Health Impact News Editor Comments:

The science and history of the polio vaccine is written by Dr. Viera Scheibner. The entire article, History and Science Show Vaccines Do Not Prevent Disease, can be read here.

This was extracted from her research presented in A critique of the 16-page Australian pro-vaccination booklet entitled “The Science of Immunisation: Questions and Answers” –You can read the entire report here.

While the polio vaccine is often referred to by those who believe in vaccines as the ultimate example of a vaccine that eradicated a terrible disease that is no longer with us, the science and history of this vaccine tell a vastly different story.

From Dr. Scheibner’s research below, we can clearly see certain facts in the history of polio vaccination:

1. There has been more than one type of polio vaccine through its history, due to the fact that earlier versions were found to be ineffective and harmful.

2. The occurrence of polio was trending downward prior to the introduction of polio vaccines.

3. The reported effectiveness accredited to polio vaccines can actually be easily accounted for by data manipulation and not actual decreases of occurrence. (See also Dr. Suzanne Humphries’ excellent treatment of this subject here:  Did Vaccines Really Eradicate Polio?)

4. The history of the polio vaccine is a history of contamination of the vaccines responsible for the injury and deaths of countless people.

Update: The New York Times published a story about new strains of the polio vaccine being developed. Here is what they wrote concerning the current strain of the polio vaccine:

The Sabin vaccine has drawbacks, however: it contains a still-live virus that was mutated long ago so that it is usually too weak to produce disease. In rare cases, it can mutate back into a dangerous form that paralyzes or kills. And the vaccine is risky in children with immune-system problems. For those reasons, the World Health Organization plans to eventually phase it out.

Source: http://www.nytimes.com/2013/02/19/health/new-polio-strains-that-protect-vaccine-factory-workers.html

The sordid history of Poliomyelitis vaccination

By Dr. Viera Scheibner (PhD)
International Medical Council on Vaccination

When the Salk injectable “formaldehyde killed” polio vaccine was tested on some 1.8 million American children in 1954‐55, cases of paralysis in the vaccinated and some of their contacts started occurring within days.(43)

The Cutter Laboratories were accused of distributing vaccines containing live polioviruses. Disasters with the Salk vaccines causing vaccine associated paralytic poliomyelitis (VAPP) seem to have been one of the main motivations behind development of an oral “live attenuated” Sabin vaccine, which was believed to simulate the natural infection. However, VAPP cases continued occurring with the Sabin vaccine.

I spent many hours locating and reading the older and more recent articles addressing the effectiveness, or otherwise, of combining IPV and OPV vaccines. I established that the results are not straightforward. Abraham reported that shedding of virulent poliovirus revertants, during immunization with oral poliovirus vaccines, after prior immunization with inactivated polio vaccines, continued.(44)

He also documented that prior immunization with EIPV (enhanced potency IPV) does not prevent faecal shedding of revertant polioviruses after subsequent exposure to OPV. (45)

Mensi and Pregliasco wrote:

In recent years great alarm has been generated by outbreaks of  paralytic poliomyelitis in vaccinated populations…epidemics were observed in Finland in 1984, Senegal and Brazil in 1986, and Israel and Oman in 1988, all countries in which vaccination is widely deployed. Four epidemics were reported between 1991 and 1992. The  first, in 1991, was in Bulgaria, which uses oral vaccination. Forty-three subjects developed paralytic type 1 polio; 88% of them belonged to a normal community and had not completed or even started a vaccination schedule. The second epidemic occurred in The Netherlands, where inactivated polio vaccine (IPV) is used, and involved 68 patients with type 3 poliovirus, members of the Amish…(46) [In The Netherlands they are called members of orthodox religion and in fact use the polio vaccination (compliance between 40‐50% and higher)].

Schaap et al. published a graph (figure 14) correlating the number of reported poliomyelitis cases with the vaccination rates in seven areas in The Netherlands.(47) Interestingly, the areas with the lowest compliance had the lowest number of cases and vice versa. The compliance ranged from 40‐49% to 90‐95%. In the 1992 epidemic, the first two cases occurred in a 14‐year old boy and 23‐year old male nurse, both vaccinated members of the orthodox religious group.

Sutter et al described an Oman outbreak as:

. . . evidence for widespread transmission among fully vaccinated children.(48)

Incidence of paralytic disease was highest in children below 2 years:

. . . despite an immunisation programme that recently had raised coverage with 3 doses of oral poliovirus vaccine (OPV) among 12-months-old  children  from  67%  to  87%…  with  transmission  lasting  for  more  than  12  months.  Among  the  most  disturbing  features  of  this  outbreak  was  that  it  occurred  in  the  face  of  a  model  immunisation   programme  and  that  widespread  transmission  had  occurred  in  a  sparsely  populated,  predominantly  rural  setting. (49)

One  of  the  interesting  reasons  quoted  was:

.  .  .  rapid  increases  in  vaccination  coverage  before  the  outbreak  may  have  reduced  or  interrupted  endemic  circulation  of  indigenous  strains,  diminishing  the  contribution  of  natural  infection  to  overall  immunity  levels  in  the  general  population. (50)

The  same  reason  was  given  by  Biellik  et  al.  in  1994  when  they  described  the  situation  in  Namibia.  They  wrote:

Endemic  wild  poliovirus  circulation  has  continued  uninterrupted  in   Angola  and  the  two  northern  regions  in  Namibia  across  the  well-travelled  border  since  1989,  when  cases  were  last  reported.  Although  OPV3  cover  age  was  fairly  low  in  northern  compared  with  southern  Namibia,  a  higher  proportion  of  northern  children  might  have  been   protected,  at  least  to  type  1,  by  natural  immunity,  thus  suppressing  epidemics  .  .  .  the  apparent  interruption  of  [natural]  poliovirus  circulation [by  vaccination] limited  the  acquisition  of  natural  immunity. (5)1

Control  of  polio  in  the  US  shows  the  same  phenomenon  as  the  control  of  pertussis,  namely  downward  trend,  which  stopped  when  individual  states  in  the  US  mandated  DPT  and  polio.

An  interesting  example  of  manipulation  of  data  is  polio  “eradication”  in  the  Americas.  Figure  16(52) shows  the  effect  of  reclassification  of  poliomyelitis  which  allowed  the  ever  increasing  number  of  “notified”  cases  to  morph  into  an  ever  decreasing  number  of  “confirmed”  cases.

Dr  HV  Wyatt (53) quoted  Hanlon  et  al.  as  stating:

…injections  during  an  epidemic  may  provoke  poliomyelitis  in  children  already  infected  with  poliovirus,  [and]  …provocation  poliomyelitis  occurs  with  injections  of  diphtheria/pertussis/tetanus  vaccine,  which,  I  am  told,  gives  rise  to  unease  among  vaccinators.  The  risk  of   provocation  poliomyelitis  with  the  killed  poliovaccine…occurred  in  the  Cutter  incident. 

During  a  poliomyelitis  outbreak  in  Taiwan,  Kim  et  al.  reported  that  65%  of  VAPP  developed  within  28  days  of  the  first  vaccine  dose  This  report  confirmed  observations  of  others  that  two  thirds  of  vaccine‐targeted  diseases  occur  after  the  first  dose  of  relevant  vaccines,  including  the  polio  vaccine,(54) and  it  also  unwittingly  confirmed  the  original  and  true  definition  of  herd  immunity  that  has  nothing  to  do  with  vaccines:  Epidemics  occur  during  the  accumulation  of  two  thirds  of  susceptibles.

Once  natural  immunity  is  2/3  of  susceptibles  get  the  disease,  the  epidemic  stops.  Yet,  the  authors  excluded  (as  unvaccinated)  all  paralytic  cases  (65%  of  all  cases)  from  calculations  of  efficacy. Ogra  evaluated  vaccination  with  live  attenuated  and  inactivated  poliovirus  vaccines:

While  the  combination  schedule  employing  EP-IPV  followed  by  OPV  should  result  in  a  decline  of  vaccine-associated  (VAP)  decease  in  OPV  recipients,  such  immunization  schedule  may  have  little  or  no  impact  on  the  development  of  VAP  in  susceptible  contacts.  Furthermore,  the  logistics  and  the  cost  of  combination  schedule  must  be  considered before  current  recommendations  based  on  the  use  of  OPV  or  EP-IPV  alone  are  revised.(55) 

Combined  OPV  and  IPV  recommendations 

Continuing  failures  of  polio  eradication  by  OPV  led  to  the  proposals  of  using  a  combination  of  killed  followed  by  oral  polio  vaccine  delivery.  However,  such  proposals  are  flawed  and  based  on  the  ignorance  of  the  documented  past  experience.

Simian  Virus  40  contamination  of  polio  vaccines

Perhaps  the  worst  thing  about  polio  vaccines  is  their  continued  contamination  by  monkey  viruses  of  which  SV  40  is  the  best  researched  one.  According  to  ample  medical  research  evidence,  polio  vaccines  of  any  kind  cause  VAPP.

However,  there  are  other  major  problems  with  the  polio  vaccine  that  justify  scepticism  about  its  benefits,  one  of  which  is  the  well‐documented  and  continuous  contamination  by  monkey  viruses  SV1‐SV40. Soon  after  the  poliovirus  mass  vaccination  programmes  started  in  the  US,  a  number  of  monkey  viruses  and  amoebas  were  found  in  the  vaccine  seed  brews.

Hull,  Milner  et  al. (56) and  Hull,  Johnston  et  al.  (1955)  encountered  numerous  filterable,  transferable  cytopathogenic  agents  other  than  polio  virus  in  “normal”  monkey  renal  cell  cultures.

Even  though  these  agents  completely  destroyed  culture  tissues,  and  even  caused  serious  diarrhoea  in  laboratory  animals,  all  of  which  died,  their  possible  pathogenesis  in  humans  was  ignored  or  glossed  over.

The  central  nervous  system  was  particularly  susceptible  to  the  pathogenic  properties  of  such  viruses;  the  histopathological  lesions  observed  in  the  intracerebrally  inoculated  monkeys  revealed  necrosis  and  complete  destruction  of  the  choroid  plexus.

Findings  included  generalised  aseptic  type  meningitis.  The  isolated  agent  was  called  simian  virus  or  SV  and  classified  into  4  groups  based  on  the  cytopathogenic  changes  induced  in  monkey  kidney  cell  cultures  infected  with  these  agents.

Hilleman  and  Sweet (57) reported  on  the  “Vacuolating  virus  S.V.  40”,  which  became  the  best  researched  among  dozens  of  known  monkey  viruses.

Gerber  et  al. (58) demonstrated  that  Sweet  and  Hilleman’s  method  of  inactivation  of  SV40  by  10  day  treatment  using  1:  4000  solution  of  formaldehyde  was  inadequate,  since  it  took  longer  than  10  days  to  establish  that  the  process  was  a  subject  to  the  asymptotic  factor  and  hence  incomplete.  Fenner’s  research (59) has  also  established  that  even  the  inactivated  portion  of  the  viruses  reverts  back  to  the  original  virulence.

Dr  Bernice  Eddy  documented  the  carcinogenic  properties  of  these  simian  viruses:  they  caused  tumours  in  hamsters  injected  with  Rhesus  monkey  kidney  cell  extracts. (60) As  established  by  many  subsequent  researchers,  in  humans  SV40  causes  characteristic  brain  tumours,  bone  sarcomas,  mesotheliomas  and  an  especially  virulent  form  of  melanoma  cancer.

The  stage  was  ready  for  a  world‐wide  [admitted]  contamination  of  hundreds  of  millions  of  children  with  an  oncogenic  monkey  virus  via  polio  vaccines.  SV40  has  been  directly  or  indirectly  implicated  in  an  epidemic  of  great  number  of  conditions  and  brain,  lung,  bone,  renal  and  other  tumours  in  all  ages. (61,62,63,64,65)

Dr  Stanley  Kops  is  a  modern  day  advocate  for  SV40  truth,  and  he  wrote:

To  date,  the  scientific  literature  and  research  examining  SV40  and  cancer-related  diseases  has  been  based  upon  an  assumption  that  SV40  was  not  present  in  any  poliovirus  vaccines  administered  in  the  United  States  and  was  removed  from  the  killed  polio  vaccines  by  1963.  The   presumption  has  been  that  the  regulation  for  live  oral  polio  vaccine  required  that  SV40  be  removed  from  the  seeds  and  monovalent  pools  ultimately  produced  in  the  manufacturing  process…The  confirmation of  the  removal  by  one  manufacturer,  Lederle,  has  been  made  public  at  an  international  symposium  in  January  1997,  where  its  representatives  stated  that  all  Lederle’s  seeds  had  been  tested  and  screened  to  assure  that  it  was  free  from  SV40  virus.  However,  in  litigation  involving  the  Lederle  oral  polio  vaccine,  the  manufacturer’s  internal  documents  failed  to  reveal  such  removal  in  all  its  seeds.  The  absence  of  confirmatory  testing  of  the  seeds,  as  well  as  testimony  for  SV40  of  a  Lederle  manager  indicate  that  this  claim  cannot  be  fully  substantiated…(66)

The  scientific  community  should  not  be  content  with  assurances  to  the  contrary.  The  continuing  occurrence  of  the  above  characteristic  SV40  tumours  in  younger  and  especially  quite  recent  generations  of  vaccinees  should  not  be  ignored  or  treated  with  indifference.

Contamination  of  polio  vaccines  by  chimpanzee  coryza  virus,  or  RSV.   

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).

In  1956,  Morris  et  al.  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). (67)

In  1957,  Chanock  et  al.  wrote  on  the  association  of  a  new  type  of  cytopathogic  myxovirus  with  infantile  croup. (68)

Chanock  and  Finberg  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  in  1956.

A  person  working  with  the  infected  chimpanzees  subsequently  experienced  respiratory  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  wildfire  all  over  the  world  and  continues  causing  serious  lower  respiratory  tract  infections  in  infants.

Beem  et  al.  isolated  the  virus  from  inpatients  and  outpatients  in  the  Bob  Robert  Memorial  Hospital  for  Children  (University  of  Chicago)  during  the  winter  of  1958‐1959,  in  association  with  human  acute  respiratory  illness. (69)

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  isolation  rate  (46%)  was  particularly  high  among  infants  below  six  months.

In  Australia,  Lewis  et  al.  isolated  further  viral  specimens  identical  with  CCA. (70)

Prior  to  July  1960,  the  influenza  and  parainfluenza  viruses  predominated  in  infant  epidemic  respiratory  infections;  in  July  1961  the  pattern  changed  abruptly  with  sudden  increases  in  bronchiolitis  and  bronchitis,  that  were  previously  infrequent.  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  observations  on  antibiotic  ineffectiveness,  and  new  serious  additional  problems  fell  on  deaf  ears.  He  wrote  that  life‐threatening  microbial  infections  continued  to  occur  despite  antibiotics,  and  that  the  previous  microbial  landscape  also  shifted  by  1957‐1958.  There  was  streptococcal  predominance  from  1938‐1940,  and  then  an  “impressive”  increase  in  the  number  of  life‐threatening  enterobacterial  infections  post  antibiotic.

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. (71)

Levy  et  al.  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. (72) [Clearly  implicating  vaccination.]

RSV  vaccine  developed  in  the  late  1960s  failed  miserably.  It  is  no  mystery  why  there  is  no  RSV  vaccine  recommended  today.  Fulginiti  and  others  showed  the  vaccine  was  ineffective,  and  induced  an  exaggerated,  altered  clinical  response…  causing  RSV  illness  requiring  hospitalisations  among  vaccinees,  and  led  to  delayed  dermal  hypersensitivity. (73)

Simoes  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. (74)

 It  should  surprise  nobody  that  data  from  ten  developing  countries – with  intense  polio  vaccination,  revealed  that  RSV  was  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  vaccination  and  brain-eating  amoebas. 

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

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.(75)

Amoebas  are  unicellular  protozoan  microorganisms.  According  to  Ma  et  al.(76),  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.(77) 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  phagocytised  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 (78,79) confirmed  that  amoebas  caused  brain  disease  and  death  within  days,  in  monkeys  and  mice.      The  reports  showed,  that  following  inoculations,  “extensive  chorio‐meningitis  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  was  babies  below  the  age  of  crawling  –  between  2  and  ten  months.

Live  amoebas  were  isolated  from  the  air (80) 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” (81) by  Pereira,  and  later  also  noted  in  a  post‐mortem  bronchial  swab  of  another  seven‐months  old  baby  boy  with  RSV  bronchiolitis.

Pereira’s  paper  describes  the  course  of  illness:  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  cultured  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  identified  the  Ryan  virus  as  Hartmanella  castellanii. (82)  They  had  no  doubt  that  these  amoebas  came  from  the  human  respiratory  tract.  In  Australia,  Fowler  and  Carter(83) Carter(84),  and  Carter  et  al.(85)  described  a  number  of  cases  in  children  and  adults.      Many  cases  all  over  the  world  occurred  in  children  and  adults,  with  and  without  histories  of  swimming  in  lakes  and  public  swimming  pools. (86)

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.

The entire article, History and Science Show Vaccines Do Not Prevent Disease, can be read here.

Extracted from: A critique of the 16-page Australian pro-vaccination booklet entitled “The Science of Immunisation: Questions and Answers” –You can read the entire report here.

About the author

Dr Viera Scheibner is Principal Research Scientist (Retired) with a doctorate in Natural Sciences from Comenius University in Bratislava. After an eminent scientific career in micropalaeontology during which she published 3 books and some 90 scientific papers in refereed scientific journals in Australia and overseas, she studied babies’ breathing patterns with the Cotwatch breathing monitor developed by her late husband Leif Karlsson in the mid 1980s. Babies had alarms after vaccination, indicating stress. This introduced her to the subject of vaccination. She then started systematically studying orthodox medical papers dealing with vaccination issues. To this day she has collected and studied more than 100000 pages of medical papers.

Despite such extensive research of orthodox medical papers published on vaccines over the past 100 years, she established that there is no scientific evidence that these injections of highly noxious substances prevent diseases, quite to the contrary, that they increase susceptibility to the diseases which the vaccines are supposed to prevent and also to a host of related and unrelated viral and bacterial infections. Vaccines are involved in a great number of modern ills of childhood such as immunoreactive diseases (asthma, allergies), autoimmune diseases (diabetes, multiple sclerosis, lupus erythematosis), cancers, leukaemia, degenerative diseases of bone and cartilage, behavioural and learning problems, to mention just the most important conditions.

Her research into vaccination has culminated so far in two books and a number of shorter and longer individual papers published in a variety of scientific and medical publications. She has also conducted frequent international lecture tours to present the results of her research to parents, health and medical professionals and anyone else who is interested. She has also provided a great number of expert witness reports for court cases relating to deaths and injuries caused by vaccines, such as so-called “shaken baby” syndrome.

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References

43  Peterson et al. VACCINATION-INDUCED POLIOMYELITIS IN IDAHO: PRELIMINARYREPORT OF EXPERIENCE WITH SALK POLIOMYELITIS VACCINE. JAMA. 1955;159(4):241-244

44 Abraham R, Minor P, Dunn G, Modlin JF, Ogra PL. Shedding of virulent poliovirus revertantsduring immunization with oral poliovirus vaccine after prior immunization with inactivated poliovaccine.J Infect Dis. 1993 Nov;168(5):1105-9.

45 Carolina Mensi and Fabrizio Pregliasco. Poliomyelitis: Present Epidemiological Situation andVaccination Problems. Clin Diagn Lab Immunol. 1998 May; 5(3): 278–280.

46 Mensi C, Pregliasco F. Poliomyelitis: present epidemiological situation and vaccination problems.. Clin Diagn Lab Immunol. 1998 May;5(3):278-80.

47 Schaap GJ, Bijkerk H, Coutinho RA, Kapsenberg JG, van Wezel AL. The spread of wild poliovirusin the well-vaccinated Netherlands in connection with the 1978 epidemic. Prog Med Virol.1984;29:124–140

48 Sutter RW, Patriarca PA, Brogan S, Malankar PG, Pallansch MA et al. Evidence for widespreadtransmission among fully vaccinated children Lancet. 1991 Sep 21;338(8769):715-20

49 Ibid.

50 Ibid.

51 Biellik RJ, Lobanov A, Heath K, Reichler M, Tjapepua V et al. Poliomyelitis in Namibia. Lancet.1994 Dec 24-31;344(8939-8940):1776

52 De Quadros CA, Andrus JK, Olivé JM, Da Silveira CM, Eikhof RM et al. Eradication  of  poliomyelitis:  progress  in  the  Americas. Pediatr Infect Dis J. 1991 Mar;10(3):222-9.

53 Wyatt HV. Poliovaccination in the Gambia. Lancet. 1987 Jul 4;2(8549):43.

54 Kim-Farley RJ, Rutherford G, Lichfield P, Hsu ST, Orenstein WA, Schonberger LB, Bart KJ, LuiKJ, Lin CC. Outbreak of paralytic poliomyelitis, Taiwan. Lancet. 1984 Dec 8;2(8415):1322–1324.

55 Ogra PL. Comparative evaluation of immunization with live attenuated and inactivated poliovirusvaccines.Ann N Y Acad Sci. 1995 May 31;754:97-107.

56 HULL RN, MINNER JR, SMITH JW. New viral agents recovered from tissue cultures of monkeykidney cells. 1956. Am J Hyg;63:204-215.

57 Sweet, B. H., and M. R. Hilleman. The vacuolating virus, SV40. Proc Soc Exp Biol Med. 1960 Nov;105:420-7.

58 GERBER P, HOTTLE GA, GRUBBS RE. Inactivation of vacuolating virus (SV40) byformaldehyde. Proc Soc Exp Biol and Med; 108: 205-209.

59 Fenner F. Reactivation of Animal Viruses. Br Med J. 1962 July 21; 2(5298): 135–142.

60 EDDY BE, BORMAN GS, BERKELEY WH, YOUNG RD. Tumors induced in hamsters byinjection of Rhesus monkey kidney cell extracts. 1961. Proc Soc Exp Biol and Med; 107; 191-7.

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62 Bergsagel DJ, Finegold MJ, Butel JS, Kupsky WJ, Garcea RL.DNA sequences similar to those of simian virus 40 in ependymomas and choroid plexus tumors of childhood. N Engl J Med. 1992 Apr 9;326(15):988-93.

63 Carbone M, Rizzo P, Grimley PM, Procopio A, Mew DJ Simian virus-40 large-T antigen binds p53in human mesotheliomas. Nat Med. 1997 Aug;3(8):908-12.

64 Butel JS and Lednicky JA. Cell and molecular biology of simian virus 40: implications for humaninfections and disease.J Natl Cancer Inst. 1999 Jan 20;91(2):119-34.

65 Weiner LP, Herndon RM, Narayan O, Johnson RT, Shah K Isolation of virus related to SV40 from patients with progressive multifocal leukoencephalopathy. 1972. NEJM;286(8):385-390.

66 Kops, SP. Oral polio vaccine and human cancer: a reassessment of SV40 as a contaminant basedupon legal documents. Anticancer Res. 2000 Nov-Dec;20(6C):4745-9.

67 Blount, R. E., Jr., J. A. Morris, and R. E. Savage. 1956. Recovery of cytopathogenic agent fromchimpanzees with coryza. Proc. Soc. Exp. Biol. Med. 92:544-549.

68 CHANOCK R, FINBERG L. Recovery from infants with respiratory illness of a virus related tochimpanzee coryza agent (CCA). II. Epidemiologic aspects of infection in infants and young children.Am J Hyg. 1957 Nov;66(3):291-300

69 BEEM M, WRIGHT FH, HAMRE D, EGERER R, OEHME M. Association of the chimpanzeecoryza agent with acute respiratory disease in children. N Engl J Med. 1960 Sep 15;263:523-30.

70 Lewis et al.. A syncytial virus associated with epidemic disease of the lower respiratory tract ininfants and young children. 1961. Med J Australia: 932-933 and Forbes (1961. Ibid: 323-325).

71 ROGERS DE. The changing pattern of life-threatening microbial disease. N Engl J Med. 1959 Oct1;261:677-83.

72 Levy BT, Graber MA. Respiratory syncytial virus infection in infants and young children.J Fam Pract. 1997 Dec;45(6):473-81.

73 Fulginiti VA, Eller JJ, Sieber OF, Joyner JW, Minamitani M et al. Respiratory virus immunization. I.A field trial of two inactivated respiratory virus vaccines; an aqueous trivalent parainfluenza virusvaccine and an alum-precipitated respiratory syncytial virus vaccine.Am J Epidemiol. 1969Apr;89(4):435-48.

74 Simoes EA. Respiratory syncytial virus infection.Lancet. 1999 Sep 4;354(9181):847-52.

75 Ibid Hull 1958.

76 Ma P, Visvesvara GS, Martinez AJ, Theodore FH, Daggett PM et al. Naegleria and Acanthamoebainfections: review. Rev Infect Dis. 1990 May-Jun;12(3):490-513.

77 JAHNES WG, FULLMER HM. Free living amoebae as contaminants in monkey kidney tissueculture. Proc Soc Exp Biol Med. 1957 Nov;96(2):484-8.

78 CULBERTSON CG, SMITH JW, MINNER JR. Acanthamoeba: observations on animal pathogenicity. Science. 1958 Jun 27;127(3313):1506.

79 CULBERTSON CG, SMITH JW, COHEN HK, MINNER JR. Experimental infection of mice andmonkeys by Acanthamoeba. Am J Pathol. 1959 Jan-Feb;35(1):185-97.

80 D. Kingston and D. C. Warhurst.. Isolation Of Amoebae From The Air J Med Microbiol February 1969 vol. 2 no. 1 27-36.

81 Pereira MS, Marsden HB, Corbitt G, Tobin JO. Ryan virus: a possible new human pathogen.Br Med J. 1966 Jan 15;1(5480):130-2.

82 J. A. Armstrong and M. S. Pereira. Identification of “Ryan Virus” as an amoeba of the genusHartmannella. Br Med J. 1967 January 28; 1(5534): 212–214.

83 M. Fowler and R. F. Carter.Acute Pyogenic Meningitis Probably Due to Acanthamoeba sp.: aPreliminary Report. Br Med J. 1965 September 25; 2(5464): 734-2, 740-742.

84 Carter RF. Primary amoebic meningo-encephalitis: clinical, pathological and epidemiologicalfeatures of six fatal cases. J Pathol Bacteriol. 1968 Jul;96(1):1–25.

85 Carter RF, Cullity GJ, Ojeda VJ, Silberstein P, Willaert E. A fatal case of meningoencephalitis dueto a free-living amoeba of uncertain identity–probably acanthamoeba sp.Pathology. 1981 Jan;13(1):51-68.

86 Scheibner 1999. Brain-eating bugs: the vaccine connection. Nexus Magazine;(whale.to/vaccines/amoebas.html).

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