The disease in animals was early recognized to have some of the features of diseases that are clearly infectious. Mention is frequently made of the fact that the disease may be carried from one animal to another by feeding the flesh of a diseased animal. In 1843, Heeringen wrote "I am compelled to believe that trembles belongs to the anthrax family." This was twelve years before the discovery of the anthrax bacillus.

In 1877, Philips reports finding "spiral bacteria" in the blood of a typical case, and the same organism, with cocci, in the urine of the same case. He encountered similar organisms in the urine of other

cases.

Gardner (1880) reported finding in the blood of a heifer suffering from the trembles, organisms "that bore in size and behavior a striking resemblance to the form of bacteria called by naturalists bacilla subtilissima." He found the same organism in the water of a spring that had supplied a family in which milk sickness was present. Dogs suffering from slows acquired by eating the flesh of the heifer also had the organism in the blood. He also found the organism in milk. No bacteriologic investigations aided by the advantages of modern methods have been made upon this disease.

Graff (1841) reported some very remarkable experimental work with trembles. He found the flesh of animals not to differ materially in appearance from that of sound animals. Salting meat he says does not impair its poisonous properties. The milk of a cow was poisonous, as shown by feeding it to dogs for eight days after she was reinoved from the infected pasture; but a test made a week later showed the milk to be harmless. He found small amounts of meat or butter sufficient to cause the disease. "One ounce of butter or cheese or 4 ounces of beef, either raw or boiled, administered three times a day, will certainly prove fatal within six days, and often earlier." All these experiments were upon dogs and the flesh of his experimentally killed dogs was as poisonous as the beef that conveyed the disease.

Graff found that treating the flesh with dilute sulphuric acid for two hours did not destroy the poison; even heating had no effect. He says butter heated "to such a degree as to cause it to inflame lost none of its poisonous properties." He failed to extract the poisonous agent from meat by prolonged boiling. He failed in attempts to communicate the disease "by an inoculation with any portion of the body or secretions from infected animals." These experiments lack confirmation.

Milk cows seldom show any symptoms so long as they are regularly inilked, even though they are secreting milk fatal to man and to other animals; in a herd the steers and heifers always show symptoms

before the cows that are giving milk. Buttermilk is generally regarded as harmless. Graff thought differently however.

Apparently not all are equally susceptible, as it has frequently been noted that of several persons who partake of the poisonous milk or meat, some may escape while others, usually the majority, will contract the disease.

A recent outbreak which I have investigated had some of the conditions of an experiment on human beings. The record, unfortunately, is based entirely upon nonprofessional observation but is, I believe, fairly accurate. In brief, it is as follows: Seven persons partook of a meal, 6 of whom used milk and butter and became ill with characteristic symptoms of milk sickness and subsequently died. The only person who escaped was a woman who never used either milk or butter. One of the 6 was a guest and had only this one meal in this house. This individual sickened on the day after partaking of that meal. The other 5 persons became ill at different times; the last one about ten days after eating the meal that apparently poisoned the guest. A calf using the same milk sickened with "trembles" soon after the earliest cases in the family. The cow accused of imparting the disease developed "trembles" and died. The cow showed no symptoms until milking was neglected on account of illness in the family. It was believed that this cow had been on milk sick land about two weeks prior to the outbreak. This outbreak seems to have been a typical one, the sickening of the cow only after she was no longer milked, the sickening of the calf at about the same time that some of the persons were attacked, the onset of the illness at a varying period after the use of the suspected milk and butter, finally, the exemption of the one woman who did not partake of the milk or butter, all agree with the older descriptions. As trembles and milk sickness are both so rare at present, an occurrence like this points strongly to a most intimate relation between them.

The few recorded post-mortem examinations throw no light upon the nature of the disease. Horne (1844), who examined three human cases, found inflamed patches in the small intestine. The mesenteric glands were red and greatly enlarged.

In animals, Graff found the brain" suffused with a large quantity of blood, which from the amount contained within the cranium, must have made great pressure on every part." In one human case he found softening of the brain and evidence of meningitis. Graff tells us that this autopsy was conducted "by stealth at night in the open air, and by the light of a single candle."

contracted to the size of a

Barbee (1840) found the colon in man common candle." The mucous membrane of the stomach was red and thickened in spots; the remainder presented a pale and softened ap

pearance. The peritoneal coat of the small intestines was inflamed. Symptoms. Philips (1877) and others thought that an interval of days or even weeks elapsed between the exposure on infected areas and the development of symptoms of trembles in cattle. Drake describes the symptoms of trembles in animals as follows:

The animal begins to mope and droop, and to walk slower than its fellows, to falter in its gait. If under these circumstances it should be driven, and attempt to run, the debility and stiffness of its muscles are immediately apparent. It fails rapidly, trembles, pants, and sometimes seems blind, as it runs against obstacles, but this may arise from vertigo; at length it falls down, lies on its side quivering, and is not, perhaps, able to rise for several hours, sometimes never

He also mentions a chronic form.

The characteristic symptom, trembling, may always be brought out by exercising the suspected animal. It is related that cattle buyers never purchased animals from milk sick districts until they had given them a run of half a mile or more to ascertain if they had trembles. When a cow is regularly milked no symptoms are likely to develop. In at least some instances a period of several days appears to intervene between the consumption of the poisoned milk or meat and the onset of symptoms in man. Spalding (1881) reports an outbreak where three days in one case and six days in another, intervened between suspending the use of the suspected milk and the onset of the symptoms. He also speaks of the onset in some cases as being "almost instantaneous when milk or beef is taken." It would appear that such cases, with very early onset, may be due to decomposition products belonging to the class of poisons usually called ptomaines. As judged by the description of most writers, the symptom complex in man appears to be fairly uniform. In describing it I will use freely the account of Way (1893). The onset is gradual, the individual tires easily, there is loss of appetite, in a day or two vomiting begins, the bowels are obstinately constipated, there is great abdominal distress, the tongue becomes large and flabby, the breath acquires a foul odor that is regarded as highly characteristic of the disease, the abdomen is scaphoid, there is marked visible pulsation of the abdominal aorta, the temperature is not elevated; in fact, it is generally subnormal, there is always great thirst. The mind usually remains clear, but in fatal cases, coma for several hours may precede dissolution. The average duration of cases is about one week. The cases referred to in the recent outbreak in Tennessee died in from two to ten days after the onset of symptoms.

A common sequel of milk sickness is a lasting debility. I have seen a considerable number of persons who claimed that since an attack of the disease, they were incapacitated for hard work, especially in warm weather.

The mortality is quite high. Physicians who have had a large experience with this disease, tell me that at least half the cases will perish, even when carefully treated. Numerous family outbreaks are recorded where the mortality has been 100 per cent, as was the case in the last outbreak in Tennessee.

Treatment. The early settlers had worked out the very successfu! preventive treatment of keeping their animals from lands known to be dangerous, or what is better, to use for purposes of pasture in endemic foci, only "tame " lands; that is, land from which the timber had been cut. It is even better to bring the land under cultivation but this does not appear to be essential.

With our present knowledge the treatment of the disease should be purely symptomatic. We have no specific remedy. Rest in bed, abstinence from food, stimulating enemeta, and a judicious use of stimulants would appear to be indicated.

The treatment of cases in the early days was somewhat vigorous in accordance with the therapeutic customs of the day. Graff recqmmended free drawing of blood and the use of calomel not to exceed 5 grains every two or three hours. Some advised a much more liberal use of calomel. Counter irritation over the abdomen was a favorite measure used to allay abdominal pain and vomiting. It was generally regarded as essential to secure a free movement of the bowels, and when this had been accomplished the case was regarded as offering a favorable prognosis.

Drake (1841) considered blood letting of doubtful value, but advised the free use of cathartics. Enemeta were frequently used. Philips (1877) used a purely expectant plan of treatment and urged against the use of strong purgatives. He used strychnine in liberal doses, apparently with benefit.

Borland. An essay on the Milk sickness," 1845.

Byford. Nashville Jour. Med. & Surg., 1855, p. 460.

Candler. Am. Jour. Clinical Med., 1907, p. 914.

Coleman. Phila. Jour. of the Med. and Phys. Sci., 1822, p. 322.

Crookshank. Observations on the Milk Sickness, 1840. Phila. Jour. of the Med.

and Phys. Sci., 1826, p. 252.

Drake. Memoir on the disease called by the people the trembles, etc.. 1841. Elder. Transactions Ind. State Med. Soc., 1874, p. 133.

Gardner.

St. Louis Med. and Surg. Jour., 1880, p. 288. Graff. Am. Jour. Med. Soc., 1841, p. 351.

Heeringen. A discovery of the cause of the disease called by the people trem

bles or milk sickness, 1843.

Horne. Western Lancet, 1844, p. 454.

Johnson. Atlanta Med. and Surg. Jour., 1866, p. 289.

Law. The Vet. Jour. and Ann. of Comp. Anat., 1877, p. 161.

McCall. Am. Med. Recorder, 1823, p. 254.

McIlhenny. A Treatise on the Disease Called the Milk Sickness, 1843.

Nagel. Nashville Jour. of Med. and Surg., 1859, p. 289.

Palmer. Chicago Clinic, 1904, p. 267.

Philips.

Cincinnati Lancet and Observer, 1877, p. 130.

Pusey. Louisville Med. News, 1886, p. 16.

Schuchardt. Die Milch-Krankheit der Nord-Amerikaner in ihrer geschichtlichen Entwickelung und in ihrem gegenwärtigen Bestande. Janus, Amst., 1897-8, ii, pp. 437; 525.

Seaton. A Treatise on the Disease Called by the People the Milk Sickness, 1841. Simon. Eclectic Med. Jour., 1888, p. 256.

Spalding. West. Med. Reporter, 1881, p. 266.

Way. Am. Jour. Med. Sc., 1893, p. 307.

Wagaman. West. Jour. Med. and Surg., 1841, p. 234.

Woodfin. North Carolina Med. Jour., 1878, p. 13.

Yandell. Transylvania Jour. of Med., 1828, p. 309. West. Jour. of Med. and

Surg., 1852, p. 374. Proc. Kentucky Med. Society, 1867-8, p. 88.