CHAPTER III

POISONOUS PLANTS AND ANIMALS

Some normal plant and animal tissues contain substances poisonous to man and are occasionally eaten by mistake for wholesome foods.

POISONOUS PLANTS

Poisonous plants have sometimes figured conspicuously in human affairs. Every reader of ancient history knows how Socrates "drank the hemlock," and how crafty imperial murderers were likely to substitute poisonous mushrooms for edible ones in the dishes prepared for guests who were out of favor. In our own times the eating of poisonous plants is generally an accident, and poisoning from this cause occurs chiefly among the young and the ignorant.

According to Chesnut[13] there are 16,673 leaf-bearing plants included in Heller's _Catalogue of North American Plants_, and of these nearly five hundred, in one way or another, have been alleged to be poisonous. Some of these are relatively rare or for other reasons are not likely to be eaten by man or beast; others contain a poison only in some particular part, or are poisonous only at certain seasons of the year; in some the poison is not dangerous when taken by the mouth, but only when brought in contact with the skin or injected beneath the skin or into the circulation. There are great differences in individual susceptibility to some of these plant poisons. One familiar plant, the so-called poison-ivy, is not harmful for many people even when handled recklessly; it can be eaten with impunity by most domestic animals.

The actual number of poisonous plants likely to be inadvertently eaten by human beings is not large. Chesnut[14] has enumerated about thirty important poisonous plants occurring in the United States, and some of these are not known to be poisonous except for domestic animals.[15] Many of the cases of reported poisoning in man belong to the class of exceedingly rare accidents and are without much significance in the present discussion. Such are the use of the leaves of the American false hellebore (_Veratrum viride_) in mistake for those of the marsh-marigold[16], the use of the fruit pulp of the Kentucky coffee tree (_Gymnocladus dioica_) in mistake for that of the honey-locust[17], the accidental employment of daffodil bulbs for food, and the confusion by children of the young shoots of the broad-leaf laurel (_Kalmia latifolia_) with the wintergreen.[18] One of the most serious instances of poisoning of this sort is that from the use of the spindle-shaped roots of the deadly water hemlock (_Cicuta maculata_) allied to the more famous but no more deadly poison hemlock. These underground portions of the plant are sometimes exposed to view by washing out or freezing, and are mistaken by children for horseradish, artichokes, parsnips, and other edible roots. Poisoning with water hemlock undoubtedly occurs more frequently than shown by any record. Eight cases and two deaths from this cause are known to have occurred in one year in the state of New Jersey alone.

An instance of food poisoning to be included under this head is the outbreak in Hamburg and some thirty other German cities in 1911 due to the use of a poisonous vegetable fat in preparing a commercial butter substitute.[19] In the attempt to cheapen as far as possible the preparation of margarin various plant oils have been added by the manufacturers. In the Hamburg outbreak, in which over two hundred cases of illness occurred, poisoning was apparently due to substitution of so-called maratti-oil, derived from a tropical plant (_Hydrocarpus_). This fat is said to be identical with oil of cardamom, and its toxic character in the amounts used in the margarin was proved by animal experiment. Increasing economic pressure for cheap foods may lead to the recurrence of such accidents unless proper precautions are used in testing out new fats and other untried substances intended for use in the preparation of food substances.[20]

Investigators from the New York City Health Department have found that certain cases of alleged "ptomain poisoning" were really due to "sour-grass soup."[21] This soup is prepared from the leaves of a species of sorrel rich in oxalic acid. In one restaurant it was found that the soup contained as much as ten grains of oxalic acid per pint!

By far the best-known example of that form of poisoning which results from confounding poisonous with edible foods is that due to poisonous mushrooms.[22] There is reason to believe that mushroom (or "toadstool") intoxication in the United States has occurred with greater frequency of late years, partly on account of the generally increasing use of mushrooms as food and the consequently greater liability to mistake, and partly on account of the growth of immigration from the mushroom-eating communities of Southern Europe. Many instances have come to light in which immigrants have mistaken poisonous varieties in this country for edible ones with which they were familiar at home. In the vicinity of New York City there were twenty-two deaths from mushroom poisoning in one ten-day period (September, 1911) following heavy rains. The "fly _Amanita_"[23] (_Amanita muscaria_) in this country has been apparently often mistaken for the European variety of "royal _Amanita_" (_A. caesaria_).[24] Such a mistake seems to have been the cause of death of the Count de Vecchi in Washington, D.C., in 1897.

The Count, an attache of the Italian legation, a cultivated gentleman of nearly sixty years of age, considered something of an expert upon mycology, purchased, near one of the markets in Washington, a quantity of fungi recognized by him as an edible mushroom. The plants were collected in Virginia about seven miles from the city of Washington. The following Sunday morning the count and his physician, a warm personal friend, breakfasted together upon these mushrooms, commenting upon their agreeable and even delicious flavor. Breakfast was concluded at half after eight and within fifteen minutes the count felt symptoms of serious illness. So rapid was the onset that by nine o'clock he was found prostrate on his bed, oppressed by the sense of impending doom. He rapidly developed blindness, trismus, difficulty in swallowing, and shortly lost consciousness. Terrific convulsions then supervened, so violent in character as to break the bed upon which he was placed. Despite rigorous treatment and the administration of morphine and atropine, the count never recovered consciousness and died on the day following the accident. The count's physician on returning to his office was also attacked, dizziness and ocular symptoms warning him of the nature of the trouble. Energetic treatment with apomorphine and atropine was at once instituted by his colleagues and for a period of five hours he lay in a state of coma with occasional periods of lucidity. The grave symptoms were ameliorated and recovery set in somewhere near seven o'clock in the evening. His convalescence was uneventful, his restoration to health complete, and he is, I believe, still living. On this instance the count probably identified the fungi as _caesaria_ or _aurantiaca_. From the symptoms and termination the species eaten must have been _muscaria_.

_A. muscaria_ contains an alkaloidal substance which has a characteristic effect upon the nerve centers and to which the name muscarin and the provisional chemical formula C{5}H{15}NO{3} has been given. The drug atropin is a more or less perfect physiological antidote for muscarin and has been administered with success in cases of muscarin poisoning. It is said that the peasants in the Caucasus are in the habit of preparing from the fly _Amanita_ a beverage which they use for producing orgies of intoxication. Deaths are stated to occur frequently from excessive use of this beverage.[25]

The deadly _Amanita_ or death-cup (_A. phalloides_) is probably responsible for the majority of cases of mushroom poisoning. Ford estimates that from twelve to fifteen deaths occur annually in this country from this species alone. This fungus is usually eaten through sheer ignorance by persons who have gathered and eaten whatever they chanced to find in the woods. A few of these poisonous mushrooms mixed with edible varieties may be sufficient to cause the death of a family. Ford thus describes the symptoms of poisoning with _A. phalloides_:

Following the consumption of the fungi there is a period of six to fifteen hours during which no symptoms of poisoning are shown by the victims. This corresponds to the period of incubation of other intoxications or infections. The first sign of trouble is sudden pain of the greatest intensity localized in the abdomen, accompanied by vomiting, thirst, and choleraic diarrhoea with mucous and bloody stools. The latter symptom is by no means constant. The pain continues in paroxysms often so severe as to cause the peculiar Hippocratic facies, _la face vultueuse_ of the French, and though sometimes ameliorated in character, it usually recurs with greater severity. The patients rapidly lose strength and flesh, their complexion assuming a peculiar yellow tone. After three to four days in children and six to eight in adults the victims sink into a profound coma from which they cannot be roused and death soon ends the fearful and useless tragedy. Convulsions rarely if ever occur and when present indicate, I am inclined to believe, a mixed intoxication, specimens of _Amanita muscaria_ being eaten with the _phalloides_. The majority of individuals poisoned by the "deadly Amanita" die, the mortality varying from 60 to 100 per cent in various accidents, but recovery is not impossible when small amounts of the fungus are eaten, especially if the stomach be very promptly emptied, either naturally or artificially.

A number of other closely related species of _Amanita_ (e.g., _A. verna_, the "destroying angel," probably a small form of _A. phalloides_) have a poisonous action similar to that of _A. phalloides_. All are different from muscarin.

The character of the poison was first carefully investigated by Kobert, who showed that the _Amanita_ extract has the power of laking or dissolving out the coloring matter from red blood corpuscles. This hemolytic action is so powerful that it is exerted upon the red cells of ox blood even in a dilution of 1:125,000. Ford[26] has since shown that in addition to the hemolytic substance another substance much more toxic is present in this species of _Amanita_ and he concludes that the poisonous effect of the fungus is primarily due to the latter ("_Amanita_ toxin"). The juice of the cooked _Amanita_ is devoid of hemolytic power, but is poisonous for animals in small doses, a fact that agrees with the observation that these mushrooms, after cooking, remain intensely poisonous for man. Extensive fatty degeneration in liver, kidney, and heart muscle is produced by the true _Amanita_ toxin. In the Baltimore cases studied by Clark, Marshall, and Rowntree[27] the kidney rather than the liver was the seat of the most interesting functional changes. These authors conclude that the nervous and mental symptoms, instead of being due to some peculiar "neurotoxin," are probably uremic in character. No successful method of treatment is known. An antibody for the hemolysin has been produced, but an antitoxin for the other poisonous substance seems to be formed in very small amount. Attempts to immunize small animals with _Amanita_ toxin succeed only to a limited degree.[28]

POISONOUS ANIMALS

While the muscles or internal organs of many animals are not palatable on account of unpleasant flavor or toughness, there do not seem to be many instances in which normal animal tissues are poisonous when eaten. As pointed out elsewhere (chapter vi), the majority of outbreaks of meat and fish poisoning must be attributed to the presence of pathogenic bacteria or to poisons formed after the death of the animal. This has been found especially true of many of the outbreaks of poisoning ascribed to oysters and other shellfish; in most, if not all, cases the inculpated mollusks have been derived from water polluted with human wastes and are either infected or partially decomposed.

In some animals, however, notably certain fish, the living and healthy organs are definitely poisonous. The family of Tetrodontidae (puffers, balloon-fish, globe-fish) comprises a number of poisonous species, including the famous Japanese _Fugu_, which has many hundred deaths scored against it and has been often used to effect suicide. Poisonous varieties of fish seem more abundant in tropical waters than in temperate, but this is possibly because of the more general and indiscriminate use of fish as food in such localities as the Japanese and South Sea Islands. It is known that some cool-water fish are poisonous. The flesh of the Greenland shark possesses poisonous qualities for dogs and produces a kind of intoxication in these animals.[29]

Much uncertainty exists respecting the conditions under which the various forms of fish poisoning occur. One type is believed to be associated with the spawning season, and to be caused by a poison present in the reproductive tissues. The roe of the European barbel is said to cause frequent poisoning, not usually of a serious sort. The flesh or roe of the sturgeon, pike, and other fish is also stated to be poisonous during the spawning season. Some fish are said to be poisonous only when they have fed on certain marine plants.[30]

There is little definite knowledge about the poisons concerned. They are certainly not uniform in nature. The _Fugu_ poison produces cholera-like symptoms, convulsions, and paralysis. It is not destroyed by boiling. The effect of the Greenland shark flesh on dogs is described as being "like alcohol." It is said that dogs fed with gradually increasing amounts of the poisonous shark's flesh become to some degree immune. Different symptoms are described in other fish poisoning cases.[31]

FOOTNOTES:

[13] _Science_, XV (1902), 1016.

[14] _U.S. Dept. of Agric., Div. of Botany, Bull. 20_, 1898.

[15] Among the plants that seem to be most commonly implicated in the poisoning of stock are the larkspur (_Delphinium._ _U.S. Dept. of Agric., Bull. 365_, September 8, 1916), the water hemlock (_Cicuta maculata_) and others of the same genus, the lupines (_U.S. Dept. of Agric., Bull. 405_, 1916), some of the laurels (_Kalmia_), and the Death _Camas_ or _Zygadenus_ (_U.S. Dept. of Agric., Bull. 125_, 1915). The famous loco-weed of the western United States (_U.S. Dept. of Agric., Bull. 112_, 1909) is less certainly to be held responsible for all the ills ascribed to it (H. T. Marshall, _Johns Hopkins Hosp. Bull._, XXV [1914], 234).

[16] Chesnut, _U.S. Dept. of Agric., Div. of Botany, Bull. 20_, 1898, p. 17.

[17] _Ibid._, p. 28.

[18] _Ibid._, p. 45. The seeds of the castor-oil bean, which contain a very powerful poison (ricin) allied to the bacterial toxins, have been known to cause the death of children who ate the seeds given them to play with.

[19] Mayer, _Deutsche Viertelj. f. oeffentl. Ges._, XLV (1913), 12.

[20] Cf. an instance of palmolin poisoning, _Centralbl. f. Bakt._, I, Ref., LXII (1914), 210.

[21] _Weekly Bull., N.Y. Dept. of Health_, September 16, 1916.

[22] Seventy-three species of mushrooms known or suspected to be poisonous are enumerated in a bulletin of the United States Department of Agriculture, Patterson and Charles ("Mushrooms and Other Common Fungi," _Bull. 175_, 1915). This bulletin contains descriptions and excellent illustrations of many edible and of the commoner poisonous species.

[23] Used in some places as a fly poison.

[24] Ford, _Science_, XXX (1909), 97.

[25] Another species of mushroom occurring in this country and commonly regarded as edible (_Panaeolus papilionaceus_) has on occasion shown marked intoxicating properties (A. E. Verrill, _Science_, XL (1914), 408).

[26] _Jour. Infect. Dis._, III (1906), 191.

[27] _Jour. Amer. Med. Assoc._, LXIV (1915), 1230.

[28] W. W. Ford, "Plant Poisons and Their Antibodies," _Centralbl. f. Bakt._, I Abt., Ref., LVIII (1913), 129 and 193, with full bibliography.

[29] A. H. Clark, _Science_, XLI (1915), 795.

[30] See W. M. Kerr, _U.S. Nav., Monthly Bull._, VI (1912), 401.

[31] _Ibid._