The art of medicine
Polio provocation: solving a mystery with the help of history
In 1998, State University of New York researchers Matthias Gromeier and Eckard Wimmer published a pioneering article on the mechanism of injection-induced polio paralysis. Through their laboratory work, they discovered that tissue injury produced by an injection aided the poliovirus to infect the body and readily journey to the spinal cord. For the first time, health professionals working in polio endemic regions had scientific evidence that paediatric injections could incite paralysis.
Substantiation of the theory seemed to vindicate the cautious policies of the 1950s and the importance of maintaining herd immunity against polio. In countries where the virus was controlled through vaccination programmes, the risk of polio provocation was insignificant. However, in regions where polio was endemic, immunisation sequence mattered until eradication of the virus was achieved. The discovery showed that polio vaccination was vital to the wider success of public health programmes and that it needed to be undertaken before other paediatric immunisations to reduce the risk of provoking polio.
One of the first medical procedures implicated in the causation of polio was tonsil surgery. A study of more than 2000 case histories in the 1940s by the Harvard Infantile Paralysis Commission concluded that tonsillectomies led to a significant risk of respiratory paralysis due to bulbar polio. Although proponents of the theory did not entirely oppose tonsillectomies, they cautioned that such interventions should be avoided during epidemics. Reflecting the growing body of evidence that tonsillectomies could provoke polio, many doctors in the USA adjusted their surgical procedures to account for disease-endemic factors. “The policy of the United States Army”, Major-General E A Noyes acknowledged in 1948, “has been to stop tonsil and adenoid operations during epidemics”. Even though laboratory technology at the time was not sufficiently advanced to unravel the mechanism, published evidence affected clinical practice.
Concerns about tonsillectomies coincided with indications that paediatric injections could also incite polio paralysis. Evidence of this correlation was first published by German doctors, who noted that children who had received treatment for congenital syphilis later became paralysed in the injected limb. Although further studies from Italy and France corroborated this link, it was not until the end of World War II that injection-induced polio emerged as a public health concern.
The application of epidemiological surveillance and statistical methods enabled researchers to trace the steady rise in polio incidence along with the expansion of immunisation programmes for diphtheria, pertussis, and tetanus. A report that emerged from Guy’s and Evelina Hospitals, London, in 1950, found that 17 cases of polio paralysis developed in the limb injected with pertussis or tetanus inoculations. Results published by Australian doctor Bertram McCloskey also showed a strong association between injections and polio paralysis. Meanwhile, in the USA, public health researchers in New York and Pennsylvania reached similar conclusions. Clinical evidence, derived from across three continents, had established a theory that required attention.
Several ideas were posited by health professionals in an effort to understand how immunisations for diphtheria, tetanus, and pertussis seemed to provoke polio infection. One theorist posited that injections injured human tissues and predisposed them to viral infection. A further theory advanced by Harold K Faber of the Stanford University School of Medicine argued that the ubiquitous poliovirus, already present on the skin of many children, was being driven into the body during immunisations and thus seeded deep into the tissue.
Meanwhile, American newspapers advised parents to postpone vaccinations during warm weather or epidemics, citing evidence that some children developed polio within a month of injection. As debates swirled and publicity mounted, parents were asked to weigh the potential risks of immunisations with their benefits.
… the American Public Health Association, accommodated the possibility of polio provocation and encouraged health professionals to avoid “indiscriminate” injections and “booster shots” during epidemics.
Most health professionals reformed their immunisation practices and accepted that seasonal factors and cycles of disease were important to consider before immunising children.
Although medical scientists failed to understand the epidemiological mechanism behind polio provocation, the Salk and Sabin vaccines pushed the issue to the margins of clinical attention.
Chronic Neuroimmune Diseases
Chronic Fatigue Syndrome
A polio by another name
But a body of evidence is growing linking Chronic Fatigue Syndrome (CFS), also called myalgic encephalomyelitis (ME), to this terrible disease, largely caused by attempts to eradicate polio. An alternative polio seems to be upon us.
The proceedings of the first intemational scientific conference on the Post-Polio Syndrome in the US have been collated in the Annals of the New York Academy of Science. It includes 50 papers written by 118 contributors from a wide range of specialties, including clinical neurology.
In particular, papers by Dr Richard Bruno, assistant professor at the New Jersey Medical School’s department of physical medicine and rehabilitation and director of Post-Polio Rehabilitation and Research Service at the Kessler Institute for Rehabilitation in New Jersey, and four other specialists compare Chronic Fatigue Syndrome and Post-Polio Syndrome (Dalakas, et al, ed. The Post Polio Syndrome: Advances in the Pathogenesis Treatment,Annals, NY Academy, Sciences, 1995: 273: 1-409). Post-Polio is developing in those who had polio 25-30 years previously. Clinically, it is indistinguishable from CFS.
Other researchers demonstrate that CFS is just another form of polio, which has increased with the advent of polio vaccination. As one type of gut virus has been eradicated, so other forms have had the space to proliferate. Up to one in every 500 Americans may have CFS, according to the Centers for Disease Control.
To understand the link one needs to understand the microbiological habits of both polio and other enterovirus disease-that is, gut bugs.
A historical accident has led to various names being given to viruses, all of which share physical , chemical and epidemiological characteristics of what we consider the classic polio virus, which science refers to as polio viruses 1, 2, and 3 (Dowsett: Journal of Hospital Infection, 1988:11:103-15). ln 1948, a polio-like illness in New York state prompted scientists to culture the virus. But what grew looked to them at that time like a new virus.
They called it “Coxsackie’ after the small town up the Hudson River where it was found. And they called the disease “Atypical Polio” because its symptoms identified it as a kind of polio, despite the virus being apparently different.
This kind of polio, “Atypical Polio,’ has since been renamed, ‘Chronic Fatigue Syndrome,’ or ME. But it remains a kind of poIio despite the change of name. and newer technology has shown up the generic similarities of the most frequent agent that causes it.
These techniques place Coxsackie, the virus most often implicated in CFS, in the polio family tree, along with so-called echo viruses. Coxsackie has been further divided into Coxsackie type A (with 24 viruses) and Coxsackie type B (six viruses ). There are 34 echo viruses. In total, there are at least 72 enteroviruses in all, with new ones still being discovered.
All this has been unnecessarily confusing and complicated, even for doctors. These days newly discovered enteroviruses are just given a new number, not a new name, since their inter-relationship is recognized.
Had the techniques been available that we now have at our disposal, all these viruses might simply have been called “Polio 1 through 72.”