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— CH. 1 · INTRODUCTION —

Polio

13 min listen · Ch. 1 of 7
7 sections
  • Polio has been leaving its mark on human bodies for at least four thousand years. The earliest known physical evidence comes from the remains of a teenage girl unearthed at a burial site in the United Arab Emirates, her bones carrying the characteristic signs of a disease that would go on to paralyze hundreds of thousands of people every year at its peak. In ancient Egypt, paintings and carvings show otherwise healthy individuals with withered limbs, walking on canes. The word for the condition we now call poliomyelitis derives from the Ancient Greek words for grey matter and inflammation, a name first put to paper in 1874 by the German physician Adolf Kussmaul. What followed that naming was a century of fear, paralysis, and ultimately one of the most ambitious public health campaigns in human history. How did a disease once dismissed as a mild childhood ailment transform into the most dreaded epidemic of the twentieth century? And how close are we, really, to finishing it off?

  • Poliovirus belongs to a group of RNA viruses called enteroviruses, and its structure is deliberately simple: a single strand of genetic material wrapped in a protein shell called a capsid. That capsid is not decorative. It allows the virus to latch onto a specific receptor on cell membranes, a protein called CD155, and from there it hijacks the host cell's machinery entirely.

    The virus enters through the mouth, colonizes the pharynx and intestinal walls, and divides within gastrointestinal cells for roughly a week. From there it spreads to the tonsils, intestinal lymphoid tissue, and the deep cervical lymph nodes, multiplying all the while. It then enters the bloodstream, a stage known as viremia, and can survive and replicate in the blood and lymph for as long as seventeen weeks.

    In about one percent of infections, poliovirus migrates from the gastrointestinal tract into the central nervous system. Scientists acknowledge that this step confers no known benefit to the virus itself. It appears to be, in the source's own framing, an incidental deviation from a normal gut infection. Whether the virus crosses into the nervous system seems to depend largely on chance, not on the age, sex, or economic status of the individual.

    Three serotypes of poliovirus exist: types 1, 2, and 3. All three cause the same disease, but type 1 is the most commonly encountered and the one most tightly linked to paralysis. Wild poliovirus type 2 was certified eradicated in 2015, and type 3 followed in 2019. Type 1 is the last holdout.

  • Roughly 72 percent of people infected with poliovirus never know it. Another 24 percent develop minor symptoms: a sore throat, a low fever, fatigue that resolves within one to two weeks. The disease declares itself as something far more serious in only a small fraction of cases.

    When the virus reaches the central nervous system, it most commonly causes nonparalytic aseptic meningitis, with headache, neck stiffness, and pain in the back and limbs. Paralytic disease, the outcome most associated with polio in public memory, develops in about one to five cases per thousand. In those cases, the virus preferentially destroys the motor neurons of the spinal cord, brain stem, or motor cortex. Without signals from these neurons, the muscles they once governed atrophy and go limp. Paralysis typically sets in one to ten days after the first neurological symptoms and progresses over two to three days.

    The form of paralysis depends on which part of the nervous system the virus attacks. Spinal polio, which accounts for about 79 percent of paralytic cases, most commonly affects the legs. Bulbar polio, about two percent of paralytic cases, destroys nerves within the brain stem and can impair swallowing, breathing, and heart function. Bulbospinal polio, accounting for around 19 percent of paralytic cases, attacks the upper cervical spinal cord and paralyzes the diaphragm, often requiring mechanical ventilation to keep the patient alive.

    Age shapes the odds in a significant way. In children under five, paralysis of one leg is the most common outcome when paralysis occurs at all. In adults, paralysis can extend to the chest, abdomen, and all four limbs. Children face a case fatality rate of 2 to 5 percent from paralytic disease; in adults, that figure rises to between 15 and 30 percent.

  • For many who do develop paralysis, recovery is possible but follows its own timetable. Nerve impulses can return to a paralyzed muscle within a month, and in those cases full recovery generally comes within six to eight months. Half of patients with spinal polio recover completely; one-quarter recover with mild disability; the remaining quarter are left with severe permanent disability.

    The mechanism behind the best recoveries is striking. Surviving motor neurons can grow new branches, called axonal sprouts, that reach out to muscle fibers left without nerve connections by the dying neurons. A single motor neuron that previously controlled around 200 muscle cells may end up controlling 800 to 1,000 cells. The muscles also adapt through a process called myofiber hypertrophy, where exercise causes muscle fibers to enlarge, partially compensating for what was lost.

    But this compensation carries a long-term price. Between 25 and 50 percent of people who recovered from paralytic polio in childhood go on to develop post-polio syndrome, sometimes decades later. The syndrome brings new muscle weakness and extreme fatigue, thought to result from the eventual failure of those oversized motor units that carried extra load during recovery. Post-polio syndrome is not infectious, and those experiencing it do not shed the virus. There is no specific treatment. It progresses slowly, but it does progress.

    Complications of long-term paralysis extend beyond the muscles themselves. Asymmetric limb paralysis can slow the growth of an affected leg, causing scoliosis and gait problems. Equinus foot, in which the foot drops permanently toward the ground because the muscles that lift it are destroyed while those that pull it down remain intact, is a characteristic complication. The Achilles tendon retracts if the condition goes untreated, and the person can no longer walk on a flat foot.

  • Before the twentieth century, major polio epidemics were essentially unknown. Polio was an endemic disease spread by poor sanitation, which meant most infants encountered it early in life, suffered mild symptoms, and acquired lasting immunity. Mothers who had survived infection passed temporary protection to their babies through the placenta and through breast milk.

    The paradox of progress: as sanitation improved in Western countries during the late nineteenth and early twentieth centuries, herd immunity declined. Children grew up without early exposure, reaching an age when the disease struck harder. By 1950, the peak age for paralytic polio in the United States had shifted from infants to children aged five to nine, when the risk of paralysis is substantially greater. A third of all US cases by that point were occurring in people over fifteen.

    The worst single outbreak in US history came in 1952. Of nearly 58,000 reported cases that year, 3,145 people died and 21,269 were left with some degree of permanent paralysis. That crisis forced medical innovation in an unexpected direction: the first respiratory centers for patients who could not breathe independently, established that same year by Danish anesthesiologist Bjorn Ibsen at the Blegdam Hospital of Copenhagen, became the direct predecessors of the modern intensive care unit. A year later, Ibsen would open the world's first dedicated ICU.

    The iron lung, a large metal cylinder that kept patients alive by creating negative pressure around the body to force air in and out of the lungs, became the defining image of the epidemic era. It was designed as a temporary measure, typically needed for one to two weeks. For some patients, it became a permanent home.

  • In 1950, William Hammon at the University of Pittsburgh extracted gamma globulin from the blood plasma of polio survivors, demonstrating in a large clinical trial that it was about 80 percent effective at preventing paralytic disease. The supply was never enough to scale broadly, and attention turned to vaccines.

    Jonas Salk, also at the University of Pittsburgh, developed the first successful vaccine using poliovirus grown in monkey kidney tissue and chemically inactivated with formalin. On the 12th of April 1955, the results were announced to the world. Two doses of Salk's injected vaccine produced protective antibodies against all three serotypes in 90 percent or more of recipients. Three doses brought that figure to at least 99 percent.

    Albert Sabin took a different approach. His oral vaccine contained live but weakened poliovirus, produced by repeatedly passing the virus through nonhuman cells at low temperatures until it could no longer efficiently infect nervous system tissue. A single dose of Sabin's trivalent oral vaccine provided immunity to all three serotypes in about 50 percent of recipients. Three doses raised protection above 95 percent. Human trials began in 1957, the US National Institutes of Health selected Sabin's vaccine in 1958 over competing live-attenuated candidates, and it received its license in 1962.

    The oral vaccine had one crucial advantage and one dangerous flaw. It was cheap, easy to give, and replicated in the gut exactly where wild poliovirus lives. But the attenuated virus could be shed in the stool and transmitted to unvaccinated contacts, which was actually beneficial in communities with good coverage. In communities with poor coverage, that same virus could mutate over successive transmissions and revert to a form capable of causing paralysis. By 2017, cases of circulating vaccine-derived poliovirus outnumbered wild poliovirus cases for the first time, a direct consequence of wild polio falling to historic lows. An improved oral vaccine with greater genetic stability, called nOPV2, received full WHO licensure and prequalification in December 2023.

  • In 1988, when the Global Polio Eradication Initiative launched under the leadership of the World Health Organization, UNICEF, and the Rotary Foundation, there were an estimated 350,000 cases of wild poliovirus annually. The initiative would eventually employ 4,000 people across 75 countries and operate with a budget of nearly one billion US dollars per year, drawing roughly 30 percent of its funding from the Gates Foundation, 30 percent from developed governments, and 27 percent from countries at risk of infection.

    By 2001, wild case counts had fallen to 483. Progress was not linear. In 2003, religious leaders in northern Nigeria issued a fatwa declaring the vaccine was designed to sterilize children. Polio returned to Nigeria and spread outward to neighboring countries. In 2013, nine health workers administering the vaccine were killed by gunmen in Kano. Local traditional leaders and polio survivors rebuilt the campaign, and Nigeria was removed from the endemic list in September 2015 after more than a year without any cases. Africa as a whole was declared free of wild polio in August 2020.

    Afghanistan and Pakistan remain the last places on earth where wild poliovirus type 1 circulates naturally. In Afghanistan, the Taliban banned house-to-house vaccination between 2018 and 2021. In Pakistan, the CIA ran a fake hepatitis vaccination clinic in Abbottabad in 2011 to try to locate Osama bin Laden, an operation that severely damaged trust in vaccination programs across the region. Sixty-six vaccination workers were killed in 2013 and 2014 alone.

    The Americas were declared polio-free in 1994, the last known case being a boy in Peru in 1991. Europe followed in 2002. Southeast Asia was certified free on the 27th of March 2014. By that point, 80 percent of the world's population lived in certified polio-free regions. In 2022-30 confirmed wild cases were recorded worldwide, all in Pakistan and Afghanistan. The Polio Hall of Fame, dedicated in 1957 at the Roosevelt Warm Springs Institute for Rehabilitation in Warm Springs, Georgia, honors fifteen scientists and two laypeople whose work shaped the campaign. World Polio Day falls each year on the 24th of October, the birth date of Jonas Salk.

Common questions

What percentage of polio cases result in paralysis?

About one to five in 1,000 cases of poliovirus infection progress to paralytic disease. Approximately 72 percent of infections produce no symptoms at all, and another 24 percent cause only mild, temporary illness such as sore throat and fever.

Who developed the first polio vaccine and when was it announced?

Jonas Salk developed the first successful polio vaccine at the University of Pittsburgh, using chemically inactivated poliovirus grown in monkey kidney tissue. It was announced to the world on the 12th of April 1955.

What is post-polio syndrome and who gets it?

Post-polio syndrome is a slow, progressive condition that affects between 25 and 50 percent of people who recovered from paralytic polio in childhood. It produces new muscle weakness and extreme fatigue decades after the original infection, thought to result from the eventual failure of the enlarged motor neurons that compensated during recovery. There is no specific treatment.

How many wild polio cases were there in 2022?

In 2022, there were 30 confirmed wild poliovirus type 1 cases worldwide, with two in Pakistan and 20 in Afghanistan, plus eight in Mozambique - the first cases there since 1992. All were caused by a strain of Pakistani origin.

Which countries still have endemic wild poliovirus?

Afghanistan and Pakistan are the only two countries where wild poliovirus type 1 still circulates naturally. Wild poliovirus types 2 and 3 have been certified eradicated, in 2015 and 2019 respectively.

What is vaccine-derived poliovirus and why does it occur?

Vaccine-derived poliovirus (cVDPV) occurs when the weakened live virus in the oral polio vaccine spreads in communities with low vaccination coverage and mutates over successive transmissions, reverting to a form that can cause paralysis. By 2017, cases of vaccine-derived poliovirus outnumbered wild poliovirus cases for the first time. An improved oral vaccine with greater genetic stability, nOPV2, received full WHO licensure in December 2023 to address this risk.

All sources

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