The Fantastic Laboratory of Dr. Weigl: How Two Brave Scientists Battled Typhus and Sabotaged the Nazis

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The Fantastic Laboratory of Dr. Weigl: How Two Brave Scientists Battled Typhus and Sabotaged the Nazis Page 2

by Arthur Allen


  Arriving at Block 50 in Buchenwald in late 1943, he joined a group of prisoners who were trying to grow typhus germs in the lungs of living, immune-compromised rabbits. This was a task of great importance, for if they could cultivate the germs, the cultures would be used to make a vaccine, which would be immensely valuable to the German military. As long as the lab was contributing to the immunological defense of its soldiers, the Nazi regime would presumably keep the lab open and refrain from murdering its staff. The boss, the SS Dr. Erwin Ding, would be happy, too, because producing a vaccine would secure his position, keeping him far away from battle duty at the eastern front. And after the war, he hoped, the vaccine would win him a university professorship.

  But there were problems with producing a sophisticated vaccine within the thoroughly corrupted confines of a concentration camp. Rickettsia, the intracellular bacteria that cause typhus, had bedeviled biologists for decades. Indeed, their somewhat mysterious existence—for no one knew just what they were—is one of the keys to understanding how Fleck developed his questioning, skeptical view of science. These germs were extremely difficult to grow artificially, though they thrived in lice and sick people. The prisoners in Block 50 knew nothing about how to prepare rickettsial cultures of the type one used to make vaccine. Yet everyone was desperate for success—Ding to further his career, the inmates in order to survive. Those in the thought collective of Block 50—a biologist, a baker, a politician, and a physicist, among others—convinced themselves that they were making a vaccine, and put the fluid substance into vials that were sent off to Hamburg and Paris, where German scientists, men of renown, responded with words of praise. How was this possible? Like 1,000 monkeys with typewriters and time, a group of desperate amateurs had learned how to prepare a devilishly complicated vaccine in the space of a few months. Or had they? Fleck, who arrived when the group was well advanced in its labors, was the only one among them with the appropriate specialized knowledge. He was the only one who knew whether the vaccine they were making was real.

  To most of the inmates of Buchenwald, in any case, the vaccine was not the most interesting thing about the rabbits that were used to grow it. On the night of the big raid, as the Goethe oak burned, the prisoners—French scientists from the Pasteur Institute, tough Polish resistance men, German Communists, Russian peasants, Dutch Jews, and Fleck—all joined in singing the “Marseillaise.” Then they had a feast of rabbit stew.

  CHAPTER ONE

  LICE/WAR/TYPHUS/MADNESS

  Typhus is an unfamiliar disease to most everyone alive today, but it left an indelible mark in past centuries, shaping the fate of empires from Napoleon to Lenin. And no one who has lived through a typhus epidemic will ever forget it. The disease is transmitted by tiny arthropods that live snugly in the seams of warm clothing, which they do not leave, unless evicted, except to suck blood or—when the body they occupy has gone cold, or too hot with fever—to find a new human host. Lice have been seen crawling as far as five feet in an hour. Head lice lay their nits, or eggs, on hair; body lice, in underwear and shirts. The body louse evolved from the head louse when people started wearing clothes and is distinguished from its progenitor by its dislike for the temperatures of the head, our hottest surface.

  Humans and lice have a long, intimate relationship. In one of the earliest sections of Exodus, Aaron “stretched out his hand with his rod and smote the dust of the earth, and it became lice on man and on beast. All the dust of the land became lice throughout all the land of Egypt.” Expressions such as “nitwit” (for those who feel dull, sullen, and “lousy,” after scratching their infected or allergic skin through sleepless nights) and “nitpicking” attest to this, as does the “fine-toothed comb” we use to examine things with care. It has even been hypothesized that the seven-day week and the Sabbath arose in recognition of body louse reproductive patterns—for if clothes are changed each week consistently, a person’s lice and their eggs will die. Yet until a few centuries ago, people in colder climates nearly always carried lice in their clothes and rarely bathed. An account of the 12th-century funeral of Thomas à Becket notes that as his body cooled, the vermin living in the archbishop’s many layers of clothing began to crawl out and “boiled over like water in a simmering cauldron, and the onlookers burst into alternate weeping and laughter.”

  In the modern world, though, the body louse is the louse of refugees, soldiers, and other desperate people. Typhus epidemics occur when a population is at the end of its tether. Starvation, cold, fear, and exhaustion are the normal prerequisites. Typhus corresponds with social collapse. Typhus “will continue to break into the open,” wrote Hans Zinsser, author and Harvard typhus researcher, “whenever human stupidity and brutality give it a chance.” By the time Zinsser wrote these lines in his famous book Rats, Lice and History, published in 1935, typhus was a distant memory to most Americans and Western Europeans, who were too clean for permanent louse infestation. Yet there were parts of the world where it was still an acute danger. At the end of World War I, the worst epidemic in history swept across Russia from Siberia all the way through Poland, causing 30–40 million cases of disease, and killing perhaps three million people. It was in the anteroom of this great catastrophe that Dr. Rudolf Weigl and his assistant Ludwik Fleck earned their stripes as typhus researchers. Working on the basis of new evidence that lice were the vectors of the disease, Fleck and Weigl were on the cutting edge of scientific efforts to tame it.

  When the Austro-Hungarian Empire called up its male subjects to fight in 1914, Weigl was 31 years old, Fleck just 18. Both left their homes in the city of Lviv—which was known to the Poles as Lwów, to German speakers as Lemberg—to become medics in the kaiser’s army. After some training in Vienna, they quickly joined the fight against typhus, which they encountered mostly in Russian prisoner-of-war camps in Bohemia and in western Galicia—around the cities of Lwów, Tarnów, and Przemyl. From 1917 to 1921, Weigl was in charge of a military laboratory—at first under the Habsburgs, and from 1919 for the Polish state—in Przemyl, which straddled the San River. This was a fortress town, now located at the border between Poland and Ukraine, and by some cultural maps a dividing line between Eastern and Western Europe. The Przemyl complex of forts, the third largest in Europe in 1914, fell to the czar’s army in March 1915, after a six-month siege that led to starvation among the poor Jews who lived there. It was retaken three months later, then lost its strategic significance and became something of a warehouse and a way station for troop movements and a center of military medicine, including a modern microbiological laboratory.

  Rudolf Stefan Weigl was born in 1883 in Perov, a picturesque Moravian town now located in the Czech Republic, and was the child of ethnic Germans. His father, who designed and produced vehicles of various sorts, died after crashing a large-wheeled bicycle of his own invention when Weigl was seven. His mother remarried a few years later to a Polish schoolteacher named Józef Trojnar. The family moved frequently from town to town until Trojnar became director of a middle school in Stryj, a wealthy town south of Lwów. The marriage was a happy one, and Rudolf, his older brother, Friedrich, and sister, Lilly, grew up in an atmosphere in which Polish language and culture predominated. After passing his examinations, Weigl enrolled at the University of Lwów, where in 1907 he received his doctoral degree under the zoologist Józef Nusbaum-Hilarowicz, a leading Polish proponent and translator of Darwin’s ideas.

  In the waning years of the Habsburg realm, the monarch had granted Polish autonomy to Galicia, a district stretching from Kraków in the west to east of Lwów and including areas of plains, forests, and mountains. The majority of peasants in the countryside were Ukrainians, the cities inhabited mostly by Poles and Jews. Those who chose to assimilate often learned Polish, the language of government and culture. This contrasted with the Russian- and Prussian-occupied areas of Poland, where assimilated Jews tended to speak German. Perhaps because of the light hand of the Austrian kaiser, the anti-Semitism and ethnic conflict that would
characterize Poland following its independence in 1919 were not as close to the surface in wartime Galicia. Anti-Semitism was evident in the professions, but had not been codified, and was not universal. Thus Weigl was simultaneously a Czech, an Austrian, and a Pole, while his doctorate adviser, Nusbaum-Hilarowicz, was a Jew who had decided to accept a Catholic baptism in 1907, viewing it as a necessary step to achieve promotion to full professor. Weigl’s boss in the military service, Filip Pincus Eisenberg, was also Jewish. A Pasteur Institure–trained bacteriologist, Eisenberg ran a laboratory that was as multiethnic as the empire it served. In 1919, Weigl hired Fleck, who had begun his studies of medicine in Lwów before the war, as his assistant in Przemyl. Fleck was also from an assimilated background. He was the son of Sabina Herschdörfer and of Maurycy Fleck, a craftsman with socialist tendencies who owned a small house-painting business. Though not rich, the Fleck parents were ambitious for their children and sent them to Polish rather than Hebrew high schools, with hopes of offering them a way into the mainstream of Polish society. Maurycy earned enough money to send Fleck and his two sisters, Antonina and Henryka, to university. While Fleck earned his doctorate at Lwów University under Weigl, the girls studied arts and pedagogy in Vienna.

  Eisenberg’s expertise was microscopy, and he was skilled at identifying bacteria in their confusingly variable forms. Weigl, who was extremely adept in the laboratory arts, had already invented a device for improving microscopic lenses—a secondary focus adjustment knob. Fleck would also gain a reputation as a razor-sharp practitioner. In visible terms, the three of them represented the evolution of fashions in facial hair. Eisenberg was balding, with a long beard of the type seen on the waistcoat-with-tails-wearing professors in movies like The Cabinet of Dr. Caligari and The Blue Angel. From his 20s, Weigl had sported a distinctive goatee in the manner of The Three Musketeers, and sartorially he favored open-necked, wide-collared shirts. Fleck liked to dress in neatly pressed suits. He was clean-shaven, increasingly the style as the century went on, in part because of the nascent popular obsession with germs, which were thought to favor beards over smooth skin (an idea encouraged by Gillette and other razor makers).

  Their prey, typhus, was an extremely difficult organism to understand and manipulate. Most successful human pathogens are relatively benign. Cold viruses, to give a classic example, spread far and wide because the humans they infect remain hardy enough to distribute them among their fellow men and women. Malaria doesn’t kill mosquitoes, and Borrelia bacteria, the cause of Lyme disease, harm neither the deer tick nor the deer. Over time, pathogenic organisms generally become less virulent, or they fade away, or have limited success. (Or, as in the case of HIV and tuberculosis, they infect slowly, giving the patient plenty of time to transmit the germ before becoming incapacitated.) The deadly Ebola virus sowed terror when it appeared in Africa in the 1980s, but has proven of little global significance because it infects and kills quickly, before the patient has time to spread it efficiently. This trait is characteristic of new pathogens that haven’t yet adapted to their hosts. At the other end of the spectrum is, for example, Streptococcus pyogenes, known also as Group A strep, which can cause strep throat, toxic shock, rheumatic fever, and scarlet fever, but usually colonizes, quietly, the throats of healthy three- to five-year-old children—at least 15 percent of whom harbor the organism in any given year.

  Rickettsia prowazekii, according to this logic, must be a young disease, for it has not “learned” to occupy a sturdy ecological niche. Experts believe that American natives may have transmitted the disease to Spanish colonists in the 16th century, although some argue it was already present in Europe. R. prowazekii has definite shortcomings. Although it generally kills fewer than 20 percent of the humans it infects, leaving plenty of others alive to transmit it, typhus relies upon a single avenue—the louse—for its spread. And lice not only spread typhus—they are its victims. Sick insects can transmit the disease to humans for up to 10 days. Then they die, and they do not pass along the disease to their eggs. When there are no typhus patients around to sicken the lice, they stop transmitting the disease. The end of a typhus epidemic should thus mean the end of typhus. However, the germ has a few more survival tricks. First, a contaminated louse’s feces contain high concentrations of R. prowazekii and remain infectious for several months. More importantly, human typhus survivors sometimes maintain latent infections for years. Just as a case of chicken pox in childhood can reappear as shingles in old age, typhus patients sometimes experience recurrences as their immune systems weaken. An American physician, Nathan Brill, first discovered such cases among Eastern European immigrants in New York’s Lower East Side in 1913. They seemed especially common among elderly men and women mourning the death of a spouse, which led Brill to call it “bereavement disease.” Hans Zinsser isolated the organism and indentified it as typhus. As old typhus patients die off, Brill-Zinsser disease becomes increasingly rare. But a senior with Brill-Zinsser who became lousy could infect his or her lice, and thus begin the cycle once again. This mechanism keeps typhus alive between epidemics. And if, as scientists believe, these are the only ways that typhus spreads, then the disease will disappear from earth when the last person who ever had it passes away.

  A century ago, typhus’s unique life patterns posed a thorny challenge to researchers. How were they to maintain a steady supply of the organism for study? It was hard to keep typhus bacteria alive in artificial cultures or in the bodies of mice or guinea pigs; there was no way to infect lice with typhus other than to feed them on the bodies of people sick with the disease. But patients were generally available only during typhus epidemics. Even the wobbly medical ethics of those days forbade intentionally infecting people with typhus. After many discussions with Eisenberg about this problem, Weigl hit upon an idea in 1916. Out of concern for his assistant’s future career, Eisenberg had been urging Weigl to drop typhus research and concentrate on cholera, an organism that was easier to culture and grow.

  “Tell me, Sir, where are you going to get the cultures?” Eisenberg asked. “You won’t have access to the typhus organism until you have patients. And you won’t get patients when there is no disease. So how is this going to work?”

  Weigl thought for a moment, then with characteristic earthiness replied, “Well, if we can’t get the louse to eat the germs, we’ll stick them up its ass.”

  Eisenberg did not understand and was not amused. Weigl told him, “Have a look.”

  Whereupon he strode to his workbench and, using a bunsen burner, drew out a long, thin glass pipette. After pinning a louse down on a piece of blotting paper, he proceeded to stick the pipette into its anus, and injected the louse with a tiny droplet of water. Weigl knew from his anatomical work that the insect’s rectum was made of a stiff, chitinous material that would not be easily damaged, if the tube was carefully inserted and its tip carefully rounded.

  Rudolf Weigl, left, Filip Eisenberg, seated, with other lab workers in Przemyl, around 1916. (Courtesy of National Museum, Przemyl. Photograph of original by S. Kosiedowski.)

  And thus a new experimental animal was born—the louse. Grotesque though it was, this was one of the true eureka moments in typhus research, and an important one for the expansion of research into viruses as well. Never before had an insect been used as an experimental animal; Weigl owed his ability to take advantage of this idea to a marvelous manual dexterity. “To watch him tenderly section an insect or create a microscope slide was an intense aesthetic pleasure,” one colleague noted.

  For Weigl, as well as Fleck and the scores of other medics in the employ of the Austrian crown, there was considerable urgency in the work. Austria was largely free of typhus before the war, and the troops of the empire, lacking natural immunity, were ripe for contagion. The crown lands whose health they defended soon burned with typhus, which erupted first in the Balkans, then in Ukraine and Russia.

  The word “typhus” comes from the Greek typhos, which means “smoky” or “hazy,” and ref
ers to the hallucinatory symptoms that arise in the sick mind. The disease is distinct from typhoid fever, whose symptoms can be similar but are caused by an intestinal bacterium present in contaminated food or water. Typhoid fever (in the early days of bacteriology, scientists tended to add the suffix “-oid” or the prefix “para-” to name a “new” organism that they had previously mistaken for another) was distinguished from typhus in the mid-19th century, but the original mistake left a linguistic muddle. In German, for example, Tyfus describes the disease that English speakers call typhoid fever, while the German word for typhus is Fleckfieber, literally “spotted fever.” In English, “spotted fever” may refer to typhus or to Rocky Mountain spotted fever, caused by similar bacteria spread by the bite of certain ticks. To add to the confusion, epidemic louse-borne typhus has less deadly cousins—murine typhus and scrub typhus—spread by fleas and chiggers and ticks in parts of Asia and the Americas, including Texas.

  The body louse bites in order to attach itself to the skin, then feeds by poking a tiny tube called a stylet through the outermost layer. It uses a mechanical pump to draw out blood, and as it eats, it excretes. The bite of the typhus-infected louse does not transmit typhus; rather, the bite and the bug’s saliva cause itching, which leads the human to inoculate himself with the typhus-laden feces by scratching where the louse bit. Typhus germs can live in human cells contained in dried louse waste for up to four months, and some unknown but small percentage of infections occur when the excrement infects people through the lungs, eyes, and nose.

 

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