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.

TRICHINIASIS

This disease is due to the introduction of the _Trichina spiralis_ into the human body. The encysted worm is found embedded in the fibres of all the striped muscles of the trunk and limbs, and even in the heart, where it appears in the form of white ovoid bodies or capsules, the capsules being sometimes calcareous. The worm passes the greater part of its existence in the chrysalis state in the muscular system of one animal, and only reaches its mature condition in the stomach of another. Virchow and Zenker assert that the trichina not only frequently presents itself in the human organism, but that this organism is most favourable for its full development. Once in the stomach, the period of incubation is about three to eight days, and then propagation rapidly begins and continues, so that Dr. Kellen estimates that in about seven days after the ingestion of half a pound of meat the stomach and intestines may contain thirty millions of the worms. The worms when introduced into the stomach leave their capsules, become free, produce young, and these leave the stomach through its coats for the muscles, where they become encysted. The trichina is most frequently found in pork, seldom in sheep, horses, or oxen--the last being the most free.

_Symptoms._--Intestinal irritation, loss of appetite, sickness, malaise, general weakness of the limbs, and diarrhœa. The eyelids swell as well as the joints, the skin is bathed in cold, clammy sweat, and a low form of fever sets in. Death may be due to peritonitis, paralysis of the muscles--the result of their destruction--or to irritative fever. During the perforation of the coats of the stomach and bowels by the worms, the mucous membrane becomes inflamed, pus is formed on the surface, and the stools become bloody.

TOXICOHÆMIC, SNAKE POISONS, ETC.

Under this head may be classed all those effects produced by the sting or bite of various insects and reptiles, and also by the bite of the mad dog and wolf.

No medico-legal question is likely to be raised on this subject, at least in this country, where, with the exception of the common viper or adder, all our reptiles are harmless enough.

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