Epidemiology and Etiology

In 1811, an anonymous author wrote that milk sickness was a true poisoning because it involved no fever. He also believed that it was caused by poisonous milk that had a peculiar taste and smell. The source of the poison, he wrote, was vegetation eaten by the cows. He further advised that finding the offending plant would remove a major stumbling block to emigration westward.

In the years that followed, the theories as to the cause of milk sickness were numerous. One suggested that the cause was arsenic; another claimed it was a mysterious soil organism, whereas another attributed the disease to a mysterious exhalation from the soil. Still others incriminated various poisonous minerals and springs. Nonetheless there was no definite identification of one specific toxic plant during the nineteenth century. In the 1880s, the medical revolution following the discoveries of Louis Pasteur in France and Robert Koch in Germany led to the expectation that many obscure diseases such as milk sickness would prove to be of bacterial etiology. This expectation appeared to have been realized when Edwin Jordan and Norman Harris (1909) reported that Bacillus lactimorbi was the cause of milk sickness in humans and trembles in cattle. Needless to say, they were wrong.

Beginning in 1905, however, Edwin Moseley of what is now Bowling Green State University in Ohio began a scientific study of the white snakeroot that lasted for over three decades. In careful animal-feeding trials, he established the toxic dose of snakeroot for animals at 6 to 10 percent body weight. He also found that the stems were less poisonous than the leaves and that neither freezing nor drying destroyed the poison. His book, published in 1941, is the definitive work on milk sickness.

Finally James Couch (1928) reported that he had isolated three poisonous substances from the white snakeroot: a volatile oil and a resin acid that did not produce trembles, and an oily liquid with the characteristics of a secondary alcohol that did. The last he identified as C16H2203 and, drawing on the Latin tremere meaning "tremble," named it tremetol.

Heating reduces somewhat the toxicity of poisoned milk, and oxidation readily destroys the toxic properties of tremetol. Because only a small number of cows are likely to be secreting toxic milk at one time, human illness is seen chiefly when milk from a single animal or herd is consumed. It is now thought that the dilution that occurs in the usual dairy collection and distribution of milk from a large milk source, rather than pasteurization, is the reason for the failure of milk sickness to develop in urban areas. For that reason, milk sickness has become extremely rare. Moreover, in rural areas, farmers are now well aware that to avoid trembles or milk sickness, one need only abandon woodland grazing, for the white snakeroot is a woodland plant and almost never found in bright and open pastures.

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