Polio

Polio eradication: a complex end game

BMJ 2012; 344 doi: http://dx.doi.org/10.1136/bmj.e2398 (Published 2 April 2012)
Cite this as: BMJ 2012;344:e2398

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Eradication of polio by vaccination - Part 4

Contamination of monkey kidney tissue cultures (used in the production of polio vaccines) by live amoebas.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Competing interests: None declared

Dr Viera Scheibner (PhD), Scientist/author retired

n/a, Blackheath, Australia

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Eradication of polio by vaccination? Part 3

Another important consideration in attempts to eradicate poliomyelitis by vaccination is the contamination of polio vaccines by chimpanzee coryza virus, renamed respiratory syncytial virus (RSV).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Competing interests: None declared

Dr Viera Scheibner (PhD), Scientist/author retired

n/a, Blackheath, Australia

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Eradication of polio by vaccination? Part 2.

According to ample medical research evidence, polio vaccines of any kind cause VAPP. However, there are other major problems with polio vaccine that justify scepticism about their benefits, one of which is the well-documented and continuous contamination of polio vaccines by monkey viruses SV1-SV40.

Soon after the poliovirus mass vaccination programmes started in the US, a number monkey viruses and amoebas were found in the vaccine seed brews. Hull, Johnston et al. (1955) and Hull, Minner et al. (1958) encountered numerous filterable, transferable cytopathogenic agents other than polio virus in “normal” monkey renal cell cultures. Even though they 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. 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, plus caused generalised aseptic type meningitis. The isolated agent was called simian or SV virus and classified into 4 groups based on the cytopathogenic changes induced in monkey kidney cell cultures infected with these agents.

Hilleman and Sweet (1960. Proc Soc Exp Biol and Med; 105: 420-427) reported on the “Vacuolating virus S.V. 40”, which became the one monkey virus best researched. Gerber et al. (1961. Inactivation of vacuolating virus (SV40) by formaldehyde. Proc Soc Exp Biol and Med; 108: 205-209) demonstrated that Sweet and Hilleman’s (1960) method of inactivation of SV40 by 10 day treatment by 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 (1962. Reactivation of animal viruses. BMJ; July 21: 135-142) research has also established that even the inactivated portion of the viruses reverts back to the original virulence.

Eddy et al. (1961. Tumours induced in hamsters by injection of Rhesus monkey kidney cell extracts. Proc Soc Exp Biol and Med; 107; 191-197) documented the carcinogenic properties of these simian viruses: they caused tumours in hamsters injected with Rhesus monkey kidney cell extracts.

As established by many subsequent researchers, in humans SV40 causes characteristic brain tumours, bone sarcomas, mesothelioma and even especially virulent form of melanoma cancers.

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 (Weiner et al. 1976. Isolation of virus related to SV40 from patients with progressive multifocal encephalopathy. NEJM; 286 (8): 385-389; Carbone et al. (1994) Simian virus 40-like DNA sequences in human pleural mesothelioma. Oncogene; 9: 1781-1779; Bergsagel et al. 1992. DNA squences similar to those of simian virus 40 in ependymomas and choroid plexus tumours in childrern. NEJM; 326: 988-993; Carbone et al. 1997. Simian virus-40 large T antigen binds p53 in human mesotheliomas. Nature Medicine; 3 (8): 908-912; Butel and Lednicky.1999. Cell and molecular biology of simian SV40: implications for human infections and disease. J Natl Cancer Inst; 91: 119-134).

Kops (2000. Oral polio vaccine and human cancer: a reassessment of SV40 as a contaminant based upon legal documents. Anticancer Res; 26: 4745-4750) 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, 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 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..." [and] 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.

Competing interests: None declared

Dr Viera Scheibner (PhD), scientist/author retired

n/a, Blackheath, Australia

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Response to Neeru Gupta’s, and colleagues’ comments to my RR (10 April 2012); a combination of killed followed by oral polio vaccine delivery

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 (Peterson et al. 1955. JAMA; 159 (4): 241-244). 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 formaldehyde inactivated” Sabin vaccine, which was believed to simulate the natural infection. However, VAPP cases continued occurring with the Sabin vaccine.

While writing this response to “A combination of killed followed by oral polio vaccine delivery may be an option to protect from VAPP by the former and maintaining the herd immunity by the latter” I spent many hours locating and reading the older and more recent articles addressing the effectiveness, or otherwise, of combining IPV and OPV vaccines and established that the results are not straighforward. Moreover, as established by Abraham et al. (1993. J Infect diseases; 168: 1105-1009, “Shedding of virulent poliovirus revertants during immunization with oral poliovirus vaccines after prior immunization with inactivated polio vaccines continued” and “...the prior immunization with EIPV does not prevent fecal shedding of revertant polioviruses after subsequent exposure to OPV”.

Mensi and Pregliasco (1998, Clinical and diagnostic Laboratory Immunology; 5 (3): 278-280) wrote “In recent years great alarm has been generated by outbreaks of paralytic poliomyelitis in vaccinated populations in which the levels of immunity against poliovirus are not adequate or controlled [the meaning unclear]…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 (31). 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…” [? 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. 1984 (Prog Med Virol; 29: 124-140) published a graph (figure 4) correlating the number of reported poliomyelitis cases with the vaccination rates in seven areas in The Netherlands. Interestingly, the areas with the lowest compliance had the lowest number of cases and vice versa. The compliance ranged from 40-49% to 90-95%. In the 1992 epidemic, the first two cases occurred in a 14-year old boy and 23-year old male nurse, both vaccinated members of the orthodox religious group.

Sutter et al. (991) described the Oman outbreak as “evidence for widespread transmission among fully vaccinated children (Lancet; 338: 715-720). 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”, one of the interesting reasons quoted as “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”. The same reason was given by Biellik et al. (1994. Lancet; 344: 1776) for the polio vaccine failure in Namibia.

Wyatt (1987. Poliovaccination in the Gambia; Lancet, July 4: 43) quoted Hanlon et al. (ibid 1987) [who] “suggest that booster dose of killed poliovaccine might be more effective than oral stopping an epidemic…” “but injections during an epidemic may provoke poliomyelitis in children already infected with poliovirus…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 poliomyelitis outbreak in Taiwan (Kim-Farley et al. 1984. Lancet; 8 Dec: 1322-1324) 65 % of VAAP developed within 28 days of the first vaccine dose, thus confirming observations of others that two thirds of vaccine-targeted diseases occur after the first dose of relevant vaccines, including the polio vaccine. Yet, the authors excluded (as unvaccinated) all paralysis case (65% of all cases) from calculations of efficacy. This unwittingly confirmed the original definition of herd immunity, “epidemics occur with the accumulation of two thirds of susceptibles”. Or, “when 2/3 of susceptibles get the disease, the epidemic stops”.

Ogra (1995. Ann NY Acad Sci; 764: 97-107) 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 bases on the use of OPV or EP-IPV alone are revised.”

Furione et al. (1993. Virology; 196: 199-208) demonstrated that recombination alone, or together with mutation, might be one of the mechanisms of the reversion toward neurovirulence of attenuated vaccine strains and of natural evolution of poliovirus.

James A. Shannon famously said “The only safe vaccine is a vaccine that is never used.” Neetu Vashisht and Jacob Pulliel (2012. Indian Journal of Medical Ethics; IX (2): wrote “Vertical [vaccination] programmes have unwittingly increased the incidence of other diseases and broken the first rule of medicine – primum non nocere – first do not harm”; and, “Polio programme: let us declare victory and move on.” [And stop vaccinating.]

Competing interests: None declared

Dr Viera Scheibner (PhD), scientist/author retired

n/a, Blackheath, Australia

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Replying to Dr Viera Scheibner

The difference between small pox and polio is that vaccine virus is replacing the wild virus in the environment to increase the herd immunity in case of polio. But the vaccine virus had its problems in both the diseases.

In 1988, the World Health Assembly resolved to eradicate poliomyelitis worldwide. The live, attenuated oral poliovirus vaccine (OPV) has many advantages favoring its use in polio eradication: it is administered easily by mouth; confers intestinal immunity, making recent OPV recipients resistant to infection by wild polioviruses (WPVs); provides long-term protection against paralytic disease through durable humoral immunity; and is inexpensive. Despite its many advantages, OPV use carries the risk for occurrence of rare cases of vaccine-associated paralytic poliomyelitis among immunologically normal OPV recipients and their contacts and the additional risk for emergence of vaccine-derived polioviruses (VDPVs)1. This is because Polio virus is an enterovirus which is an RNA virus that are notorious for mutation. Attenuated strains of Sabin poliovirus vaccine replicate in the human gut and, in rare cases, may cause vaccine-associated paralytic poliomyelitis (VAPP). The genetic instability of Sabin strains constitutes one of the main causes of VAPP, a disease that is most frequently associated with type 3 and type 2 Sabin strains, and more rarely with type 1 Sabin strains2.

Killed vaccine will protect the individual and will not have the problem of VAPP. Whereas, the oral polio vaccine (Sabin) not only protects the individual but also the community by replacing wild virus with vaccine virus and hence increase the herd immunity by getting transmitted through oral faecal route, but a rare disadvantage of VAPP. In my opinion the killed vaccine should be given first as it will protect against all three strains and is non-neurovirulent and does not cause VAPP. In fact it will have protective levels against VAPP for subsequent delivery of oral polio vaccine.

Because of these risks, OPV use will be discontinued worldwide once the goal of eradicating all WPV transmission is achieved. VDPVs can cause polio outbreaks in areas with low OPV coverage and can replicate for years in immunodeficient persons; therefore, strategies to strengthen global polio immunization and surveillance are needed to limit emergence of VDPVs2.

A successful program of poliomyelitis control is described in the literature using a combination of killed and live polio vaccines over a 10-year period in two developing areas, the West Bank and Gaza, adjacent to a relatively developed country, Israel. During the 1970s, immunization using live trivalent oral polio vaccine (OPV) in these areas covered more than 90 percent of the infant population. During this period, nevertheless, the incidence of paralytic polio continued to be high, with many cases occurring in fully or partially immunized persons3. That time the reason thought was that this could be due to interference with OPV take by other enteroviruses present in the environment due to poor sanitary conditions in these areas. A new policy combining five doses of OPV with two doses of inactivated polio vaccine (IPV) was adopted then and implemented in 1978. It was reported that in the 10 years since then, immunization coverage of infants increased to an estimated 95 percent and paralytic poliomyelitis has been controlled, despite exposure to wild poliovirus from neighboring countries including an outbreak in Israel in 1988. This experience suggested that wide coverage using the combination of IPV and OPV is an effective vaccination policy that may make eradication of polio possible even in developing areas3.

References:

1. Update on vaccine-derived polioviruses--worldwide, July 2009-March 2011. MMWR Morb Mortal Wkly Rep. 2011 Jul 1;60(25):846-50.

2. Pliaka V, Kyriakopoulou Z, Tsakogiannis D, Ruether IG, Gartzonika C, Levidiotou-Stefanou S, Krikelis A, Markoulatos P. Correlation of mutations and recombination with growth kinetics of poliovirus vaccine strains. Eur J Clin Microbiol Infect Dis. 2010 Dec;29(12):1513-23. Epub 2010 Sep 5.

3. T Tulchinsky, Y Abed, S Shaheen, N Toubassi, Y Sever, M Schoenbaum, and R Handsher. A ten-year experience in control of poliomyelitis through a combination of live and killed vaccines in two developing areas. Am J Public Health. 1989 December; 79(12): 1648–1652.

Competing interests: None declared

Neeru Gupta, Scientist E

Manju Rahi, KK Jani

Indian Council of Medical Research, Ansari Nagar, New Delhi-110029

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Smallpox versus polio eradication

In my previous response to the question of smallpox and polio eradication (BMJ.com; 28.2.2012; and BMJ.com; 10 April 2012; re: assaulting alternative medicine: worthwhile or witch hunt?) I omitted to comment on smallpox. I am addressing the relevant issues of smallpox eradication now in responding to Neeru Gupta’s, Manju Rahi’s and Nivedita Gupta’s assertions.

Deleterious effects and ineffectiveness of smallpox vaccination have been among the main smallpox issues discussed in medical papers for a long time. In 1928, the British Medical Journal (21 January: 115-116) published an article by Dr Garrow showing that the fatality rate among the vaccinated cases of smallpox in England and Wales in 1923 and 1926, in those over 15 years of age, was higher than among the unvaccinated. Dr Parry, one of the contributors to the discussion, summarised the questions raised by Dr Garrow:

1. How is it that small-pox is five times as likely to be fatal in the vaccinated as in unvaccinated.
2. How is it that, as the percentage of people vaccinated has steadily fallen from about 85 in 1870 to about 40 in 1925, the number of people attacked with variola has declined pari passu and the case mortality has progressively lessened? The years with least vaccination have been the years of least small-pox and of least mortality.
3. How is it that in some of our best vaccinated towns – for example Bombay and Calcutta – small-pox is rife, while in some of our worst vaccinated towns, such as Leicester, it is almost unknown?
4. How is it that something like 80 percent of the cases admitted into the Metropolitan Asylum Board small-pox hospitals have been vaccinated whilst only 20 percent have not been vaccinated?
5. How is it that in Germany, the best vaccinated country in the world, there are more deaths [from smallpox] in proportion to the population than in England – for example, in 1919, 28 deaths in England, 707 in Germany; in 1920, 30 deaths in England, 354 in Germany. In Germany, in 1919 there were 5,012 cases of small-pox with 6 deaths. What is the explanation?
6. Is it possible to explain the lessened incidence and fatality of small-pox on the same grounds as the lessened incidence and fatality of other infectious fevers – namely, as due to improved hygiene and administrative control?

The editorial comment to the above discussion accused Dr Parry of introducing assumptions of fact into the framework of his questions, while he was the one referring to the well-known facts. Indeed, his letter was factual, logical and to the point which would still stand up to scrutiny today.

Interestingly, the contributions of the other participants in the above debate used the same questionable tactics as many provaccinators today: accusing their opponents of expressing personal opinions, while it is the other way around: it is the antivaccinators who study orthodox medical literature and document their statements with published facts. Characteristically, provaccinators resort to argumenta ad hominem avoiding argumenta ad rem.

Besides reporting on outbreaks of smallpox in the vaccinated, numerous authors reported on serious reactions to smallpox vaccine: neurological complications, encephalitis, multiple sclerosis, recurrent herpes simplex at the smallpox vaccination site, anaphylaxis and many others.

Spillane and Wells (1964. Brain; 87:1-44) in their voluminous account of postvaccinal encephalomyelitis stated that it has only been recognised as such after 70 years of compulsory smallpox vaccination in England.

However, this opened a floodgate of reports on smallpox vaccine reactions and indeed, was the motivation behind the decision to proclaim smallpox eradicated: the adverse effects of vaccination were much worse than the disease itself.

Smallpox was pronounced officially eradicated on 8 May 1980. Arita and Gromyko (1982. Bull WHO; 60 (3): 367-375), considered the main benefit of official eradication of smallpox that the smallpox vaccination could be discontinued in all countries. By 1 March 1982, 150 of the 158 WHO Member States had officially terminated their smallpox vaccination programmes and the requirement for an international certificate of smallpox vaccination have been abolished in all countries.

The early 2003 decision to reinstitute smallpox vaccination for selected segments of the US population on the basis of concern that smallpox could be used as an agent of bioterrorism, had to be discontinued: many recipients of smallpox vaccine developed serious cardiac events (MMWR; March 28, 2002 and MMWR October 3, 2003; 52 (39), myopericarditis (JAMA; 2003; 289 (24): 3283-3289), and there was also a multistate outbreak of what was called monkeypox (MMWR; 2003; 52 (24): June 20).

BMJ (BMJ.com newsroundup; 18 May 2002) quoted Dr DA Henderson, who led the worldwide smallpox eradication programme of 1970s, citing “many problems if the smallpox vaccine were to be offered to all Americans. People with compromised immune systems, such as those with AIDS, and those with a history of eczema or atopic dermatitis are at risk from vaccination. A recipient of smallpox vaccine can infect another person by transfer of the virus by hand or through bathing. Other complications include post-vaccination encephalitis.”

Needless to say, small, largely ignored, outbreaks of monkeypox, buffalopox, whitepox (indistinguishable from classical smallpox) have continued occurring without posing any problems (Scheibner 2012. Smallpox was declared eradicated, yet still infects humans today. International Medical Council on vaccination). All outbreaks are self-limiting, anyway.

In contrast, vaccination drives with smallpox and other vaccines trigger outbreaks of all so called “vaccine-preventable” diseases, as amply documented by orthodox medical and immunological research, published in reputable peer-reviewed medical journals.

Conclusions. Based on now more than 120 years of published orthodox medical research, vaccines of any kind, smallpox and polio including, not only increase their recipients’ susceptibility to the targeted diseases, but also to related and unrelated bacterial and viral infections. Hence outbreaks mainly in the vaccinated who also infect contacts. The best way to stop epidemics is to stop vaccinating and let nature do its own thing.

The specifics of manipulation of poliomyelitis “eradication” are also discussed by Mr Ron Law of Auckland (New Zealand) in his BMJ.com rapid response dated 10 March 2012.

Competing interests: None declared

Dr Viera Scheibner (PhD), scientist/author retired

n/a, Blackheath, Australia

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Smallpox had only one reservoir of infection i.e. human beings and for some time contaminated fomites whereas, Polio survives in environment in drains etc.

Smallpox had mild subclinical cases which won’t transmit the disease. Whereas, Polio has subclincal cases which continue to be reservoir.

Smallpox vaccine was good with lasting immunity and thermostable, whereas polio vaccine itself can cause polio and requires cold chain. Polio vaccine if effective (no vaccine virus induced polio), also has life long immunity.

Small pox case is a spot diagnosis and has no differential diagnosis whereas polio has all the differential diagnosis of acute flaccid paralysis.
Therfore, surviellence of small pox was easier and the subsequent action of ring immunization was very effective.

International co-operation was the key to small-pox success, while polio campaign suffers from un-cooperation, e.g. muslims in Afganistan.

The strategy of Polio eradication is replacement of wild polio virus with vaccine virus whereas in small pox it was total extermination of virus (except the samples stored in Russia and the USA).

So, in spite of above disparities we are still hopeful that polio eradication will be a dream come true in near, foreseeable future.

Competing interests: None declared

Neeru Gupta, Scientist E

Manju Rahi, Nivedita Gupta

Indian Council of Medical Research, Ansari Nagar, New Delhi-110029

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Polio eradication by vaccination?

Let me quote some original seminal medical research.

Anderson et al. (1951) in his article “Poliomyelitis occurring after antigen injections” (Pediatrics; 7(6): 741-759) wrote “During the last year several investigators have reported the occurrence poliomyelitis within a few weeks after injection of some antigen. Martin in England noted 25 cases in which paralysis of as single limb occurred within 28 days of injection of antigen into that limb, and two cases following penicillin injections. In Australia, McCloskey, during a study of the 1949 outbreak, recorded 38 cases that developed within 30 days of an antigen injection, finding an association between the site of paralysis and that of the recently antecedent injection. His findings, contrary to Martin’s suggested a greater association with pertussis vaccine than with other antigens. Geffen, studying the 1949 poliomyelitis cases in London, observed 30 patients who had received an antigen within four weeks, noting also that the paralysis involved especially the extremity into which the injection had been given. In a subsequent survey of 33 administrative areas in England, Hill and Knowelden found 42 children who had been immunized within a month [of injections]…Banks and Beale3 observed 14 cases that followed within two months after immunization noting also a correlation between site of injection and location of paralysis, as well as increased severity of residual paralysis…In the discussion of this problem during the April 1950 meeting of the Royal Society of medicine, Burnett and others stressed the apparent relationship to multiple antigens containing a pertussis component”. [undoubtedly reflecting the increasing use of pertussis-containing vaccines].

Peterson et al. (1955) reported on vaccination induced poliomyelitis in Idaho as part of the trial of the Salk (injectable) vaccine (Vaccination-induced poliomyelitis in Idaho. Preliminary report of experience with Salk poliomyelitis vaccine. JAMA; 159 (4): 241-244).

The Cutter laboratories were accused of distributing vaccines containing live polioviruses, and singled out, even though vaccines produced by other manufacturers also caused paralysis (Nathanson and Langmuir 1963. The Cutter incident: poliomyelitis following formaldehyde-inactivated poliovirus vaccination in the United States during the spring of 1955 III. Am. J Hyg; 78: 61-81

Wyatt (1981) summarised cases of provocation poliomyelitis caused by multiple injections in his article “Provocation poliomyelitis: neglected clinical observations from 1914 to 1950” (Bull Hist Med; 55: 543-557).

Wyatt et al. (1992) and Wyatt (1993) warned against the unnecessary injections causing paralytic poliomyelitis in India (Trans Roy Soc Trop Med Hyg; 86: 546-549 and Lancet 341: 61-62, respectively).

Sutter et al. (1992) published an article “Attributable risk of DTP (Diphtheria and Tetanus toxoids and Pertussis toxoid vaccine injection in provoking paralytic poliomyelitis during a large outbreak in Oman”. (J Infec Dis; 165: 444-449).

According to Strebel et al. (1994. Paralytic poliomyelitis in Romania, 1984-1992. Am J Epidemiology; 140 (12: 111-124) ) although poliomyelitis due to wild virus had virtually disappeared from Romania (no cases reported between 1984-1989), the vaccine-associated paralytic poliomyelitis (VAPP) was reported at very high rates for over two decades. The overall risk of VAPP in Romania was up to 17 times higher than the reported risk in the USA.

In November 1990, to decrease the risk of VAPP, oral poliomyelitis vaccine produced in Romania was replaced by imported OPV produced by “Western European manufacturer”. However, the risk of PAPP continued unabated with that vaccine.

The history continued repeating itself all over the world wherever the poliomyelitis vaccines were used. Paralysis developed after both injectable and oral polio vaccines.

It comes as no surprise that the most recent mass polio vaccination programs fuelled by Bill and Melinda Gates Foundation resulted in increased cases of VAPP. In India, two paediatricians, Dr Neetu Vashisht and Dr Jacob Pulliel of the Department of Paediatrics of St Stephens Hospital in Delhi noted that another major ethical issue raised by the campaign is the failure to thoroughly investigate the increase in incidence “of non-polio acute flaccid paralysis (NPAFP)” in areas where many doses of vaccine were used, while noting that these cases are clinically indistinguishable from polio paralysis and twice as deadly.

They also noted that while India was declared polio-free in 2011, at the same time there were 47500 cases of NPAFP, which increased in direct proportion to the number of polio vaccine doses received. Independent studies showed that children identified with NPAFP “were at more than twice the risk of dying than those with wild polio infection”.

According to their report, nationally, the NPAFP rate is now twelve times higher than expected. In the states of Uttar Pradesh and Bihar – which have pulse polio vaccination every month – the NPAFP rate is 25 and 35 fold higher than the international norms (Ramesh Shankar, Mumbai 2012).

Ron Law (Assaulting alternative medicine: worthwhile or witch hunt? BMJ.com 10 March 2012) recently addressed the polio situation in India: eradication has been achieved by re-naming the disease. Poliomyelitis paralysis which occurs even after 30+ vaccination doses, is now called acute flaccid paralysis (AFP) or polio-like paralysis; hardly a great success of vaccination or comfort to the parents of the more than 60 000 affected children.

Earlier redefinition of poliomyelitis had been introduced in the US: a disease with residual paralysis which resolves within 60 days changed into a disease with residual paralysis which persists for more than 60 days. Cases of paralysis which resolve within 60 days (99% of cases) are diagnosed as viral or aseptic meningitis.

According to MMWR (1997; 32[29]: 384-385), there are 30 000 to 50 000 cases of viral/aseptic meningitis per year in the US. Considering that in the pre-vaccine era the vast majority (99%) of the reported cases were non-paralytic (corresponding to aseptic or viral meningitis), vaccination has actually increased the incidence of poliomyelitis. Before mass vaccination there were a few hundred or few thousand cases of polio in some outbreaks, while now it is up to 50 000 cases every year.

Figure 1 in Schonberger et al. (1984. Control of poliomyelitis in the United States. Rev infect dis; 6 (Suppl 2: S424-S426) shows the steady downward trend in the incidence of poliomyelitis stopping, and indeed increasing, when DPT and P vaccination became mandatory in the US in the mid-seventies.

The experience in northern Namibia showed that with no polio vaccination children developed natural immunity to the wild polio virus without developing paralysis (Biellik et al. 1994. Poliomyelitis in Namibia. Lancet 344: 1776).

The vaccine viruses inactivation by a 14-day treatment with 1:4000 formaldehyde solution is the subject to asymptotic factor making the inactivation incomplete (Gerber et al. 1961. Inactivation of vacuolating virus (SV 40) by formaldehyde, Proc Soc Exp Biol & Med; 108: 205-209), and, Fenner (1962. The reactivation of animal viruses. BMJ; July 21: 135-142) showed that the process is also reversible.

Evans et al. (1985. Nature ; 314: 548-550) demonstrated “Increased neurovirulence associated with a single nucleotide change in a noncoding region of the Sabin type 3 poliovirus genome”.

The only way to eradicate paralytic poliomyelitis is to stop vaccinating.

Competing interests: None declared

Dr Viera Scheibner (PhD), scientist/author retired

n/a, Blackheath, Australia

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It is important that every country takes note of the need for and continuation of the polio eradication program so diligently followed in many countries, including India. Pulse Polio, the slogan of Rotary International, had a crucial role in the immunization program. I was President of a Rotary Club and was involved in implementing the Pulse Polio program, in which all Rotarians and family members participated. I remember the enthusiasm with which Fatima Sultan took part as an individual to make citizens aware of the need for polio eradication and immunization.

The technicalities and the choice of vaccine are the responsibilities of Government and Health Authorities. It is right time to be introspective about this vital immunization program and make it very successful. dhastagir

Competing interests: None declared

dhastagir Sultan sheriff, Professor

Faculty of Medicine, Benghazi University, Benghazi

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