Explaining Polio, pt. 2
The circumstantial case for injections as the cause of polio epidemics.
Polio series table of contents:
A summary and introduction is provided in Part 1, which also deals with the peculiar etiology of injection-provoked increased susceptibility to (paralysis from) polio virus.
Pt. 2: The advent of medical injections and the emergence of polio epidemics
iii.Polio and injections
Overview
Polio epidemics — large clusters of cases in different cities, states, and nations — did not occur before the late 19th century. Among many technological and social changes in this era, medicine transformed radically.
Needle injection in particular went from being almost unheard-of to a nearly ubiquitous tool of delivering medicine “overnight” at the turn of the century. The fad for injecting tonics was soon followed by the development of fantastic new serums and drugs to inject, producing cures more effective than anything dreamed of before — and these developments influenced the likelihood of children receiving injections.
The polio era proper begins in 1905, when just over a thousand cases are recorded in Sweden, resulting in a case rate of 19.5 per 100,000, whereas no previous epidemic compares. This is quickly followed by similar rates in the northern United States (which are diluted by inclusion of the overall population necessary to capture the increases of later decades).
The most significant medical development in history, in terms of first expanding needle injections to pediatric medicine and making the injection of children routine instead of rare, was the advent of clinical-grade diphtheria antitoxin in 1894.
This early watershed is quickly followed by reinforcing developments in injection medicine which are adopted at different rates in different countries: Diphtheria vaccines (1916-1926), tropical medicine in continental and island contexts (1920-1950), and other early modern vaccines (1940-1945), and finally penicillin (1943-1950).
It is only at the very end of this transition to routine injection of children, in 1949 and 1950, that an obvious relationship between injection and polio paralysis is noticed. If humans had been injecting children with things since the beginning of time, we might need to struggle to understand why such a link “suddenly” developed in 1949. Obviously, it is more likely that the link was there from the very beginning of the injection era in 1895, and simply went unnoticed.
Therefore, the default explanation for the emergence of polio epidemics is the novel practice of injection of children in pediatric medicine.
Early days: A novelty in human experience
The modern reader might simply take it for granted that children had always been injected, and therefore no immediate questions regarding the consequences of injection in childhood need be raised. In fact, the development of diphtheria antitoxin precedes the advent of injected vaccines and is seminal to the field of knowledge that would soon be termed immunology. For describing antitoxin in 1890, von Behring was awarded the first Nobel Prize for medicine eleven years later. For elaborating from studies on antitoxin to theories on the specificity of immune responses, Ehrlich received the prize a few years later.
Behind these technological leaps was a revolution in medical care for children. Previously, “vaccination” had meant simple scraping of shoulders with infected animal pus. Everything which was added later, to form the modern landscape of constant injection of children in the name of protecting them from every threat, was individually redundant to “the antitoxin era” which was already underway in the early 1900s. Thus, the antitoxin era is the injection era, and, is the polio era.
It is for this reason that some focus must be given to antitoxin despite the problem of timing. Diphtheria was a disease of the winter. If antitoxin injections were received in winter, then any provocation of polio which followed must have taken place the following summer — a delay which far exceeds the accepted, statistically-observed 30-day interim for polio provocation after injections. On the other hand, the eventual use of prophylactic antitoxin delayed natural immunity by preventing infections to begin with. This may have resulted in some disruption of diphtheria seasonality and a higher incidence of late injections as time went on.
Imprecise beginnings
Of course, the transition to routine use of diphtheria antitoxin injections does not immediately follow recognition of their value as a curative. Production of antitoxin is roughly comparable to vaccine preparation, with attendant difficulties regarding potency, purification, etc. — and the technology arrives only a few years after cities have begun to establish the types of laboratories capable of the work. For example, WH Park’s lab, which is able to produce a consistent antitoxin product in 1895 after beginning development in September of 1894,1 was located at the NYC Department of Health diagnostic laboratory — which had only been established the previous year in response to a cholera outbreak. Some time must therefore pass before substantial numbers of children experiencing diphtheria are likely to receive the novel treatment in all places.
Frederick S. Crum, in a 1917 statistical review of diphtheria, inserts over a decade into the division between the “pre-antitoxin period” and “antitoxin period” of various countries in the West and elsewhere, this division therefore representing the transition from what we might loosely term “rare” to “routine” antitoxin use. For Sweden, the “pre” period ends in 1893 and the antitoxin period begins in 1907; for a selection of cities in the US, it begins in 1910.
However, debate on the efficacy of serum is already underway in Swedish medical journals in 1895.2 Recorded deaths from diphtheria fall sharply around 1900 (some are skeptical of the role of antitoxin in this and other declines observed elsewhere; I am not). It can be inferred that antitoxin would have been used substantially in Sweden in 1905 and probably for several years before then.
The above visually offensive composite attempts to give a sense of the scale of diphtheria treatment compared to polio cases. Circa 1911, perhaps 250 to 340 individuals per 100,000 received an antitoxin injection annually in Sweden, based on the prevailing death rates in the immediate pre-antitoxin era.
This is roughly consistent with Crum’s survey of New York City in the same era. (I am inferring all of the weekly rates below to be annualized, as was a common presentation style of the time — thus a bit over 250 cases per 100,000 population are recorded per year.)
These of course would almost all be children. If the rate of polio in 1911 was 70 per 100,000 in Sweden, this would only be a portion of the number of children likely to have received an antitoxin injection the winter before — or later. In the New York City record, cases persist year-round.
Therefore diphtheria antitoxin injections alone, either in winter or afterward, are potentially sufficient to account for polio case rates up to 70 per 100,000 — a peak rarely exceeded in the West any time afterward.
This is an extremely crude treatment of diphtheria statistics; more detailed local records could be used. But it suffices, since drawing a precise relationship between antitoxin use and the initial emergence of polio epidemics is impossible, because epidemics were at the time not being measured precisely. Thus, the following comparison between Crum’s figures for antitoxin use in Pennsylvania and early polio cases recorded by Frost, et al., is offered merely to show the reader that such numbers that exist likely do not provide an accurate understanding of early polio.
The problem of early, small epidemics
1905 is the dawn of the polio age proper, but the novelty of polio epidemics being observed at all demands that earlier, smaller epidemics (e.g. in the Nordic states, and Vermont and Massachusetts) be explained.
Likewise, diphtheria antitoxin is a watershed in the use of injections in pediatric medicine, but it takes place during an era of widespread, general experimentation with injections of all sorts. It would have been the case that some local doctors in the West took up injection of children before the advent of antitoxin, applying tonics already in more widespread use among adults to respond to childhood illnesses. Despite its rural populace, Sweden in the late 19th century was home to a statistically literate medical class vying for political influence with the clergy and Crown. Upon the advent of antitoxin, skeptical opinion in Swedish journals in 1895 scolds other doctors, in Marie C. Nelson’s words, “not to fall for every new fashion that came along”3 — and so of course it must have already been the case that some doctors, somewhere in Sweden, were already wont to do exactly that as of 1895. And such “new fashions” would have included injection of tonics. It is no great stretch to imagine that some doctors in New England — itself a pioneer in public health intrusiveness — also went for some injection-related fads in the years immediately prior to the advent of antitoxin. Antitoxin merely “democratizes” a problem, namely injection of children, that was likely already taking place in obscure medical practices beforehand. And so it is probably because of antitoxin that polio epidemics transition from a remote curiosity to a universal headache in the West.
Antitoxin did not displace the likely growing practice of medically injecting children generally. In fact, it may have increased faith in pediatric injection, including for diphtheria treatment. One possible example of such an effect comes from a 1906 monograph:4
In severe cases, and in all cases treated on the third day or later, 8,000 units should be given immediately, and this dose repeated at intervals of 12 hours if the membrane is not separating and signs of improvement are not apparent. In some cases a third injection may be necessary, and rarely a fourth. […]
In addition to being used as a curative agent, diphtheritic antitoxin can also be used as a prophylactic remedy in persons exposed to infection, an injection of 500 units being sufficient to protect for three weeks.
Antitoxin should always be injected and never given by mouth, either side of the abdomen being the most suitable site. […]
Strychnine should be injected hypodermically on the occurrence of symptoms of heart failure. Rolleston recommends adrenalin chloride 1 in 1,000 in doses of five to ten minims, four hourly
It is unlikely, in general, that the most severe and heavily-treated cases of diphtheria are responsible for most polio cases. For example, when it comes to such invasive procedures as tracheotomy, little suspicion is warranted, because a good portion of children who reached this state died before recovery anyway.
Still, the above quote provides an example of a case where the logic “injection follows injection” seemed to direct thinking; even milder cases frequently featured multiple injections in short duration. Given the stark difference in paralysis rates in Bodian’s experiments for macaques injected twice or just once with inert needles,5 this could explain an outsized and prolonged provocation danger from early antitoxin care.
To make some sort of sense of these nuances, we will here draw comparisons between countries and regions with distinct injection regimes over the entire polio age, to show that areas with more injections of children had more polio epidemics.
First, some basic facets of the relationship between polio virus ecology and observed paralysis epidemics deserve attention.
iv. The ecology of polio virus
Upon the turn and throughout the first half of the 20th Century, some “mysterious agent” was rendering humans of all ages more susceptible to paralysis from polio virus infection. (As previously noted, this series will deal with the concept in this fashion to point out features of the polio problem that are implacable, rather than a burden created specifically by the injection theory.)
The mere existence of this “mysterious agent” is implied by the emergence of polio paralysis epidemics, and at the same time the agent provides satisfactory explanation for their mere existence: Whereas the virus had been with humans for some time, one might as well say “forever,” the essential rareness of post-infection paralysis meant that seasonal patterns of polio infection did not lead to substantial numbers of local children becoming paralyzed in certain months anywhere on Earth.
The “mysterious agent,” by making post-infection paralysis more common, led to precisely this observation in certain locales. And once it had been observed in some place for the first time, it was with few exceptions routinely observed in the future, rendering the seasonality of the polio virus obvious.
There ends the most straight-forward conclusion. Anything further is complicated by the differences in regional polio virus exposure (the natural ecology of the virus and its host) and exposure to whatever our “mysterious agent” is. Polio exposure can either be individually protective or harmful — depending on whether, for a given individual, it precedes or follows exposure to the mysterious agent which confers susceptibility. The local ecology of the virus makes different outcomes more or less likely for any given individual.
The virus detection tool
Still, a significant insight is available to help guide predictions of what would be observed in different places and different times: The “mysterious agent” is itself a method for detecting polio virus. When the agent is applied to a population, the natural ecology of the polio viruses becomes visible in the “reflection” of paralysis cases, which correspond to a larger mass of seasonal infections which are free of any serious outcome:
It is for this reason, as well as a historical accident, that so much of the ecology of polio was correctly described in the early deductions of Frost and others. Early thinkers reached for insights recently made possible from the improved detection of diphtheria via culture, and diphtheria immunity via the subcutaneous application of professionally prepared toxin (the Schick test): Diphtheria was readily detected in apparently healthy children; adults possessed widespread immunity; immunity was attained later in life in rural children compared to those in cities. Diphtheria cases were thus merely a reflection of a universal childhood infection that typically does not result in clinically recognized illness. In rural areas, such infections occurred less frequently and therefore later in childhood. From the fact that most polio cases occurred in the young, but in rural areas older children as well, therefore, polio was predicted to follow the same ecology, over a decade before the virus and immunity could be detected in a widespread fashion like diphtheria.
Once more sensitive methods became available to detect polio virus and antibodies, these early inferences, along with later speculations that there were multiple iterations of polio virus (three serotypes in all), were validated.
Staying invisible
The point above is that once the “mysterious agent” arrived in a certain region, the local ecology of the virus was reliably reflected in paralysis cases — or so it would seem. But it also follows that in some regions the mysterious agent could have been present without revealing the local ecologies, because unless the agent is applied to a substantial number of individuals before natural polio infection occurs, paralysis epidemics would not be observed. Applying the mysterious agent to the already-immune, say to adults alone, is harmless, and prevents detection of the local virus ecology.
For this reason, the ecology of the virus in tropical areas remained (mostly) invisible until the advent of other methods of detection, e.g. cell culture. (This transition has already been discussed in “What Polio Was Not.”)
The question therefore is at what age did polio find un-immune hosts in different regions, and were individuals at this age within the “reach” of the unknown agent that conferred susceptibility to paralysis. If only individuals who were probably already naturally immune were within the same reach, then the local ecology of polio would remain invisible. In short, it will be true for most regions that if the agent is applied to children, epidemics follow; if only to adults, epidemics are less likely.
Finally, in regions where natural polio infections are delayed for many years by isolation — namely in islands — this age divide will not be observed, and paralysis epidemics will follow whether or not children are (also) within reach of the mysterious agent.
From problem to solution
The ground is now set to offer different models for what should have been observed if needle injections of children provoked polio epidemics beginning with the local advent of injections like diphtheria antitoxin (i.e. if, per the needle theory, provocation can occur for several months after injection). We need not be comprehensive, but merely establish a few templates:
v. The circumstantial evidence, generally and in NYC, the Solomon Islands, and the UK / Germany
Before and after antitoxin
The following is a rough overview of medical developments which influenced pediatric injection before and after the advent of antitoxin:
With regards to the West, general observations are that injections in preschool age children may have declined in the 1920s, and that the United Kingdom and Germany were unexpected holdouts to embracing early vaccines.
Now for specifics.
New York City: An early leader
In New York City, the newly-formed diagnostic laboratory of the Department of Health appoints WH Park a director’s position to work on diphtheria in 1894. Along with Anna Williams, Park cultivates a strain of diphtheria capable of producing toxin efficiently, which begins three decades of world leadership in toxin and antitoxin research. In January of 1895, forty horses are already under treatment with toxin in order to produce antitoxin serum, and the resulting product is soon shipped to health departments elsewhere in the anglosphere.
Park, along with testing of prophylactic antitoxin injection of contacts, begins testing of his toxin-antitoxin vaccine in New York in 1913, and this seems to be the only active investigation outside of Germany for the next decade.
Von Behring in 1913 first introduced toxin-antitoxin mixtures for human use. Since 1913, Park and his collaborators in New York have, by their combined clinical and laboratory studies, and through large scale employment of such mixtures, led in the campaign for the control of diphtheria through specific prevention.6
Park’s vaccination campaigns reach a scale equaled nowhere else for several years.7 Still, they are unlikely to have been very relevant in the major early epidemics in the city in 1907 and 1916. And by the time that polio epidemics arrive in the city in the early 20th Century, antitoxin treatment for acute cases is widespread throughout the West.
Therefore, more suspect is Park’s antitoxin injection campaigns of family contacts of diphtheria cases, though he is unclear on the year in which these begin:
The next important means of controlling diphtheria [since 1892] was diphtheria antitoxin. […] The two most striking instances in our own experience in the control of diphtheria occurred one in 1894 and the other in 1915. In the first an outbreak in a large children’s institution was controlled by giving every inmate a dose of 300 units of antitoxin. The other was a large insane asylum where some forty cases had developed within twenty-four hours. […] For a number of years our inspectors in New York City yearly injected between ten and fifteen thousand children belonging to families in which diphtheria occurred.8
The language obviously allows for a wide range of starting dates for this aggressive yearly treatment of “ten to fifteen thousand children” in the city. Was it after 1894? After 1915?
At all events, at least the 1916 polio epidemic (9,345 cases) and perhaps the 1907 epidemic (2,500 cases) in New York City, both which resulted in global record numbers, may have been related to Park’s family contact injection campaigns.
It is however the case that abundant other routes of “provocation” likely prevailed in 1916 in the city. These resulted from the botched public health response, which sought to identify, hospitalize, and medically “treat” every polio case possible, even though no benefit had ever been demonstrated from any such interventions. (It would seem to have simply been assumed that “So goes diphtheria treatment, goes polio treatment.”)
In general, it may be said that WH Park’s New York City was a hotspot for injection in the diphtheria antitoxin era, and it was a hotspot for polio epidemics as well. This at least weakly supports the injection theory. Nothing can really be satisfactory here, without knowledge of whether children experiencing paralysis in New York’s epidemics had actually been injected.
It has already been mentioned (in regard to the toxin theory) that this same WH Park was later instrumental in a successful polio vaccine trial, which was wrongly ignored in 1935. One can only speculate if Park’s motivations were personal — if he had recognized, but not published, some link between his efforts to thwart diphtheria in New York City, and trends in paralyzed kids during polio epidemics.
Solomon Islands?: Another early leader
While polio epidemics were blooming throughout industrialized nations in the early 20th century, a few remote islands also reported epidemic outbreaks of paralysis.
Here the background history and “expected” ecology of the paralytic polio should be reviewed. The tropical islands in question had already been “crashed” by European explorers in the colonial era, likely resulting in the introduction of long-unknown viruses, but without any recorded outbreaks of polio paralysis.
In terms of the “expected” ecology of the polio viruses, it is likely that all such early contact with Europeans introduced long-unknown polio to tropical islands where the viruses had gone extinct. And, during and after the colonial era, the virus would continue to die out and be reintroduced into these populations, and yet paralysis epidemics did not occur. In fact, no-occurrence of epidemics likely remains the “norm” in remote communities until the twilight of the polio age. It is only the exceptions — those islands where the “mysterious agent” has arrived — which begin to experience epidemics before the polio vaccine era.
Per, again, our “expected” ecology, it would only be after the local introduction of needle injection that subsequent reintroductions of polio virus to tropical islands would result in paralysis epidemics, due to injection provocation. These would be limited to whichever particular islands had come under the bullseye of tropical medicine.
In absence of a thorough investigation of preceding injection practices in each-and-every island outbreak, we may consider the isolated case of the Solomon Islands, a Polynesian nation colonized by Britain (and briefly Japan) which experienced several polio epidemics after 1925.
The first and second of these took place in 1925 and 1929 and were retroactively described by AB Cross.9 Cross’s figures for the both epidemics, as it happens, can be interpreted in the context of overall prevalent diseases described by TR Ritchie and N Crichlow in the same years.10 This results in the clear association of an early island polio epidemic with a recent injection campaign:
Cross, 1977
The recorded history of the Solomon Islands begins with their discovery in 1568 by the Spaniard Alvaro de Mendana [no polio epidemics resulted] […] In the late 1700s, with the upsurge of Pacific exploration, the islands renewed their contact with Europe [no polio epidemics resulted] […]
The first medical practitioner to study the Solomon Islands was Guppy, the surgeon on H.M.S. Lark in the 1880s, who in his book on the islands, in the section on prevalent diseases, does not mention any condition suggestive of poliomyelitis […] The naturalist and later resident commissioner, C. M. Woodford, writing in the 1890s on his three visits to the islands, states: “. . . Cripples and deformities of longstanding are seldom seen”. […]
The 1925 Epidemic
The first well-documented epidemic suggestive of acute anterior poliomyelitis was recorded in the Annual report of the Medical Department for 1925. […] As far as can be ascertained there were fifty-six cases […] thirteen known deaths.
The 1929 Epidemic
In 1929 there is no doubt that there was a severe epidemic of acute anterior poliomyelitis. […] totalling 276 confirmed cases of whom sixty-three died. […]
[A} table in a unsigned report on the epidemic gives the age incidence as follows: 1-3 years 8 per cent, 4-12 years 44 per cent, 13-20 years 16 per cent, 21-40 years 30 per cent and above 40 years 2 per cent.
Before reading Ritchie and Crichlow’s remarks on injections in the years before these epidemics, it may be noted that the low rate of polio paralysis in natives above 40 years old in 1929 suggests that the virus which spread on the island this year had also sparked an outbreak some decades prior, but without causing paralysis, due to the lack of injections.
Now, for the relevant injection campaign histories:
TR Ritchie, 1925
I have the honour to submit the annual report of the Department of Health for the year ended 31st March, 1925. […]
Yaws (Frambœsia tropica).—In April, 1923, as a result of the Natives agreeing to a medical tax of £1 per adult male, free medical treatment was instituted, and steps were immediately taken to organize a systematic campaign against this disease. Although a considerable amount of work had been done before that date, systematic work was impossible, as most of the Natives were not prepared to pay the charges made for treatment. This preliminary work was of value in disseminating amongst the population a knowledge of the (to them) miraculous results obtained from injections of novarsenobillon. It was found impossible to cover the whole Territory in the year, but in those districts attended to 32,366 injections were given. This year the whole area was covered, and 21,222 injections given. […]
During the first round numbers of small children with primary and commencing secondary lesions were not offered for treatment, but during the year under review such children were offered much more freely.
Crichlow, 1929
Yaws is the commonest disease. On Malaita the infection-rate is 60, on Makria 65, per cent. […] Yaws is one of the greatest factors in producing the heavy sick-rate and high infant mortality.
During the year 1928, 900 injections of N.A.B. [/ novarsenobillon] were given at Tulagi hospital, 5,000 injections among free natives by the Traveling Medical Officer, and 30,000 injections by the Rockefeller Foundation Campaign on Malaita.
In sum: Several thousand injections were given to treat Yaws in the Solomon islands immediately before the island’s first two polio epidemics, in 1925 and 1929.
The UK (and Germany): Late hold-outs
No major polio epidemics occur in the UK or Germany until after WWII. Coincidentally, both countries (despite geopolitical animus) are nests of robust anti-vaccine sentiment. Additionally, the public health culture in the UK insists on a progressive-era-vintage viewpoint that disease is a problem of the lower classes; as such, British MOsH emphasize treatment and confinement of those already ill with diphtheria over prevention of novel infections via vaccination.
Diphtheria vaccination is not embraced in Germany until 1935. The UK follows suit in the early years of WWII.
Both nations therefore are holdouts to injection of children in the 1930s; and do not experience large-scale polio epidemics until after WWII.
This is consistent with the injection theory. Only the delay in “punishment” for the UK’s embrace of diphtheria vaccination — the first epidemic is not until 1947 — dampens an obvious proof that the embrace of pediatric injection in 1941 is to blame.
Two points shore up the injection theory in this regard. First of all, British soldiers are among the first (between the UK, New Zealand, and the United States) to be observed to experience high rates of polio paralysis on deployment to the Middle East in WWII. This offers an earlier “punishment” for Britain’s embrace of injections than the local 1947 epidemic. Second, when polio epidemics do hit home in the UK, the link between recent injections and epidemic paralysis is rapidly noticed (whereas it had gone unnoticed for decades in America and continental Europe). Thus: When the country most reluctant to embrace pediatric injection finally did so (in 1941), only two years passed between the first polio epidemic (in 1947) and the recognition of injection provocation (in 1949).
To repeat from the summary above:
If humans had been injecting children with things since the beginning of time, we might need to struggle to understand why such a link “suddenly” developed in 1949. Obviously, it is more likely that the link was there from the very beginning of the injection era in 1895, and simply went unnoticed.
If you derived value from this post, please drop a few coins in your fact-barista’s tip jar.
Park, WH. Williams, AW. “The Production of Diphtheria Toxin.” J Exp Med. 1896 Jan 1; 1(1): 164–185.
Marie C. Nelson (1994). Diphtheria in late-nineteenth-century Sweden: policy and practice. Continuity and Change, 9, pp 213-242 doi:10.1017/ S0268416000002277
ibid.
Miller, JW. “The Treatment of Diphtheria.” Hospital (Lond 1886). 1906 Aug 4; 40(1037): 313–315.
FitzGerald, JG. “Diphtheria Toxoid as an Immunizing Agent.” Can Med Assoc J. 1927 May; 17(5): 524–529.
Park, WH. Schroder, MC. Zingher, A. “The Control of Diphtheria.” Am J Public Health (N Y). 1923 Jan; 13(1): 23–32.
ibid.
Cross, AB. “The Solomon Islands tragedy--a tale of epidemic poliomyelitis.” Med Hist. 1977 Apr; 21(2): 137–155.
Ritchie, TR. “Mandated Territory of Western Samoa: Annual Report of the Department of Health for the Year Ended 31st March, 1925.”
Crichlow, N. “The Prevalent Diseases of the British Solomon Islands.” Transactions of the Royal Society of Tropical Medicine and Hygiene. Volume 23, Issue 2, August 1929, Pages 179-184 https://doi.org/10.1016/S0035-9203(29)90568-X
Tangentially related:
Deposition rates of viruses and bacteria above the atmospheric boundary layer
https://www.nature.com/articles/s41396-017-0042-4
I am reminded of this.... I listened to a Twitter space a few months ago. A doctor was relaying conversations she had had with some colleagues who were plastic surgeons. It was a bit gruesome but may be of interest to you wrt 'it's repeat injection' as described in your recent posts. It went like this.
These plastic surgeons sometimes carry out lower body surgery for various reasons a bit of tightening, or filler or remodelling. What they said was that patients were getting necrosis of said lower regions and it seemed to be linked to them having had covid injections and Botox injections close together and that the time between injections was a factor. They were recommending I think 6 weeks apart to reduce the chances of necrosis.
They didn't speculate on any mechanism for this and thankfully no pictures (!)