“Infectious Causation of Disease: An Evolutionary Perspective”, Gregory M. Cochran, Paul W. Ewald, Kyle D. Cochran2000 (; backlinks; similar)⁠:

Over the past two centuries, diseases have been separated into three categories: infectious diseases, genetic diseases, and diseases caused by too much or too little of some noninfectious environmental constituent. At the end of the 19th century, the most rapid development was in the first of these categories; within three decades after the first cause-effect linkage of a bacterium to a disease, most of the bacterial causes of common acute infectious diseases had been identified. This rapid progress can be attributed in large part to Koch’s postulates, a rigorous systematic approach to identification of microbes as causes of disease. Koch’s postulates were useful because they could generate conclusive evidence of infectious causation, particularly when (1) the causative organisms could be isolated and experimentally transmitted, and (2) symptoms occurred soon after the onset of infection in a high proportion of infected individuals. While guiding researchers down one path, however, the postulates directed them away from alternative paths: researchers attempting to document infectious causation were guided away from diseases that had little chance of fulfilling the postulates, even though they might have been infectious. During the first half of the 20th century, when the study of infectious agents was shifting from bacteria to viruses, Mendel’s genetics was being integrated into the study of disease. Some diseases could not be ascribed to infectious causes using Koch’s postulates but could be shown to have genetic bases, particularly if they were inherited according to Mendelian ratios. Mendel’s genetics and Koch’s postulates thus helped create a conceptual division of diseases into genetic and infectious categories, a division that persists today.The third category—diseases resulting from noninfectious environmental causes—has a longer history. The known associations of poisons with illness provided a basis for understanding physical agents as causes of disease. The apparent “contagiousness” of some chemical agents, such as the irritant of poison ivy, led experts to consider that diseases could be contagious without being infectious. Even after the discovery of causative microbes during the last quarter of the 19th century, many infectious diseases were considered contagious through the action of poisons, but not necessarily infectious1.

…This tendency to dismiss infectious causation has occurred in spite of the recognition that (1) infectious diseases are typically influenced by both host genetic and noninfectious environmental factors, and (2) some chronic diseases, such as tuberculosis and syphilis, have long been recognized as being caused by infection. In this essay we analyze the present conceptions of disease etiology from an historical perspective and within the framework offered by evolutionary biology. We begin by analyzing the degree to which infectious causation has been accepted for different categories of disease over the past two centuries with an emphasis on (1) characteristics that make the infectious causes of different diseases conspicuous or cryptic, and (2) the need to detect ever more cryptic infectious causes as a legacy of the more rapid recognition of the conspicuous infectious causes. We then consider principles and approaches that could facilitate recognition of infectious diseases and other phenomena that are not normally considered to be of infectious origin.