During spring 1817, rumours floated towards the English that virulent form of cholera morbus was attacking British ports in India, and was heading towards Asia. This vicious nature of cholera was the first wave in a series of epidemics during the nineteenth century, and Europeans held their breath as the disease continued its journey, hitting Europe by 1827. Fears of the disease hitting England was well absorbed, as on September 15, 1830, Lord Heytesbury, Russian Ambassador, wrote to the Early of Aberdeen, His Majesty’s Secretary of State for Foreign Affairs, claiming that “the accounts of the progress of cholera morbus are now becoming rather alarming. It is making rapid advances towards Moscow…If the disease once reaches Moscow there can be little doubt that it will spread to St. Petersburg, Warsaw and hence into Germany…It appears to be of a very deadly nature and to have all the character of real Indian cholera.”[1] Nevertheless, the second wave was even more lethal than the first, and English citizens first felt the brunt of the disease during 1831-1832 as the epidemic hit the United Kingdom.  A third wave would follow during 1848-1849, a fourth, 1853-1854, a fifth 1866, before disappearing.

The magnitude of cholera’s impact was well known. Mainly helpless during the first English epidemic, during 1831-1832, English scholars, doctors, and members of government attempted to understand the nature and cause of the disease, in order to combat the affliction it provided. Between the years of 1845-1856, a stunning 700 works on cholera were published in London alone.[2] Introducing the battle against the disease, Frank Mort emphasizes that the “history of the disease is largely preserved within the narrative of the public health and other reform movements in early Victorian Britain. Health, housing, sanitation, the emergence of preventive medicine, the foundations of a national system of education, the reform of industrial conditions – these objects have formed the classic terrain for histories of government and public administration.”[3] Though the during the epidemic of 1831-1832, attention was mainly focused on living urban conditions, and the link of medicine to social factors in order to advocate sanitary reform, the 1840s were spent on focusing on the pathology and mode of communication of cholera itself. Cholera, Chloroform and the Science of Medicine explains that though the 1830s were dominated by the Reform Movements which led to unemployment, poverty, hunger and unrest, and placed Industrial England into unsanitary conditions, a pure contagious version of cholera nevertheless dominated the medical picture; the theory lost its ground to modified versions and non-contagion theories by the second and third epidemics. By the mid-1840s, an intense debate occurred between two parties intent on proving their explanation of cholera: the anticontagionists, and the contagionists.

Disagreements about pathology and cause resided within the contagionist camp, which explained pathological explanations by virtue of infectious agents, such as “viruses,” and the non-contagionist camps, which advocated miasma theories of atmospheric conditions as a cause of the disease. Vinten-Johnasen et al also classify the camps into “pure contagiosness” – contact (with infected skin), formities (e.g. infected bedding), and infection (“virus”) – and “pure non-contagiousness” – Sydenham’s theory of epidemic constitution (atmospheric changes/seasonal pressures), miasmas, and inhaling of poisons. Margaret Pelling also notes that during the Chadwickian period of public health, with Edwin Chadwick’s New Poor Law, historians note the conflict between the miasmatic theory of the sanitarians and what she calls the contagium virum theories as a sharp polarization upon which by the late 1840s, the sanitarians received victory. She argues that this story is not historically accurate, and attempts to destroy the simplicity of the account in Cholera, Fever and English Medicine 1825-1865 (though a very difficult and often confusing book). She presents the thesis denying the sharp polarization between the two camps, and rejects ideas that the contagionists were forebears of later germ theory and provided foundations for modern bacteriology, or that their theories—especially John Snow’s (1813-1858)—about cholera were ignored due to external and socio-political factors from the opposite camp. Rather, she argues that there were several theories of contagium virum, a subtlety picked up by Vinten-Johansen et al, as they note the development of the “contingent Contagionism” camp, and its initial London proponent, James Johnson.[4] The contingent Contagionism camps attempted to merge the problems of the contagionists and the anticontagionists, and merged favoured perspectives of both: from the miasmaists, the chemical curative agent for cholera resides from vegetable and animal matters, and from the contagionists, the transmission of infections and “virus” produced from sick bodies. The contingent contagionists also provided an environmental predisposition for cholera, arguing that crowded populations, concentrated filth were forbearers for the spread of cholera, and thus were also able to advocate sanitary reforms.

The contingent contagionists were widely perceived, and Vinten-Johansen et al provide other supporters of the theory, including E.O. Spooner, William Farr, Justus Leibig and John Snow. Since history grants John Snow credit for solving the transmission of cholera, or least setting the stage for later germ theory, Vinten-Johansen et al implies that based on Snow’s analogy between smallpox and cholera, he was a contingent Contagionism, though by fall 1848, he had changed his mind. Thus, merging his own view with the contingent contagionists, John Snow’s theory was widely received, and even led to governmental support in removing the handle from the Broad Street water pump. Pelling, on the other hand, denies initial success of Snow’s theory, and argues instead that there existed a delayed reception to both John Snow’s theory, and a similar proponent in William Budd’s version, which was mainly due to the lack of explanatory power of their hypothesis.