Wild Barley or Squirrel Tail (Hordeum jitbation). la. Agr. Exp. Sta. A Manual of Poisonous Plants Chiefly of Eastern North America, with Brief Notes on Economic and Medicinal Plants, and Numerous Illustrations By L. H. PAMMEL, Ph. D. Professor of Botany, Iowa State College Agriculture and Mechanic Arts THE TORCH PRESS CEDAR RAPIDS, IOWA 1910 tl1 QK loo Wo COPYRIGHT BY Iv. H. PAMMEL 1910 FOREWORD During the last decade, there has been much interest manifested in regard to plants injurious to live stock. Numerous contributions have been made along this line, notably by Dr. Chesnut, formerly of the United States Department of Agriculture, Drs. True and Wilcox and their co-workers also of Washington, Dr. Schaffner of the Ohio State University, Dr. Jones of the Vermont Agri- cultural Experiment Station, Dr. Kennedy of the Nevada Experiment Station, Dr. Nelson of the Wyoming Station, Dr. Nelson of Washington, and Drs. Peters and Bessey of Nebraska. Other station botanists have also contributed to the same line of work. Much of the literature is scattered, however, hence an effort has been made to bring together in the following pages the results obtained. Much information on this line of investigation has also been obtained from such works as Millspaugh's Medicinal Plants of North America, Dr. Johnson's Manual of the Medical Botany of North America, Lloyd's Drugs and Medicines of North America, Winslow's Veterinary Materia Medica and Therapeutics, Sayre's Organic Materia Medica and Pharmacognosy, Fliickiger and Hanbury's Phar- macographia, Greenish's Materia Medica, Ellingwood's Materia Medica, Thera- peutics and Pharmacognosy, Pereira's Materia Medica, Luerssen's and Czapek's publications and many others which give details in regard to the effects of poisonous plants. Many persons may object to the great number of plants which are here regarded as poisonous or described as such in this work. I have placed the broadest interpretation on the subject and have, therefore, included all plants that are injurious although many of these are not known to produce poisons, some even being most useful economic plants and yet injurious to some people. It has been thought best to arrange the manual so as to consider the plants in the same order as that given in Erigler and Prantl's Die Pflanzen- familien. The Schizomycetes were contributed by my colleague, Dr. R. E. Buchanan, who has also favored me in many other ways. The parts concerning the blue-green algae and algae, taking up the higher algae and their relation to the water slimes are given in their sequence under the Schizophyceae and Euphyceae. The Eumycetes or true fungi are considered chiefly from the pathogenic standpoint; while other fungi are referred to and briefly considered under their respective groups. In regard to the higher fungi, such as the toadstools, much valuable information may be obtained from the works of Dr. Farlow, Prof. Peck and Prof. Atkinson. The so-called Blastomycetic fungi have been arranged under the group of the imperfectly known forms. There are also brief characterizations of other groups of the cryptogams such as lichens, mosses, ferns and their allies. iv FOREWORD The flowering plants or Spermatophyta are described more fully than the previous groups, and under the various orders and subdivisions we have also added notes on economic and medicinal plants. Those who desire fuller in- formation in regard to other American species of the different orders described should consult the latest editions of Gray's or Britton's Manuals, in which the descriptions are full and complete. Of course, one cannot expect to add much to the excellent descriptions given in these treatises. I have freely made use of published literature in the systematic portions as well as in the more technical matter pertaining to poisons, and I wish to acknowl- edge my assistance from these sources. In order that the species named may be more readily recognized, a large number have been figured. In addition to the descriptive part of the work there has been added a chapter on the active principles of plants, by my colleague, Prof. A. A- Bennett. I am also greatly indebted to Miss Harriette S. Kellogg who has carefully read the manuscript and assisted me in other ways besides preparing the bibliography. To Dr. Trelease of the Missouri Botanical Garden, I am indebted for the use of a number of books on the subject. Miss Charlotte M. King, Miss Ada Hayden, Mr. W. S. Dudgeon, and my daughter, Lois, have made drawings especially for this work. Other illustrations are taken from special works, due credit being given in each case. I am indebted for the use of cuts to the following persons : Dr. C. F. Curtiss of the Iowa Agricultural Experiment Station, Dr. B. D. Halsted of the New Jersey Agricultural Experiment Station, Profs. S- B. Green and Washburn of the Minnesota Station and Prof. A. D. Selby of the Ohio Station, and to the United States Department of Agriculture. Some have been reproduced from Baillon's Diet., and from Bentham's Handbook of British Plants. I have endeavored in each case to give credit for the drawing or cut. I am indebted to Drs. R. R. Dykstra and C. H. Stange, Profs. L. G. Michael, C. V. Gregory and A. A. Bennett for proof reading and to Dr. W. H. Stuhr for some matter in Part I. The work does not pretend to be complete; we hope, however, that it may prove useful to the Veterinarian, Physician and Layman. Ames, Iowa, June 1, 1909. CONTENTS CHAPTER I . POISONS AND STATISTICS ON POISONS 1 Ancient Use of Poisons, 2; The Rise of Chemistry and Poisons, 3; Ratze- burg on Poisonous Plants, 4; Statistics of Poisoning, 5; Statutes on Poisoning and Actions of Poisons on Different Animals, 6. CHAPTER II. BACTERIAL POISONS 8 Impure Water the Source of Disease, 8; Bacterial Poisons, 10; Botulism, 11; Maidismus or Pellagra, 11. CHAPTER III. DERMATITIS 12 Dermatomycosis, 12; Dermatophytes of Domestic Animals, 13; Favus, 17. CHAPTER IV. FORAGE POISONING, ERGOTISM, AND ASPERGILLOSIS . . 20 Forage Poisoning, 20; Poisoning from Silage, 24; Ergotism, 28; Aspergil- losis, 29. CHAPTER V. POISONING FROM FUNGI 31 Toadstools — Amanita muscaria, 31; Amanita phalloides, 31. CHAPTER VI. POISONING FROM OTHER PLANTS. EQUISETOSIS, LOCOISM, AND LUPINOSIS Equisetosis, 37; Lccoism, 37; Lupinosis, 40. CHAPTER VII. DELPHINOSIS, LATHYRISMUS (LATHYRISM), ACONITISM, VERATRISM, UMBELLI FERAE, CONIUM, CICUTA . . 44 Delphinosis, 44; Lathyrismus, 45; Aconitism, 46; Veratrism, 46; Poisoning from Umbelliferae, 49; Cowbane, 49; The Poison Hemlock, 51. CHAPTER VIII. FISH AND ARROW POISONS, HYDROCYANIC POISONING — TOXALBUMINS — BLACK LOCUST, CASTOR OlL, AND JEQUIRITY 52 Fish and Arrow Poisons, 52; Hydrocyanic Poisoning, 53; Poisoning from Toxalbumins, Black Locust, Ricinus and Abrus, 55. CHAPTER IX. POISONING FROM OPIUM, SOLANACEAE AND PLANTS THAT CONTAIN SAPONINS 59 Opium, 59; Poisoning from Solanaceae; Jimson Weed; Hyoscyamin, 60; Poisoning from Plants that Contain Saponin; Bouncing Betty; Corn- cockle, 62. CHAPTER X. POISONING FROM FLOWERS, POISONING FROM HONEY, ME- CHANICAL INJURIES 64 Poisoning from Flowers, 64: Poisoning from Honey, 64; Mechanical In- juries; Wild Barley; Cheat; Needle Grass; Greasewood; Crimson Clover, 66. CHAPTER XI. CLASSIFICATION OF POISONS, SYMPTOMS, AND ANTIDOTES 72 Poisons which Cause Coarse Anatomical Changes of the Organs, 72; Classi- fication of Poisons and Poisonous Symptoms According to Bernard H. Smith — Narcotics, 73; Deliriants, 73; Inebriants, 74; Convulsives, 74; Depressants, 74; Asthenics, 75; Purgatives, 75; Abortives, 76; Irritants with Nervous Symptoms, 76; Simple Irritants, 76. Table of Symptoms Observed After the Administration of Poisons, Adapted from Cattell After the Work of Robert, 77; Treatment for Poisoning, 79. CHAPTER XII. THE PRODUCTION OF POISON IN PLANTS .... 82 The Use and Actions of Poisons on Plants, 82; Distribution of Poisonous Substances in Plants, 82; Light, 83; Heat, 83; Seasons, 83; Climatic, 85; Culture, 87; Related Species and Toxic Substances, 88; Distribu- tion of Chemical Substances, 88; Saponins, 89; Hydrocyanic Acid, 89; Cumarin, 90; Cytisin, 90. vi CONTENTS CHAPTER XIII. ALGAE IN WATER SUPPLIES 91 How Growth of Algae in Water May Be Prevented, 94; The Use of Algiciies, 94. CHAPTER XIV. A CATALOGUE OF THE MORE IMPORTANT POISONOUS PLANTS OF THE UNITED STATES AND CANADA ... 96 Literature, 96; Euthallophyta, Schizophyta, Schizomycetes. Bacteria, 97; Euphyceae — Algae, 98; Eumycetes — Fungi; Phycomycetes. Black Molds and Downy Mildews, 98; Smuts, 98; Rusts, 99; Toadstools, 99; Ascomycetes, 100; Fungi Imperfecti, 100; Embryophyta, Pteridophyta, 100; Embryophyta siphonogama; Flowering Plants; Gymnospermae, Con- ifers and Allies, 101; Angiospermae, 102; Monocotyledoneae, 102; Grass Family, 102; Lily Family, 103; Dicotyledoneae, 105; Nettle Family, 106; Pink Family, 107; Crowfoot Family, 108; Poppy Family, 112; Rose Family, 115; Pulse Family, 117; Spurge Family, 121; Poison Ivy Family, 122; Carrot Family, 126; Heath Family, 127; Nightshade Family, 131; Composite Family, 137. CHAPTER XV. CHEMISTRY OF ALKALOIDS, GLUCOSIDES, ETC. . . .143 Composition and General Properties of Alkaloids, 143; Occurrence of the Alkaloids, 144; Classification of the Alkaloids, 145; On Alkaloids, 147; Glucosides, 148; Gluco-Alkaloids, 149; Saponins, 149; Picrotoxin, Cicu- toxin and Toxins, 149; Other Vegetable Poisons, 149; Amins, 149; Or- ganic Acids, 150. CHAPTER I POISONS AND STATISTICS ON POISONS A poison has been defined as "Any substance that, when taken into the system acts in a noxious manner by means not mechanical, tending to cause death or serious detriment to health." Kobert and other physicians define a poison as "A non-organized body, either organic or inorganic, which under certain conditions, affects temporarily or permanently one or more organs of the body, when in a state of health or in a healthy condition." Such poisons may develop in the body or may come from without. Some substances act injuriously in a mechanical way, that is, they may set up disturbances by irritating some parts of the body. Other sub- stances, while poisonous to one who is ill, may be entirely harmless to persons or animals in a state of health. Kobert also defines poisons from a pharmacological standpoint as "All pharmacological agents which, in a given case, do not act beneficially but in- juriously." Toxicology is the science of poisons, the word being derived from the ancient word "tox," meaning bow, or arrow, probably from the ancient use of the arrow to kill. In tracing the application of the word "tox;" "arrow," to its later appli- cation, poison, Blyth says : "Perchance the savage found that weapons soiled wth the blood of former victims made wounds fatal; from this observation, the next step naturally would be that of experiment, — the arrow or spear would be steeped in all manner of offensive pastes, and smeared with the vegetable juices of those plants which were deemed noxious; and as the ef- fects were mysterious they would be ascribed to the supernatural powers, and covered with a veil of superstition." The different tribes of Indians in South America have from early days been skilful in preparing arrow poisons, the majority of which contain strych- nin in some form. The following plants have, at various times, furnished poisons for arrow tips, not only in South America, but also in other countries : Strychnos toxifera (Strychnine), perhaps the most generally used of any; Antiaris toxicaria, an arrow poison of Java, Borneo, and North Africa; various Leguminosae, as Erythrophloeum in Angola, Sierra Leone, and Seychelles, a different species being used in each place; Pithecolobium, Afzelia, and Derris elliptica of Borneo; of the Menispermaceae, two species of Abuta are used. Perhaps in this connection, it would not be out of place to mention several fish-poisons, many of which are also legumes. Of this order are Albidizzia, Afzelia, Bauhinia, Enterolobium, Leucaena, Milletia, Piscidia, Acacia, Abrus precatorius, Clitoria, Mundelia, Derris, Lonchocarpus, and Tephrosia. In pre- paring the last named, the leaves are crushed and mixed with quicklime before using. Among the Menispermaceae are the Indian Berry, Fish-berry or Levant Nut (Anamirta paniculata} of the East Indies which contains picrotoxin; and 2 MANUAL OF POISONOUS PLANTS P achy gone ovata, used also by the Malays to poison crocodiles. Of the Rhamnaceae, Kraemer mentions Tapura, Gouania, and Zisyphus. Among the Tiliaceae, Kraemer, also mentions species of Greivia which are used as fish- poisons. The same authority adds species of Barringtonia of the order Lecy- thidiaceae and Laportea stimulans of the Urticaceae to the above list. ANCIENT USE OF POISONS In his work on "Poisons: their Effects and Detection," Blyth writes an excellent account of their history from which a few of the following more im- portant data have been taken for the present work. Their early history is involved in myth. Hecate was said to have been the discoverer of poisonous herbs and her knowledge passed in turn to Medea. The Egyptian kings, Menes and Attalus Philometer, not only had a knowledge of plants but the latter was also familiar with the uses of such plants as hyoscyamus, aconite, conium, and others of similar character. He experimented with poisons and compounded medicines. The Egyptians knew prussic acid, which was extracted from the peach and by means of which those who re- vealed religious secrets were put to death. The ancient Romans also must have been familiar with this poison, since a Roman knight once took poison and fell dead immediately at the feet of Samolus. The ancient Greeks knew about poisons and it was not considered a dishonorable thing to commit suicide. Nicander of Colophon (204-138 B. C.) wrote two treatises on poisons, in one of which he described the effect of snake venom ; in the other, henbane, aconite, conium, and fungi, were discussed. As antidotes for poisoning from any of these substances, he recommended such remedies as lukewarm oil, in order to excite vomiting. Dioscorides (40-90 A. D.) divided poisons into (1) Animal poisons, as cantharides, poisonous snakes, the blood of an ox (probably putrid) ; (2) Poi- sons from plants, as opium, hyoscyamus, conium, aconite (the latter coming from Akron in Heraclea), and colchicum; (3) Mineral poisons like arsenic and mercury (cinnabar). Pliny mentions that the Gauls dipped their arrows in a preparation of veratrum. Toffana of Naples sold under the name of Acquetta di Napoli a solution of arsenious acid, by which, it is said, 605 persons were poisoned, among them the popes, Pius III and Clement XIV. Poisoning was much practiced in India for the purpose of revenge, robbery and suicide, every little quarrel being liable to end in assassination of one of the parties. Such poisons as arsenic, aconite, opium, and extracts derived from plants of the Solatium family, were also used in India to destroy cattle. It is said that gipsies used Phycomyces nitens, having knowledge of its properties from the same country. The spores of the fungus were administered in warm water and death, accompanied with all the symptoms of tuberculosis, followed in a few weeks. The Hebrews seem to have been familiar with certain poisons, as arsenic, aconite and, possibly, ergot. The deaths of Socrates, Demosthenes, Hannibal, and Cleopatra, were due to the administration of poisons. In the early part of the Christian era, there were many professional poison- ers and their business flourished, kings, emperors, popes, and members of the nobility being among their victims. There were two great criminal schools POISONS AND STATISTICS ON POISONS 3 in Venice between the tenth and seventeenth centuries, the government secretly recognizing the operations of these criminals and paying a sum of money for the execution of prisoners of note. However, these efforts were not often success- ful. J. Baptisa Porta, in the sixteenth century, wrote under the title of "Natural Magic," a work devoted partly to cookery and partly to poisons and how to use them. The early methods of detecting the presence of poisons were crude; the surroundings were always noted; the suspected poison was generally admin- istered to an animal and, if it died, poison was sure to be diagnosed without further investigation, since the early church forbade postmortem examination. Later, however, doctors were permitted to dissect and thus become familiar with pathological changes. THE RISE OF CHEMISTRY AND POISONS At the close of the eighteenth and the beginning of the nineteenth cen- turies, chemistry had advanced sufficiently to test for arsenic and the more important mineral poisons. Scheele discovered prussic acid; other chemists, as Berthollet, Lavoisier, and Stahl, added to the chemical knowledge of poisons The father of modern toxicology, however, was Bonaventura Orfila, whose work was published in 1814. Derosne discovered the alkaloids of narcotin and morphin in 1818. Pelletier and Cavantou discovered strychnin in 1818. Giesecke discovered coniine in 1827, and Geiger and Hesse separated atropin and hyoscyamin in 1833. The modern aspect of the subject began with treatises on poisons by such workers as Vogel * and Richard Mead,2 and writings on the subject of chemistry through the works of Stahl, Scheele, Berthollet, Priestly and Lavoisier. Bot- anists, too, at this time began to be greatly interested in a study of poisonous plants. Thus we have the work of Bulliard 3 and the work of Gmelin.4 The work of Bulliard discusses a large number of poisonous plants with excellent il- lustrations, and Gmelin treats quite fully of the then known poisonous plants of Europe. The works of Gmelin, Bulliard and Plenck5 on Toxicology, and Buchner's Toxicology 6 were frequently quoted by the older writers. The greatest of the older writers, however, was Orfila 7 whose great work on toxicology became the recognized authority on toxicology. This work was first published in 1814, and passed through many editions. Orfila conducted actual experiments with differ- ent plants. This work of Orfila was also translated into different languages,8 Orfila was preceded by Fodere.9 About that period other toxicologies were published in France and Germany, such as those of Sobernheim and Simon,10 1 The Usefulness of Natural Philosophy. 1654. 2 Mechanical Theory of Poisons. 3 Historic des plantes veneneuses et suspectes de la France. Paris 1784. Folio X, 177 p., 72 tab. col. — Ed. II: Paris 1798. 4 Abhandlung von den giftigen Gewachsen. Ulm. 1775. Allegemeine Geschichte der Pffanzengifte. Nurnberg 1777. 5 Toxicolgia, seu doctrina de venenis et antidotis. Viennae, Graeffer. 1785, 338 p. 6 Toxicologie. Nurnberg. 1827. 7 Traite des poisons, ou Toxicologie generate. Paris, 1813. Ed. Ill, ib. 1826. Orfila and Bonaventura. Traite des Poisons ou Toxicologie Generale. Paris, 1814. (Ed. 5) 1852. 8 Toxicologie. Seemann & Karls. 2 Vols. Berlin 1829-1831. 9 Nedec leg. Ed. 2. 10 Handbuch der praktischen Toxicologie. Berlin, 1838. Toxicologie. Nurnberg, 1827, 2nd Ed. 4 MANUAL OF POISONOUS PLANTS Taylor,4 Hoffman,5 Th. Husemann & A. Husemann,6 von Pragg,7 and Opwyrda Rebuteau,8 Selmi,9 Bohm and von Boeck,^ Dragendorff,11 Falck,12 and more recent works by Joshua Nunn,13 Smith,14 H.utyra and Marck,1^ to say nothing of the recent contributions occurring in the American Veterinary Review, the Journal of the Chemical Society, American Journal of Pharmacy, besides treat- ises in many chemical and pharmaceutical journals. The modern work of Blyth, though a somewhat exhaustive treatise on the subject of poisons, is not comprehensive so far as a large number of the poison- our plants are concerned. Many popular treatises on the subject of poisonous plants have appeared in nearly every European language both in ancient and mod- ern times, but perhaps no one has contributed more to the subject of poisons than Kobert, who has published several treatises, and one of his works "Practical Toxicology for Physicians and Students" was translated into English by Dr. Friedburg. Such men as Dr. M. Greshoff of Haarlem, published a number of ex- tended treatises on the subject "Poisons, especially Hydrocyanic Acids and Saponins, in Plants." His monograph on fish poisons and subsequent mono- graphs two and three, really survey most of the poisonous plants of the world. Nor should we omit to mention the many treatises by Prof. Power of Well- come laboratory and his students who have investigated a large number of poi- sonous plants or the work of Prof. Maiden of New South Wales, or of Cornevin of France. RATZEBURG ON POISONOUS PLANTS. Between 1834 and 1838 there appeared the first part of the work of Brandt and Ratzeburg on Phanerogamous poisonous plants of Germany, and in the year 1838 in the same work the poisonous Cryptogams by Phoebus. This like other works of the time contained numerous fine colored plates. This work pertaining to the flowering plants, lists the following plants of Germany as poisonous. Darnel (Lolium temulentum) Juniperus Sabina, Yew (Taxus baccata) Arum maculatum, Colchicum autumnale, Fritillaria imperialis, Narcissus pseudonar, sissus, Paris quadrifolia, Veratrum album, Aconite (Aconilum Anthcra, A Lycoctonum, A. Cammarum, A. altigaleatum, A. variable) Anemone nemorosa, Caltha palustris, Helleborus niger, H. foetidus, H. viridis, Pulsatilla vulgaris, Crowfoot (Ranunculus sceleratus, R. acris, R. alpestris, R. repens, R. bulbosus, R. flammula, R. Thora), Papaver somniferum, Euphorbia palustris, E. Cyparis- sias, Rhus Toxicodendron, Acthusa Cynapium, Cicuta virosa, Conium maculatum, Coronilla varia, Oenanthe fistulosa, Sium latifolium, Ledum palustre, Cyclamen curopaeum, Daphne Mezereum, Nerium, Oleander, Cynanchum, Vincetoxicum, Atropa Belladonna, Datura Stramonium, Hyoscyamus niger, Mandragora verna- iis, Scopolina atropoides, Solanum nigrum, Digitalis purpurea, G ratio la officina- 4 Principles and Practice of Medical Jurisprudence. 3 vols. London, 1873. 5 Hoffmann, lyebrbuch der gerichtlichen Medicin. 5th ed. Wien, 1890-91. 6 Husemann & Husemann, Handbuch der Toxicologie. Berlin, 1862. 7 L,eerboek voor practische giftleer. In Swee Theilen. Utrecht, 1871. 8 Elemens de Toxicologie et de Medecine Regale, appliquees a MEmpoisonnement. Paris, 1873. 2nd ed. by Ed. Bpurgoing, Paris, 1888. 9 Studi di Tossicologio Chimica. Bologna, 1871. 10 Bohm and von Boeck. Handbuch der Intoxicationen. (Bd. 15 of the German edition of Ziemssen's Cyclopaedia). 11 Die gerichtlichchemische Ermittelung van Giften in Nahrungsmitteln, Luftgemischen, Speiseresten, Korpertheilen, etc. St. Petersburg, 1868. 3rd ed. Gottingen, 1888. 12 Die Klinischtigen Intoxicationen (Handbuch der spec. Pathologic u. Therapie red. von' R. Virchow, Bd. 2.) Erlangen, 1854. 13 Veterinary Toxicology. Wm. R. Jenkins & Co., N. Y., 1901, 1907. 14 A Manual of Veterinary Hygiene. 5th ed. Wm. R. Jenkins & Co., N. Y., 1035 pages^ 15 Specielle Pathologic and Therapie der Hausthiere. POISONS AND STATISTICS ON POISONS 5 Us, and L&ctuca virosa. Many poisonous fungi are enumerated in the second part. It is interesting here to note their classifications of poisons. Sobernheim classifies the poisons into, A. vegetable poisons, B. nervous poisons, C. blood poisons. Orfila clasifies poisons into four classes, (1) irritant, acrid, corrosive, (2) narcotic, (3) narcotic acrid, (4) septic poisons. In 1834 Brandt and Ratze- burg classified poisons as to their origin into (1) mineral, (2) plant, (3) animal. Brandt and Ratzeberg in their treatise on plant poisons make three divisions (1) narcotic (stupefying), (2) acrid (inflammatory), (3) narcotic (inflammatory). They use the classification of Buchner which is as follows:- (1) narcotic, a HCN Prunus, b, volatile narcotic, Lolium, c, narcotic alkaloidal, Poppy; (2) acrid narcotic, Cicuta, Conium, Ruta, Digitalis; (3) irritant narcotic, a, Aconite,. Oleander, Rhus, Smartweed, b, more volatile, hot acrid, Dirca, Pepper; (4) acrid, a, drastic resins, Bryonia, Hypericum, Melia, b, drastic coloring matter, Abrus, Spartium, Pokeweed, c, emetic alkaloids, Iris, Colchicum, Narcissus, d, unknown poisons, Agaricus, Boletus, Phallus, Lycoperdon. Fodere divided poisons into septic, narcotic, narcoacrid, acrid, irritant and astringent. STATISTICS OF POISONING. The use of poisons for criminal purposes, although not nearly so extensive at the present time as during the middle ages, still plays an important part in criminal law. The following statistics afford some indication of the use of poisons for suicidal and homicidal purposes. According to the last census of the United States, the number of persons reported as poisoned was as follows : By Active Poisons By Gas 1 1902 1374 950 1903 1551 1715 1904 1632 2167 1905 1269 1306 1906 1734 1276 Intentional cases of poisoning in live stock are not nearly so frequent as are those in the human family, although there are many cases of the former on rec- ord. Poisoning of live stock is generally accidental, caused by consuming plants that are poisonous. Large losses occur annually in this way. In 1900 Prof. Ches- nut and Dr. Wilcox investigated the conditions in Montana relative to this subject and published the following statistics resulting from their studies. They state- that probably not more than one fourth of the actual cases occurring came under their observation. i These numbers include deaths during, or as a result of conflagrations. The annual average was 1412 from active poisons and 1365 from gas. From 1900-1904, the number of deaths by poison averaged 4.5 per 100,000. Poisoning cases among cattle, horses, and sheep in Montana observed dur- ing the season of 1900: SHE EP CAT! %E HOR5 5ES tj I a 8 I »d B Q Poisoned 3 s Poisoned | 3 Zygadenus venenosus 3030 636 Zygadenus elegans 40 . 15 6 2 4 3 Lupine 3000 1900 4 3 Delphinium bicolor 2 2 Delphinium glaucum 100 56 Cicuta occidentalis 105 80 36 30 Loco weeds 3550 700 3 150 3 Total I 9725 3331 147 90 154 Nearly every veterinarian has frequent calls to attend cases of poisoning from obscure causes. These can often be traced to plants that occur in the pasture or feed lot. Accidental cases of poisoning from such wild plants as jimson weed and others are frequent in the United States, several cases occurring annually from cowbane in Iowa. Statistics in regard to such cases are, however, difficult to obtain. H. W. Cattell, as senior coroner physician in Philadelphia, performed 799 postmortems, in 155 of which, death was due to poisoning. The poisons used were listed as f oUows : aconite, 1; ammonia, 1; arsenic, 5; carbolic acid, 10; chloroform, 1; creosote, 1; cyanide of potassium, 1; hydrocyanic acid, 2; il- luminating gas, 12; lead, 1; oil of merbane, 1; opium, 11; oxalic acid, 1; phosphorus, 1; silver nitrate, 1; stramonium, 1; strychnin, 2; sulphuric acid, 1. In his work on poisons, Blyth states that the deaths from poisons in England and Wales during the ten years ending December, 1903, were 11,035. Deaths from laudanum were 1,505; cocaine, 12; atropin, 96; prussic acid and oil of almonds, 328; potassic cyanide, 207; strychnin and nux vomica, 244; aconite, 45; alcohol, 87; petroleum, 23; belladonna, 95; cocain, 12. STATUTES ON POISONING AND ACTION OP POISON ON DIFFERENT ANIMALS. The statutes do not as a general rule define poisons, but in most of the codes the sale of certain poisonous substances is regulated by law. The fol- lowing extract from the Iowa code illutrates this: Sale regulated of substances under Schedule A. Arsenic and its preparations, corrosive sublimate, white precipitate, red precipitate, biniodide of mercury, cyanide of potassium, hydro- cyanic acid, strychnia and other poisonous vegetable alkaloids and their salts, essential oil of bitter almonds, opium and its preparations, except paregoric and other preparations of opium containing less than two grains to the ounce. Schedule B. Aconite, belladonna, colchicum, conium, nux vomica, henbane, savin, ergot, cotton root, cantharides, creosote, digitalis, and the pharmaceutical preparations, croton oil, chloroform, chloral hydrate, sulphate of zinc, mineral acids, carbolic acid, and oxalic acid. Not all poisons act in the same way, some acting more quickly than others. Quality and quantity are prime factors in the results obtained. As an illustra- tion of this fact, we may mention ricin which is obtained from the cas- POISONS AND STATISTICS ON POISONS 7 tor oil bean, one gram of which, if properly diluted, is estimated as suffi- cient to cause the deaths of 1,500,000 guinea-pigs. The characteristics of the animal affected by the poison is also an important factor in the result. For instance, a fatal dose of strychnin in case of ruminants, when given by mouth is varying; when given hypodermically, it is a little larger than for horses; the minimum fatal dose for a horse being \l/2 to 3 grains when given hypodermically, and 3/5 grains (or ^2 ounce of nux vomica) when given by mouth, but as much as 2 grains is permissible. The snail is said to be capable of withstanding more strychnin than an adult man. The minimum dose for man is l/2 a grain, while 4/7 grains con- stitute a lethal quantity. Cardiac poisons produce no action upon insects. The rabbit can stand more morphin than a man. Kobert says: "Amygdatitt does not affect dogs, but it kills rabbits. The hedgehog takes, with apparent enjoyment, a dose of canthar- ides that would kill several persons under excruciating pains. The bite of the most venomous snake does not harm him; he can even accommodate no in- considerable quantity of hydrocyanic acid. Whereas the frog is extraordinarily susceptible to the digitalis poisons, they have no effect on the toad." "Poisons act more powerfully when absorbed from the subcutaneous connective tissue than when administered internally, with the following exceptions : The neutral crotonolglycerid which is found in large quantities in the fresh seeds of Croton Tig Hum, but which is often lacking in commercial croton oil, is inactive when introduced under the skin. It possesses, however, terrific action when taken into the stomach. Myronic acid of mustard as an alkaline salt has no effect when it is injected under the skin ; it has, on the other hand, a strong action when taken per os by herbivora ; the same is true of amygdalin. "In all three of the foregoing cases, the apparent exception to the rule is explained by the fact that the substance, in itself not poisonous, is split up in the intestinal tract, giving off, amongst others, a toxic substance. In the instance first mentioned, crotonilic acid is the poison thus freed; in the second, ethereal mustard oil', and in the third, hydrocyanic acid. Some substances, such as salts of manganese, iron, tungsten, have no poisonous action when introduced into the intestinal tract, because under these conditions only very minute quantities are absorbed; others are rendered inert because they are excreted almost as quickly as they are taken up, curare being an example; and yet others, such as snake poison, spider poison, quillaic acid, sapoto.rin, ergotinic acid, are converted into non-poisonous substances within the intestines." Persons may become accustomed gradually to the use of poisons. Thus individuals who consume opium or its alkaloids may take large doses without apparent injury, although children are particularly susceptible. The former statement is equally true of those who daily use such poisons as hashish, nicotin, caffein, cocain, alcohol, or morphin. They must have the drug in order to keep up their condition. Many people exhibit idiosyncrasies with reference to food substances or drugs. Some people cannot inhale the odor of morphin, turpentine, or tobacco without becoming ill. Others are uncom- fortably affected if the flowers of the common bird cherry or the haw are left in the room. Others become sick when in the presence of the flowers of the tuberose. Coming in contact with the castor-oil plants sometimes causes illness. CHAPTER II BACTERIA!, POISONS Impure Water In all ages great stress has been laid upon the value of the Source a pure water supply. In ancient times, wherever there were of Disease. great centers of population, a large amount of labor as well as of money was employed to furnish water. Of this the Claudian aqueduct, built in Rome in the year 50 A. D., is an illustration. Prof. W. P. Mason says : "Not only was a generous daily per capita allowance sought for, but we note in the centuries gone by unmistakable evidences of a keen appreciation of the dangers lurking in a polluted supply; and upon this point many of the ignorant consumers of our day and generation would be benefited did they consult the wisdom of the past." Of the value placed by the ancients upon the quality of water, Prof. Mason also says : "In ancient times, the valleys of the Euphrates and Tigris, now almost a desert, were densely populated. Four thousand years ago the rulers of Assyria had converted those sterile plains and valleys into gardens of ex- treme productiveness by the construction of immense artificial lakes for the conservation of the flood-waters of the rivers, and as great distributing canals for irrigation. One of these canals, supplied by the Tigris, was over 400 miles long and from 200-400 feet broad, with sufficient depth for the navigation of the vessels of that time." "In India, tanks, reservoirs, and irrigating canals were constructed many centuries before the Christian era, and a great part of that country was kept in the highest state of cultivation. Some of the tanks or artificial lakes covered many square miles, and were often fifty feet in depth. A great de&l of interest has been manifested recently in all parts of the United States concerning water supplies. This has not been confined to the cities but the interest is manifested in the villages and rural districts as well. We are now demanding more than ever before, not only that a good wholesome supply of water be provided to the citizens of a city or village, but also that as good a supply be furnished the farmer. That such diseases as typhoid and cholera are water borne can not be doubted. Many others, as anthrax, hog cholera, and tuberculosis may also be conveyed by water. Animal parasites are also water borne. In addition to these, there are some poorly defined in- testinal disorders that are caused by poor water. That typhoid fever is quite as prevalent in the country as in the city admits no denial. A record of the cases of typhoid occurring during the fall and winter in any of our rural communities shows that the disease is as widely spread in the country as in the city. A certain class of animal diseases is produced not by the invasion of micro- organisms, but is caused by the water supply being contaminated by the decomposing products of animals. The water may, for example, be highly charged with colon bacilli or other bacteria that produce poisonous products. BACTERIAL POISONS 9 Several years ago Dr. Stalker traced an epidemic of horses, cattle, and pigs, all of which had been affected with similar symptoms, the animals uni- formly dying after an illness of about two days. The disease was not con- tagious; the farm buildings were fairly comfortable and clean, and the trouble was, evidently, not due to the food consumed by the animals on the farm. Most of them, however, had been in the habit of drinking from a small creek which ran through the premises. The stream was supplied by a series of springs, and in ordinary seasons flowed for a portion of its course over a gravelly bed. This season the rainfall was light, and it so reduced the supply of water that it ceased to flow. Investigation made on these premises and on the adjoining farms indicated that dead animals were thrown down the steep bluffs into the bed of the stream. During the summer, chickens which had died from cholera and hogs dead from hog cholera had been dumped into the creek. In addition, the creek received the drainage from manure heaps. This was the kind of water that these animals had had to drink. Stock which did not have access to the creek but were watered from a well escaped the disease, while stock on other farms having access to the creek water suffered from the disease. Dr. Lewis and Mr. Nicholson, in Bulletin 66 of the Oklahoma Agricultural Station, refer to certain troubles of live stock due to faecal contamination. In many cases the pond from which stock is watered is situated where plowed debris is carried into it by heavy rains, partially or completely filling it up, while the stock tramping down the banks soon complete the process. Stock standing in the pond also foul the water with excrement, and in hot weather, when the water is low, such a pond certainly can not afford a very satisfactory water supply. During the winter and spring months, when the rainfall is abundant, this condition is not so noticeable since the water is being continually changed by fresh water running in. One of the dangers that follow allowing stock of all kinds to stand in a pond is that when the water is at a low stage, and foul, as it becomes in summer seasons, the cattle will not drink a quantity of the hot, foul, surface water, sufficient to prevent certain derangements of the digestive system such as impaction, "dry murrain," and other conditions that are usually ascribed to dry feed, but which are, in a large measure, brought about by insufficient water. A type of injury resulting from the use of polluted water is illustrated in volume 19, page 74, of the "Journal of Comparative Pathology and Therapeutics." This record is in the form of evidence given in a case in which the plaintiff is the tenant of a farm on which is kept a dairy herd of from 30-35 cows. In 1903, there was no complaint but in 1904 the cows were put to grass in the middle of May and their condition became unsatisfactory at the end of July. Early in September, one of the cows aborted, six others lost their calves be- tween that date and the 7th of October. On the 19th of November, another cow aborted; seventeen of the remaining ones carried their calves the full term and four were barren. The cows drank water from a small lake about one and a half acres in extent, which the town council of Maybole, who were the defendants in the action, used for the deposit of rubbish from the town. About the 18th of October, the cows were removed to another pasture with different water supply, and only one cow slipped her calf. (This occurred Nov. 19). The expert testimony was very conflicting. The plaintiff and expert 10 MANUAL OF POISONOUS PLANTS testimony held that septic poisoning resulted from the use of this water and thus caused abortion, Prof. Williams maintaining that water holding a large amount of vegetable matter is dangerous to pregnant cows, while the defendants held that this would not be a sufficient cause for the action. Judgment was rendered for the plaintiff. Bacterial poisons are produced by two classes of bac- Bacterial Poisons, teria : the first includes such as are parasitic or pathogenic ; the second, those which form poisonous products by the breaking down of dead animal or plant tissues. An illustration of the first class is seen in the products resulting from the tetanus bacillus and diptheria bacillus which produce an extra-cellular toxin. Another type is the toxin known as endo-toxin. In the extra-cellular form, toxin exudes through the bacterial cell-wall and is found in the body; while in the endo-toxin form, the toxin remains wholly, or in part, in the cell during the life of the organism and is liberated only on the death of the bacteria. There are on record numerous cases of poisoning as a result of eating certain foods of animal origin, and the same statement may be made in regard to foods of plant origin. Such foods as meats, fish, cheese, and milk, some- times become injurious because of the products of bacterial growth which they contain. These products are classified as either ptomains or toxins ; a third class, the leucomains, result from the breaking down of tissues of the living animal body, being proteid bodies which have been broken down by enzymes, secreted by the cells of the body. These leucomains produce auto-intoxication. Ptomains are soluble, basic substances formed by the action of bacteria on protein material. Dr. Holland illustrates the action as follows : "The amino- acids, ornithin and lysin, constituents of pure protein, subjected to bacterial action, split off CO2, and change to putrescin and cadaverin." Some of these products, as methylamin, are harmless, while others are active poisons. The ptomains are strongly basic, combining with acids to form salts. They are precipitated with chlorides of mercury and are of various kinds. Some are free from oxygen, while others contain that element; some, as typhotoxin, tetanin, pyocyanin, are unclassified; several are injurious in foods; some are produced in fresh oysters and mussels. Ptomain poisoning. Symptoms : Gastro-enteritis is the most prominent symptom, with depression and nervous disturbances. In most cases, there are, also, marked thirst, salivation, nausea, and vomiting, diarrhoea, cramps in the legs, great prostration, feeble pulse, dilated pupils, delirium, paralysis, and col- lapse. The postmortem examination generally, but not always, shows in- flammation of the stomach and bowels. Cholin, in large doses, nervin, diamin, amanitin, muscarin, all act as poisons; nervin is much more powerful than cholin, the symptoms being those accompanying obstruction of the bowels, to- gether with nausea, pain, and depression; the diamins are all actively poison- ous, dilated pupils, convulsions, diarrhoea, and paralysis being prominent symp- toms. Muscarin, found in Fly Agaric and certain putrid products, is a much more powerful poison than cholin or nervin and produces vomiting, griping pains in the stomach and intestines, slow pulse, arrested action of the heart, contraction of the pupils and fatal collapse. Toxins. These are poisonous bases produced by living bacteria or by saprophytic bacteria in the animal body and in higher plants. Holland arranges the food toxins in two classes: (1) The poisonous BACTERIAL POISONS 11 products of specific bacteria, not putrefactive, growing in meat after slaughter, (2) Products of specific bacteria infecting the tissues of food-animals before slaughter. To these should be added: (3) Toxins of higher plants (phyto- toxins}, in which class would be placed ricin, a product of the castor-oil plant, abrin of the Jequirity plant, crotin of the croton, and robin from the black locust. This belongs to the first group and is caused by the Bacillus Botulism. botulinus, which contaminates ham, sausage, and fish, and is so poisonous that it frequently is the cause of death in the person using the affected meat or fish. Rabbits, guinea pigs, and cats are very sensi- tive to the poison and die when given the fluid culture, rabbits succumbing in 36-48 hours after injection of 0.0003-0.001 c. c. Proteus vulgaris, growing in pork and beef sausage produces a similar poisoning. Symptoms. "Epigastric discomfort, belching nausea, vomiting, gripes, diar- rhoea followed by constipation ;" nervous symptoms appear in a few days ; these are dilated pupils, paralysis of the tongue and pharynx, loss of voice; death may follow delirium and coma, or, after some time, recovery may take place. Poisoning from this cause manifests itself within a half hour occasionally, generally within twenty-four hours, although it may be delayed a week. The toxins of the second class come from pathogenic bacteria and are due to their growth in living animals. The meat and milk from animals that have had septicaemia or pyaemia may cause such symptoms as headache, vomiting, profuse diarrhoea, gripes, chills and fever, the usual symptoms of these diseases. In some of the European countries, and occasionally in the Maidismus or United States, there occurs a disease known as Maidismus or Pellagra. Pellagra. It is common in Northern Italy and Bessarabia and appears at times in France, Portugal, Spain, Roumania, and Wallachia. Etiology. The disease results from the exclusive use of bread made from spoiled maize or Indian corn. It is caused by an unknown toxic substance, partly basic in its nature, called pellagrocein. When maize is kept in a moist place, this poison is likely to develop, probably through the presence of organ- isms, possibly bacteria or moulds. Symptoms- The disease produces debility, reddening and swelling of the skin, an antipathy to food, profuse diarrhoea, delirium and raving mania, ataxic walk, spasms and contractions, debility of muscles, and paraplegia. Sui- cide is not infrequent. In chronic cases, the central nervous system, the skin and digestive tract become the seat of this disease. Postmortem. The intestines show multiple small ulcers and extensive catarrh. The posterior column and motor area of the lateral tract of the spinal cord show a diseased condition. Treatment. Change of diet. Use wheat or rye bread or if maize is used it should be thoroughly dried. A large percentage of cases prove fatal. CHAPTER III DERMATITIS Skin diseases are produced by a variety of causes, some resulting from pathogenic organisms and others through the ingestion of food. On account of these differences, we have two classes sometimes given : parasitic skin diseases and urticarial diseases. Under the second class are placed such eruptions as those produced by buckwheat and smartweed, known technically as fagopyrismus and rhus venenata (dermatitis}, and urticaria, the latter being produced by a large number of plants, especially the nettles. Or there may be internal causes due to innervation of vaso- motors. Of the parasitic skin dis- eases known under the general name of dermatomycoses, we have sever- al types, the co-called Tinea ton- surans and the Favus organ- isms, the former occurring in cattle, dogs, horses, sheep, swine, and poul- try. This term is derived Dermat- from two Greek words omycosis. meaning skin and fun- gus. The classification of the fungi concerned is not at all satisfactory; at present, however, they are generally included in the groups known as Fungi Imperfccti, the Mucoraceae and Ascomycetes. The Fungi Imperfecti include a cause of dermatitis or" Rhus poisoning (U. S. large group of fungi whose life his- pt' gr tory has not been worked out completely. The fungi of this class are form- genera, such as the favus fungus. The so-called Achorion and Trichophyton of various authors represent such form genera, the Oidium albicans being another type; of these, some, perhaps, never produce any other kind of spore than the one commonly seen. Many of these genera undoubtedly belong to the Ascomycetes, in which the spores are produced in little sacs called asci, the spores being known as ascospores. A kind of ringworm of the dog (Eidamella spinosa} belongs to (Rhus Toxicodendron) DERMATITIS 13 this group, also the forms that produce aspergillosis, one type of which oc- curs in the ear. The Mucoraceae produce an unsegmented mycelium and septa only where the reproductive bodies are formed; the spores usually occur in sporangia, or occasionally small spores may be found in the mycelium ; zygospores which result from fertilization also occur in some species. Several species produce surface lesions. According to Neumann, the dermatophytes of domestic animals belong to six distinct genera of fungi as follows: Trichophyton, Eidamella, Microsporon, Achorion, Lophophyton, and Oospora. These genera are not, however, all accepted by botanists. Trichophyton was established by Malmsten in 1848 and is characterized by having a mycelium consisting of simple or dichotomously branched filaments and producing spores from 4-9 ^ long. Sabouraud, however, divides the genus into several species depending on the position of the fungus with regard to the invaded hair. The T. endothrix lives inside the hair; the T. ectothrix develops outside of the hair, forming a sheath around it, and the T. endo-ecto- thrix develops both inside and outside the hair. This classification is scarcely tenable from either clinical or cultural characters. We have placed this genus with Sporotrichum. The Eidamella spinosa described by Matruchot and Dassonville in 1901, has a much branched mycelium, 1.5 ^ in diameter, divided into short segments and splitting into somewhat squarish oval bodies ; it is found on the dog. The Microsporon discovered by Gruby in 1843, has a branched mycelium, the latter branches bearing conidia from 2-3 p in diameter. This fungus has also been placed with Sporotrichum. The Lophophyton, described by Matruchot and Dassonville in 1899, pro- duces a mycelium with some tortuous filaments, others short curved, with thick curved walls ; no spores produced ; it occurs on fowls and is also referred to Sporotrichum. The Achorion was described by Remak in 1833. The filaments of the mycelium are from 2-3 p. in diameter, flexuose or straight, variously branched; finally breaking up into spores. This fungus has been placed with the genus Oospora. Oospora was described by Wallroth in 1833. Its mycelial threads are 2-3 fji in diameter, arranged in irregular chains. The best expert account of dermatomycosis so far as it affects lower animals will be found in the treatise by Neumann *• who includes also an excellent bibliography on the subject. Hutyra and Marek have a German text which devotes considerable space to the subject. The work by Hyde and Montgomery treats the subject from a human standpoint. The work by Plaut is also an exhaustive treatise. Etiology. The cause has been ascribed to various fungi which will be described later in the present work. The predisposing causes are unclean- liness, weakness of animals (those that are worn out may offer a favorable medium for the attacks of the fungus). In the case of cows, Fleming observes that the disease is common in the winter when the stables are dirty, and disappears in the spring when the animals are turned out to i "A Treatise on the Parasites and Parasitic Diseases of the Domesticated Animals." English Translation by George Fleming. Second Edition Revised and Edited by James MacQueen. 697. 365 f. 1907. New York. 14 MANUAL OF POISONOUS PLANTS pasture, the new condition being opposed to contagion. In the case Jof the cat, early age seems to be an essential condition. In the case of the rabbit, a similar condition seems to hold true. In the dog, early age is not an especially predisposing influence but inoculation is successful in young dogs only, accord- ing to Horand, so far as trichophyton is concerned. This latter statement does not hold true for favus. Contagion. In ringworm of the horse, infection may occur from horse to horse. Megnin states that in one locality 200 horses became in- fected in this way, a saddle from an infected horse having carried the disease to other animals. In each case, the disease occurred on the left side of the back. It has also been transmitted from an ox to a horse. The tinea tonsurans has been transmitted from the horse to calves, and the tinea of the horse from horse to dogs, sheep, and pigs, and even to man. Neumann says : "The infection of man is exceptional when the frequency of tinea ton- surans in the horse is considered, as there is scarcely a regiment in which it is not always on some young horse." Grooming is the usual way in which the infection is carried and rubbing facilitates inoculation. The ease with which infection occurs on man depends on the character of the fungus, some forms adapting themselves to the conditions present more readily than others. In the case of the bovines, the contagion may be direct. The virus may be preserved a long time in parts of stables where calves were affected with the tinea tonsurans. The infection spreads less readily to sheep and pigs but may be transmitted from bovines to man. In the case of the dog, it is transmitted from dog to dog, from rats and mice to the dog, and, occasionally, from dogs to man. In cats, favus is largely transmitted from mice and it is certain that this form can be transmitted to man. In general, it may be said that the transmission of favus from the rat or mouse is frequently brought about through the domestic cat. The tinea of the fowl is transmitted by contact with a diseased fowl. The favus fungus of the fowl * cannot be inoculated on the rat or dog but when inoculated on man, it produces lesions similar to favus. Man may be inoculated very easily by handling a fowl on which large erythematous patches occur. Similar patches have occurred in man when inoculation from a fowl was very probable. Symptoms. Two forms of skin dermatomycosis in the horse have been recognized: (1) called microsporosis, and (2) trichophytosis. The more important symptoms of the first as given by Neumann are: "It appears in patches which are more especially seated on the upper part of the body — on the shoulders, back, loins, croup, sides, and flanks. These patches may, however, be met with on any part of the body, though they are rare on the lower parts of the legs. What are first noticed are the circular patches, the diameter of which is generally about that of a shilling; they are distinguished from the healthy skin by the dullness and erectness of the hairs covering them. Some time before the circular patches appear, a very small tuft of hairs — probably from half a dozen to a dozen — may be seen slightly, but markedly, raised in the form of a fine pencil, and feeling as if they had a somewhat hard base, or were matted together at the bottom, when the finger is passed over them. These tufts may be several in number, and are usually best seen in hindquarters at the very commencement of the disease, or in the vicinity of the patches, of which they are the initial symptom. The hairs fall off in a 1 Lophophyton gallinae, Megnin — Trichophyton Megnini, Blanchard. — Sporotrichum. DERMATITIS 15 few days, and this is often the first symptom that attracts attention. The epi- dermis of the patch falls off at the same time as the hairs ; it appears to be softened, and the surface of the skin has then a dark-grey tint and is slightly moist, which might be attributed to the rupture of vescicles, though their pres- ence has never been demonstrated. It cannot, therefore, be said, as Raillet remarks, that the disease presents itself in the form of herpes, as what is so called in human pathology includes a phase marked by the appearance of vesicles. The humidity of the patch is ephemeral. Its surface generally soon dries, and is covered with epidermic scales of varying thickness, which are agglutinated into flat crusts that are shed and renewed incessantly. These crusts have — more frequently than in the ox — a shinning appearance and a grey or yellowish color like flax. At the same time, the lesion progresses by per- ipheral extension until it attains the diameter of a five-shilling piece or more, and on each zone invaded, successive symptoms are observed. Pruritis is nearly absent in Microsporosis, and is scarcely even shown to exist, except by move- ments indicating satisfaction on the part of the animal when the patches are gently scratched. "2. Trichophytosis (S p or o trie hum). A. — Trichophyton jlavum. — The lesions consist of large patches, at least 8 to 10 cm. broad, of a more or less regular form, greyish, and quite smooth. The hairs, raised and matted at their base by a greyish-yellow crust, fall away very rapidly with the crust. The naked surface is not prominent, and shows no trace of suppurative folliculitis (Bodin). "B. Trichophyton equinum occurs usually in numerous patches, some isolat- ed, scattered over the croup and shoulders, and attaining at the most 3 cm. in diameter. At first they can be detected only by touch, but later they become visible by the flattening of the hair. The least traction or slight friction carries off a scaly crust which brings away the diseased hairs. The skin then appears smooth, moist, pinkish, or light grey. Very soon the patch becomes dry, scaly, or powdery, and at its base a slaty grey. The lesions spread by the falling out of the marginal hairs (Matruchot and Dassonville). "C. Trichophyton verrucosum, var. equi, occurs in numerous patches which average 5-6 cm. in diameter, and are localized on the shoulders, neck, withers, flanks, in fact, everywhere where the harness touches. By their confluence, these patches may produce large, irregular lesions. At first the hairs are raised, not broken, and are matted together at the base by a soft grey crust. This crust falls off in less than a week, carrying away the hairs, and having an absolutely bald, grey surface covered more or less with dry, greyish scales, and without follicular suppuration. In young horses, however, the shedding of the crust leaves a vesicle or pustule, then the surface of the patch is slightly raised, red, and indurated (Bodin). "D. Trichophyton verrucosum, var. asini. — The lesions are the same as in the preceding Trichophytosis of the Horse, but are generally confined to the neck, head, and ears (Bodin). "E. Trichophyton mentagrophytes. — This Trichophytosis occurs usually on the nostrils or head. It forms patches up to 5 or 6 cm. in diameter, which may be mistaken for pustules of horse-pox undergoing regression. Over the whole of these patches the hairs are matted together at their base by a soft, brownish crust of unequal thickness. Slight traction on the hair brings away the crust, exposing a bare, slightly raised surface, which is red, inflamed, and pitted with 16 MANUAL OF POISONOUS PLANTS small depressions, grey at their base. These result from the opening of the pustules, of which some may be found at the margin of the patch. The hairs are not broken, but shed, and the condition is, in fact a suppurating folliculitis." The symptoms observed in the bovine, as described by Neumann, are as follows: "The commencement is manifested by a slightly salient ring, on the surface of which the hairs are erect. An active proliferation of the epidermis causes the rapid formation of scales more or less adherent to each other, and crusts of 2 mm. to 7 mm. thick — hence; the name dartre crouteuse was given to the affection by the older (French) veterinarians. According to Gerlach, the crusts are thicker on dark skins, on which they have a greyish-white, fibrous appearance, resembling the amianthus (porrigo asbestinea) on white skins, which are usually finer, the crust is thinner and a little yellow in color." Diagnosis. The diagnosis based on clinical symptoms should be veri- fied by microscopical examinations. It is best to take material from the younger and deeper parts of the crust which may be moistened with water, or a better examination can be made if it is boiled with a 40 per cent solution of potash after which the particles can be dissected and the fungus threads and spores made out. The different forms cannot readily be distin- guished except by cultural methods. The organism grows readily on nutrient media that are neutral or with slightly alkaline reaction. Sabouraud recom- mended the following: Pure glycerine, glucose, lactose, or maltose 4 grammes Granulated petone 1 gramme Distilled water 100 grammes Gelose 1 . 50 grammes Solid media like potato, agar, and peptonized bouillon are favorable media while liquid media are less favorable. Growth may occur at 15°C, the optimum being 30°C. Prognosis. The duration of the disease depends on circumstances, it grad- ually diminishes and may disappear without medical aid. The average length of time of the disease is 40-50 days. Cleanliness has much to do with its disap- pearance. It lasts longer in thick coated animals than in those with thin coats. Treatment. Cleanliness and sanitary surroundings, disinfection of stables, careful and regular grooming (all articles used in this process having been thoroughly disinfected, especially when they have previously been used on a diseased animal), avoiding any substance that causes irri- tation. The following preparations have been used with success : Mercury 1-500; carbolized glycerine; alcohol; an ointment composed of 1 part of carbolic acid, hard and soft soaps, each 20 parts. Fourie and La Calve recommend pure carbolic acid, tincture of iodine, and chloral hydrate in equal parts. The ap- plications should be made once or twice a day or every other day depending upon the irritant properties of the preparations used. For bovines, the remedies named above will prove efficacious; for the dog, application of an ointment prepared from 1-5 per cent of nitrate of silver, is satisfactory. DERMATITIS 17 Dr. Stuhr has contributed the following account of favus in ani- Favus mals: "Favus is a contagious, vegetable-parasitic disease of the skin, characterized by the formation of more or less circular, cup-shaped crusts, varying in size from very small up to that of a dime. It has been observed in almost every species of domestic animals. The disease is quite rare among horses and cattle although dogs and cats are frequent sufferers. The domestic fowl and pigeon are also susceptible. Of the laboratory animals, mice, rats, rabbits, and guinea pigs, harbor the Fig. 2. Favus and Herpes Fungus. A. Spores germinating, grown in gelatine. JB. Hypha breaking into segments. C. Formation of spores in chains (a) formation of buds (fc) chlamydospores. D. Herpes, threads of the mycelium and formation of spores. E. Oidium lactis spore with germ tubes. After Grawitz. disease. Young age, thin skin, and debility predispose. Favus is communicable from lower animals to man and vice versa. Man frequently contracts the disease from cats, the latter becoming infected from eating mice and rats. Etiology. Favus is caused by a vegetable parasite, (Oospora porriginis) which invades the cutaneous structures, especially the epidermal portion. The Achorion Schoenleinii was first discovered by Schoenlein in 1839, 18 MANUAL OF POISONOUS PLANTS although Remak was the first to demonstrate its pathogenic character by direct inoculation. It consists of mycelium and spores, existing in such profusion that it is readily detected. Skin abrasions are an important accessory cause. Symptoms. The disease is characterized by dry scabs, brownish or yellowish, gray or silver white on the surface, and white or sulphur yellow in their deep layer. These scabs have a circular form, with a diameter not to exceed that of a dime, and a thickness varying up to one-fifth of an inch. They occasion atrophy of the hair and a slight depression of the skin. These scabs are usually found on the forehead, cheeks, ears, face, abdo- men, external side of the hind legs and in the neighborhood of the claws. At first the scabs are perforated by hairs which soon fall out. Later the skin exfoliates under the scab and leaves a pit. In the horse the scabs may become confluent and form bands as wide as the finger. Itching is observed in the dog. In most cases the progress of the disease is quite rapid although the prognosis is favorable unless the disease has become too far advanced. Lesiotis. According to Robinson the parasite first obtains a lodgment in the funnel-shaped depression in the epidermis, through which the hair shaft emerges upon the surface. It grows luxuriantly in the upper part of the hair-sac and insinuates itself on all sides between the superficial layers of the epidermis. When it reaches a short distance on all sides of the hair follicle it breaks up the looser layers and appears on the surface producing the characteristic cup-shaped bodies. It also invades the hair shaft itself, pene- trates between the cellular layers of the root sheath and by its mechanical pres- sure upon the papillae interferes with the nutrition of the hair and causes it to fall out. If the pressure is sufficient to cause atrophy of the papilla, a new growth does not occur. In the skin the parasite usually confines itself to the upper corneous cells and does not extend to the living tissues. In cases where the surface is covered by irregular confluent masses of the parasites, the entire upper layer of the epidermis will be found infiltrated with the achorion. The corium itself is usually in a state of chronic inflammation, and suppuration, which may be quite abundant, often occurs under crusts. Even in the absence of pus, the pressure of the parasite causes atrophy of the skin, and at last pit-like depressions or more extensive reddened scars are left. The disease ends with the destruction of the glandular structures of the skin. Treatment. This is purely local except when debility complicates the disease, in which instance tonics should be administered to build up the system. As for the local treatment, its aim is to destroy the para- site and relieve the cutaneous irritation. The dry scabs may be softened and removed by thoroughly washing with soft soap and water. The removal of the hairs, by extraction, from the affected part has been attended with good success since, in so doing, many of the parasites are disposed of. A liniment composed of liquid tar and green soap two parts and alcohol one part will prove beneficial since it is antiparasiticide, disinfectant, dessicating, emollient and cleansing. Mercuric chlorid in one to two per cent aqueous solution tincture of iodine, sulphur iodid ointment, red iodid of mercury ointment 1-8, sulfur ointment, etc., are all useful applications. It is advisable to clip the hair from unaffected parts adjacent to the diseased foci, so that any spread of the malady may be immediate- ly detected. Whatever the treatment, it is a good plan to wash daily with soft DERMATITIS 19 soap and water before applying it. Cleanliness is extremely essential." Hyde and Montgomery state that the parasiticides are corrosive sublimate in the strength of 1-4 grains (0.066-0.266) to the ounce; formalin (1-4 per cent); sodium hyposulfite in saturated solution; spirit of green soap. CHAPTER IV FORAGE POISONING, ERGOTISM, AND ASPERGILLOSIS We have several excellent illustrations of how other Forage Poisoning external known parasitic organisms may produce disease. Catarrhal stomatitis, for instance, may be produced by the ingestion of fodder which has become infected with any one of several fungi belonging to distinct orders. Among these are the rust of clover, bacteria, mil- dew of grass, and the rape-destroying fungus, Polydesmus exitiosus; even the common grass rust and other rusts upon grasses as well as the bunts and smuts are known to produce this form of disease. Among higher plants, such products as the pungent spices of pepper and of the roots of horseradish and radish are treated at length in such pathologies as the Friedburger and Frohner Veterinary Pathology. Serious diseases of the stomach are caused not only by pathogenic germs but also by the ingestion of various foods. Many foods, such as unclean, or damaged fodder, poor water, musty hay, mouldy corn, decomposing potatoes, are responsible for gastro-intestinal catarrh; many fodders, also, contain irritant substances. There are several forms of gastro enteritis. Among forms of the third class (including those caused by ingestion of lower organisms such as fungi or poisonous substances) we may mention botulism, fish poisoning, injuries produced by mould fungi, smuts, rusts, and, finally, the so-called toxic gastro-enteritis produced by numerous poisons. These have sometimes been classed as irritant poisons and narcotic irritant poisons. The vegetable poisons under this head are numerous and have been treated under the different plants. Some pathologists, however, mention especially lupinosis of sheep and equisetosis. The terms applied to this disease are Cryptogamic Poisoning, Forage Poison- ing, Enzootic Cerebritis, Epizootic Cerebro-Spinal Meningitis, Leuco-Encaphali- tis, etc. Characterization. So-called forage poisoning among horses and mules is a non-communicable disease, which undoubtedly belongs to a group of cryptogamic poisonings. Horses seem to be slightly more susceptible than mules, although it usually terminates fatally in both species. The disease is characterized by symptoms which are referable to a disturb- ance in the central nervous system, and by lesions which, if present, are also found there. The course of the disease may be very acute, or it may be greatly lengthened, depending upon the suddenness of the onset. The mortality is very high and but few well developed cases ever recover. Suckling foals do not contract the disease. History. This disease has prevailed quite generally throughout the Eastern and Central parts of the United States for many years, but until recently has not attracted any considerable attention. During the past few years, however, it has occurred with unusual frequency in the Central West, and, because of the extensive losses directly attributable to it, has FORAGE POISONING ERGOTISM 21 become of great economic importance. In various parts of Iowa, for instance, individual stock-owners have lost several thousand dollars from its ravages. In the different localities the disease has been known by various names, such as "grass staggers," "choking distemper," and "putrid sore throat," and because it apparently presents some of the distinguishing characters of a specific infec- tious disease, has been frequently recognized as "infectious cerebro-spinal meningitis." A noteworthy fact however is, that thus far no evidence has been discovered which would indicate that the disease is transmissable from animal to animal, or that it is even inoculable. On the other hand, an outstanding feature in every outbreak is, that the affected animals have had access to unwholesome food, either while at pasture or in the stable. Fig. 3. Common Aspergillus on mouldy corn. 1. General appearance, showing long conidiophore and sterigmata: on end. 2. Perithecium with one of its asci and ascospores. 3. Contents from an unripe perithecium. 4. A small part of the mycelium with conidio- phore c and spore bearing sterigmata; young ascogonium as. 2, 3, 4 after DeBary. Geographical distribution. The disease has been reported from nearly every part of the United States. It never becomes epizootic, but is usually confined to isolated localities. While forage poisoning is not necessarily peculiar to low, poorly drained districts, it is at least most frequently observed in those places where conditions are most favorable for the development of cryptogamic growth. Etiology. The disease seems especially likely to appear when horses or mules are fed on grain or fodder which has become overgrown with 22 MANUAL OF POISONOUS PLANTS moulds, or when at pasture, they have had access to grass which, for various reasons, has become fermented or mouldy. Various micro-organisms have been found to be associated with the disease, but as yet none have been proven to possess any etiological significance. Cultural and histological studies have all proved negative. Dr. Moore has in one instance succeeded in obtaining a pure culture of the colon bacillus from the brain. symptoms. Depending upon the severity of the attack, tne disease may manifest itself in any one of three forms, namely; acute, subacute and abortive. It is possible to observe all of these forms in a single outbreak, as the sudden- ness of the onset is apparently regulated by the amount of the poison laden food which the animal has ingested. The acute type is characterized by the abruptness of its appearance, and the grave general disturbances which immediately manifest themselves. There is sometimes violent trembling and twitching of the muscles over the entire body, but most commonly the acute form is ushered in by stupor. There is manifested a weak, staggering gait and the pharynx is either partially or completely paralyzed. The tongue may also be partially paralyzed and protrude from the mouth, and saliva falls in strings from the lips. The pupil is dilated and the conjunctiva is, as a rule, highly congested. The pulse is variable and may be very rapid and hard, or scarcely perceptible; the respira- tion is hurried and jerky. The temperature may be slightly elevated, but is most frequently subnormal. Intestines and bladder are paralyzed. In this form there may be slight muscular rigidity affecting the muscles of the back, neck and jaws, although in many cases this symptom never mani- fests itself. There is no rigidity of the ocular muscles. The animal soon becomes so weak that he is no longer able to support himself and falls. Delirium may manifest itself, in which the patient may perform a series of movements as if trotting, or become so violent as to do himself serious injury, but most often coma and complete paralysis supervene and death results in from four hours to two days from the commencement of the attack. The subacute form is much the same as the preceding, except that it developes more slowly and the symptoms are not so violent. It is first noticed by a slowness in mastication and a difficulty in swallowing. A further indication of approaching paralysis is seen in the frequent knuckling and the loss of control over the tail. The temperature is subnormal and the pulse and respira- tion are but slightly altered. The bowels and bladder are inactive and it is seldom that voidance of urine and faeces occurs voluntarily. There is but slight rigidity of the muscles if indeed there is any, and no evidence of pain is apparent. These symptoms may last two or three days, when gradual improve- ment takes place, or the paralysis becomes more complete, the general weakness more marked, paroxyms of delirium develop, with inability to stand, breathing becomes more labored, coma comes on and death results apparently without a struggle. This form lasts from six days to two weeks. In the abortive form there are no well marked constitutional symptoms. The appetite may be somewhat lessened, the ability to swallow slightly impaired, and the animal's movements a little uncertain, but no very noticeable symptoms appear to attract the attention. Improvement usually takes place on the third or fourth day, and recovery is the usual result. Lesions. As a rule, post-mortem examination reveals no naked eye changes in the tissues of animals dead of forage poisoning. There FORAGE POISONING ERGOTISM 23 may be congestion of the brain and cord with extensive effusion into the ventricles and subarachnoid spaces. Few small hemorrhages and parenchyma- tous degenerations within the various organs have been mentioned. MacCallum and Buckley have found in the brains of horses dying of this disease, areas of softening "in the frontal region on each side, anterior to the motor region of the cortex." This lesion was practically confined to the white matter immediately under the cortex. In the affected areas there was "complete destruction of the brain substance, in which the anatomical structures are disintegrated and largely replaced by a colloid-like material. The neighboring blood vessels were acutely inflamed, with cellular infiltration of leucocytes and red corpuscles into the perivascular spaces and tissues. In a later outbreak these writers failed to find the brain lesion, but did observe the vascular changes above described. McCarthy and Ravenel, in a study of fifteen animals found certain lesions in the upper gastro intestinal tract and in the central nervous system. These were: (1) In the intervertebral and Gasserian ganglia, where a pericapsular, small round cell accumulation was present. The cells were all of the same type, the nucleus and protoplasm being about the size of a red corpuscle. There was no evidence that these cells were the result of proliferation of the original layer of capsular cells. (2) Cortical lesions. — These consisted of congestion of the cerebellar and cerebral cortex. There were also capillary hemorrhages. The meninges were normal. (3) Changes in the choroid plexus. — In three cases the choroid plexus was changed into a triangular tumor-like mass, of a yellowish red color and of a firm consistency. The increase in size was found to be due to a proliferation of the elastic tissue surrounding the vessels. (4) Changes in the nerves. — There was a distinct degeneration of the nerves supplying the larynx and neck. This was present in the nerve up to the ganglion, but was not found in the posterior roots. Other slight changes were detected. Moore failed to find any gross lesions in the nervous system and other organs in the cases examined by him. In one case the brain, spinal cord, and organs were studied histologically with negative results. Differential diagnosis. A very important point in the recognition of forage- poisoning is the history which has been referred to previously. It must be distinguished from inflammations of the brain and meninges, and from rabies. Treatment. In the acute cases this is seldom successful, although quick- acting stimulants to arouse the patient may be tried. In the subacute cases a purge should always be given to rid the intestines of the poison. Strychnin in large doses, to overcome the extreme depression of the nerve centres, and atropin to support a failing circulation may be administered hypodermically at frequent intervals with benefit. In the very mild cases, all that is necessary is to empty the bowels with a purge. It is of the utmost importance, in all cases, with the return of the appetite, to supply only such food and water concerning the wholesomeness of which there can be no question. Prevention. Since it seems to be quite generally accepted that this disease is brought about by the ingestion of mould-contaminated food 24 MANUAL OF POISONOUS PLANTS the prophylaxis is apparent. Whenever the disease makes its appear- ance either in a stable or a pasture, the animals should be immediately removed from further exposure by changing the food supply. The food should come, preferably, from a clean, new source and the water should not be contaminated by surface drainage. It is also well to thoroughly disinfect the mangers and feed-boxes, and render inocuous the soiled litter. There is no known means of artificial protection, and the disease will recur if the animals are again allowed access to spoiled food. (Stuhr). . . History. During the winter of 1908-1909, several cases of poisoning from spoiled silage were reported to Dr. Stange of the Iowa State College. Other cases have no doubt been en- countered. In every instance, as in the case reported by Dr. Beaumont, below, moulds occurred in the silage. Dr. Beaumont says : "I am sending you under separate cover by mail a specimen of corn silage upon which you will notice is growing some form of mould which in my opinion is accountable for a very peculiar disease, existing among a herd of young horses and mules belonging to a farmer living here." Dr. R. E. Buchanan found these moulds occurring in spoiled silage to be a species of Monascus. Other moulds, Mucor, Penicillwm glaucum, and Verticil- Hum were also present; but there was a preponderance of Monascus. Symptoms. "The first animal, a three year old filly, was taken sick about April 1st, showing symptoms as follows: Gaunt, depressed, stiffness of gait. When lying was unable to rise, but when assisted to rise would stand and show inclination to eat but was unable to masticate and swallow food. Temp. 103.5 F. Pulse 86, Respiration 36; friction sounds distinctly heard at each heart beat. A whistling sound was emitted during expiration and there was also a suppressed painful cough. Animal died in about five days. "A two-year-old mule and one two-year-old filly were attacked with disease. The mule is improving and will recover but the two-year-old filly shows exactly the same symptoms as Case No. 1, aside from being especially stiff and lame in one fore shoulder, and I think will die within two days." Treatment. The treatment as followed by Dr. Beaumont is described in detail in his paper before the Missouri Valley Veterinary Association, June 16-17, 1909. Briefly, the method was as follows: Tincture Strophanthus in two-dram doses, every two hours (given as a cardiac stimulant, the heart action being very weak). 1 quart of raw linseed oil given in two doses, six hours apart (as general laxative). Potasii Nitras in half to one ounce doses, dissolved in water and given as a drench, every three hours (alterative diuretic, and respiratory stimulant). After the first twenty-four hours the Tr. Strophanthus was discontinued and he began giving Iron Quinine and Strychnin tonic in one-ounce doses three times daily. This was continued with the Potasii Nitras until the animal showed marked im- provement when both remedies were discontinued and he prescribed Fowler's Solution (Liquor Potasii Arsenitis) in half-ounce .doses three times daily during convalescing stage of the disease which lasted about ten days or two weeks. Dr. C. H. Stange has contributed the following on forage poisoning and especially with reference to silage : "Numerous cases have been reported of an affection of the central nervous system, the symptoms being in general quite similar but different and varying FORAGE POISONING ERGOTISM 25 causes are assigned. Dr. Francis reports that in the fall of '03, spring of '04, four to five thousand horses and mules died with a nervous disorder character- ized by structural changes in the brain which cause incoordination, delirium, coma and usually death. He concludes that the disease is not caused by moulds but is the result of animals having free access to a labor diet when kept in idleness. He was unable to find the germ described by Wilson and Brimball. "Professor Harrison of the Ontario Agricultural College reported several cases and as a result of his investigations he concluded that the disease was due to a coccus insolated from the meningeal fluids. Pearson studied an out- break in seven horses, five of which died. The outbreak occurred soon after opening a new silo, the ensilage from which was mouldy. The symptoms ob- served were very similar to those observed by Professor Harrison and he emphasized the paralysis of the pharynx and great muscular weakness. He concluded as a result of feeding experiments that the so-called cerebro-spinal meningitis was a forage poisoning. Dr. Dow of Connecticut describes two cases which were attributed to watering from a tub containing a mouldy slime. Dr. Ferguson of Texas describes three cases of forage poisoning due to smutted corn. There was vertigo, coma, low temperature, pulse in later stages rapid and irregular. In 1901 Dr. Hickman investigated an outbreak among horses in North Carolina in which a large number of horses died. In 1906 another outbreak occurred at the same place (Hyde Co.) in which about forty horses and mules died in about three weeks. The cause in these cases seemed to be moulds on vegetation. On the whole the country is low and swampy. The pathological changes of Epizootic Leuco-Encaphalitis were described by McCal- lum and Buckley in 1902. Muller of Germany reported an outbreak among horses, cattle and sheep due to mouldy straw. (Berliner-Tierarztliche Wochen- schrift). Drs. McCarrol and McMullen describe an outbreak of cryptogamic poisoning in horses due to feeding mouldy beet tops. Dr. Lockhart describes several cases in Canada. The prominent symptom seemed to be the inability to swallow. "Two outbreaks have come under our observation during the past year. The first consisted of eleven head of horses, two horses were being fed for market, the others were fed in the same manner during the nights and turned out during the day. The first animal affected was one being fed for market. It ate part of its feed in the morning but in a few hours showed symptoms of ptyalism, depression and paresis of the hind quarters. By noon the animal was down, unable to rise and struggling some, and died that night. The next animal to show symptoms was its mate. The symptoms shown in this case were similar to acute cases of the so-called cerebro-spinal meningitis, coming on with trembling and weakness causing the animal to stagger. An early symptom in all cases coming under our observation is the ptyalism due to inability to swallow. (Dyspagia). As a result the saliva collects in the mouth and hangs from it in strings. Muscles of different regions of the body are liable to con- tract. The breathing is rapid and in some cases may be of the Cheyne-Stokes variety. The temperature in this case was sub-normal. In some of the more chronic cases and when the animal has been down for some time with con- siderable struggling the temperature was somewhat elevated. The pulse was variable, being about normal in some cases and rapid and almost imperceptible in others. The animal became quite violent at times and finally died living but a few hours longer than the first animal. The other seven animals showed 26 MANUAL OF POISONOUS PLANTS a more chronic course, showing inability to swallow, slow, weak pulse, difficult, noisy respiration, weakness and paralysis, spasm of muscles of head, neck and back, death taking place in from two to six days. The other two animals showed a mild type of the disease as slight loss of control, some exophthalmia, loss of appetite and thirst and loss of condition. These animals were placed on potassium iodid and nux vomica and recovered. "This outbreak was attributed to mouldy silage, which was being fed to the horses, but in order to be more certain 150 pounds of silage were ship- ped to the college and fed, first to one horse which died in two days from an acute form of the disease. Another horse was fed but would not eat the silage so well, consequently did not die quite so soon, living for several days. In both cases the symptoms resembled those seen in the original outbreak. Post mortem revealed no changes except a few petechia along the small in- testine, a few infarcts in the kidney and slight softening of the brain. This however was not very marked, probably due to the fact that they were acute cases. Microscopic examination revealed the presence of mould in the niucosa and submucosa of the intestine, also mycelial threads growing between and around the renal tubules. "The other outbreak consisted of four horses, three of which died of an acute form of the disease, the symptoms being similar to those already des- cribed. The fourth being of a more chronic nature was placed on potassium iodid and nux vomica and recovered. In this outbreak the hay was found to contain a fine mould and was cut from an old pond which had been plowed up and seeded. The water had overflown this, however, and stood for some time. The symptoms and post mortems were similar to those described in the first outbreak, with the exception that no histological examinations were made. "A form of cerebro spinal meningitis is quite common in Germany. It has also been described in Australia, Great- Britain and Russia. It may be that these outbreaks are due to other causes than those already described. Sid- amgrotzky and Schlegel found a form of coccus in the sub-arachnoid fluid, but it was necessary to make sub-dural injections of cultures of this organism to cause meningo encephalitis. Johne found a diplococcus in the cerebro-spinal fluid of affected horses. "Ostertag found a diplococcus similar to the one found by Johne in the cerebro-spinal fluid in the so-called Borna's disease. They were pathogenic for horses and sub dural injections produced symptoms and death similar to cases of Borna's disease. Hutyra and Marek call attention to the fact that bacter- iological investigations have not been followed by the same result but possibly the several investigators were working with the same organism. Nevertheless it remains to be shown whether all cases of cerebro-spinal meningitis are due to the same cause and resemble Borna's disease. On the other hand it is possi- ble that epizootic cerebro-spinal meningitis of domestic animals has no specific cause. "It is apparent that mouldy food and water has caused several outbreaks in this country. Natural infection in European outbreaks is also supposed to take place through infected food and drinking water. The disease is not trans- mitted from one animal to another. Mohler calls attention to the very inter- esting work of Schlegel and the Berliner Tierarztliche Wochenschrift who FORAGE POISONING ERGOTISM 27 ERGOT ON VARIOUS GRASSES Figr, 4—1. Manna Grass (Glyceria nervata.}. 2. Blue Grass (Poo). 3. Spikelet of Bottle Grass (Asprella Hystrix). 4. Reed Canary Grass (Phalaris Arundinacea) . 5. Wild Rye (Ely- mus robustus). 6. Koeleria cristata. 7. Wheat Grass (Agropyron Smithii}. 8. Red Top (.Agrosttt alba). 9. Blue Joint (Calamagrostis canadensis). 10. Timothy (Phleum pratense). 28 MANUAL OF POISONOUS PLANTS associates with the affection an organism which he termed Streptococcus mel- anogenes. Mohler states, however, that whether the disease is of microbian origin or an intoxication has not yet been definitely established." Ergotism is a disease of bovines caused by the ingestion of Ergotism considerable quantities of food contaminated by ergot. Equines are apparently less susceptible than bovines, although the horses have been known to suffer severely from the disease. Ergotism in man is not an uncommon occurrence, and in nearly every instance it has resulted from eating bread made of ergotized grain. The disease makes its appearance among cattle chiefly in the winter and spring seasons and has at times been the cause of serious losses throughout the central and western states. Ergot is the sclerotium of a parasitic fungus, Claviceps purpurea, which infests many species of native and cultivated grasses, and appears on some of our grains, especially rye. The sclerotium represents a stage in the life history Of the fungus, which is intermediate between that of the mycelium or spawn, and that of the spore-bearing thallus. It flourishes particularly well on rich soil and in warm, damp seasons. The chemistry of ergot is not exactly known, although Kobert succeeded in separating three bodies; namely, ergotinic acid, cornutin, and sphacelinic acid. Ergotinic acid is a protoplasmic poison, and when injected intravenously produces inflammation of serous and mucous membranes, disintegration of red blood cells, and wide-spread ecchymoses; cornutin excites the central nervous system and causes general convulsions; and sphacelinic acid induces gangrene. Symptoms. Ergotism manifests itself among animals chiefly in the chronic form, since, as a rule, the poison is acquired in small amounts and accumulation takes place slowly. Two distinct types of the disease are recognized, namely: spasmodic and gangrenous. Symptoms referable to the digestive tract, such as nausea, vomiting, colic, diarrhoea or constipation appear in both forms. Pregnant animals very frequently abort. In the spasmodic type of the disease, symptoms due to over stimulation of the central nervous system, appear. These are tonic contraction of the flexor tendons of the limbs, anaesthesia of the extremities, muscular trembling, general tetanic spasm, convulsions and delirium. Death usually occurs from secondary causes. Gangrenous ergotism is attributed to prolonged constriction of the arterioles, and more directly perhaps to degenerative changes in the vessel walls, and the consequent formation of hyaline thrombi. It is characterized by coldness and anaesthesia of the extremities, followed ultimately by dry gangrene of these parts. The effects of this dry gangrene are often very serious and amount to sloughing of the feet, tips of the ears, tip of the tail, shedding of the hair, teeth, etc. Death takes place from exhaustion. Lesions. With the exception of the gangrene which may vary greatly in severity, there are no lesions of especial significance. Degenerative changes in the sensory area of the cord and in the vessel walls have been observed in animals slowly poisond with ergot. Treatment. The first essential in the treatment of ergotism is to remove the cause. In well established cases treatment does not as a rule prove satisfactory. Tannic acid is the chemical antidote, and should be given to neutralize the unabsorbed portion of the poison. Chloral is the physiological antidote. In FORAGE POISONING ERGOTISM 29 addition to giving the antidote, the treatment is entirely symptomatic. (Stuhr). Fig. 5. A. Aspergillus fumigatus showing coniliophore on right with sterigmata and spores attached on left. B. A. niger showing conidiophore, sterigmata, and spores attached in chains. After Siebenmann. Pneumonomycosis is a not uncommon disease of domestic Aspergillosis animals caused chiefly by the mould, Aspergillus fumigatus, although the Aspergillus niger is also pathogenic for birds. This disease is most frequent in birds, both domestic and wild, occasionally observed in horses and cattle, and rarely in man. Respiratory diseases and lowered vital- ity predispose. In all species the disease is characterized by purulent local inflammations in the lungs or other tissues, and a purulent and necrotic pseudo- membrane upon the bronchial, tracheal, and other mucous membranes upon which it grows. The appearance of the pulmonary lesions sometimes resembles tubercle, sometimes actinomycosis. Pneumonomycosis has been experimentally produced in birds (pigeons and geese) by compelling them to inhale aspergillus spores for a few minutes, after which they usually die of pneumonia in a few days. Rabbits have also been successfully inoculated by intravenous injection of spores. Etiology. In mammals the Aspergillus fumigatus and in birds the Asper- gillus fumigatus, niger and jlavescens seem to be pathogenic species. Infection takes place most commonly by inhalation of the spores which often are suspended in the air, or by taking them in with the food. Intestinal infection has not been observed. The spores are widely distributed in nature and exist in vegetable matter and grain abundantly. They possess remarkable vitality and exhibit considerable resistance to destructive agencies. The patho- genic power of the mould does not depend upon any product which it elaborates but upon the reactions which result from its penetration into the tissues. Peck observed the disease in seven subjects, in a stable where horses were fed on mouldy hacked hay. Symptoms. The disease is of slow development in the larger animals and may not be observed until well advanced. In general the symptoms are of a pneumonic nature and in addition there is progressive emaciation. A case in a 30 MANUAL OF POISONOUS PLANTS Jersey cow, described by Pearson and Ravenel presented the following symp- toms; the animal had been in poor condition for six months before it was examined. It was weak and depressed, did not eat, breathed with difficulty and, at times, coughed violently. Percussion of the chest gave sounds clearer and louder than normal and auscultation revealed the lung and bronchial sounds much intensified. Six days later these symptoms became more pronounced, the respiration and pulse very rapid. The animal grew rapidly weaker and died ten days after first being seen. The symptoms in birds are much the same as those in mammals except, that the disease runs a more rapid course. Emacia- tion advances rapidly and fetid diarrhoea may set in and continue until death in from a week to two months. At times emaciation is the only symptom. Fowls emit a glairy discharge from the nostrils which may contain the spores. In the prevention of the disease in fowls therefore, it is necessary to isolate or destroy the sick fowls together with the carcasses and fumigate the poultry houses. The roosts may be whitewashed. Lesions. The lesions take the form of a miliary suppurative process, the foci varying in size from very small up to that of a pea. These may exist in large numbers and be scattered throughout the entire lung. Sometimes they become confluent and produce large areas of disease. The process starts in the bronchial mucous membrane, and later involves the bronchioles and alveoli. A very important feature is the intense amount of emphysema which is apparent on external examination of the lung. The lobules are often widely separated and can be readily seen in outline when a portion of the tissue is examined by transmitted light. In these emphysematous interlobular spaces, and in the air passages are seen whitish, mouldy looking patches. They are composed of denuded epithelium, inflammatory exudate, fruit hyphae and spores. The lesions spread by penetration of the mycelium causing a destruction of tissue. Spores are not found within the tissues. In rare cases there is diffuse pneumonia characterized by hepatization and interstitial infiltration. On this latter account the disease has been described as being similar to contagious pleuro pneumonia of cattle. There may be pulmonary gangrene from secondary invasion of putrefactive organisms acting upon the devitalized tissue. An interesting feature is that this disease may interfere with the tuberculin test. This was shown in the case, above referred to, in which the test was used without success, and lesions of tuberculosis found in the lung on postmortem examination. Treatment. This must of necessity be unsatisfactory since it is quite impossible to destroy the moulds which have penetrated the lungs. (Stuhr). CHAPTER V POISONING FROM FUNGI That fungi of various kind are injurious, was known to the ancients. Prof. Ford * says, "The most interesting cases of mushroom or, as commonly described, toadstool poisoning and one of the first authentic cases on record, occurred in the family of the Greek poet, Euripedes, who lost in one day, wife, daughter, and two sons, who in the poet's absence partook of the deadly species. Among the great ones whose lives were sacrificed to the same ignorance may be mentioned Pope Clement VII., the Emperor Jovian, the Emperor Charles VI., Berronill of Naples and the widow of Tsar Alexis. The death of the Emperor Claudius is also assigned to this cause, but the reason and manner of the accident are not certain. In addition to poisoning from toadstools, it has long been known that Ergot (Claviceps pur pur ea} is injurious to man and lower animals. In recent years Ergotism has not been so serious as formerly. Other fungi also may be responsible for the death of animals by poisoning. The Fly Agaric (Amanita muscaria}, a beautiful species, is common in many parts of the United States. I have described it in detail in another part of this work. In this connection I shall quote freely from the detailed and excellent account of poisoning as given by Prof. V. K. Chesnut, and the excellent report given, of A. phalloides by Prof. Ford, who has written the most recent account of poisoning from this fungus. The symptoms and treatment are thus described by Mr. V. K. Chesnut: "The symptoms of poisoning from the fly amanita, as deduced from a number of cases, are varied. In some instances they begin only after several hours, but usually in from one-half to one or two hours. Vomiting and diarrhoea almost always occur, with a pronounced flow of saliva, suppression of the urine, and various cerebral phenomena beginning with giddiness, loss of confidence in one's ability to make ordinary movements, and derangement of vision. This is succeeded by stupor, cold sweats, and a very marked weaken- ing of the heart's action. In case of rapid recovery the stupor is short and usually marked with mild delirium. In fatal cases the stupor continues from one to three days and death at last ensues from the gradual weakening and final stoppage of the heart's action. "The treatment for poisoning by Amanita muscaria consists primarily in removing the unabsorbed portion of the amanita from the alimentary canal and in counteracting the effect of muscarin on the heart. The action of this organ should be fortified at once by the subcutaneous injection, by a physician, of atropin in doses of from one one-hundredth to one-fiftieth of a grain. As a stimulant emetic, mustard is particularly valuable. If this is not effective apomorphin should be administered by a physician. In case of profound stupor, however, even this may not produce the desired action. Tannin is of little l Science N. S. 30: 97. 98. 32 MANUAL OF POISONOUS PLANTS or no value in rendering the muscarin insolu- ble in the stomach. If vomiting has not taken place, recently burned charcoal or two grains of a one per cent alkaline solution of perman- ganate of potash may then be administered, in order, in the cases of the former substance, to absorb the poison, or, in case of the latter, to decompose it. This should be followed by oils and oleaginous purgatives, and the in- testines should be cleaned and washed with an enema of warm water and turpentine. "Experiments on animals poisoned by the fly amanita and with pure muscarin show very clearly that when the heart has nearly ceased to beat it may be stimulated to strong action almost instantly by the use of atropin. Its use as thus demonstrated has been the means of saving many lives. We have in this alkaloid an almost perfect physiological antidote for muscarin, and therefore in such cases of poi- soning its use should be pushed as heroically as the symptoms will warrant. The presence of phallin in Amanita muscaria is possible, and its symptoms should be looked for in the red color of the blood serum discharged from the intestines. Its treatment, which is difficult, is discussed under Amanita phalloides. "It is well known that in some parts of Europe the fly amanita, after the removal of the poison by treatment with vinegar, is a common article of food. It was interesting to discover not long since that among some of our own people a similar practice prevails. Though most of the colored women of the markets look upon the species with horror, one of them recited in detail how she was in the habit of cooking it. She prepared the stem by scraping, the cap by removing the gills and peeling the upper surface. Thus dressed the mushrooms were first boiled in salt and water, and afterwards steeped in vinegar. They were then washed in clear water, cooked in gravy like ordinary mushrooms and served with beefsteak. This is an exceedingly interesting operation from the fact that although its author was wholly ignorant of the chemistry of mushroom poisons, she had nevertheless been employing a process for the removal of these poisons which was scientifically correct. The gills, according to various pharmacological researches, are the chief seat of the poisonous principles in this plant and their removal at once takes away a large part of the poison. The salt and water would remove phallin or any other toxalbumin the mushroom contained, and although the presence of phallin or any of this class of poisons has not been demonstrated in Amanita muscaria, there is a strong suspicion that it may occur in slight amount. The vinegar, secondly, removes the alkaloid poison, muscarin, and the mushroom after the two treatments is free from poisons. This process is cited, not to recommend its wider use, but as a matter of general interest. The writer's recommenda- Fig. 6. Deadly Amanita (Am- anita phalloides}. U. S. Dept. Agrl. POISONING FROM FUNGI 33 tion is that a mushroom containing such a deadly poison should not be used for food in any form, particularly at a season when excellent non-poisonous species may be had in abundance. "It is surprising that cases of poisoning are not more frequent. At Tacoma Park, D. C., on November 9, of last year, a lady who has a thorough knowl- edge of edible and poisonous mushrooms met a family, consisting of a man, woman, and two children, who had just completed the gathering of a basket- ful of the fly amanita and the death cup, described below, which they were taking home to eat. In reply to questions the woman stated that they had often eaten this kind purchased dry at an Italian store, but that they had never gathered fresh ones before. Of course they had mistaken the species, or pos- sibly the dried ones were fly amanitas from which the poison had been re- moved by treatment with vinegar. After considerable persuasion the people consented to throw the lot away. Figr. 7. Fly Agaric (Amanita muscaria). U. S. Depf. Ag.l. ''It is impossible to say what amount of the fly amanita would prove fatal, but in this connection it is of interest to note the custom reported by Krashen- innikoff, a Russian who travelled in Siberia and Kamchatka from 1733 to 1743, namely that the natives of the latter country, particularly the Koraks, used the fly amanita as an intoxicant, three or four specimens constituting a moderate dose for one habituated to its use, but ten being required for a thorough drunk. 34 MANUAL OF POISONOUS PLANTS The same observations, with varied details, have been made by others, par- ticularly by Langsdorff, who traveled around the world with the Russian navigator Krusenstern from 1803 to 1806, and in more recent times by Kennan in his first Siberian journey of 1865-67. "The plant may be taken fresh, but its taste is so disagreeable that only with great difficulty can a sufficient amount be eaten to produce the intoxicating effect. The Koraks have two principal methods of taking it : First, by swallow- ing pieces of the dried caps without chewing them; second, by boiling the dry caps in water and then drinking the liquor thus produced mixed with the juice of berries or herbs to disguise the taste. The intensity of the poisonous character of the fly amanita undoubtedly varies at different ages, with different individuals, and with different methods of preparation. The amount of the poison that can be taken into the system with impunity varies, too, with the person who takes it. The fact that a Korak, who has long used the plant as an intoxicant, can eat ten specimens and merely become drunk, does not prove that a similar number would not be fatal to an American who had never eaten it before. "Very diverse statements concerning the properties of this fungus have been recorded. While some have attributed to it edible qualities, others have as- serted that it is a most active poison and has caused numerous accidents by being confused with the Orange amanita. It is said to have caused death even when eaten in small quantities, and again it is said to have been eaten in abundance without any evil results. According to Quelet, it acts as a cathartic if eaten in small quantity, but causes death if eaten freely. One of my own correspondents assures me that he has eaten of the yellow variety, Var. formosa, without evil results, and that he regards it as very good. But there is no disputing the fact that the species possesses intoxicating and poisonous prop- erties. It has long had the reputation of possessing properties fatal to flies that sip its juice. This suggests the names muscaria, Fly amanita, Fly agaric and Fly killer by which it is known. I have myself seen the cap of a single specimen surrounded by a circle of lifeless flies that had sipped the viscid juice from its moist surface and fallen victims to its virulent properties before leaving the place of their fatal repast. "Some have attempted an explanation of the contradictory statements concerning this plant by supposing that its poisonous properties are not always developed, that in some localities or under favorable circumstances it is harm- less. This explanation violates our sense of the constancy of Nature, and is not at all satisfactory. In the case of my own correspondent, the caps were peeled before cooking. May it not be that much of the noxious quality resides in the epidermis and the viscid substance upon it, and that by discarding this the dish is rendered less dangerous? In some cases it is said that those who eat it freely and without harm boil it a long time in water and throw away the water. In this way, doubtless, much of the poison is abstracted. Long soaking in salt and water, also in vinegar, have been recommended as a means of rendering suspected or noxious species harmless, and may have been prac- ticed in some of the cases in which this fungus has been eaten with impunity. Whatever may be the explanation of the contradictory statements, the only safe way is to consider this species as deleterious and avoid its use under all circumstances. There is no need of taking any risks, with suspected species, POISONING FROM FUNGI 35 since there are so many good ones against which no charge of evil has ever been established." A second very poisonous species is the White or Deadly Amanita (Amanita phalloides), common also in some parts of the United States. This species is described in another part of this work. This and allied species are eaten ignorantly by persons who do not know the nature of the powerful poison found in the plant. Prof. Ford says, "A small amount of the fresh material is sufficient to cause profound illness with fatal outcome, so potent is the poison contained in its meshes, and the raw plant seems usually more toxic than the cooked specimens. "Two or three 'deadly amanitas' suffice to bring on disastrous results, and Plowright reports the death of a child of twelve from eating a third of the pileus of a small raw plant. The extreme toxicity of this species illustrates the dangerous consequences which the admixture of two or three specimens to a dish of edible mushrooms entails. ''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 located 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 Hypocratic facies, "la face vulteuse" 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 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." Kobert isolated from the fungus, a substance which he called phallin, and which had the property of disolving the red blood corpuscles. Such substances are called hemolysins. Prof. Ford says, v'Very minute traces of this substance brought in contact with the red blood cells of man or with those of animals, produced within a short space of time, fifteen minutes to one or two hours, a complete solution of these corpuscles — a laking of the blood. So powerful was the hemolytic action that even in a dilution of 1-125,000 it was still operative upon the red cells of ox blood." In a recently published statement by Prof. Ford it appears that * the fungus always contains another poison which differs from hemolysin in being resistent to heat and digestion, "the blood-laking substance phallin, being destroyed by heating to 70° C., and by the action of the digestive ferment. This substance he called Amanita-toxin, and the blood-laking substance Amanita-hemolysin. Abel and Ford 2 have shown that the so-called phallin, regarded by Kobert as 1 Science N. S. 30:101. 2 Jour. Biol. Chem. 2:273; 1907. 36 MANUAL OF POISONOUS PLANTS a toxalbumin is a glucoside. Prof. Ford has obtained an anti-poison or an anti-hemolysin with a high grade of immunity. According to Schlesinger and Ford * the Amanita-toxin in a purified state is one of the most powerful of organic poisons — four tenths of one milligram killing a guinea pig within twenty-four hours. Ford believes that the hemolysin plays no part in human intoxication, but that the toxin is the active principal which resists the action of the gastric juice and boiling. He finds that the Amanita rubescens considered an edible species by some, contains an hemolysin as powerful as the Deadly Amanita. He found a toxin and an hemolysin in Amanita inrosa. The latter substance in a dilution of 1-200 killed a guinea pig. The A. spreta produced in- toxication and according to Ford must be classified with the "deadly poisonous'* as the A. verna. The A. strobiliformis, A. chlorinosma, A. radicata, and A. porphyria, do not contain hemolysins but small quantities of a toxin probably identical with amanita-toxin. The Amanita solitaria, regarded as edible, causes the blood corpuscles to adhere in clumps much as agglutination occurs with typhoid bacilli when brought in contact with the blood of a typhoid patient. Jour. Biol. Chem. 3:279. 1909. o CHAPTER VI POISONING FROM OTHER PLANTS. EQUISETOSIS, LOCOISM, AND UJPINOSIS Equisetosis. It has been recently proven by direct experimentation that the common horsetail (Equisetum arvense) when ingested in sufficient amount, is capable of producing fatal poisoning among horses. This discovery is of great importance since the plant has a wide distribution, and at times is the cause of extensive losses. The common horsetail thrives best in- moist sandy soils or in low, damp meadows, which are not frequently cultivated, and often constitutes a large part of wild hay. The dried plant alone seems to be poisonous. Young horses seem to be the most susceptible. Sheep are supposed to be slightly susceptible although cattle eat the hay in which the plant occurs in large proportion, with impunity. The toxic principle of the plant has not been determined. Symptoms. The effects of poisoning from eating horsetail appear at times varying from two to five weeks, depending upon the age of the animal, and the amount of contaminated hay ingested. The first symptoms are usually unthriftiness, general bodily weakness and emaciation. The animal seems to have a depraved appetite, preferring the plant to wholesome feed. As the disease progresses the muscular weakness becomes more pronounced, the animal loses muscular control and exhibits in- coordinate movements. During this stage the pulse and temperature are de- pressed, extremities are cold and the visible mucosae are pale. Appetite usually remains good until the end and consciousness is apparently retained. Finally the animal falls, manifests nervous excitement, paroxysms of convulsions appear and death results from exhaustion. In the final stage the pulse becomes ac- celerated and the temperature elevated. Hypostatic pneumonia is a frequent complication. Treatment. The first step in the treatment is the removal of the cause. A cathartic should be administered to rid the bowels of the irritant and nerve and heart stimulants given to combat the symptoms of depression. In case the patient is unable to stand, it would be advisable to give some support. When the animal is down it becomes necessary to guard against the develop- ment of hypostatic pneumonia. Where cases are not too far advanced and appropriate treatment is in- stituted, recovery is the usual result. (Stuhr). Stock-poisoning by the loco weed is a frequent and serious con- Locoism. dition with which the stock-owners of the western half of the United States have to contend. Montana and Colorado, especially, sustain heavy annual losses. Similar diseases occur in other parts of the world. In Australia other plants of the order Leguiminosae like Gastrolobium produce similar symptoms. Maiden * states that the "Nenta Lessertia disease of S. Africa is identical with a disease of the Pea-eating animals of Australia and i Miscell. Pub, Dept. Agrl. N. S. Wales, 477: 11. 38 MANUAL OF POISONOUS PLANTS with the Loco disease of the United States. Many forage plants of excellent repute such as white clover, alfalfa, lotus and other plants, may produce tympanites. Fig. 8. Common Horsetail (Equisetum arvense), the plant causing Equisetosis. 1. Fer- tile stems terminating in cones a. 2, Sterile stem. a. rhizome tubers. 3. Sporophyl with sporangia. 4. Sporangia opened to discharge spores. 5, 6, 7. Spores with spiral elaters. After Wossidlo. Symptoms: difficult breathing; the poison enters the circulation and stops the action of the lungs and heart when the animals stagger and die. POISONING FROM OTHER PLANTS 39 In the advanced stages the animals become frantic, hence the name "loco" or crazy. Horses and sheep are the most susceptible, although cattle are also affected. Of the various species of loco weed, the stemless loco Oxytropis Lamberti Pursh), and the woolly loco weed (Astragalus mollisismus Torr}, are the most injurious. These weeds grow luxuriantly on sandy ranges and appear early in the spring when other vegetation is scarce, and since they retain their fresh Fig. 9. Loco Weed (Astragalus mollissvmus) , U. S. Dept. Agrl. green color during the entire summer they prove especially attractive to stock. Recently the poisoning has been attributed by Dr. Crawford and others of the U. S. Dept. of Agrl., to mineral salts in the plant. The period of greatest danger is chiefly during the month of May. Symptoms. The symptoms, which are referable to the nervous system, are attributable to the narcotic effect of the plant. They appear slowly and are ap- parently divisible into two stages. The first stage is characterized by the follow- ing symptoms : Stupor, defective vision, unnatural movements and apparent hal- lucinations. When excited the animals become frenzied. The coat becomes shaggy, the teeth grow long and become loose, and a depraved appetite which is very marked, is developed. The animals prefer the loco weed to wholesome food, and will dig up the roots and eat them to satisfy their craving. In the second stage there is emaciation, exhaustion, feeble movements and finally death from starvation. The course of the disease is quite variable 40 MANUAL OF POISONOUS PLANTS and may last from a few months to one or two years. Sheep manifest symp- toms very similar to those above described. Treatment. When the disease has reached the advanced stage, treatment is of no avail as recovery does not occur. If, however, the afflicted animals are taken early in the course of the disease and placed on pasture where loco weeds do not exist, and are given good nourishing food, there is hope of re- covery. Prevention, which of course is the most desirable, is not always practicable. Animals do not as a rule become addicted to the loco habit when they have plenty of wholesome food and salt. There are no demonstrable lesions other than emaciation. (Stuhr). The recent investigations of Marsh and Crawford lay considerable stress on the presence of barium in the plants and the Bureau of Animal Industry, Washington, D. C., recommends the following treatment : for cattle, strychnin in doses of three-twentieths to four-twentieths of a grain daily, administered hypodermically ; for horses, Fowler's solution of arsenic in half-ounce doses daily in the drinking water or in the grain. This treatment should be continued for at least a month. To correct the constipation which is almost universal in locoed animals, magnesium sulphate (Epsom salt) may be administered as a drench in two-ounce doses. Epsom salt may also serve to some extent as an antidote to the poison produced by the weeds. Beneficial results have also been obtained by giving horses daily a drench containing two ounces of Epsom salt with ten drops of dilute sulphuric acid, and by giving cattle tri-weekly three or four ounces of Epsom salt with a proportional increase in the quantity of dilute sulphuric acid. As the foregoing treatments are in the experimental stage, the Bureau of Animal industry of Washington, D. C., would be glad to receive reports from their use. The value of keeping stock away from these poisonous plants is indicated in some investigations that have been carried on by the Bureau of Forestry and the Bureau of Plant Industry. In many cases the ranges are becoming practical- ly useless on account of these poisonous plants and if used the losses are so heavy as to materially reduce the profits of the business. In the Manta Forest Reserves in Utah for instance, it was found that the death of sheep was due to their browsing upon the chokecherry. Certain portions of the old trail were abandoned, and along other portions the chokecherry bushes were cut out. The method of handling the sheep was also changed. Instead of large bands which could be moved but slowly, smaller bands were trailed, and so far as possible they were allowed to fill up on healthy forage before entering the dangerous area. The trail was also improved wherever practicable and by this means it was possible to get the sheep through in much better shape and with little or no loss. The Department has also, in some instances, adopted the plan of flagging the area in which these injurious plants occur. This is a disease of sheep and horses especially, caused by Lupinosis. eating the seeds and straw of the lupine. Cattle and goats are also susceptible and the dog has been poisoned experimentally. There are many species of the lupine growing in various parts of the United States, although the yellow lupine (Lupinus luteus) is the most toxic. The nature of the toxic agent found in the lupines has not as yet been determined. Arnold and Schneidemuhl succeeded in isolating a chemical poison and POISONING FROM OTHER PLANTS 41 (D Fig. 10. lyupine (Lupinus leucophyllus) causes lupinosis U. S. Dept. Agrl, 42 MANUAL OF POISONOUS PLANTS gave to it the name lupinotoxin. They described its physical properties but failed to determine its chemical composition. Attempts to associate a fungus with the plant have failed. Lupinosis is characterized by jaundice, acute yellow atrophy of the liver, and parenchymatous inflammation of other in- ternal organs. Symptoms in Sheep. The disease appears in either the acute or chronic form, depending upon the amount of poison ingested. These two forms have been experimentally reproduced by giving carefully regulated amounts of lupinotoxin. In the acute form the disease appears suddenly. There is loss of appetite, fever, hurried and difficult breathing, rapid pulse, stupor, vertigo, and not in- frequently swelling of the lips, ears or face. The initial temperature may be as high as 104° to 106° Fahr., but is intermittent and gradually falls just before death. The pulse may reach 130 per minute and the respirations 100. A bloody froth may issue from the nostrils. Icterus which may be detected in the conjunctiva and the urine, usually appears on the second or third day. In certain cases this latter symptom fails to manifest itself and therefore is not constant. There is grinding of the teeth and sometimes trismus. The animal apparently prefers the recumbent position, extends the head on the ground and seems entirely oblivious to all surroundings. At first there is constipation, the faeces being hard and scanty and covered with yellow mucous. Later diarrhoea may set in and the excreta be tinged with blood giving them a dark brown color. Emaciation develops rapidly. In case of recovery the symptoms grad- ually abate and improvement takes place slowly. Cachexia.is a common sequel. In the chronic form the symptoms are not so violent. Jaundice may be en- tirely absent and emaciation and anemia may be the chief signs. Inflammatory tumefaction of the lips, eyelids, and ears with the formation of ulcers and scabs is described by various writers. Course. Death may supervene within twenty-four to forty-eight hours, although frequently the disease lasts four or five days. The immediate cause of death is rapid emaciation and extreme weakness. Horses contract the dis- ease from eating oats contaminated with the seeds or from eating the straw of the plant. The symptoms which they manifest are essentially the same as those above described. Horses seldom die from the effects of lupines. Lesions. The cadavers are emaciated and decompose rapidly. The muscles are of a grayish yellow color, the fibers having become fatty and having lost their striations. The subcutaneous tissue of the abdomen and the omentum and mesentery are yellowish. The most important lesion in both the acute and chronic forms is found in the liver. The alterations in this organ are those of acute hepatitis. The liver cells have become swollen and granular on ac- count of the parenchymatous change, or they may be more or less completely degenerated into fat. The gland is soft and friable and may be somewhat swollen. The interlobular connective tissue is greatly increased in amount due to inflammatory hyperplasia. In the course of a few days the liver under- goes acute yellow atrophy as a result of the absorption of the degenerated cells and the contraction of the hyperplastic stroma. In the chronic form the changes are those of chronic interstitial hepatitis. The icterus is of hepatic origin and due to catarrh of the bile ducts. The gall bladder is distended with bile and its lining membrane is congested and swollen. The kidneys and blad- der may show changes, more or less marked, due to inflammation. The blad- POISONING FROM OTHER PLANTS 43 der is, as a rule, empty. In the digestive tract we observe frequently yellowish discoloration of the mucosa, hemorrhages in the small intestine with catarrhal lesions of the entire canal. The heart is pale and friable and the blood which it contains is dark and thick. Capillary hemorrhages are quite generally ob- served throughout all of the tissues. Treatment. This is chiefly preventive since there is no specific antidote. Attempts should be made at once to prevent further absorption of poison by administering some acid as acetic or hydrochloric, well diluted with water. Alkalis should be strictly avoided as the poisonous principle is very soluble in alkaline solutions. It is advisable to evacuate the bowels by giving a purga- tive, preferably oil. Potassium permanganate is recommended by some as an antidote. Further than this the treatment is entirely symptomatic. (Stuhr). Fig. 11. A. Larkspur (Delphinium tricorne). B. D. Carolinianum. Larkspur poison- ing (Delphinosis) is caused by various species of Delphinium. A. U. S. Dept. Agrl. B. Ada Hayden. CHAPTER VII DEI-PHINOSIS, LATHYRISMUS (l,ATHYRISM) , ACONITISM, VERATRISM, UMBELLIFERAE, CONIUM, CICUTA. The purple larkspur (Delphinium Menziesii D C.), and Delphinosis. other species which are found in the northwestern part of this country and especially in Montana are plants very dangerous to stock. Drs. Chesnut and Wilcox have proven the toxicity of the above species by direct experiment and have called attention to the serious losses which they occasion annually. The latter experimenter has fatally poisoned a yearling lamb within two hours by administering, per os, the extract made from less than an ounce of the dried leaves. The weed appears early in spring, in advance of the forage plants and it is during this period that the greatest harm results. The poison is found both in the leaves and the roots although the latter are not frequently eaten on account of their woody fibrous nature. The poisonous principle has not been isolated. Cattle and sheep are most susceptible although horses frequently suffer. Symptoms. The first indication of poisoning is a general stiffness and a straggling gait, especially in the posterior limbs. Walking appears to be diffi- cult, and is evidently painful. At this stage the pulse and respiration are much depressed, and the temperature is lowered. The appetite is retained in most cases until the appearance of the final stage of the poisoning. This is man- ifested by irregular muscular twitching of all of the muscles which finally be- comes frequent and violent, and by incoordinate movement. There are attempts at vomiting and the animal froths at the mouth. Finally all of the muscles of the body contract spasmodically, the animal falls and dies in violent spasms. The pulse and respiration become very weak and rapid just before death. There is no aberration of the special senses. The course of the poisoning is quite rapid and death usually takes place within a few hours. Lesions. The direct cause of death from larkspur poisoning is probably failure of respiration due to paralysis of the centre and the alterations there- fore are those of asphyxia. The lungs are congested and dark-colored and the right heart, veins and capillaries are distended with dark colored blood. Other organs and tissues are normal with the exception of the general venous and capillary congestion. Treatment. Potassium permanganate is the chemical antidote and should be given as early as possible in doses of fifteen to twenty grains to horses, thirty to fifty grains to cattle, and five to ten grains to sheep, dissolved in a copious amount of water. To combat the extreme depression of the cir- culation and respiration, atropin sulphate has proven very efficacious. Even after the final convulsions have begun this drug has been of good service. It should be hypodermically administered in doses of three-fourths to one grain to the larger animals and one-twentieth to one-fifteenth of a grain to sheep. In the late stages sheep should be given as much as one-sixth to one- DELPHINOSIS LATHYRISMUS 45 fourth of a grain. In the convulsive stage when there is impending failure of respiration, inhalations of ammonia may be resorted to with good results. A feature of the treatment quite as important as the medication is the care of the animals. Complete rest and freedom from excitement are very essential since exercise or fright is likely to induce fatal spasms. Finally the danger from poisoning can be largely obviated by preventing access to the young plant in the early spring. In ancient times, this disease was quite common, affecting Lathyrisrnus. both man and the horse. It is very frequent today in Spain, Italy, Russia, and India. Etiology, It is caused by eating bread made of flour derived from some species of Lathyrus or Vetch (L. Cicera, L. Clymenum, or L. sativus), or, in case of horses, by the consumption of Fodder Pea. The seeds of these species contain a toxic substance formed without the action of bacteria. Man, the horse and the pig are subject to this disease. Symptoms. In domestic animals, the symptoms are debility of the rear and lower extremities, producing motor paralysis. In lower animals, the normal functions of the larynx become impaired because of paralysis. Treatment. Change of fodder, providing good food, application of massage and electric treatment. Fig. 12. Aconite {Aconitum uncina- tum). Aconitism is caused by this and other species of Aconitum. Charlotte M. King. Fig. 13. Green Hellebore (.Veratrum viride). Common Eastward. (U. S. Dept. Agrl.). 46 MANUAL OF POISONOUS PLANTS Prognosis. Fatal cases are not frequent. Post-mortem. The ganglion cells of the anterior horns are atrophied; also the recurrent nerves and the muscles of the larynx. (Adapted from Friedberger and Frohner). Various species of aconite (Aconitum) are known to be Aconitism. poisonous. One species, the A.conitum Napellus, has long been used in medicine. The most common species in North America is the Columbia Aconite (A. coluinbianum), which is found in the Rocky Mountains and on the Pacific coast. Several other species occur in North America, one extending into northeastern Iowa; the European Aconite (A. Napellus*) is frequently cultivated in gardens. Cases of poisoning are largely due to the administration of over doses in medicine. In the Rocky Mountains accidental poisoning among live stock is confined to animals that graze at higher altitudes. All parts of the plant are poisonous; one tenth of a grain of the drug is a poisonous dose for some animals. The smallest fatal dose recorded in man is a teaspoonful of the tincture of aconite, which is equivalent to about XXX gr. of the crude drug. The minimum lethal quantity is 1-16 of a gr. for man. Symptoms. The effects of the poisoning are a tingling sensation on the end of the tongue, which shortly gives rise to a burning sensation followed by pronounced constriction in the throat. It reduces the pulse and frequency of the cardiac pulsations. The action of the heart is lessened and the pulse is weak, irregular and intermittent, at first slow and then rapid; tingling and prickling over the entire body is characteristic; vision is confused, there are abdominal pains, vomiting and diarrhoea. Death is caused by the stoppage of respiration, but is preceded by numerous twitchings; in the case of the horse the animal falls and is unable to rise. The symptoms are different in cats and rabbits. Treatment. No specific antidote is known, but physicians use atropin or digitalis and nitrite of amyl. The stomach should, however, be evacuated at once; cardiac and respirative stimulants are given subcutaneously. The Hellebores belonging to the genus Veratrum are common Veratrism. in the mountain regions of the west and one species is abundant in the east. They are found in swampy places, in wet meadows and along brooks. The most frequent cases of poisoning come through the administration of the drug; although in the Rocky Mountains considerable quantities of the plant are consumed by sheep where grazing is close. All parts of the plant are poisonous although the root is more poisonous than the seeds and leaves which contain several alkaloids. Symptoms. Veratrin is a powerful irritant and when inhaled in minute quantities produces sneezing. When injected under the skin it causes restless- ness, when consumed in large quantities it produces salivation, frequent vomit- ing with purging pain, and collapse, the temperature falls. Veratrin is a drug poisonous to the motor and sensory nerves. Death is caused by paralysis of the heart; 1/16 of a grain has produced alarming symptoms in man and 1 gr. injected subcutaneously produces poisonous symptoms in a horse. Treatment. The stomach should be emptied immediately, then give stim- ulants, such as brandy and strong coffee. DELPHINOSIS LATHYRISMUS 47 Fig. 14. Larkspur (Delphinium glaucitm) causes Delphinosis (U. S. Dept. Agrl.). 48 MANUAL OF POISONOUS PLANTS Fig. 15. Cowbane (Cicuta occidentalism, a deadly poisonous plant. (U- S. Dept. Agrl.). DELPHINOSIS LATHYRISMUS 49 The Cowbane (Cicuta maculata} and related species be- Poisoning from long to the Carrot family. The Cowbane is common in low Umbelliferae. grounds in the Northern States and in the Rocky Mountains; another species (C. vagans) occurs on the Pacific Coast; and a third species (C. bulbifera) is a common bog plant in the Northern States. The Cowbane is frequently mis-called Wild Parsnip. The latter, however, has a conical root and is the feral form of our cultivated species, and, although it may be somewhat injurious, as indicated elsewhere, is not poisonous like the Cowbane (Cicuta maculata). Cowbane is a smooth, marsh perennial plant from 2-5 feet high, with fleshy, fascicled roots and a pungent odor; leaves are pinnately compound with coarsely-serrate leaflets ; flowers are white and small ; fruit broadly ovate to oval and small. The European species has long been recognized as poisonous. Many cases of poisoning of man and lower animals by this plant are on record. Cases of poisoning of children by Cowbane are not of infrequent occur- rence, several being reported each year in the daily press. The following item appeared in the Des Moines Register and Leader of May 23, 1909, and is but one of many that have come under the observation of the writer during the last twenty years. Boone, May 22. — "Virgil Hyatt, a high school boy, was poisoned last night while walking to the Ledges, a summer resort near Boone. He fell to the ground unconscious, and a companion carried him to a nearby farm house, and summoned medical aid and his mother from Boone. The trip was made in an automobile at record breaking speed. The boy was brought to a hospital here (Boone) but died just as he was being carried into the institution." It seems that the young man, while walking across a plowed field with a companion picked up some of the weed whose roots had been exposed and ate freely of them. In an hour he complained of illness, and fell into the creek from which his companion rescued him. However, as reported above, all at- tempts to save his life were unavailing and he died from convulsions in a few hours. As a sequel to the above, the daily papers of June 3, of the same year report a second death in the same locality from the same cause. In this case a young man who was sent to secure some of the weed for examination, be- came poisoned in some way, possibly by the juice of the plant coming in con- tact with some abrasion of the skin. The lad died after a short illness, having shown symptoms similar to those of the previous case. Symptoms. The first symptoms are pain in the bowels, urging to ineffectual attempts to evacuation, burning in the stomach, nausea, vomiting, tetanic con- vulsions which may be severe resembling those produced by strychnin, or there may be coma without convulsions. Dr. Hazeltine says that, in one case, he found the patient "showing con- vulsive agitations consisting of tremors, violent contractions and distortions with imperfect relaxations of the whole muscular system, astonishing mobility of the eyeballs and eyelids, with wide dilated pupils, frothing at the mouth and nose mixed with blood, and, occasionally, genuine, violent epilepsy." The convulsive agitations were so violent that the pulse could not be ex- amined with sufficient accuracy to determine its character. There is a profuse sweat. In fatal cases, the respiration is stertorious, the pulse small, and the face cyanotic. Not many cases among animals have been recorded. In a case 50 MANUAL OF POISONOUS PLANTS reported to the writer by an Iowa farmer, a cow which had eaten freely of the roots, fell into a spasm when brought into the barnyard. The animal, how- ever, rose, walked one hundred feet and fell again, got up again, walked about thirty rods, fell and died in about thirty minutes. In a second case, a yearling owned by the same man had been in good healthy condition but began to dis- play the same symptoms and died in twenty minutes. Dr. E. S. McCord, on September 31, of the same year, gave an old horse six drachms, hypodermically, of a strong decoction of the root. In fifteen minutes the animal showed uneasiness; pulse was full and fast; in a short time the animal laid down, and the pulse decreased; the horse was in great pain and kept moving the extremities ; the pulse was weak but the patient finally recovered. The botanist of the Oregon Experiment Station found that the root has less of the toxic substance in the summer than in the winter and spring, which may account for the failure in this last case to produce death. In frogs, frequency of breathing is increased, tetanic convulsions follow, grad- ually paresis of the extremities, and lastly full paralysis and death. Cicutoxin, Fig. 16a. Poison Hemlock (Conium mac- ulatum), native to Europe; naturalized in the U. S. (U. S. Dept. Agrl.). the characteristic poison of Cicuta, acts especially upon the medulla oblongata; the brain and spinal cord are merely secondary seats of its action. Treatment. The stomach should be effectually evacuated by the use of the stomach pump or by a strong emetic. External and internal stimulants such as whisky should be applied; anaesthetics and narcotics used to control the spasms; hypodermic injection of morphin aids in recovery. It usually hap- DELPHINOSIS LATHYRISMUS 51 pens, however, that the veterinarian or physician is called too late to ac- complish much. The Poison Hemlock (Conium maculatum) is indigenous to The Poison Europe and has long been known as a poisonous plant. It is Hemlock. a fetid smelling herb from 2-5 feet high, with a spotted stem, compound leaves, and small, white flowers in umbels. The plant is not uncommon in waste places in the East and in the Rocky Mountains, especially in Utah. It has long been used as a poison. Symptoms. In lower animals, there is observed a dilatation of the pupil, followed by weakness of the limbs, passing into paralysis; labored respiration, frequency of breathing diminished, heart action irregular; death preceded by convulsions. In man, there are weakness in the lower extremities, staggering gait, in two hours paralysis of upper and lower extremities and slight con- vulsions; death occurs in a few hours usually caused by cessation of respiration. Treatment. The stomach should be evacuated by means of a pump or tube; or a hypodermic injection of 4-5 drops of a solution of apomorphin given; or emetics of sulphate of zinc or mustard administered. The tempera- ture of the body should be kept up by hot applications. Stimulants may be given, and, if necessary, artificial respiration applied. As a drink, strong tea, tannin, or any harmless vegetable decoction containing tannin may be administered. CHAPTER VIII FISH AND ARROW POISONS, HYDROCYANIC POISONING — TOXALBUMINS — BLACK LOCUST, CASTOR OH,, AND JEQUIRITY. Fish and arrow poisons have played an important part Fish and Ar- with the aborigines of all countries and they are still used row Poisons, to a considerable extent by primitive people. Thus Merrill * mentions the use of the Antiaria toxicaria in the Philippines and other plants used in the same way which are being worked up by Dr. R. F. Bacon. Radlkofer2 some years ago published a long list of plants which are used to poison fish, and added a history of the earlier literature. He lists some 154 species which have been used in various parts of the world for this purpose and these plants belong to the following orders and genera. The species are listed under the poisonous species in another part of this work. Dilleniaceae (Tetracera), Menispermaceae (Anamirta, Abuta, Pachygone) ; Cruciferae (Lepidium), Capparideae (Cleome), Bixaceae (Pangium, Hydno- carpus), Ternstroemiaceae (Caryocar), Tiliaceae (Grewia), Meliaceae {Wai- sura) ; Chailletiaceae (Chailletia Tapura) ; Rhamneae (Gouania) ; Sapindaceae (Serjania, Paullinia, Sapindus, Dodonaea, Harpullia, Magonia) ; Hippocastaneae (Pavia) ; Leguminosae (Tephrosia, Milletia, Orobus, Abrus, Centrosema, Cli- toria, Camptosema, Phaseolus, Lonchocarpus, Derris, Piscidia, Bowdichia, Cas- sia, Bauhinia, Leucaena, Albizzia) ; Myrtaceae (Barring tonia, Gustavia) ; Com- positae (Clibadiuin, Ichthyothere) ; Campanulaceae (Tupa) ; Ericaceae (Rhodo- dendron) ; Primulaceae (Cyclamen) ; Myrsineae (Aegiceras, Jacquinia) ; Sapotaceae (Bassia) ; Ebenaceae (Diospyros) ; Apocyneae (Melodinus, Thevetia, Ccrbera, Aspidosperma) ; Loganiaceae (Buddleia, Strychnos) ; Solanaceae (Hy- oscyamus, Nicotiana) ; Scrophularineae (Verbascum, Digitalis); Bignoniaceae (Bignonia, Tecoma, Jacaranda) ; Labiatae (Ercmostachys) ; Chenopodiaceae (Cheno podium) ; Polygoneae (Polygonum) ; Aristolochiaceae (Aristolochia) ; Piperaceae (Piper) ; Thymelaeaceae (Daphne, Wilkstroemia) ; Buphorbiaceae (Euphorbia, Phyllanthus, Securinega, Piranhca, C rot on, Joannesia, Manihot, Jatropha, Hxcoecaria, Hura) ; Coniferae (Taxus) ; Liliaceae (Veratrum). Ernst 3 lists only sixty species that are used as fish poison. There must, however, be considerably more as indicated by Radlkofer. W. M. I. Brost Pauwels 4 in his contribution on the Surinamic fish poison- ing 5 contributes an interesting article on the subject. Pauwels who made an investigation of Nekoe (Lonchocarpus viola- ceus) states that it is a powerfully toxic substance. He found that Nekoeid will poison fish in proportion of 1,5,000,000, and that a second substance B. 1 Philip. Journ. of Sci. 2:111, Sect. C. 2 Sitz. Math-Phys. Classe k. b. Akad. d. Wiss. Munchen., 1886, 379. 3 Memorio Bot. el £mbarbascar o sea la Pesca por media de Plantis venenosas, 4 Bijdrage tot de Kermis der Surinaamsche Vischvergiften. M. Greshoff has likewise published a number of works on fish poisoning plants. 5 Hart and Swatters found in the Piscidia Brythrina piscidin CisHjaCU, and Greshoff found in Pachyrhizus angulatus, pachyrhizid CasHigOg (OCH3)2. FISH AND ARROW POISONS 53 Nekoeid will poison fish in proportion of 1-10,000,000. The poison will take ef- fect in one hour. The water poisoned with the substance will cause the fish to make an effort to get away from the poison, they are in a horizontal position, breathe heavily, come to the surface of the water and try to jump out and finally breathing becomes, increasingly difficult and at last they turn on their backs and die. Under poisoning from cherry, sorghum and a few other Hydrocyanic plants, an account has been given of poisoning from hydro- Poisoning, cyanic acid. It may be convenient to bring together some of the plants from which the very poisonous substance, prussic acid, has been obtained. Maurits Greshoff of the Colonial Museum in Holland has taken the pains in a paper on Cyanogenesis to give the distribution of Prussic acid in the vege- table kingdom, the Hydrocyanic acid being found in a great many different plants. The following list gives the orders in which this substance occurs. Ranunculaceae (Aquilegia vulgaris, Thaliclrum aquilegi folium). Berberi- daceae (Nandina domestica). Cruciferae (Lepidium sativum), Bixaceae (Gyno- cardia odorata, Hydnocarpus venenata, Kiggelaria africana, Pangium edule, Ryparosa caesia, Taraktogenos Blumei, Trichadenia zeylanica) ; Sterculiaceae (Sterculia) ; Tiliaceae (Hchinocarpus) ; Linaceae (Linum usitatissimutn) ; Rutaceae (Citrus medico) ; Dichopetalaceae (Chailletia cymosa) ; Olacaceae (Ximenia americana) ; Celastraceae (Kurrimia zeylanica) ; Rhamnaceae (Rham- nus Frangula) ; Sapindaceae (Cupania, Schleichera trijuga) ; Anacardiaceae (Coryno carpus laevigata) ; Leguminosae-Papilionaceae (Lotus arabiscus, In- digofera galegoides, Phaseolus lunatus, Vicia saliva, Dolichos Lablab) ; Rosaceae (Amelanchier vulgaris, Chamaemeles, Coloneasler inlegerrima, Cratae- gus Oxyacantha, Eriobotyra japonica, Nuttallia cerasiformis, Osteomeles, Pho- tinia, Pyrus, Prunus Amygdalus, Pygeum africanum, Spiraea Aruncus) ; Saxi- fragaceae (Ribes aurcum) : Combretaceae (?Combretum constrictum) ; Myrt- aceae (?Psidium monlanum) ; Melastomaceae (Memecylon) ; Samydaceae (Homalium) ; Passifloraceae (Passiflora quadrangularis, Tacsonia) ; Caprifoli- aceae (Sambucus nigra) ; Rubiaceae (Pleclronia dicocca) ; Compositae (Char- dinia xeranlhemoides, Xcranthemum annuum) ; Sapotaceae (Isonandra, Lucuma bonplandia, Payena latifolia) ; Asclepiadaceae (Gymnema latifolium) ; Convol- culaceae (Ipomoea dissecla) ; Bignoniaceae (Osmohydrophora noclurna) ; Euphorbiaceae (Bridelia ovala, Elateriospermum Tapos, Hevea brasiliensis, Ja- tropha auguslidens, Manihot ulilissima, Ricinus communis) ; Urticaceae (Sponia virgata) ; Araceae (Arum maculalum, Colocasia giganlea, Cyrlospcrma lasioides, Lasia aculeala) ; Gramineae ( Glyceria aquatica, Panicum, Sorghum vulgare, Slipa hystricina) ; Fungi (Hygrophorus agathosmus, Marasmius oreades, Phaliota radicosa, Russula foelens). He makes the following statement with regard to the presence of this substance in plants : "Many plant physiologists in Europe, with more experience with Prunus or amygdalin than with the tropical Pangium, incline to the view that hydrocyanic acid in these plants has nothing to do with either the building-up or the break- ing-down of proteids, but that this substance is made by the plant from sugar and nitrate by a special process, and serves no other purpose than to defend the plants against the attacks of animals. It is above all the incompleteness of our physiological knowledge which makes decision between these theories difficult. 54 MANUAL OF POISONOUS PLANTS "In the study of this question it is important to remember the possible diversity of origin of this body, and every cyanogenetic plant will be required to be examined on the lines laid down by Treub." The wide distribution of glucosides that yield hydrocyanic acid is evident from the list above. Dunstan and Henry * discovered three glucosides, dhurrin C17H1TO7N in the common sorghum, lotusin C.,8H31O16N in a species of lotus of Egypt and phaseo-lunatin C10H17O6N in wild beans of Phaseolus lunatus, the common lima bean. Brunnich 2 attributed death from the feeding of immature sorghum to dhurrin. Power and Lees 3 isolated from the seeds of Gynocardata odorata a glucoside to which they gave the name gynocardin C13HlgO9N. All of the above glucosides yield on hydrolysis, hydrocyanic acid. The most important and best known of all the glucosides that yield hydro- cyanic acid is amygdalin. Greshoff discovered an amygdalin-like glucoside in two tropical trees, Pygeum paruiflorum and P. latifolium. The same author found glucosides. in a member of the milkweed family Asclepidaceae. The Pang mm edule of the tropics contains a large quantity of a glucoside capable of being converted into hydrocyanic acid and a large amount can be prepared from a single plant. ,The Hydnocarpus inebrians also contains a large quantity of a glucoside which yields hydrocyanic acid. It is used to destroy fish. The common linseed cake contains a glucoside which yields prussic acid. Francis found prussic acid in the sweet cassava root, .0168 per cent, and in the bitter cassava .0275 per cent. It is well known that fresh bitter cassava root is bitter poison. The above facts are brought together by Blyth in his work on poisons and may be con- sulted for more of the details. The statistics on poisoning seem to indicate that it occupies third place among poisons in the order of frequency in Great Britain. In that country there are about forty deaths annually from this poison according to Blyth. It is responsible for the loss of a great many cattle in sections of the country where the wild cherries are abundant and also from sorghum poisoning. It is frequently used for criminal poisoning, at one time more frequently than now. It is nearly always taken by the mouth into the stomach, but occasionally the vapors produce death. It is generally used by Entomologists to kill insects. Blyth gives the symptoms of poisoning as follows : Cold blooded animals require a larger relative dose than warm blooded animals except the birds which are slightly less sensitive but the action is essentially the same. Hydro- cyanic acid acts in two ways : 1. It profoundly interferes in the ordinary metabolic changes in animals. 2. It causes a paralysis of the nerve centers. Normal blood decomposes with great ease hydrogen peroxide into oxygen and water. If it is normal venus blood and a little hydrogen is added it becomes bright red, but if a trace of prussic acid be present it is a dark brown color. The blood corpuscles lose their power of conveying oxygen to all parts of the system and asphyxia results. The main symptoms in animals are as fol- lows : The main differences between the symptoms induced in cold-blooded and warm-blooded animals, by a fatal dose of hydric cyanide, are as follows: The respiration in frogs is at first somewhat dyspnoeic, then much slowed, and at length it ceases. The heart, at first slowed, later contracts irregularly, and at length gradually 1 Proc. Roy. Soc. Ixviii and Ixxii (See Blyth "Poisons" p. 204). 2 Ib., Ixxxiii. (See Blyth "Poisons" p. 204). Sjourn. Cham. Soc. Ixxxix. (See Blyth "Poisons" p. 204). FISH AND ARROW POISONS 55 stops; but it may continue to beat for several minutes after the respiration has ceased. But all these progressive symptoms are without convulsion. Among warm-blooded animals, on the contrary, convulsions are constant, and the sequence of the symptoms dyspnoea, slowing of the pulse, giddiness, falling down, then convulsions with expulsion of the urine and faeces. When the dose is short of a fatal one, the symptoms are as follows: Evident giddiness and distress; the tongue is protruded, the breath is taken in short, hurried gasps, there is salivation, and convulsions rapidly set in, preceded, it may be, by a cry. The convulsions pass into paralysis and insensibility. After remaining in ths state some time, the animal again wakes up, as it were, very often howls, and is again convulsed; finally, it sinks into a deep sleep, and wakes up well. Dr. K- Winslow in his work on Veterinary Materia Medica and Thera- peutics, gives the Toxicology of Hydrocyanic Acid as follows : "Three stages may be distinguished in fatal poisoning. First : a very short period elapses before the symptoms appear. There are giddiness, difficult breathing, and slow pulse in this stage. Second : the pupils dilate, vomiting may occur, and the animal utters loud cries. Spasmodic defacation, micturition and erections may be present, with con- vulsions and unconsciousness. Third : the last stage is characterized by col- lapse, spasms, general paralysis and death. The subacute form of poisoning may ensue and prove fatal, or, owing to the volatile character of the drug,, complete recovery may take place within one-half or three-quarters of an hour. Occasionally dogs continue to be paralyzed for several days and get well. The minimum fatal dose recorded in man is 9/10 of a grain of pure acid, or about 50 drops of the medicinal solution. Four to five drachms of the diluted acid frequently, but not invariably, causes subacute poisoning and death, in horses, within an hour. One or two drachms of the pharmacopoeial prepara- tion usually kills dogs within ten minutes." Poisoning from Toxalbumins, Black Locust, Ricinus and Abrus. In recent years much work has been done with a class of poisons, known as toxalbumins. These are of especial interest because many of the bacteria pro- duce such poisons. Some of the fungi responsible for "forage poisoning" pro- duce, it is thought, toxalbumins. In recent years a number of cases of horse poisoning from Black Locust bark have been reported. The poisoning from castor oil bean (Ricinus') and from Abrus are also of this class. Castor Oil Seed and Abrus. One of the best known of the toxalbumins is that occurring in the castor oil seed, known as ricin. This albuminous sub- stance is very poisonous, more so than strychnin and prussic acid. Ricin coagulates the blood. Blyth in his work on poisons states : If castor-oil seeds are eaten, a portion of the poison is destroyed by the digestive processes; a part is not thus destroyed, but is absorbed, and produces in the blood-vessels its coagulating property. Where this takes place, ulcers naturally form, because isolated small areas are de- prived of their blood supply. These areas thus becoming dead, may be digested by the gastric or intestinal fluids, and thus, weeks after, death may be produced. The symptoms noted are nausea, vomiting, colic, diarrhoea, tenesmus, thirst, hot skin, frequent pulse, sweats, headache, jaundice, and death in convulsions or from exhaustion. Animals may be made immune by feeding them carefully with small doses, gradually increased. The post-mortem appearances are ulceration in the stomach and intestines. In animals the appearances of haemorrhagic gastro-enteritis with diffuse nephritis, haemorrhages in the mesen- tery, and so forth have been found. A toxalbumin also occurs in the Jequirity seed (Abrus precatorius) which causes similar effects and symptoms. That the poisons are not the same have been shown by experiments with animals. It is known that animals may become immune by repeated doses of Jequirity against abrin and the principle of castor oil does not produce immunity against abrin, nor does abrin confer immunity against the ricin of the castor oil bean. The abrin when applied to the con- 56 MANUAL OF POISONOUS PLANTS junctiva causes coagulation in the vessels and a secondary inflamation. The disease is known as Jequirity opthalmia. More details in regard to the poisons of these plants are given under the plants of the families in which they occur. Black Locust Poisoning, The Black Locust which is commonly planted as an ornamental tree has in a number of instances caused death. Dr. Waldron in the American Veterinary Rewiew, writes thus of locust bark poisoning, referring' es- pecially to the beating of the heart of a horse that had been poisoned by the locust bark. This beating shook the horse and could be heard outside the stable. The sound was caused by the action of the diaphragm. It was greater when the ribs were at their fullest expansion and could be heard most distinctly at a distance of ten feet. I tried to locate or rather find out what pro- duced the sound, but in that I am as ignorant as I was then. ... In questioning where the team was hitched at the mill, it was found that the driver had tied them to a young lo- cust tree that had been cut down a few years before. This was a sapling of about four inches in diameter and had probably made a very rapid growth and the bark, from this reason was tender and easily peeled They had done a good job of peeling, but as they had their bits in they were not able to swallow much. The poison obtained from this bark is, in my opinion, the cause of the trouble. Dr. Waldron says that the symptoms otherwise are about the same as those occurring in cases of belladonna poisoning and are about as follows : Extreme lassitude, which includes almost imperceptible pulse and which, when found, is weak and prolonged; respiration less than normal by one-third and sonorous; temperature normal; no pain, no appetite, mucous membrane congested, of a blue, rusty, or yellow color. Mucous membrane of the mouth some swollen, caused by the congestion of the capillaries; slight ptyalism, and above all, the dilation of the pupil of the eye; in fact I should judge, we have nearly the same symptoms we get in belladonna poison. He also says that he had not known before that locust bark was poisonous and although he had searched for literature upon the subject had found but one reference, that being in the U. S. Pharmacopoeia ,which records a case re- ported in Jan., 1887, when 33 children were said to have been poisoned by chew- ing locust bark. In mild cases there were "flushed faces, dryness of the throat and mouth, and dilation of the pupils. In severe cases, were added epigastric pain, extremely intermittent heartbeats, and stupor." It is evident from the fact that there is not much literature on the subject that such poisoning does not occur often. Dr. H. S. Murphy has kindly contributed the following case on locust bark Fig. 16b. Castor oil plant (Ricinus corn- munis'). The seeds furnish the castor oil of commerce, and also contain an acrid poison. (Chestnut, U. S. Dept. Agr.). poisoning: Anamusis: Gray mare twelve years old, pregnant ten months, has been at light work FISH AND ARROW POISONS 57 continuously, is driven to town afternoon of March 31, and tied to a locust tree which is 6-8 inches in diameter; owner noticed that animal had peeled bark from tree also noticed animal pant on road home. Anorexia and stupidity were all owner noticed until 8 p. m. when a faint noise was heard this gradually grew worse until I arrived at 7 a. m. April 1. Symptoms: 1. Animal stands back from manger with legs well apart resting nose and mouth on floor, most of the time, a part of the time head is held 18-24 inches from floor. 2. A continual "thud" is heard which is not synchronous with respiration but is synchronous with a vibration of thorax. 3. Animal will not obey commands and when pushed over in stall loses balance and nearly falls. 4. Fetus is seen kicking in mare's left hypo-chondriac region. 5. Temperature 99.C Farh. 6. Pulse 54 full, bounding. 7. Respiration, 14, very feeble. Fig. 16c. Black Locust (Robinia Pseud-acacia) Bark, leaves and flowers poisonous. (After Faguet). 8. Mucous membranes dry, very yellow a dirty yellow (in distinction from bright yel- low of icterus) swollen, only moderately sensitive (probably due to general depression). 9. Intense dilation of pupil. 10. No evacuation of feces; auscultation reveals paresis of bowels; ropy urine is passed. 11. Internal cause of thud was determined as due to heart beat in the following manner: 1. Pulse over maxillary artery is synchronous with "thud" and thoracic vibration. 2. Owner counts aloud while auscultation of heart is conducted and heart beat is synchronous •with thud. 3. Ausculation of heart and radial pulse are synchronous, also heart sounds are muffled but very loud. (Palpitation). Treatment: (Symptomatic) J^ gr. of Digitalin (P. D.) every fifteen minutes subcutan- 58 MANUAL OF POISONOUS PLANTS eously until four doses are given, also £ I potassi iodidum is given per orem at once and the following prescription left. Ex Strychnini sulphatis gr. IV. Fid. ext. digitalis £1. Potassi iodidum II. Aqua £XVI. Sig. : A table spoon full every 2 hours. Result: After the second hypodermic was given a slight improvement noticed (lessening in force and frequency of thud, which was quite marked after fourth hypodermic. Owner reports thud gone at end of 24 hours but stupidity still present though not so marked. Recovery uneventful and at end of gestation parturition proceeds normally, and foal lives. Toxicity of bark proven in the following manner: Two cc of 10% tincture (bark grated) killed half grown kittens which showed above symptoms in an aggravated form. One ounce necessary to kill a 25 pound dog. This tincture dropped in eye acted much as atropin but no toxic symptoms developed. Simply a dilation of pupil. Grated root in lard produced slight symptoms in two dogs. P. m. on cats revealed a generalized dirty m. m. but only a very slight yellow on cartilages. Swollen liver and a few petechia on serous membranes. Blood quite dark. The cadaver, resembled somewhat that of one dead of septicaemia. CHAPTER IX POISONING FROM OPIUM, SOLANACEAE AND PLANTS THAT CONTAIN SAPONiNS. The use of opium by Chinese and other races is as Fliickiger and Han- bury say, "in the words of Pereira, the most important and valuable used in medicine of the whole Materia Medica; and we may add, the source by its judicious employment of more happiness by mankind." Blyth in his work on Poisons, states that in England and Wales 1505 deaths were attributed to the use of opium or its active constituents between the years 1898-1903. Of these 882 were accidental or because of negligence, 621 were suicidal. In France opium and morphin poisons are said to cause about 1 per cent of the cases of poisoning. Various patent medicines contain opium or some of its products and in the past have been the cause of frequent cases of poisoning. The use of the drug in patent medicines for children in the United States in the form of soothing syrups was once more common than now. The use of opium for infants is a common practice in India, according to Blyth who quotes from Dr. Chevers.1 In general the opium and morphin poisoning are as follows : The beats of the heart are at first accelerated and then diminished. Large doses introduced into the circulation diminish the pulsations without acceleration and may even cause heart paralysis. "The arterial blood pressure, at first increased is after- wards diminished. If morphin is in sufficient quantity thrown into the circula- tion, then tetanus at once occurs. Depression and stimulation depend on dosage. The common form occurring in 99 per cent of the cases; excitement, narcosis, and coma, bowels nearly always constipated. (2) A very sudden form in which death occurs rapidly, the person sinks into a deep sleep almost immediately. (2) An abnormal form in which there is no coma but convulsions. Blyth in referring to opium eating says : The consumption of opium is a very ancient practice among Eastern nations, and the picture, drawn by novelist and traveler, of poor, dried-up, yellow mortals addicted to this vice, with their faculties torpid, their skin hanging in wrinkles on their wasted bodies, the conjunctivae tinged with bile, the bowels so inactive that there is scarcely an excretion in the course of a week, the mental faculties verging on idiocy and imbecility, is only true of a percentage of those who are addicted to the habit. In the case of opium poisoning the stomach tube should be used to empty the stomach, and wash with warm water, then coffee may be given. Per- manganate of potash is a perfect antidote and should be given when at hand. The alkaloid codein also found in opium produces sleep but its effects are different. Large enough doses produce death and cause epilepti-form convul- sions. Thebain found in opium produces symptoms that resemble those pro- duced by strychnin, namely tetanic spasms. Apomorphin found in opium is an active emetic. Papaverin causes paralysis of respiration in guinea pigs. 1 Jurisprudence 232 (3rd ed.). 60 MANUAL OF POISONOUS PLANTS Fig. 16d. Garden Poppy (Papaver somniferum). A poisonous plant produc- ing a large number of alkaloids like morphin, codein, etc., (Strasburger, Noll, Schenck and Schimper). Poisoning from Solanaceae. A number of plants of the Solanaceae are known to be poisonous; among them the common thorn-apple or Jimson weed (Datura Stramonium), the atropa (Atropa Belladonna) and hyoscyamin (Hyoscyamus niger) besides such suspected plants as the common black nightshade (Solanum nigrum), horse nettle (Solan- urn carolinense) , bittersweet (Solatium dulcamara) and scopiola. The cases of poisoning from atropin are more frequent, perhaps, than statistics seem to in- dicate. The English death statistics for ten years, ending 1903, according to Blyth show 95 per cent of the deaths from atropin; 35 per cent were suicidal. Most of the accidental cases arise from mistakes made by the pharmacist or physician. Criminal poisoning is carried on to a less extent in Europe and America than in India. Blyth states that of the 120 cases recorded in works on Indian toxicology no less than 63 per cent were criminals, 19 per cent suicidal, and 18 per cent accidental. The most important alkaloids found are atropin, hyoscyamin, scopalamin and solanin. Solanin is poisonous and is regarded as a nitrogenised glucoside. In man the symptoms of atropin poisoning are: Dilating of the pupils, dryness of the mouth and throat; the POISONING FROM OPIUM 61 mucous membrane is reddened, inability to swallow, deranged vision, breath at first a little slow and then rapid; the nervous system is affected in a marked degree; the lower extremities are often partly paralyzed. There is want of coordination. "The person reels like a drunken man." In adults this takes on a hilarious pleasing form. The symptoms of poisoning from hyoscyamin are similar to those of atropin. The absence of delirium and excitement, however, makes it decidedly different. The symptoms in animals for both of these sub- stances do not differ essentially from those given above 1C3 Fig. 16e. Nightshade (Solatium nigrum) From Darlington's Weeds and Useful Plants. Fig. 16f. Jimson Weed (Datura Stramo- nium), a, leaf and flowers; b, fruiting capsule. (U. S. Dept. Agrl.). Atropin may be absorbed by the skin, and enough may be absorbed, if it is broken, to cause death. Blyth quotes Ploss * to the effect that atropin sulfate applied as an ointment to the abraded skin was fatal. Atropin has also been absorbed from the bowel as recorded by Blyth: A clyster containing the active principles of 5.2 grms. (80 grains) of belladonna root was administered to a woman 27 years of age, and caused death. Allowing the root to have been carefully dried, and to contain .21 per cent of alkaloid, it would seem that so little as 10.9 mgrms. (.16 grains) may even prove fatal, if left in contact with the intestinal mucous membrane. Belladonna berries and stramonium leaves and seeds are eaten occasionally by children. A remarkable series of poisoning by belladonna berries occurred in London during the autumn of 1846. l Zeitschr f. Chir. 1863. Blyth, Poisons; Their Effects and Detection. 62 MANUAL OF POISONOUS PLANTS Poisoning from Plants that contain Saponin. In recent years our knowledge of the Saponins has been greatly extended; many of these studies have been made by Kobert or his students in the lab- oratory at Dorpat. The term saponin has been applied to a class of substances of a glucosidal nature which are poisonous and when dissolved in water form a solution which froths much like soap-suds. These substances are not all the same chemically, but have the general formula CnH2nO10. Blyth gives the fol- lowing list with their formulae : Saponin 1. Saponin senegin \ Quillaja sapotoxin r Sapindus sapotoxin ( C17H96O10. Gypsophila sapotoxin I Agrostemma sapotoxin/ Saponin 2. Asamin ) Digitonin saporubrin ) is 2* 10* Saponin 3. Quillagic acid Polygalic acid Herniaria saponin Cyclamin Sarsaparilla saponin Sarsa saponin C22H36O10 Parillin C06H uPio Melanthin C~>oHr,o°io The suggestion is made that possibly dulcamarin C00H01Olftl and syringin — — *~> 1 1 U C17H50O10 may belong to the same series. One of the oldest of the known saponins was isolated from the Bouncing Betty, Saponaria officinalis, and later from the corn cockle Agrostemma Githago and many other plants. This saponin is a white amorphous powder, very soluble in water, is neutral and reacts without odor ; it causes sneezing when applied to the mucous membrane of the nose ; tastes at first sweetish, then becomes sharp and acrid. The saponin when rubbed on the skin exerts no action be- cause not absorbed; when injected subcutaneously into frogs it becomes quickly absorbed and acts upon the nerves and muscles. In warm blooded animals there is little or no absorption because of an aseptic abscess which forms. Intravenous injections in small amounts in the laboratory of Kobert proved fatal for cats and dogs. It acts injuriously on the striated muscle and heart muscle. The sensor and motor nerve fibers are also affected in a serious way. On the digestive tract it causes inflammation and peristalsis. The saponin substances dissolve the blood corpuscles of all animals and thus penetrate the corpuscles. It is thought that the haemolytic action of these substances is due to the lique- faction of the cell membrane. Ransom found that the saponin may become bound to the corpuscles and the serum. That this action depends on the cholosterin, saponin so bound will not act on the red corpuscles. The saponin cholosterin mixture exerts no ac- tion on dog's blood.1 Dr. R. F. Bacon and H. T. Marshall who made a study i The toxic action of saponin. Phil. Jour. Sci. 1:1037. Dr. R. F. Bacon and H. T. Mar- shall. POISONING FROM OPIUM 63 of the saponin found in Entada scandens proved that it was highly toxic for rabbits and guinea pigs. When diluted with normal salt solution to a concentrated form 1-200 and injected into the peritoneal cavity, 2-5 mgrms. of saponin to 100 grms. of animal was uniformily fatal, while a quarter of this amount killed in several cases. Where smaller quantities were used and animals living for a longer period of time localized peritotinitis was found. "The saponin is powerfully haemolytic" 0.005 cubic cm. of l/2 of \% solu- tion (0.025 mgrms.) completely dissolved one cubic cm. of a 5% suspension of rabbits corpuscles which were freed from serum and the half of this amount produced haemolysis of the serum of the free corpuscles of the guinea pig. "Saponin, however, loses its haemolytic power after the addition of serum." Immunity could not be produced in rabbits or guinea pigs recently treated with intraperitoneal doses of saponin or saponin serum mixture. Blyth has studied the general action of saponin on kittens. He states that when 13 to 22 mm. (1/5 to l/2 gr.) is injected underneath the skin of a kitten immediately symptoms of local pain occur, in 5 to 10 minutes the respiration is quicker and the animal falls into a lethargic condition with signs of muscular weakness; just before death breathing became rapid with all the signs of asphyxia. The appearances after death were fullness in the right side of the heart and congestion of the intestinal canal. In man the taking of saponin causes an increase of mucus secretion and nausea. Saponin or saponin-like substances occur in the following families : Phytolaccaceae, (Phytolacca abyssinica) ; Caryophyllaceae, (Gypsophila struthium, Agrostemma Githago, Lychnis, Saponaria officinalis, S. rubra, Herni- aria) ; Berberidaceae, (Caulophyllum thalictroides) ; Leguminosae, (Entada scandens, Gymnocladus dioica, Gleditschia, Enterolobium) : Oleaceae, (Chio- nanthus virginica, Syringa vulgaris) ; Amaryllidaceae, (Agave) ',Liliaceae, (Yucca glauca?, Chlorogalum pomeridianum) ; Rosaceae, (Quillaja Saponaria) ; Sapin- daceae, (Sapindus trifoliatus, S. saponaria, Pometia pinna-fa, Magonia) ; Hip- pocastanaceae, (Aescula Hippocastanum, A. Pavia) ; Theaceae, (Thea Sasan- qua, T. assanica) ; Sapotaceae, (Omphalocarpum procerum) ; Polygalaceae, (Poly gala Senega). In all more than 200 species of plants contain saponin. See Chapter XIV, and Pt. II, for a list of others. CHAPTER X POISONING FROM IXOWERS, POISONING FROM HONEY, MECHANICAL INJURIES Poisoning from Flowers. The odors from a large number of flowers are more or less injurious, especially to some individuals. The flowers of the com- mon wild black cherry (Prunus serotina} when past their prime give off a cyano- gentic odor that is quite objectionable to many people, causing headache. The carion-like odors, like those produced by Stapelia, the carion flower (Smilax herbacea) and Aristolochia are sickening to many people, causing headache and a depressing feeling. Many flowers that are ordinarily sweet scented like the tuberose (Polyanthes tuberosa) often give people the headache if the flowers are abundant in the room they are sitting in. The flowers of Wistaria are in- jurious to some people- The flowers of Magnolia grandiflora are "overpower- ing" according to some authorities. Poisoning from Honey. The honey obtained from the flowers of some plants is said to be poisonous; for instance the honey collected by insects from the oleander was long ago recorded as being injurious, and it is said that the honey collected from the mountain laurel (Kalmia latifolia} appears to be poisonous under some conditions according to Chesnut. According to Chesnut the honey collected from the flowers of the snow-on-the-mountain, {Euphorbia marginata} is bitter and disagreeable, but does not appear to be a serious poison. Several cases of poisoning from the nectar of the flowers of Datura metel and D. Wrightii are on record and the flowers of the Brazilian magonia of the family Sapindaceae produces poisonous honey; also the flowers of Rhododendron are said to contain andromedotoxin. Toxic honey has also been gathered from the flowers of Black Locust (Robinia pseud-acacia) and Lily of the Valley (Con- vallaria majalis). Prof. Lyman F. Kebler who has made a somewhat extended investigation with poisonous honey x has given an excellent bibliography with reference to the earlier literature on the subject. It has been known for centuries that the honey collected from Ericaceae acts as a narcotic irritant, producing giddiness, vomiting, and purging. Poisonous honey was described by Xenophon. He gives a fairly accurate description of how the soldiers of his army acted that ate honey that was poisoned. He states that they lost their senses, vomited and were af- fected with purging, and those who had eaten but little were intoxicated, but when they had eaten much they were like mad men. Strabo and Pliny spoke of poisonous honey, the latter writer, an early naturalist noted for his accurate ob- servations, records poisonous honey which he called "aegolethron" (goat's death), which bees collected at Heraclea. He gives a description of the honey which is said to have had a peculiar smell and produced sneezing. It is generally supposed that this honey came from a species of Rhododendron, the R. pontica. This and allied species are the chief source of poisonous honey in Asia and Asia Minor, l Poisonous Honey. Proc. Amer. Pharm. Assoc. 1896: 167-173. POISONING FROM FLOWERS 65 but it may be said in this connection that honey collected from the Heather in Scotland is not poisonous. Barton, an early American botanist, reported poisonous honey in New Jersey as early as 1794. Subsequently Coleman reported a large number of cases in 1852, and Gammer in Gleanings in Bee Culture and several writers in the Amer- ican Bee Journal reported poisonous honey. Other writers like Chesnut and Crawford have reported on the occurrence of poisonous honey in the United States and Kebler reports no less than eight cases for New Jersey in 1896 and believes that it is much more common than the records seem to indicate. Kebler was fortunate enough to investigate some of the poisonous honey following a case of poisoning in New Jersey. He examined a part of the comb of the dark honey which had a light brown color and a nauseating odor, pungent taste, caused a burning sensation in the back of the mouth similar to that of aconite. Persons who partook a small amount of this honey began to cough immediately. He also made a chemical analysis of the non-suspicious honey, digesting with alcohol then evaporated, the residue was again treated to alcohol and evaporated and administered to two cats. One received a small dose and the other a larger one. The results from the cats were so interesting that I quote from Prof. Kebler.1 The small dose produced partial exhaustion, relaxation of the voluntary muscles and gen- eral depression. The large dose in a short time produced restlessness, vomiting, purging, prostration and almost complete loss of the voluntary muscles, showing that the honey con- tained a prompt and potent poison. The animal could scarcely be induced to move, and when motion was attempted, first the fore-limbs would fail, and then the back limbs would give way. First one portion of the body would sway in one direction, then the other portion in another, reminding one of a highly intoxicated person. Had the entire dose been retained, death un- doubtedly would have followed. As it was, the cat had regained her normal condition only at the end of twenty-four hours. Along with this we may append the symptoms as recorded by the physician who attended the persons who were poisoned: Mr. and Mrs. Chambers took but a small quantity, yet each noticed a peculiar, pungent, burning taste in the comb as soon as it had passed their lips. In fifteen or twenty minutes afterwards, Mrs. C. was taken with nausea, abdominal pain, and vomiting, soon followed by loss of consciousness, coldness of extremities, feebly acting heart, and complete collapse. While ministering to her, Mr. Chambers, who had also experienced the initiatory symptoms of pain and nausea, suddenly exclaimed, "I cannot see," and soon sank in a state of syncope to the floor. In each case the symptoms were similar. Retching, vomiting, purging, acute gastric and abdominal pain, and continued cramps for some hours, with surface coldness, and deadly pallor, and the general symptoms of collapse. Kebler was, however, unable to definitely locate the andromedotoxin found by Plugge.2 This author recorded it for a large number of plants as follows : Andromeda japonica, A. polifolia, A. Catesbaei,, A. calyculata, Kalmia latifolia, Monotropa uni flora, Pieris formosa, P. ovalifolia, Rhododendron grande, R. barbatum, and R. fulgens. It has been recorded for additional plants by Greshoff who mentions the following plants which produce poisonous honey, Nerium oleander, Cytisus Laburnum, Pieris ovalifolia, Callotropis procera, Daphne, Pontica, Buxus balearica, Clcrodendron serratum, C. Bhramaramari, Sapindus emarginatus. (It is said that thousands of bees are killed by this honey.) Centaur ea scabiosa, Carduus natans, Scabiosa succisa. A South African species of Euphorbia also produces a poisonous honey which was not noted by Greshoff. 1 Proc. Amer. Pharma. Assoc., 1896:170. 2 Arch, d, Pharm., 229; 552, 1891; Am. Jour. Pharm. 63:603. Shresh, J. C. Notes on Trebizonde Honey. Pharm. Jour, and Trans., 18:397, 404. 1887-88. 66 MANUAL OF POISONOUS PLANTS Fig. 16g. The flowers of Black Locust (Robinia pseud-acacia) produces a toxic nectar. (Ada Hayden). Fig. 16h. The wilted and old flowers of Wild Cherry (Prunus) produce a cyanogentic poisonous odor. (Ada Hayden). We have a long list of plants that act injuriously Mechanical Injuries in a mechanical way. Among the best known of these are Wild Barley or Squirrel-tail Grass (Hordcum juba- tuin) and the related species, which, by mechanical means, injure sheep, horses, and cattle. The awned heads, when eaten with hay or grass, break up into sections, the awns working their way into the mucous membrane, insinuating themselves around the teeth, thus causing inflammation and deep ulcerating sores, with the formation of pus. The teeth may consequently become loosened and fall out. A Cheat or Brome Grass (Bromus tectorum) which is common in Utah, parts of Colorado, and westward, produces similar injuries. The Needle Grass, common in the dry gravelly hills and sandy plains of Northern Mississippi Valley has a fruit with a sharp pointed callus, with hairs above the pointed callus projecting upwards. The sharp-pointed callus of the "seed" enters tie skin, especially of sheep, where it produces an irritation which is sometimes followed by death. This has sometimes been eaten with forage, thus entering the intestinal tract, perhaps perforating it, causing death, especially when they have pierced the walls of the intestines. Several allied species as Black Oat (Stipa avenacea) produce similar injuries. The Western Needle Grass (Stipa comata}, however, is less injurious than our Common Needle Grass. POISONING FROM FLOWERS 67 (b) Fig. 16i. Wild Barley (Hordeum jubatum). b. Wild Barley (H. nodosum), cause of mechanical injuries to animals. Similar and allied species in other parts of the world are known to be injuri- ous in the same way. Other plants are injurious by means of their sharp-point- ed fruit. Among those of the last named type are members of the Geranium fam- ily notably the Stork's bill (Er odium cicutarium}, common in the west, which fre- quently gets into the wool of sheep and may produce local irritation. Mechanical injuries are also produced by the Sand Bur (Cenchrus tribuloides} whose spiny involucre may work into the flesh of animals and induce an irritation followed by inflammation, and the formation of pus. Hogs and cattle often receive mechan- ical injuries from the Cocklebur (Xanthium canadense} and allied species. A recent number of Horticulture (Jan. 1, 1910) notes that rose thorns have caused the poisoning of the hands of clerks who handle the roses. Prof. J. Davy states that in South Africa the burrs of a clover Trifolium terrestris var hispidissimus are said to injure young lambs. The Burdock (Lappa major} sometimes produces no little irritation, and the same may be said of the Spanish Needle (Bidens frondosa). The sharp, stiff 68 MANUAL OF POISONOUS PLANTS B E D Fig. 17. A. Fruit of the Cocklebur (Xanthium canadense), causes mechanical in- juries to hogs when eaten by them. B. Sandbur (Cenchrus tribuloides). C. Burdock (Arctium major). D. Boot Jack (Bidcns frondosa). E. One of the Borages (Cynogtossum). F. Carrot (Daucus Carota). branches of Greasewood (Sarcobatus vermiculatus) easily penetrate the skin and sometimes induce pus infection. The bristles and spines of the rose and stiff bracts of the Russian Thistle may be the cause of injury to animals and men. The small, barbed trichomes of the calyx of Crimson Clover (Trifolium incarnatum}, according to Prof. Coville, produce phytobezoars similar to those commonly produced by hair. Dr. Trelease has described similar bezoars from the barbed trichomes and spines of cacti. Millet and barley awns are known to produce similar balls in horses as well as in cattle. Corn stalks, when eaten with an insufficient amount of water, produce impaction. This has, however, been attributed to other causes also. Bloat is known to follow the use of such forage as white and red clover, alfalfa, pigweed and many other plants con- sumed under the same conditions. POISONING FROM FLOWERS 69 Fig. 17 a. Fresh water cord grass (Spartina cynosuroides') with sharp leaves often injuri- ous. 17b. Sand Bur (Cenchrus tribuloides) U. S. Dept. Agrl. 70 MANUAL OF POISONOUS PLANTS Fig. 18. Needle Grass (.Stipa comata). U. S. Dept. Agrl. Fig. 18a. Needle Grass (.Stipa spartea) inflicting mechanical injuries. U. S. Dept. Agrl. POISONING FROM FLOWERS 71 Fig. 18b. Urticating hairs and cutting leaves, a. Urticating hair of nettle, b. Bristles of bugloss. c. barbed margin of a leaf of sedge, d. barbed margin of a leaf of grass. CHAPTER XI CLASSIFICATION OF POISONS, SYMPTOMS AND ANTIDOTES Blyth classifies poisons as follows: A. POISONS CAUSING DEATH IMMEDIATELY OR IN A FEW MINUTES. PrUSSic acid, cyanides, oxalic acid and occasionally, strychnin. B. IRRITANT POISONS. Symptoms mainly pain, vomiting, and purging. Savin, ergot, digitalis, colchicum, yew, laburnum, and putrid substances. C. IRRITANT AND NARCOTIC POISONS. Symptoms of an irritant nature, with more or less cerebral indications. Oxalic acid or oxalates. D. POISONS MORE ESPECIALLY AFFECTING THE NERVOUS SYSTEM. 1. Narcotics. Chief symptoms: insensibility which may be preceded by more or less cerebral excitement. Opium. 2. Deliriants. Delirium, for the most part, a prominent symptom: Bella- donna, hyoscyamus, stramonium, and other Solanaceae, poisonous fungi, Indian hemp (Cannabis), darnel (Lolium temulentum), camphor and Ocnanthe crocata. 3. Convulsives. Almost every poison has been known to produce con- vulsive effects, but the only true convulsive poisons are the alkaloids of the strychnin class. 4. Complex nervous phenomena. Aconite, digitalis, poison hemlock, Cala- bar bean, tobacco, Lobelia inflata, and curare. Robert's classification is as follows: I. POISONS WHICH CAUSE COARSE ANATOMICAL CHANGES OF THE ORGANS. A. Those which especially irritate the part to which they are applied. 1. Acids. 2. Caustic alkalies. 3. Caustic salts, especially those of the heavy metals. 4. Locally irritating organic substances which neither can be classified as corrosive acids nor alkalies, nor as corrosive salts; such are: cantharadin phrynin, and others in the animal kingdom, croton oil and savin in the vege- table kingdom; locally irritating colors, such as the anilin dyes. 5. Gases and vapors which cause local irritation when breathed; such as ammonia, chlorin, iodin, bromin, and sulphur dioxid. B. Those which have but little effect locally, but change anatomically other parts of the body; such as lead, phosphorus, and others. II. BLOOD POISONS. 1. Blood poisons interfering with the circulation in a purely physical manner; such as perox'id of hydrogen, ricin, abrin, 2. Poisons which have the property of dissolving the red corpuscles ; such as the saponins. 3. Poisons which, with or without primary solution of the red blood corpuscles, produce in the blood methaemoglobin ; such as potassic chlorate, hydrazine, nitrobenzene, anilin, picric acid, carbon disulphid. CLASSIFICATION OF POISONS 73 4. Poisons having a peculiar action on the coloring matter of the blood, or on its decomposition products; such as hydric cyanid, and the cyanides and carbon monoxid. III. POISONS WHICH KILL, WITHOUT THE PRODUCTION OF COARSE ANATOMICAL CHANGE. 1. Poisons affecting the cerebro-spinal system; such as chloroform, ether, nitrous oxid, alcohol, chloral, cocain, atropin, morphin, nicotin, coniin, aconitin, strychnin, curarin, and others. 2. Heart poisons; such as digitalis, helleborin, muscarin. IV. POISONOUS PRODUCT OF TISSUE CHANGE. 1. Poisonous albumin. 2. Poisons developed in food. 3. Auto-poisoning, e. g. uraemia, glycosuria, oxaluria. 4. The more important products of tissue change; such as, fatty acids, oxy-acids, amido-fatty acids, amines, diamines, and ptomaines. CLASSIFICATION OF POISONS AND POISONOUS SYMPTOMS, ACCORDING TO BERNHARD H. SMITH POISONS ACTING ON THE BRAIN NARCOTICS Symptoms. Giddiness; dimness of sight; contracted pupils; headache; noises in the ears; confusion of ideas, and drowsiness, passing into insensibility. Treatment. (Immediate) : EMETICS (especially mustard, a tablespoonful in half a tumbler of warm water). STOMACH TUBE. (Wash out at half-hourly intervals with Potash Per- manganate solution B. P. 1 per cent solution diluted three times with warm water). Dash cold water on face and chest. Ammonia or Amyl Nitrite to nostrils. (Later:) TANNIN. (Hot, strong coffee, tea, or infusions of nut-galls or oak-bark). Strychnin solution B. P. (Iper cent solution) two minims subcutaneously. Atropin, half grain subcutaneously, repeated if necessary. Faradic current. Oxygen. Artificial respiration if necessary. DEMULCENTS. (Milk, eggs, oil, etc., swallowed and injected). Note — All vegetable poisons act more quickly on the empty stomach; our treatment therefore is directed towards (1) diluting and evacuating the poison by means of washing out with warm water containing powdered charcoal; (2) neutralising the poison by means of an antidote such as Tannin. Plant producing poisons that act on the brain as narcotics — Poppy (Papaver somniferum). II DEWRIANTS Symptoms. Spectral illusions; delirium; dilated pupils; thirst, and dryness of the mouth; inco-ordination. Occasionally, though rarely, there are paralysis and tetanoid spasms. 74 Treatment. ( Immediate : ) EMETIC and STOMACH TUBE. Pilocarpin Nitrate, one-third of a grain subcutaneously, repeated if neces- sary. Ammonia or Amyl Nitrite to nostrils. TANNIN. (Later:) Stimulants, Castor Oil. DEMULCENTS (swallowed and injected). Note — Muscarin poisoning give Belladonna Tincture B. P. fifteen minims Plants furnishing poisons that act as deliriants — Thorn Apple (Datura Stramonium). Black Nightshade (Solanum nigrum), Hemp (Cannabis sativa), Darnel (Lolium temulentum), Several Fungi as Fly Agaric (Amanita muscaria). Ill INEBRIANTS Symptoms. Excitement of cerebral functions, and of the circulation ; loss of power of co-ordination, and of muscular movements, with double vision; leading to profound sleep, and deep coma. Treatment. ( Immediate : ) EMETIC and STOMACH TUBE. TANNIN. (Later:) Epsom Salts. DEMULCENTS (swallowed and injected). Plants furnishing poisons that act on the brain as inebriants : Wormwood (Artemisia Absinthium), Jamaica Dogwood (Piscidia Erythrina). POISONS ACTING ON THE SPINAL CORD CONVULSIVES Symptoms. Clonic (intermittant) spasms, extending from above down- wards. Opisthotonos very violent; but trismus (lock-jaw) rare. Swallowing' spasmodic. Death, usually, in less than three hours, or rapid recovery. Treatment. (Immediate:) EMETIC and STOMACH TUBE. TANNIN. Chloral Hydrate five grains subcutaneously (a weak solution as it is an irritant), repeated if necessary. Chloroform inhalation. Artificial respiration. Potassium Bromide, one drachm in water every half -hour. Morphia (?). (Later:) DEMULCENTS (swallowed and injected). Castor Oil. Chloroform inhalation if convulsions return. Plants furnishing poisons that act upon the spinal cord as convulsives: Nux-vomica Tree (Strychnos Nux-vomica), St. Ignatius's Bean (Strychnos Ignatii). POISONS ACTING ON THE HEART I DEPRESSANTS Symptoms. Vertigo; vomiting; abdominal pain; confused vision; convul- sions; occasional delirium; paralysis; syncope; sometimes asphyxia. CLASSIFICATION OF POISONS 75 Treatment. ( Immediate : ) EMETIC and STOMACH TUBE. TANNIN. STIMULANTS. Strychnin solution B. P., two minims subcutaneously. Atropin, half a grain subcutaneously, repeated if necessary. (Later:) Stimulants. Hot fomentations. Artificial respiration if necessary. Castor Oil. DEMULCENTS (swallowed and injected). Plants furnishing poisons that act on the heart as depressants : Tobacco (Nicotiana Tabacum), Hemlock (Conium maculatum), Indian Tobacco (Lobe- lia inflata). II ASTHENICS Symptoms. Numbness, and tingling in the mouth; abdominal pain; vertigo; vomiting; purging; tremor; occasional delirium; paralysis; dyspnoea, ending in syncope. Treatment. (Immediate:) KMETIC and STOMACH TUBE. TANNIN. STIMULANTS. Cold affusion. Faradic current. Atropin, half a grain subcutaneously. (Later:) DEMULCENTS (swallowed and injected). Continued recumbent position. Artificial respiration if necessary. Castor Oil. Note — In Aconite poisoning inject Digitalis Tincture B. P., twenty minims subcutaneously (\2l/2 per cent strength). Plants furnishing poisons that act on the heart as asthenics: Lima Bean (Phaseolus lunatus), Tapioca (Jatropha manihot}, Aconite (Aconitum Napel- lus), Cohosh (Cimicifuga racemosa), Oleander (Nerium Oleander), Fox-glove (Digitalis purpurea}, White Hellebore (Veratrum album}, Green Hellebore ( Veratrum viride} . VEGETABLE IRRITANTS PURGATIVES Symptoms. Abdominal pain; vomiting, and purging; cramps; strangury and tenesmus, followed by collapse, and sometimes accompanied by drowsiness, and slight nervous symptoms. Treatment. (Immediate:) EMETIC and STOMACH TUBE. TANNIN. (Later:) Opium to relieve pain. Stimulants to counteract collapse. DEMULCENTS (swallowed and injected). Plants producing poisons that act as purgatives: Castor Bean (Ricinus communis), Green Hellebore (Helleborus viridis), May Apple (Podophyllum peltatum), Marsh Marigold (Caltha palustris}. 76 MANUAL OF POISONOUS PLANTS II ABORTIVE Symptoms. Nausea; vomiting; stupor; polyuria; sometimes tenesmus. Abortion may or may not occur; coma. Treatment. ( Immediate : ) EMETIC and STOMACH TUBE. TANNIN. Ammonia or Amyl Nitrite to nostrils. (Later:) Opium to relieve pain. Stimulants to counteract collapse. DEMULCENTS (swallowed and injected). Plants producing poisons that act as abortives: Ergot (Claviceps pur- purea), Herb of Grace (Ruta graveolens} , Cotton root (Gossypium herbaceum), Pulsatilla (Anemone patens, and its variety). Ill IRRITANTS WITH NERVOUS SYMPTOMS Symptoms. Abdominal pain; vomiting and purging; dilated pupils; head- ache ; tetanic spasms ; occasional convulsions ; sometimes rapid coma. Treatment. ( Immediate : ) EMETIC and STOMACH TUBE. TANNIN. Opium to relieve pain. Stimulants to counteract collapse. Bleeding if necessary. (Later:) Castor Oil. DEMULCENTS (swallowed and injected). Plants furnishing poisons that act as irritants, causing also nervous symp- toms: Indian Pink (Spigelia marilandica) , Cut-leaved Water Parsnip (Berula erecta), Fool's Parsley (Aethusa Cynapium). IV SIMPLE IRRITANTS Symptoms. Burning pain in the throat and stomach; thirst; nausea; vom- iting; tenesmus; purging; dysuria; dyspnoea and cough occasionally. Death through shock; convulsions; exhaustion; or starvation due to injury to throat or stomach. Some few (i. e. the Nettles) cause smarting pain on the merest contact with the secretions of the plant; quickly followed by erythema and urticarial rash, which slowly subsides. Treatment. (Immediate:) EMETIC and STOMACH TUBE. TANNIN. Opium to relieve pain. Stimulants to counteract collapse. Chloral and Bromides if convulsions. (Later:) Castor Oil. DEMULCENTS (swallowed and injected). Plants producing, poisons that cause the above symptoms : Arrow Root CLASSIFICATION OF POISONS 77 (Arum maculatum), Wood Anemone (Anemone nemorosa), Cursed Crowfoot (Ranunculus sceleratus), Buttercup (Ranunculus acris), Bouncing Betty (Sap- onaria officinalis), Kinnikinnik (Arctostaphylos Uva-ursi), Sundew (Drosera rotundi folia}, Poison Ivy (Rhus Toxicodendron), Nettle (Urtica dioica U. gracilis), Wood Nettle (Laportea canadensis) , Bull Nettle (Jatropha stimu- losa). V SIMPLE IRRITANTS WHEN TAKEN IN LARGE QUANTITIES Symptoms. Burning pain in throat and stomach. Vomiting; purging; dif- ficulty in swallowing. Recovery usual. Treatment. (Immediate:) EMETIC and STOMACH TUBE. TANNIN. Opium to relieve pain. Stimulants to counteract collapse. (Later:) Castor Oil. DEMULCENTS (swallowed and injected). Plants affording poisons that act as simple irritants when taken in large quantities only: White Mustard (Brassica alba), Black Mustard (B. nigra"), Black Pepper (Piper nigrum), Common Ginger (Zingiber officinalis), Cay- enne Pepper (Capsicum annuum). TABLE OF SYMPTOMS OBSERVED AFTER THE ADMINISTRA- TION OF POISONS, ADAPTED FROM CATTELL AFTER THE WORK OF ROBERT. ACUTE SYMPTOMS PRESENT 1. Death within a few sec- onds or minutes. 2. Deep coma. 3. Collapse. 4. Feverish rise of tempera- ture. 5. Mania; furious delirium; psychic excitement. 6. Mental disturbance of the most diverse kind. 7. Violent at times, tetanic convulsions. 8. General paralysis, for the most part ascending. 9. Dilation of the pupil. 10. Contraction of the pupil. 11. Aneurosis. 12. Diplodia and ptosis. 13. Conjunctivitis. WE SHOULD THINK OF Hydrocyanic acid; potassium cyanid; car- bonic acid; carbolic acid. Alcohol ; morphin ; opium. Nicotin; colchicin. Cocain ; enzymes. Chronic alcoholism; atropin; camphor; phy- sostigmin; veratrin. Alcoholism; morphinism; cocainism; pella- gra; ergotism. Strychnin ; toxin of tetanus ; cytisin ; cornu- tin ; picrotoxin ; cicutoxin ; active principle of digitalis ; cocain ; santonin ; aconitin ; gelse- min; filicic acid. Coniin; curarin; colchicin. Atropin; hyoscyamin; scopolamin; cocain; ephedrin ; aconitin. Muscarin ; pilocarpin ; nicotin ; codein ; opi- um ; physostigmin. Quinin; extract of male fern; belladonna; uraemic poisoning. , Sausage (botulism) and fish poisoning. Irritating vapors; ethereal oil of mustard; 78 MANUAL OF POISONOUS PLANTS 14. Moist skin. 15. Skin conspicuously dry even in a warmed bed. Mouth and throat parch- ed. 16. Urticaria or scarlatiniform erythema. 17. Eczematous eruptions of skin. 18. with the Diffuse dermatitis perspiration of hands. 19. Acne pustules. 20. Blisters on the skin or the mouth, containing clear serum. 21. Gangrenous ergotism; car- bolism. 22. Cyanosis. 23. Yellowish-brown discolor- ation of the conjunctiva, in combination with that of the skin. 24. Discoloration primarily of the tongue and mucous membrane of the mouth. 25. Salivation. 26. Metallic cough and apho- nia. 27. Oedema of the glottis. 28. Oedema of the lungs. 29. Increased dullness of the liver. 30. Diarrhoea with vomiting. 31. Vomiting without diarr- hoea. 32. Diarrhoea without vomit- ing. 33. Pulse continuously and markedly becoming slow- er. 34. Pulse first slower, then ir- regular, finally accelerat- ed. 35. Pulse greatly accelerated. 36. Abortion. croton oil vapor; irritating kinds of dust as roots of ipecac, quillaja bark, pepper, forma- lin, etc. Opium ; morphin ; aconitin ; pilocarpin ; ni- cotin; physostigmin ; lobelin. Atropin; belladonna; stramonium; hyoscya- mus ; hyoscyamin ; scopalamin ; sausage and fish poisoning. Atropin ; hyoscyamin ; antipyrin ; quinin ; bal- sam of copaiba; cubebene; morphin; hand- ling of nettles; buckwheat; smartweed. Croton oil; curcas oil; cardol; Rhus Toxi- codendron; powdered cinchona bark; carbolic acid; tar. Anilin colors; aurantia; butter yellow. Powdered ipecac. Ranunculus acris ; R. sceleratus. etc. Ergot. Antif ebrin ; exalgin ; anilin. Helvellic acid; lupinotoxin (ictrogen) Carbolic acid. Pilocarpin ; muscarin ; arecolin ; nicotin ; cornutin ; physostigmin ; cytisin ; saponin. Atropin ; hyoscyamin ; scopolamin ; sausage poisoning. All caustic poisons. Muscarin ; morphin ; pilocarpin ; nitric acid vapors. Agaricus bulbosus ; poley oil ; alcohol. Digitalin ; pilocarpin ; nicotin ; muscarin ; col- chicin ; corrosive poisons ; colocynthin ; emetin ; cephalin; croton oil. Apomorphin; lobelin; cytisin. Jalap ; podophyllotoxin ; croton oil ; calomel. Opium ; morphin ; muscarin ; arecolin ; phy- sostigmin ; all narcotics. Digitalin; hellebore; adonis; coronilla; cheirathin; nervin; scilla; strophanthus ; con- vallaria ; pilocarpin ; nicotin ; scopolamin. Belladonna ; hyoscyamin ; atropin. Sabina; thuja, rue; mentha.; pulegium ; er- got; cotton root. CLASSIFICATION OF POISONS 79 37. 6-12 hour period of good health between the pois- oning and the appear- ance of the symptoms. Most of the poisonous fungi, but especially Amanita phalloides. TREATMENT FOR POISONING. (CHIEFLY AFTER ROBERT). KIND OF POISON Aconite. Alcoholism, acute. Aspergillosis Atropin Carbolic acid. Cicuta virosa. cowbane. Cicutoxin. Cocain. Colchicin. Coniin. Conium. Cytisin. Delphinosis. Dermatitis. Rhus. C. maculata TREATMENT. Use stomach pump at once; give emetics of sulphate of zinc, or a hypodermic injection of apomorphin; patient should recline; when stomach has been evacuated, give atropin (4 drops U. S. P. solution) hypodermically or by the mouth, or 20 drops of tincture of bella- donna ; if there is a tendency to heart-syncope, give tincture of digitalis, in y2 drachm doses by mouth, or hypodermically in doses from 10 drops upwards ; apply mustard plasters to pericardium; aid vomiting by plenty of water; if necessary apply artificial respiration. Wash out the stomach with a siphon tube; cause vomiting by emetics, cold and hot ef- fusions alternated; strychnin hypodermically. Treatment unsatisfactory; moulds that have entered lungs cannot be destroyed. Wash out the stomach with a solution of tannic acid or cause evacuation with an emetic ; hypodermic injection of strychnin to stimulate respiration ; administer tea or whiskey. A liberal dose of whiskey or alcohol as a diluent; use soft stomach tube to wash out the stomach with sodium sulfate; sodium sul- fate, raw eggs, milk and saccharate of lime are antidotes. Tannin and narcotics according to symptoms, especially chloral hydrate. Chloroform, chloral hydate, artificial respira- tion, stimulants like whiskey. Evacuate the stomach; then give vegetable astringents, iodin 1 gr. and potassium iodid 10 gr. dissolved in water; digitalis and amyl nitrite are given for syncope; give stimulants like oxygen and whiskey for cyanosis. Mucilaginous potions, morphin, warm com- presses on the abdomen. Wash out the stomach after giving tannic acid or some other astringent; strong coffee and whiskey; strychnin hypodermically; apply artificial respiration if necessary. Tannin, stimulants, especially camphor. When spasms occur, give narcotics ; artificial respiration in case of paralysis of the organs of respiration. Potassium permanganate is the antidote; in extreme depression of circulation and respira- tion, atropin sulfate administered hypodermic- ally. Antidote is acetate of lead. 80 MANUAL OF POISONOUS PLANTS Dermatomycosis. Digitalis. Equisetosis. Ergotism. Fagopyrism. Forage Poisoning. Formic Acid. (In stinging net- tles). Gelsemin. Helleborus niger. tlydrocyanic Acid. Lathyrism Locoism. Lupinosis. Maydism. Morphin. Muscarin. Nicotin. Phallin. Picrotoxin. Pilocarpin. Cleanliness; sanitary surroundings; disinfec- tion; preparation of bichloride of mercury. No antidote; treat symptomatically. Administer cathartic; also nerve and heart stimulants to combat symptoms of depression; change of food. Administer purgatives and stimulants, es- pecially camphor; tannic acid is chemical an- tidote and will neutralize unabsorbed portions of poison; chloral is physiological antidote; further treatment symptomatic. Change of food. Change of food. Cooling compresses externally ; chalk, soda, or magnesia internally. Wash out the stomach thoroughly ; give stim- ulants and hot applications to the epigastrium and extremities; digitalis to strengthen the heart action and atropin to increase respira- tion. Use stimulants, especially camphor. Wash stomach with 0.5 per cent potassium permanganate solution or with hydrogen per- oxid ; the latter may be given hypodermically in small doses but with great caution ; arti- ficial respiration. Treat paralyzed parts electrically; massage. In advanced stage of disease, treatment of no avail; in early stage, removal to an un- infected pasture with plenty of good nourish- ing food besides may benefit. Chiefly preventive; no specific antidote; to prevent further absorption of poison, admin- ister an acid; also give purgative. Change of diet; transfer to hospital. Wash out stomach with siphon tube using water containing potassium permanganate in the proportion of 20 gr. of the permanganate to 1 tumbler full of water; or use in the same manner an infusion of tea or tannic acid; emetics like mustard, using one or two tea- spoons of each; apomorphin 5-10 minims of a 2 percent solution ; hypodermic doses of strychnin 1-20 gr. or sulphate of atropin 1-60 gr. Atropin used hypodermically; stimulants like strychnin may be given; wash out stomach. If free vomiting has not occurred, wash out stomach with warm water or tea ; give stim- ulants like whiskey or use hypodermic injec- tion of strychnin nitrate 1-25 gr. No known antidote; undigested material should be removed from stomach and same remedies as those suggested in muscarin poi- soning may be administered. Chloroform; chloral hydrate; artificial res- piration. Evacuate the stomach and wash out with so- CLASSIFICATION OF POISONS 81 Physostigmin. Ranunculus. Santonin. Strychnin. Toxins. Veratrin. lution of tannin; atropin is antagonistic, give 1-60 gr. hyppdermically ; use whiskey and am- monia as stimulants. Scopalamin hypodermically ; artificial res- piration. According to symptoms; tannin. Chloroform; chloral hydrate; artificial res- piration. Control spasms by inhalation of chloroform ; use stomach tube with warm water containing potassium permanganate, 4 gr. in 11 fl. oz. water. Botulism produced in sausage poisoning may be treated by removing the poison, by giving free potations of warm water and salt, irriga- tion of intestines with enemas ; vomiting and purging can be relieved by hypodermic injec- tions of morphin; inject normal salt solutions. Wash out stomach thoroughly with the si- phon tube, or give emetics; give tannic acid or vegetable astringents which will precipitate the alkaloids; atropin or strychnin will coun- teract the cardiac depression.1 i In the above table use has been made of the English translation of Robert's Practical Toxicology by Friedburg, as well as the original. CHAPTER XII THE; PRODUCTION OF POISON IN PLANTS THE USE AND ACTION OF POISONS ON PLANTS An extraordinarily large number of poisonous substances belonging to the alkaloids, glucosides, saponins, and toxins, occur in the vegetable kingdom- In addition there is a larger number of substances not strongly poisonous which are curative in their nature. These substances so widespread in the vegetable kingdom are the products of metabolism and probably in some cases, waste products, although according to Weevers, may act as reserve food substances. Treub 1 states that the hydrocyanic acid in the Pangium edule is of importance in the metabolism of the plant. It occurs not only in certain parts of the fibro- vascular bundle but in the cells from the leaf and certain specialized cells of the epidermis, occurring both in a free and in an unstable combination. His con- clusion is that the hydrocyanic acid is the first recognizable product of nitrogen assimilation. It is certainly true that in some cases the poisonous products formed in the plant do not undergo any further change. Undoubtedly the sub- stances serve as a protection to the plant and it may be interesting to note that large quantities of these substances may be excreted and occur in an insoluble form in the cell sap and do no injury to the plant- Digitalin, morphin, atropin, eserin, muscarin, and veratrin, seem to exert little or no poisonous action on most plants; while strychnin may act as a strong poison.2 There are also other alkaloids that when applied to the plant are poisonous to the plants from which they have been obtained. Morphin is said to poison the poppy, and the motile spores are speedily killed by the same substance according to Strasburger. Too little, however, is known about this subject to make any extended remarks. It is interesting, however, to observe in this connection that as in the case of man and other animals, plants can be gradually accustomed to doses which would probably prove fatal in many cases. The Blue Mould (Penicillium glaucum) and some species of Aspergillus can accommodate themselves to strong solutions of copper and formalin. There are some reasons for believing that the proto- plasm of different plants is not a uniform substance but varies, and that one substance may be toxic to the plant while harmless to another and even act as a stimulant- DISTRIBUTION OF POISONOUS SUBSTANCES IN PLANTS The seed may contain a toxic substance and upon the germination the poisonous material may occur not only in its juvenile stage but at maturity. In some cases the seed and the juvenile form may be non-poisonous, but as the plant becomes older the poisonous substance is elaborated as in the latex of some plants that contain narcotic principles. In some cases the seed is poisonous and the young plants apparently do not contain a toxic material; the 1 Ann. du Jardin Bot. de Buitenzorg 13. Pharm. Review. 14:278. 2 Pfeffer, Physiology of Plants. English Translation. 2:260; Schwarz, Wirkungen von Alkaloiden auf Pflanzen, Erlanger Dissertation. 1897. THE PRODUCTION OF POISON IN PLANTS 83 poisonous substance apparently being broken up to serve as a nourishing material for the growth of the plants. Cornevin * in his work upon poisonous plants says : In one group "the poison- ous substance does not exist in the plants themselves, but, in some parts or tissue, elements are present which are not really poisonous in themselves but become so when the parts or tissues come in contact with one another. An example is seen in the glucoside amygdalin which in contact with emulsin forms hydrocyanic acid." The activity of vegetable poisons may depend upon the age of the plant producing them. No definite rule can be established in regard to the age at which a plant produces its poisonous substance. Sometimes a younger plant is more actively poisonous than when older, sometimes, also, the poison is stored in certain tissues. Poisonous principles are found in various parts of the plant, such as the root, stem, flowers, fruit, leaves, bark, tubers, seed and bulbs. In many aerial parts of plants the poisonous substances are more ephem- eral than they are in organs of the plant that serve as store houses of food. Cornevin says : It sometimes happens that the subterranean part only is poisonous as in Atractylis gum- mifera. This is true, also, of the common European Violet. On the other hand, when sub- terranean organs of certain plants come in contact with the light a poisonous substance may be produced. This is true of the tuber of potato which when green is poisonous. Poisonous substances are elaborated both in evergreen and deciduous leaves; no rule of comparison has, however, been established. Certain variations of the plant are dependent upon its environment, certain conditions of which play an important part especially in the elaboration of poisonous substances. These conditions are light, heat, season, climate, soil, culture and fertility. LIGHT. It is a well knewn fact that light seriously interferes with the growth of parasitic fungi and bacteria so that pathogenic species may become quite harmless when placed in direct sunlight. The poison atractylin is formed only in darkness, on the other hand solanin is formed only in the light, as in the case of the green potato. HEAT. Cornevin says : The action of heat upon plants should be considered with that of light, of the seasonal variation, and of climate, and not as an isolated cause. When it is prolonged it induces dessi- cation of the plant and as a consequence evaporation follows and destruction of the poison when it is volatile. This result is produced in some Ranunculaceae, Chenopodiaceae, etc. Moist heat, that is boiling, conduces to the same result in some poisons. Three-seeded mercury (Mercurialis annua) becomes inoffensive when it has been submitted to the action of heat, because of the volatilization of its toxic substance mercurialin. SEASONS. Seasons cause considerable variation in the poisonous material produced in plants, the amount of poison contained often varying with the ad- vance of the season. In aconite the poison, at first contained in the leafy or- gans becomes concentrated little by little in the seed. The time of the year may have an important bearing upon the amount of poisonous material found in the plant. According to Prof. Hedrick the Cow- bane or Musquash root (Cicuta vagans) of the west is much more toxic in the fall, winter, and spring, than in the summer, and this is partially confirmed by an experiment conducted with our common Cowbane {Cicuta maculata}- It is also well known that the mature bulbs of Colchicum contains a much larger amount of the toxic substances than the growing bulbs and that for medicinal l Des plantes veneneuses et des empoisonnements qu'elles deterrminent, 524. Paris, 1893. 84 MANUAL OF POISONOUS PLANTS purposes the bulbs are usually collected between the decay of the foliage and the production of the flowers. Opium is obtained from the capsules of the opium plant a few days after the petals have fallen, the seed containing comparatively little of the narcotic substances. It is well-known also that the poisonous principles of the Lark- spurs are much more active in the spring than in the summer. Dr. Albert C. Crawford * says referring to the Delphinium camporum, with which he con- ducted some experiments and was able to kill several guinea pigs with toxic material obtained from the plant collected on April 26th and May 16th, but failed to get positive results of material collected in June. There is no question as to the fact that Delphinium when injected subcutaneously will kill, and these experiments also establish the fact that the plant loses much of its toxicity as it approaches the flowering stage. It has been noted that Delphinium consolidcfi is also less active when mature. Just after flowering, the purple larkspur turns yellow and ceases to be attractive, so that there is less danger of poisoning, although Chesnut and Wilcox report death in cattle from eating Delphinium glaucum in September. The great danger early in the season seems to arise from the fact that the Delphinium appears early in the spring, and the ground may again be covered with snow, so that it is the only green plant in sight, and therefore when in an especially poisonous stage it is eaten by cattle. Botanical and other writers have frequently called attention to the fact that the greatest amount of poisoning in the west occurs in early spring- Of course, this may be because there is less green food and live stock may consume more of this plant than at other seasons. However, there seems scarcely any reason to doubt that the plant does contain a larger amount of the acrid toxic sub- stances in! the spring than in the summer, as proved by the experiments of Dr. Crawford. The same author who investigated the Mountain Laurel 3 calls attention to the well-known fact that most of the cases of poisoning from Mountain Laurel occur in the winter. Undoubtedly the animals will eat more of the tough and leathery leaves in the winter because there is very little green for them; but may they not also have a larger amount of the toxic material? The plant is evidently also poisonous in the summer, as indicated by numerous re- ports of the experiments by Dr. Crawford, who conducted an experiment with material collected in the summer, in May and June, death occuring in a sheep weighing 49 Ibs-, that had received 90 grams of powdered dried laurel leaves. The late lamented Dr. Greshoff has called attention to the peculiar distribu- tion of hydrocyanic acid in plants. In referring to a species of Hydrangea of the Saxifragaceae he states that he sometimes found considerable quantities of hydrocyanic acid in some of the well-known ornamental plants like the //. hortensia and sometimes he did not find it. He surmises that the cyanogentic principle disappears from the leaves in the autumn and that the young leaves have much more of the HCN than the older ones. In the case of the Plane Tree (Platanus) he found considerable of the same acid in the young leaves but as the leaves grow older the HCN content falls off to small traces. He states further that in the ordinary plane tree of the London Streets there is so much HCN that the amount from each London Plane Tree leaf would be enough to kill a London sparrow. 1 Bull. Bur. Plant Ind., U. S. Dept. of Agric. Ill: Part II; 7. 2 Dammann, C. Gesundheitspflege. 1886:1072. 3 Bull. U. S. Dept. of Ag., Bur. Plant Industry. 121:21. THE PRODUCTION OF POISON IN PLANTS 85 Miss Alice Henkel in a paper on American Root Drugs 1 notes the im- portance of collecting medicinal plants and drugs at the right time. The roots of the American Hellebore (Veratrum viride) should be collected in the autumn after the leaves are dead. Generally speaking the drugs contain more of the medicinal virtues after the period of cessation of growth of the plant. Dr. C- Mueller 2 calls attention to the fact that Colchicum is much better if the rhizome is collected at time of flowering. On this point all authorities do not agree. Cornevin who has made a study from month to month of the migration of poison in plants such as the Laburnum found the following conditions : On May 20th, 2 grammes of the dried leaves of Cytisus Laburnum, administered to some carnivorous animal, were sufficient to induce vomiting. On June 10 (at which time pods were forming) 4 grammes were required to produce the same result. July 28 (when the pods were fully formed) 12 grammes were required. September 28 (pods were beginning to dry) 20 grammes were required. The experiments show that at all periods the leaves were poisonous but as the poison became concentrated in the pod the leaves became less toxic. Similar experiments resulted in demonstrating that while the poison con- centrates in the pod it also loses toxicity as the season advances, enormous doses taken from dried seed in October failing to produce death, while a 2- gramme dose from a June pod proved fatal. CLIMATIC. Latitude has an influence upon the formation of poisons- There are more poisonous plants in tropical regions than in colder regions. Certain plants which are poisonous in temperate regions lose their poisonous properties when taken into colder regions. Examples of this are aconite and cherry laurel. It is difficult to make a comparison between the total number of poisonous plants in tropical and temperate regions, but it is probable that the warmer regions will show the greater number of poisonous species. It might be well, however, to note in this connection that the poisonous properties of Rhododendron Chrysanthemum and R. catawbiense as well as of Aconitum are developed in colder regions while such toxic plants as the calabar bean (Physostigma venenosum), Strychnos nux-vomica, the Upas tree (An- tiaris toxicaria) and numerous others are inhabitants of warm climates. It is well known that the sorghum grown in dry climates produces a greater amount of a glucoside which is capable of being, converted into hydro- cyanic acid than in more moist regions. Some writers even assert that in dry seasons the drought depauperates the plant and that in the nodes there are considerable quantities of potassium nitrate.3 Again Dr. Ludwig Bernegau notes that the amount of alkaloid in Cola Nut varies considerably, it depending upon the source of the nut. With reference to the presence of alkaloids in different kinds of opium, it is known that the Smyrna opium is of superior quality for medicinal pur- poses. It is said to be superior to the opium obtained from India, which is in part attributed to climatic conditions, and probably in part to the method of collection. According to Blyth, the amount of morphin varies as follows : Crude morphin (containing about 7-10 of pure morphin). Highest, 12.30; lowest, 6.76; mean, 9.92 per cent, which equals 12.3 per cent of the dried drug. 1 Bull. U. S. Dept. Agrl., Bur. Plant Industry, 107. Farmers Bull. 188. 2 Pharm. Review. 14:113. Die Natur. 44:550. 3 An English writer, Pease, attributed the death of animals to this substance rather than to the hydrocyanic acid. Pharm. Review, 15:208. 86 MANUAL OF POISONOUS PLANTS The nicotin of tobacco depends largely on climatic and soil conditions, The Havana, Porto Rico, Sumatra, Connecticut Seed Leaf and Wisconsin have qualities all peculiarly their own. Blyth records the following percentages of nicotin in various tobaccos as given by Cox.1 Variety examined Nicotin per cent 1. Syrian leaves (a), ....... .612 2. Syrian leaves (b), . . . . . .1.093 3. Gold Flake (Virginia), . . . . . .2.501 10. "Navy-Cut" (Light colored), . . . . . .3.640 15. "Best Shag" (b), 5.000 17. Algerian tobacco (a), . . . . . . 8.813 According to Professor Garner 2 the nicotin contents vary as follows : Nicotin soluble in petroleum ether in domestic filler tobacco 2.20 percent; Imported Cuban Santa Clara tobacco 1.33 percent. That climate plays an important part in connection with chemical products is illustrated in the essential oils. The most important of these such as bergamot, cassia, cinnamon, jasmine, fennel, lavender, orange, rosmary, attar of roses, and many of the others are imported into the United States. These are pro- duced in localities that are more favorable for their production than in many parts of this country. However, some of the essential oils like those from pep- permint, sweet birch, and sassafras are produced extensively in the United States. The time of collecting and many other factors as well as the matter of labor enter into the production of these oils. The variation in composi- tion has been indicated by Dr. Edward Kremers and his students in various publications.3 It is well known that the locality for attar of roses which supplies most of the commerce of the world is a small district of country on the southern side of the Balkan Mountains. The best localities according to those best informed on the subject are those occupying southern or southeastern slopes. The flowers attain perfection in April or May and are gathered before sunrise. It is concluded from some experiments carried on in some of the northern countries in Europe, that a cool northern climate is not conducive to the production of highly odorous oils.4 It is interesting to note that the oil of orange flowers comes chiefly from the southern part of France, and that the flowers of sweet orange afford about one-half the amount of oil that those of the bitter orange do. Lavendar oil, made from Lavandula vera, is very variable in quantity, depending upon its source, although not grown to any great extent in England. Fliickiger and Hanbury state that the Mitcham oil grown in the Surrey, is of a superior and high quality. The above is used here to illustrate the fact that the chemical products of plants vary depending upon the different climatic conditions. 1 Pharm. Journ., Jan. 20, 1894. Blyth, Poisons; Their Effects and Detection. Ed. 2.274. 2 Bull. U. S. Dept. Agr., Bur. Plant Ind. 141; Pt. I, 12. 3 Kremers and Schreiner. The Quantitative Estimation of Carvone in Volatile Oils. Pharm. Review. 14:76. Edward Kremers and Florence M. Gage. Notes on Two Oils Containing Pulegeone. Pharm. Review. 16:412. Kremers and Sievers. Oils from Milfoil. Pharm. Review. 25:215. The Volatile Oils, by E. Gildemeister & Fr. Hoffman. English Translation, E- Kremers. 4 Fliickiger & Hanbury, 262. THE PRODUCTION OF POISON IN PLANTS 87 Dr. Rodney H. True in an article in the Cyclopedia of American Agricul- ture,1 says : The sources of our crude drugs and condiments are very widely separated, depending in large part on climatic conditions. Common drug plants belonging to the temperate zone, such as digitalis, burdock and caraway, are in very large part produced in northern and central Europe, frequently in more or less localized regions. Caraway comes chiefly from Holland, in small quantities from Norway, east Prussia and southern Germany. Fennel is cultivated in Saxony, Galicia, Macedonia and Italy. Digitalis leaves and belladonna reach the market of northern Germany, Austria, Belgium, Holland and England. Peppermint oil is produced chiefly in Japan and the United States. Other plants demanding tropical conditions are ob- tained from regions in which their culture has been undertaken. Cinchona bark, from which quinine is obtained, came formerly from the slopes of the Andes. Cultivation of this plant in India, Java, and other parts of the Orient has succeeded in so far as to cause the practical disappearance of the wild barks of South America from the market. Ipecacuanha, likewise a native of northern South America, is apparently repeating this history. Black and white pepper are chiefly produced in southeastern Asia, coming on the market through Singapore and Penang. Cloves are in large part supplied by Zanzibar, where the crop constitutes one of the royal monop- olies. Some products are derived from still more localized regions, as buchu leaves from the vicinity of Cape Town, South Africa, and aloes from South Africa, the island of Socotra in the Red Sea, and the Barbadoes islands. Some are cultivated, as may be seen in numerous cases cited above, and some are wild products. Camphor until recently has been derived from an essentially wild tree growing in Japan, China and Formosa. The great depletion of the natural forests has led the Japanese government to make extensive plantings. Several African sorts of the red peppers of the market are collected by natives from the wild plants and brought long distances to market. CULTURE. Cultivation often affects the amount of poison contained in a plant. A wild vetch of Europe (Laythrus} is extremely bitter, but through cultivation the poisonous material has been largely eliminated and the vetch has become a useful cultivated forage plant. It is stated also that the aconite (Aconitum Napellus) when cultivated loses some of its toxic properties and that this loss of toxic action occurs in a few generations. Prof. S. M. Tracy informs me that the cultivated forms of the Cassava are not injurious to stock but the wild form, as is well known, contains toxic materials. The wild forms of the lima bean (Phaseolus lunatus) contains much more HCN than the cultivated forms. Dr. Rodney H. True in speaking of the physiological action of the betel nut states that its physiological action 2 depends on several factors. The green nuts produce temporary dizziness. The poisonous variety according to Indian, authorities is one that is reverted to its former wild condition, while the common or ordinary betel nut which has been cultivated for hundreds of years is a mild narcotic stimulant bringing about a feeling of general comfort, good humor and exhilaration. It is also well known that when certain toxic bacteria as Streptococcus pyogenes are cultivated they lose some of their pathogenic properties. We must not, however, conclude that because a plant is cultivated it loses its poisonous properties, because there are certain cultivated ornamental plants that are as poisonous in their cultivaed form as when grown wild. For ex- ample the tobacco which has been cultivated for several hundred years contains as much nicotin in its cultivated as in its primitive form. SOIL. It is believed also that the soil plays an important part in connection with the amount of poison produced in the plant. There can be no question that the soil plays an influence upon the quality of the fruit as well as upon 1 Cyclopedia of American Agriculture. 2:458. 2 Pharm. Review, 14:130. 88 MANUAL OF POISONOUS PLANTS the quality of the grain. Why should it not also influence the poisonous con- stituents of the plant? Cornevin mentions that soil affects the color of Digitalis, it being much paler when grown in calcareous than when grown in granitic soil. RELATED SPECIES AND TOXIC SUBSTANCES. In some cases the same toxic substance is widely distributed in different families of plants. On the other hand closely related plants frequently have entirely different amounts of toxic substances. The bitter and sweet almond illustrate this in a very marked degree, the bitter almond having considerable amounts of the glucoside amygdalin, while the sweet almond is entirely harmless. Frank Rabak x has made an investigation of the amount of the chemical substances found in the kernels of the fresh apricot and plum, in which it ap- pears that the amount of hydrocyanic acid by per cent contained in these plants is as follows :- Per Cent Peach ......... 2.20 Apricot . . . . . . . . .2.40 Apricot ......... 2.05 Prune . . . . . . . . .1.75 Bitter Almond . . . . . . . .4.80 According to Dohme and Engelhardt 2 the thin green or young bark of Prunus serotina is richer in hydrocyanic acid, than the dark brown or older bark. It may be interesting to note that certain species of Cacti are used for stock food,3 and others contain powerful drugs. For instance, the Mescal Bean, which is derived from several species of Anhalonium which contain pel- iotin, is a narcotic of considerable potency.4 According to Dr. Peinemann 5 the alkaloidal-content of Datura varies as follows; the seeds, 0.541 percent.; root, 0.315; leaves, 0.41 percent, of atropin, The Datura alba is richer in alkaloids than the native species, D. Stramonium. Dunstan and Henry6 are authorities for the statement that two forms of Mandrake, the American (Podophyllum peltatum} and the Indian (P. emodi), produce the same principle podophyllotoxin C1(.H14O6 a strong purgative and also the so-called podophyllin which consists of a resin. The podophyllotoxin occurs in the Indian plant from 9-12% and in the American plant from 4-5%. DISTRIBUTION OF CHEMICAL SUBSTANCES. The same chemical sub- stance is frequently found in plants that are not closely related. For instance, Edward Kremers and many other pharmaceutical chemists have found the essential oils in widely separated families, and Greshoff states that a leaf of Five-finger (Potentilla davurica of China) which is closely related to our shrubby Cinquefoil (P. fruticosa) produces a powerful odor of roses. Ger- anoil occurs, for instance, in the young foliage of willow and many other plants. The substance berberin is found in a large number of plants like the Bar- berry, the Mandrake, Twin Leaf (Jeffersonia diphylla), Meadow Rue (Thai- ictrum flavum), Toddalea aculeata, Hydrastis canadensis, Argemone mexicana, etc. 1 Bull. U. S. Dept. Agr., Bur. Plant Industry. 133. 2 Pharm. Review. 14:13. 3 Griffiths and R. F. Hare, The Tuna as Food for Man. Bull. U. S. Dept. Agrl. Bur. Plant Ind. 116. 4 Pharm. Review. 14:153. 5 Pharm. Review. 14:233. 6 Proc. Chem. Soc. 189:42-44. THE PRODUCTION OF POISON IN PLANTS 89 Greshoff x has indicated that a species of Thymus, the Thymus Serpyllus can be readily distinguished from the variety album phytochemically ; the com- mon form of this species (Thymus Serpyllus) produces thymol in its leaves, whereas the other has the odor of lemons. SAPONINS. We may note here the very wide distribution of saponins in different plants. Greshoff in several papers 2 gives a long list of the orders in which saponin occurs,1 many of the others are mentioned in the list of species at the end of this manual. The substance saponin occurs in many different plants of which the fol- lowing is a partial list: Amaryllidaceae : Agave, Fourcroya. Araceae : Arum. Araliceae : Aralia. Begoniaceae: Begonia. Berberidaceae : Berberis, Caulophyllum, Leontice. Bromeliceae: Bromelia. Caryophyllaceae : Acanthophyllum, Arenaria, Dianthus, Gypsophila, Lychnis, Melandryum, Polycarpaea, Saponaria, Silene. Chenopod- iaceae: Chenopodium. Commelinaceae : Tradescantia. Compositae: Arnica, Grindelia, Mutisia. Convolvulaceae : Ipomoea. Cucurbitaceae : Echinocystis, Luff a, Trichosanthes. Dioscoreaceae : Dioscorea. Euphorbiaceae : Phyllanthus? Ficoideae : Trianthema. Filices : Polypodium. Gramineae : Panicum, Lolium. Hippocastanaceae : Aesculus. Illecebraceae : Herniaria. Leguminosae: Acacia, Albiszia, Caesalpinia, Hntada, Enterolobium, Gleditschia, Gymnocladus, Milletia, Mimosa, Pithecolobium, Prosopis, Calliandra, Tetrapleura, Xylia e. a. Lili- aceae: Chamaelirium, Chlorogalum, Helonias, Medeola, Muscari Paris, Poly- gonatum, Smilax, Trillium, Yucca, e. a. Loganiaceae : Buddleia. Magnoli- aceae: IHicium. Meliaceae: Trichilia, Walsura. Melianthaceae : Bersama. Menispermaceae : Stephania? Cocculus? Cosciniumf Myrtaceae : Barringtonia, Careya. Oleaceae: Chionanthus, Syringa. Passifloraceae : Carica? Modecca. Phytolaccaceae : Pircunia. Pittosporaceae : Pittosporum. Polemoniaceae : Can- tua. Polygalaceae : Monnina, Polygala. Primulaceae: Anagallis, Androsace, Cyclamen, Primula, Soldanella, Trientalis, e. a. Ranunculaceae : Ficaria, Nigel- la. Rhamnaceae: Gouania, Zizyphus. Rosaceae: Quillaja, Spiraea. Rubiaceae: Basanacantha, Cephalanthus, Mitchella, Mussaenda, Randia. Rutaceae: Zan- thoxylum. Sapindaceae : Blighia, Dodonaea, Ganophyllum, Koelreuteria, Ma- gonia, Nephelium, Paullinia, Pancovia, Pometia, Sapindus Serjania. More than 100 species of this family contain saponin. Sapotaceae : Achras, Bassia, Lucuma, Omphalocarpum. Saxif ragaceae : Hydrangea. Scrophulariaceae : Digitalis, Leptandra, Limosella. Simarubaceae : Balanites. Solanaceae: Ac- nistus, Lycopersicum, Scopolia, Solanum. Ternstroemiaceae : Camellia, Cary- ocar. Tiliaceae Grewia. Urticaceae : Ficus. Zygophyllaceae : Guapacum, Tri- bulus. HYDROCYANIC ACID. A list of the plants containing a glucoside cap- able of being converted into HCN has been given in another connection, but we may note in this connection plants belonging to many different orders like the Compositae, Huphorbiaceae or Spurge Family, Gramineae or Grass Family, Ranunculaceae or Buttercup Family, Fern, Filices, Droseraceae or Sundew Fam- ily, Saxifragaceae or Saxifrage Family. A common Rocky Mountain shrub, the Jamesia, of this family, is said to contain considerable quantities of HCN, and the Mountain Mahogany (Cercocarpus parvifolius} of the Rose Family (Rosa- 1 Bull. Misc. Information, Royal Bot. Gardens Kew. 1909:415. 2 Kew Bot. Garden 1909:397. Phytochemical Information at Kew. Mededeelingen uit 'S Lands Plantentuin. 29:1909. 90 MANUAL OF POISONOUS PLANTS ceae), contains HCN, and Greshoff says must henceforth be counted among the poisonous plants. Of the Grass Family (Gramineae) quite a number of species such as the Stipa lessingiana, are now known to contain HCN. Some of them like our Stipa robusta, have been known to be toxic for a long time, but such genera as the Quaking Grass, Briza (Catabrosa), Wild rye {Elymus}, Manna Grass (Glyceria), Salt Grass Holcus lanatus all contain HCN. CUMARIN: The substance cumarin also occurs in many different plants which we may list as follows : Talauma (Magnoliaceae) ; Phoenix (Palmae) ; Dipteryx, Toluifera, Mel- ilotus (Leguminosae) ; Prunus (Rosaceae) ; Ceratopetalum (Saxifragaceae) ; Asperula, Basanacantha, Borreria, Diodia, Galiuni, Mitracarpum, Spermacoce (Rubiaceae) ; Ageratum, Chrysanthemum, Eupatorium, Humea, Trilisa, Liatris (Compositae) ; Alyxia (Apocynaceae) ; Hemidesmus (Asclepiadaceae) ; Rhina- canthus (Acanthaceae), Aceras, Angraecum, Orchis (Orchidaceae) ; Hierochloe, Anthoxanthum (Gramineae) ; Adiantum, Cheilanthes, Polypodium (Filices) ; Lactarius, Russula (Fungi). CYTISIN. Greshoff reports cytisin as occuring in the following plants of the Pulse family: Cytisus Adanii; C. alpinus; C. Alschingeri; C. biflorus; C. hirsutus; C. Laburnum, seed 1.8 per cent; C. nigricans; C. polytrichus; C. pro- liferus; C. Weldeni; C. Attleanus; C. candicans; C. formosissimus; C. monspcs- sulanus; C. Ruthenicus; C. scoparius; Ulex europaeus, seed 1 per cent; U. Jussiae; Genista ephedroides; G. monosperma, seed 1.9 per cent; G. florida; G. germanica; G. spicata; G. tinctoria; G. ramosissima; Sophora secundiflora, seed 3.5 per cent; S. tomentosa; S. flavescens; S. sericea; Baptisia perfoliata; B. tinctoria; B. alba; B. australis; B. leucantha; B. versicolor ; Huchresta Hors- fieldii, Anagyris faetida, Rauwerda reported it in 28 species of Lotus, L. suaveolens; Thermopsis Caroliniana; and Th. montana. In some instances apparently the same alkaloidal substance was first reported in some plants, but later investigations have shown that these substances are not identical. For instance Schlotterbeck who investigated the alkaloids found in the poppy family, especially Argemon'ia Mexicana, reported that this plant does not contain morphin but protopin and berberin. CHAPTER XIII IN WATER SUPPLIES Algae have long been known to be injurious to water supplies and numerous papers in the United States and Europe have discussed some of the problems arising therefrom. Algae are generally small, microscopic plants found in water and belong to the great class known as Thallophyta. These frequently cause the pollution of water supplies and are therefore of first importance in this connection. Some algae contain a green coloring matter called chlorophyll and hence they are able to make their own food out of water and carbon dioxid. Many of the algae, however, are not green, some being blue, others red, and still others brown. The Sea Mosses are algae also, and occasionally attain great size and length. Some algae are supposed to be injurious to stock, Mr. George Francis in Australia having attributed a disease of horses, sheep, dogs, and pigs to some blue-green algae. The organism causing the trouble in this case was referred to Nodularia spumigera, which floats on the water and, being wafted to the lea shores, forms scums from two to six inches thick. He says that, when animals drink the water, it acts as a rapid poison and causes death. It first produces stupor and unconscioueness, the animal falling and remaining quiet, as if asleep, unless touched, when convulsions come on, with head and neck drawn back by rigid spasms which subside before death. This, in sheep, takes place in from 1-6, or 8 hours; in horses, in 8-24 hours; in dogs, in 4-5 hours ; and in pigs, in 3-4 hours. A post mortem was made on a sheep that had 30 ounces of fresh scum administered by mouth, death occurring in 15 hours. The post mortem, 6 hours later, showed that the stomach had none of the green scum left, all having been absorbed; the abdominal cavity contained 2 pints of yellowish material; the heart was flaccid with effusion of serum around it ; lungs, liver, kidneys, and brain normal ; dura mater enlarged ; blood of ventricles and arteries black. It was thought that poisoning was due to the decomposition of the algae which smelled like putrid urine, previous to this it had an odor like butyric acid. Account was not taken of the products of decomposition by bacteria. The trouble may have been caused by the poison- ous products of bacteria rather than these algae. This seems not have occurred to Dr. Francis. Many of the algae, especially the following, Anabaena, Clathrocystis and bacteria-like Beggiatoa, produce what is known as the working of the lakes and pig pen odors. Dr. Farlow has described these from Massachusetts and Dr. Trelease has described them for the lakes about Madison, Wisconsin. The greenish-yellow scum occurs on the surface of the lakes, especially noticeable during hot weather of the summer. Dr. Trelease says : When a lot of it is present, it appears as fine granules suspended in the water, scarcely visible to the naked eye except as they reflect the light, when they call to mind the dancing motes in a beam of sunlight. Under the influence of a gentle, but continuous breeze, these particles are collected into fleshy masses and are driven ashore, so that they accumulate along the margins of the lake, forming a slimy scum, which quickly putrefies, giving off a very disagreeable odor. During this change, its color changes to a decided 92 MANUAL OF POISONOUS PLANTS Fig. 19. Algae found in water supplies, a. Protococcus. b, c. Cosmarium, one of the desmids. d. Pediastrum. e. Oscillatoria. f. Nostoc paludosum. g. Closterium, chr — chromatophore. h. Pandorina; 1, gelatinous envelope; 2, cilia, i, j. (Anabaena flos-aquae). k. Botrydium granulatum; 2, rhizoids. I and m. Diatoms, n. Zygnema; 1, chromatophore; 2, zygospores. o. Spirogyra; 1, 2, 3, 4, different stages in the formation of the zygospores. p. Draparnaldia', 2, thallus. q. Stone-worts (Chara) ; 1, antheridium; 3, archegonium; 5, nodal cells, r. Portion of antheridium with sperm cells. ALGAE IN WATER SUPPLIES 93 blue green, which stains the pebbles, sticks, etc., over which it is smeared. The appearance of this scum is sometimes spoken of as the working of the lakes, from the resemblance to the collection of scum on cider, etc., when fermenting, or, as an idiom expresses it, "working." The odor given off by this putrefaction can be detected from some distance. In speaking of the water bloom, Prof. Dwight C. Marsh says : This phenomenon is especially marked in Lake Winnebago in some summers. It is due, of course, to the enormous growth of the plants of the plankton, that growth being particularly fostered by the hot weather of midsummer. The plants especially concerned in forming the bloom are Clathrocystis, Anabaena, Aphanizomenonfi Oscillaria, Lyngbya, and Gloiotrichia. .The times of occurrence of these plants have already been noticed in the dis- cussion of the individual constituents of the plankton. At the middle of August, in some summers, on a still day, the surface of Lake Winnebago is apparently a solid, opaque green. Some of this material decomposes, and as the currents slowly move along the surface material, it shows a wavy streaked appearance like the surface of polished malachite. Its intrinsic beauty, however, does not attract the average person, for he looks upon it as "scum," and he thinks of it simply as an evidence of filth. This material is thrown upon the shores by the waves until the rocks alongshore are completely covered with it, and it may in its decay become very offensive. Following the maximum period of the "bloom," Cladophora appears and covers the littoral rocks with a thick mat of green. This great growth of "bloom" naturally attracts the attention of the non-scientific observer, and many absurd explanations of its appearance are given. The most common one in Oshkosh is that it is a mass of seeds coming from the marshy shore of the Fox and Wolf above Ohkosh. Doubtless the Anabaena and Gloiotrichia have given rise to the supposition that the bloom is a mass of seeds. The decomposition of Gloiotrichia produces a blood red coloring matter which is sometimes very noticeable on the shores of Lake Winnebago, and has led people to question as to whether the lake is not affected by one of the plagues of Egypt. When the water is still the plants of the bloom are in greatest abundance, close to the surface, and are distributed very uniformly over the lake. Frequently, in the latter part of July and in August, there may be seen floating about yellowish green masses of a more or less spherical outline, perhaps as much as three inches or more in diameter. These masses, which are composed of aggregations of Aphanizomenon mingled with scattered fronds of Gloiotrichia and Anabaena, have very little coherence and elude the collector by falling in pieces almost at a touch. As is evident from the discussion of the occurrence of the algal constituents of the plankton, the bloom is not a prominent feature of the deep lakes, — in fact, in some years the growth of these algae is hardly noticed by the ordinary observer,— and of the shallow lakes few seem to produce as large an amount as is seen in Lake Winnebago. Of the lakes under observation, Shawano and Pelican were the only ones that could be compared at all with Lake Winnebago. Odors produced by the decomposition of organic matter in water are easily detected. Sometimes they are grassy and sometimes mouldy or musty. Some- times the odor is decidedly fishy, which is especially true of some of the higher plants like Myriophyllum or Potamogeton. Mr. Whipple* says that the cucum- ber taste found in the Boston water supplies was due to a fresh water sponge. He made a series of experiments with oil of peppermint and other oils and he found that the oil of peppermint could be recognized when the dilution was 1 to 50,000,000; oil of cloves, 1 to 8,000,000; cod liver oil, 1 in 8,000,000. Kerosene oil could not be detected when diluted to 1 in 8,000. Accord- ing to Whipple, aromatic odors are produced by certain diatoms ; grassy odors are produced by certain blue-green algae like Anabaena and Rivularia; the sweet grassy odor is produced by Clathrocystis; Volvox produces a fishy odor, while Pandorina and Eudorina produce a faintly fishy odor. Certain protozoa produce fishy and oily odors. Perhaps the most extensive investigation of microscopical organisms in water are those reported by the Massachusetts State Board of Health. Special methods for determining the amount of impurities found in water are given in these reports. Prof. Parker has shown that when the odors are pronounced the organisms are always? present in considerable numbers. He says : 94 MANUAL OF POISONOUS PLANTS The majority of organisms which have been recorded are of microscopic size. At first sight it might appear that these organisms would be insignificent in proportion to their mass, and that more attention should have been devoted to the larger plants and animals. Very few cases have been observed, however, in which really serious trouble in water supplies can be referred directly to the growth of large plants or animals; whereas, in many in- stances, waters with very objectionable qualities contain nothing to which these qualities can be attributed except microscopic organisms. Further, although the organisms here dealt with are of such small dimensions, the immense numbers in which they occur more than counterbalance their small size; and I am therefore, of the opinion that, of those organisms which cause objectionable qualities in water, the microscopic ones are the more important. HOW GROWTH OF ALGAE IN WATER MAY BE PREVENTED The growth of algae may be prevented by covering the reservoir; since light is essential for their growth, they will not develop in a closed reservoir, and we hear of little complaint under such conditions. Large reservoirs for public water supplies are not generally covered. Often reservoirs are much troubled by algal contamination ; in some cases it becomes necessary to remove these by a laborious method. The removal of organic matter by keeping the source of the water supply in as pure condition as possible will no doubt do something toward keeping algae out, but nearly all water contains sufficient organic matter for the growth of algae, especially water coming from water sheds. THE USE OF ALGICIDES Within recent years much work has been done in preventing the growth of algae and bacteria by copper sulphate solutions. Moore and Kellerman in a recent paper arrive at the following conclusions: The disagreeable odors and tastes so often present in drinking water are due almost exclusively to algae, although the economic importance of studying these plants has not been recognized until recent years. These algal forms are widely distributed, and reservoirs in many states have been rendered unfit for use by their presence. It has been found that copper sulphate in a dilution so great as to be colorless, tasteless, and harmless to man is sufficiently toxic to the algae to detroy or prevent their appearance. At ordinary temper- atures one part of copper sulphate to 100,000 parts of water destroys typhoid and cholera germs in from three to four hours. The ease with which the sulphate can then be elimin- ated from the water seems to offer a practical method of sterilizing large bodies of water when this becomes necessary. The cost of material for exterminating algae will not exceed fifty to sixty cents per million gallons and will usually be less. The destruction of patho- genic bacteria requires an expenditure of from $5.00 to $8.00 per million gallons, not including the cost of labor. It has been found that Spirogyra will die in water containing one part of copper to one billion parts of water. Some of the algae like Anabaena are destroyed in dilutions from one to five million, although Moore and Kellerman found that one species of Spirogyra requires a greater strength of solution. There is a wide-spread opinion that metallic copper and copper salts are in- jurious, which is certainly true when the same are taken in larger quantities. According to Tschirsch, .05 to .2 of copper sulphate causes vomiting and diar- rhoea. In the paper cited, Moore and Kellerman write as follows : It is evident that there is still a considerable difference of opinion among eminent authorities as to the exact amount of copper which may be injurious, but as a «very con- servative limit we may accept 0.02 gram as the amount that may with safety be absorbed daily. According to Merck's Index, the National Dispensatory, and the United States Dispensatory, the dose of copper sulphate for tonic and astringent purposes is one-fourth grain, or 0.016 gram; as an emetic, a dose of five grains, or 0.33 gram. Thus it is seen that even if the maximum concentration of copper sulphate necessary to destroy algae in reservoirs were maintained indefinitely, the absorption from daily use would be very far below an amount that could produce the least unpleasant effect. Taking a dilution of one ALGAE IN WATER SUPPLIES 95 to one million, which in all cases would be sufficient to prevent the growth of a polluting algal form, it would be necessary to drink something over twenty quarts of water a day before an amount which is universally recognized as harmless would be introduced into the system, while more than fifty quarts would have to be consumed before there would be danger of producing an unpleasant or undesirable effect. As will be seen from the pre- ceding tables the use of copper sulphate at this maximum strength of one to one million would need to be resorted to only in extreme cases, and for a very short length of time, for, the reservoir once entirely free from the organisms, a very much weaker solution would be sufficient should any further application be necessary. The Report of the Massachusetts State Board of Health for 1905 stated as follows : The objectionable tastes and odors of pond and reservoir waters, which are often at- tributed to decaying fish and other causes, are, in practically all cases which have been brought to the attention of the Board, caused by the presence of organisms, in some cases of kinds which attach themselves to the sides and bottom of the reservoir, but in the majority of cases of those kinds which live in suspension in the water. Early in 1903, Dr. George T. Moore formerly Algologist of the United States Department of Agriculture, brought to the attention of the Board the results of investigations which he had made, indicating that the microscopic organisms which are the chief cause of objectionable tastes and odors in the waters of ponds and reservoirs could be destroyed by applying sulphate of copper or blue vitrol to the water in very small quantities; and information was also submitted tending to show that bacteria were also destroyed in water brought in contact with metallic copper. The results of some of the experiments and investigations so far as obtained tend to support the conclusions which had been reached when the matter was first brought to the attention of the Board as to the practicability of the copper treatment for the removal of growths of organisms and bacteria, but the results of other experiments conflict with some of these conclusions. Further study and experiment are necessary before the probable results of the use of copper in preventing objectionable conditions resulting from growths of or- ganisms, or the probable effect of the use of this substance in public water supplies upon the public health can be conclusively determined. Dr. Moore states that : Spirogyra is often the cause of considerable trouble in a mechanical v/ay, and on account of its method v of forming resting spores is usually able to withstand the most unfavorable conditions to which it may be subjected in a pond or reservoir. In at least one instance this alga has been the cause of the loss of thousands of dollars by the damage it produced in smothering out the young water-cress plants in the artificial beds constructed for the winter propagation of this vegetable. When the cress is cut for market, it necessarily leaves the plants in a weakened condition, and if the Spirogyra gets a start it will form a thick, heavy mat over the water, which is sufficient to prevent the growth, if not entirely to kill, the cress plants. CHAPTER XIV A CATALOGUE OF THE MORE IMPORTANT POISONOUS PLANTS OF THE UNITED STATES AND CANADA For the purpose of facilitating a study of the poisonous plants of this coun- try a partial catalogue is given here. It is based in part on a catalogue of the poisonous plants of Iowa,* issued by the writer and Estelle D. Fogel (Buchan- an). To further facilitate the study of the poisonous plants the following papers on the subject should be mentioned: Chesnut,1 Chesnut & Wilcox,2 Wilcox,3 Nelson,4 O'Gara,5 Kennedy,6 Peters, Slade & Avery,7 Glover,8 Crawford,9 Heald & Peters,™ White," John- son,12 Bessey,:3 Rusby,z4 Guttenberg^s, Pammel,16 Millspaugh,1? Coville,18 Peck,'9 J. U. & C. G. Lloyd,2o Stebler & Schroeter,2i Schaffner,22 R. Schimpfky.23 Winslow,24 Farlow,25 Maiden,26 Atkinson,2? Greshoff,2* Wilson,2^ Cor- nevin,3Q Halsted,3i Kobert,32 Crawford,33 and Marsh.34 *Proceedings of the Iowa Academy of Science. 14:147-172. Contributions, Department of Botany, Iowa State College. 37:147-176. 1 Principal Poisonous Plants of the United States, Div. Bot. U. S. Dept. Agr. 20-60, £34. Thirty Poisonous Plants of the United State, U. S. Dept. Agr. Farmers Bull. 86:32, f24. Rep. Bu. An. Ind. 15:387-420, f69. 2 The Stock Poisoning plants in Montana, Bull. Div. Bot. U. S. Dept. Agr. 26:150, pi. 36 3 Rep. Bu. An. Ind. 17:91-121, p. 32. 4 Feeding Wild Plants to Sheep, Rep. Bu. An. Ind. 15:421-425. 5 Rep. Nebr. Agr. Expt. Sta. 16:14-84, f. 13. 6 Bull. Nev. Agr. Expt. Sta. 51-57, pi. 26. 7 Poisoning of Cattle by Common Sorghum and Kafir Corn, Neb. Agr. Expt Sta. 77-16 8 Bull. Col. Agr. Expt. Sta. 113:24, pi. 8. 9 The Poisonous Action of Johnson Grass, Bull. Bur. Pi. Ind. 90, part 4. 10 Ergot and Ergotism, Press Bull. Nebr. Agr. Expt. Sta. 24, f. 3. 11 Dermatitis Venenata, An Account of the Action of External Irritants upon the Skin 216:1887. 12 A Manual of the Medical Botany of N. Amer. p. 292, pi 9, f 160 13 Bull. Dept. Bot. 1884. Proc. Soc. Prom. Agr. Sci. 23:35-41. 14 Poisonous Plants of the Vicinity of New York City, 19. 15 Poisonous Plants which Grow in and around Erie, 21:25 Q* 9Q%?cV»i<