90 Milk Sickness (Tremetol Poisoning)
Milk sickness, usually called milksick by early nineteenth-century American pioneers, denotes what we now know to be poisoning by milk from cows that have eaten either the white snakeroot or the rayless goldenrod plants.
The white snakeroot, common in the Midwest and upper South, is a member of the Compositae called Eupatorium Urticaefolium. It is also known as white sanicle, squaw weed, snake weed, pool wort, and deer wort. A shade-loving plant, it is frequently seen growing on roadsides, in damp open areas of the woods, or on the shaded north side of ridges. The rayless goldenrod, Haplopappus heterophyllus, is the cause of the disease in southwestern states, such as Arizona and New Mexico.Milk sickness has been called variously alkali poisoning, puking disease, sick stomach, the slows or sloes, stiff joints, swamp sickness, tires, and trembles (when it occurs in animals). It is now known as tremetol poisoning after an identified toxic ingredient of the white snakeroot and rayless goldenrod. Tremetol, obtained from the leaves and stems of these plants by extraction with ether, is an unsaturated alcohol with the empirical formula C16H22O3. In consistency and odor, it resembles turpentine.
Distribution and Incidence
Milk sickness was unknown in Europe or in any other region of the world except North America. It appeared in North Carolina as early as the American Revolution near a mountain ridge named Milk Sick. Its highest incidence was in dry years when cows wandered from their brown pastures into the woods in search of forage. As more forests were cleared so that cattle had more adequate pasture, and as fences were built, the incidence of milk sickness decreased rapidly.
The disease wrought havoc in the Midwest, especially in Illinois, Indiana, and Ohio, and in the upper southern states of Kentucky, North Carolina, Tennessee, and Virginia.
Milk sickness was, in some years and some localities, the most important obstacle to settlement by the pioneers. Beginning about 1815, a flood of pioneers moved west. As they penetrated the forest wilderness of the Midwest they all too frequently came upon evidence of epidemics of the disease as several villages were abandoned. Physicians in Kentucky and Tennessee described milk sickness as being so widespread that the Kentucky legislature appointed a committee in 1827 to investigate its cause. A few years later, the state medical society of Indiana also attempted a similar investigation. Interestingly, in that state it has been noted that “Evansville, Indiana, owes its prominent position... today, in part at least, [to] the fact that its early competitor, Darlington, was abandoned” because of milk sickness (Snively 1967).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 Ofbacterial etiology. This expectation appeared to have been realized when Edwin Jordan and Norman Harris (1909) reported that Bacillus Iactimorbi 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 animalfeeding 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 C16H22O3 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.
Clinical Manifestations
When milk sickness occurs in animals, chiefly cattle, it is called trembles. The animals suffer from anorexia, weakness, falling, stiffness, and trembling.
In humans the symptoms of milk sickness include anorexia, Iistlessness, severe constipation, and - most important of all, and underlying most of the symptoms - profound acidosis; the latter, if untreated, leads to coma and death.
Because of the acidosis, the breath smells of acetone, described in the past as an overpowering “fetor.” The weakness is thought to be due chiefly to hypoglycemia, and death, to ketoacidosis and marked fatty degeneration of the liver, kidney, and muscles. The disease can be chronic or latent, and is likely to recur if the patient is subjected to fatigue, starvation, intercurrent infection, or vigorous exercise.The lethargy that characterizes the patient who has not completely recovered from an attack of milk sickness helped give it the name of slows (or sloes). Abraham Lincoln knew it by that name, and, annoyed by the desultory progress of the Army of the Potomac in the early months of the Civil War, he once tartly remarked that General McClellan “seemed to have the slows.”
History and Geography
Milk sickness has vanished from the list of major concerns of modern Americans. Although endemic in the Midwest and upper South, it had never been seen elsewhere in the United States, in Europe, or in any other continent. The settlers along the Atlantic seaboard knew nothing of it, and if the Indians or their cattle suffered from the disease, they did not inform the early settlers. Not until the pioneers began to push westward beyond the Alleghenies did the disease attract attention.
The first sporadic cases to be recognized occurred in North Carolina in the years preceding the Revolution. It was generally known that on the western side of the Allegheny Mountains from Georgia to the Great Lakes a disorder called trembles prevailed among cattle, and that wherever it appeared, the settlers were likely to get a disease, which from its most prominent symptom received at first the name “sick stomach” and from a theory concerning its cause that of “milk sickness.”
In 1811, the Medical Repository of New York contained an anonymous report entitled “Disease in Ohio, Ascribed to Some Deleterious Quality in the Milk of Cows.” This appears to be the earliest surviving reference to a disease that was to become a frequent cause of death and a major source of misery and mystification in the rural South and Midwest through a large part of the nineteenth century.
William Snively and Louanna Furbee (1956) described a discovery made in 1834 by Anna Pierce Hobbs, a pioneer doctor, in southeastern Illinois. Having learned from a Shawnee medicine woman that white snakeroot caused trembles and milk sickness, she had a calf fed several bunches of the root. The calf developed typical trembles, enforcing her conviction that she had found the cause of milk sickness. John Rowe, a farmer of Fayette County, Ohio, wrote in 1838 that he had discovered through similar experimentation that trembles was caused by ingestion of white snakeroot.
During the second half of the nineteenth century, milk sickness occurred sporadically, which made sequential observations difficult to make, and the reason for its cause was lost in the widely held medical belief in miasmas and exhalations from the ground. Moreover, because milk sickness was limited to the Midwest, upper South, and Southwest, influential eastern physicians tended to ignore it or even discount the possibility that it really existed as a disease sui generis.
Nonetheless, the solution was eventually found when attention was turned back to the poisonous plant theory advanced during the first half of the century. Although many plants were suspected, such as poison ivy, water hemlock, Virginia creeper, coralberry, spurge, mushrooms, and march marigold, scrutiny finally centered once again on white snakeroot. Yet it was not until 1928 that the white snakeroot was established with certainty as the cause of milk sickness - over a century after the anonymous 1811 article appeared.
The question that Snively has asked remains: “How could a disease, perhaps the leading cause of death and disability in the Midwest and Upper South for over two centuries, go unrecognized by the medical profession at large until 1928?”
Thomas E. Cone, Jr.
Bibliography
Anon. 1811. Disease in Ohio ascribed to some deleterious quality in milk of cows. Medical Repository [N.Y.] 3: 92-4.
Couch, James F.
1928. Milk sickness, result of richweed poisoning. Journal of the American Medical Association 91: 234—6.Furbee, Louanna, and William D. Snively, Jr. 1968. Milk sickness, 1811-1966: A bibliography. Journal of the History of Medicine 23: 276—85.
Hartmann, Alexis F., Sr., et al. 1963. Tremetol poisoning — not yet extinct. Journal OftheAmerican Medical Association 185: 706-9.
Jordan, Edwin 0., and Norman MacL. Harris. 1909. Milk sickness. Journal OfInfectious Diseases 6: 401-91.
Jordan, Philip D. 1944. Milk sickness in the western country together with an account of the death of Lincoln’s mother. Ohio State Medical Journal 40: 848-51.
McKeever, George E. 1976. Milk sickness: A disease of the Middle West. Michigan Medicine 72: 775-80.
Moseley, Edwin L. 1941. Milk sickness caused by white snakeroot. Ann Arbor, Mich.
Snively, William D., Jr. 1967. Mystery of the milksick. Minnesota Medicine 50: 469—76.
Snively, William D., Jr., and Louanna Furbee. 1956. Discovery of the cause of milk sickness. Journal of the American Medical Association 196: 1055-60.