Health Impact News Editor Comments:

In the vaccine debate currently raging in modern society, seldom, if ever, is the basic presupposition that vaccines prevent diseases ever questioned. It is assumed by the government and the medical system that this presupposition is a scientific fact.

Without this presupposed “fact”, the justification to force people to receive vaccinations completely falls apart. The acceptance of sacrificing certain children and others due to vaccine harm for “the greater good” also loses its justification, if vaccines actually do not prevent disease.

So it is easy to see why those who profit from vaccines, which includes both the manufacturer and the U.S. government, do not want to debate this issue.

What is the actual history and science behind this belief in vaccines? Dr. Viera Scheibner has done everyone a favor in critiquing the current scientific rationale for such a belief, taking a comprehensive look at history and peer-reviewed studies on the subject.

We have extracted this from her 50 plus page response to the Australian Academy of Science pro-vaccine report entitled: 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.

We have extracted the relevant information regarding the history and science of vaccines, so that the comprehensive report by Dr. Scheibner can be used by anyone interested in the topic.

This is the research you want to print out and give to your doctor if they are uneducated on the facts and science of vaccines. If you are involved in a lawsuit over refusing mandatory vaccines, you will want to give this to your attorney who can enter the information into the court record and start educating judges.

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

Science simply means an organised system of knowledge. It does not mean infallibility, superiority, or eternal validity, and it is subject to changes and revisions. Many a crime has been committed in the name of science, starting with the medieval inquisition, through Nazi Germany’s perversion of just about everything, including medicine, and now, continuing into the present day with harmful excesses of medicine.

In the following [research] I provide documented facts, describing the reality of vaccines/vaccination, as published in reputable peer‐reviewed medical journals.

The documented effects of vaccines as shown by orthodox medical research:

Sensitisation after vaccination.

At the turn of the twentieth century, medical researchers tested vaccines on themselves and other surgeons and medical students and established that vaccine injections result in the so‐called negative phase of lowered bactericidal power of the blood, in other words, a measurable immune‐suppression.(7)

Dr Parfentjev, an employee of Lederle Laboratories (one of many well‐known vaccine manufacturers), reported that vaccination of mice with pertussis vaccine sensitised them, i.e. caused anaphylaxis (as opposed to prophylaxis), and increased their susceptibility to infection with several unrelated species of Gram negative bacteria and viruses.(8)

Sensitisation (anaphylaxis) was achieved with injection of 15 billion cells of commercial pertussis vaccine. Compared with controls (normal, unvaccinated mice) the lethal dose of virus for sensitised mice was much smaller than for normal mice of the same age group. In other words, vaccination with pertussis vaccine increased the susceptibility of mice to lethal shock.

In another benchmark seminal work, Kind demonstrated that pertussis vaccines also sensitised the mice to the lethal effects of subsequent injections of pertussis vaccine as well as a variety of agents and conditions such as anaphylaxis, histamine, serotonin, and endotoxins, and certain proteins of “related” and “unrelated” organisms, such as Escherichia coli and Shigella dysenteriae.(9)

Craighead reported that the same effects as observed in mice were also observed in children given inactivated microbial vaccines. He also wrote that during the past five years, significant advances were made in the understanding of the natural history of a number of common infections, among which he mentioned the apparent states of altered host reactivity consequent to vaccination.

Immunisation with inactivated vaccines could  “sensitise” the recipients and result in an accentuated pattern of disease upon natural or experimental exposure.(10)

Meaning, if a child did not react much to the first dose of vaccine, it may react seriously to subsequent doses.

Evidence for delayed hypersensitivity in recipients of “killed” vaccine is demonstrated by local skin reactions after the injection of live or inactivated microorganisms. The dermal response may also be caused by nonmicrobial constituents such as adjuvants and preservatives, which by themselves are highly toxic: aluminium and mercury compounds, formaldehyde, phenol, propylene glycol among others.

Modern immunological research regards vaccines as foreign antigens; indeed, vaccines represent superantigens, which are typified as multiple vaccines administered at the same session.

Earlier researchers have observed the many problems with antigenic stimulation by vaccines, such as the vaccine induced enhancement of viral infections which is known to occur with several vaccines.(11,12) This phenomenon was well described with the failed RSV (Respiratory Syncytial Virus ) vaccines. However, as of 2009, scientists are still unsure of the exact mechanism.(13) As a result, vaccine development for lentivirus infections in general, and HIV/AIDS in particular, has been little successful.(14) Many trials of HIV vaccines, including the latest ones, confirmed this phenomenon: the trials had to be abandoned because a number of human volunteers contracted AIDS from the tested vaccines.

Equally unsuccessful are vaccines against bacterial infections such as whooping cough, diphtheria and Haemophilus influenzae as shown later in this critique.

Sabath documented antigen‐induced transient hypersusceptibility to infections in mice and infants.(15) In mice they determined onset of infection and death due to influenza virus challenge at different times after antecedent monovalent influenza vaccine administration. In infants hospitalised for purulent meningitis there was a clustering of time intervals between routine vaccination and the onset of symptoms, proving the causal link.

Daum demonstrated a decline in serum antibody to the capsule of Haemophilus influenzae type b in the immediate postvaccination period in children.(16) They wrote that this increases the risk of invasive disease if it occurred during a period of asymptomatic colonization with H. influenzae type b, which, of course is a rule rather than an exception, because the bacterium is a ubiquitous commensal living on tonsils.

Effectiveness of vaccination.

Outbreaks and epidemics of measles, whooping cough and poliomyelitis diseases in unvaccinated and fully vaccinated populations.

The Amish are a religious community living across the USA that claim religious exemption to vaccination. Thus, the vast majority are not vaccinated.

They had not reported a single case of measles between 1970 and 1987.(17) At the same time, non‐Amish highly‐vaccinated communities still reported 2‐3 year epidemics. Despite this obvious vaccination failure, pro‐vaccinators claimed success with the measles vaccine.

In 1982, just when the US Secretary of State Joseph A. Califano Jr. planned to announce eradication of measles, the well‐vaccinated non‐Amish populations started reporting huge outbreaks. The unvaccinated Amish did not have large epidemics of measles until much later, starting in early December 1987.

Outbreaks in the fully vaccinated American children continued with increasing frequency and severity. Without disclosing the vaccination status of children in measles epidemics, claiming victory over measles is just empty jabbering.

Moreover, vaccinated children started developing an especially vicious form of atypical measles. Fulginiti described the occurrence of atypical measles in children given formaldehyde‐treated, aluminium precipitated measles vaccine, also referred to as “killed” measles.(18) He explained the problem as due to the altered immunological host response caused by vaccination.

Later on, when live‐attenuated measles vaccine was introduced, the recipients starting developing atypical measles from it, as well.

Rauh and Schmidt described nine cases, which occurred in 1963 during a measles epidemic in Cincinnati.(19) The authors followed 386 children who had received three doses of killed measles virus vaccine in 1961. Of these 386 children, 125 had been exposed to measles and 54 developed it. The authors concluded that:

it is obvious that three injections of killed vaccine had not protected a large percentage of children against measles when exposed within a  period of two-and a half years after immunization.

Even when vaccination rates in the UK dropped in the 1990s and early 2000s, when confidence in the vaccine fell, measles deaths never exceeded 4 per year, and remain today at that level. Increasing laboratory‐confirmed measles continue to occur in England and Wales even since vaccination rates have gone back to former levels. (Figure 1.)(20) This is evidence that measles vaccines at best interrupt transmission, but do not confer reliable immunity no matter how much of the herd is vaccinated.

Figure 1: Laboratory confirmed measles cases, London and the rest of England and Wales, 1995‐2008

Outbreaks of whooping cough (pertussis) in the vaccination era.

Right after the intense DPT vaccination that started in the mid 1970s, and right through the first decade of 2000, whooping cough outbreaks hit several US states, accompanied by similar outbreaks in all other countries that adopted intensive vaccination including Australia.

In addition to pertussis (and measles) outbreaks in fully‐vaccinated children, the outbreaks in the last thirty‐odd years have been occurring increasingly in very young babies, born to mothers who were vaccinated when they were babies and as a result they lack transplacentally‐transmitted immunity (TTI). Before the vaccine era, TTI protected babies and young children for up to two years against any infectious diseases of childhood.

Lennon and Black demonstrated that hemagglutinin‐inhibiting and neutralizing antibody titers are lower in younger women who have been vaccinated than they are in older women.(21) The same applies to measles and pertussis.(22)

Breastfed infants of vaccinated mothers in the USA have nearly three times the risk of measles infection compared to those of naturally immune mothers, even in the era of vaccination when there is supposedly less measles virus in the environment.

Infants whose mothers were born after 1963 had a measles attack rate of 33%, compared to 12% for infants of older mothers. Infants whose mothers were born after 1963 are more susceptible to measles than are infants of older mothers. An increasing proportion of infants born in the United States may be susceptible to measles. . . the adjusted odds ratio for maternal year of birth (born after 1963) was 7.5 (95% confidence interval 1.8, 30.6).(23)

This is most likely the result of lower levels of virus‐specific immunity in the serum and milk in vaccinated mothers compared to naturally immune mothers. While the overall clinical case rate may have declined with measles vaccination, the most sensitive members of the herd are at an increased risk today‐ because of vaccination.

Hutchins et al. described pertussis epidemiology in the US. They wrote:

During the period 1980-1986, a total of 17,396 cases of pertussis were reported to CDC… The annual incidence of reported pertussis rose  from 0.5 cases per 100,000 population to 1.7/100,000. Infants less than 12 months old had the highest average annual incidence… Children 1-4 years of age accounted for 25% of all cases but had an average annual incidence only 1/7th that of infants.(24)

Figure 2 (25) reveals a steady downward trend in the incidence and mortality from pertussis between 1922 and until about 1975‐6; thereafter the downward trend in pertussis morbidity stopped and went sharply upwards, while pertussis mortality remained high but stationary. What could have caused such increase in the disease incidence seen in figure 3?

Figure 2: Pertussis, United States, 1922‐1987

Hutchins et al. showed the reason for the increase, unwittingly, when they also wrote:

In 1978 a nationwide childhood immunization initiative was begun. Individual States passed legislation requiring proof of immunization  for school entry at 5-6 years of age.

The vaccination age started at 6‐8 weeks (and not at 5‐6 years), and large numbers of very young babies were vaccinated within a short period of time; hence the observed major increase of whooping cough in those babies straight after the first dose.

Figure 3: Number of Pertussis Cases Reported to MMWR and Incidence of Disease per 100,000 Population, United States, 1980‐1986.

This also coincided with a sudden upsurge in cot deaths, of which the so‐called Tennessee deaths were widely publicised. Bernier(26), Walker(27), and Griffin(28) all described a number of such tragedies. Their data showed a clear clustering of these deaths along the critical days as documented by data collection of babies breathing with Cotwatch breathing monitor.(29)

Figure 4: Record of alarms as recorded by the mother of a baby on the Cotwatch breathing monitor.

Figure 5: A “raw” record of breathing of baby one, as printed from the microprocessor Cotwatch breathing monitor. Every vertical line represents a histogram of events for one hour. Events from 6 to 15 seconds are mostly apneas (pauses in breathing), while the events above 15 seconds are mostly hypopneas (low volume breathing, which is only 5% of the volume of unstressed breathing). Hypopneas occur at critical hours in clusters of several shorter episodes within 10‐15 minutes and are associated with exposure to a great variety of stressors. The entire record represents 21 days of non‐stop monitoring in sleep. The arrow indicates the day when the DPT vaccine was administered. A marked change in the pattern and duration of events in breathing occurred after the injection.

Figure 6: First and second charts: Record of events in breathing in two babies, as printed from the microprocessor Cotwatch breathing monitor. ‐ baby one had been given the third DPTP (diphtheria‐pertussis‐tetanus) and OPV (oral polio) vaccines and ‐ baby two had been give the first DPT and OPV vaccines. Third chart: Actual deaths ‐ 41 randomly listed in deaths in relation to when the last DPT vaccine had been administered.


Figure 7: Record of events in breathing in two babies, as printed from the microprocessor Cotwatch breathing monitor ‐ baby one had been given the third DPT (diphtheria‐pertussis‐tetanus) and OPV (oral polio) vaccines ‐ baby three had been given the first DPT and OPV vaccines.

Figure 8: Relative* risk of SIDS in days after vaccination. *Note: The risk is not relative to the risk of SIDS in unvaccinated babies. What is important to note here is the recognisable pattern of critical days.


Figure 9: Links age, number of deaths and the time taken to die after vaccination (Source: Griffin et al. 1988)

Due to the 1975 UK television program reporting on brain damage linked to DPT vaccine, the vaccination compliance fell down to 30%, or even 10% in some areas, in the UK. This was followed by the longest inter‐epidemic period with the lowest incidence of whooping cough on record.

Fine and Clarkson wrote:

Though overall pertussis incidence fell in England and Wales subsequent to the introduction of vaccination on a national scale in 1950s, pertussis epidemics have continued to occur regularly every 3-4 years. Since epidemic frequency is a function of the rate of influx of susceptibles, it is suprising that the interepidemic period did not decrease after the 1974 fall in vaccine uptake. One explanation for this paradox may be that pertussis vaccines are more effective in  protecting against disease than in protecting against infection.(30)

Figure 10: Weekly number of pertussis cases notified to Office of Population Censuses and surveys, from week 1 of 1950 to week 3 of 1982.

It is my opinion that the incidence of whooping cough fell worldwide in the mid 1970s due to natural dynamics, similar to those of measles, and not due to increasing levels of vaccination.

When vaccination stops, the incidence of the targeted disease returns back to normal dynamics. This explanation is supported by another observation in the UK and former West Germany. Miller and Farrington wrote:

In the West Germany unlike the UK, there are no national statistics on  pertussis incidence, no national vaccination policy and no figures for vaccine uptake. . . vaccination rates are low and pertussis is prevalent,  particularly in the 2-4 year age group, which is typical of a country with low vaccination uptake; similarly serotype 2 predominates. . . The age distribution was similar to that of cases reported in the UK during 1978 when vaccine uptake was at it’s lowest with the highest  proportion occurring in children aged 2-4 years.(31)

Figure 11 (32) is very instructive. The facts point strongly against the presumed benefits of vaccination.

Figure 11: Age distribution of pertussis cases in West Germany and England & Wales.

The dynamics of vaccine uptake as described above are also reflected in the dynamics of infant deaths after four weeks in England and Wales. According to Macfarlane:

The postneonatal mortality rate fell markedly in 1976, the year in which a sharp decline in perinatal deaths began. Between 1976 and 1979, however, neither the later neonatal nor the postneonatal mortality rate fell any further. Indeed, the postneonatal mortality rate increased slightly among babies born in 1977.(33) [when the vaccination compliance started climbing up.]

Figure 12: Age‐specific incidence of bacteriologically confirmed pertussis. Massachusetts. 1981‐1991. JID 1994:169 (June)

In contrast, Marchant et al. described inter alia the age incidence of pertussis in Massachusetts in a ten year period 1981‐1991(34) and demonstrated in figure 12 that the highest incidence of bacteriologically‐confirmed pertussis was below the age of one; however, the breakdown in months showed the highest incidence was just after the first and second doses of DPT, with rapid decline afterwards. Equally revealing was the high incidence of pertussis below the vaccination age, in small babies (0 to 6 weeks), this being due to the lack of TTI documentedly caused by the deleterious generational effect of vaccination.(35)

Sutter and Cochi studied pertussis hospitalisations and mortality in the United States between 1985 and 1988 and concluded that there was substantial under‐reporting of pertussis in the US.(36) This of course would have inflated the perceived effectiveness of vaccination. They wrote that based on their indicators, the national health impact of pertussis is considerably higher than previously published reports suggested. Applying the age‐specific hospitalisation rates, 187,867 to 515,930 cases of pertussis may have occurred during the study period, instead of only 14,057 cases reported to the CDC. They concluded that using different methods of estimation, approximately 121,340 cases of pertussis may have occurred during the study period, indicating 11.6% vaccine efficacy. Considering that the pre‐vaccine era pertussis occurrence was in the order of 240,000 cases, vaccination has made no inroads into the pertussis incidence.

Williams et al, made a statement about infants who died:

Infants were less than six weeks of age and died from overwhelming cardiovascular respiratory compromise despite intensive care support. . .The excessive infant mortality from a preventable disease demonstrated the need for better pertussis immunity in the community and for erythromycin treatment of all suspected cases and  family contacts.(37)

But, their own data showed something completely different! All four babies were doing OK until they were admitted in hospitals and put on intravenous broad‐spectrum antibiotics. The causal link to the administered antibiotics was clearly shown because the downhill slide followed closely the days when the offending antibiotics were administered.

Moreover, some of the mothers and siblings had whooping cough at the time of the infant’s births, despite being fully vaccinated. One sibling’s vaccination status was uncertain, but he was very likely vaccinated as part of the highly vaccinated generation.

This confirmed two phenomena:

  • The increased incidence of whooping cough (and measles) in babies below the vaccination age reflects the lack of transplacentally‐transmitted immunity in the era of vaccinated mothers as predicted by Lennon and Black.(38)
  • A well documented phenomenon, that many cases (up to 65%) of infectious diseases develop straight after the first dose of the relevant vaccine in very young children.

Romanus et al. wrote that discontinuation of pertussis vaccination in 1979 in Sweden was followed by a low endemic level of pertussis for 3 years.(39) Thereafter the incidence gradually increased and there were two outbreaks in 1982‐1983 and 1984‐1986. In epidemic years, however, the incidence in infants and small children below the age of one year was very low (11%). The majority of cases (69%) occurred in older children up to 6 years, meaning: when Sweden stopped pertussis vaccination between 1979‐1990, the disease incidence returned back to normal, with most cases occurring at the optimal age.

In contrast to this, when Sweden trialled the acellular pertussis vaccines for the second time (1990‐ 1995), as soon as the trial babies were vaccinated, there was a major outbreak of pertussis in those very young babies.(40) Since 82% of the entire live birth cohort participated in this trial, the pertussis epidemic reached noticeable proportions.

The acellular pertussis vaccine failed to make any inroads into pertussis incidence, as witnessed in Sweden: already during the [second] trials of that vaccine, the infant recipients contracted whooping cough which prompted discontinuation of the trial well before the planned date.(41) This is particularly instructive since during the eleven years without usage of pertussis vaccines (1979‐1990) – babies under one year of age did not contract whooping cough and 90% of cases occurred in the ideal age group between 5‐10 years.(42)

Despite high vaccination compliance, there remained a high persistent level of pertussis in regular 3.5 year epidemics. Vaccines made no inroads into incidence of pertussis as demonstrated in figure 13:


Figure 13: Pertussis notifications 1991‐2009 (Australia).

The sordid history of Poliomyelitis 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.

Figure 14: Number of places with polio cases, by average vaccination acceptance rate for birth cohorts 1971‐1975 (Shaap/Bijkerk/Coutinho/Kapsenberg/van Wezel).

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.

Figure 15: Annual reported paralytic poliomyelitis case rates, United States, 1951‐1982 (Paralytic case rate/100,000 population.) The 1982 data are preliminary.


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.

Figure 16: Polio cases notified and confirmed: The Americas. 1985-1989.


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.

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.

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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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49 Ibid.

50 Ibid.

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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;(

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