The Polio Vaccine - Neil Z Miller. Part - 1
The polio vaccine: a critical assessment of its arcane history, efficacy,
and long-term health-related consequences
By: Neil Z. Miller, medical research journalist and Director of the Thinktwice Global Vaccine Institute
1. What is polio?
Polio is a contagious disease caused by an intestinal virus that may attack nerve cells of the brain and spinal cord. Symptoms include fever, headache, sore throat, and vomiting. Some victims develop neurological complications, including stiffness of the neck and back, weak muscles, pain in the joints, and paralysis of one or more limbs or respiratory muscles. In severe cases it may be fatal, due to respiratory paralysis.
2. How is polio contracted?
Polio can be spread through contact with contaminated feces (for example, by changing an infected baby’s diapers) or through airborne droplets, in food, or in water. The virus enters the body by nose or mouth, then travels to the intestines where it incubates. Next, it enters the bloodstream where “anti-polio” antibodies are produced. In most cases, this stops the progression of the virus and the individual gains permanent immunity against the disease [1].
Polio can be spread through contact with contaminated feces (for example, by changing an infected baby’s diapers) or through airborne droplets, in food, or in water. The virus enters the body by nose or mouth, then travels to the intestines where it incubates. Next, it enters the bloodstream where “anti-polio” antibodies are produced. In most cases, this stops the progression of the virus and the individual gains permanent immunity against the disease [1].
Many people mistakenly believe that anyone who contracts polio will become paralyzed or die. However, in most infections caused by polio there are few distinctive symptoms [2].In fact, 95 percent of everyone who is exposed to the natural polio virus won’t exhibit any symptoms, even under epidemic conditions [3,4]. About 5 percent of infected people will experience mild symptoms, such as a sore throat, stiff neck, headache, and fever—often diagnosed as a cold or flu [3,5]. Muscular paralysis has been estimated to occur in about one of every 1,000 people who contract the disease [3,6]. This has lead some scientific researchers to conclude that the small percentage of people who do develop paralytic polio may be anatomically susceptible to the disease. The vast remainder of the population may be naturally immune to the polio virus [7].
Injections: Several studies have shown that injections(for antibiotics or other vaccines) increase susceptibility to polio. In fact, researchers have known since the early 1900s that paralytic poliomyelitis often started at the site of an injection [8,9]. When diphtheria and pertussis vaccines were introduced in the 1940s, cases of paralytic poliomyelitis skyrocketed (Figure 1) [10]. This was documented in Lancet and other medical journals [11-13]. In 1949, the Medical Research Council in Great Britain set up a committee to investigate the matter and ultimately concluded that individuals are at increased risk of paralysis for 30 days following injections; injections alter the distribution of paralysis; and it did not matter whether the injections were subcutaneous or intramuscular [14,15].
Figure 1. Polio cases skyrocketed after diphtheria and pertussis vaccines were introduced
Several studies show that injections increase susceptibility to polio. When diphtheria and pertussis vaccines were introduced in the 1940s, cases of paralytic poliomyelitis skyrocketed. This chart shows the average number of polio cases per 100,000 people during five year periods before and after the vaccines were introduced.
Source: National Morbidity Reports taken from U.S. Public Health surveillance reports; Lancet (April 18, 1950), pp. 659-63.
A 1992 study, published in the Journal of Infectious Diseases, validated earlier findings. Children who received DPT (diphtheria, tetanus, and pertussis) injections were significantly more likely than controls to suffer paralytic poliomyelitis within the next 30 days [16]. According to the authors, “this study confirms that injections are an important cause of provocative poliomyelitis [16:444].”
In 1995, the New England Journal of Medicine published a study showing that children who received a single injection within one month after receiving a polio vaccine were 8 times more likely to contract polio than children who received no injections. The risk jumped 27-fold when children received up to nine injections within one month after receiving the polio vaccine. And with ten or more injections, the likelihood of developing polio was 182 times greater than expected [17]. Why injections increase the risk of polio is unclear [18]. Nevertheless, these studies and others [19-24] indicate that “injections must be avoided in countries with endemic poliomyelitis [18].” Health authorities believe that all “unnecessary” injections should be avoided as well [18:1006;24].
Nutritional deficiencies: A poor diet has also been shown to increase susceptibility to polio [25]. In 1948, during the height of the polio epidemics, Dr. Benjamin Sandler, a nutritional expert at the Oteen Veterans’ Hospital, documented a relationship between polio and an excessive use of sugars and starches. He compiled records showing that countries with the highest per capita consumption of sugar, such as the United States, Britain, Australia, Canada, and Sweden (with over 100 pounds per person per year) had the greatest incidence of polio [26]. In contrast, polio was practically unheard of in China (with its sugar use of only 3 pounds per person per year) [26].
Dr. Sandler claimed that sugars and starches lower blood sugar levels causing hypoglycemia, and that phosphoric acid in soft drinks strips the nerves of proper nourishment. Such foods dehydrate the cells and leech calcium from the body. A serious calcium deficiency precedes polio [26-29]. Weakened nerve trunks are then more likely to malfunction and the victim loses the use of one or more limbs [26:146].
Researchers have always known that polio strikes with its greatest intensity during the hot summer months. Dr. Sandler observed that children consume greater amounts of ice cream, soft drinks, and artificially sweetened products in hot weather. In 1949, before the polio season began, he warned the residents of North Carolina, through the newspapers and radio, to decrease their consumption of these products. That summer, North Carolinians reduced their intake of sugar by 90 percent– and polio decreased by the same amount! The North Carolina State Health Department reported 2,498 cases of polio in 1948, and 229 cases in 1949 (data taken from North Carolina State Health Department figures) [26:146;29].
One manufacturer shipped one million less gallons of ice cream during the first week alone following the publication of Dr. Sandler’s anti-polio diet. Soft drink sales were down as well. But the powerful Rockefeller Milk Trust, which sold frozen products to North Carolinians, combined forces with soft drink business leaders and convinced the people that Sandler’s findings were a myth and the polio figures a fluke. By the summer of 1950 sales were back to previous levels and polio cases returned to “normal” [26:146;29].
3. Can polio be treated? Paralytic polio is rarely permanent. Usually there is a full recovery [30-34]. Muscle power begins to return after several days and continues to improve during the next 12-24 months [30-34]. A small percentage of cases will experience residual paralysis. In rare cases, paralysis of the muscles used to breathe can lead to death [5:108;30-34].
Treatment mainly consists of putting the patient to bed and allowing the affected limbs to be completely relaxed. If breathing is affected, a respirator or iron lung can be used. Physical therapy may be required.
4. Does a polio vaccine exist?
In 1947, Jonas Salk, an American physician and microbiologist, became head of the Virus Research Laboratory at the University of Pittsburgh. He was interested in developing a polio vaccine. In 1952, Salk combined three types of polio virus grown in cultures made from monkey kidneys. Using formaldehyde, he was able to “kill” or inactivate the viral matter so that it would trigger an antibody response without causing the disease. That year he began his initial experiments on human subjects. In 1953, his findings were published in the Journal of the American Medical Association. And in April of 1954 the nation’s first polio immunization campaign, directed at school children, was launched [35]. However, shortly thereafter hundreds of people contracted polio from Salk’s vaccine; many died. Apparently, his “killed-virus” vaccine was not completely inactivated [1]. The vaccine was redeveloped, and by August 1955 over 4 million doses were administered in the United States. By 1959, nearly 100 other countries were using Salk’s vaccine [1,35].
In 1947, Jonas Salk, an American physician and microbiologist, became head of the Virus Research Laboratory at the University of Pittsburgh. He was interested in developing a polio vaccine. In 1952, Salk combined three types of polio virus grown in cultures made from monkey kidneys. Using formaldehyde, he was able to “kill” or inactivate the viral matter so that it would trigger an antibody response without causing the disease. That year he began his initial experiments on human subjects. In 1953, his findings were published in the Journal of the American Medical Association. And in April of 1954 the nation’s first polio immunization campaign, directed at school children, was launched [35]. However, shortly thereafter hundreds of people contracted polio from Salk’s vaccine; many died. Apparently, his “killed-virus” vaccine was not completely inactivated [1]. The vaccine was redeveloped, and by August 1955 over 4 million doses were administered in the United States. By 1959, nearly 100 other countries were using Salk’s vaccine [1,35].
In 1957, Albert Sabin, another American physician and microbiologist, developed a live-virus (oral) vaccine against polio. He didn’t think Salk’s killed-virus vaccine would be effective in preventing epidemics. He wanted his vaccine to simulate a real-life infection. This meant using an attenuated or weakened form of the live virus. He experimented with thousands of monkeys and chimpanzees before isolating a rare type of polio virus that would reproduce in the intestinal tract without penetrating the central nervous system. The initial human trials were conducted in foreign countries. In 1958, it was tested in the United States. And in 1963 Sabin’s oral “sugar-cube” vaccine became available for general use [1,35].
5. Which vaccine is in use today?
In 1963, Sabin’s oral vaccine quickly replaced Salk’s injectable shot. It is cheaper to make, easier to take, and appears to provide greater protection, including “herd immunity” in unvaccinated people. However, it cannot be given to people with compromised immune systems [1,35]. Plus, it is capable of causing polio in some recipients of the vaccine, and in individuals with compromised immune systems who come into close contact with recently vaccinated children [1,35-38]. As a result, in January 2000, the CDC “updated” its polio vaccine recommendations, reverting back to policies first implemented during the 1950s: Children should only be given the killed-virus shot. The oral polio vaccine should only be used in “special circumstances [39-41].
In 1963, Sabin’s oral vaccine quickly replaced Salk’s injectable shot. It is cheaper to make, easier to take, and appears to provide greater protection, including “herd immunity” in unvaccinated people. However, it cannot be given to people with compromised immune systems [1,35]. Plus, it is capable of causing polio in some recipients of the vaccine, and in individuals with compromised immune systems who come into close contact with recently vaccinated children [1,35-38]. As a result, in January 2000, the CDC “updated” its polio vaccine recommendations, reverting back to policies first implemented during the 1950s: Children should only be given the killed-virus shot. The oral polio vaccine should only be used in “special circumstances [39-41].
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References:
[1] Okonek BM, et al. Development of polio vaccines. Access Excellence Classic Collection, February 16, 2001:1. www.accessexcellence.org/AE/AEC /CC/polio.html
[2] Volk WA, et al. Basic Microbiology, 4th edition. Philadelphia, PA: J.B. Lippincott Co., 1980:455.
[3] Physician’s Desk Reference (PDR); 55th edition. Montvale, NJ: Medical Economics, 2001:778.
[4] Burnet, M., et al. The Natural History of Infectious Disease New York, NY: Cambridge University Press, 1972:16.
[5] Neustaedter R. The Vaccine Guide. Berkeley, California: North Atlantic Books, 1996:107–8
[6] Baby Center. The Polio Vaccine (0-12 months).http://www.babycenter.com/0_the-polio-vaccine_1566.bc [7] Moskowitz R. Immunizations: The Other Side. Mothering Spring 1984:36.
[8] Houchaus. Ueber Poliomyelitis acuta. Munch Med Wochenschr 1909; 56:2353–55.
[9] Lambert SM. A yaws campaign and an epidemic of poliomyelitis in Western Samoa. J Trop Med Hyg 1936; 39:41–6. [10] Lindsay KW, et al. Neurology and Neurosurgery Illustrated. Edinburgh/London/New York: Churchill Livingston, 1986:100. Figure 15.2. Polio incidence rates obtained from National Morbidity Reports.
[11] McCloskey BP. The relation of prophylactic inoculations to the onset of poliomyletis. Lancet, April 18, 1950:659–63.
[12] Geffen DH. The incidence of paralysis occurring in London children within four weeks after immunization. Med Officer 1950;83:137–40.
[13] Martin JK. Local paralysis in children after injections. Arch Dis Child 1950; 25:1–14.
[14] Hill AB, et al. Inoculation and poliomyelitis. A statistical investigation in England and Wales in 1949. British Medical Journal 1950; ii:1–6.
[15] Medical Research Council Committee on Inoculation Procedures and Neurological Lesions. Poliomyelitis and prophylactic inoculation. Lancet 1956; ii:1223–31.
[16] Sutter RW, et al. Attributable risk of DTP (Diphtheria and Tetanus Toxoids and Pertussis Vaccine) injection in provoking paralytic poliomyelitis during a large outbreak in Oman. Journal of Infectious Diseases 1992; 165:444–9.
[17] Strebel PM, et al. Intramuscular injections within 30 days of immunization with oral poliovirus vaccine—a risk factor for vaccine-associated paralytic poliomyelitis. New England J of Med, February 23, 1995:500+.
[18] Editorial. Provocation paralysis. Lancet 1992; 340:1005.
[19] Wyatt HV. Provocation poliomyelitis: neglected clinical observations from 1914-1950. Bulletin of Historical Medicine 1981; 55:543–57.
[20] Townsend-Coles, W.F and Findlay, G.M. Poliomyelitis in relation to intramuscular injections of quinine and other drugs. Trans R Soc Trop Med Hyg 1953; 47:77–81.
[21] Guyer B, et al. Injections and paralytic poliomyelitis in tropical Africa. Bull WHO 1980; 58:285–91.
[22] Bodian D. Viremia in experimental poliomyelitis. II. Viremia and the mechanism of the >provoking= effect of injections of trauma. Amer J Hyg 1954; 60:358–70.
[23] Wyatt HV. Incubation of poliomyelitis as calculated from time of entry into the central nervous system via the peripheral nerve pathways. Rev Infect Dis 1990; 12:547-56.
[24] Wyatt HV, et al. Unnecessary injections and paralytic poliomyelitis in India. Trans R Soc Trop Med Hyg 1992; 86:546–9.
[25] Chandra RK. Reduced secretory antibody response to live attenuated measles and poliovirus vaccines in malnourished children. British Medical Journal 1975; ii:583–5.
[26] McBean E. The Poisoned Needle. Mokelumne Hill, California: Health Research, 1957:116.
[27] Sandler B. American Journal of Pathology, January 1941.
[28] Sandler B. Diet Prevents Polio (Milwaukee: Lee Foundation for Nutritional Research, 1951).
[29] Allen H. Don’t Get Stuck: The Case Against Vaccinations. (Oldsmar, Florida: Natural Hygiene Press, 1985:166.
[30] Harry NM. The recovery period in anterior poliomyelitis. British Medical Journal 1938; 1:164–7.
[31] Sharrard W. Muscle recovery in poliomyelitis. J Bone Joint Surgery 1955; 37B:63–79.
[32] Affeldt JE, et al. Functional and vocational recovery in severe poliomyelitis. Clin Orthop 1958; 12:16–21.
[33] Hollenberg C, et al. The late effects of spinal poliomyelitis. Can Med Assoc J 1959; 81:343–6.
[34] Ramlow, J., et al. Epidemiology of the post-polio syndrome. American Journal of Epidemiology 1992;136:783.
[35] A Science Odyssey: People and Discoveries. Salk produces polio vaccine.www.pbs.org/wgbh/aso/databank/entries/dm52sa.html [36] Strebel PM., et al. Epidemiology of poliomyletis in U.S. one decade after the last reported case of indigenous wild virus associated disease, Clinical Infectious Diseases CDC, February 1992:568–79.
[37] Gorman C. When the vaccine causes the polio. Time October 30, 1995:83.
[38] Shaw D. Unintended casualties in war on polio. Philadelphia Inquirer June 6, 1993:A1.
[39] Morbidity and Mortality Weekly Report (MMWR): CDC. 2000; 49:1–22.
[40] Reuters Medical News. CDC publishes Updated Poliomyelitis prevention recommendations for the U.S., May 22, 2000.www.id.medscape.com/reuters/prof/2000/05/05.22/20000522plcy001.html
[41] The Associated Press. Polio cases caused by vaccine. The Santa Fe New Mexican, January 31, 1997.
[2] Volk WA, et al. Basic Microbiology, 4th edition. Philadelphia, PA: J.B. Lippincott Co., 1980:455.
[3] Physician’s Desk Reference (PDR); 55th edition. Montvale, NJ: Medical Economics, 2001:778.
[4] Burnet, M., et al. The Natural History of Infectious Disease New York, NY: Cambridge University Press, 1972:16.
[5] Neustaedter R. The Vaccine Guide. Berkeley, California: North Atlantic Books, 1996:107–8
[6] Baby Center. The Polio Vaccine (0-12 months).http://www.babycenter.com/0_the-polio-vaccine_1566.bc [7] Moskowitz R. Immunizations: The Other Side. Mothering Spring 1984:36.
[8] Houchaus. Ueber Poliomyelitis acuta. Munch Med Wochenschr 1909; 56:2353–55.
[9] Lambert SM. A yaws campaign and an epidemic of poliomyelitis in Western Samoa. J Trop Med Hyg 1936; 39:41–6. [10] Lindsay KW, et al. Neurology and Neurosurgery Illustrated. Edinburgh/London/New York: Churchill Livingston, 1986:100. Figure 15.2. Polio incidence rates obtained from National Morbidity Reports.
[11] McCloskey BP. The relation of prophylactic inoculations to the onset of poliomyletis. Lancet, April 18, 1950:659–63.
[12] Geffen DH. The incidence of paralysis occurring in London children within four weeks after immunization. Med Officer 1950;83:137–40.
[13] Martin JK. Local paralysis in children after injections. Arch Dis Child 1950; 25:1–14.
[14] Hill AB, et al. Inoculation and poliomyelitis. A statistical investigation in England and Wales in 1949. British Medical Journal 1950; ii:1–6.
[15] Medical Research Council Committee on Inoculation Procedures and Neurological Lesions. Poliomyelitis and prophylactic inoculation. Lancet 1956; ii:1223–31.
[16] Sutter RW, et al. Attributable risk of DTP (Diphtheria and Tetanus Toxoids and Pertussis Vaccine) injection in provoking paralytic poliomyelitis during a large outbreak in Oman. Journal of Infectious Diseases 1992; 165:444–9.
[17] Strebel PM, et al. Intramuscular injections within 30 days of immunization with oral poliovirus vaccine—a risk factor for vaccine-associated paralytic poliomyelitis. New England J of Med, February 23, 1995:500+.
[18] Editorial. Provocation paralysis. Lancet 1992; 340:1005.
[19] Wyatt HV. Provocation poliomyelitis: neglected clinical observations from 1914-1950. Bulletin of Historical Medicine 1981; 55:543–57.
[20] Townsend-Coles, W.F and Findlay, G.M. Poliomyelitis in relation to intramuscular injections of quinine and other drugs. Trans R Soc Trop Med Hyg 1953; 47:77–81.
[21] Guyer B, et al. Injections and paralytic poliomyelitis in tropical Africa. Bull WHO 1980; 58:285–91.
[22] Bodian D. Viremia in experimental poliomyelitis. II. Viremia and the mechanism of the >provoking= effect of injections of trauma. Amer J Hyg 1954; 60:358–70.
[23] Wyatt HV. Incubation of poliomyelitis as calculated from time of entry into the central nervous system via the peripheral nerve pathways. Rev Infect Dis 1990; 12:547-56.
[24] Wyatt HV, et al. Unnecessary injections and paralytic poliomyelitis in India. Trans R Soc Trop Med Hyg 1992; 86:546–9.
[25] Chandra RK. Reduced secretory antibody response to live attenuated measles and poliovirus vaccines in malnourished children. British Medical Journal 1975; ii:583–5.
[26] McBean E. The Poisoned Needle. Mokelumne Hill, California: Health Research, 1957:116.
[27] Sandler B. American Journal of Pathology, January 1941.
[28] Sandler B. Diet Prevents Polio (Milwaukee: Lee Foundation for Nutritional Research, 1951).
[29] Allen H. Don’t Get Stuck: The Case Against Vaccinations. (Oldsmar, Florida: Natural Hygiene Press, 1985:166.
[30] Harry NM. The recovery period in anterior poliomyelitis. British Medical Journal 1938; 1:164–7.
[31] Sharrard W. Muscle recovery in poliomyelitis. J Bone Joint Surgery 1955; 37B:63–79.
[32] Affeldt JE, et al. Functional and vocational recovery in severe poliomyelitis. Clin Orthop 1958; 12:16–21.
[33] Hollenberg C, et al. The late effects of spinal poliomyelitis. Can Med Assoc J 1959; 81:343–6.
[34] Ramlow, J., et al. Epidemiology of the post-polio syndrome. American Journal of Epidemiology 1992;136:783.
[35] A Science Odyssey: People and Discoveries. Salk produces polio vaccine.www.pbs.org/wgbh/aso/databank/entries/dm52sa.html [36] Strebel PM., et al. Epidemiology of poliomyletis in U.S. one decade after the last reported case of indigenous wild virus associated disease, Clinical Infectious Diseases CDC, February 1992:568–79.
[37] Gorman C. When the vaccine causes the polio. Time October 30, 1995:83.
[38] Shaw D. Unintended casualties in war on polio. Philadelphia Inquirer June 6, 1993:A1.
[39] Morbidity and Mortality Weekly Report (MMWR): CDC. 2000; 49:1–22.
[40] Reuters Medical News. CDC publishes Updated Poliomyelitis prevention recommendations for the U.S., May 22, 2000.www.id.medscape.com/reuters/prof/2000/05/05.22/20000522plcy001.html
[41] The Associated Press. Polio cases caused by vaccine. The Santa Fe New Mexican, January 31, 1997.
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