Last time we went over a brief history of the polio vaccine and the disease itself. This time we’re going to focus on some of the diagnostic issues and some other factors that may have contributed to the increase in polio cases.
What is AFP?
Before moving on, let’s look closer at the paralysis caused by polio. Specifically it is called acute flaccid paralysis (AFP), and it’s a term which describes the weakening or paralysis of a muscle and/or loss of muscle tone. Polio is not the only cause. It can be caused be several different things. In fact, Marx et al compiled a list of 26 possible causes of AFP.(1)
Here is a list of possible causes for AFP:
2) Enterovirus (non-polio)
3) VAPP (vaccine associated paralytic poliomyelitis)
4) Rabies virus
5) Varicella-zoster virus
6) Japanese encephalitis virus
7) Guillain-Barre syndrome
a) Acute inflammatory polyradiculoneuropathy
b) Acute motor axonal neuropathy
c) Cytomegalovirus polyradiculomyelopathy
8) Intramuscular gluteal injection
9) Acute transverse myelitis
10) Epidural abscess
11) Spinal cord compression; trauma
12) Exotoxin of Corynebacterium diphtheriae
13) Toxin of Clostridium botulinum
14) Karwinskia humboldtiana, K. calderoni
15) Tick bite paralysis
16) Lyme borreliosis
17) Myasthenia gravis
18) Nondepolarizing drugs
20) Viral myositis
22) Toxic myopathies
23) Hypokalemic periodic paralysis
24) Gossypol, licorice
25) Critical illness polyneuropathy
26) Thick filament myopathy
Diagnostic/Data Problems in the US
Why does it matter that AFP has other causes? It has to do with diagnosis of polio, and how that can affect the perceived effectiveness of a vaccine. In order to accurately assess the effectiveness of the polio vaccine, we need to know how many cases there were before the vaccine was introduced, and how many there are after. The CDC would have you believe that we have this information. But unfortunately if we actually look closely, we find that we do not. Sure we have numbers of reported cases, but the problem lies with the diagnosis of the disease, and how the diagnosis criteria changed from pre 1954, to post 1961. Let’s take a look at some of these diagnostic issues.
How were cases of polio counted before and during 1954? The diagnostic criteria were based on the WHO definition at the time:
“A patient is considered clinically to have poliomyelitis for purposes of notification if the symptoms and signs correspond with the following descriptions:
(a) Non-paralytic poliomyelitis
An illness characterized by fever, headache, vomiting, sore throat, listlessness, stiffness of neck and pack; pains in the back, neck trunk, or limbs, and hyperaesthesia; cerebrospinal fluid changes are usually found. The diagnosis is often strongly supported by epidemiological evidence; for example, known contact with a paralytic case or residence in an epidemic area.
(b) Spinal paralytic poliomyelitis
Signs and symptoms of non-paralytic poliomyelitis with the addition of partial or complete paralysis of one or more muscle groups, detected on two examinations at least 24 hours apart.”(2)
Here’s another source:
“There has been a decided shift in clinical concepts during the past twenty-five years as to what constitutes a case of poliomyelitis. For instance, more cases of non-paralytic poliomyelitis are so designated in the 1930’s and 1940’s than was the situation in the 1920’s. But, on the other hand, it has become increasingly difficult to define a case of non-paralytic poliomyelitis. For instance, in the present day when extensive muscle testing is performed, transient weaknesses lasting only a day or two have been designated as “paralytic cases” and thus the problem of definition has again shifted with a tendency for an increase in the relative percentage of paralytic cases.(emphasis added)”(3)
So all it takes for a diagnosis of polio in 1954 was partial paralysis of a muscle group tested twice at least 24 hours apart accompanied by signs and symptoms of nonparalytic poliomyelitis. Now the CDC has already said concerning nonparalytic poliomyelitis: “These syndromes are indistinguishable from other viral illnesses.”(4)
How about in 1955? What were the diagnostic criteria used?
“In 1955 the criteria were changed to conform more closely to the definition used in the 1954 field trials:residual paralysis was determined 10 to 20 days after onset of illness and again 50 to 70 days after onset”. (5)
That’s a big change in diagnostic criteria. We’ve already seen from the CDC that “Many persons with paralytic poliomyelitis recover completely and, in most, muscle function returns to some degree.”(4)By changing the diagnostic criteria from paralysis 24 hours apart, to 2 months apart, they have pretty much guaranteed that the number of paralytic polio cases would decrease, regardless of whether the vaccine was used or not.
Here’s an interesting quote from Paul Meier, a statistician who has written on the 1954 Salk trials, which affirms the over diagnosis of polio:
“Next, we said, the diagnosis of polio is tricky, but we need to have the entire country’s physicians participate, because we can’t look over every case where there’s some kind of paralysis. So physicians reported the cases they thought were polio according to the protocol, and we accepted those cases. Now about half those cases were probably not polio at all, but still, we did have total reported cases, compared with paralytic and nonparalytic cases.”(6)
Now by 1960, how is poliomyelitis diagnosed? By this time in order for a diagnosis to be confirmed as polio, there must be a positive virus test on a stool sample.
“The diagnosis is made by identifying poliovirus in clinical specimens (usually stool) obtained from an acutely ill patient.”(7)
Below you’ll find a chart of reported cases of paralytic poliomyelitis by year from the CDC.
There are a couple of things to be aware of in this chart. From 1955 to 1960, only the Salk vaccine was being used. This was a killed virus vaccine. In 1961, the Sabin oral polio vaccine was introduced, which quickly replaced the IPV. If you look closely at this data, you’ll find that from 1957 to 1958, there is a 48% increase in paralytic cases reported. Between 1958 and 1959, there is another 70% increase in paralytic cases reported!
Due to the drastic change in diagnostic criteria, comparing the pre 1954 polio numbers to the post 1961 numbers is dishonest. You’re comparing apples and oranges. Yet this is exactly what the mainstream medical community does. They use these numbers to demonstrate how amazing mass vaccination campaigns are. To get an accurate view of the polio vaccine, we need to do one of two things. Either we need to compare pre-vaccine numbers to current levels that include all causes of AFP, or we can only look at data after 1961 to assess the effectiveness of the vaccine.
We’ve already gone over the fact that there are 25 other causes of AFP, other than the wild polio virus, so in order to make a valid comparison, it would be nice if we could compare the total number of cases of AFP that occurs today to the number of polio cases diagnosed in the pre-vaccine era. This is easier said than done, because a lot of these causes aren’t tracked, so nobody knows how prevalant they may be. Take tick paralysis as an example.
“There is no national surveillance system for tick paralysis and reliable information on incidence does not exist”(8)
Nevertheless, let’s look at a few examples of the other causes in order to get a general idea of the scope of the issue.
Guillain-Barre syndrome – The annual incidence globally is 1-2 per 100,000 population.(1) The incident rate really varies by age from .62 to 2.66 per 100,000.(9) The current US population is estimated to be about 316 million. So for Guillain-Barre syndrome, there are between 3160 and 6320 new cases every year. A study done in 2003 suggested that the symptoms exhibited by Franklin Delano Roosevelt, who was thought to suffer from poliomyelitis, were more likely to be Guillain-Barre syndrome.
“The diagnosis at the onset of the illness and thereafter was paralytic poliomyelitis. Yet his age and many features of the illness are more consistent with a diagnosis of Guillain-Barré syndrome”(10)
Acute transverse myelitis – There are 1,400 new cases of transverse myelitis diagnosed each year in the United States.(11)
Myasthenia gravis – There are estimated to be between 3 and 30 new cases of myasthenia gravis per million population every year. McGrogan et al said “However, it is thought that the rates at the upper end of this range, reported by the prospective studies, provided the most accurate estimates.”(12) So 30 cases per million is likely the more accurate number. In the US, that would be between 948 and 9480 new cases every year.
|BOX 1It is interesting to note that the cited list of AFP causes may not be exhaustive. That study which was done in the year 2000 does not mention West Nile virus, which is now known to cause a polio-like illness in some infected individuals. The incident rate of neuroinvasive disease from West Nile Virus varies by state. There are 3 states with a greater than 1 in 100,000 incidence, and 10 more states with an incidence between 0.25 and 0.99 per 100,000.(13) It is unclear how many of these neuroinvasive West Nile cases resulted in AFP.West Nile Virus Neuroinvasive Disease Incidence by State – United States, 2013
If we add up just the three causes of Guillain-Barre syndrome, acute transverse myelitis, and myasthenia gravis, we get the annual incidence of AFP in the US to be 5508 – 17200. That doesn’t include the other 22 causes of non-polio AFP listed in the 2000 study, or the cases of AFP caused by West Nile virus! I’m not claiming that all of these cases of acute flaccid paralysis would have been diagnosed as polio, but it is reasonable to believe that the majority of the cases could have been.
We can’t come to any solid conclusions about the effectiveness of the polio vaccine for getting rid of polio based on this data. However, we can say that based on the diagnostic criteria in 1954, ‘polio’ still exists today.
Worldwide polio and AFP
We’ve seen how the lack of consistent diagnostic criteria in the US has led to a huge difficulty in assessing the true effectiveness of the polio vaccine. So what about worldwide data? Surely we can get more accurate numbers to evaluate the vaccine by looking at the cases in vaccine programs around the world. Alas, that is not the case. Doctors used lameness surveys, looking for people with deformed or shriveled legs, presuming that such problems were caused by polio, and then extrapolated that data to cover the surrounding areas which weren’t directly surveyed. Here is a case definition for the lameness surveys:
“The case definition used most frequently consists of (1) flaccid paralysis with atrophy, (2) no decrease in sensation, and (3) a history of acute onset with no subsequent progression of disease.”(14)
This source also states
“Some variation is to be expected, but the specificity of the case definition is a reasonable concern. Also, the case definition has not been applied uniformly.”(14)
And here is the WHO’s recommended surveillance standard:
“Highly sensitive surveillance for acute flaccid paralysis (AFP), including immediate case investigation, and specimen collection are critical for the detection of wild poliovirus circulation with the ultimate objective of polio eradication.”(15)
What the WHO and the lameness surveys do is try to ascertain all cases of acute flaccid paralysis, with the reasoning that polio will be a part of that group, and so they can target that area for vaccination programs. This is very similar to what happened in the US, in that we start with all cases of AFP, rather than just cases due to polio, so we can’t compare data from these surveys to outcomes of the vaccination programs.
According to the WHO:
“In 1988, when the Global Polio Eradication Initiative began, polio paralysed more than 1000 children worldwide every day.”(16)
That means that polio paralyzed over 350,000 kids every year! This statistic has been called into question however. In 2007, Dr. Jacob Puliyel, head of pediatrics at St Stephens hospital in Delhi said:
“WHO claims five million children have been saved from polio paralysis. It is instructive to see how this figure is arrived at. In 1988, there were 32,419 cases of paralytic poliomyelitis. The WHO arbitrarily raised this number ten-fold to 350,000 claiming incomplete reporting. In 2004 with the changed definition, only culture positive paralysis was considered polio and there were 2000 such cases. Subtracting 2000 from 350,000, the WHO calculated that 348,000 children were saved from paralysis that year.”(17)
The WHO has done a nice job of monitoring cases of polio and AFP in several countries since 1996. So let’s take a look at an example of the effectiveness of these worldwide polio eradication campaigns. (18)
What the heck is going on with this huge increase in AFP? It looks like polio was finally eradicated in 2012, but what would it look like if they used the same lameness surveys as outcome markers for their campaign? Again, Puliyel examines this situation in 2012 in the Indian Journal of Medical Ethics:
“It has been reported in the Lancet that the incidence of AFP, especially non-polio AFP has increased exponentially in India after a high potency polio vaccine was introduced (25). Grassly and colleagues suggested, at that time, that the increase in AFP was the result of a deliberate effort to intensify surveillance and reporting in India (26). The National Polio Surveillance Programme maintained that the increased numbers were due to reporting of mild weakness, presumably weakness of little consequence (27). However in 2005, a fifth of the cases of non-polio AFP in the Indian state of Uttar Pradesh (UP) were followed up after 60 days. 35.2% were found to have residual paralysis and 8.5% had died (making the total of residual paralysis or death – 43.7%) (28). Sathyamala examined data from the following year and showed that children who were identified with non-polio AFP were at more than twice the risk of dying than those with wild polio infection (27).”(19)
So Dr. Puliyel points out that the increase in AFP is not due to better surveillance that picked up more cases of mild weakness, as had been claimed, but rather these AFP cases are even more deadly than wild polio. Puliyel goes on to say:
“Data from India on polio control over 10 years, available from the National Polio Surveillance Project, has now been compiled and made available online for it to be scrutinised by epidemiologists and statisticians (29). This shows that the non-polio AFP rate increases in proportion to the number of polio vaccine doses received in each area.”(19)
There are a couple of takeaways from this assessment. Non-polio AFP seems to be twice as deadly as paralytic polio, and cases of non-polio AFP go up in relation to the number of polio vaccines received. It is beyond the scope of this book to look into the reasons for this. However, this will hopefully serve as a reminder to us all that disease control is typically not a single factor issue. If we look at the US, we see that polio disappeared rather quickly especially compared to developing countries. We should not underestimate the role that sanitation plays in the control and eradication of disease.
Data from 1961 to the present
So we’ve seen that it is impossible to make a good comparison by using data from 1954 and prior. Even during the rest of the 1950’s, it may be difficult to trust the data. Observer bias can greatly affect the reported cases. For example, if you’re a doctor during this time period, and you’re told that the vaccine is 80-90% effective at preventing paralytic polio, then what do you do when you examine somebody who is exhibiting signs of paralytic polio (acute flaccid paralysis). The first thing you would likely do is to ask them if they received the polio vaccine. If they say yes, and you believe in the effectiveness of the vaccine, you would likely come up with a different diagnosis.
“In fact, I am certain that many health officers and physicians here will ask routinely if a child has been vaccinated when signs of poliomyelitis are present during the summer months. We have been conditioned today to screen out false positive cases in a way that was not even imagined prior to 1954”(5)
This is one of the reasons why it is imperative for us to only compare confirmed cases of polio. By 1960, testing for the poliovirus in stool samples was required in order for a case to be confirmed as polio.
Ignoring the possibility that some of these paralytic cases were in fact VAPP (paralysis caused by the vaccine), let’s assume that these were all confirmed cases of wild polio. Using this data, the best case scenario for the vaccine would be that it was able to reduce paralytic polio from 2525 cases per year to zero. That’s still pretty good, but it’s about 12% of the number that is typically cited by the CDC:
“Polio reached a peak in the United States in 1952, with more than 21,000 paralytic cases.”(4)
It’s definitely possible that the number of paralytic cases prevented by the vaccine is higher than this, however it’s difficult to have any confidence in the data prior to the polio cases being confirmed via testing of stool samples. Even though it’s not nearly as impressive as is often stated, it does appear that the polio vaccine was effective at getting rid of polio. However, before we come to any conclusions, it would be wise to further explore any other factors which may have played a role in the sudden appearance of epidemics of poliomyelitis.
What other factors may be linked to the rise in polio in the 20th century?
We’ve already gone over the sanitation theory, which is the main argument for the epidemics of polio we experienced in the mid 20th century. We’ve also seen how the sanitation theory fails to explain why developing countries began to experience epidemics of polio despite any advancements in their sanitation. So what are some other factors that may help to explain the sudden increase in paralytic polio?
There are several studies that point to something called provocation polio.(1, 20-24) Basically what they say is that getting an intramuscular injection while having a polio infection can cause a relatively benign infection to become paralytic. The virus will typically multiply in the nose, throat, and GI system without causing any symptoms. Normally, this type of infection will lead to immunity to the polio virus. However, if a muscular injury is sustained during this time, specifically a medical injection, it can cause the polio virus to spread to the central nervous system (CNS). The reason for this is that the injection causes retrograde axonal transport to occur, which then facilitates invasion of the CNS by the polo virus. A study was done in 1998 by Gromeier and Wimmer, trying to simulate provocation poliomyelitis in mice.
“Muscle injury due to injection of vaccines or therapeutic agents is common in medical practice. It has been observed that, if concurrent with PV infection, such injury may increase the risk of neurological complications …we have shown that muscular trauma induced by multiple injections can lead to rapid progression of PV-induced paralysis”(24)
Looking back on the data from 1957-1959, there was a 48% increase of paralytic polio cases reported between 1957 and 1958, and another 70% increase between 1958 and 1959. Was this increase caused by the polio vaccine? I believe that the Salk vaccine likely contributed to the increase in polio, because it was administered via an injection, and thus caused provocation polio. However it was not necessarily (except for the Cutter Incident) the ingredients in the vaccine that caused the increase. Wild-polio was still circulating widely at the time, and the mass vaccination programs created a lot of muscular trauma. This is why we don’t have an increase in polio today even though we’ve been using the injected IPV since 2000. There is no circulating polio virus.
The thing to remember is that it doesn’t have to be injection with the polio vaccine to cause this provocation polio. It can be any injection, whether it be another vaccine, antibiotics, medications, or whatever. In fact, if we look at history, we find that the diphtheria and pertussis vaccines were introduced and recommended in the 1940’s. And by the mid 1940’s they were in regular use.
Per the CDC’s pinkbook chapter on Pertussis:
“[Pertussis vaccine] was developed in the 1930s and used widely in clinical practice by the mid-1940s.” (25)
As we can see from this graph, cases of polio were steadily rising in the 1940’s.
It’s a little bit easier to visualize the steady rise in polio cases in the above graph. Unfortunately, before 1951 polio cases were not separated into paralytic and non-paralytic cases, so we’re unable to get a more accurate view of the effects of these other vaccines on paralytic cases. Several studies(26-28) have been done which corroborate the fact that the risk of paralysis is greater following some sort of injection. Here’s an excerpt from one such study:
“Seventeen cases are described in which paralysis of a single limb has occurred within 28 days of receiving an injection. Of these fifteen followed immunization and two penicillin.”(28)
Another study by Greenberg et al, demonstrates this concept very well:
“This investigation corroborates the published findings of other investigators that there is a relationship between recent inoculation with diphtheria toxoid, tetanus toxoid or pertussis vaccine (DPT) and the development of paralytic poliomyelitis.”(29)
Anybody familiar with the polio scare back in the mid 20th century will surely think of the iron lung. The iron lung was used for those people who suffered from the most severe type of polio infection called bulbar polio. This occurs when the polio virus makes its way to the brain stem, which can lead to difficulties speaking, swallowing and breathing, and can ultimately result in death. Having your tonsils removed has been shown to significantly increase your risk for developing bulbar polio. For a long time, tonsils were thought of as being nothing more than vestigial organs that the body no longer needed. They were taken out on a whim. It is a little bit less common today than it was back in the mid 20th century, but it is still a fairly common procedure.(30)
There are quite a few sources supporting this idea that tonsillectomy contributes to a higher risk of developing bulbar polio.(31-35) In fact in 1938, Albert Sabin, replicated bulbar polio in monkeys who had received a tonsillectomy. (31)
From the American Journal of Public Health, we find this:
“The results of these studies are singularly consistent in demonstrating that a history of tonsillectomy is from two to three times more frequent in patients with bulbar than it is with patients having spinal or nonparalytic poliomyelitis.”(35)
Writing about the pros and cons of tonsillectomy, AH Gale had this to say:
“But a more important matter is that of the possible association between tonsillectomy and poliomyelitis of severe bulbar type. Everyone has heard of the five children of one family in Akron, Ohio, who had their tonsils removed in August, 1941, and all developed bulbar poliomyelitis, of which three died. The sixth and youngest child, who was not operated upon, did not develop poliomyelitis, although excreting poliomyelitis virus in the faeces.”(36)
And just how common were tonsillectomies?
“Between 1915 and the 1960s, [tonsillectomy/adenoidectomy] was the most frequently performed surgical procedure in the United States.”(37)
“In 1959, 1.4 million tonsillectomies were performed in the United States. This number had dropped to 260,000 by 1987, when it was the 24th most common indication for hospital admission”(30)
There is a theory (the toxin theory/DDT theory) which postulates that cases of poliomyelitis may actually have been caused by exposure to pesticides such as DDT, and had nothing to do with the polio virus. The problem with this theory is that it fails to account for the reduction in poliomyelitis cases following the introduction of the vaccine, and prior to DDT being banned in the United States. On the other hand, the viral theory (the idea that the polio virus is the sole cause of poliomyelitis) fails to explain why prior to the 19th century, epidemics of poliomyelitis were practically unheard of, even though the polio virus was highly endemic in humans. Instead there is intriguing evidence that insecticides such as DDT and the lead arsenate used before it, were important co-factors in the development of epidemics of paralytic polio. It was environmental toxins combined with the circulating virus which ended up causing these epidemics of polio. There is a lot of information to digest with this theory, and Dan Olmstead and Mark Blaxill do an excellent job of breaking it down.(38) I highly recommend taking the time to read through their presentation in it’s entirety. Below is an interesting graph from their presentation:
Dr. Morton Biskind had early concerns about DDT, and stated in 1950:
“… it is known that not only can DDT poisoning produce a condition that may easily be mistaken for polio in an epidemic but also being a nerve poison itself, may damage cells in the spinal cord and thus increase the susceptibility to the virus.”(39)
There is some evidence that shows exposure to DDT may increase the replication of the polio virus. Janis Gabliks looked at the replication effects of various insecticide compounds on the vaccinia and polio viruses:
“In the poliovirus tests the cell response was not uniform. In comparison to the controls the virus yield in the DDT-treated cultures was slightly increased”(40)
Olmstead and Blaxillbelieve it was a different mechanism than that stated by Dr Biskind, which caused the increasing polio epidemics:
“… our fundamental idea is that both the poliovirus and the pesticide enter the body by the same route — they are ingested — and both end up in the stomach. There, the toxin could damage the stomach lining in such a way that the virus gains access to peripheral nerves. This kind of virus-toxin interaction (perhaps with arsenic or lead acting alone as the toxin) took place sporadically before 1890 and increased dramatically, we propose, with the invention of more potent insecticides like lead arsenate. With the advent of DDT, the interaction became even more dangerous, dramatically increasing the number of cases.”(38)
Regardless of the causative mechanism, more research needs to be done in this area in order to come to a better understanding of the role of environmental toxins, such as lead arsenate and DDT, on the emergence of poliomyelitis epidemics.
From the preceding information, it seems pretty clear that multiple factors were involved in the sudden emergence of poliomyelitis epidemics. An interesting question that remains to be answered is what would happen to the prevalence of paralytic polio infections, if all of the other risk factors besides the virus were eliminated? We know that before the 20th century, these epidemics were pretty much unheard of, so was the chance of a paralytic infection during this time period still 1 in 200 cases? I’m inclined to believe that without being exposed to these other risk factors, the chance of a paralytic infection is probably much lower. To my knowledge, no study has been done to examine this idea, and I doubt one will be done anytime soon given the fact that the poliovirus has been eradicated from the Western Hemisphere.
(1) Differential Diagnosis of Acute Flaccid Paralysis and Its Role in Poliomyelitis Surveillance, Arthur Marx, Jonathan D. Glass, and Roland W. Sutter. Epidemiologic Reviews, Vol. 22, No. 2, 2000. http://epirev.oxfordjournals.org/cgi/reprint/22/2/298.pdf
Yale Journal of Biology and Medicine p 327-340 Julian Irving Pichel
Yale J Biol Med. 1950 March; 22(4): 327–340.
(4) Epidemiology and Prevention of Vaccine-Preventable Diseases, The Pink Book: Course Textbook, 11th Edition (May 2009), Chapter 16, Poliomyelitis. http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf
(5) The Present Status of Polio Vaccines (a panel discussion), Illinois Medical Journal, August, 1960.
(6) A Conversation with Paul Meier, Harry M. Marks. Clinical Trials 2004, 1, 131. http://www.hopkinsmedicine.org/histmed/people/faculty/papers/meier.pdf
(10) Goldman.2003.”What was the cause of Franklin Delano Roosevelt’s paralytic illness?” J Med Biog, 11:233-240.
(14) Some Observations on Poliomyelitis Lameness Surveys, Roger H. Bernier, Reviews of Infectious Diseases, Vol. 6, Supplement 2. International Symposium on Poliomyelitis Control (May – Jun., 1984), pp. S371-S375
(17) Polio eradication & the future for other programmes: Situation analysis for strategic planning in India (Editorial), Jacob S. Puliyel, Manoj Anand Gupta, Joseph L. Mathew, Indian J Med Res 125, January 2007, pp 1-4 http://jacob.puliyel.com/download.php?id=132
(18) WHO, Immunization Monitoring, Diseases, Poliomyelitis Case Count, accessed multiple times between May 1 and June 1, 2010. http://apps.who.int/immunization_monitoring/en/diseases/poliomyelitis/case_count.cfm
(19) http://www.issuesinmedicalethics.org/202co114.html Indian J Med Ethics. 2012 Apr-Jun;9(2):114-7.Polio programme: let us declare victory and move on.Vashisht N, Puliyel J.
(20) The Relation Between Recent Injections and Paralytic Poliomyelitis in Children. Morris Greenberg, Harold Abramson, Helen M. Cooper and Helen E. Solomon. American Journal of Public Health, 1952, 42, 142-152. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1525737/pdf/amjphnation00407-0031.pdf
(21) Intramuscular Injections Within 30 Days of Immunization with Oral Poliovirus Vaccine – A Risk Factor for Vaccine-Associated Paralytic Poliomyelitis. Peter M. Strebel, Nicholae Ion-Nedelcu, Andrew L. Baughman, Roland W. Sutter, and Stephen I. Cochi. New England Journal of Medicine, 1995, 332, 8, 500-506. http://www.nejm.org/doi/pdf/10.1056/NEJM199502233320804
(22) Poliomyelitis: 20 years–the Pondicherry experience. Mahadevan S, Ananthakrishnan S, Srinivasan S, Nalini P, Puri RK, Badrinath S, Rao RS. The Journal of Tropical Medicine and Hygiene. 1989 Dec;92(6):416-21. http://www.ncbi.nlm.nih.gov/pubmed/2558226
(23) Outbreak of poliomyelitis due to type 3 poliovirus, northern India, 1999–2000: injections a major contributing factor. Kathryn A Kohler, W Gary Hlady, Kaushik Banerjee and Roland W Sutter, International Journal of Epidemiology, 2003, 32, 272-277. http://ije.oxfordjournals.org/content/32/2/272.full.pdf+html
(24) Mechanism of Injury-Provoked Poliomyelitis, Matthias Gromeier and Eckard Wimmer. Journal of Virology, June 1998, p. 5056-5060. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC110068/pdf/jv005056.pdf
(26) McCloskey BP. The relation of prophylactic inoculations to the onset of poliomyletis. Lancet, April 18, 1950:659–63.
(27) Geffen DH. The incidence of paralysis occurring in London children within four weeks after immunization. Med Officer 1950;83:137–40.
(28) Martin JK. Local paralysis in children after injections. Arch Dis Child 1950; 25:1–14.
(29) The Relation Between Recent Injections and Paralytic Poliomyelitis in Children. Morris Greenberg, Harold Abramson, Helen M. Cooper and Helen E. Solomon. American Journal of Public Health, 1952, 42, 142-152. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1525737/pdf/amjphnation00407-0031.pdf
(31) Experimental Poliomyelitis by the Tonsillopharyngeal Route: With Special Reference to the Influence of Tonsillectomy on the Development of Bulbar Poliomyelitis. Albert B. Sabin.J Am Med Assoc, Aug 1938; 111: 605 – 610. http://jama.ama-assn.org/cgi/content/summary/111/7/605
(32) Studies on a Long Range Association Between Bulbar Poliomyelitis and Previous Tonsillectomy. R. V. Southcott. The Medical Journal Of Australia. 1953. Aug 22;2(8):281-98. http://www.ncbi.nlm.nih.gov/pubmed/13098558
(33) Occurrence of Poliomyelitis in Relation to Tonsillectomies at Various Intervals. Franklin H. Top. Journal of the American Medical Association. 1952, 150(6) 534-538. http://jama.ama-assn.org/cgi/content/summary/150/6/534
(34) Absence of Tonsils as a Factor in the Development of Bulbar Poliomyelitis, Gaylord W. Anderson, Jeanne L. Rondeau. The Journal of the American Medical Association, 1954, 155 (13) 1123-1130. http://www.ncbi.nlm.nih.gov/pubmed/13174358
(35) Tonsillectomy and Poliomyelitis. American Journal of Public Health, 1954, 44 (8) 1065-1067. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1620872/pdf/amjphnation00361-0092.pdf
(36) “Pros and cons of Tonsillectomy” A. H. Gale. BMJ 1951, 20 January. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2068074/?page=1
(39) Morris S. Biskind, M.D., “Statement on Clinical Intoxication From DDT and Other New Insecticides, Presented before the Select Committee to Investigate the Use of Chemicals in Food Products, United States House of Representatives, December 12, 1950.” Journal of Insurance Medicine, May 1951.
(40) Arch Environ Health. 1967 May;14(5):698-702.Insecticidal compounds. Effects on replication of vaccinia and polio viruses in human chang-strain liver cells. Gabliks J.