LEPROSY IN THE AMERICAN
MIDWEST
Leprosy in the Midwest? How was that possible?
It entered from Scandinavia, predominantly from Norway. Present in Norway since at least the time of the Vikings, leprosy resurged in the early 1800s along with scabies, tuberculosis, and other diseases associated with poverty and poor hygiene. Severe economic hardships in Norway had followed the Napoleonic wars of the early 19th century, providing a setting for poverty-related diseases. Before long, Norway, with a new constitution and elevated social awareness, began to tackle the problems with studies of health and poverty. One such survey, done in 1836, identified 659 leprous patients and acknowledged it as an incomplete count.
Carl Wilhelm Boeck, a dermatologist (whose nephew is
Carl Wilhelm Boeck
(Wikipedia)
associated with Boeck’s sarcoid), and Daniel C. Danielssen published a thorough study of leprosy, Om Spedalskhed (On Leprosy), in 1847, in which the investigators described the two basic clinical types of “nodular” and “anesthetic” leprosy (diffuse skin infiltration of disease and peripheral nerve involvement), a classification still in use today. The study was a factor spurring the government to open, in 1849, a hospital in Bergen devoted solely to research on leprosy, Lungegaard Hospital. It supplemented the old St. 
D. C. Daniellsen
(Wikipedia)
Jørgen’s Hospital for leprosy, dating from the 15th century, that provided what care was available. Daniellsen was appointed the first chief physician at Lungegaard Hospital.
A few years later, in 1856, the country established a national Leprosy Registry, the first of its kind, to track all patients and help guide public health measures.
Lungegaard Hospital, taken between 1900-1920 (courtesy K. Knudsen & Co: https://marcus.uib.no/instance/photograph/ubb-kk-1824-4307.html)
Poverty in Norway, particularly in the western parts, also drove migration to the United States. The bulk of Norwegians settled in Illinois, Iowa, Minnesota, and the Dakotas, engaging mainly in farming. Some brought leprosy with them. News of leprosy in America prompted Norwegian Drs. Jean Holmboe and Wilhelm Beck to visit the area. Both noticed that the overall health of the immigrants had improved and in occasional cases their leprosy seemed to have resolved. Boeck credited the improved living conditions in America, saying “They have settled on fertile lands, where they certainly have to work hard to make a living, but they, generally, never undergo hardships, as we, in Norway, understand the term.” They also found cases developing after arrival, but all had come from endemic areas in Norway and most from families with leprosy, suggesting they were incubating the disease on arrival. Most authorities at the time considered the disease to be hereditary though some favored contagion or miasmas.
Minnesota was an early state to develop a public health department, opened in 1873. (California’s, the second in the U.S., opened in 1870). In Minnesota, Dr. Christian Grönvold, a Norwegian immigrant with university degrees from Norway and a medical 
Christian Grönvold (courtesy Goodhue County
Historical Society, Minnesota)
degree from Humboldt University in the U.S., settled in Minnesota, joined the Health Department, and took an interest in leprosy. His careful detective work confirmed that the cases appearing after arrival in Minnesota all came from endemic regions in Norway, usually with affected family members. Leprosy in settlers without such background was non-existent. To Grönvold, theories of heredity and contagion were both plausible.
Back in Bergen, the Lungegaard Hospital had taken on a young physician, Armauer Hansen, as a pathologist and researcher. He had just returned from a stint above the arctic circle caring for fishermen and native peoples. Interested in the new findings of bacteriology, Hansen searched leprous tissues microscopically and found faint clusters of thin rods, difficult to see because of the inadequate staining techniques at the time. In 1874, Hansen published his findings, promoting the idea of a bacterial cause of leprosy, though nothing grew in cultured material. 
Bust of Amauer Hansen (Wikipedia)
Danielssen, under whom Hansen worked, persisted in his belief that leprosy was a hereditary disease. He injected lepromatous material into his own tissue and no disease resulted, affirming his belief. The difference of opinion, though, did not prevent Hansen from marrying his daughter. And the new son-in-law gave leprosy another name: Hansen’s disease.
The issue of the hereditability of leprosy persisted despite the bacteriologic findings. In 1887, Hansen wrote to the then Secretary of the Board of Health of Minnesota, Dr. Charles N. Hewett, saying that the heredity question would be difficult to resolve in Norway because of leprosy’s high prevalence. However, in America, by tracing the offspring of lepers in an environment with fewer cases, several would be ill if the disease was inherited. The following year, Hansen, on a trip to America, was able to report that among the numerous offspring of Scandinavian lepers (some were Swedish), including grandchildren and great-grandchildren, none showed signs of the disease. As a result, the State avoided strict isolation policies and required only that leprous patients staying home must occupy their own bedroom and bed and not share utensils. Up to 1948, Minnesota reported 108 lepers, the vast majority from Scandinavia.
Leprosy in neighboring states, such as Illinois, Wisconsin, Iowa, and the Dakotas, was not tracked as well, but the pattern was similar. In Wisconsin, bedroom and utensil isolation were recommended. Some states refused entry of immigrants with leprosy, but physicians realized that many cases were asymptomatic on arrival, developing features of the disease over time. Data from the other states are sparse. Gradually, the disease died out in the upper Mississippi Valley area. Overall, the number of lepers in this region may have numbered around two hundred, perhaps more.
Studies of the leprous patients in the upper Mississippi Valley, particularly the work of Christian Grönvold in Minnesota, helped end theories of a hereditary basis for leprosy, allowed for the relatively liberal isolation policies adopted, and provided a model for international cooperation.
SOURCES:
Gussow, Z, Leprosy, Racism, and Public Health: Social Policy inChronic Disease Control. 1989, Westview Press.
Washburn, W L, “Leprosy among Scandinavian Settlers in the Upper Mississippi Valley, 1864-1932.” Bull Hist Med 1950; 24 (1): 123-148.
Grönvold, C, “Leprosy in Minnesota.” Chicago Medical J and Examiner, 1884; 48: 133-39.
Hewitt, C, “Leprosy and its Management in Minnesota.” Public Health Papers and Reports 1890; 16: 172-5.
Feldman, W H, “Gerhard Henrik Armauer Hansen: What Did He See and When?” 1965; Int J Leprosy33 (3): 412-16.
Irgens, L M, “Leprosy in Norway: An Inte3rplay of Research and Public Health Work.” 1973; Int J Leprosy 41 (2): 189-198.
Esson, A, “Faces of the Past: Dr. Just Christian Grönvold.” Accessible at: https://www.republicaneagle.com/news/community/faces-of-the-past-dr-just-christian-gronvold/article_ce4c2711-90ed-501e-a22f-3e6ff1ed457a.html
A full index of past essays is available at: https://museumofmedicalhistory.org/j-gordon-frierson%2C-md
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