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Saturday, January 28, 2017

Poliovirus and Zika: What’s Past is Prologue by Marco Cáceres

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Poliovirus and Zika: What’s Past is Prologue

poliovirusStory Highlights
  • Proper scientific studies have not been done to prove a causal relationship between the Zika virus and microcephaly.
  • Similarly, proper scientific methodology may not have been followed to prove the existence of a poliovirus.
  • Consequently, there may not exist what has come to be widely known and accepted as the poliovirus.
In December 2015, formalin-fixed, paraffin-embedded (FFPE) tissue from two newborn babies and two miscarriages in Brazil diagnosed with microcephaly were provided by the Brazilian government to the U.S. Centers for Disease Control and Prevention (CDC) for “histopathologic evaluation and laboratory testing” for “suspected Zika infection.”1 The newborns, which had been born at 36 and 38 weeks gestation, died within 20 hours of birth. The miscarriages were from fetuses at 11 and 13 weeks.1 
Samples included brain and other autopsy tissues from the two newborns, a placenta from one of the newborns, and products of conception from the two miscarriages.1 
CDC scientists determined that the placenta samples from two fetal miscarriages tested positive for the Zika virus, and that the tissue samples from the two newborns also showed evidence of Zika.
FFPE tissues were tested by Zika virus reverse transcription-polymerase chain reaction (RT-PCR) targeting the nonstructural protein 5 and envelope genes using general methods for RT-PCR, and by immunohistochemistry using a mouse polyclonal anti-Zika virus antibody, using methods previously described. Specific specimens from all four cases were positive by RT-PCR, and sequence analysis provided further evidence of Zika virus infection, revealing highest identities with Zika virus strains isolated from Brazil during 2015. In the newborns, only brain tissue was positive by RT-PCR assays. Specimens from two of the four cases were positive by immunohistochemistry: viral antigen was noted in mononuclear cells (presumed to be glial cells and neurons within the brain) of one newborn, and within the chorionic villi from one of the miscarriages.1
Lyle Petersen, MD, director of the CDC’s division of vector-borne diseases, said that the results of these tests offered the “strongest evidence to date of a possible link between Zika virus and microcephaly and other congenital abnormalities.” But Dr. Petersen stopped short of declaring a causal relationship.2
The fact that the tissue from the two newborns with microcephaly tested positive for the Zika virus is not evidence that the virus caused the microcephaly. By the same token, the fact that the tissue from the two miscarriages tested positive for Zika is not evidence that the virus caused the miscarriages or that the two fetuses had microcephaly, or that the virus would have been the cause of the microcephaly had it been determined that the fetuses showed signs of the birth defect. Correlation is simply not the same as causality.
The mere presence of a virus is not scientific evidence that the virus caused something to occur. Before a causal relationship can be established between Zika and microcephaly, in depth studies must be conducted on thousands of babies—both those born with microcephaly and without microcephaly—and studies enrolling pregnant women prospectively and monitoring their health and fetal development throughout pregnancy should be conducted. There must also be conclusive laboratory evidence. None of this has yet taken place.
This kind of scientific research did not take place in 1908 when Austrian physicians Karl Landsteiner, MD and Erwin Popper, MD are said to have discovered the poliovirus. In that landmark year in the history of poliomyelitis, or “polio,” Drs. Landsteiner and Popper “deduced the viral nature of polio by carefully filtering preparations of spinal cord fluid” from a 9-year old boy who had been paralyzed and was thought to have apparently died of severe complications of a four-day viral infection at the Children’s Clinic in the Wilhelminen Hospital in Vienna, Austria, an infection that would eventually be called poliomyelitis.3 4 5
These preparations, as investigative journalist Janine Roberts has described it, were a “suspension in water of minced diseased spinal cord…”6
They had tested this noxious suspension by injecting one or two cups of it directly into the brains of two monkeys. The monkeys fell severely ill (as might have been predicted). One died and the other had its legs paralysed. The scientists then dissected the monkeys and found damage in their central nervous tissues similar to that found in human cases of infantile paralysis.6
By this reasoning, Drs. Landsteiner and Popper claimed that they had found some sort of “invisible virus” that ultimately came to be known as the “poliovirus.” Remember, though, Drs. Landsteiner and Popper never actually saw the virus, but rather “deduced” it. They did not see the virus because they did not have the technology to do so. The first electron microscope with the ability to view viruses was not invented until 1931,7 8 and the first image of what has become known as the poliovirus was not taken until 1953.8
Reviewing these historical facts, three questions arise. The first is, “How did Drs. Landsteiner and Popper know that the 9-year old boy from which they had taken spinal cord fluid samples actually had polio?”
Prior to the 1950s when the first polio vaccine was developed by Jonas Salk, MD, “many distinct diseases were naively grouped under the umbrella of ‘polio,'” according to Suzanne Humphries, MD and Roman Bystrianyk in their book Dissolving Illusions: Disease, Vaccines, and The Forgotten History.9 
Only after the vaccine was widely accepted was there an effort to distinguish poliovirus from other types of paralytic disease. The following list represents a few that could have been categorized and documented as polio prior to 1958: Enteroviruses such as Coxsackie and ECHO; Undiagnosed congenital syphilis; Arsenic and DDT toxicity; Transverse myelitis; Guillain-Barré syndrome; Provocation of limb paralysis by intramuscular injections of many types, including a variety of vaccines; Hand, foot, and mouth disease; Lead poisoning.9
For all Landsteiner and Popper knew in 1908, the paralysis suffered by the 9-year old boy may have been caused by any number of factors. The paralysis could easily have been caused by arsenic or lead poisoning. Arsenic, in particular, was a big killer throughout the 1800s and early-1900s. During the late-1800s and early-1900s, arsenic was added to foods as a preservative.10 During the 1890s and early-1900s, throughout the United States and Europe, there were frequent epidemics of lead poisoning from contaminated water in pipes.11
So perhaps the 9-year old boy became paralyzed in much the same way that many children were paralyzed during the 1940s and 1950s by the toxic pesticide DDT (dichlorodiphenyltrichloroethane).12 As Dr. Humphries and Bystrianyk note, “The diagnostic criteria for polio were very loose prior to the field trials for the [polio] vaccine in 1954.”9
Drs. Landsteiner and Popper diagnosed the boy as having a communicable viral infection that caused paralysis (eventually called polio). They assumed he had polio. But there was no way for them to scientifically demonstrate that the boy was infected with poliovirus. This leads to the second question, which is, “What caused one of the monkeys to die and the other to become paralyzed?”
The first monkey became violently ill on the sixth day and died on the eighth. He lay on the floor of his cage and his power to move his limbs was not investigated. After death changes typical of anterior poliomyeletis were found. The second monkey was noted to have lost all power in the hind legs on the seventeenth day. No paralysis was present on the twelfth, although it may have been present before the seventeenth in some degree. He was killed on the nineteenth day and again typical pathological changes were found in the central nervous system. From the spinal cord of this monkey inoculations were made into two other monkeys with negative results. The conclusion of these authors is that ‘a so-called invisible virus, that is, one belonging to the class of the protozoa, is the cause of the disease.’
The spinal cord fluid concoction that Drs. Landsteiner and Popper injected into the two monkeys could have had lots of harmful ingredients that may have caused neurological damage.
The fluid they injected must have contained much human cellular debris, any toxins involved in the child’s illness, and probably several kinds of viruses. So, it was no wonder the monkeys fell so desperately ill. Such a soup could in no way be considered an ‘isolate’ of the tiny organism we now call a virus. It was also strangely non-infectious for a so-called virus, for the monkeys were not paralysed when made to drink it or when one of their limbs was injected with it, nor did they pass it on to other monkeys. The experiment, in fact, shed no light on what had paralysed the monkeys, and for that matter, the children.6 
The death of one of the monkeys and the paralysis of the other may have been caused, not by any specific virus, but rather by having needles stuck in their brain and being injected with foreign cellular tissue, toxins from whatever the boy was suffering of, as well as any number of unknown viruses or bacteria.
So if there was no way to scientifically know for sure that the 9-year old boy had polio virus infection, and it is just as possible that the boy could as easily have suffered from arsenic or lead poisoning, and it is entirely possible that the two monkeys became ill (one paralyzed) from the injection of many harmful substances, then the so-called discovery of a the poliovirus itself  becomes open to question. The entire process appears to have developed less through scientific methods proving causation and more byway of a series of personal assumptions and correlations.
Yet, the belief in the discovery of the poliovirus took hold and grew during the first half of the 20th century. The belief was seldom questioned within the medical and scientific communities. But the belief was not based on solid evidence that qualifies as good science. In his commencement address, at McGill University in Montreal, Canada in June 1990 titled “The Germ Theory of Disease and The Hunt for the Poliovirus,”13 John C. Polanyi, PhD, a Hungarian-Canadian chemist who won the 1986 Nobel Prize in Chemistry, questioned how any scientist could “credibly claim that injecting cellular debris into the skull of a monkey proves a virus to cause polio?”13
The more I read of what are supposed to be the victories of polio research, the more I have been, quite frankly, appalled. During the 1920s and 1930s all kinds of biological materials-spinal cord, brain, faecal matter, even flies-were ground up and injected into monkey brains to induce paralysis, causing great harm to many animals—all in the hope that such experiments would explain why humans were getting summer polio.
The method they used to exclude bacteria from their injected sample of backbone was also quite extraordinary. They put some of the backbone suspension into a dish and watched to see what happened.  They reported: ‘If there was no [bacterial] growth after approximately 22 hours of incubation at 37 C., the specimen was considered suitable for inoculation into monkeys. This was not a sterility test, since growth would usually occur on longer incubation; it was rather an indication of the amount of bacterial contamination in the specimen.’ Slow growing bacteria were thus deliberately not removed—and no toxin was looked for —yet they knew these might well be present.13
Dr. Polanyi did not believe that Drs. Landsteiner and Popper and other polio researchers who followed up their work had succeeded in isolating a poliovirus or any other kind of virus.
From all I read, I was forced to conclude that these ‘scientists’ shared a doctrinal conviction that the cause of polio must be a particular virus and could be nothing else. They routinely described as ‘isolated virus’ what was nothing much more than fluid from a cell culture contaminated with many diverse particles and possibly toxins. What else but an irrational belief in a theory could so blind these scientists?13

Finally, the last question—”Then what did scientists see in 1953 when they took an image of the ‘poliovirus’ with their electron microscope?” According to Janine Roberts, in the late-1940s, Jonas Salk “found among the debris and toxins of ‘viral isolates’ from monkey brain experiments what he believed to be the poliovirus.”6

What Dr. Salk found was the product of experiments conducted by Gilbert Dalldorf, MD and Grace M. Sickles, MD of the New York State Department of Health in 1948-49. According to Dr. Polanyi, Drs. Dalldorf and Sickles “claimed to have ‘isolated’ in the faeces of paralyzed children an ‘unidentified, filterable agent’ or ‘virus’ that might be the cause of polio.”
They had done so by diluting the excrement of polio-victims.  They said they took a ‘20% faecal suspension, prepared by ether treatment and centrifugation.’ (Ether to kill bacteria and centrifugation to remove large particles.) This they had injected ‘intracerebrally into mice’—meaning into the living brains of mice. The result was ‘suckling mice, 3-7 days of age, became paralyzed…’
So what had they proved with this experiment? Surely, only that paralysis could be induced in young mice by injecting diseased human excrement into their young brains?  I was utterly shocked that serious scientists could get away with describing this as the successful ‘isolation’ of a virus that they had thus proved to cause polio in humans.
Dr. Polanyi cited polio research pioneer Claus W. Jungeblut, MD as having expressed serious reservations about the scientific methodology of Drs. Dalldorf and Sickles.
The highly respected bacteriologist Claus Jungeblut critically stated that such ‘viral isolates,’ including those developed by Salk and other vaccine scientists, had not been proved to cause polio—as they had not been shown to give monkeys the disease found in human cases of infantile paralysis—and thus had failed to meet the Koch Postulates.
In fact quite the contrary had been demonstrated. Jungeblut said the virus would be so changed or mutated by the way these vaccine scientists passaged it through monkey cells that it would be quite unlike the wild virus by the time it was used for a vaccine.  He concluded: ‘The highly specialized … virus which has been maintained in the past by intra-cerebral passage in rhesus monkeys is more likely a laboratory artefact than the agent which causes the natural disease in man.’
Dr. Polanyi also noted that Drs. Dalldorf and Sickles had reason to believe there was another “agent” apart from their poliovirus that could have been a factor in causing paralysis.
It also might not be the only agent at work. Dalldorf and Sickles thought at one point that they had detected an agent at work alongside the ‘poliovirus,’ helping to cause polio. ‘The patients we studied may possibly have been coincidentally infected with the new agent and classical poliomyelitis virus.’  They tried to test the putative ‘new agent’ but it was ‘not successful in [causing disease in] the rhesus monkey.13
In short, even though the medical and scientific communities credit Drs. Landsteiner and Popper for the “discovery” of the “poliovirus,” the image of what we have come to recognize as the “poliovirus” is owed to the work of Drs. Dalldorf and Sickles.
This tiny particle, some 24-30 nm (thousand millionths of a meter) in width, isolated from excrement, thus became the basis of our polio vaccine. Dr Salk developed the first commercial polio vaccine with virus found in ‘the pooled faeces of three healthy children in Cleveland. It was not found in the victims of polio.13
It is this kind of “science” based on assumptions that is now being pursued in what appears to be a frantic, irrational campaign to tie the Zika virus to microcephaly at all cost, and then invest what could end up being billions in tax dollars to research, develop and test a Zikca vaccine that public health officials will subsequently recommend, or even mandate, that all pregnant women receive.
It’s funny how often what is past can so easily become prologue.


1 comment:

  1. Both Aedes and Culex are #ZIKV vectors. In Culex and in vertebrates (like birds and possibly humans) I believe #Wolbachia is playing an inordinate role in the amplification of the #Zika virus.

    I think Zika could be behaving like a bacteriophage. I just hope it's not too late to restore ecological balances.

    The most likely reservoir host: Red-Whiskered Bulbuls. For more: http://www.infobarrel.com/Red-Whiskered_Bulbul_Zikas_Ideal_Reservoir_Host