areas on the rabbits' skin were shaved and scarified. One of the areas was smeared with the emulsion, the other was used as a control. An eye of each rabbit was also inoculated … Both corneas were scarified with a cataract knife (cocaine anesthesia was always used); one was inoculated with the testicular emulsion, the other was used as a control …
The first few animals in each series showed little reaction other than that which might be expected to follow the trauma of the inoculations. The skin and cornea healed rapidly. The scrotum was edematous at times for 24 to 48 hours…
The testicles, when removed, were slightly swollen. Necrotic areas and often remains of the material injected studded the tissue in various places. This reaction was no more striking than that caused by the injection of an emulsion of normal testicles.
The first few rabbits in each series and all the rabbits in the series from which no virus was recovered served as excellent controls for the work. After four to eight transfers of the virus from rabbit to rabbit, however, in certain series, the testicles became tense and firm on the 3rd or 4th day after the inoculation, and the scrotum often remained edematous.
In the inoculated eye a roughness of the cornea and a circumcorneal redness appeared on the 3rd or 4th day following the inoculation. An erythema and swelling not present in the control occurred along the lines of scarification in the skin 4 to 6 days after the inoculation (Fig. 6). Occasionally, in addition to the reaction in the skin inoculated with the testicular emulsion, discrete, papular lesions appeared 5 to 11 days after the inoculation in the control areas (Fig. 7).”
At this stage, are we allowed to ask; why the testicles? Why the eyes? Why are these steps necessary, when their ‘virus’ allegedly spreads through ‘aerosol’ and skin contact? Of course, no ‘virus’ particle was isolated in these studies, so it’s difficult to know whether the results of these experiments are due to the ‘virus’ particle, or any number of other contaminants present in the inoculated substances.
Indeed, Rivers concludes his paper by stating that; “in working with material supposed to contain a virus which is invisible, or not recognizable, and about which practically nothing is known experimentally, one can easily be mistaken about the identity of the virus or even in regard to its presence … Further evidence must be obtained, however, before one can think and speak definitely of this virus as the etiological agent of varicella … The ultimate proof depends upon the type of reaction this virus will cause in man and upon the possibility of protecting against varicella by inoculations of the virus.”
Smallpox is said to be caused by a different ‘virus’, known as ‘variola’. It belongs to another family of ‘viruses’ known as ‘poxviruses’, which also includes the ‘monkeypox virus’.
Once again, other than touting the success of ‘vaccination’ in ‘eradicating it’, the WHO doesn't provide us with an awful lot of useful information. WebMd state that; “Smallpox and chickenpox might seem similar. They both cause rashes and blisters. They both have ‘pox’ in their names. But other than that, they’re completely different diseases. You really don’t need to know how to tell them apart”.
They go on to list some of the key differences, starting with the following: “Chickenpox is still around. Smallpox is pretty much extinct”. In other words, they are different because one, apparently no longer exists, whilst the other does. A perfect example of circular reasoning. And this example isn’t unique; in 2014 the Washington Post ran a story on a mysterious ‘polio-like’ doing that rounds, where they stated that; “since polio has been eradicated in the United States and the patients in California were vaccinated against it, the suspicion has fallen on other members of the enterovirus family, to which poliovirus belongs”. In other words; it wasn’t ‘polio’ – not because they tested for ‘it’, and the tests came back negative – no, it wasn’t ‘polio’, because they decided it couldn’t possibly be – because ‘polio’ was ‘eradicated’ by ‘vaccination’.
WebMD then state that “doctors can tell chickenpox and smallpox apart” – which makes you wonder why, then, did we have to wait until the “end of the 19th century” for these ‘diseases’ to be accepted as different. Furthermore, given that ‘smallpox’ is said to have been ‘eradicated’, one wonders how it’s possible for doctors to tell them apart with such ease, given that most of them will never have seen a case for themselves in the flesh. This difference between the two is illustrated for us with the following image:
One can't help but wonder why they didn't choose to compare two similarly pigmented skins. Perhaps no photographs were available. But the last fatality attributed to ‘smallpox’ in the UK, is said to have been a certain Janet Parker in 1978. In fact, this same article includes a photo of an alleged smallpox victim that appears to be white.
The affliction certainly looks severe, but one wonders then how it is possible for ‘chickenpox’ and ‘smallpox’ to have ever been confused for one another. WebMD also state that: “while they may look similar to the untrained eye, smallpox rashes are different [to chickenpox]”. Furthermore, they appear to suggest that the rashes do not differ much in their appearance, only their location.
So, where did ‘smallpox’ come from? According to the CDC, “the origin of smallpox is unknown”. However they are able to confidently assert that it’s been around for “at least 3,000 years”. Evidence for this statements is provided to us in the form of this picture of Pharaoh Ramses V, on whom one can allegedly see “traces of smallpox pustules”.
But anyway, just like in the case of ‘polio’, the idea that this proves the existence of a ‘virus’ is quite clearly, absurd.
On the subject of contagion, Nightingale, in her book, ‘Notes on Nursing’ that: “I was brought up ... distinctly to believe that small-pox, for instance, was a thing of which there was once a first specimen in the world, which went on propagating itself, in a perpetual chain of descent. Since then I have seen with my eyes and smelt with my nose small-pox growing up in first specimens, either in close rooms or in overcrowded wards, where it could not by any possibility have been ‘caught,’ but must have begun”. It is clear that she did not think of ‘smallpox’ as a contagious disease.
Monkeypox and more
An in-depth look at ‘monkeypox’ is available here. At the time of writing, the CDC, and other medical authorities were stating that ‘lymphadenopathy’ (swollen lymph nodes) is the main difference between ‘monkeypox’ and ‘smallpox’. It would now appear that the CDC have scrubbed any mention of this from their fact sheet.
It is also interesting to note that the ‘disease’ was in one instance found in monkeys that had been irradiated. According to the researchers, the symptoms were not caused by the fact these monkeys were, essentially, poisoned, but by the fact that “irradiation, by decreasing host resistance, may lead to the appearance of clinical disease”.
As discussed, ‘smallpox’, ‘chickenpox’ and ‘shingles were all once confused for one another. ‘Monkeypox’ has also been confused for ‘chickenpox’. According to some, two can be told apart in the following way; “in the case of monkeypox, the eruptions may also manifest on the palms and soles of the feet, which is not the case in chickenpox”. This, however, is contradicted by other health authorities, who state that ‘chickenpox’ postules can be “can be anywhere on the body”, including “on the palms of the hands” and the “soles of the feet”.
Recently, a new ‘disease’ – ‘tomato flu’ – was allegedly detected in India. According to reports, this one is said to ‘mimic’ not just ‘monkeypox’, but also ‘dengue fever’, ‘chikungunya’ and ‘hand foot and mouth disease’.
We are also told that ‘scarlet fever’ was previously often confused with ‘diphtheria’ and ‘measles’, and that “the measly rash cannot always be distinguished from true measles, instances of which may be mistaken for the initial smallpox rash”. Physician Al Razi, was the first to describe the symptoms and signs of ‘smallpox’ and ‘measles’. According to his account; “back pain was more severe in smallpox, while it might be slight or absent in measles” and “distress, syncope and anxiety were more prominent in measles.” ‘Syphilis’ was also confused for ‘smallpox’; “when syphilis was first recognized at the end of the fifteenth century it became necessary to distinguish it from smallpox which it occasionally resembled to a most striking degree”.
There are many other such conditions that all appear to ‘mimic’ each other, including Sweet’s syndrome, Rickettsial pox (said to be caused by Rickettsia, a bacteria that is allegedly spread by mites and is said to be the causative agent of typhus). In 2003, several volunteers taking part in clinical trials for a ‘smallpox vaccine’ broke out in a “curious acne-like rash … samples of the lesions … tested negative for the virus, ruling out vaccinia and possibly establishing a new, less serious, reaction to the vaccine: folliculitis, benign eruptions like pimples”. The researchers also note that “we wanted to see if this eruption was common in adults after vaccination, and if it could be mistaken for general vaccinia Talbot said. The paper, he said, was an effort to lessen anxiety and provide some clarity for physicians who might see the rash on patients and confuse the less serious reaction with a fatal one”.
In the case of COVID, we find that certain patients appear to have developed ‘papulovesicular exanthems’ said to be “varicella-like”. Some researchers have rejected this sort of terminology and “proposed a term which was more suitable in their view: “COVID-19-associated acantholytic rash.”
In this most interesting case study, we are told of an individual who developed ‘bullous pemphigoid’, which consisted “of numerous tense blisters containing fluid on both an erythematous and an urticated background, erosions were also noted with haemorrhagic crusts”. The contents of these blisters “were positive for varicella zoster virus on both culture and immunofluorescence”. According to the researchers: “whether this was reactivation of the latent virus or a primary varicella zoster infection is not known”.
What causes these rashes?
It is not immediately obvious from reading these accounts that we are dealing with, as we are lead to believe, distinct entities, and that one or more ‘infectious viruses’ are to blame. As discussed here, there is good reason to believe that a great many of these ‘diseases’ may be linked to some form or other of poisoning – arsenic being the prime suspect. In ‘The Arsenic Century’, we are told of ‘arsenic pock’;
“‘Arsenic pock’ was the name workers gave to the eruptions resulting from the poison sticking to sweat-moistened skin, pus-filled eruptions that could break out anywhere on the body but were particularly common on the scrotum (Fig. 8), the depression between the lower lip and chin, along the border where the hat pressed upon the forehead, or, simply, ‘every crevice or fold where the arsenic can accumulate, unless frequently and carefully washed out’”.
And indeed, we find that on occasion, arsenic poisoning is said to cause a rash that is said to be indistinguishable from ‘chickenpox’; “that is, I think, the most accepted theory, but it still remains almost incredible that arsenic can ‘produce’ a common infectious disease such as chickenpox”.
In a recent report, researchers documented a case of arsenic poisoning whereby “on day 3 of chelation therapy, a vesicular rash developed on the upper arm, which became generalized over the next 48 hours. Swab specimens were positive for VZV, and the patient was treated with acyclovir”. They also note that “there is an association between arsenic poisoning and reactivation of varicella–zoster virus”, which is consistent with what others have documented; “clinical reports observe the reactivation of varicella zoster virus (VZV) in people who have recovered from arsenic poisoning”. Rashes are also commonly found in cases of exposure to ionising radiation, and these include ‘bullous pemphigoid’.
What purpose, if any, do these rashes serve? In the previous article, we discussed the fact that scientist have now discovered that symptoms such as diarrhoea and fever, are in fact, triggered by the body itself in an attempt to rid itself of toxins. The toxins are always thought to be ‘viruses’ of bacteria, but the exact same principle applies to any substance the body considers toxic.
‘Detox rashes’ are apparently a phenomenon that individuals can on occasion experience when going on a ‘detox diet’; “your skin plays an active role in the elimination process through your pores, and since we sweat through our pores, a common skin reaction that is described with certain detox regimens or elimination diets is a red, bumpy, itchy skin rash”.
As discussed in the previous article, if we accept the premise that many of the symptoms said to be caused by contagious ‘viruses’ or bacteria, are in fact, ‘detox symptoms’ following exposure to one or more toxins (or some form of emotional trauma, as per the GNM school of thought), then it is perhaps no surprise that we find that “there is an association between arsenic poisoning and reactivation of varicella–zoster virus”.
Re-introducing these toxins into test subject by means of injection, as done by Rivers and others, may then, on occasion lead to ‘localised rashes’, as observed in their experiments. In the case of ‘polio’, Popper and Landsteiner hypothesised that the effects they were seeing in their experiments may have been the result of a “a transferred poison”. And this isn’t altogether unreasonable given that arsenic, for instance, can break down into nanoparticles that are roughly the same size as ‘viral’ particles.
It would be very interesting to repeat the sort of experiments Rivers conducted (preferably using cell culture to avoid tormenting any more rabbits), having carried out some form of chemical and toxicological analysis of the materials being inoculated. Curiously, no such study appears to exist, and this appears to be the case for virtually all experiments that involve ‘viral isolation’.
Thank you as always to Caroline for her help in pulling this material together, and Dr Andy Kaufman for sharing the papers that document the similarities between ‘chickenpox’ and arsenic poisoning.