A history of the building’s unsavory reputation and abandoned sixth floor.
This is part one of a three-part series.
For 50 years, Science Hall was an important center of medical research and education on the University of Wisconsin’s Madison campus. The building was home to the various departments of the medical school from its founding in 1907 until 1956, when the anatomy department finally moved out. Facilities included a mechanically cooled cadaver room in the basement, a cluster of dissecting rooms in an attic wing, and an elevator to convey body parts between floors.
It’s no wonder the building gained an unsavory reputation. A sophomore writing in the January 1928 edition of the Alumni Magazine made special mention of the “the smell of the place.” Medical students at the time purportedly scattered the cremated remains of cadavers behind the building on university property. As late as the 1970s students were still discovering mummified human remains tucked behind the walls. Adding to the ominous mood is the building itself, with its foreboding red-brick façade, looming towers and chimneys, and eccentric Victorian ornamentation. It looks like the kind of place that harbors dark secrets.
The medical school grew rapidly in the first few decades of its existence, expanding into previously unoccupied areas of Science Hall. When the building was completed in 1887, its fourth, fifth, and sixth floors were not heavily used. As demand for space increased, these floors were renovated to accommodate additional uses. After the medical school moved out, new tenants repeatedly adapted and modified these parts of the building. Today the fourth and fifth floors are occupied by classrooms, offices, and labs. Only the sixth-floor attic remains vacant and unused.
The sixth-floor attic of Science Hall sits under the pyramidal roof and gabled wall dormers of the building’s central tower. On the east dormer, two small rectangular windows stare down onto Langdon Street and let in a little filtered sunlight. The attic walls slope dramatically up to the peak of the central tower some 20 or more feet above the wooden floor. Mechanical air handling equipment dominates the center of the room, but otherwise it seems deserted, the floor dusty and littered with odds and ends: old doors and windows, a few chairs and some empty boxes. It is quiet except for the squeaking of the wooden floor beneath one’s feet and the cooing of pigeons nesting in some secluded corner. It feels cut off from the world.
One hundred years ago the impression would have been very different. In the 1920s, the attic housed an important research laboratory with large numbers of small mammals—rabbits, mostly—used in medical experiments. The main focus of the research was finding a cure for syphilis. The timing coincided with the return of veterans from the First World War who were suffering from sexually transmitted diseases, or venereal disease as it was then called. In the U.S. Army during the war, venereal disease was the second-most common reason for disability and absence from duty, and was responsible for the discharge of more than 10,000 men.
The research effort was led by Dr. Arthur S. Loevenhart, the first chair of the Department of Pharmacology and Toxicology in the University of Wisconsin’s Medical School. Born in Lexington, Kentucky, in 1878, Loevenhart earned his B.S. and M.S. degrees in chemistry from the University of Kentucky, then known as Kentucky State College. He received his M.D. from Johns Hopkins in 1903, when he was just 25. He advanced rapidly as a professor of physiological chemistry and pharmacology at Johns Hopkins until 1908, when he came to Wisconsin.
To work on a cure for syphilis, Loevenhart needed laboratory space to house animals and conduct experiments. Space was in short supply. The eventual location chosen for his lab, according to a July 1926 Alumni Magazine article, was “an unused attic in the very top of the tower of Science Hall.” The space had been converted to “one of the most attractive laboratories of its kind in the country” and which contained “a large number of animals infected with syphilis.”
Today only remnants of the lab remain: several standing-height cabinets from which the tops have been removed, a network of galvanized steel pipes to supply water and gas, a gutter for liquid waste, and shelving to hold supplies. Typewritten labels describe what was once stored here: ether, intravenous supplies, spinal fluid devices, and other medical equipment. On the wall an iron bracket marks the one-time location of a Kohler sink. Sheetrock, an early form of plaster wall paneling, covers the walls. The installation directions for the Sheetrock are still visible and help date the lab to the decade of the 1920s.
The fact that Science Hall has an abandoned syphilis lab in its deserted attic is newsworthy enough, but it is not the whole story. The experiments conducted by Loevenhart and his students greatly improved the prognosis for syphilis patients, especially those with an advanced form of the disease known as neurosyphilis. But the work also had implications for another disease, African sleeping sickness, which at the time was the subject of intense medical research in Europe and America. While Loevenhart’s neurosyphilis work focused on patients in Wisconsin, the extension of his research to sleeping sickness had global implications.
Sleeping sickness and syphilis
The causes and symptoms of syphilis and sleeping sickness are unrelated, but both diseases respond to some of the same chemotherapeutic remedies, including arsenicals, or compounds containing the poison arsenic. During the first few decades of the 20th century, labs around the globe tested hundreds of arsenicals to determine their potential therapeutic effects for syphilis and sleeping sickness. The two diseases are historically linked through the work of labs like Loevenhart’s, where researchers sought cures for one disease only to discover a remedy for the other.
Human African trypanosomiasis—more commonly known as sleeping sickness—is an infectious disease caused by a protozoan parasite (genus Trypanosoma) transmitted by the bite of infected tsetse flies. The linkage between the disease and the fly was made in the middle of the 19th century by Scottish missionary, explorer, and Victorian-era hero David Livingstone. Fifty years later, scientists first observed trypanosomes, the parasite causing the disease, in human blood and cerebrospinal fluid. The connection between the parasites, the disease, and the tsetse fly was thus established.
The distribution of sleeping sickness is limited to the range of the tsetse fly in tropical Africa between about 12 degrees North and 20 degrees South latitude. Infection leads to joint pain, headaches, and fever. The victim becomes drowsy and the lymph nodes on the neck begin to swell. Once the parasite infects the central nervous system, the patient goes into a coma and dies.
While sleeping sickness would have been endemic in tropical Africa in pre-modern times, it is generally agreed that the African slave trade and colonialism caused the disease to become widespread. Increases in human interaction and migration, coupled with the opening of new areas for agricultural production, contributed to several devastating epidemics of sleeping sickness that erupted in the early part of the 20th century. A particularly severe epidemic broke out in 1901 in Uganda in the area around Lake Victoria. Within a few years over 200,000 inhabitants, one-third of the population of the region, had died of the disease. Other epidemics occurred in areas that are now part of South Sudan, Tanzania, Zimbabwe, Malawi, Democratic Republic of the Congo, and Central African Republic.
Alleviation of the disease became a priority. At first, the primary health objective was the protection of Europeans who became ill during stints in colonial administration or as immigrants and settlers. Efforts soon shifted to include the local population. While there was no doubt a humanitarian element to these efforts, the rationale was also economic. For the colonial powers, sleeping sickness exacerbated labor shortages associated with the production and transport of agricultural and mineral commodities. Cheap indigenous labor supplied workers for diamond and copper mines, stevedores for river steamers, and bearers for pack trains. With laborers incapacitated or killed by sleeping sickness, economic exploitation was compromised and a cure for the disease became a priority.
The country to first find a cure for the disease would be at a considerable advantage. The race to find a cure began. Soon, trained scientists and doctors were being sent to Africa on research missions to study the disease. Between 1901 and 1913, no fewer than 15 missions went to Africa. A favored location, especially for British and German delegations, was the Lake Victoria region, then sandwiched between British East Africa (roughly modern Kenya and Uganda) and German East Africa (roughly modern Tanzania, Rwanda, and Burundi).
It might seem odd that Loevenhart would be interested in a disease whose geographical reach was limited to tropical Africa.. The United States had played a major role in the African slave trade—until it was banned by Congress in 1808—and participated in the colonial partitioning of Africa to protect its perceived commercial and political interests. But, unlike many European powers, the United States did not lay claim to any African territories; its imperial interests at the time were focused more on Latin America, Hawaii and the Philippines.
And yet Loevenhart consciously became an actor in the geopolitical drama unfolding in Africa at this time, especially Germany’s struggle to reclaim its place as a colonial power in the aftermath of the First World War. Germany had lost its African colonies (essentially modern-day Namibia, Cameroon, Togo, Tanzania, Rwanda, and Burundi) in that war, and was anxious to leverage its medical and scientific discoveries—especially new treatments for sleeping sickness—as a bargaining chip to regain its lost territory. Meanwhile, researchers like Loevenhart sought to neutralize Germany’s advantage by developing even better drugs. It was sort of an arms race, but one where the arms were medicines, not weapons.
Like his contemporaries, Loevenhart’s interest in a sleeping sickness remedy was driven by a combination of factors: humanitarianism, professional aspiration, national pride, and the desire—shared by the citizens of most industrialized nations—to open Africa to further development and commercial exploitation. Unfortunately for Loevenhart, events conspired against him. While his neurosyphilis cures continued to be used until penicillin became widely available after the Second World War, his sleeping sickness remedies were never fully tested and to this day their effectiveness is unknown. He never received the scientific acclaim or financial rewards other researchers gained from their medical discoveries, and the impact he and his students had on medical research in Africa after the First World War was ultimately a minor one.
But given the lamentable role scientists from the industrialized nations played in that research, perhaps this failure was for the best.
Coming in part two: How the search for a sleeping sickness cure instead led to the development of salvarsan, the first effective treatment for syphilis; Arthur S. Loevenhart’s toxicology research at the University of Wisconsin; Use of the arsenic-containing drug tryparsamide to treat neurosyphilis; Drug trials on First World War veterans at Wisconsin Memorial Hospital and the Wisconsin State Hospital for the Insane; Controversies over the effectiveness of tryparsamide, its tendency to cause blindness, human drug testing and the university’s acceptance of external funding for medical research.