By W. T. OLIVER*
Toxicology, the science of poisons, is the facet of pharmacology dealing with source, chemical and physical properties, actions, and detection of poisons. In this article, a poison is considered to be any substance which by its direct and usual chemical action on body tissues, internally or externally, can disturb health or destroy life. This arbitrary definition excludes infectious and mech- anical agents and those compounds which, like water, are noxious only in massive doses. Sources: The sources of poisonous substances are many and varied. A partial list includes: a) paints - chromium, boiled linseed oil, lead; b) batteries - lead, corrosives; c) insecticides - arsenic, sodium fluoride, organophosphates (lindane, parathion); d) rodenticides -Antu, thallium, Warfarin, squill, phosphorus, strychnine; e) fertilizers - nitrates, phosphates; f) venoms - snake, toad; g) roofing paper - coal tar products; h) drinking water - arsenicals, fluorides, sulfates, nitrates, nitrites; i) noxious gases - carbon monoxide, carbon dioxide; j) disinfectants - coal tar (phenol, cresol), lye, chlorines; k) shot - lead; 1) fungicides - copper sulfate, mercurials; m) herbicides - chlorates, sodium fluoride; n) depilatories - sulfides; o) dry cleaning agents - chlorinated hydro- carbons; p) moth crystals - naphthalene; q) bleaches - chlorine; r) gasoline - lead, petroleum products; s) Lye - sodium hydroxide; t) antifreeze - diethylene glycol; u) therapeutic agents - ointments, laxatives, liniments, etc; v) toxic plants and algae - cyanogenes, glycosides, alkaloids. The poison content of plants depends, among other factors, upon the age of the plant. Sorghum and cocklebur are most poisonous when the plant is young whereas the swamp sunflower and lupen are more toxic when mature. Plants such as wild cherry, sweet clover, cornstalk, and rape, are dangerous after wilt or some other degen- erative change has occurred. Materials The materials submitted for analysis should be selected on the basis of history, symptoms, and pathology. Tissues should be frozen if possible and shipped in sealed, chemically-clean containers. Preserving sealers are suitable for this purpose. Since conditions which produce putrefaction have little effect on the majority of poisons, preservatives are not required and must not be added to the specimens. Such agents have the disadvantages of reacting with many chemical compounds and of hardening tissues, making them less susceptible * Ontario Veterinary College, Guelph, Canada. [382] Canadian Journal of October, 1956 rQQQl Comparative Medicine Poisons and PoisoningPiongVol. XX, No. 10 L383J to the action of solvents used for extraction of the poison. It is recommended that a separate container be used for each tissue. Inclusion of ingesta and, for example, liver, in the same container may result in a mechanical transfer of a toxic agent from the ingesta to the liver and so indicate to the analyst that absorption of the compound had occurred prior to death. The brain, liver, and kidney, are valuable for analyses in cases of suspected poisoning by volatile and non-volatile compounds. The latter two organs are particularly important in poisoning by heavy metals. Stomach contents should be submitted in cases of poisoning. The contents can be used for screening procedures, the detection of corrosives by pH estima- tion and, at times, to indicate the amount of poison which was ingested by the animal. Urine may be included if acute fluorosis or lead is suspected; or bone, if there is evidence of chronic fluorosis. Blood is a convenient medium for the determination of sulfonamides and barbiturates. Hair can be used for the de- termination of chronic arsenic poisoning. Lung tissue is chiefly of value in cases of poisoning by volatile agents, rare in veterinary medicine. Symptoms: The diagnosis of poisoning usually is not simple. Although a poison may produce particular symptoms, none is characteristic for that poison to the exclusion of all other agents. The sudden and almost simultaneous onset of similar symptoms among a number of animals, previously in good health, especially in the absence of an elevated temperature, suggest poisoning. The condition may be associated with a change of pasture, water supply, or feed; it may follow therapeutic measures or the handling of certain pesticides. The symptoms produced by a drug depend upon its mechanism of action. Arsenic and Warfarin affect the vascular system, the former by destroying the in- tegrity of the capillaries, the latter by interfering with the clotting mechanism. Nicotine and the organo-phosphate insecticides affect nerve impulse transmis- sion, the former by raising the refractive threshold of the ganglionic cells to acetylcholine, the latter by competing with acetylcholine for cholinesterase. Among the systems and tissues which may be affected by the more common poisons are: Central Nervous System. (a) stimulated: cyanide, ergot, strychnine, picrotoxin, caffeine, DDT, lindane.,. nicotine. (b) depressed: barbiturates, chloroform, cannabis, chloral, opium, mercV1r7 carbon disulfide, carbon tetrachloride. (c) sensory disturbance: 1384] CoanadianveJournalCmaaieMedicineof Poisons and Poisoning Vol.October,XX. No.195610 1. pain: acids, alkalis, arsenic, lead, mercury, organophosphate insecticides. 2. vision: arsenic, lead, aspidium, sodium chloride. 3. paraesthaesia: cannabis, mercury, thallium. Mucus membranes. (a) eroded: acids, alkalis, nicotine coal tar disinfectants (cresols). (b) anaemic: arsenic, cocaine, lead, sulfonamides, ergot, amphetamine. (c) haemorrhagic: dicumarol, Warfarin, corrosives. (d) cyanotic: barbiturates, cyanide nitrites, chlorates, nitrobenzene, sulfo- nilamide. (e) icteric: phosphorus, carbon tetrachloride, arsenic. Skin, and appendages. (a) eroded: acid, alkalis. *(b) depilated: selenium, sulfides, thallium. (c) wounds: snake bite, shot. (d) exostoses: fluorine, selenium. Alimentary tract. (a) diarrhoea: arsenic, mercury, organophosphate insecticides. (b) constipation: lead, opium, ergot. (c) vomition: antimony, mercury, copper, zinc, nicotine, strychnine, carbon bisulfide. (d) colour: red - phenothiazone greenish - copper sulfate, copper arsenate, phenothiazine fluorescence - phosphorus black - lead. Urine. (a) frequency: 1. polyurea: mercury, digitalis, nitrates, caffeine. 2. oligourea: arsenic, cantharides, sulfonamides. (b) haematurea: arsenic, cantharides, mercury, sulfonamides. (c) colour: red (phenothiazone), orange (santonin), green (phenothiazine). (d) odour: violets (turpentine). Pupil. (a) dilated: atropine, barbiturates, morphine (dog and rabbits), cocaine. (b) constricted: organophosphates, opium, ergot, morphine (cat). Lesions: Post mortem lesions constitute an important guide for the analyst. A poison usually produces particular structural changes but since its pathogenesis is dependent upon such variables as concentration of the poison, chemical form, route of absorption, individual and species susceptibility, not all of the char- acteristic alterations may be present in a single animal. At times the autopsy Canadian Journal of Poisons and Poisoning Vol. Xe, No. 10 Comparative MedicineVo.X N.0 [385 findings may give little indication of the toxic substance. Animals which are persistent refuse eaters may develop a chronic gastritis. Should such an animal die of strychnine poisoning and the only report available to the analyst be one on gross pathology, it is improbable that the agent would be suspected since death by strychnine, as by most alkaloids, is characterized by a lack of dis- tinctive gross lesions. For this reason, history (including habits), and symp- toms are valuable adjuncts to a thorough post mortem examination. The lesions which may be observed during necropsy are: Rapid rigor mortis: fluorides, strychnine Haemorrhage: (a) general - coumarin, Warfarin (b) discrete: arsenic, mercury, lead, phosphorus, benzol, ergot, benzene, bracken, cyanide, nitrate, nitrite, chlorinated hydrocarbons, magnesium sulfate. Inflammation: (a) gastro-intestinal tract: acids, alkalis, heavy metals, chlorine, coal tar dis- infectants, bismuth, chloroform, formaldehyde, nicotine, halogens, croton oil, castor oil, squill, carbon bisulfide, Antu, ergot, sodium chloride, cyanide, aspidium, copper, arsenic. (b) liver: carbon tetrachloride, DDT, mushroom (Amanita phalloides), phosphorus. (c) kidney: coal tar disinfectants, (phenol, cresol), bromates, chlorates, arsenic, camphor, lead, mercury. Oedema: (a) gastrointestinal: arsenic, ergot, oak buds. (b) lungs: opium, chlorine, chloral, Antu, organophosphate insecticides, pitch, selenium. (e) brain: arsenic, lead, fluoride, sodium chloride, chenopodium, iodine. Necrosis: (a) liver: benzene, heavy metals, diethylene glycol, fluorine, thallium, wood alcohol, carbon bisulfide, barbiturates, chloral, alum, magnesium sulfate, iodoform, carbon tetrachloride, chenopodium, chlorates, nitrites, DDT, Antu, iodine, pitch, arsenic, lead, mercury, selenium, bracken, rotenone. (b) kidney: coal tar disinfectants, chlorates, diethylene glycol, alkali, mercury bichloride, bismuth, sulfonamides, fluorine, thallium, DDT, barbiturates, chenopodium, iodine, bromates, chlorates, nitrites, methy- lene blue, colchicine. (c) CNS: arsenicals, cyanide, carbon disulfide, barbiturates. (d) bone: phosphorus, mercury. (e) brain: DDT, sodium chloride. Canadian Journal of October, [3861 Comparative Medicine Poisons and Poisoning Vol. XX, No.196610 (f) spleen: arsenic. (g) lungs: phosgene, mercury. (h) heart: mercury, arsenic, chloral, selenium, sodium, nitrite, phenol. Blood: (a) colour: cherry red (cyanide borates), dark brown (benzene, alkalis, colchicine, sodium fluoroacetate, nicotine), tarry (phosphorus). (b) low viscosity: chloral, cyanide, trichloroethylene, colchicine. (c) hemolysed: arsine, aspidium, snake venom. (d) delayed clotting: cyanide, fluoride, phosphorus, mercury, Warfarin., di- coumarol. Odour: phenols (carbolic); phosphorus, tellerium, selenium (garlic) ; hydrogen cyanide (almonds); camphor, alcohol, benzene, and many others have a characteristic and individual odour. SUMMARY Sources of common poisons and their effects upon various systems and tissues together with methods for selection and shipping of specimens have been considered. RESUME L'auteur traite de la source des poisons les plus communement rencontres et des effets de ces poisons sur les divers appareils et tissus de l'economie. II traite aussi du choix des prelevements et de leur mode d'expedition au labo- ratoire.
OMEGA TAU SIGMA Fraternity Grand Council Meeting November 2nd, 1956 at the Ontario Veterinary College, Guelph, Ontario
Wm. Barnes, 51 Dundas Rd., Guelph, Ont. Secretary. CALCIUM VERSENATE IN TREATMENT OF LEAD POISONING Chelating agents are being increasingly used in human and veterinary -medicine. Calcium versenate (EDTA), one of these complexing agents, appears to be of value in the treatment of lead poisoning in man, horses, and cattle, Holm et al (J. Amer. Vet. Med. Assoc. 123: 528, 1953) and Lewis and Meikle (Vet. Rec. 68: 98, 1956). In the presence of lead which is ionised or loosely absorbed to protein, the calcium in the calcium versenate is replaced by the lead to form a non-ionisable, non-toxic compound. Recovery may be expected even from acute lead poisoning.
LYMPHOMATOSIS REVIEW The laboratory staff of the Regional Poultry Research Laboratory, East Lainsing, Michigan, have prepared a circular (U.S.D.A. No. 970) on lympho- matosis in chickens, in which they review the literature, discuss the various manifestations of the disease, and emphasize the importance of selective breed- ing and control. Forty references are included.
CONGENITAL INFECTION WITH JOHNE'S BACILLI The finding of Johne's bacilli in foetuses from a certain proportion of cattle with Johne's disease, has been reported recently by Pearson and McClel- land (Vet. Rec. 67: 615, 1955) and Lawrence (Vet. Rec. 68: 312, 1956). One of the five positive foetuses examined by Lawrence was from a cow from a Johne's disease-infected herd, which showed neither clinical symptoms nor detectable lesions at post-mortem.
EXUDATIVE DERMATITIS IN PIGS Jones (Amer. J. Vet. Research, 17:179, 1956) has described a study of acute dermatitis involving 3055 immature swine, 5 to 35 days old, from 20 droves in the State of Iowa; the morbidity was 28.8 per cent, the mortality 19.5 per cent. The condition was characterized by hyperhidrosis, excess seba- ceous secretion, exfoliation and exudation, and was usually accompanied by secondary bacterial infection. The disease is being reported with increasing frequency. [387]