circumstances that were ideal for spread of the disease; and the mobility inherent in urbanization and industrialization meant that infected individuals could carry the disease more rapidly and further afield to more individuals (Holmberg, 1990). A third factor was the commercialization of food production, which led to increased movement of animals and animal products between farms and population centers. This allowed contaminated milk from one herd to be mixed with the milk of many herds and thus reach larger numbers of people (Collins and Grange, 1983). During this period it is estimated that 25 percent of European cattle were infected with M. bovis. The confluence of these factors contributed to long-term interrelated epidemics of tuberculosis in cattle and humans.
In 1882 Robert Koch, a general practitioner in Germany, isolated an organism he called the “tubercle bacillus” (Myers, 1940). He was specifically interested in tuberculosis because it accounted for one-seventh of all his cases (Sakula, 1979). Koch's proof that this organism M. tuberculosis, was the causative agent of what we know as tuberculosis is the basis for all modern causal associations (Myers, 1940; Daniel and Janicki, 1978; Koch, 1932). The organism that caused tuberculosis in cattle (M. bovis) was found to differ from M. tuberculosis and to cause some tuberculous disease in humans (Collins and Grange, 1983).
In an attempt to devise a cure for human tuberculosis, Koch produced a sterile filtrate of the tubercle bacillus culture. He believed that this material would be therapeutic if injected into tuberculous patients. Unfortunately, there was no therapeutic effect from Koch 's tuberculin, although it was observed that patients infected with tuberculosis developed fever, chills, and vomiting after being injected, while nontuberculous patients showed no response after injection (Daniel and Janicki, 1978). Eventually tuberculin was used as a tool to diagnose tuberculosis in animals and humans.
Cattle were introduced to North America in the 1500s by Spanish explorers arriving through the Caribbean and Mexico. One hundred years later cattle from Britain and northern Europe were being imported to the east coast of North America; 25 to 50 percent of these cattle were infected with tuberculosis. At the same time, the majority of human immigrants from Europe had active tuberculosis or had been infected at some time in their life and thus were potential carriers.
Through the 19th century 20 percent of all deaths were caused by tuberculosis (Holmberg, 1990). In 1800 in New England, deaths caused by tuberculosis in humans peaked at the estimated rate of 1 percent of the population per year. This rate began to decline in New England after 1820, but peak rates in other population centers followed the development of urbanization.
The highest rates in the Midwest occurred in the 1840s and in San Francisco in 1870. After the Civil War the death rate caused by tuberculosis was highest in the African American population as they moved to urban areas and became more mobile (Grigg, 1958). These peaks all related to the spread of the disease among susceptible populations living in crowded conditions.
Since peaking in the 1800s in the United States, the prevalence of tuberculosis has declined steadily at a rate of about 5 to 6 percent per year. Several contributing factors have been suggested for this decline. Natural selection has had an opportunity to act on the U.S. population over the past 2 centuries and it is argued that individuals today have greater natural resistance than did their ancestors. Improved housing with a decrease in the number of individuals per housing unit may have