Vaccine Contamination

tonto

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Just started learning about this line of research. Respiratory syncytial virus (RSV) appears to emerge in 1950s through contamination of polio vaccine. In addition, amoebic infection appears related to polio vaccine.

Recent interview Judy Mikovits revealed that Eastern Equine Viruses exist in modern vaccines (see review). Interesting Eastern Equine Encephalitis used to be a disease of children, now increasing in adults.


Sources:
Re: Polio eradication: a complex end game
Another important consideration in attempts to eradicate poliomyelitis by vaccination is the contamination of polio vaccines by chimpanzee coryza virus, renamed respiratory syncytial virus (RSV).

Morris et al. (1956. Recovery of cytopathogenic agent from chimpanzees with coryza. Proc Soc Exp Biol Med; 92: 544-549) described monkey cytopathogenic agent that produced acute respiratory illness in chimpanzees at the Walter Reed Army Institute of Research and named it chimpanzee coryza virus (CCA).

Chanock et al. (1957. Recovery from infants with respiratory illness of vius related to chimpanzee coryza agent (CCA). I. Am, J Hyg; 66: 281-290) wrote on the association of a new type of cytopathogic myxovirus with infantile croup.

Chanock and Finberg (1957. Recovery from infants with respiratory illness of virus related to chimpanzee coryza agent. II. Am J Hyg; 66: 291-300) reported on two isolations of similar agents from infants with severe lower respiratory illness (bronchopneumonia, bronchiolitis and laryngotracheobronchitis). The two viruses were indistinguishable from an agent associated with the outbreak of coryza in chimpanzees (CCA virus) studied by Morris et al. (1956). A person working with the infected chimpanzees subsequently experienced repiratory infection with a rise in CCA antibodies during convalescence. They proposed a new name for this agent “respiratory syncytial virus” (RSV). RSV has spread via contaminated polio vaccines like a wildfire all over the world and continues causing serious lower respiratory tract infections in infants.

Beem et al. (1960. Association of the chimpanzee coryza virus agent with acute respiratory disease in children. NEJM; 263 (11): 523-539) isolated the virus from inpatients and outpatients in the Bobs Robert Memorial Hospital for Children (University of Chicago) during the winter of 1958-1959, in association with human acute respiratory illness. The virus (named Randall) had an unusual cytopathic effect characterised by extensive syncytial areas and giant cells. Soon, 48 similar agents were isolated from 41 patients. There were antigenic similarities between RV and Long and Sue strains of CCA; it produced illness in humans (the age range 3 weeks to 35 years): acute respiratory diseases, croup, bronchiolitis, pneumonia and asthma ranging from mild coryza to fatal bronchiolitis. The isolatation rate (46%) was particularly high among infants below six months.
In Australia, Lewis et al. (1961. A syncytial virus associated with epidemic disease of the lower respiratory tract in infants and young children. Med J Australia: 932-933) and Forbes (1961. Ibid: 323-325) isolated further viral specimens identical with CCA.

Prior to July 1960, the influenza and parainfluenza viruses predominated in infant epidemic respiratory infections; in July 1961 the pattern changed abruptly with sudden increase in bronchiolitis and bronchitis, infrequent before. 58% were under 12 months, and patients under 4 years predominated. Infants with bronchiolitis and severe bronchitis yielded RCA, not previously isolated. Deaths have occurred.

Rogers (1959. The changing pattern of life-threatening microbial disease. NEJM; 261 (14): 678-683) wrote that life-threatening microbial infections continued occur despite antibiotics. Microbial agents have also changed in 1957-1958 compared with the streptococcal predominance during 1938-1940).

An “impressive” increase in the number of life-threatening enterobacterial infections has occurred. “During the preantimicrobial era most infections were acquired before admission to hospital, while in the postantimicrobial era the vast majority of infections arose in hospital.”

“Mycotic infections, especially with Candida albicans, became a major problem. Unusual serious generalised clostridial infections arose and antibiotics have not dramatically altered the risk of, or mortality resulting from, endogenous infections” in sick, hospitalised patients.

Rogers’s (1959) observations on antibiotics ineffectiveness, and new serious additional problems outlined above, fell on deaf ears.

Levy et al. (1997. Respiratory syncytial virus infection in young infants and young children. J Family Practice; 45 (6): 473-481) wrote “Respiratory syncytial virus (RSV) is the most prevalent cause of lower respiratory tract infections (LRTI) in infants and young children. Infections with RSV is a major health problem during early childhood and primary RSV infections occurs most often between the ages of 6 weeks and 2 years. Approximately one half of all infants become infected with RSV during the first year of life and nearly all infants by the end of their second year of life…in the US each year, approximately 100,000 children are hospitalised at an estimated cost of $300 million. More than half of those admitted for RSV bronchiolitis are between 1 and 3 months of age.” [Clearly implicating vaccination.]
And, “In the US each year, approximately 100,000 children are hospitalised at an estimated cost of $300 million. More than half of those admitted for RSV bronchiolitis are between 1 and 3 months of age.”

RSV vaccine developed in late sixties clearly failed. Fulginiti et al. (1969). Respiratory virus immunizations. I A field trial of two inactivated respiratory virus vaccines…Am J Epidemiology; 80 (4): 435-448) and others showed the vaccine ineffective, inducing exaggerated, altered clinical response…causing RSV illness requiring hospitalisations among vaccines and delayed dermal hypersensitivity.

Simoes (1999. Respiratory syncytial virus infection. Lancet; 354: 847-852) wrote “Since it was identified as the agent that causes chimpanzee coryza in 1956, and after its subsequent isolation from children with pulmonary disease in Baltimore, USA, respiratory syncytial virus (RSV) had been described as the single most important virus causing acute respiratory-tract infections in children. The WHO estimates that of the 12.2. million annual deaths in children under 5 years, a third are due to acute infections of the lower respiratory tract. Streptococcus pneumoniae, Haemophilus influenzae, and RSV are the predominant pathogens… vaccinated children were not protected from subsequent RSV infection. Furthermore, RSV-naïve infants who received formalin-inactivated RSV vaccine, and who were naturally infected with RSV later, developed more severe disease in the lower respiratory tract than a control group immunized with a trivalent parainfluenza vaccine”.

Data from ten developing countries, with intense polio vaccination, showed RSV the most frequent cause of LRT infections (70% of all cases).

Polio vaccines are not only ineffective in preventing paralysis, they carry the risk of contamination with many harmful adventitious microorganisms, of which only some monkey viruses have been researched in more detail. Many other potentially dangerous microorganisms remain unaddressed.

Polio eradication: a complex end game
Contamination of monkey kidney tissue cultures (used in the production of polio vaccines) by live amoebas.

In 1996, while watching a TV news report on the death of two 5-year olds in Australia from brain-eating amoebae, I remembered a note in Hull et al.'s paper (1958. New viral agents recovered from tissue culture of monkey kidney cell. Am J. Hyg; 68: 31-44): “Recently, an amoeba was isolated from monkey kidney tissue cultures and was identified as belonging to the genus Acanthamoeba. It grew readily in tissue cultures…It appeared to have the ability to infect and kill monkeys and mice following intracerebral and intraspinal inoculation.”

Amoebas are unicellular protozoan microorganisms. According to Ma et al. (1990. Naegleria and Acanthamoeba infections: Review. Rev Infec Dis; 12 (3): 490-513), they are classified in the phyllum Sarcomastigophora and belong to Rhizopoda, equipped by propulsive pseudopodia and/or protoplasmic flow without production of pseudopodia. Acanthopodina, a suborder of Amoebida, form two families, Vahlkampfiidae and Acanthoamoebididae, with two genera Naegleria and Acanthamoeba respectively, with a number of species. Naegleria species form three life-stages, trophozoites, flagellates and cysts and Acanthamoeba species only two, trophozoites and cysts.

Jahnes et al. (1957. Free-living amoebae as contaminants in monkey kidney tissue cultures. Proc Soc Exp Biol. Med; 96: 484-488) isolated two strains of apparently the same amoeba which looked like round bodies, similar in appearance to cells manifesting changes induced by certain simian (monkey) viruses. On closer examination, they proved to be amoebic cysts. They varied in size, from 10 to 21 microns in diameter. In one experiment, the cysts were treated with 10% formalin, washed and inoculated into monkey kidney tissue culture tubes. The monkey kidney cells fagocytised the cysts. The trophozooites turned into cysts under refrigeration down to 4 degrees C. These were resistant even under –50 degrees C for months and survived in the pH range 5.0-9.0. Their tissue cultures were not affected by streptomycin and penicillin.

Culbertson et al. (1958. Acanthamoeba: observations on animal pathogenicity. Science 1958; 127: 1506) and Culbertson et al. (1959. Experimental infection of mice and monkeys by Acanthamoeba. Am J Pathology; 35: 185-197) confirmed that amoebas caused brain disease and death within days in monkeys and mice.

Following inoculations “extensive choriomeningitis and destructive encephalomyelitis occurred” and killed monkeys in four to seven days and mice in three to four days. Intravenous injections of the amoebas resulted in perivascular granulomatous lesions. Intranasal inoculation in mice resulted in fatal infections in about four days. These mice exhibited ulceration of the frontal lobes of the brain. There were amoebas in the lungs, and they caused severe pneumonic amoeba reaction. Haemorrhage was a common feature. Sections of the kidney showed amoebas present in the glomerular capillaries.

Amoebas showed the ability to migrate through the tissues. The size of the inoculum did not matter: both small and large inoculums produced amoebic invasions. Intragastric inoculations were unsuccessful most probably because amoebic cysts were dissolved by bile.

Researchers, as a rule failed to address the seriousness of the introduction into children of Acanthamoeba via the polio vaccines, even though they were aware of their origin from monkey kidney tissue cultures used in the production of polio vaccines. However they noted that the most contaminated age group were babies below the age of crawling – between 2 and ten months.

Live amoeabas were isolated from the air (Kingston and Warhurst 1969. Isolation of amoebae from the air. J Med Microbiol; 2: 27-36) in the UK, together with respiratory syncytial virus, and from the surfaces in hospital cubicles in which infants with acute bronchiolitis were being nursed,

The amoebas were isolated at Booth Hall Children’s Hospital in the cubicle occupied by a ten-week-old infant with acute bronchiolitis. First, only RSV was isolated and the child sent home, but later an unidentified cytopathic effect was noticed in the tissue cultures and was provisionally called “Ryan virus1” (Pereira et al. 1966, Ryan virus: a possible new human pathogen. BMJ 1Jan 15: 130-132), and later also in post-mortem bronchial swab of another seven-months old baby boy with RSV bronchiolitis.

Six days before admission, the baby developed a sore throat and ulcers in the mouth which later spread over the face; he was unwell, could not suck and developed loose stools. The day before admission, he developed a cough and started vomiting. He was drowsy and dyspnoeic, made jerky movements and died soon after admission. Necropsy showed some emphysema, petechiae and small areas of congestion and alveolar haemorrhaging in the lungs, a fatty liver, prominent mesenteric nodes, and mucopus in the ears. Escherichia coli bacteria were cultures from his ears. Death was diagnosed as due to a respiratory infection associated with encephalomyelitis and hepatitis. Vaccination status was not disclosed, although considering the age, the baby could have received up to three doses of DPT and OPV vaccines.

Armstrong and Pereira (1967. Identification of “Ryan virus” as an Amoeba of the genus Hartmanella. BMJ; 28 Jan: 212-214) identified the Ryan virus as Hartmanella castellanii. They had no doubt that these amoebas came from the human respiratory tract.

In Australia, Fowler and Carter (1965. Acute pyogenic meningitis probably due to Acathanoeba sp.: a preliminary report. BMJ; September 25: 740-742), Carter (1968. Primary amoebic meningoencephalitis: clinical, pathological and epidemiological features of six fatal cases. J Pathol, Bacteriol; 96 (1): 1-25) and Carter et al. (1981. A fatal case of meningoencephalitis due to a free living amoeba of uncertain identity, probably Acanthamoeba sp. Pathology; 13: 31-48) described a number of cases in children and adults.

Many cases all over the world occurred in children and adults, with, or without the history of swimming in lakes and public swimming pools. (Scheibner 1999. Brain-eating bugs: the vaccine connection. Nexus Magazine; (whale.to/vaccines/amoebas.html).

Even if polio vaccines were effective in preventing polio paralysis, their potentially continued contamination by undesirable microorganisms (monkey viruses and amoebas) should encourage the abandonment of their use.

Well-meaning Rotarians should study the relevant medical research first, before engaging in global polio vaccination.

Eastern equine encephalitis in Massachusetts
We studied the case records of 16 patients with eastern equine encephalitis (EEE) in Massachusetts from 1970 to 1984 and compared their presentations, courses, and outcomes with the data available from previous epidemics. In recent years, there has been a greater frequency of EEE in adults, whereas in the past it was considered a disease of children. Also, prognosis for a good functional recovery seems to be correlated with age over 40 years, a long prodromal course (5 to 7 days) of constitutional symptoms, and the absence of coma. Previous reports did not mention these significant correlations. We also stress the positive and negative diagnostic correlations, in order to distinguish between EEE and herpes simplex encephalitis.
 

Gone Peating

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Sep 16, 2018
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yea it's quite obvious that a lot of evil people have been attempting to depopulate and gain control over what's leftover for some time now

in their minds, however, they think this is progress and that they are doing good
 

aodg

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Jan 23, 2020
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Hi, what's up with RSV these days ?

Seems to be abnormally high in some regions. Is it telling of something else to come ?

Influenza B too, for that matter. Up a fair bit when it otherwise wouldn't come till later in the season, no ?


 

Lollipop2

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Hi, what's up with RSV these days ?

Seems to be abnormally high in some regions. Is it telling of something else to come ?

Influenza B too, for that matter. Up a fair bit when it otherwise wouldn't come till later in the season, no ?


Sounds like ADE to me...
 

aodg

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Jan 23, 2020
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"respiratory syncytial virus (RSV) infection induces bacterial biofilm formation through a mechanism of dysregulated iron homeostasis of the airway epithelium"


Parsifaler has been shining a light on the spike protein and it's affect on Iron.

Perhaps there's a connection. Dysregulated Iron leads to a higher prevalence of RSV or something like that.
 

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