The End of Epidemics: The Looming Threat to Humanity and How to Stop It

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To the memories of

Dr. D. A. Henderson, a tenacious and ultimately victorious

leader in the battle to end the scourge of smallpox.

and

Nurse Salome Karwah, an Ebola survivor who saved many lives

and later was left to die in childbirth, a victim of stigma.

Unless otherwise specified, all dollar amounts are U.S. currency.

ACRONYMS

PROLOGUE

A FEAR I’D NEVER FELT BEFORE

What can be done to stop the next killer virus from destroying millions of lives?

Following a frightening meeting with my staff at the peak of the West Africa Ebola crisis, I asked myself, What would it take to prevent such devastating epidemics? A new pandemic could kill more than 300 million people worldwide. It could also reduce global GDP by 5 to 10 percent—an impact equivalent to the financial crisis of 2008. There will always be new outbreaks of infectious diseases. But as a medical doctor and a global health leader, I know that by following the prescriptions laid out in this book, it is within the power of modern public-health leaders to keep such outbreaks from exploding into catastrophic epidemics that kill thousands or millions.

I was more alarmed than I had ever been in my 35 years of working in public health. The world was facing a potentially global catastrophe unlike anything I, or any of my colleagues, had ever seen. In response to the fears of my far-flung staff, I knew I had to be straightforward and talk frankly and calmly about the crisis.

It was a rainy Thursday morning, October 9, 2014, and 100 of us were stuffed into a classroom-sized room where I was hosting a videoconference for the global health nonprofit that I led, Management Sciences for Health (MSH). More than 500 staff members from our home office near Boston, and those in field offices in Africa, Asia, and Latin America, were huddled around our various communication devices, listening intently. We had all read or heard appalling reports from medical teams on the ground in West Africa, where the Ebola virus was spinning out of control, condemning thousands of people—including some of our own beloved colleagues—to horrific deaths. At this moment, some team members were reporting in from ground zero in Liberia, where the epidemic was rampaging.

The treatment facilities are overrun with cases, they told us. Whole parts of the health system are at a standstill. Staff and patients are scared away. Patients refuse to go to community health centers; they see them as places to die. Corpses are lying in the streets. Women were delivering babies without trained help. Malaria cases were going untreated, adding to the death toll. In defiance of ancient traditions in which families lovingly touch and swaddle the dead, villagers were being instructed by strange people in alien-looking plastic moon suits not to hug each other, shake hands, or touch their loved ones.

With the risk to our staff, why are we there? someone sitting near me asked.

It was an obvious question. And we all wondered about the follow-on: Where would Ebola travel next, given all the remote places MSH operated in around the planet? Thomas Duncan, the first Ebola patient in the U.S., had died just the day before at Texas Health Presbyterian Hospital in Dallas. Which city would be next? Paris? Tokyo? Moscow? Mexico City? Right here, where some of us were sitting, in Boston? Symptoms didn’t show up for several days. Unknowingly infected people who had been in West Africa could be coming to our offices.

I was especially worried for our staff in the hot zone. Ian Sliney, our stiff-upper-lipped British colleague, candidly admitted that, despite taking all precautions, he was worried. What could I tell him and the others? Ian and hundreds like him were real heroes, first responders on the front lines of the outbreak. They were taking their temperatures constantly and dousing their hands, arms, feet, and everything else in chlorine.

I know there is a lot of fear out there and also among you, I said. But, in good conscience, we can’t not be involved. I then read a letter from Niniola Soleye, a staff member in Nigeria. Her aunt, a doctor, had died trying to stop the spread of the disease. My aunt’s death is painful, she had written, but it comforts me to know that I’m part of an organization that’s truly committed to saving lives. I hoped her words offered at least a bit of salve.

In that meeting, we were all asking the big question of how? How could we help bring this horror to a halt? Better organization, better communication, better local community action, better leadership, more money, more global engagement? After all, our organization’s mission is to save lives by closing the gap between knowledge and action in global public health. But with Ebola, we were all staring hard at that yawning gap. We didn’t know enough, so we didn’t know what actions to take. As experts, we were doing everything in our combined experience that we knew how to do to treat the sick and prevent the spread of disease, but the challenge was like trying to swim in a tsunami.

After that meeting, I also kept asking myself another big question: Why? Why had it taken months for the World Health Organization (WHO) to declare a global public-health emergency? Why was there still no Ebola vaccine after more than 20 outbreaks of the disease since it was discovered in 1976? Why had the director of the Centers for Disease Control and Prevention (CDC) and the governor of Texas insisted the public was safe from this terrible disease, only to find days later that two nurses had contracted it at a Texas hospital from an infected man who had apparently come in from West Africa under the radar, potentially spreading the disease to an entire American city?

I began to reflect on what I had experienced firsthand or learned through colleagues about AIDS, avian influenza, severe acute respiratory syndrome (SARS), and other infectious-disease outbreaks. I also studied credible scenarios of the magnitude and impact of future epidemics. And I became more and more frightened.

What frightened me? Certainly the prediction by Bill Gates and his team that an epidemic like the 1918 influenza pandemic that killed 50 million people could happen again today—and that in the first 200 days it could kill 33 million people.¹ That’s almost as many people as AIDS has killed over four decades. Even scarier was the Bank of America/Merrill Lynch assessment that the threat of a global pandemic is arguably higher than at any time in human history and that a severe pandemic could claim more than 300 million lives and cost the global economy as much as $3.5 trillion.²

We already know how to stop local outbreaks before they spread. But time and time again, our human failings—various mixtures of fear, pride, complacency, hubris, denial, and financial self-interest—have created, worsened, or delayed the response to past epidemics. I asked myself, why does this keep happening?

Yet I’ve also seen how, at our smartest, we have overcome our human failings. I know of myriad inspiring examples of intelligent, compassionate people—from presidents to paupers—who, throughout history, did the right thing. I have worked closely with colleagues and studied the success stories of those who eradicated smallpox, transformed AIDS from a death sentence into a treatable disease, contained the avian influenza outbreak in the late 2000s—and, of course, handled the nearly two dozen Ebola outbreaks in Africa that preceded the West Africa epidemic of 2014–15. Based on my observations and experience, I firmly believe that achieving the impossible is possible.

I was a little kid in May 1961 when President John F. Kennedy committed the U.S. to achieving the goal, before the decade is out, of landing a man on the moon and returning him safely to the earth. Over the next eight years, along with millions of other kids, I became more and more enthralled with all things astronaut. Like everyone else, I was awestruck on July 20, 1969, when Apollo 11 astronaut Neil Armstrong became the first person to put a foot onto the lunar surface and radio back to earth his famous line, That’s one small step for man, one giant leap for mankind.

When Kennedy set his famous goal in 1961, the technology that would take the three Apollo 11 astronauts to the moon did not exist. Neil Armstrong once observed that during the years of strategizing, innovating, and testing that led up to his landing, NASA engineers and scientists repeatedly ran into ferocious, unscalable walls. They often thought they would have to halt the mission. Nevertheless, each time the moon shot looked like a certain failure, they were firmly told: We are going to the moon. They went back, reimagined the impossible, and made it happen.

By contrast, when leaders shrug their shoulders in resignation, nothing happens. World Health Organization director-general Dr. Marcolino Candau spent most of his career in public health believing that smallpox eradication was impossible. After all, smallpox had been around for at least 3,000 years and was fatal in 30 percent of cases. That’s probably one of the reasons why, when WHO finally committed to smallpox eradication in 1966, Dr. Candau’s home country of Brazil was the only one in the Western Hemisphere that hadn’t yet dedicated itself to joining WHO’s mission. It had taken global health leaders fifteen years to decide to rid the world of smallpox for good. But once they did so, it took just over ten years to eradicate the scourge.³

In late April 2003, at the height of an epidemic of the new respiratory disease known as SARS, reporters asked then–CDC director Dr. Jeffrey Koplan whether SARS could be eliminated in Hong Kong. He said he would be shocked if it was. To be realistic, what we can hope for is the suppression and a minimization of the disease and viral spread, he told them.⁴ A mere two months later, Hong Kong was declared SARS-free—ahead of Toronto, Beijing, and Taiwan. The virus has never returned. The impossible had again happened.

In this book, through examples and evidence, I will establish the seven fundamental sets of actions needed for preventing epidemics: (1) ensuring bold leadership at all levels; (2) building resilient health systems; (3) fortifying three lines of defense against disease (prevention, detection, and response); (4) ensuring timely and accurate communication; (5) investing in smart, new innovation; (6) spending wisely to prevent disease before an epidemic strikes; and (7) mobilizing citizen activism. I’m convinced that a combination of these actions could be achieved within a decade. Working together, The Power of Seven would put us well on the path to an epidemic-free world.

Dangerous microbes will always be out there, and small outbreaks that kill tens or hundreds of people will continue to occur. But if we can send people to the moon, if we can eradicate smallpox, if we can mount the largest public-health treatment effort in history as we did for AIDS, surely we can end epidemics.

In response to skepticism about sending a man to the moon, John F. Kennedy said, We choose to go to the moon. We choose to go to the moon in this decade and do the other things, not because they are easy, but because they are hard. Pursuing the vision of making the world’s last epidemic the very last one will be hard. To the skeptics who believe we cannot end epidemics, I say, Let’s imagine the impossible—then make it happen. Humanity simply cannot afford not to do this.

My sense of hope springs from my four-decade journey in global health. As a third-year medical student, I traveled to Latin America, Africa, Asia, and the Western Pacific to document pioneering efforts to bring modern medicines to the world’s poor and underserved. As a family physician at the U.S. Public Health Service hospital in Talihina, Oklahoma, I delivered babies, treated snakebites, and healed gunshot wounds. I lived in Pakistan and Kenya, where I helped to strengthen local primary health care. As a director at WHO headquarters in Geneva, I worked to expand access to quality essential medicines, including AIDS treatment. And as former president and CEO and now senior fellow at Management Sciences for Health, I have worked with inspiring local leaders around the world to build strong health systems.

Throughout my journey, I have witnessed intense suffering, but I have also seen the stunning results of concerted effort in turning around public-health catastrophes. My experience as a family physician has put me face-to-face with the profound human pain experienced by families who lose a child, a beloved parent, or a sibling. Yet I have also observed the remarkable impact on entire countries when government officials, public-health leaders, activists, and average citizens galvanize action against a global health threat like AIDS, maternal mortality, or a preventable childhood illness. This book is driven by my personal response to the human anguish caused by missed opportunities to help, and by the intense joy I feel when our work saves lives. In it, I’ll describe what happens when disease takes hold and spreads due to all-too-human failings, and how the heroic actions of others help to slow or stop viruses. I’ll suggest how forward thinking could save us from global threats like Ebola, Zika, and pandemic influenza.

At the end of that MSH global staff videoconference, Ian Sliney spoke again from his hotel room in Liberia. His fatigued but stalwart voice was the last one we heard. Wish us the very best of luck, he said. Pray that we get this right.

With this book, I hope that we can all work to get this right.

PART I

THE PANDEMIC THREAT

CHAPTER 1

STOP EPIDEMICS WITH THE POWER OF SEVEN

We can end epidemics with seven sets of concrete actions proven over a century of epidemic response.

The enormous health and financial impacts of epidemics are made worse through human foibles like fear, denial, panic, complacency, hubris, and self-interest. But we can end epidemics by facing up to them and applying concrete actions I call The Power of Seven: (1) ensuring bold leadership at all levels; (2) building resilient health systems; (3) fortifying three lines of defense against disease (prevention, detection, and response); (4) ensuring timely and accurate communication; (5) investing in smart innovation; (6) spending wisely to prevent disease before an epidemic strikes; and (7) mobilizing citizen activism.

I had my first lesson in epidemic forecasting back in 1975, when I was 24 years old. As a second-year medical student at the University of Rochester in upstate New York, I was fascinated by the stories one of my young professors, Dr. Steve Kunitz, told of his search for predictors of the bubonic plague outbreaks, which occurred every few years in the American Southwest. Six hundred years after the Black Death killed half the population of Europe and swept through Asia and Africa to claim roughly 50 million lives worldwide, Native Americans and others in the Southwest endured sporadic outbreaks of this ghastly disease, Kunitz said. They suffered abdominal pain, bleeding, blackening of the extremities, and other awful but classic symptoms. The question is: How were these Native Americans getting infected with plague?

Fleas on rats, somebody said.

You’re half right, Kunitz replied. The disease came from fleas, but not rat fleas.

Dog fleas? another student suggested.

Close, the professor said. Prairie dog fleas hitchhiking on dogs. Native American families kept as many as ten domesticated dogs. These dogs often would hunt prairie dogs, picking up prairie dog fleas along the way.

We were perplexed. So where did the human plague come from?

Kunitz was a clever investigator. When he and a colleague visited the Navajo Reservation at Tuba City, Arizona, to discover how nature might signal when the next outbreak would occur, they began interviewing the locals. They suggested that clusters of dead prairie dogs (die-offs) might carry a clue.

In class, we students learned that plague is caused by the Yersinia pestis bacteria, which is transmitted by the bite of an infected flea from a rat or other small rodent, like the prairie dog of the Southwest. The fleas that infested the prairie dogs came from rats that migrated on steamships from China, which suffered a plague epidemic in the 1860s. Over generations, the infected fleas migrated from ship rats to San Francisco squirrels, and the insects then made their way to the American Southwest. Kunitz and his colleague found that local domestic dogs regularly came in contact with prairie dogs and their fleas but rarely became visibly sick themselves.

Kunitz wondered whether the dogs might be getting a mild illness and developing antibodies to the disease. Could he measure that possibility by asking veterinarians to take blood samples when dogs came in for rabies shots? And what if the level of antibodies to plague among dogs meant that an outbreak of human plague was not far behind? If both were true, he told us, then regular testing of dogs could be used as an early warning alert for human plague.

Kunitz’s research confirmed both of these hypotheses. Soon after, public-health officials began taking annual surveys of antibodies in dog populations. When dog antibody levels increased, community health representatives would spread the warning via local radio and TV and intensify education programs that teach people to protect themselves from fleas and recognize plague symptoms. The effort continues today, albeit with some modifications (such as sampling from coyotes instead of domestic dogs).

I was mightily impressed by this medical Sherlock Holmes. As a student, I had no idea how an epidemic disease could migrate around the world over centuries while occasionally jumping from its animal host to humans, inflicting death on tens, thousands, or millions of people. Nor did I have any inkling that, many years later, I would take on the challenge of preventing epidemics from starting.

Three Tales from Killer Diseases

The 1918 Spanish flu that sickened a third of the world’s population almost a century ago still exists in weaker, seasonal strains today. For a tiny view of what could happen with a new pandemic, let’s take a look at the moment when twentieth-century modernity was taking hold and World War I was winding down.

Based on clinical reports and genomic studies, scientists today believe that the influenza virus had been circulating within the armies of the World War for a long time—even years—before the pandemic of 1918–19.¹ Like all influenza viruses, the Spanish version mutated. In the western trenches, that flu likely took hold among those who had no immunity to it and were living in filthy, wet, cold conditions. It then erupted in far-flung port cities: Freetown, Sierra Leone; Brest, France; and Boston, Massachusetts.²

In the summer of 1918 in the U.S., the Spanish influenza first touched someone in Philadelphia. Americans were hoping for an end to the war and the return of their surviving fathers and sons. Many of the nearly 2 million citizens of Philadelphia flocked to theaters to see vaudeville, plays, and big events and concerts, exchanging occasional coughs. Nobody had paid attention to the fact that 8 million Spaniards were sick and dying from a strange new disease named the Spanish influenza or that people in Boston had come down with the same thing. The alarm bells were silent.

But by the time early autumn arrived, the coughing had spread the disease throughout the city. The coughed-upon developed fevers and pneumonia; the mortally ill suffocated because their lungs and organs collapsed, their bodies turning a hideous blue-black. By October 4, there were 636 new cases of the Spanish flu in Philadelphia; 139 people died. In less than a week, there were an astounding 5,531 new cases. In response, officials closed all the vaudeville and picture theaters, saloons, schools, and churches in the city. Most of the city’s doctors had been sent to Europe to tend to soldiers while the flu was raging. Many remaining healthcare workers succumbed too. The most common treatment was whiskey, the stronger the better. But as whiskey ran out, frantic shoppers stripped pharmacy shelves bare. Medical care was in very short supply. Snake-oil salesmen advised patients to treat themselves with oil of balsam or to try Munyon’s Paw Paw pills.

By mid-month, parents were so sick that they could not care for their children. Hospitals were so full that beds were set up in the armory. When volunteers showed up to hospitals to help, they could do little more than to carry away the dead. People died so fast that the coroner’s office could not keep up with the demand for death certificates. Like some nightmare from plague-ridden fourteenth-century Europe, volunteers drove horse-drawn carts through the city streets, calling for people to bring out the dead. Cemetery directors in Philadelphia raised prices for a plot by 50 percent and charged families an exorbitant $15 for the privilege of digging their loved ones’ graves themselves.

In the streets, little girls jumped rope to a grim new rhyme:

I had a little bird / and its name was Enza / I opened the door / And in flew Enza. ³

Before it was over, the Spanish flu of 1918 wiped out 13,000 people in Philadelphia and between 50 and 100 million worldwide. It remains the most deadly flu outbreak in history.

*   *   *

Gaëtan Dugas was a handsome, charming Air Canada flight attendant who claimed to have had more than 2,500 sexual partners. For years, epidemiologists considered him patient zero in the AIDS epidemic. Early researchers believed he contracted AIDS while in Africa. In his iconic 1987 history of AIDS, And the Band Played On, Randy Shilts portrayed Dugas as recklessly spreading AIDS through unprotected sex even after he was diagnosed. Dugas died from his illness in 1984.⁴

As is the case with most epidemics, the first two decades of AIDS were rife with conspiracy theories about the origin of this other twentieth-century Black Death. Some people blamed smallpox immunization; others blamed a polio vaccine grown in chimpanzee cells; still others claimed that AIDS was a government-sponsored genocide weapon used against the black or gay communities. Over the last decade, however, gene sleuths have unraveled the mystery. Scientists have now found proof that five successful species jumps of the simian immunodeficiency virus (SIV) from primates to humans occurred in Africa during the last century. Successful means that the SIV virus adapted, through rapid mutation, to a form of human immunodeficiency virus (HIV) that would thrive and multiply in humans. The first species jump happened around 1910 in southeastern Cameroon. The biology of the HIV virus subtype tells us that it came from a chimpanzee, which a human probably killed to eat or barter as bushmeat, ultimately igniting the AIDS pandemic.

A Century of Deadly Outbreaks

Influenza and HIV/AIDS have been among the most deadly of the viral pathogens of the last 100 years.

SOURCE: Bean A, Baker M, Stewart C et al. Studying immunity to zoonotic diseases in the natural host—keeping it real. Nature Reviews: Immunology 2013; 13:851–61.

From the first human infections in Cameroon, the HIV virus spread down the Sangha River—probably through sexual contact among those living near and traveling along the river—to the bustling city of Leopoldville (modern-day Kinshasa in the Democratic Republic of Congo). Leopoldville became the cauldron in which the pandemic slowly cooked over the next decades.⁵ In the early 1960s, following the end of the Belgian colonial government, the HIV virus was carried from the Congo to Haiti—most likely via Haitians returning from Africa after working for the colonial government. Around 1970, a single infected person or a container from a plasma-donation clinic brought the AIDS virus from Haiti to the U.S. and from the States to Europe.

Gaëtan Dugas certainly contributed to the spread of AIDS. But he was not patient zero. The HIV virus was already in North America when he contracted AIDS. AIDS had smoldered virtually unnoticed for more than 50 years in Africa before one strain passed into Western countries via Haiti, while other strains were carried from Africa to Asia and beyond. By 2014, the HIV virus had infected almost 78 million people.⁶

*   *   *

The recent Ebola epidemic in West Africa also began with an animal. In late December 2013, a two-year-old named Emile Ouamouno had been playing in a hollow tree, grabbing and poking insect-eating bats. Shortly afterward, he grew seriously ill and died in a small Guinean village near the great rainforest where Guinea, Liberia, and Sierra Leone come together. His family mourned the little one with all the appropriate traditional rites, including holding and kissing his corpse.⁷

There had been 22 previous Ebola outbreaks in Africa, all of which had been contained. In none did the caseload exceed 425, and there were rarely more than 50 deaths. Just months before the West Africa outbreak, experts had even declared Ebola to be a dead-end event because it burned out too quickly to spread very far.

But within weeks of little Emile’s death, the Ebola virus that killed him had exploded into a three-country epidemic. By late 2015, it had infected nearly 30,000 people, killed more than 11,000, and touched people in Africa, Britain, France, Germany, Italy, the Netherlands, Norway, Spain, Switzerland, and the U.S.⁸ The conventional wisdom about Ebola had proven fatally wrong.

*   *   *

These three stories of devastating sickness—and others that I draw into this book—illustrate how murderous diseases erupt when a microbe jumps species from animals to humans, as in the cases of plague, AIDS, influenza, and Ebola, and then spread from human to human. The majority of new infectious diseases with pandemic potential actually result from these animal-to-human species jumps. Infectious-disease outbreaks also happen whenever humans are exposed to a virus, bacteria, or other microbe against which they have little or no immunity—just as Europeans, who had long endured smallpox, introduced the disease to the indigenous populations of the New World, very nearly exterminating them. Outbreaks also occur when a microbe to which humans have developed immunity mutates, as often happens with influenza.

A Gigantic Threat

Somewhere out there a dangerous virus is boiling up in the bloodstream of a bird, bat, monkey, or pig, preparing to jump to a human being. It’s hard to comprehend the scope of such a threat, for it has the potential to wipe out millions of us, including my family and yours, over a matter of weeks or months. The risk makes the threat posed by ISIS (Islamic State in Iraq and Syria), a ground war, a massive climate event, or even the dropping of a nuclear bomb on a major city pale by comparison.

A new epidemic could turn into a pandemic without warning. (For definitional purposes, an outbreak refers to a localized epidemic—something that affects hundreds, sometimes thousands; an epidemic refers to an illness or infection that is in excess of normal; and a pandemic is an epidemic that occurs over a very wide area, crosses international boundaries, and touches thousands or millions.) It could be born in a factory farm in Minnesota, a poultry farm in China, or the bat-inhabited elephant caves of Kenya—any place where infected animals are in contact with humans. It could be a variation of the 1918 Spanish flu, one of hundreds of other known microbial threats, or something entirely new, like the 2003 SARS virus that spread globally from China. Once transmitted to a human, an airborne virus could pass from that one infected individual to 25,000 others within a week, and to more than 700,000 within the first month. Within three months it could spread to every major urban center in the world. And by six months, it could infect more than 300 million people and kill more than 30 million.

This is not alarmist science fiction or tabloid fearmongering. It is one of several highly plausible scenarios—and far from the worst—developed by infectious-disease specialists working with disease-modeling experts. Just ask Bill Gates, who funds a group that uses computer simulations to predict the spread of diseases. In an interview with Vox, Gates said, The Ebola epidemic showed me that we are not ready for a serious epidemic, an epidemic that would be more infectious and would spread faster than Ebola did. This is the greatest risk of a huge tragedy. This is the most likely thing by far to kill over 10 million people in a year. He put the likelihood of a catastrophic epidemic at well over 50 percent in his lifetime. Gates’s model estimates that a perilous virus, carried via cars, planes, ships, and trains, and spreading quickly in packed cities, could kill up to 33 million people in just over 200 days.⁹ Some experts put the potential first-year death rate at over 300 million people. To imagine what such a catastrophe would look like, imagine what happened in Philadelphia in 1918 occurring again, on a much larger scale, throughout the world. We would be in a world where scrappy, ravaged survivors struggle for life in a zombie-movie wasteland.

In the last century alone, smallpox killed 300 to 500 million people. The 1918 Spanish flu killed 50 to 100 million in a two-year period, and AIDS has taken 40 million lives since it was first recognized in 1981. The annual influenza outbreak still claims half a million people a year worldwide. The West African Ebola crisis took more than 11,000 lives—seven times the total of the 22 Ebola epidemics that preceded it. But widespread death isn’t the only threat. For those who survive the initial infection, an epidemic leaves its own particular trail of disfigurement and disability. People who contracted smallpox suffered characteristic, sometimes horrific, scars along with blindness, limb deformities, and other disabilities. As