Henrietta Lacks' Cells Enabled Medical Breakthroughs. Is It Time to Finally Retire Them?
Henrietta Lacks, (1920-1951) unknowingly had her cells cultured and used in medical research.
For Victoria Tokarz, a third-year PhD student at the University of Toronto, experimenting with cells is just part of a day's work. Tokarz, 26, is studying to be a cell biologist and spends her time inside the lab manipulating muscle cells sourced from rodents to try to figure out how they respond to insulin. She hopes this research could someday lead to a breakthrough in our understanding of diabetes.
"People like to use HeLa cells because they're easy to use."
But in all her research, there is one cell culture that Tokarz refuses to touch. The culture is called HeLa, short for Henrietta Lacks, named after the 31-year-old tobacco farmer the cells were stolen from during a tumor biopsy she underwent in 1951.
"In my opinion, there's no question or experiment I can think of that validates stealing from and profiting off of a black woman's body," Tokarz says. "We're not talking about a reagent we created in a lab, a mixture of some chemicals. We're talking about a human being who suffered indescribably so we could profit off of her misfortune."
Lacks' suffering is something that, until recently, was not widely known. Born to a poor family in Roanoke, VA, Lacks was sent to live with her grandfather on the family tobacco farm at age four, shortly after the death of her mother. She gave birth to her first child at just fourteen, and two years later had another child with profound developmental disabilities. Lacks married her first cousin, David, in 1941 and the family moved to Maryland where they had three additional children.
But the real misfortune came in 1951, when Lacks told her cousins that she felt a hard "knot" in her womb. When Lacks went to Johns Hopkins hospital to have the knot examined, doctors discovered that the hard lump Henrietta felt was a rapidly-growing cervical tumor.
Before the doctors treated the tumor – inserting radium tubes into her vagina, in the hopes they could kill the cancer, Lacks' doctors clipped two tissue samples from her cervix, without Lacks' knowledge or consent. While it's considered widely unethical today, taking tissue samples from patients was commonplace at the time. The samples were sent to a cancer researcher at Johns Hopkins and Lacks continued treatment unsuccessfully until she died a few months later of metastatic cancer.
Lacks' story was not over, however: When her tissue sample arrived at the lab of George Otto Gey, the Johns Hopkins cancer researcher, he noticed that the cancerous cells grew at a shocking pace. Unlike other cell cultures that would die within a day or two of arriving at the lab, Lacks' cells kept multiplying. They doubled every 24 hours, and to this day, have never stopped.
Scientists would later find out that this growth was due to an infection of Human Papilloma Virus, or HPV, which is known for causing aggressive cancers. Lacks' cells became the world's first-ever "immortalized" human cell line, meaning that as long as certain environmental conditions are met, the cells can replicate indefinitely. Although scientists have cultivated other immortalized cell lines since then, HeLa cells remain a favorite among scientists due to their resilience, Tokarz says.
"People like to use HeLa cells because they're easy to use," Tokarz says. "They're easy to manipulate, because they're very hardy, and they allow for transection, which means expressing a protein in a cell that's not normally there. Other cells, like endothelial cells, don't handle those manipulations well."
Once the doctors at Johns Hopkins discovered that Lacks' cells could replicate indefinitely, they started shipping them to labs around the world to promote medical research. As they were the only immortalized cell line available at the time, researchers used them for thousands of experiments — some of which resulted in life-saving treatments. Jonas Salk's polio vaccine, for example, was manufactured using HeLa cells. HeLa cell research was also used to develop a vaccine for HPV, and for the development of in vitro fertilization and gene mapping. Between 1951 and 2018, HeLa cells have been cited in over 110,000 publications, according to a review from the National Institutes of Health.
But while some scientists like Tokarz are thankful for the advances brought about by HeLa cells, they still believe it's well past time to stop using them in research.
"Am I thankful we have a polio vaccine? Absolutely. Do I resent the way we came to have that vaccine? Absolutely," Tokarz says. "We could have still arrived at those same advances by treating her as the human being she is, not just a specimen."
Ethical considerations aside, HeLa is no longer the world's only available cell line – nor, Tokarz argues, are her cells the most suitable for every type of research. "The closer you can get to the physiology of the thing you're studying, the better," she says. "Now we have the ability to use primary cells, which are isolated from a person and put right into the culture dish, and those don't have the same mutations as cells that have been growing for 20 years. We didn't have the expertise to do that initially, but now we do."
Raphael Valdivia, a professor of molecular genetics and microbiology at Duke University School of Medicine, agrees that HeLa cells are no longer optimal for most research. "A lot of scientists are moving away from HeLa cells because they're so unstable," he says. "They mutate, they rearrange chromosomes to become adaptive, and different batches of cells evolve separately from each other. The HeLa cells in my lab are very different than the ones down the hall, and that means sometimes we can't replicate our results. We have to go back to an earlier batch of cells in the freezer and re-test."
Still, the idea of retiring the cells completely doesn't make sense, Valdivia says: "To some extent, you're beholden to previous research. You need to be able to confirm findings that happen in earlier studies, and to do that you need to use the same cell line that other researchers have used."
"Ethics is not black and white, and sometimes there's no such thing as a straightforward ethical or unethical choice."
"The way in which the cells were taken – without patient consent – is completely inappropriate," says Yann Joly, associate professor at the Faculty of Medicine in Toronto and Research Director at the Centre of Genomics and Policy. "The question now becomes, what can we do about it now? What are our options?"
While scientists are not able to erase what was done to Henrietta Lacks, Joly argues that retiring her cells is also non-consensual, assuming – maybe incorrectly – what Henrietta would have wanted, without her input. Additionally, Joly points out that other immortalized human cell lines are fraught with what some people consider to be ethical concerns as well, such as the human embryonic kidney cell line, commonly referred to as HEK-293, that was derived from an aborted female fetus. "Just because you're using another kind of cell doesn't mean it's devoid of ethical issue," he says.
Seemingly, the one thing scientists can agree on is that Henrietta Lacks was mistreated by the medical community. But even so, retiring her cells from medical research is not an obvious solution. Scientists are now using HeLa cells to better understand how the novel coronavirus affects humans, and this knowledge will inform how researchers develop a COVID-19 vaccine.
"Ethics is not black and white, and sometimes there's no such thing as a straightforward ethical or unethical choice," Joly says. "If [ethics] were that easy, nobody would need to teach it."
Dr. Barry Marshall (along with a collaborator) discovered that the bacteria H. Pylori, pictured, caused stomach ulcers.
[Editor's Note: Welcome to Leaps of the Past, a new monthly column that spotlights the fascinating backstory behind a medical or scientific breakthrough from history.]
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Until about 40 years ago, ulcers were a mysterious – and sometimes deadly – ailment. Found in a person's stomach lining or intestine, ulcers are small sores that cause a variety of painful symptoms, such as vomiting, a burning or aching sensation, internal bleeding and stomach obstruction. Patients with ulcers suffered for years without a cure and sometimes even needed their stomachs completely removed to rid them from pain.
"To gastroenterologists, the concept of a germ causing ulcers was like saying the Earth is flat."
In the early 1980s, the majority of scientists thought that ulcers were caused by stress or poor diet. But a handful of scientists had a different theory: They believed that ulcers were caused by a corkscrew-shaped bacterium called Helicobacter pylori, or H. pylori for short. Robin Warren, a pathologist, and Barry Marshall, an internist, were the two pioneers of this theory, and the two teamed up to study H. pylori at the Royal Perth Hospital in 1981.
The pair started off by trying to culture the bacteria in the stomachs of patients with gastritis, an inflammation of the stomach lining and a precursor to developing an ulcer. Initially, the microbiologists involved in their clinical trial found no trace of the bacteria from patient samples – but after a few weeks, the microbiologists discovered that their lab techs had been throwing away the cultures before H. pylori could grow. "After that, we let the cultures grow longer and found 13 patients with duodenal ulcer," said Marshall in a later interview. "All of them had the bacteria."
Marshall and Warren also cultured H. pylori in the stomachs of patients with stomach cancer. They observed that "everybody with stomach cancer developed it on a background of gastritis. Whenever we found a person without Helicobacter, we couldn't find gastritis either." Marshall and Warren were convinced that H. pylori not only caused gastritis and peptic ulcers, but stomach cancer as well.
But when the team presented their findings at an annual meeting of the Royal Australasian College of Physicians in Perth, they were mostly met with skepticism. "To gastroenterologists, the concept of a germ causing ulcers was like saying the Earth is flat," Marshall said. "The idea was too weird."
Warren started treating his gastritis patients with antibiotics with great success – but other internists remained doubtful, continuing to treat their patients with antacids instead. Making matters more complicated, neither Warren nor Marshall could readily test their theory, since the pair only had lab mice at their disposal and H. pylori infects only humans and non-human primates, such as rhesus monkeys.
So Marshall took an unconventional approach. First, he underwent two tests to get a baseline reading of his stomach, which showed no presence of H. pylori. Then, Marshall took some H. pylori bacteria from a petri dish, mixed it with beef extract to create a broth, and gulped it down. If his theory was correct, a second gastric biopsy would show that his stomach was overrun with H. pylori bacteria, and a second endoscopy would show a painfully inflamed stomach – gastritis.
Less than a week later, Marshall started feeling sick. "I expected to develop an asymptomatic infection," he later said in an interview published in the Canadian Journal of Gastroenterology. "… [but] after five days, I started to have bloating and fullness after the evening meal, and my appetite decreased. My breath was bad and I vomited clear watery liquid, without acid, each morning."
At his wife's urging, Marshall started on a regimen of antibiotics to kill off the burgeoning bacteria, so a follow-up biopsy showed no signs of H. pylori. A follow-up endoscopy, however, showed "severe active gastritis" along with epithelial damage. This was the smoking gun other clinicians needed to believe that H. pylori caused gastritis and stomach cancer. When they began to treat their gastritis patients with antibiotics, the rate of peptic ulcers in the Australian population diminished by 70 percent.
Today, antibiotics are the standard of care for anyone afflicted with gastritis.
In 2005, Marshall and Warren were awarded the Nobel Prize in Physiology or Medicine for their discovery of H. Pylori and its role in developing gastritis and peptic ulcers. "Thanks to the pioneering discovery by Marshall and Warren, peptic ulcer disease is no longer a chronic, frequently disabling condition, but a disease that can be cured by a short regimen of antibiotics and acid secretion inhibitors," the Nobel Prize Committee said.
Today, antibiotics are the standard of care for anyone afflicted with gastritis – and stomach cancer has been significantly reduced in the Western world.
Isaac Asimov on the History of Infectious Disease—and How Humanity Learned to Fight Back
Children in Mississippi get vaccinated against polio with the Salk vaccine in 1956.
[EDITOR'S FORWARD: Humanity has always faced existential threats from dangerous microbes, and though this is the first pandemic in our lifetimes, it won't be the last our species will ever face. This newly relevant work by beloved sci-fi writer Isaac Asimov, an excerpt from his 1979 book, A Choice of Catastrophes, establishes that reality in its historical context and makes clear how far we have come since ancient times. But by some measures, we are still in the earliest stages of figuring out how to effectively neutralize such threats. Advancing progress as fast as we can—by leveraging all the insights of modern science—offers our best hope for containing this pandemic and those that will inevitably follow.]
Infectious Disease
An even greater danger to humanity than the effect of small, fecund pests on human beings, their food, and their possessions, is their tendency to spread some forms of infectious disease.
Every living organism is subject to disease of various sorts, where disease is defined in its broadest sense as "dis-ease," that is, as any malfunction or alteration of the physiology or biochemistry that interferes with the smooth workings of the organism. In the end, the cumulative effect of malfunctions, misfunctions, nonfunctions, even though much of it is corrected or patched up, produces irreversible damage—we call it old age—and, even with the best care in the world, brings on inevitable death.
Civilization has meant the development and growth of cities and the crowding of people into close quarters.
There are some individual trees that may live five thousand years, some cold-blooded animals that may live two hundred years, some warm-blooded animals that may live one hundred years, but for each multicellular individual death comes as the end.
This is an essential part of the successful functioning of life. New individuals constantly come into being with new combinations of chromosomes and genes, and with mutated genes, too. These represent new attempts, so to speak, at fitting the organism to the environment. Without the continuing arrival of new organisms that are not mere copies of the old, evolution would come to a halt. Naturally, the new organisms cannot perform their role properly unless the old ones are removed from the scene after they have performed their function of producing the new. In short, the death of the individual is essential to the life of the species.
It is essential, however, that the individual not die before the new generation has been produced; at least, not in so many cases as to ensure the population dwindling to extinction.
The human species cannot have the relative immunity to harm from individual death possessed by the small and fecund species. Human beings are comparatively large, long-lived, and slow to reproduce, so that too rapid individual death holds within it the specter of catastrophe. The rapid death of unusually high numbers of human beings through disease can seriously dent the human population. Carried to an extreme, it is not too hard to imagine it wiping out the human species.
Most dangerous in this respect is that class of malfunction referred to as "infectious disease." There are many disorders that affect a particular human being for one reason or another and may kill him or her, too, but which will not, in itself, offer a danger to the species, because it is strictly confined to the suffering individual. Where, however, a disease can, in some way travel from one human being to another, and where its occurrence in a single individual may lead to the death of not that one alone but of millions of others as well, then there is the possibility of catastrophe.
And indeed, infectious disease has come closer to destroying the human species in historic times than have the depredations of any animals. Although infectious disease, even at its worst, has never yet actually put an end to human beings as a living species (obviously), it can seriously damage a civilization and change the course of history. It has, in fact, done so not once, but many times.
What's more, the situation has perhaps grown worse with the coming of civilization. Civilization has meant the development and growth of cities and the crowding of people into close quarters. Just as fire can spread much more rapidly from tree to tree in a dense forest than in isolated stands, so can infectious disease spread more quickly in crowded quarters than in sparse settlements.
To mention a few notorious cases in history:
In 431 B.C., Athens and its allies went to war with Sparta and its allies. It was a twenty-seven-year war that ruined Athens and, to a considerable extent, all of Greece. Since Sparta controlled the land, the entire Athenian population crowded into the walled city of Athens. There they were safe and could be provisioned by sea, which was controlled by the Athenian navy. Athens would very likely have won a war of attrition before long and Greece might have avoided ruin, but for disease.
In 430 B.C., an infectious plague struck the crowded Athenian population and killed 20 percent of them, including the charismatic leader, Pericles. Athens kept on fighting but it never recovered its population or its strength and in the end it lost.
Plagues very frequently started in eastern and southern Asia, where population was densest, and spread westward. In A.D. 166, when the Roman Empire was at its peak of strength and civilization under the hard-working philosopher-emperor Marcus Aurelius, the Roman armies, fighting on the eastern borders in Asia Minor, began to suffer from an epidemic disease (possibly smallpox). They brought it back with them to other provinces and to Rome itself. At its height, 2,000 people were dying in the city of Rome each day. The population began to decline and did not reach its preplague figure again until the twentieth century. There are a great many reasons advanced for the long, slow decline of Rome that followed the reign of Marcus Aurelius, but the weakening effect of the plague of 166 surely played a part.
Even after the western provinces of the empire were torn away by invasions of the German tribes, and Rome itself was lost, the eastern half of the Roman Empire continued to exist, with its capital at Constantinople. Under the capable emperor Justinian I, who came to the throne in 527, Africa, Italy, and parts of Spain were taken and, for a while, it looked as though the empire might be reunited. In 541, however, the bubonic plague struck. It was a disease that attacked rats primarily, but one that fleas could spread to human beings by biting first a sick rat and then a healthy human being. Bubonic disease was fast-acting and often quickly fatal. It may even have been accompanied by a more deadly variant, pneumonic plague, which can leap directly from one person to another.
For two years the plague raged, and between one-third and one-half of the population of the city of Constantinople died, together with many people in the countryside outside the city. There was no hope of uniting the empire thereafter and the eastern portion, which came to be known as the Byzantine Empire, continued to decline thereafter (with occasional rallies).
The very worst epidemic in the history of the human species came in the fourteenth century. Sometime in the 1330s, a new variety of bubonic plague, a particularly deadly one, appeared in central Asia. People began to die and the plague spread outward, inexorably, from its original focus.
Eventually, it reached the Black Sea. There on the Crimean peninsula, jutting into the north-central coast of that sea, was a seaport called Kaffa where the Italian city of Genoa had established a trading post. In October, 1347, a Genoese ship just managed to make it back to Genoa from Kaffa. The few men on board who were not dead of the plague were dying. They were carried ashore and thus the plague entered Europe and began to spread rapidly.
Sometimes one caught a mild version of the disease, but often it struck violently. In the latter case, the patient was almost always dead within one to three days after the onset of the first symptoms. Because the extreme dangers were marked by hemorrhagic spots that turned dark, the disease was called the "Black Death."
The Black Death spread unchecked. It is estimated to have killed some 25 million people in Europe before it died down and many more than that in Africa and Asia. It may have killed a third of all the human population of the planet, perhaps 60 million people altogether or even more. Never before or after do we know of anything that killed so large a percentage of the population as did the Black Death.
It is no wonder that it inspired abject terror among the populace. Everyone walked in fear. A sudden attack of shivering or giddiness, a mere headache, might mean that death had marked one for its own and that no more than a couple of dozen hours were left in which to die. Whole towns were depopulated, with the first to die lying unburied while the survivors fled to spread the disease. Farms lay untended; domestic animals wandered uncared for. Whole nations—Aragon, for instance, in what is now eastern Spain—were afflicted so badly that they never truly recovered.
Distilled liquors had been first developed in Italy about 1100. Now, two centuries later they grew popular. The theory was that strong drink acted as a preventive against contagion. It didn't, but it made the drinker less concerned which, under the circumstances, was something. Drunkenness set in over Europe and it stayed even after the plague was gone; indeed, it has never left. The plague also upset the feudal economy by cutting down on the labor supply very drastically. This did as much to destroy feudalism as did the invention of gunpowder. (Perhaps the most distressing sidelight of the Black Death is the horrible insight into human nature that it offers. England and France were in the early decades of the Hundred Years War at the time. Although the Black Death afflicted both nations and nearly destroyed each, the war continued right on. There was no thought of peace in this greatest of all crises faced by the human species.)
There have been other great plagues since, though none to match the Black Death in unrivaled terror and destruction. In 1664 and 1665, the bubonic plague struck London and killed 75,000.
Cholera, which always simmered just below the surface in India (where it is "endemic") would occasionally explode and spread outward into an "epidemic." Europe was visited by deadly cholera epidemics in 1831 and again in 1848 and 1853. Yellow fever, a tropical disease, would be spread by sailors to more northern seaports, and periodically American cities would be decimated by it. Even as late as 1905, there was a bad yellow fever epidemic in New Orleans.
The most serious epidemic since the Black Death, was one of "Spanish influenza" which struck the world in 1918 and in one year killed 30 million people the world over, and about 600,000 of them in the United States. In comparison, four years of World War I, just preceding 1918, had killed 8 million. However, the influenza epidemic killed less than 2 percent of the world's population, so that the Black Death remains unrivaled.
What stands between such a catastrophe and us is the new knowledge we have gained in the last century and a half concerning the causes of infectious disease and methods for fighting it.
[…] Infectious disease is clearly more dangerous to human existence than any animal possibly could be, and we might be right to wonder whether it might not produce a final catastrophe before the glaciers ever have a chance to invade again and certainly before the sun begins to inch its way toward red gianthood.
What stands between such a catastrophe and us is the new knowledge we have gained in the last century and a half concerning the causes of infectious disease and methods for fighting it.
Microorganisms
People, throughout most of history, had no defense whatever against infectious disease. Indeed, the very fact of infection was not recognized in ancient and medieval times. When people began dying in droves, the usual theory was that an angry god was taking vengeance for some reason or other. Apollo's arrows were flying, so that one death was not responsible for another; Apollo was responsible for all, equally.
The Bible tells of a number of epidemics and in each case it is the anger of God kindled against sinners, as in 2 Samuel 24. In New Testament times, the theory of demonic possession as an explanation of disease was popular, and both Jesus and others cast our devils. The biblical authority for this has caused the theory to persist to this day, as witness by the popularity of such movies as The Exorcist.
As long as disease was blamed on divine or demonic influences, something as mundane as contagion was overlooked. Fortunately, the Bible also contains instructions for isolating those with leprosy (a name given not only to leprosy itself, but to other, less serious skin conditions). The biblical practice of isolation was for religious rather than hygienic reasons, for leprosy has a very low infectivity. On biblical authority, lepers were isolated in the Middle Ages, while those with really infectious disease were not. The practice of isolation, however, caused some physicians to think of it in connection with disease generally. In particular, the ultimate terror of the Black Death helped spread the notion of quarantine, a name which referred originally to isolation for forty (quarante in French) days.
The fact that isolation did slow the spread of a disease made it look as though contagion was a factor. The first to deal with this possibility in detail was an Italian physician, Girolamo Fracastoro (1478–1553). In 1546, he suggested that disease could be spread by direct contact of a well person with an ill one or by indirect contact of a well person with infected articles or even through transmission over a distance. He suggested that minute bodies, too small to be seen, passed from an ill person to a well one and that the minute bodies had the power of self-multiplication.
It was a remarkable bit of insight, but Fracastoro had no firm evidence to support his theory. If one is going to accept minute unseen bodies leaping from one body to another and do it on nothing more than faith, one might as well accept unseen demons.
Minute bodies did not, however, remain unseen. Already in Fracastoro's time, the use of lenses to aid vision was well established. By 1608, combinations of lenses were used to magnify distant objects and the telescope came into existence. It didn't take much of a modification to have lenses magnify tiny objects. The Italian physiologist Marcello Malpighi (1628–94) was the first to use a microscope for important work, reporting his observations in the 1650s.
The Dutch microscopist Anton van Leeuwenhoek (1632–1723) laboriously ground small but excellent lenses, which gave him a better view of the world of tiny objects than anyone else in his time had had. In 1677, he placed ditch water at the focus of one of his small lenses and found living organisms too small to see with the naked eye but each one as indisputably alive as a whale or an elephant—or as a human being. These were the one-celled animals we now call "protozoa."
In 1683, van Leeuwenhoek discovered structures still tinier than protozoa. They were at the limit of visibility with even his best lenses, but from his sketches of what he saw, it is clear that he had discovered bacteria, the smallest cellular creatures that exist.
To do any better than van Leeuwenhoek, one had to have distinctly better microscopes and these were slow to be developed. The next microscopist to describe bacteria was the Danish biologist Otto Friedrich Müller (1730–84) who described them in a book on the subject, published posthumously, in 1786.
In hindsight, it seems that one might have guessed that bacteria represented Fracastoro's infectious agents, but there was no evidence of that and even Müller's observations were so borderline that there was no general agreement that bacteria even existed, or that they were alive if they did.
The English optician Joseph Jackson Lister (1786–1869) developed an achromatic microscope in in 1830. Until then, the lenses used had refracted light into rainbows so that tiny objects were rimmed in color and could not be seen clearly. Lister combined lenses of different kinds of glass in such a way as to remove the colors.
With the colors gone, tiny objects stood out sharply and in the 1860s, the German botanist Ferdinand Julius Cohn (1828–98) saw and described bacteria with the first really convincing success. It was only with Cohn's work that the science of bacteriology was founded and that there came to be general agreement that bacteria existed.
Meanwhile, even without a clear indication of the existence of Fracastoro's agents, some physicians were discovering methods of reducing infection.
The Hungarian physician Ignaz Philipp Semmelweiss (1818–65) insisted that childbed fever which killed so many mothers in childbirth, was spread by the doctors themselves, since they went from autopsies straight to women in labor. He fought to get the doctors to wash their hands before attending the women, and when he managed to enforce this, in 1847, the incidence of childbed fever dropped precipitously. The insulted doctors, proud of their professional filth, revolted at this, however and finally managed to do their work with dirty hands again. The incidence of childbed fever climbed as rapidly as it had fallen—but that didn't bother the doctors.
The crucial moment came with the work of the French chemist Louis Pasteur (1822–95). Although he was a chemist his work had turned him more and more toward microscopes and microorganisms, and in 1865 he set to work studying a silkworm disease that was destroying France's silk industry. Using his microscope, he discovered a tiny parasite infesting the silkworms and the mulberry leaves that were fed to them. Pasteur's solution was drastic but rational. All infested worms and infested food must be destroyed. A new beginning must be made with healthy worms and the disease would be wiped out. His advice was followed and it worked. The silk industry was saved.
This turned Pasteur's interest to contagious diseases. It seemed to him that if the silkworm disease was the product of microscopic parasites other diseases might be, and thus was born the "germ theory of disease." Fracastoro's invisible infectious agents were microorganisms, often the bacteria that Cohn was just bringing clearly into the light of day.
It now became possible to attack infectious disease rationally, making use of a technique that had been introduced to medicine over half a century before. In 1798, the English physician Edward Jenner (1749–1823) had shown that people inoculated with the mild disease, cowpox, or vaccinia in Latin, acquired immunity not only to cowpox itself but also to the related but very virulent and dreaded disease, smallpox. The technique of "vaccination" virtually ended most of the devastation of smallpox.
Unfortunately, no other diseases were found to occur in such convenient pairs, with the mild one conferring immunity from the serious one. Nevertheless, with the notion of the germ theory the technique could be extended in another way.
Pasteur located specific germs associated with specific diseases, then weakened those germs by heating them or in other ways, and used the weakened germs for inoculation. Only a very mild disease was produced but immunity was conferred against the dangerous one. The first disease treated in this way was the deadly anthrax that ravaged herds of domestic animals.
Similar work was pursued even more successfully by the German bacteriologist Robert Koch (1843–1910). Antitoxins designed to neutralize bacterial poisons were also developed.
Meanwhile, the English surgeon Joseph Lister (1827–1912), the son of the inventor of the achromatic microscope, had followed up Semmelweiss's work. Once he learned of Pasteur's research he had a convincing rationale as excuse and began to insist that, before operating, surgeons wash their hands in solutions of chemicals known to kill bacteria. From 1867 on, the practice of "antiseptic surgery" spread quickly.
The germ theory also sped the adoption of rational preventive measures—personal hygiene, such as washing and bathing; careful disposal of wastes; the guarding of the cleanliness of food and water. Leaders in this were the German scientist Max Joseph von Pettenkofer (1818–1901) and Rudolph Virchow (1821–1902). They themselves did not accept the germ theory of disease but their recommendations would not have been followed as readily were it not that others did.
In addition, it was discovered that diseases such as yellow fever and malaria were transmitted by mosquitoes, typhus fever by lice, Rocky Mountain spotted fever by ticks, bubonic plague by fleas and so on. Measures against these small germ-transferring organisms acted to reduce the incidence of the diseases. Men such as the Americans Walter Reed (1851–1902) and Howard Taylor Ricketts (1871–1910) and the Frenchman Charles J. Nicolle (1866–1936) were involved in such discoveries.
The German bacteriologist Paul Ehrlich (1854–1915) pioneered the use of specific chemicals that would kill particular bacteria without killing the human being in which it existed. His most successful discovery came in 1910, when he found an arsenic compound that was active against the bacterium that causes syphilis.
This sort of work culminated in the discovery of the antibacterial effect of sulfanilamide and related compounds, beginning with the work of the German biochemist Gerhard Domagk (1895–1964) in 1935 and of antibiotics, beginning with the work of the French-American microbiologist René Jules Dubos (1901–[1982]) in 1939.
As late as 1955 came a victory over poliomyelitis, thanks to a vaccine prepared by the American microbiologist Jonas Edward Salk (1914–[1995]).
And yet victory is not total. Right now, the once ravaging disease of smallpox seems to be wiped out. Not one case exists, as far as we know, in the entire world. There are however infectious diseases such as a few found in Africa that are very contagious, virtually 100 percent fatal, and for which no cure exists. Careful hygienic measures have made it possible for such diseases to be studied without their spreading, and no doubt effective countermeasures will be worked out.
New Disease
It would seem, then, that as long as our civilization survives and our medical technology is not shattered there is no longer any danger that infectious disease will produce catastrophe or even anything like the disasters of the Black Death and the Spanish influenza. Yet, old familiar diseases have, within them, the potentiality of arising in new forms.
The human body (and all living organisms) have natural defenses against the invasion of foreign organisms. Antibodies are developed in the bloodstream that neutralize toxins or the microorganisms themselves. White cells in the blood stream physically attack bacteria.
Every few years a new strain of flu rises to pester us. It is possible, however, to produce vaccines against such a new strain once it makes an appearance.
Evolutionary processes generally make the fight an even one. Those organisms more efficient at self-protection against microorganisms tend to survive and pass on their efficiency to their offspring. Nevertheless, microorganisms are far smaller even than insects and far more fecund. They evolve much more quickly, with individual microorganisms almost totally unimportant in the scheme of things.
Considering the uncounted numbers of microorganisms of any particular species that are continually multiplying by cell fission, large numbers of mutations must be produced just as continually. Every once in a while such a mutation may act to make a particular disease far more infectious and deadly. Furthermore, it may sufficiently alter the chemical nature of the microorganism so that the antibodies which the host organism is capable of manufacturing are no longer usable. The result is the sudden onslaught of an epidemic. The Black Death was undoubtedly brought about by a mutant strain of the microorganism causing it.
Eventually, though, those human beings who are most susceptible die, and the relatively resistant survive, so that the virulence of the diseases dies down. In that case, is the human victory over the pathogenic microorganism permanent? Might not new strains of germs arise? They might and they do. Every few years a new strain of flu rises to pester us. It is possible, however, to produce vaccines against such a new strain once it makes an appearance. Thus, when a single case of "swine flu" appeared in 1976, a full scale mass-vaccination was set in action. It turned out not to be needed, but it showed what could be done.
Copyright © 1979 by Isaac Asimov, A Choice of Catastrophes: The Disasters That Threaten Our World, originally published by Simon & Schuster. Reprinted with permission from the Asimov estate.
[This article was originally published on June 8th, 2020 as part of a standalone magazine called GOOD10: The Pandemic Issue. Produced as a partnership among LeapsMag, The Aspen Institute, and GOOD, the magazine is available for free online.]