Infectious diseases are diverse. They are diverse in transmission modes, diverse in their use of host tissues, and diverse in the harm they cause. Medicine understands the acute infectious diseases fairly well because the chains of infectious transmission range from being very conspicuous to pretty conspicuous. A few, such as smallpox and malaria, cause terrible problems for people. But the vast majority rarely kill, and most are so mild that the fitness costs they impose on humans would not be sufficiently high to implicate infection.
No one grasps yet the distribution of virulence among chronic infectious diseases because the health sciences are now still in the midst—or perhaps at the beginning—of discovering the scope of infectious causation of chronic diseases. The germ theory has been widely accepted since about 1880. During the first century of this period, almost all the recognized chronic infectious diseases had a distinct acute phase. Diseases like tuberculosis had chronic phases that were easy to link to infectious causes because the development of chronic disease involved a slow and observable transition from the acute phase to the chronic. The chronic phases of diseases like syphilis were a bit more difficult to recognize as being caused by infection, because of gaps
between the acute and chronic phases and because the different phases had fundamentally different symptoms. The acute phase was characterized by lesions on the genitalia, the first chronic phase by a generalized rash, and the late chronic phases by such a variety of disease states, including heart disease, insanity, and paralysis, that syphilis became known as the great imitator. A chronic disease such as shingles was still more difficult to link to its infectious cause because it surfaced after a long disease-free period had elapsed after the acute phase, which we call chicken pox; moreover, shingles does not occur in everyone who has had chicken
pox—some people die before it would have occurred, and the immune systems of other people have apparently so thoroughly controlled the virus that it cannot resurge in the form of shingles.
During the first three decades of the germ theory, from about 1880 to 1910, the scope of acute infectious diseases was quickly resolved, and hypotheses for infectious causation of chronic diseases were advanced. Chronic diseases that were the most easily linked to their acute
beginnings were broadly accepted during this period as different manifestations of specific infectious processes.
During the first half of the twentieth century, medical researchers confirmed that infections caused various chronic diseases that appeared as delayed consequences of acute diseases with entirely different symptoms. In 1909 the Hungarian pediatrician J. von Bokay provided evidence that convinced many of his colleagues that the hypothesis he first published in 1892 was true: shingles is a delayed manifestation of chicken pox. After about a half century of observation, experimentation, and debate about rheumatic fever, it was finally accepted during the 1940s as a delayed, often chronic manifestation of previous infection with Streptococcus pyogenes, the primary agent of strep throat.
By the middle of the twentieth century medical science was poised to move into an even more cryptic realm of the spectrum of infectious disease—those chronic diseases that were caused by infections that did not generate obvious acute phases. Then medical science dropped the ball. A few people noticed it, and kicked it around a bit, but for the most part it was left alone. This period strikingly parallels the three decades before the first flowering of the germ theory in the nineteenth century, when Jacob Henle’s call for investigating infectious causation of acute diseases was similarly dismissed without any evidence to justify the dismissal. It is not entirely clear why medicine dropped the ball between 1950 and 1980. In the 1940s the hypothesis for the infectious causation of peptic ulcers, cardiovascular disease, and cancer was still being considered. In some cases people were even being cured with antibiotics. A combination of developments in science and medicine were misinterpreted and misapplied as leaders failed to guard against the biases of human thought.
Ironically, one of the reasons for this slowdown was the same reason for the tremendous success in identifying infectious causation during the preceding three quarters of a century: the adherence to Koch’s postulates. In a presentation to the Tenth International Medical Congress held in Berlin in 1880, Robert Koch set out powerful guidelines for identifying infectious causation. These guidelines, which have come to be known as Koch’s postulates, were simple rules for maintaining a high standard of evidence in an area of research that was burgeoning at the end of the nineteenth century. Koch advised researchers to (i) demonstrate the putative pathogen in each patient with the disease, (ii) recover and grow the pathogen in pure culture, (iii) produce the disease in humans or laboratory animals with the cultured microbe, and (iv) recover the pathogen microbe from the diseased animals. The historical record shows that when these guidelines were met, the diseases invariably turned out to be caused by infection. This success then led many experts to insist that infectious causation be accepted only when these guidelines had been met—and that is where the logical error crept in. The goal of the experts was laudable; they were trying to ensure that medical research would be rigorous. But they presumed that if a batch of evidence is sufficient for the acceptance of the validity of an argument in one situation, then other kinds of evidence are insufficient for the acceptance of the validity of the argument in other cases. Koch did not make this error; he cautioned that researchers should not use these guidelines as the only basis for ascribing infectious causation. Unfortunately, it is easier to follow guidelines than to think critically on a case-by-case basis, and the experts of the
mid-twentieth century set in stone Koch’s postulates as the standard for ascribing infectious causation. The consequence was that even when important evidence of infectious causation was available, it tended to be dismissed if Koch’s postulates were not satisfied. This dismissal had major consequences for understanding the scope of infectious causation because for some infectious diseases Koch’s postulates can be virtually impossible to fulfill.
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