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.

[Illustration: FIG. 1.--_Conium maculatum._ The fresh juice of _Conium

maculatum_ was used in the preparation of the famous hemlock potion

which was employed by the Greeks in putting their criminals to death.

(From _Applied and Economic Botany_, by courtesy of Professor Kraemer

[after Holm].)]

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]

[Illustration: FIG. 2.--_Cicuta maculata_ (water hemlock); _A_, upper

part of stem with leaves and compound umbels; _B_, base of stem and

thick tuberous roots; _C_, cross-section of stem; _D_, flower; _E_,

fruit; _F_, fruit in longitudinal section; _G_, cross-section of a

mericarp. (From _Applied and Economic Botany_, by courtesy of Professor

Kraemer [after Holm].)]

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!

[Illustration: FIG. 3.--Fly Amanita (poisonous). (_Amanita muscaria_ L.)

(After Marshall, _The Mushroom Book_, by courtesy of Doubleday, Page &

Company.)]

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.

[Illustration: FIG. 4.--Death-cup; destroying angel (_Amanita

phalloides_ Fries); reduced; natural size: cap, 3-1/2 inches; stem,

7-1/2 inches. (After Marshall, _The Mushroom Book_, by courtesy of

Doubleday, Page & Company.)]

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._

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