Despite the antiquity of concepts that seem to be associated with the germ theory of disease, microbiology was not established as a scientiﬁc discipline until the end of the nineteenth century. In the process, scien- tists and medical reformers often cast their arguments in terms of an opposition between contagion theory and miasma theory. Although the miasma theory of disease was the primary stimulus to the public health campaigns of the nineteenth century, closer inspection of the evolution and usage of these terms in earlier periods suggests that they were not necessarily seen as mutually exclusive. Sharp distinctions between contagion and miasma models might be considered rather misleading and anachronistic when applied to the period between Girolamo Fracastoro’s On Contagion (1546) and triumph of microbiology at the end of the nineteenth century. That is, Renaissance authors and those who followed them often switched back and forth between the two terms. When contagion was deﬁned loosely enough to include harmful material that was indirectly, as well as directly transmitted, it was not incompatible with equally vague deﬁnitions of miasma as disease- inducing noxious, contaminated air. Thus, when nineteenth-century bacteriologists expressed their interest in Fracastoro as the precursor of germ theory, they were probably interpreting his views in a manner very different from the way in which Fracastoro and other Renaissance physicians saw them.
During the seventeenth century, microscopists established the
existence of tiny ‘‘animalcules,’’ infusoria, the capillary network, and certain kinds of cells. Antoni van Leeuwenhoek (1632–1723), one of the most ingenious microscopists of that period, described molds, proto- zoa, bacteria, sperm cells, and other ‘‘little animals.’’ Nevertheless, most physicians and natural philosophers regarded the notion of ‘‘disease- causing animalcules’’ as little better than ancient superstitions about elf-shot, worms, and ﬂying venom. Moreover, there was little evidence available to decide between the hypothesis that the minute entities
observed by microscopists were the product of disease, putrefaction, and fermentation and the alternative hypothesis that they were the cause of these phenomena.
The idea that disease, impurity, or corruption can be transmitted
by contact is an ancient folk belief. On Contagion (1546) by Girolamo Fracastoro is generally regarded as the earliest exposition of germ theory, but it was Giovanni Cosimo Bonomo (1663–1696) who pro- vided the ﬁrst convincing demonstration that a contagious human disease was caused by a minute parasite close to the threshold of invisibility. Bonomo proved that scabies, commonly known as ‘‘the itch,’’ was caused by a tortoise-like mite (now known as Sarcoptes scabiei var. hominis) just barely visible to the naked eye. When the female mite burrows into the skin and lays her eggs, the unfortunate host develops
a rash and intense itching. The mites can be transferred directly from person to person or by means of bedding or clothing used by ‘‘itchy’’ persons. Sarcoptes scabiei can also affect cats, dogs, horses, cattle, pigs, and wild animals, but the condition is generally referred to as mange. The itch mite, however, was regarded as an interesting curiosity rather than an example that might apply to other diseases.
Further evidence for contagion theory appeared in studies of silk- worm diseases. Agostino Bassi (1773–1857) found that he could transfer the disease called muscardine to healthy silkworms by inoculating them with material taken from worms that had died of the disease. According to Bassi, muscardine was caused by a minute living plant or parasitic fungus. Bassi suggested that other contagious diseases might be caused by similar parasites. The fungus that causes muscardine was later named Botrytis bassiana in honor of Bassi. Johann Lucas Scho¨ nlein’s (1793–1864) search for the cause of ringworm was inﬂuenced by Bassi’s work on muscardine. In 1839, Scho¨ nlein, a professor of medicine at Zurich, reported ﬁnding a fungus in the pustules of ringworm. Unlike the prolix Bassi, Scho¨ nlein set forth his case for a causal relationship between parasite and disease in barely two hundred words.
When Jacob Henle (1809–1895), Professor of Anatomy at Zurich, published On Miasmata and Contagia in 1840, several examples of microparasites as putative agents of disease had been added to scabies and muscardine. Critically evaluating the experimental evidence, Henle discussed the nature of the proofs that would be required to establish a causal relationship between microbes and disease. Although it is pos- sible to link Fracastoro’s account of contagion and miasma to Henle’s hypothesis, the context in which they worked and the centuries that separated them infused very different meanings into their use of the terms miasma and contagion.
Henle argued that physicians blamed disease on miasma, which
they deﬁned as something that mixed with and poisoned the air, but no one had ever demonstrated the existence of miasma with scientiﬁc instruments. Miasma was only presumed to exist, by exclusion, because no other cause could be demonstrated.
According to Henle’s hypothesis, contagia animata (living organ- isms) caused contagious diseases because whatever the morbid matter of disease might be, it obviously had the power to increase in the afﬂicted individual. Given the fact that a small inoculum of pus from smallpox pustules could be used to infect a multitude of people, the con- tagion must be an animate entity that multiplies within the human body. Chemicals, toxins, and venoms remain ﬁxed in amount. By deﬁnition, only living things have the power of growing and multiplying.
One could most logically explain the natural history of epidemics
by assuming that a living agent excreted by sick individuals was the cause. If this agent were excreted by the lungs, it might easily pass
to others through the air. If excreted by the gastrointestinal system, it would enter sewers and wells. Acknowledging the lack of rigorous evi- dence for the germ theory of disease, Henle argued that science could not wait for unequivocal proofs, because scientists could only conduct research in ‘‘the light of a reasonable theory.’’ Although Henle’s theory was generally ignored by his contemporaries, after the establishment of microbiology, his essay on contagion was awarded the status of a landmark.