Why did polio become lethal since the 1880s? – Part 1

Polio is a much-feared disease that has been dramatically reduced by vaccines. India is polio-free since 2014 as a result of Oral Polio Vaccine campaigns undertaken since 1995. After type 2 polio virus was globally eradicated in 2015, two types of polio virus still remain (types 1 and 3), so a modified vaccine (only for these two types) has been used since 2016 during mass immunization events. In addition, a fractional‑dose Inactivated Poliovirus Vaccine has been part of routine childhood immunization since 2016. 

The world now awaits the global eradication of all strains of polio. This doesn’t mean, though, that all forms of childhood paralysis will be eradicated. Inflammation of the gray part of the spinal cord – from which the word poliomyelitis derives its name – is caused also by other viruses, bacteria and toxins. Acute Flaccid Polio will therefore continue and will require its own separate treatments. 

In this piece, however, my focus is on something mysterious that happened 145 years ago: a puzzle which has not yet been solved. It is about the sudden rise in polio cases and lethality from around 1880. 

1. Polio was a mild disease in the past

Records show that polio cases in the past were sporadic and limited to the paralysis of lower limbs. Then, from the 1880s, large epidemics of polio, some of which were also highly lethal, started emerging. Most peculiarly – as thoroughly documented in multiple studies and early textbooks on polio – many of these epidemics were accompanied at the same time by paralysis and deaths in animals including dogs, horses, calves, pigs, fowl, sheep and cats. This happened despite the fact (which became known much later) that the polio virus is only found in humans and doesn’t jump across animals.

I outline below six theories that seek to explain this phenomenon. But before doing that, how can we be sure that polio was not actually rampant in the past but merely ignored in the midst of other diseases? That couldn’t have happened because, as Neal Nathanson noted in 2010, “The disease’s striking presentation, in which previously healthy infants underwent an acute febrile illness followed by localized paralysis, would have made outbreaks conspicuous”0F. And so, the question remains.

Records show that one of the earliest polio epidemics occurred in 1881 in Umea in north Sweden with 18 cases, followed by 43 cases in Stockholm in 1887. Epidemics then emerged across Norway, the UK, Austria, Canada and the USA. Deaths from polio were rare in the past but were now becoming common. (Polio becomes lethal mainly when the virus goes into the brain stem (bulbar polio) and paralyses respiratory muscles. Paralysis occurs when the virus focuses on the lumbar area of the spine.) 

Sweden, 3,602 died out of 23,254 polio cases between 1905 and 1944, with a case fatality rate (CFR) of 15.5%. The peak mortality was during the 1916 polio epidemic in the USA when an estimated 6,500 people died from 27,000 cases, a CFR of 24% (New York, with 2,407 deaths from 8,928 cases had a CFR of 26.9 per cent; the CFR for children under two years was 51.3%, with 83% of those who died being below the age of 5). Mortality rates then stabilised or slightly reduced, even as paralytic cases dramatically increased. In the following years, there was also a shift in the age distribution of those affected towards older ages. Franklin Roosevelt got polio in 1921 at the age of 39. 

Regarding tropical developing countries, we don’t have much information in that period. A 1914 textbook noted that 30 per cent of Nauru was struck with the polio epidemic in 1910 and in India, polio [presumably paralytic] “is very common among the native children during the hot weather” and that “these children are of a notoriously low nutritional status”. There were also sporadic reports in the first half of the 20th century that Europeans or American soldiers living in poor countries had higher rates of polio paralysis than the local population. 

2. Facts to be explained

Many questions arise. Why did polio go from being a mild, sporadic and endemic disease to epidemic? Why did it shift from a disease that rarely killed, into a lethal disease? Why did many initial epidemics occur in rural areas? Why was lethality often (not always) more in the upper classes? Why did American soldiers abroad experience more polio than the community in which they lived? Why did epidemics arise mostly in summer (but not always)? Why did the age distribution of polio cases shift towards higher age groups? Why did animals get paralysis and even die exactly at the time of the early epidemics? 

Any explanation will need strong biological logic and must also provide laboratory proof. Finally, the explanation will need to be consistent with the typical symptoms of polio: an incubation period, fever, and paralysis without loss of sensation. 

3. Theory 1: Sanitation reduced immunity to polio

The theory most widely accepted today, which Neal Nathanson called the “central dogma” of poliomyelitis epidemiology, is that improvements in sanitation led to increase in polio. Let’s call this the “excess sanitation” theory. According to this, improvements in sanitation and water supply reduced early-life exposure to poliovirus, thus delaying primary infection to older ages when the risk of severe polio is supposedly greater. The example of chickenpox is given, in which getting the disease for the first time at an older age can lead to severe outcomes.

The 14th edition (2021) of the Pink Book (published by the CDC) summarised: “Before the 18th century, polioviruses probably circulated widely. Initial infections with at least one type probably occurred in early infancy, when transplacentally acquired maternal antibodies were high and protected infants from infection-causing paralysis. In the immediate prevaccine era, during the first half of the 20th century, improved sanitation resulted in less frequent exposure and increased the age of primary infection, resulting in large epidemics with high numbers of deaths”.

END OF ARTICLE