CANTHARIDES
Cantharides—Cantharis vesicatoria (N.O. Coleoptera)—is seldom given as a poison, but is most frequently employed to procure abortion, or for its supposed aphrodisiac properties.
Cantharides is a pure irritant. Applied externally, it produces vesication; and if absorbed, strangury.
Cantharidine—the active principle of Cantharides—is insoluble in water and bisulphide of carbon. It is but slightly soluble in alcohol, but it is dissolved by chloroform, ether, and some oils. Four parts of cantharidine have been procured from a thousand parts of the flies.
Symptoms.—An acrid taste is first experienced in the mouth, followed by a burning heat in the throat, stomach, and abdomen. There is constant vomiting of bloody mucus, and the stools also contain blood. The patient complains of intense thirst, pains in the loins, and an incessant desire to void urine, which is frequently mixed with blood. Salivation in some cases is a prominent symptom. Strangury may result from the external application of cantharides as a blister, &c. Priapism is often obstinate and painful, and the fatal termination is generally ushered in by violent convulsions and delirium. In pregnant women, abortion may take place as a result of the general irritation and disturbance of the system, there being no proof that the uterus is particularly affected by the drug. The vomited matters may contain shining green particles, the presence of which indicates the nature of the poison taken. The invasion of the symptoms may in some cases be retarded.
Post-mortem Appearances.—Those of powerful irritation. The mucous membrane of the whole alimentary canal, from the mouth to the rectum, has been found in a state of acute inflammation. The uterus, kidneys, and internal organs of generation share also in the general irritation, ulceration of the bladder having been met with in some cases. Portions of the wings and elytra are sometimes found adhering to the coats of the stomach.
Fatal Dose.—One ounce of the tincture has caused death in fourteen days. This is perhaps the smallest fatal dose on record. Six ounces have been stated to have produced no dangerous symptoms. The worthlessness of the preparation may account for this result.
Treatment.—Vomiting should be promoted and warm mucilaginous drinks given. If vomiting be absent, emetics should be administered. Oil should not be given, as it dissolves out the active principle. Opium may be given with advantage.
Chemical Analysis.—The contents of the stomach should be concentrated and then treated with chloroform, filtered, and the filtrate allowed to spontaneously evaporate. A portion of the residue should then be placed on the skin, and the presence or absence of vesication noticed. Examined under the microscope, portions of the wing-cases may be detected. No change of colour is produced in cantharidine by the action of sulphuric or nitric acid, thus distinguishing this substance from any of the vegetable alkaloids.
PUTREFACTIVE OR BACTERIAL
ALKALOIDS
The processes by which complex and highly organised substances are broken up into their primary elements are largely synthetical. The putrefactive processes brought about by the action of bacteria result in the formation of special products, some of which combine with certain mineral and vegetable acids to form definite chemical salts; in this respect they correspond with inorganic and organic bases. These products are called ptomaines, a name suggested by an Italian toxicologist, Selmi, and it is derived from the Greek word πτῶμα, a cadaver or corpse.
On account of their basic properties, resembling the vegetable alkaloids, they are called putrefactive or bacterial alkaloids. They have been called animal alkaloids, but some ptomaines may be produced by the action of bacteria upon vegetable proteids; so this term is not strictly applicable, and should be restricted to those basic bodies or “leucomaines” that result from metabolism of the tissues in the animal body.
The essential element of their basic nature is nitrogen, and in this they resemble the vegetable alkaloids. Some contain oxygen, like the fixed alkaloids, while others do not, like the volatile alkaloids nicotine and conine. The kind of ptomaine formed depends upon the nature of the bacterium, the material upon which, and the conditions under which, it grows; the amount of oxygen present; the temperature and the period of growth. All ptomaines are not necessarily poisonous. Albumin is the origin from which all alkaloids, vegetable or animal, are derived. The following is a list of the principal ptomaines:
Methylamine, CH₃NH₂.—Found in herring brine and decomposing fish—non-poisonous.
Dimethylamine, (CH₃)₂NH₂.—From putrefying gelatine, yeast, fish, and sausage—non-poisonous.
Trimethylamine, (CH₃)₃N.—Various decomposing animal and vegetable tissues, ergot—poisonous in large quantities.
Ethylamine, C₂H₅NH₂.—Beet-sugar, wheat-flour—non-poisonous.
Diethylamine, (C₂H₅)₂NH₂.—Putrid fish and sausage—non-poisonous.
Triethylamine, (C₂H₅)₃N.—Putrid fish and sausage—non-poisonous.
Propylamine, C₃H₇NH₂.—From cultures of bacteria of fæces—non-poisonous.
Butylamine, C₄H₁₁N.—From cod-liver oil. Diaphoretic and diuretic—in large doses causes vomiting and stupor.
Iso-amylamine, (CH₃)₂·CH·CH₂CH₂NH₂.—Decomposing yeast and cod-liver oil—active poison, causes convulsions and death.
Caproylamine, C₆H₁₅N.—Called septicin by Hager.
Collodine, C₈H₁₁N.—The first ptomaine obtained in a chemically pure condition—from putrid horse flesh, pancreas, gelatine, and mackerel.
Hydrocollodine, C₈H₁₃N.—Putrefying horse flesh and mackerel—highly poisonous.
Parvoline, C₉H₁₃N.—Putrid horse flesh and mackerel.
Unnamed base, C₁₀H₁₅N.—From decomposing fibrin and jelly-fish. Like curare in its action.
Putrescine, C₄H₁₂N₁₂.—From human corpses—feebly poisonous.
Cadaverine, C₅H₁₆N₂.—From human corpses—causes suppuration.
Neuridine, C₅H₁₄N₂.—Common product of putrefaction—quite inert.
Neurine, C₅H₁₃NO.—From human corpses, intensely poisonous—resembles muscarin in its action.
Choline, C₅H₁₅NO₂.—From putrefying animal and vegetable substances—feebly poisonous; by giving up one molecule of water it changes to neurine—this may be brought about by bacteria or chemical agencies.
Muscarine, C₅H₁₃NO₂.—From putrid fish and horse flesh. The active principle of poisonous mushroom.
Gadinine, C₇H₁₆NO₂.—From putrefying codfish, haddock, and gelatine, in pure cultures of proteus vulgaris—poisonous in large quantities.
A Base (?), C₇H₁₇NO₂.—From decomposing horse flesh—its action is like curare: causes loss of temperature, rigors, convulsions, and general paralysis: the heart stops in diastole.
Mydaleine.—Composition not determined—from human corpses—actively poisonous.
Even after prolonged periods and with access of air, any putrefactive alkaloids which may form do so in very small quantities, and they are very unstable. In their chemical reactions they respond to many of the group-tests used for alkaloids, but they differ in their reaction to the special tests used for vegetable alkaloids. There is no test that will differentiate between putrefactive and vegetable alkaloids, as a class; at the same time no putrefactive alkaloid will give the same chemical reactions, and have the same physiological properties, as any one of the vegetable alkaloids.
Neurine was first obtained by Liebreich by boiling protagon with concentrated baryta. Since then it has been extracted from putrefying animal tissues. The free base is strongly alkaline, and gives a white cloud with the vapour of hydrochloric acid. It is intensely poisonous, resembling muscarine in its action. Very small quantities cause complete paralysis in frogs. Respiration ceases first, and the heart beats become more and more feeble, until it stops in diastole. If atropine be now injected the heart begins to beat again.
As a defence set up in cases of poisoning, when one or other of the rarer alkaloids has been used, it has been suggested that the poison discovered in the body of the deceased was due to the processes of putrefaction of the tissues themselves. In view of this it is important to know the toxic power of such putrefactive alkaloids as may be found in the human cadaver.
Two only of these are actively poisonous—neurine and mydaleine; others are toxic in so small a degree that large amounts would be required to produce lethal effects, far more in proportion to the body weight than any vegetable alkaloid for which it may be alleged they have been mistaken.
Neurine does not appear before the fifth or sixth day after death, mydaleine not until the seventh day, and only in traces; it does not appear in amount sufficient for quantitative analysis until the end of the second or third week.
At the period after death when a medico-legal analysis has generally to be made, choline is the only alkaloid present, and it is but feebly poisonous.
In rabbits neurine causes marked salivation and increased flow of secretion from the eyes and nose. The heart beats more quickly at first, but gradually slows down and stops in diastole. There is increased peristalsis of the intestines with profuse diarrhœa. There is narrowing of the pupil both after injection or local installation. Clonic spasms and violent convulsions occur, and are followed by paralysis first of the hind then of the fore legs, ending in death. The symptoms are prevented or relieved by atropine.
If atropine be injected first the poisonous effects of the neurine do not show themselves.
Mydaleine was discovered by Brieger in putrefying cadaveric organs. Small doses injected into guinea-pigs cause profuse lachrymation and coryza.
The pupils dilate and then become motionless. The temperature rises from 1° to 2° Centigrade. There is somnolence at this stage, with increased intestinal peristalsis. The pulse and respirations are quickened; later these with the temperature return to the normal, and the animal recovers. Large doses cause death with the heart in diastole and the intestines contracted.
Clonic spasms and stupor precede death.
The Extraction of putrefactive alkaloids from organic matters may be carried out by the process for alkaloid extraction ([vide p. 335 et seq.]).
Amongst the attempts made to distinguish the putrefactive from vegetable alkaloids by chemical reactions one method was based on the rapid reduction of potassium ferricyanide to the ferrocyanide. After converting the alkaloid to a sulphate, a solution of it is mixed with a drop of potassium ferricyanide and a drop of ferric chloride added: the deep blue colour of Prussian blue is produced if reduction to the ferrocyanide has taken place. However, certain vegetable alkaloids, viz. morphine, aconitine, eserine, and hyoscyamine act rapidly as reducing agents upon the ferricyanide. Emetine, igasurine, nicotine, colchicine act less rapidly. Brieger considers that when the reaction occurs with putrefactive alkaloids it is due to impurities present in them. Brouardel and Boutmy have suggested making use of the action of alkaloids upon photographic silver bromide paper as a means of distinction. The paper is written upon with a solution of the alkaloid and kept light free for half an hour; it is then fixed in a solution of sodium hyposulphite and washed in water. The putrefactive alkaloids are said to reduce and blacken the silver compound, while the vegetable alkaloids do not. Neither of these processes is to be relied upon for medico-legal purposes.
LEUCOMAINES OR
ANIMAL ALKALOIDS
Leucomaines or animal alkaloids are basic substances which originate from the metabolic processes taking place in the animal body. They closely resemble the vegetable alkaloids, and some are found in plants as well as animals. It is probable that some of them may have originated primarily from the putrefactive processes in the intestines and been absorbed into the system. The following is a list of the principal leucomaines resulting from the metabolism of the tissues of the animal body:
Adenin, C₅H₅N₅.—From thymus gland, from all tissues animal or vegetable which are rich in nucleinic acid—poisonous in large doses.
Sarkine or hypoxanthine, C₅H₄N₄O.—From urine and flesh—causes increased reflex excitability and convulsive seizures.
Guanine, C₅H₅N₅O.—From flesh and guano—it is inert.
Xanthine, C₅H₅N₄O₂.—From flesh and urine—acts as a muscle stimulant.
Heteroxanthine, C₆H₆N₄O₃.—From urine.
Methylxanthine, C₆H₆N₄O₂.—From urine.
Paraxanthine, C₇H₈N₄O₂.—From urine—destroys spontaneous muscular action, lessens reflex excitability.
Carnine, C₇H₈N₄O₃.—From fresh meat.
Gerotine, C₅H₁₄N₂.—From liver and kidneys, an isomer of cadaverine—exerts a paralysing action upon the nerve centres and cardiac ganglia.
Spermin, C₂H₅N.—From semen, testicles, ovaries, breast, thyroid, pancreas, and spleen, normal bone marrow. Poehl states that it has a tonic effect on the nervous system.
Creatinine, C₄H₇N₃O.—From urine.
Crusocreatinine, C₅H₈N₄O.—From fresh meat.
Xanthocreatinine, C₅H₁₀N₄O.—From fresh meat—causes depression, fatigue, somnolence, defæcation, and vomiting.
Betaine, C₅H₁₁NO₂.—From urine.
Mytilotoxine, C₆H₁₅NO₂.—From poisonous mussels.
The Relation of Leucomaines
to Disease
It will be necessary in considering the relation of leucomaines to disease to give the term a wider significance than that relative to the chemistry of these bodies. Autogenous diseases may be looked upon as having their origin in altered metabolism of the tissue cells, apart from the introduction of foreign cells or poisons. “It is certainly true that if we should drink only chemically pure water, take only that food which is free from all adulteration and infection, and breathe the purest air free from all organic matter living and dead, yet our excretions would contain poisons. It is true that the excretions of all living things, plants, and animals contain substances which are poisonous to the organisms excreting them” (Vaughan). Bouchard estimates that the amount of a certain poison formed in the intestines of a healthy man in twenty-four hours, if absorbed, would prove fatal. Unless free elimination takes place, elevation of temperature may follow.
The products of imperfect digestion, if absorbed, may give rise to serious disturbances. Hildebrandt has shown by his experiments that subcutaneous injection of pepsin into dogs is followed by elevation of body temperature, which he calls “ferment fever.” The fever reaches a maximum within a few hours and may last several days. Rigors are frequent. The animals suffer from trembling in the limbs, uncertainty of gait, vomiting, dyspnœa, and coma followed by death. On post-mortem examination there are found degeneration of the heart, muscles, liver, and kidneys, abundant hæmorrhages into the intestine, Peyer‘s patches, the mesenteric glands, and occasionally into the lungs. The blood is at first lessened in coagulability, afterwards increased, and thrombi formed which have been found in the lungs and kidneys.
Excessive formation of these poisonous substances within the body or insufficient elimination of them produces serious disturbances. Fatigue fever is an example. A considerable rise of temperature may follow excessive and prolonged exercise, the appetite is impaired, and insomnia is present from excitation of the brain and the senses being rendered more acute. There may be rigors simulating malaria. This fatigue fever occurs particularly amongst recruits in armies subjected to prolonged marching. From his observations of this disease in the Italian army, Mosso states that it is due to the absorption of poisonous substances into the blood from the tissues, which, if injected into the circulation of healthy animals, produces symptoms of exhaustion. The fever of prostration or exhaustion is similar but less in degree, it is more likely to be produced by prolonged exertion with insufficient food, it may resemble typhus fever, delirium may be present, and loss of muscular control over the bowels; death may result. In non-fatal cases weeks may elapse before recovery takes place.
Rachford has pointed out that an excess of paraxanthine in the blood is followed by migraine, and it may give rise to epileptic seizures, gastric neurosis, and asthma; and by injecting paraxanthine into the blood of mice and rats he has produced symptoms of certain forms of epilepsy, and others similar to the nervous symptoms of chronic lead poisoning.
CHAPTER VI
FOOD POISONING
(BROMATOTOXISMUS)
Instances have occurred from time to time of serious illness attacking individuals either separately or collectively shortly after the ingestion of food. The food may be rendered poisonous in the following ways:
1. A poisonous substance may have been added to it, intentionally or accidentally.
2. Grain may become infected with poisonous fungi, e.g. ergot.
3. Plants or animals may feed upon materials harmless to them, but which render them poisonous to man—birds that have fed on mountain laurel are said to have proved poisonous to man.
4. During periods of physiological activity of certain of their glands, the flesh of some animals becomes poisonous to man; some fish, for example, are poisonous during the spawning season.
5. Food may carry infection by contamination with germs, e.g. typhoid bacilli in milk.
6. The animal may suffer from a specific disease, and it may be transmitted to man, e.g. tuberculosis.
7. Foods may be contaminated with bacteria which produce poisons either before or after the food has been eaten.
8. The food may be infected with parasites or their ova, and which develop in the individual who partakes of it, e.g. trichiniasis.
In cases in which the poison has been added or preformed, the symptoms of poisoning come on almost immediately or within a short space of time; there may, however, in the latter, be a delay in the appearance of the symptoms in instances where the bacterial poison is formed subsequent to the ingestion of the food. This delay is bordering on the nature of a true infection. In those cases when the bacteria have been present in the animal before, or develop in it subsequent to its death, and which develop in the person who eats it as food, symptoms may not come on for some time; the condition is a true infection, and there may be an incubation period over six or seven days.
Meat Poisoning
(Kreotoxismus)
Apart from those cases of poisoning following the ingestion of food to which poison has been added, or from meat affected by parasitic disease, there have occurred outbreaks of serious illness following the partaking of meat. Vaughan, in the Twentieth Century Practice of Medicine, vol. xiii. p. 20, holds that “there can scarcely be any difference of opinion on the following points: (1) With fresh food to act upon and with normal gastric juice to act, the process of peptic digestion proceeds without the formation of any harmful substance. (2) With putrid food, containing poisons to start with, the most active digestion does not guarantee the destruction of those poisons. (3) With even the best of food, peptic digestion may proceed so slowly and imperfectly that during the process poisons may be formed by bacterial agencies.” During the process of decomposition of meat and other albuminous foods by bacterial agency, certain poisonous substances are formed prior to the production of the ptomaines or bacterial alkaloids. These are known as toxalbumoses and enzymes; they are unstable bodies, they cannot be obtained in a crystalline form, and their composition is not fully understood. They give certain reactions with a few group reagents, but they are recognised only by their effects upon living animals. As decomposition advances the more stable alkaloids are formed, but those which are poisonous, like the toxalbumoses, are readily converted by further processes of putrefaction or by chemical means into innocuous bodies. Toxins is the general term used in toxicology for these poisonous substances formed from animal tissues.
It is not necessary that complete putrefaction should have taken place for meat to prove poisonous. In fact many of the severest cases are those in which it has not fully putrefied. The most poisonous toxins are present during the early stages of decomposition, and the changes are not recognisable by the senses—smell or taste—which would ensure the rejection of the meat as food.
The poisonous effects are rarely due to the ingestion of bacterial products alone; those cases in which no bacteriological investigation of the food has been made cannot be taken into consideration. The toxalbumoses are destroyed by a few minutes‘ exposure to a temperature at boiling-point, 212° F. (Durham, B. M. J., 1898, vol. ii. p. 797).
In reference to the toxic action of the alkaloids, these have been noted only from the results following subcutaneous injection; their effects when taken per orem have not been established by experiment. In all instances where the necessary bacteriological investigation has been properly carried out a true infection has been proved to have taken place.
In cases of meat poisoning the principal bacteria concerned are not the ordinary putrefactive organisms. The Bacillus enteritidis of Gärtner, which has been found associated with twelve epidemics, and the Bacillus botulinus of Ermengem are the most important causative agents.
The Bacillus enteritidis is killed by proper cooking. It is destroyed in one minute at a temperature of 180° F. At 41° F. it will not grow, but, in meat kept at 68° F. for seventy-two hours, it flourishes abundantly. Freezing will not kill it. In meat which has been infected with the bacilli post-mortem they do not penetrate the meat more than 1 cm. in ten days. Roasting or boiling will sterilise it. In those instances in which poisoning has taken place after cooking, the bacilli have either been present in the meat beforehand, and the temperature has not been sufficiently high or the cooking sufficiently prolonged, to ensure their destruction in the deepest portions; or the meat after cooking has become contaminated, and been insufficiently warmed up again after keeping it for a day or so. Exposure to sewer gas will not affect meat and contaminate it with the Bacillus enteritidis. The chief symptoms due to the Bacillus enteritidis are vomiting and diarrhœa, herpes labialis, rashes on the skin followed by desquamation in about fourteen days, jaundice, and great thirst. The onset is sudden, with nausea, headache, pains in the back and limbs, rigors, fever lasting a few days, general weakness, and, in cases which recover, convalescence extending over a period of from three to six weeks.
The symptoms of botulismus, due to the Bacillus botulinus of Ermengem, and associated with sausage poisoning, are, as a rule, dryness of the mouth, constriction of the fauces, nausea, vomiting, purgation, vertigo, dilatation of the pupils, with dimness of vision and diplopia, and a sense of suffocation. Marked muscular weakness and nervous prostration are prominent symptoms. In fatal cases there is weakness of the pulse and cyanosis, with coldness of the surface and perspiration. The temperature is raised at first and may reach 103° F., but ultimately falls below normal. Delirium comes on late, followed by coma and death.
In dangerous cases obstinate constipation may follow after a few hours of watery stools.
On post-mortem examination of the bodies in fatal cases the following appearances have been noted: a white, dried, parchment condition of the mouth, fauces, throat, and gullet; hyperæmia of the mucous membrane of the stomach and intestines with submucous extravasations of blood. The abdominal and thoracic viscera have been found engorged with blood, with enlargement of the spleen; the former are due to failure of the heart, and cannot be regarded as characteristic of sausage poisoning. Some stress has been laid on the observation that putrefaction is unusually delayed, but Müller has shown that no reliance can be placed upon it; he says that in forty-eight autopsies it has been noted that in eleven of them putrefaction had developed rapidly.
The symptoms of meat poisoning are grouped by Dixon Mann into two divisions: (1) those due to a true infection, (2) those due to simple poisoning.
In (1) the symptoms are those of an infectious disease—they include headache, anorexia, rigors, constipation followed by diarrhœa, pains in the back and limbs, photophobia, delirium, skin eruptions, meteorism, and enlargement of the spleen. The post-mortem appearances greatly resemble those of enterica—infiltration, ulceration, and sloughing of Peyer‘s patches; hæmorrhage into the bowels, enlargement of the spleen, with possibly some pus depots.
In (2) the symptoms are those of acute gastro-enteritis—violent vomiting, purging, prostration, cramps in the legs, and collapse; the temperature is generally subnormal, but may be elevated. The post-mortem appearances are those produced by gastro-enteritis, with hæmorrhages into the intestinal mucous membrane; the spleen is frequently enlarged, and Peyer‘s patches may be infiltrated.
Meat poisoning has usually been most frequently associated with the ingestion of pork, veal, beef, meat pies, potted meat, tinned meat, sausages, and brawn. The more finely divided the meat, the more easily and completely it may become infected and poisonous. Cases of poisoning from the ingestion of canned meats are not uncommon. In some instances they may be due to metallic poisoning, in the great majority they are due to putrefactive changes having taken place in the meat. Ungefug reports a case confirmed by the celebrated chemist Heinrich Rose, in which sulphate of zinc had been used as a preservative instead of saltpetre. In some the canning may have been imperfect, and putrefaction taken place before reaching the consumer; in others decomposition may have begun after opening the can. The meat may have been taken from diseased animals, or decomposed prior to canning.
Poisoning by tinned provisions with the metal used for tinning is more likely to occur with fruits than meat. The malic acid of the juice probably dissolves the solder and forms a malate of tin. Cherries, apples, pineapples, and tomatoes are the most likely to do this.
In 1890 Luff investigated four cases of tin poisoning due to the consumption of tinned cherries. Some of the material left was analysed, and the juice contained malate of tin in solution equivalent to two grains of the higher oxide of tin per fluid ounce. It was estimated that the symptoms were produced by doses of two to four grains of malate of tin. Two of the patients nearly died from the diarrhœa and collapse.
Sulphate of copper is used to give a full green colour to peas, olives, and pickles, or it may contaminate preserved fruits if they be left in copper vessels. The copper combines with the phyllocyanic acid of the chlorophyll, and although insoluble in the surrounding liquor, is set free and absorbed by the process of digestion.
Fish Poisoning
(Ichthyotoxismus)
Fish may cause poisoning in two ways: in one the poison is a physiological product of certain glands of the animal, and is quite independent of bacteria; the other is due to the poisonous products of bacterial growth. The fish that are inherently poisonous as a rule occupy tropical waters: several of them exist in Japanese waters. Mackerel, carp, barbel, and herrings may become poisonous at times; some of these, especially mackerel, may rapidly become unfit for food after they are dead. Caviare and the roe of herrings have caused poisoning. Shell-fish, especially mussels, also may prove poisonous.
The symptoms of fish and shell-fish poisoning are variable. In some cases disturbance of the nervous system predominates, with delirium, convulsions, and paralysis. There may be dryness and constriction of the throat, dyspnœa, disturbed vision, vertigo, jerky speech or aphonia, rapid pulse, loss of co-ordination, numbness, formication, coldness of the limbs, dilated pupils, paralysis, and collapse, followed by death in a few hours. Other cases exhibit symptoms of severe gastro-intestinal irritation, with nausea, vomiting, pain, tenesmus, mucous and bloody stools; in the most dangerous cases the bowels are constipated. Cases exhibiting the nervous type of symptoms resemble poisoning by atropine, and an alkaloid—ptomatropine—is regarded as the cause. It has never been obtained in the pure state, and nothing is known of its composition. It must not be mistaken, in toxicological examination, for atropine; its presence can only be recognised by its action on the pupil.
Many cases of fish poisoning are accompanied by erythema, urticaria, and severe itching of the skin. In probably all cases there is an elevation of the body temperature.
Tinned fish has caused poisoning on many occasions. In one case of tinned salmon poisoning, which proved fatal, parts of the stomach and intestines were almost gangrenous from the intensity of the inflammation.
Stevenson (Brit. Med. Journ., 1892) records a case of sardine poisoning which proved fatal, and in which the tissues post-mortem were found to be emphysematous. He extracted an alkaloid from some of the sardines, and the stomach contents; it was highly toxic and proved fatal to rats.
It is most probable in poisoning by tinned fish that the contents of the tins have become contaminated with bacteria before being sealed up.
Shell-fish may become contaminated with bacteria and cause true infections in people who eat them. Typhoid fever has been carried in this way by oysters, and probably cockles. The fish may develop toxins and prove poisonous, and as an example of this mussels produce a powerful toxin—mytilotoxine—while they are alive, which gives rise to a serious illness termed mytilotoxismus. There are three quite different classes of symptoms induced by poisonous mussels. In one the symptoms are principally those of acute gastro-enteritis; in another skin eruptions are the principal feature; and the third is known as mytilotoxismus paralyticus, in which there is great disturbance of the cerebro-spinal nervous system, with paralysis. The two former groups of symptoms are due to putrefactive processes in the mussels, but the third or paralytic group is due to the alkaloid mytilotoxine, which is not a product of putrefaction, as it is not found in mussels that have been allowed to decay.
There is nothing to evidence the idea that mussels absorb metallic poisons—e.g. copper—from the bottoms of vessels.
Poisoning by Milk and
Milk Products
The term milk poisoning or galactotoxismus is used here to indicate the results following the drinking of milk infected with saprophytic toxicogenic bacteria, and which are mainly responsible for the high mortality from “summer diarrhœas” of artificially-fed infants. One of the products of these bacterial infections of milk is the alkaloid tyrotoxicon. It has been isolated by Vaughan from cheese, and has also been found in ice-cream, frozen custards, and cream puffs. Vaughan, however, asserts that it is not the one most frequently present, nor is it the most actively poisonous. There are others which he considers are poisonous albumins (Vaughan, Twentieth Cent. Pract. Med., vol. xiii.).
The symptoms of poisoning by tyrotoxicon are mainly those of acute gastro-enteritis, and comprise constriction of the fauces, nausea and vomiting, sharp griping intestinal pains, headache, thoracic oppression, chilliness, dizziness, and purging. In severe forms exhaustion, subnormal temperature, coma, collapse, and death may follow.