LITTLE KNOWN FACTS ABOUT POLIOMYELITIS VACCINATIONS by Viera Scheibner

LITTLE KNOWN FACTS ABOUT POLIOMYELITIS VACCINATIONS

Nexus Magazine Aug-Sept 2009 Vol 16, No.5 & Oct-Nov 2009 Vol 16, No 6.

Outbreaks of paralysis during mass vaccination programs in the USA
Paralytic poliomyelitis outbreak in Taiwan
Outbreak in Oman
Paralytic poliomyelitis outbreaks in Romania
Poliomyelitis epidemic in The Gambia
Paralytic poliomyelitis outbreak in Namibia
Mechanics of vaccine-associated paralysis
Conclusions

Pro-vaccinators claim eradication success with vaccines against two diseases: smallpox and poliomyelitis. The problem is that both these claims are not true, but many people believe them. In this article, I deal with outbreaks of paralytic poliomyelitis straight after mass vaccination programs in both developed and developing countries, as published in orthodox medical journals.

When the first, injectable, Salk polio vaccine was tested on some 1.8 million children in the USA in 1954-55, cases of paralysis in the vaccinated and some of their contacts started occurring within days (Francis et al, 1955; Peterson et al., 1955). It became known as the Cutter Incident. Cutter Laboratories was accused of distributing vaccines which contained live polioviruses. Even though paralysis also occurred after injections of other polio vaccines produced by different manufacturers, Cutter Laboratories became the scapegoat and was asked to withdraw all batches of its vaccines.

The disasters with the injectable polio vaccines causing paralysis seem to have been one of the main motivations behind developing an oral poliovirus vaccine (OPV), which was believed to simulate the natural infection. The reality proved such expectations wrong.

Henderson et al. (1964) wrote that since 1961, when oral poliomyelitis vaccines were first made available for general use in the USA, scattered cases of paralytic disease have occurred in association with these vaccines. Many of these cases have been clinically indistinguishable from paralytic poliomyelitis. Epidemiologically, the pattern of their occurrence has raised the possibility that some cases may have been caused by the vaccines. In 1962, when the existence of this problem was first appreciated, the Surgeon General of the US Public Health Service convened a Special Advisory Committee which met on a number of occasions between August and December. The committee reviewed in detail the reported cases of paralytic disease occurring within a period of 30 days following ingestion of the oral polio vaccine. Of these, 11 followed "type III vaccine" and seven followed "type I vaccine". The committee concluded that "the maximum potential risk for types I and III vaccine is in the order of one per million or less overall; but higher for those over 30 years of age".

Now we know how the much-quoted rate of these vaccine-caused cases as "one per million or less overall" was born: it was created as a typical desktop statistic by a committee and not achieved by a proper statistical study. (A proverbial camel: a horse created by a committee. Sorry, camels; only joking!)

Importantly, poliovirus type III was the one most implicated. The committee also made this allegation: "The total number of such reports [meaning paralysis after the administration of OPV] received by the Public Health Service through June 1964, is 123. This number includes those cases reviewed by the Committee in 1962. Of this total, 36 cases occurred in epidemic areas where mass immunization programs were undertaken as emergency control measures. The remaining 87 cases were widely scattered and occurred in nonepidemic areas usually following community-wide oral poliomyelitis programs."

I find it hard to believe that, in a country with some 220 million people and 2.5 million live births per year, there would only be some 200 cases of paralysis. Even if it were true, then the number certainly would be more than the much-quoted "one case in a million".

Because of the continued incidence of vaccine-associated cases, a committee was again convened by the Surgeon General to re-assess the problem and to develop recommendations for the future use of oral poliomyelitis vaccines. The committee met on 17 and 18 July 1965. Its recommendations, as far as the diagnosis of poliomyelitis is concerned, were as follows:

"1. Onset of illness between four and 30 days
following feeding of the specific vaccine in question, with onset of paralysis not sooner than six days after the feeding;
"2. Significant residual-lower-motor-neuron paralysis;
"3. Laboratory data not inconsistent with respect to multiplication of the vaccine virus fed;
"4. No evidence of upper-motor-neuron disease, definite sensory loss or progression or recurrence of paralytic illness one month or more after onset."

Of the 87 cases considered, 57 were judged "compatible" and 21 were excluded after careful consideration. In nine of the cases, the data were considered insufficient upon which to make a judgement. The "compatible" cases occurred largely among adults, 44 being 15 years of age or older and eight over 50 years of age. The onset of illness fell between four and 28 days, with the majority of cases occurring within eight to 21 days following vaccine administration. There was no apparent association of cases with specific lots of vaccine or vaccine produced by a particular manufacturer.

It is obvious to me that this committee's main motivation was to exclude as many paralysis cases associated with vaccination as possible. There was no concern for the affected recipients of the polio vaccines; they were discarded and left to fend for themselves. A truly mediaeval, feudalistic and, to say the least, unscientific attitude!

Under "Evaluation of the risk", the committee wrote that it "recognizes that it is not possible to prove that any individual case was caused by the vaccine and that no laboratory tests available can provide a definitive answer".

The committee went further and stated the following:

"1. The extent of the associated risk is sufficiently low relative to the risk of naturally occurring illness in children to warrant continuation and intensification of the poliomyelitis immunization program throughout the nation, although with some changes in emphasis;

"2. Primary emphasis should be given in all communities to the immunization of all infants during their first year of life. All communities which have not already organized continuing programs for the effective immunization of their infants and preschool children in all socioeconomic groups are urged to do so. (The success of such programs is requisite for attaining the goal of the elimination of paralytic poliomyelitis since it is primarily these younger children who serve to transmit the natural infection within the community.)

"3. Communities which have not yet embarked upon mass immunization programs are encouraged to do so during the coming fall and winter (1964-65). (Such programs will be of value only if they succeed in reaching unimmunized persons, particularly preschool children, in lower socioeconomic areas. Before embarking on mass programs, all communities should develop definite plans for continuing immunization programs to care for new susceptibles born into or moving into the community)."

The statements and conclusions in the above paragraphs are important in that they started the avalanche of denials of the causal link between the documented administration of the offending vaccines and the resultant symptoms (paralysis)—which, in my opinion, defies common sense. While it may be partially true that the contemporary methods in the 1960s may have been insufficient to prove the causal link, the obviously flawed methods and criteria for accepting causality developed soon afterwards. Moreover, the repetition in innumerable countries of documented outbreaks of polio within 30 days after vaccination drives is sufficient to see that polio vaccines of all kinds (OPV, IPV) do cause major outbreaks of paralytic poliomyelitis, following vaccination drives, in areas that have not had any polio cases for a number of years.

The most important development was the publication of Bradford Hill's 1965 paper, in which he defined nine points to be fulfilled for accepting causality. All documented outbreaks of polio after vaccination drives fulfill these nine points. Outbreaks of other infectious diseases in the vaccinated follow suit.

It is interesting that the pro-vaccinators frown upon those, including myself, who study relevant medical papers published before the 1990s, yet they try to write off such articles as automatically obsolete. As the above published information shows, they are very relevant to the present situation in vaccination. Pro-vaccinators themselves still act upon obsolete information such as outlined above (notwithstanding practising Jennerian vaccination) and keep denying that it is possible to prove causality and/or that serious vaccine reactions are in the order of one in a million. Surely, modern medicine's diagnostic methods have progressed since the 1960s—or haven't they? With modern statistical methods, it is possible to calculate the rates more precisely.

Similar "reasoning" applies to the pro-vaccinators' constant assertions that there are no known treatment methods to effectively manage , infectious diseases of childhood and therefore that's why we have to continue preventing them by vaccination. They totally overlook the vaccines' obvious and documented ineffectiveness in preventing any diseases, and the never-ending trail of disasters and very serious immune, autoimmune and degenerative diseases created in the process by modern medicine which earns billions of dollars from the vaccines.

Here, I agree with one thing, though: it is only orthodox modern medicine that does not know how to effectively and correctly treat— or, rather, handle—infectious diseases, or any other diseases for that matter. They "treat" everything with antibiotics, fever suppressants and painkillers despite the obvious uselessness inappropriateness and dangers o these drugs and without am regard for individuality.

Outbreaks of paralysis during mass vaccination programs in the USA
Besides the infamous Cutter Incident described above, outbreaks of paralysis after vaccination continued occurring in the USA.

Nathanson (1984) presented epidemiological aspects of poliomyelitis eradication. He wrote that mass vaccination with oral polio vaccine was begun in the USA in 1963, and the last outbreak of natural poliomyelitis occurred in 1972. Then he alleged that there was only one more outbreak, in 1979, due to the introduction of wild poliovirus to an undervaccinated Amish population. "Paradoxically, eradication occurred even though 5%-10% of the population zero to 1 year of age was unvaccinated and susceptible". First, this statement is inaccurate, because not even 5%-10% of the Amish population are vaccinated (they claim religious exemption to vaccination). Second, the first case of paralytic polio occurred in a nine-month-old Amish baby who became paralysed five days after being given a dose of OPV. Even though the US health authorities opened a vaccination clinic, the Amish residents shunned it. They eradicated the outbreak by giving it free rein and letting it eradicate itself. That's exactly what happened. After all, all outbreaks are self-limiting.

MMWR (1993) reported on the outbreak of 68 cases of poliomyelitis among members of religious communities in The Netherlands. Because members of an affiliated religious community in Alberta, Canada, had direct contact (i.e., travel to and from The Netherlands) with members of the affected community, health authorities in Alberta conducted an investigation during January-February 1993 to determine whether the poliovirus had been imported. The investigation focused on a small rural community in southern Alberta that reported the only cases of poliomyelitis from the province during the last poliomyelitis outbreak in Canada in 1978 (11 cases). The author of this report wrote: "The community comprises members of a religious group that generally opposes vaccination."

Interestingly, according to the MMWR report: "...wild poliovirus type 3 (PV3) was isolated from stool specimens obtained from 21 (47%) of 45 persons (primarily children). Laboratory investigations conducted by the National Center for Enteroviruses in Halifax, including application of molecular technique in collaboration with laboratories at the CDC (Centers for Disease Control), determined that this PV3 was virtually identical to the strain that caused the outbreak in The Netherlands."

Perhaps the most revealing information was unwittingly presented in an article by Schonberger et al. (1984). Their figure 1 shows the annual reported paralytic poliomyelitis case rates for the USA during the period 1951-1982. The graph shows a steady fall in the incidence of paralytic poliomyelitis until 1974-75, when it shot up threefold and remained high (with slight up and down fluctuations) until 1979; then the incidence seemingly fell down again to the 1974 level.

This graph is practically identical to the graphs of whooping cough incidence published by Hutchins et al.

(1988). Their graphs show a steady downward trend in the incidence of (and mortality from) whooping cough until 1976, when the incidence shot up threefold. This coincided with the "nationwide childhood immunization initiative", when individual states were gradually passing legislation requiring three doses of DTP (diphtheria-tetanus-pertussis) vaccine and OPV for school entry, no doubt preceded by an advertising campaign for some time beforehand and accompanied by intensified vaccination activity. The incidence of both whooping cough and polio quite obviously went up threefold when vaccination became virtually mandatory. I see it as clear evidence that the vaccinations caused the recipients to contract the diseases which the vaccines were supposed to prevent.

Paralytic poliomyelitis outbreak in Taiwan
Kim-Farley et al. (1984) described an epidemic of poliomyelitis cases (1,031) which occurred between 29 May and 31 October 1982, after seven years of freedom from major outbreaks. Already by 1 September, the outbreak had become one of the largest reported in Taiwan's history. Importantly, before this outbreak, approximately 80 per cent of infants had received at least two doses of trivalent oral polio vaccine before their first birthday. Because the outbreak occurred in the face of high community-wide vaccination levels, the CDC (Atlanta, Georgia, USA) was invited to help determine the extent of the outbreak, why it had occurred and whether OPV was an effective protective agent. (I have no doubt that the outbreak sent shock waves through the vaccinators' camp—particularly so, since it was freely admitted and publicised and could have not been swept under the carpet.)

Kim-Farley and colleagues wrote that Taiwan's total population at the end of 1980 was 18 million, with approximately 400,000 births per year. Persons under the age of five comprised 11 per cent of the population.

Polio was first reported in Taiwan in 1913 and became officially notifiable in 1955. Inactivated polio vaccine (IPV) was introduced in 1958 and OPV in 1963. At the time of the 1982 outbreak, routine vaccination in Taipei and Kao-Hsiung (the two largest cities in Taiwan) consisted of a three-dose OPV schedule before the first birthday. An additional dose at about 18 months was also recommended.

From 1975 to 1981, no fewer than nine cases of paralytic poliomyelitis were reported to the Taiwan health authorities each year. No polio deaths were recorded after 1978 Cases of polio were defined as physician-diagnosed paralytic poliomyelitis. The vaccination status of cases was determined from information supplied on case reports and, importantly, "(vjaccinations received in the 28 days before the onset were not counted because they might have been given after exposure". These represented 65 per cent of the cases. So, most cases were excluded as vaccine-caused.

It is well established that most cases of vaccine-derived paralysis occur after the first dose of any polio vaccine. Marking the cases of paralysis in the recipients of the first dose within 28 days of the vaccination date as "unvaccinated" is not only a major fraud—no doubt designed to "improve" the effectiveness of the vaccine—but it also contravenes the definition of vaccine-associated paralysis as determined by the US Special Advisory Committee (a case which occurred within 30 days of the vaccine dose; Henderson et al., 1964, as above).

The indisputable reality of what happened in Taiwan is that 65 per cent of vaccinees developed paralysis within 28 days of the first vaccine dose, thus confirming observations of others that the majority of vaccine-caused paralysis occurs after the first dose of any vaccine, the polio vaccine being no exception. The case fatality rate was nine per cent. However, this rate was calculated as per total population, even though the definition of polio is "infantile paralysis". It should have been calculated on the numbers of children in the relevant age groups.

Moreover, because before this 1982 outbreak there had been no outbreaks of polio in Taiwan for seven years, it is not likely that all those who developed paralysis within 28 days of the first vaccine dose were already incubating the disease. In addition, less than seven per cent of the surveyed population had not received any OPV.

Equally flawed is the conclusion of the authors that failure to vaccinate, rather than vaccine failure, was the most important risk factor for the polio epidemic in Taiwan.

What sends shivers down my spine is the ease with which the pro-vaccinators got away with an obviously fraudulent analysis of the vaccine-caused outbreak of paralysis. At the same, I praise both the authors and the Lancet for publishing it in a way that enables any intelligent reader to see through the smokescreen and mirrors. John (1985) wrote: "The proposed explanation— namely, pockets of low vaccination coverage sustaining poliovirus transmission and seeding an outbreak (5.8 cases per 100,000—was unconvincing. Cases did not cluster in pockets and, since the mean coverage rate was very high, pockets of low coverage could have been infrequent...Taipei and Kao-Hsiung cities had high incidence despite better vaccination efforts."

Outbreak in Oman
Virtually the same thing as described in Taiwan happened in Oman. Sutter et al. (1991) and Sutter et al. (1992) described an outbreak of paralytic poliomyelitis type I (118 cases) between January 1988 and March 1989. They wrote: "Incidence of poliomyelitis was highest in children younger than 2 years (87/100 000) 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%." Despite?

Eighty-seven per cent of case patients in Oman received at least one dose of OPV, and 50 per cent received at least three doses. The authors wrote: "Accumulation of enough children to sustain the outbreak seems to have been due to previous success of the immunisation program in reducing spread of endemic strains, suboptimum efficacy of OPV, and delay in completing the primary immunisation series until 7 months of age. Additionally, the estimated attack rate of infection among children aged 9-23 months exceeded 25% in some regions, suggesting that a substantial proportion of fully vaccinated children had been involved in the chain of transmission."

Their statement that "3 doses of OPV reduced the risk of paralysis by 91%" is facetious: if most cases occur after the first dose, there will be fewer vaccinees left to develop paralysis after the second dose and even fewer after the third.

While alleging that "(widespread use of oral poliovirus vaccine (OPV) has led to the virtual elimination of paralytic poliomyelitis in industrialised countries, in addition to substantial reduction in the incidence of the disease in the developing world", the authors also stated: "However, the efficacy of OPV in inducing humoral immunity against
poliovirus type 1 and 3 in some countries has been lower than expected. Recent outbreaks in The Gambia, Brazil, and Taiwan have also raised concern that primary reliance on routine immunisation may be inadequate to achieve the goal of eradicating wild poliovirus infection globally by the year 2000."

The authors also wrote: "...vaccination coverage with 3 doses of OPV at the time of the outbreak was 87% for children aged 12 months. Based on the number of reported cases, the overall attack rate of paralytic disease in children 9-23 months was 57/100 000. There was no correlation between vaccination coverage and attack rates by region; the region with (the] then highest attack rate (Batinah, 117/100 000) had one of the highest coverage rates (88%), whereas the region with the-lowest coverage (Capital, 71%) had a low attack rate."

No correlation? In fact, there was a perfect correlation showing that the vaccines caused the outbreak, the highest incidence of paralysis occurring with the highest compliance.

S utter et al. (1991) also wrote: "Among the most disturbing features of the [paralytic poliomyelitis] outbreak [in Oman] 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." This represents further evidence that vaccination caused the outbreak. The vaccinators had travelled into sparsely populated communities.

Sutter et al. (1992) reviewed vaccination records for 70 children aged 5-24 months with poliomyelitis and from 692 matched control children during a poliomyelitis outbreak investigation in Oman. "A significantly higher proportion of cases received a DTP vaccine injection within 30 days before paralysis onset than did controls (42.9% vs. 28.3%). The proportion of poliomyelitis cases that may have been provoked by DTP injections was 35% for children 5-11 months old." They concluded that their study confirmed that "...injections are an important cause of provocative poliomyelitis. Although the benefits of DTP vaccination should outweigh the risks of subsequent paralysis, these data stress the importance of avoiding unnecessary injections during outbreaks of wild poliovirus infection."

The fact is that previous injections of other vaccines (such as those containing a pertussis component) causing provocation paralysis was described in the 1950s (for instance, McCloskey, 1950). So, the situation in Oman was just another example of the phenomenon of provocation paralysis. However, time and again, mass vaccination programs have ignored this important fact and continued causing suffering and disability to children all over the world. Another important well-known fact is that the significant majority (65 per cent) of recipients of any vaccines actually get the disease which the vaccines are supposed to prevent, after the first dose (Hedrich, 1933). Hedrich studied outbreaks of measles for 30 years in the Baltimore (USA) area. He established that when about 63 per cent of susceptibles get measles, an epidemic stops. Strebel et al. (1992) wrote that vaccine-associated paralysis in recipients of OPV usually occurs after their first dose. In Oman (and elsewhere), those who became paralysed after the first dose were simply excluded from efficacy calculations as unvaccinated or such vaccinations "were not counted".

Sutter et al. (1993) published an article on another outbreak in Oman after the post-vaccination polio outbreak of 1988-89. For obvious reasons I cannot quote the entire article, so I highlight certain sentences which reflect the observed reality. The authors wrote: "Investigation of the outbreak suggested that its occurrence was due to several factors, including accumulation of children susceptible to poliomyelitis due to a reduction in overall immunity levels from exposure to wild poliovirus in 1987-1988, suboptimal efficacy of trivalent oral poliovaccine (OPV), provocationpoliomyelitis from antecedent injections with DTP vaccine, and participation of fully vaccinated children in the chain of transmission... A total of four laboratory-proven cases occurred in 1991. The first two cases occurred in the Batinah region in March 1991 (44- and 49-months-old children), both of whom received four doses of OPV. Two additional cases (25 and 30 months old), all after 5 doses of OPV, occurred in August and October 1991 in adjoining Eastern and Interior regions. The same genotype of wild type 3 poliovirus was isolated in all of them." They concluded that the experience in Oman indicates that uniform implementation of the present WHO strategy "may not be sufficient to interrupt transmission" and that several additional doses of OPV to all children may be needed. (Obviously, no doses would do the trick.)

Paralytic poliomyelitis outbreaks in Romania

According to Strebel et al. (1994), although

poliomyelitis due to wild virus infection had virtually disappeared from Romania, with no cases having been documented between 1984 and 1989, vaccine-associated paralytic poliomyelitis was reported at very high rates for over two decades. In November 1990, to decrease the risk of vaccine-associated paralytic poliomyelitis, oral poliovirus vaccine

produced in Romania was replaced by imported oral vaccine produced by a Western European manufacturer. The overall risk of vaccine-associated paralysis in Romania was 14 times higher than the "reported" risk in the USA. However, the risks of recipient vaccine-associated paralysis relating to the first dose of oral vaccine were similar for the Romanian and imported vaccines.

The word "reported" is crucial due to a chronic endemic underreporting of any "vaccine-preventable diseases" after the introduction of mass vaccination, which consequently seemingly improves the efficacy and masks the real risk. All this is further compounded by a new definition of the disease poliomyelitis introduced after mass vaccinations were started in the 1950s and 1960s. The classical definition of poliomyelitis is "a disease with residual paralysis which resolves within 60 days"; the new definition is "a disease with residual paralysis persisting for more than 60 days". Since only less than one per cent of the cases develop a residual paralysis persisting for more than 60 days, the new definition "eradicated" the vast majority of cases in which paralysis resolved within 60 days as not being poliomyelitis.

Strebel et al. (1994) wrote: "Cases are confirmed if they meet the following definition: an acute illness characterized by flaccid paralysis which is compatible with the clinical presentation of poliomyelitis in the acute phase and residual neurologic deficit 60 days (or later) after the onset of paralysis."

Additionally, cases were defined as "vaccine-associated" if there was no direct evidence of wild poliovirus infection and if there was a positive history of recent exposure to oral poliovirus vaccine. This definition is interesting in that it highlights the fact that vaccine-caused paralysis acquired very high significance. Just in case someone may think that vaccination eradicated the wild poliovirus in the environment (as claimed by the vaccinators), note that natural infections with wild poliovirus resulted in the development of natural immunity without paralysis. The outbreaks of paralysis were directly connected with the mass administration of a variety of vaccines, starting with smallpox and continuing with diphtheria, tetanus and, especially after World War II, all the other vaccines. A great number of articles have been published about "provocation poliomyelitis", meaning "provoked by prior injections with a variety of vaccines".

Even in the case of Romania, Strebel et al. (1995) wrote about intramuscular (IM) injections within 30 days of immunisation with oral poliovirus vaccines as a risk factor for vaccine-associated paralysis. They wrote: "In Romania the rate of vaccine-associated paralytic poliomyelitis is for unexplained reasons 5 to 17 times higher than in other countries. Long ago it was noted that intramuscular injections administered during the incubation period of wild-type poliovirus infection increased the risk of paralytic disease (a phenomenon known as 'provocation' poliomyelitis). We conducted a case-control study to explore the association between intramuscular injections and vaccine-associated poliomyelitis in Romania.

"Of the 31 children with vaccine-associated disease, 27 (87 percent) had received one or more intramuscular injections within 30 days before the onset of paralysis, compared with 77 of the 151 controls (51 percent) (matched odds ratio, 31.2; 95 percent confidence interval, 4.0 to 244.2). Nearly all the intramuscular injections were antibiotics, and the association was strongest for the patients who received 10 or more injections (matched odds ratio for more or equal 10 injections as compared with no injections, 182.1; 95 percent confidence interval)."

So, the risk of paralysis was strongly associated with injections given after the oral polio vaccine, but not with injections given before or at the same time as the vaccine. However, in all cases, OPV was given simultaneously with DPT vaccine.

Interestingly, as reported by Strebel et al. (1995), the timing of the onset of paralysis, with IM injections given after DPT and OPV, was 9-30 with a median of 16 days (the highest risk being at 8-14 days, 15-21 days and 22-30 days), and 0-7 days and 15-21 days with DPT and OPV injections given before the onset of paralysis. This reflected the phenomenon of critical days as discovered and defined by Scheibner (2004).

Poliomyelitis epidemic in The Gambia

OttenetaL (1992) and Deming et al. (1992) reported on the epidemic in The Gambia of poliomyelitis associated with type 1 poliovirus involving 305 cases (estimated 1986 population of 768,995) from May to November 1986, following a six-year non-epidemic period with only five reported cases. The highest attack rate was in one-year-old children: 394 cases per 100,000 of population. The national attack rate was 40 per 100,000 of population. A vaccination coverage survey showed that 64 per cent of one- to two-year-old children were vaccinated with at least three doses of trivalent oral polio vaccine at the beginning of the epidemic. Fifty-seven cases became paralysed more than two weeks after a national mass vaccination campaign, in which 95 per cent of children aged one to seven years old were reported to have received a dose of trivalent oral polio vaccine. The authors concluded that the mass vaccination campaign may only have been partially successful in ending the epidemic.

Wyatt (1987) addressed another well-known problem of provocation poliomyelitis caused by injections of DPT together with OPV in The Gambia. This phenomenon was addressed in the above section on Romania.

Paralytic poliomyelitis outbreak in Namibia

Van Niekerk et al. (1994) described an outbreak of paralytic poliomyelitis in Namibia. They wrote: "The last confirmed cases of poliomyelitis in Namibia had been reported in 1988. However, between November 8, 1993, and January 7, 1994, 27 cases of paralytic poliomyelitis were confirmed in the country. The outbreak was limited to the south health region; at least 80% of infants in this region have received four doses of oral poliovaccine (OPV) by the age of 1 year. The patients ranged from 13 months to 12 years; 24 were younger than 5 years. Of the 26 patients whose vaccine status was known, 14 had received four doses of OPV, 6 had one or two doses, and 6 no vaccine." The normal health services and hence vaccination in the north had been severely disrupted by a long war. Interestingly, the authors reasoned that since due to poor vaccination efforts the wild poliovirus was circulating freely in the northern health region, children developed solid immunity to it (without developing paralysis).

This interesting and important information was repeated by Biellik et al. (1994), who wrote: "In late 1993 a poliomyelitis epidemic occurred almost exclusively in residents of the south health region (the area that was highly vaccinatedj. We speculate, therefore, that endemic wild poliovirus circulation continued uninterrupted in Angola and the two north regions of Namibia across the well-travelled border since 1989, when cases were last reported. Although OPV coverage was fairly low in northern compared with southern Namibia, a higher proportion of northern children may have been protected, at least to type 1, by natural immunity, thus suppressing epidemics. In 1993 OPV3 coverage among infants aged less than 1 year was higher in the south than the north. However, evidence suggests that a substantial pool of susceptibles, especially among children aged 1-3 |years), was created when |vaccine] coverage was low, and the apparent interruption of wild poliovirus circulation limited the acquisition of natural immunity (in the well-vaccinated southern health region]."

The same situation of poliomyelitis occurring in fully vaccinated children, usually straight after mass vaccination drives, has occurred in many other countries, both developed and developing. The difference was in the truthfulness in reporting.

Mechanics of vaccine-associated paralysis

There is more than one aspect to the mechanics of vaccine-associated paralysis. One of the most important suspects is increased neurovirulence associated with a single nucleotide change in a noncoding type 3 poliovaccine genome.

Evans et al. (1985) wrote: "Most of the small number of cases of poliomyelitis which occur in countries where Sabin's attenuated poliovirus vaccines are used are temporally associated with administration of vaccine and involve polioviruses of types 2 and 3. Recent studies have provided convincing evidence that the Sabin 2 and 3 viruses themselves may revert to a neurovirulent phenotype on passage in man [meaning babies] ... a point mutation in the 5' noncoding region of the genome of the poliovirus type 3 vaccine consistently reverts to wild type in strains isolated from cases of vaccine-associated poliomyelitis. Virus with this change is rapidly selected on passage through the human gastrointestinal tract. The change is associated with a demonstrable increase in the neurovirulence of the virus."

Inherent problems with inactivation of viruses (including those contaminating polio vaccines) were already known as early as 1961 and 1962.

Gerber et al. (1961) described inactivation with formaldehyde which is subject to asymptotic factor, meaning that within about 40 hours most viruses are inactivated but afterwards there is a viable residue of live viruses indefinitely.

Fenner (1962) described reactivation of animal viruses: "It is still a common practice among medical men [and women] to speak of 'killed' and 'live' viral vaccines, and the everyday meaning of the terms is clear enough. But, as I shall demonstrate, virologists now recognise a variety of situations in which 'killed' virus may multiply and produce new infectious virus. They have therefore discarded the term 'killed' and adopted the word 'inactivated' to replace it. Even 'inactivated', however, is used in a restricted sense; it refers to the loss of viral infectivity—that is, to the inability of the virus particles to multiply and produce a new infectious virus in susceptible cells, when these cells each receive only single particles of the inactivated preparation, and no other virus particles or derivates thereof." More recently, inactivation has been used as a method of studying the structure and function of viruses. "This approach received its principal stimulus from the discovery that inactivation was sometimes reversible." (Fenner, 1962)

Little attention has been given to viral intracellular reactivation. Multiplicity of reactivation of UV-irradiated influenza virus was demonstrated in 1951, and cross-reactivation was shown to occur with the same virus in 1956 and 1961. Recently-irradiated vaccinia virus was shown to undergo both multiplicity and cross-reactivation (Fenner, 1962). (In my opinion, this shows the fallacy of irradiating food: irradiated bacteria are only temporarily weakened and revert to their original virulence.) In 1936, Berry and Dedrick (quoted by Fenner, 1962) had already demonstrated that some rabbits inoculated with a mixture of heat-inactivated myxoma virus and active fibroma virus died of myxomatosis. These data emphasise the dangers of injecting dubiously "inactivated" or "non-genetically" reactivated viruses.

Published orthodox medical literature has documented many outbreaks of paralysis connected with mass vaccination programs time and again and in many countries. In this article, I've only described a few examples, but it would be easy for the interested reader to search the existing literature for more examples.

Conclusions

Not only has mass polio vaccination not eradicated paralytic poliomyelitis, it has caused a number of outbreaks of paralysis directly linked to the administered vaccines.

These days, when a vaccinee develops poliomyelitis, it may not be called poliomyelitis; instead, it may be called viral or aseptic meningitis, ascending paralysis (Guillain-Barre syndrome), cerebral palsy (over 75 per cent of cases are not diagnosed at birth but after six months) or other such names. According to MMWR (1997; 32[29]:384-385), there are 30,000 to 50,000 cases of aseptic meningitis every year in the United States. Considering that the vast majority (99 per cent) of the reported cases in the pre-vaccine era were non-paralytic and would have corresponded to aseptic or aviral meningitis, then vaccination has actually increased the incidence of poliomyelitis. In the pre-vaccine era, such high numbers only occurred in some epidemics. Now, such numbers occur every year, year by year.

About the Author:

Viera Scheibner, PhD, born in 1935 in Bratislava in the former Czechoslovakia (now the Slovak Republic), is a retired Principal Research Scientist. Having studied medicine in 1953 and changed streams in 1954, she graduated in natural sciences in 1958 and was awarded a doctorate in this discipline (RNDR) in 1964 from Comenius University in Bratislava.

Before emigrating to Australia in 1968, she progessed to Senior Associate Professor (Docent) and lectured in biology, micropalaeontology and geology at the university. She had 35 scientific papers and one book published.

After arriving in Australia, Dr Scheibner took up a position as Research Scientist (Micropalaentologist) with the Geological Survey of New South Wales, Department of Mines (later renamed as Department of Mineral Resources). She retired as Principal Research Scientist in 1987, having published scientific findings in a further 47 papers and two books. In the late 1980s, Dr Scheibner was engaged in the study of babies' breathing with the Cotwatch microprocessor-based breathing monitor, developed in conjunction with her husband, Swedish biomedical electronics engineer Leif Karlsson (deceased in 1994). The findings with Cotwatch sparked her interest in the link between sudden infant death syndrome (SIDS) and vaccination, and resulted in her intensive research of orthodox medical literature into the dangers and ineffectiveness of vaccines which continues to this day.

Since 1990, Dr Scheibner has had numerous papers and letters published in peer-reviewed and other journals and has lectured and held seminars in Australia and internationally on vaccine dangers and ineffectiveness. Since 1996, she has provided over 100 reports and appeared as an expert witness for numerous court cases involving vaccine injuries and deaths misdiagnosed as physical injuries by parents and other carers, called "shaken baby syndrome".

Dr Scheibner is the author of Vaccination-. 100 Years of Orthodox Research Shows that Vaccines Represent a Medical Assault on the System (1993; reviewed in NEXUS, vol. 2, no. 16) and Behavioural Problems in Childhood: The Link to Vaccination (2000; reviewed in NEXUS, vol. 7, no. 5). She has previously contributed five articles to NEXUS, most recently "Vaccinations and the Dynamics of Critical Days" (vol. 12, no. 6; first published in IACNEM 2004; 23(31:10-14).

Dr Scheibner can be contacted by email at viera.scheibner@gmail.com.

References

• Biellik RJ, Lobanov A, Heath K, ReichlerM, TjapepuaVetal. (1994). Poliomyelitis in Namibia. Lancet 3AAM16.

• Bradford Hill A (1965). Environment and disease: Association or causation? PracRoy SocMed 1965:295-300.

• Deming MS, Jaiteh KO, Otten MW, Flagg EW, fallow M et al. (1992). Epidemic poliomyelitis in The Gambia following the control of poliomyelitis as an endemic disease. II. Clinical efficacy of trivalent oral polio vaccine. Am 1 Epidemiology 135(4):393-408.

• Evans DMA, Dunn G, Minor PD, Schild GC, Cann AJ et al. (1985). Increased neurovirulence associated with a single nucleotide change in a noncoding region of the Sabin type 3 poliovirus genome. Nature 314:548-550.

• Fenner F (1962). The reactivation of animal viruses. British Medical journal Jul 21:135-142.

• Gerber P, Hottle GA, Grubb RE (1961). Inactivation of vacuolating virus (SV40) by formaldehyde. Proc Soc ExpBiol&Med 108:205-209.

• Henderson DA, Witte JJ, Morris L. Langmuir AD (1984). Paralytic disease associated with oral polio vaccines. JAMA 190(l):41-48.

• Hutchins SS, Cochi SL, Brink EW,

• Hedrich AW (1933). Monthly Estimates of the Child Population "Susceptible" to Measles, 1900-1931, Baltimore, MD. Am I Hyg 17:613-635

• McCloskey BP (1950). The relation of prophylactic inoculations to the onset of poliomyelitis. Lancet Apr 18:659-663.

• Nathanson N (1984). Epidemiologic Aspects of Poliomyelitis Eradication. Rev of Infect Dis 1984 May-June; 6(Suppl2):S308- S312.

• Otten MW, Deming MS, Jaiteh KO, Flagg EW, Forgie 1 et al. (1992). Epidemic poliomyelitis in The Gambia following the control of poliomyelitis as an endemic disease. Am I Epidemiology 135(4):381-392.

• Peterson L, Benson WW, Graeber FO (1955). Vaccination-induced poliomyelitis in Idaho. Preliminary report of experience with Salk poliomyelitis vaccine. JAMA 159(4):241-244.

• Special Advisory Committee on Oral Poliomyelitis Vaccine to the Surgeon General of the Public Health Service. Oral Poliomyelitis Vaccines. JAMA 190(l):49-l.

• Schonberger LB, Kaplan J, Kim-Farley R, Moore M, Eddins DL, Hatch M (1984). Control of paralytic poliomyelitis in the United States. Rev Infect Dis 6 (Suppl2):S4240-S426.

• Sutter RW, Patriarca PA, Brogan S, Malankar PG, Pallansch MA, Kew OM, Bass AG et al. (1991). Outbreak of paralytic poliomyelitis in Oman: evidence for widespread transmission among fully vaccinated children. Lancet 338:715-720.

• Sutter RW, Patriarca PA, Suleiman AIM, Brogan S, Malankar PG, Cochi SL etal. (1992). Attributable risk of DTP (diphtheria and tetanus toxoids and pertussis vaccine) injection in provoking paralytic poliomyelitis during a large outbreak in Oman. ] Infect Dis 165:444-449.

• Sutter RW, Patriarca PA, Suleiman AIM, Pallansch MA, Zell ER, Malankar PG et al. (1993). Paralytic poliomyelitis in Oman: association between regional differences in attack rate and variation in antibody responses to oral poliovirus vaccine. Intern J Epidemiology 22(5):936-944.

• Strebel M, Aubert-Combiescu A, Ion-Nedelescu N, Biberi-Moroneanu S, Combiescu M et al. (1994). Paralytic poliomyelitis in Romania, 1984-1992. Am I Epidemiology 140(12):l 111-24.

• Strebel M, Ion-Nedelescu N, Baughman AL, Sutter RW, Cochi SL (1995). Intramuscular injections within 30 days of immunization with oral poliovirus vaccine - a risk factor for vaccine-associated paralytic poliomyelitis. NEJM 332:500-506.

• Scheibner V (2004). Dynamics of critical days as part of the dynamics of non-specific stress syndrome discovered during monitoring with Cotwatch breathing monitor. I ACNEM 23(3):10-14.

• Van Niekerk ABW, Vries JB, Baard J, Schoub BD, Chezzi C, Blackburn NK (1994). Outbreak of paralytic poliomyelitis in Namibia. Lancet 344:661-664.

• Wyatt HV (1987). Poliovaccination in The Gambia. Lancet Jul 4; 2:43.