(The) germ theory shifted the cause of disease away from internal organs to external invaders. The long-frustrated social hygiene movements could now marshal science to help their efforts to clean up the world in a joint campaign against a living “enemy.” What’s more, (the) germ theory spawned the new science of bacteriology, which more than any other form of inquiry brought pathology into the medical spotlight. Bacteriology established the microscope as a tool for doctors as well as scientists.
—Jacalyn Duffin
History of Medicine:
A Scandalously Short Introduction
The idea behind (Pasteur’s) germ theory seems simple enough today. Microorganisms such as bacteria, fungi, and protozoan parasites come from forebears of the same species; they are present in large numbers almost everywhere—in air, in water, in dust; finally, germs can therefore be understood as the causative factor in not only fermentation and putrescence but also in disease. Different diseases are caused by different microbes. It all fits together into such a neat package that it’s hard at first to understand why his germ theory was so controversial and took so long to be accepted.
—Hal Hellman
Great Feuds in Medicine: Ten of the Liveliest Disputes Ever
As a Hungarian trainee in Vienna’s great hospital, Semmelweis (1818–1865) was isolated from the easy camaraderie of Austrian medical students in the wards and autopsy rooms. Although he told of his discovery of the association between autopsies and childbed fever many different ways, he probably first noticed the too-frequent ringing of a little bell as the priest came to give last rites to a dying mother. Becoming a crusader, Semmelweis angrily attacked European obstetricians as murderers. He himself died from the skull fractures he sustained after (a forced) admission to an asylum.
Ann G. Carmichael and Richard M. Ratzan (editors)
Medicine: A Treasury of Art and Literature
The Justinian Plague, named for the Byzantine emperor Justinian I, killed 10,000 people each day. The deaths started in 541 AD and before it was over 200 million had died.
The Antonine Plague, named for one of the two Roman emperors who died from the infection, began in 165 AD, and as it gained energy it killed 5,000 people each day for 15 years, and ended up killing an estimated 27 million.
The bubonic plague (Black Death) ravaged the 14th century, killing 25 million Europeans and an additional 12 million people throughout China and India. The global total is unknown.
Eyeglasses were invented in medieval Italy. In 1590 a Dutch eyeglass maker, Zacharias Janssen, and his father, Hans, discovered that they could build on the concept of magnification using a single lens by using two lenses, and the light microscope was born.
In 1665, while looking at thin slivers of cork through a microscope, Robert Hooke observed small holes, or what he coined “cells.” Hooke later said that the cavities reminded him of monk’s quarters (thus the origin of the name). He believed that these cells had once been containers for “noble juices” or “fibrous threads” necessary for the cork tree’s survival. In addition Hooke supported the common theory of the day that only plants possessed cells; at the time no one thought to look at animal or human tissues through the microscope.
Hooke included drawings of the cells he had observed in his book, Micrographia. He also provided instructions for constructing a microscope like the one he used, presumably so that readers could make the same observations. Not happy enough to simply observe cells, Hooke calculated how many could be contained in a cubic inch. Hooke quite correctly calculated the number of cells would be: 1,259,712,000.
Known as the father of microscopy because of his superior designs of microscopes, Anton van Leeuwenhoek is lauded for his building of a microscope that could magnify up to 270 times as well as his observations and descriptions of protozoa and bacteria. People had been using single lenses, such as magnifying glasses, for centuries to observe small things. However, the single lens is limited in its magnifying power. The compound lens microscope created by the Dutch produced a system that allowed one magnified image to be magnified again!
The Dutch naturalist was the first to observe and document these one-celled organisms in 1674. His findings opened up a new field of science and revealed the world of microbiology to the biologist of his day. Additionally, van Leeuwenhoek observed yeast cells, blood cells, sperm cells, and tissue cells.
In 1716 Leeuenhoek wrote, “My work was not pursued in order to gain the praise I now enjoy, but chiefly from a craving after knowledge . . . Whenever I found out anything remarkable, I have thought it my duty to put down my discovery on paper, so that all ingenious people might be informed thereof.”
The understanding of the basis of infectious disease is thought to be one of the most important discoveries of the 19th century. Up to the middle of the 19th century the prevailing belief was that microbes could spontaneously come to life out of inanimate matter. The theory proposed to support this phenomenon was called “spontaneous generation,” and it was thought that disease was not spread from host to human host on droplets of sputum or bodily fluids, but rather was “carried on a miasma of noxious, foul-smelling air”
Scientists rejected the spontaneous generation theory grudgingly. An amateur Dutch lens grinder, Anton van Leeuwenhoek first looked at bacteria in the 1670s. It was not until the 19th century in 1840, almost 200 years later, that Hungarian physician Ignaz Semmelweis (1818–1865), developed, tested, and proved his theory that the much-dreaded childbed fever was being transmitted on the hands of Austrian physicians, who, directly from their gruesome work at the autopsy table, wiped their gory hands on their aprons and then employed them unwashed as they attended women in labor in the great Vienna hospital.
Semmelweis reported his observations in The Etiology, Concept and Prophylaxis of Childbed Fever:
Because Vienna is so large, women in labor often deliver on the street, on the glacis (earthwork), or in front of the gates of houses before they can reach the hospital. It is then necessary for the woman carrying her infant in her skirts, and often in very bad weather, to walk to the maternity hospital. Such births are referred to as street births. Admissions to the maternity clinic and to the foundling home is gratis, on the condition that those admitted be available for open instructional purposes, and that those fit to do so serve as wet nurses for the foundling home. Infants not born in the maternity clinic are not admitted gratis to the foundling home because their mothers have not been available for instruction. However, in order that those who had the intention of delivering in the maternity hospital but who delivered on the way would not innocently lose their privilege, street births were counted as hospital deliveries.
This, however, led to the following abuse: women in somewhat better circumstances, seeking to avoid the unpleasantness of open examination without losing the benefit of having their infants accepted gratis to the foundling home, would be delivered by midwives in the city and then be taken quickly by coach to the clinic where they claimed that the birth had occurred unexpectedly while they were on their way to the clinic. If the child had not been christened and if the umbilical cord was still fresh, these cases were treated as street births, and the mother received charity exactly like those who delivered at the hospital. The number of these cases was high; frequently in a single month between the two clinics there were as many as one hundred cases.
As I have noted, women who delivered on the street contracted childbed fever at a significantly lower rate than those who delivered in the hospital. This was in spite of the less favorable conditions in which such births took place. Of course, in most of these cases delivery occurred in a bed with the assistance of a midwife. Moreover, after three hours our patients were obliged to walk to their beds by way of the glass-enclosed passageway. However, such inconvenience is certainly less dangerous than being delivered by a midwife, then immediately having to arise, walk down many flights of stairs to the waiting carriage, travel in all weather conditions and over horribly rough pavement to the maternity hospital, and there having to climb up another flight of stairs. For those who really gave birth on the street, the conditions would have been even more difficult.
To me, it appeared logical to the patients who experienced street births would become ill at least as frequently as those who delivered in the clinic. I have already expressed my firm conviction that the deaths in the first clinic were not caused by epidemic influences but by endemic and as yet unknown factors, that is, factors whose harmful influences were limited to the first clinic. What protected those who delivered outside the clinic from these destructive unknown endemic influences? In the second clinic, the health of the patients who underwent street births was as good as in the first clinic, but there the difference was not so striking, since the health of the patients was generally much better . . .
In addition to those who delivered on the street, those who delivered prematurely also became ill much less frequently than ordinary patients. Those who delivered prematurely were not only exposed to all the same endemic influences as patients who went full-term, they also suffered the additional harm of whatever caused the premature delivery. Under these circumstances, how could their superior health be explained? One explanation was that the earlier the birth, the less developed the puerperal condition and therefore the smaller the predisposition for the disease. Yet puerperal fever can begin during birth or even during pregnancy; indeed, even at these times it can be fatal. The better health of patients who delivered prematurely in the second clinic conformed to the general superior health of full-term patients in the clinic.
Patients often became ill sporadically. One diseased patient would be surrounded by healthy patients. But very often whole rows would become ill without a single patient in the row remaining healthy. The beds in the maternity wards were arranged along the length of the rooms and were separated by equal spaces. Depending on their location, rooms in the clinic extended either north-south or east-west. If patients in beds along the north walls became ill we were often inclined to regard chilling as a significant factor. However, on the next occasion those along the south wall would become ill. Many times those on the east and west walls would become diseased. Often the disease spread from one side to the other, so that no one location seemed better or worse. How could these events be explained, given the same patterns did not appear in the second clinic where one encountered the disease only sporadically?
I was convinced that the greater mortality rate at the first clinic was due to an endemic but as yet unknown cause. The fact that the newborn, whether female or male, also contracted childbed fever convinced me that the disease was misconceived. I was aware of many facts for which I had no explanation. Delivery with prolonged dilation almost inevitably led to death. Patients who delivered prematurely or on the street almost never became ill, and this contradicted my conviction that the deaths were due to endemic causes. The disease appeared sequentially among patients in the first clinic. Patients in the second clinic were healthier, although individuals working there were no more skillful or conscientious in their duties. The disrespect displayed by the employees towards the personnel of the first clinic made me so miserable that life seemed worthless. Everything was in question; everything seemed inexplicable; everything was doubtful. Only the large number of deaths was an unquestionable reality.
The reader can appreciate my perplexity during my first period of service when I, like a drowning person grasping at a straw, discontinued supine deliveries, which had been customary in the first clinic, in favor of deliveries from a lateral position. I did this for no other reason than that the latter were customary in the second clinic. I did not believe that the supine position was so detrimental that additional deaths could be attributed to its use. But in the second clinic deliveries were performed from a lateral position and the patients were healthier. Consequently, we also delivered from the lateral position, so that everything would be exactly as in the second clinic.
I spent the winter of 1846–47 studying English. I did this because my predecessor, Dr. Breit, resumed the position of assistant, and I wanted to spend time in the large Dublin maternity hospital. Then, at the end of February 1847, Dr. Breit was named Professor of Obstetrics at the medical school in Tubingen. I changed my travel plans and, in the company of two friends, departed for Venice on 2 March 1847.
On 20 March of the same year, a few hours after returning to Vienna, I resumed, with rejuvenated vigor, the position of assistant in the first clinic. I was immediately overwhelmed by the sad news that Professor Kolletschka, whom I greatly admired, had died in the interim.
The case history went as follows: Kolletschka, Professor of Forensic Medicine, often conducted autopsies for legal purposes in the company of students. During one such exercise, his finger was pricked by a student with the same knife that was being used in the autopsy. I do not recall which finger was cut. Professor Kolletschka contracted lymphangitis and phlebitis in the upper extremity. Then, while I was still in Venice, he died of bilateral pleurisy, pericarditis, peritonitis, and meningitis. A few days before he died, a metastasis also formed in one eye. I was still animated by the art treasures of Venice, but the news of Kolletschka’s death agitated me still more. In this excited condition I could see clearly that the disease from which Kolletschka died was identical to that from which so many hundred maternity patients had also died. The maternity patients also had lymphangitis, peritonitis, pericarditis, pleurisy, and meningitis, and metastases also formed in many of them. Day and night I was haunted by the image of Kolletschka’s disease and was forced to recognize, ever more decisively, that the disease from which Kolletschka died was identical to that from which so many maternity patients died.
Earlier, I pointed out that, autopsies of the newborn disclosed results identical to those obtained in autopsies of patients dying from childbed fever. I concluded that the newborn died of childbed fever. I concluded that the newborn died of childbed fever, or in other words, that they died from the same disease as the maternity patients. Since the identical results were found in Kolletschka’s autopsy, the inference that Kolletschka died from the same disease was confirmed. The exciting cause of Professor Kolletschka’s death was known; it was the wound by the autopsy knife that had been contaminated by cadaverous particles. Not the wound, but contamination of the wound by the cadaverous particles caused his death. Kolletschka was not the first to have died this way. I was forced to admit that if his disease was identical with the disease that killed so many maternity patients, then it must have originated from the same cause that brought it on in Kolletschka. In Kolletschka, the specific causal factor was the cadaverous particles that were introduced into his vascular system. I was compelled to ask whether cadaverous particles had been introduced into the vascular systems of those patients whom I had seen die of this identical disease. I was forced to answer affirmatively.
Because of the anatomical orientation of the Viennese medical school, professors, assistants, and students have frequent opportunity to contact cadavers. Ordinary washing with soap is not sufficient to remove all adhering cadaverous particles. This is proven by the cadaverous smell that the hands retain for a longer or shorter time. In the examination of pregnant or delivering maternity patients, the hands, contaminated with cadaverous particles, are brought into contact with the genitals of these individuals, creating the possibility of resorption. With resorption, the cadaverous particles are introduced into the vascular system of the patient. In this way, maternity patients contract the same disease that was found in Kolletschka.
Suppose cadaverous particles adhering to hands cause the same disease among maternity patients that cadaverous particles adhering to the knife caused in Kolletschka. Then if those particles are destroyed chemically, so that in examinations patients are touched by fingers but not by cadaverous particles, the disease must be reduced. This seemed all the more likely, since I knew that when decomposing organic material is brought into contact with living organisms it may bring on decomposition.
To destroy cadaverous matter adhering to hands I used chlorine liquida. This practice began in the middle of May 1847; I no longer remember the specific day. Both the students and I were required to wash before examinations. After a time I ceased to use chlorina liquida because of its high price, and I adopted the less expensive chlorinated lime. In May 1847, during the second half of which chlorine washings were first introduced, 36 patients died—this was 12.24 percent of 294 deliveries. In the remaining seven months of 1847, the mortality rate was below that of the patients in the second clinic.
Louis Pasteur, the Germ Theory, and the Science of Microbiology
Louis Pasteur was born in Dole in eastern France, a tanner’s son. He attended school at Arbois and Besancon with grades sufficient to be recommended for taking the entrance exam for the prestigious Ecole Normale Superieure in Paris. Pasteur failed to pass the exam on his first attempt but his second try was successful. His academic path started with the physical sciences; he did very well in his first degree and progressed to a dual doctorate in physics and chemistry with a major in crystallography.
Five avenues of investigation defined Pasteur’s scientific and research methods:
1. Skill and tenacity as a researcher
2. Microscopy
3. The uniqueness of the chemistry of life
4. Ability to capitalize on raw luck
5. High public impact from his research
In 1849 Pasteur took a position with the University of Strasbourg as a professor of chemistry, continuing to study asymmetry of crystals and reveled in his growing scientific reputation. Pasteur’s personal situation changed following his marriage to Marie Laurent, the daughter of the rector of the university who gave devoted and practical support to his career. Six years later, Pasteur moved to the University of Lille as dean of the new Faculty of Science, with a mission to support the university’s goal of joining teaching and research with the participation of local industries through the application of science. Pasteur taught bleaching, refining, and brewing, although his research continued to investigate asymmetric compounds and their optical properties.
Pasteur’s interest in the chemistry of living organisms directed his investigations of fermentation, particularly the part played by yeast in the production of alcohol. In 1857 Pasteur published the results of research on lactic acid, which was a common by-product of abnormal fermentation, and on amyl alcohol. Pasteur was convinced that the asymmetric optical properties of amyl alcohol came from the process of fermentation, which confirmed his belief that it was a product of living creatures.
Pasteur’s beliefs flew in the face of accepted dogma that fermentation was a chemical process. In 1860 Pasteur was called back to Ecole Normale to be director of scientific studies. At this time he published a significant study that showed unequivocally that fermentation was in fact a biological phenomenon. Pasteur then redirected his microscopic studies from crystal structures to looking at wine fermenting and sour milk, observing that yeast and other “ferments,” which historically had been looked at as large molecules, were in fact yeast that had changed shape during fermentation—thus confirming that yeast were living cells or their “germs.”
Pasteur’s view that fermentation was a biological process rather than a chemical reaction, pulled him into a high profile public debate with Felix-Archimede Pouchet, who was a vocal supporter of the theory of spontaneous generation that states that life can begin from nothing.
Pouchet spoke out in support of the theory of spontaneous generation until the end of 1850s. Pasteur first spoke out against the theory in February 1860, and then published a prize winning essay arguing that life always arose from existing life. Pasteur used fermentation and decomposition (putrefaction) in infusions of natural organic substances as his growth medium. Pasteur always maintained that new life in the laboratory was always due to contamination by living ferments. Pouchet still argued that they could arise spontaneously without contamination.
The two scientists joined in a scientific duel, sharing experimental results and polemics, in which fine matters of technique in sterilization were mixed with reflections on the religious implications of whether life was constantly being created. Pasteur sided with the view that life had been created in the “distant past by God’s creation” and could not arise simply by mixing inorganic materials and physical forces. The contest was decided in Pasteur’s favor and against spontaneous generation, not only through the emerging consensus of the scientific community, because in a highly unusual move judgments in Pasteur’s favor were awarded by committees of the French Academy of Sciences.
The controversy drew Pasteur toward new and unusual investigation of disease in animals and humans. Medical doctors had long posed that the development of fevers and septic infections were similar to fermentation and putrefaction; thinking of these processes as a result of invasion by living organisms or their “germs,” rather than a chemical process, posed new and highly controversial questions. Initially, the connection between small unseen organisms and disease was a theory. However, Pasteur was able to successfully package the idea as the “germ theory of disease.”
The term “germ” carried the message that the organisms were protein, widely dispersed in the environment (in air, water and soil), and potentially infectious via multiplication. The designation “theory” inferred that the germ’s connection to disease was still to be proved. Typical of Pasteur’s method of thinking, he employed practical applications of his germ theories of fermentation and putrefaction by demonstrating that by heating wine to 50C, one killed the yeast cells and prevented the deterioration of wine to vinegar—the same process used to prevent milk from spoiling became known as “pasteurization.”
The most highly regarded medical use of Pasteur’s germ theories were employed by Joseph Lister, a British surgeon, who posed that septic infection of wounds was due to contamination of the wound, either surgical or traumatic, by putrefying germs and developed methods of antisepsis. Lister became a vociferous supporter of the wider use of germ theories to all infections and contagious diseases, while always crediting Pasteur for the basic discovery.
In 1865 Pasteur’s reputation for successfully applying science to solve common problems caused the French government to draft him to head a team to investigate a devastating disease in the silk industry. After three years of investigation, Pasteur showed that the disease was caused by a parasite, and changes in management were produced to keep the silk worms parasite and germ-free and healthy.
Pasteur’s broad success continued to give more exposure to germ theories for the genesis of disease. Because of wide public interest in the germ theory, medical investigators across the world incorporated the germ theory into their research procedures and private medical practices.
Pasteur suffered his first stroke that produced a partial paralysis on his left side and which continued for the remainder of his life. However, the stroke did not slow the energy or pace of his research; in fact, Pasteur enjoyed the most productive time of his career following the stroke.
Pasteur’s first study of an infectious disease was one that was primarily a threat to the French livestock: anthrax, although on rare occasions it could also infect humans.
The bacterial cause of anthrax was established by Robert Koch in 1876. Although Pasteur questioned Koch’s experimental procedures, he is famous for his creation of a vaccine for anthrax by using the principle employed for creating the vaccine for smallpox, which is that contracting a mild infection can protect against a more serious infection.
The anthrax bacillus (Bacillus anthracis) is an anaerobic bacteria, one that flourishes in a low oxygen environment, so Pasteur reduced the virulence of the bacillus by exposing it to the oxygen in open air. In the laboratory trials Pasteur was immediately successful. He then took his “attenuated” vaccine to Pouilly-le-Fort near Paris in 1881.
Twenty-five sheep were vaccinated and twenty-five sheep were used as unvaccinated controls. Two weeks later, all fifty sheep were inoculated with viable anthrax bacillus—germs! A majority of the vaccinated sheep survived and almost all of the unvaccinated sheep died of anthrax.
In addition to providing an immediate benefit for the French farmer, Pasteur’s success demonstrated that vaccination can be employed to defend a population against all infectious diseases. Pasteur was immediately “lionized” at the International Medical Congress in 1881 and was blessed with the continuing support of the French government.
Pasteur’s prestige continued to grow as he successfully took on more complicated projects, including the production of a post-exposure vaccine for rabies. While rabies is rare in a human population, it produced a high public anxiety because no one survived the disease—once symptoms of clinical rabies appeared, a predictable path to a horrible death was inevitable.
Pasteur and his team produced rabies in laboratory dogs and rabbits. The early trials of the vaccine on dogs were successful and were then tested on humans for safety. The idea was to use the extended incubation period of the rabies virus to help the patient build up a defense, an immunity to the causative virus before irreversible symptoms and death occurred.
The first public trial was Joseph Meister, a boy who had been bitten by a rabid dog in eastern France. The boy was brought to Paris by his parents who had read of Pasteur’s attempts to find a cure for rabies. The boy survived and the vaccine was used on a second rabies infected boy with great success. Following the release of these successes to the public in 1885, rabies victims from France, Europe and around the world came to Pasteur’s laboratory for the treatment.
The popular press of the day made Pasteur’s rabies cure a front page story, lauding him as one of the greatest scientists and humanitarians of the time and whose research was destined to deliver man from the terrors of epidemics of infectious diseases—germs had been defeated!
Additional awards and rewards flowed to Pasteur, but the greatest of them was a public grant to fund an institution to pursue his research on a grand scale. A grand opening of the Pasteur Institute occurred in November 1888.
At his death in 1895, Louis Pasteur was viewed as a French national hero and an international celebrity. He was best known to the general public for his research and public service in the science of infectious disease. To academia, Pasteur was an icon in the fields of stereochemistry, the biological basis of fermentation. Pasteur personally defeated the theory of spontaneous generation, proved the germ theory of infectious disease, and proved the economic benefits and human safety benefits of laboratory research.
Pasteur’s elevated public image is thought to be due to a combination of self-promotion and well-respected skills in the theory and practical application of the science of microbiology.
When Louis Pasteur conducted his famous experiment in 1859, the idea that germs could infect and make people sick and even kill them was generally accepted, although it was meeting extreme resistance from those who still believed in the theory of spontaneous generation.
Pasteur’s experiments finally answered the question of whether spontaneous generation is possible. He created flasks of broth covered with filters or fitted with narrow, downward-curving stems that admitted air but excluded the tiniest of organisms and particles—and these devices failed to grow bacteria by spontaneous generation.
Robert Koch, disturbed by “physician’s new and widespread belief that all disease was caused by infectious organisms,” established a set of postulates that needed to be satisfied before one could say that a disease was caused by an infectious organism:
1. An organism must be isolated from a patient with the disease
2. The suspected agent must be able to be grown on artificial medium
3. The pure organism must injected into a susceptible host and the disease reproduced
4. The agent must be able to be re-isolated from the infected susceptible host
5. The agent collected from the experimentally infected host must be able to be grown on an artificial medium and identified as the original organism
After satisfying all of the postulates the recovered organism can with confidence can be called the causative agent.
Pasteur apparently enjoyed success because he lived his own and frequently quoted maxim:
“In the fields of observation, chance favours only prepared minds.”
—Louis Pasteur
Quoted from a speech at the University of Lille, 1854
Alexander Fleming and the Discovery of Antibiotics
When Scottish biologist Alexander Fleming returned from his 1928 summer vacation, he noticed a mold growing in one of his culture dishes of bacteria. The bacterial population covered the surface of the growth media except for a bacteria-free zone around the mold. Fleming deduced correctly that the “molds juice” was toxic to the pathogenic Staphylococcus spp.
Fleming understood very well the potential of the agent he called penicillin. He retested the new drug against additional disease causing organisms with positive results. However, the mold was difficult to grow and the active drug was difficult to isolate. Ten years later during World War II Allied governments joined forces and found a way to solve the manufacturing problems and determined that the mechanism of action of the antimicrobial substance was the prevention of the development of the bacterial cell wall.
In the middle of the 20th century, the pharmaceutical industry produced numerous families of antibiotics. These rapidly replaced the old standbys of tincture of iodine, hydrogen peroxide, and grandma’s collection of herbs, colloidal silver, and aroma therapy oils that had been employed as wound disinfectants and systemic killers of germs for centuries, in some instances they had used for millennia—particularly against bacteria.
In the decades following World War II, “super-bugs” appeared that had adapted and biochemically learned how to survive treatments with the new antibiotics. The “miracle drugs” that had been created by the pharmaceutical giants were defeated by single celled organisms. A common example of these successful germs is known as Methicillin-Resistant Staphylococcus aureus (MRSA).
According to the Centers for Disease Control, each year in the United States, 94,000 patients, contract MRSA infections. Of these 19,000 patients, almost 20%, die.
A 1998 study published by the Centers for Disease Control stated that American doctors annually inflict 2 million infections upon American hospital patients and 90,000 of these infected patients die each year.
A common bowel bacteria, Clostridium difficile, infected 87,000 and killed 30,000 American hospital patients in 1993. The annual infection numbers in American hospital patients from “C. diff” rose to 487,000 by 2010, a 400 percent increase in 17 years, hardly a sign that doctors were vigorously trying to solve problems.
“Taming the new drug-resistant pathogens requires ever more toxic, expensive, and time consuming therapies, such as a class of last resort antibiotics called carbapenems, which must be administered intravenously in hospitals. In the United States alone, fighting drug-resistant infections costs up to eight million additional patient hospital days at a cost of $34 billion every year . . . Now, the emergence in India of a particularly nasty form of antibiotic-resistant bacteria, which renders even the last-resort drugs obsolete could bring about an era of unstoppable infections . . .”
—The Economist (March 31, 2011)