Not only pathogenic bacteria but certain kinds of animal parasites sometimes enter the human body in or upon articles of food. One of the most important of these is the parasite causing trichiniasis.
Trichiniasis or trichinosis is a disease characterized by fever, muscular pains, an enormous increase in the eosinophil blood corpuscles, and other more or less well-defined symptoms; at the onset it is sometimes mistaken by physicians for typhoid fever. The responsible parasite is a roundworm (Trichinella spiralis, formerly known asTrichina) which is swallowed while in its encysted larval stage in raw or imperfectly cooked pork.[90]The cysts or envelopes in which the parasites live are dissolved by the digestive fluids and the young larvae which are liberated develop in the small intestine to the adult worm, usually within two days. The young embryos, which are produced in great numbers by the mature worms, gain entrance to the lymph channels and blood stream, and after about ten days begin to invade the muscles—a procedure which gives rise to many of the most characteristic symptoms of the infection. It is estimated that in severe cases as many as fifty million embryos may enter the circulation.The parasites finally quiet down and become encysted in the muscle tissue and the symptoms, as a rule, gradually subside. Ingestion of a large number of parasites at one time often results fatally, the mortality from trichiniasis being on the average somewhat over 5 per cent and rising in some outbreaks to a much higher figure (30 per cent). On the other hand, many infections are so light as to pass unnoticed. Williams[91]foundTrichinellaembryos present in 5.4 per cent of the bodies of persons dying from other causes. Such findings are considered to indicate that occasional slightTrichinellainfections even in the United States are quite common. This might indeed be expected from the frequent occurrence of infection in swine, about 6 per cent of these animals being found to harbor the parasite.
Fig. 7.Fig. 7.—Trichinae encysted in intercostal muscle of pig. (About 35×1.) (After Neumann and Mayer.)
Fig. 7.—Trichinae encysted in intercostal muscle of pig. (About 35×1.) (After Neumann and Mayer.)
The specific symptoms (such as the muscular pain) of trichiniasis may be due in part to mechanical damage of the muscle tissue, but it is also probable that they are partly due to toxic products exuded by the worms and partly to the introduction of alien protein material—the protein of the worm—into the tissues. Secondary bacterial infection is also a possibility, but there islittle evidence to prove that this is an important factor in most cases of trichiniasis. The various stages observed in the progress of the disease are plainly connected with the different phases of the worm's development—the initial localization in the intestines, the invasion of the muscles, and the final encystment.
Swine become infected with this parasite by eating scraps of infected meat, or the offal of their own kind, or by eating infected rats. The rat, through its cannibalistic propensities, becomes infected frequently, and is one of the chief factors in the wide dissemination of the disease. Human infection is practically accidental and self-limited; biologically speaking, man as a host does not enter into the calculations of the parasite.
Treatment of established trichiniasis infection is palliative, not truly remedial. The parasites, once inside the body, cannot be materially affected by the administration of any drug. While cure of trichiniasis is thus difficult, if not impossible, prevention is very simple. The thorough cooking of all food is sufficient to preclude infection. This relatively simple means of destroying the larvae is a more certain as well as less expensive method of preventing infection than is the laborious microscopic examination of the tissues of every slaughtered hog. In Germany between 1881 and 1898 over 32 per cent of 6,329 cases of trichinosis that were investigated were traced to meat that had been microscopically examined and passed as free from trichinae.[92]On the other hand, thorough cooking removes all possibility of danger.
Various tapeworm or cestode infections are contracted by eating meat containing the parasite. Particular species of tapeworm usually infest the flesh of specific hosts, asTenia saginatain the beef andTenia soliumin the hog. The dwarf tapeworm,Hymenolepis nana, develops in rats, and the human infections with this parasite occasionally observed are probably caused by contamination of food by these animals.
Fig. 8.Fig. 8.—Cysticercus cellulosaein pig's tongue. (After Neumann and Mayer.)
Fig. 8.—Cysticercus cellulosaein pig's tongue. (After Neumann and Mayer.)
Sometimes the existence of the tapeworm in man is restricted to the alimentary tract and the symptoms vary from trivial to severe, but sometimes (Tenia solium) the larval stage of the tapeworm invades the tissues and becomes encysted in various organs (brain, eye, etc.), where, as in the case of cerebral infection, it may result fatally. The encysted larva ofTenia soliumwas at one time regarded as an independent animal species and namedCysticercus cellulosae. The condition known as "measly pork" is produced by the occurrence of this encysted parasite.
So-called hydatid disease is due to the cystic growth produced by the larva of a species of tapeworm (Echinococcus) inhabiting the intestine of the dog. Human infection may be caused by contaminated food as well as more directly by hands soiled with petting infected dogs. Several varieties of tapeworms infesting fish, especially certain fresh-water species, may be introduced into the human body in raw or partly cooked fish.
Methods for the prevention of tapeworm infection include the destruction of the larvae by heat—that is, the thorough cooking of all meat and fish—and the minimization of close contact with those animals, such as the dog and cat, that are likely to harbor parasites. Cleanliness in the preparation and serving of food, and attention to hand-washing before meals, and especially after touching pet animals, are necessary corollaries.
Hookworm infection (uncinariasis, ankylostomiasis) is commonly caused by infection through the skin of the feet, but the possibility of mouth infection cannot be disregarded, and in regions where hookworm disease exists methods of guarding against food contamination should be practiced, as well as other precautions. Billings and Hickey[93]believe that hookworm disease is contracted by unconscious coprophagy (from raw vegetables) much more frequently than is generally supposed.
A number of other parasitic worms (e.g.,Strongyloides,Ascarisor eelworm, andOxyuriaor pinworm) may conceivably enter the human body in contaminated food, and while, as in hookworm disease, other modes of infection are probably more important, the liability to occasional infection by uncooked food must not be overlooked.
Fig. 9.Fig. 9.—Lamblia intestinalis.(After Neumann and Mayer.)
Fig. 9.—Lamblia intestinalis.(After Neumann and Mayer.)
Various forms of dysentery or diarrhea have been attributed to infection withGiardia (Lamblia) intestinalis. Observations made by Fantham and Porter[94]upon cases contracted in Gallipoli and Flanders have given support to this view. Strains of this parasite of human origin have been shown to be pathogenic for mice and kittens. It is considered possible that these animals may act as reservoirs of infection and spread the disease by contamination of human food.
In close relation to the cases of infection with animal or plant parasites which have been discussed, there are certain well-established instances of poisoning by substances that have been generated in food while it is still outside of the body. This is the common type of food poisoning in popular estimation, but in point of fact the proved cases of this class are much less frequent than the instances of true infection with bacteria of theparatyphoid-enteritidisgroup (chapter vi). Thus far the best-known examples of poisoning by the products of micro-organisms are botulism and ergotism.
Ergotism or ergot poisoning is due to the use of rye that has become diseased through the attack of a fungus,Claviceps purpurea. It occurred frequently in the Middle Ages when in times of famine the ergot or spurred rye (O.Fr.argot, "a cock's spur") was often used in default of better food. In Limoges in 922 it is said that forty thousand persons perished from this cause. Improvement in the facilities for transportation of food into regions where crops have failed, and the use of special methods for separating the diseased grain from the wholesome have greatly reduced the prevalence of ergotism. In Western Europe poisoning from this cause has practically ceased, although Hirsch recordedsome twenty-eight outbreaks in the nineteenth century; in parts of Russia the disease is said still to occur in years of bad harvest.[95]
The poison ergot itself has long been used as a drug in obstetrics, but its composition is complex and is still not completely understood. Several constituents of ergot have been extracted, and these have been shown to possess different physiological effects.[96]The symptoms observed in the outbreaks of ergotism of mediaeval times are not wholly reproduced experimentally by the drug and are thought to have been in part due to the semi-starvation engendered by the use of rye from which the nutritious portions had been largely removed by the growth of the fungus.
The best established case of poisoning by means of bacterial products taken in with the food is the serious malady known somewhat inappropriately as botulism (botulus, sausage).[97]This kind of food poisoning, which has a characteristic set of symptoms, seems to have been first recognized and described in 1820 by theGerman poet and medical writer Justinus Kerner. In two articles (1820-22) he enumerates 174 cases with 71 deaths occurring in Württemberg between 1793 and 1822 and apparently in most cases connected with the useof insufficiently smoked sausage. Mayer[98]tabulates about 600 additional cases observed in various parts of Germany down to the end of 1908, the total mortality in the 800 cases being about 25 per cent. In France botulism is said to be very rare.[99]In Great Britain Savage[100]declares that he has been unable to trace the occurrence of a single outbreak. In the United States several instances of botulism poisoning are on record (Sheppard,[101]1907, 3 cases, 3 deaths, canned pork and beans; Peck,[102]1910, 12 cases, 11 deaths; Wilbur and Ophüls,[103]1914, canned string beans, 12 cases, 1 death; Frost,[104]1915, 3 cases, 3 deaths). Professor Stiles[105]has given a graphic description of his own attack of probable botulism due in all likelihood to minced chicken.
Fig. 10.Fig. 10.—Claviceps purpurea:1, ergot on rye-grass; 2, ergot on rye; 3, section of a portion of the conidial form of fruit, ×300; 4, a sclerotium or ergot; 5, head of ascigerous form of fruit; 6, an ascus, ×300; 7, a single spore, ×300. (After Massee,Plant Diseases, by courtesy of the Macmillan Company.)
Fig. 10.—Claviceps purpurea:1, ergot on rye-grass; 2, ergot on rye; 3, section of a portion of the conidial form of fruit, ×300; 4, a sclerotium or ergot; 5, head of ascigerous form of fruit; 6, an ascus, ×300; 7, a single spore, ×300. (After Massee,Plant Diseases, by courtesy of the Macmillan Company.)
Symptoms.—The description of a case seen by Wilbur and Ophüls,[106]is so typical that it may be cited:
Girl, aged 23, Tuesday evening, Nov. 23, 1913, ate the dinner including the canned string beans of the light green color together with a little rare roast beef. The following day she felt perfectly normal except that at 10:00 in the evening the eyes felt strained after some sewing. Thursday morning, thirty-six hours after the meal, when the patient awoke, the eyes were out of focus, appetite was not good, and she felt very tired. At night she had still no appetite, was nauseated, and vomited the noon meal apparently undigested. Friday morning, two and one-halfdays after the meal, the eyes were worse, objects being seen double on quick movement, and it was noticed that they had a tendency to be crossed. A peculiar mistiness of vision was also complained of. She was in bed until late in the afternoon, when she visited Dr. Black. She had had some disturbance in swallowing previous to this time and stated that it felt as if "something came up from below" that interfered with deglutition. The fourth day she remained in bed, was much constipated, and noticed a marked decrease in the amount of urine voided. There was at no time pain except for occasional mild abdominal cramps, no headache, subnormal temperature, and a normal pulse. The fourth and fifth days the breathing became difficult at times and swallowing was almost impossible. The patient complained of a dry throat with annoying thirst. The sixth day there were periods of a sense of suffocation with a vague feeling of unrest and as if there might be difficulty in getting the next breath. The upper lids had begun to droop. The voice was nasal. When the attempt was made to swallow liquids they passed back through the nose. The patient felt markedly weak.
Physical examination at this time showed ptosis of both upper eyelids, dilatation of the right pupil, sluggish reaction to light of both pupils, apparent paralysis of the internal rectus of the left eye, normal retina, inability to raise the head, control apparently having been lost of the muscles of the neck, inability to swallow, absence of taste. The tongue was heavily coated and the throat was covered with a viscid whitish mucus clinging to the mucous membrane. The soft palate could be raised but was sluggish, particularly on the right side. The exudate on the right tonsil was so marked that it resembled somewhat a diphtheritic membrane. The seventh day there was some change in the condition; occasional periods occurred when swallowing was more effective, and there was less tendency to strangle. On the eleventh day there was some improvement of the eyes, still strangling on swallowing, sensation of taste was keener, and the general condition improved. The twelfth day the patient was able to move her head, but was unable to lift it except when she took hold of the braids of her hair, and pulled the head forward. The eyes could be opened slightly, speech was less nasal andmore distinct, and improvement in swallowing was marked. At the end of two weeks the patient was able to take soft diet freely, and at four weeks she was up in a chair for a couple of hours complaining only of general weakness and inability to use her eyes. At the end of five weeks she was able to leave the hospital and return to her home and later to resume her regular work.
In all cases the nervous system is strikingly affected in this form of food poisoning. Dizziness, double vision, difficulty in chewing and swallowing, and other symptoms of nervous involvement occur with varying intensity and may persist for a long time after the first signs of the attack. Temperature, pulse, and respiration remain practically normal. In contrast with the traditional type of food poisoning gastro-intestinal symptoms may be slight or altogether lacking. Freedom from abdominal pain is usually noted; diarrhea is the exception and constipation the rule; vomiting sometimes occurs, but may be absent. In the cases described by Sheppard there was "an entire absence of the usual gastro-intestinal symptoms from first to last, no pain or sensory disturbance and no elevation of temperature." The visual disturbances are very characteristic. Stiles relates his own experiences as follows:
Vertigo and nystagmus developed [a few hours after eating] in a startling degree, the car [in which he was being taken to his house] seemed to be ascending an endless spiral, the stars made circles in the sky, and the houses by the wayside reeled. The lighted doorway of my house seemed to approach and surround me as I was carried in. My bed for the moment presented itself as a vertical surface which I could not conceive to be a resting place.... Whenever I opened my eyes on this day [the next day] the impression of gyration of the room was appalling.... To turn my head even very slowly from one side to the other brought an accession of the overpowering giddiness.... [eightdays after the beginning of the attack]. The nystagmus now became limited to momentary onsets, but in its place I became aware of a peculiar diplopia. The image of one retina was not merely displaced from the position of its fellow but was tilted about 15 degrees from parallel.... This fantastic diplopia gradually gave place to the familiar variety and this occurred less and less often as my convalescence proceeded. From [this date] my recovery pursued a course which was dishearteningly slow but free from any setbacks. Among the persistent symptoms were ... the visual difficulties mentioned. The left pupil was usually smaller than the right and I thought I detected a slight failure to relax accommodation with the left eye. Reading was difficult for several weeks and the ability to write, as requiring closer fixation, was still longer in returning.
In the cases reported by Sheppard visual symptoms were the initial signs of trouble, double vision, mistiness, and inability to hit the mark in shooting being the first complaint.
The time elapsing between eating the implicated food and the onset of the earliest symptoms is usually between twelve and forty-eight hours, but may be much less. In Stiles's case the interval was apparently less than three hours.
Anatomical lesions.—In fatal cases no characteristic gross changes are observed in the various organs. It has been stated by some writers that microscopic degenerative changes occur in the ganglion cells, involving especially the so-called Nissl granules, but in the carefully studied case reported by Ophüls[107]the Nissl granules were quite normal in size, arrangement, and staining qualities. There was, in fact, no evidence to substantiate the hypothesis of a specific action of the toxin on the nerve-cells. On the other hand, Ophülsfound numerous hemorrhages in the brain-stem and multiple thromboses in both the arteries and veins. He holds, consequently, that the indications of severe disturbances of brain circulation associated with hemorrhages and thrombosis in medulla and pons are sufficient to explain the symptoms of botulism poisoning without having recourse to the assumption that the poison has a specific action on certain ganglion cells.
Bacteriology.—The cause of botulism poisoning was discovered by Van Ermengem to be the toxin produced by a bacillus which he namedB. botulinus. This organism was isolated from portions of a ham that had caused fifty cases of poisoning (1895) at Ellezelles (Belgium), and also from the spleen and gastric contents of one of the three fatal cases. The bacillus grows only in the absence of oxygen (strict anaërobe), stains by Gram's method, forms terminal spores, and develops best at 22°C. Unlike most bacteria dangerous to man, it appears unable to grow in the human body, and its injurious effect is limited to the action of the toxin produced in foodstuffs outside the body. Botulism is an intoxication—not an infection. The fact that the bacillus can grow in nature only when the free oxygen supply is cut off explains in part at least the relatively rare occurrence of botulism since all the conditions necessary for the production of the botulism toxin do not commonly concur. Next to nothing is known as to how widelyB. botulinusis distributed. Except in connection with the cases of poisoning it has been reported but once in nature.[108]The botulism poisonis a true bacterial toxin, chemically unstable, destroyed by heating at 80°C. for 30 minutes, capable of provoking violent symptoms in minute doses, and possessing the property characteristic of all true toxins of generating an antitoxin when injected in small, non-fatal doses into the bodies of susceptible animals. In animal experiments the toxin formed byB. botulinushas been found capable of reproducing the typical clinical picture of this form of food poisoning. Symptoms of paralysis are produced in rabbits, guinea-pigs, and other animals by the injection of so small a dose as 0.0001 c.c. of a filtered broth culture.
Fig. 11.Fig. 11.—Bacillus botulinuswith spores. Pure culture on sugar-gelatin. Van Ermengem preparation. (Kolle and Wassermann.)
Fig. 11.—Bacillus botulinuswith spores. Pure culture on sugar-gelatin. Van Ermengem preparation. (Kolle and Wassermann.)
Epidemiology.—The conditions under whichB. botulinusoccurs and is given opportunities for multiplying are not completely known. It is possible that there are localities where this bacillus is particularly abundant in the soil or in the intestinal contents of swine or other domestic animals, but on the whole it seems more probable that the organism is widely distributed, but that it does not often find suitable conditions for entrance into, and multiplication in, human food. Practically all the reported cases of botulism have been caused by food which has been given some sort of preliminary treatment, as smoking, pickling, or canning, thenallowed to stand for a time, andeaten before cooking. Since both the bacillus, including the spore stage, and its toxin are destroyed by relatively slight heating, it is clear that a rather unusual set of factors must co-operate in order that botulism poisoning shall take place. These are evidently: (1) the presence of the bacilli in sufficient numbers in a suitable foodstuff; (2) the initial preparation of the food by a method that does not destroy theB. botulinus—inadequate smoking, too weak brine,[109]or insufficient cooking; (3) the holding of this inadequately preserved food for a sufficient length of time under the right conditions of temperature and lack of oxygen; (4) the use of this food, in which conditions have conspired to favor the production of toxin byB. botulinus, without final adequate cooking. It seems as reasonable to suppose that the infrequency with which these several factors coincide is responsible for the relative uncommonness of botulism as to suppose it due to the rarity of the specific bacillus. In the Belgian outbreak studied by Van Ermengem the poisonous ham had lain at the bottom of a cask of brine (anaërobic conditions) while the other ham of the same animal lay on top of it but was not covered with brine, and was eaten without producing any poisonous effect. In this instance the presence or absence of favorable conditions for anaërobic growth seemed to be the decisive factor.
Prevention and treatment.—The food in whichB. botulinushas grown does not seem to be altered in a waythat necessarily arouses suspicion. In the case described by Römer the incriminated ham showed bluish-gray areas from whichB. botulinuscould be isolated, but this condition does not seem to have attracted attention before the poisoning occurred and was an observation made only after the event. So far as can be learned the meat that has caused botulism has always come from perfectly sound animals. In some cases the accused article of food is said to have had a rancid or acrid taste (due to butyric acid?), but there is nothing definitely characteristic about this, as the majority of anaërobes produce butyric acid. If, as in the Darmstadt[110]and Stanford University[111]epidemics, the food (canned beans) is served with salad dressing, a sour taste might pass without notice or even add to the relish. In the instance reported by Sheppard the canned beans were good in appearance, taste, and smell.
The obvious precaution to take against poisoning of this sort is first the use of adequate methods of food preservation. To judge from the recorded outbreaks, domestically prepared vegetables and meats are more likely to give rise to botulism than those prepared commercially on a large scale. The general use of steam under pressure in the large canning factories affords a high degree of protection against the anaërobic bacteria and their resistant spores. Whatever the method of treatment, all canned or preserved food having an unnatural appearance, taste, or odor should be rejected. Reheating of all prepared foods immediately before use is an additional safeguard. Foods, such as salads,composed wholly or in part of uncooked materials should not be allowed to stand overnight before being served.
If symptoms of botulism, such as visual disturbances, become manifest, the stomach should be emptied with a stomach pump, cathartics administered, and strychnine and other stimulants given as required. Since one of the noteworthy features of this disease is the paralysis of the intestinal tract by the toxin absorbed, the guilty food may lie for a long time in the stomach (cf. Stiles,loc. cit.). Consequently, measures to empty the stomach should be taken even if the patient does not come under observation until several days after the poisonous food has been eaten.
An antitoxic serum has been prepared at the Koch Institute in Berlin. This serum has given successful results in animal experimentation, but has not been used, so far as I can learn, in any human outbreak. It is not available at any point in this country.
The interesting case reported by Barber[112]shows that there are other possibilities of food poisoning by formed bacterial poisons. Acute attacks of gastro-enteritis were produced in several individuals by the use of milk containing a poisonous substance elaborated by a white staphylococcus. This staphylococcus occurred in almost pure culture in the udder of the cow from which the milk was derived. The milk when used fresh was harmless and the poison was generated in effective quantities only when the milk stood some hours at room temperaturebefore being used. The symptoms were similar to those usually ascribed to "ptomain poisoning."
There is a general belief that food is unwholesome whenever the evidence of the senses shows it to be more or less decomposed. This opinion finds expression in civilized countries in many legal enactments forbidding traffic in decomposed meats, vegetables, and fruits. There is unfortunately lack of evidence as to what kinds or degree of visible decomposition are most dangerous. In fact, some foods of high nutrient value, notably cheeses, are eaten only after somewhat extensive decomposition processes (termed ripening) have taken place. The characteristic flavors or aromas of the various hard and soft cheeses are due to the substances formed by certain species of molds and bacteria and are just as properly to be regarded as decomposition products as the unpleasant stenches generated by decomposing eggs or meat. Indeed, some of the decomposition products formed in the ripening of Brie, Camembert, or Limburger are similar to, if not identical with, those which are associated with spoiled foods. Sour milk, again, is recommended and commonly used as a food or beverage for persons in delicate health, and yet sour milk contains many millions of bacteria and their decomposition products. Some of the bacteria commonly concerned in the natural souring of milk are closely related to pathogenic types. The partial decomposition of meats and game birds is often considered to be advantageous rather than otherwise. Even eggs, a food whose "freshness" is marred for most persons by the initialstages of decomposition, are ripened in various ways by the Chinese and eaten as a delicacy after the lapse of months or years. The preserved ducks' eggs known as pidan are stored for months in a pasty mixture of tea, lime, salt, and wood ashes. "They are very different from fresh eggs. The somewhat darkened shell has numerous dark green dots on the inner membrane. Both the white and yolk are coagulated; the white is brown, more or less like coffee jelly...."[113]Increase of ammoniacal nitrogen has taken place to an extraordinary degree in these eggs, indicating much decomposition of the egg protein. The ammoniacal nitrogen in pidan is considerably higher than in the eggs known by egg candlers as black rots.
It is evident, therefore, that bacterial growth in substances used as food is not necessarily injurious and may in some cases increase the palatability of food without destroying its wholesomeness. Little or nothing is known about the correlation of visible signs of decomposition with the presence of poisonous products, and it is at present impossible to say at what point in the process of decomposition a food becomes unfit to use owing to the accumulation of poisonous substances within it. There seems to be no connection between the natural repugnance to the use of a food and its unwholesomeness. Under ordinary conditions the nauseous character of very stale eggs is proverbial, and yet few nitrogenous foods have so clear a health record as eggs or have been so infrequently connected with food poisoning outbreaks.
It might seem tempting to conclude on the basis of the available evidence that spoiled or decomposed foods possess poisonous qualities only when certain specific bacteria, like theB. botulinusalready discussed, have accidentally invaded them and formed definite and specific poisons. But we have no right to assume that the everyday decomposition products of the banal bacteria are in all cases without injurious effects. Even though no sharply defined acute form of poisoning may be laid at their door, it does not follow that an irritating or perhaps slightly toxic action of the ordinary decomposition products is altogether absent. Our present knowledge of the nature and degree of danger to be apprehended from the use of spoiled food is imperfect and unsatisfactory. That fact, however, does not release us from the obligation to continue measures of protection based even to a limited extent on experience.
While many and diverse causes of food poisoning have been discussed in the foregoing pages, there remain certain affections definitely connected with food that are still of obscure or doubtful causation.
This disease, common to man and some of the higher animals, is characterized by a definite symptom-complex, the salient features being excessive vomiting and obstinate constipation accompanied usually by a subnormal temperature. Many cases result fatally. At the present time it is known to occur only rarely in some of the southern and central western states in this country, but during the period of pioneer settlement it was quite common in districts that are now seldom affected. A great many references to milksickness are found in the writings of the early travelers and physicians in the Middle West, one observer predicting that "some of the fairest portions of the West in consequence of the prevalence of this loathsome disease must ever remain an uninhabitable waste unless the cause and remedy can be discovered." In certain regions it is estimated that "nearly one-fourth of the pioneers and early settlers died of this disease." The mother of Abraham Lincoln fell a victim to this malady in 1818 in southern Indiana.
The disease appears to be usually contracted in the first instance by grazing cattle or sheep that have accessto particular tracts of land; "milksickness" pastures are, as a rule, well known locally for their dangerous qualities. Milksickness is communicated to man through the medium of raw milk, or butter and possibly of meat. Although some of the earlier observers make the statement that the disease is self-propagating and can be passed on without limit from one animal to another, later experiments cast doubt on this view.[114]
Many different theories have been advanced to account for the origin of the disease. The belief that mineral poisons such as arsenic or copper might be taken up by grazing animals and eliminated in the milk finds no justification either in analytical or in clinical data. Many plants, known or suspected to be poisonous, have been accused of furnishing the substance that imparts the poisonous quality to the milk of animals suffering from trembles, but there is no agreement as to the responsible species. Feeding experiments with suspected plants have in no case given unambiguous results. While some facts have been supposed to indicate that living micro-organisms are the cause of milksickness, other facts are opposed to this view, and the most recent experiments in this direction did not lead to conclusive results.[115]The true cause of milksickness is at present quite unknown.
Although diseased conditions due to the absence rather than the presence of certain constituents in the food are not perhaps to be properly classed as foodpoisoning, they may be mentioned here to illustrate the complexity of the food problem. At least one disease,—pellagra—is attributed by some observers to the presence of an injurious substance or micro-organism in the food, and by others to the absence of certain ingredients necessary to the proper maintenance of life.
Beriberi.—One of the best established instances of a disease due to a one-sided or defective diet is beriberi. This affection is prevalent among those peoples subsisting chiefly or wholly on a diet of rice prepared in a certain way. As a matter of trade convention milled white rice has long been considered superior to the unpolished grain. The process of polishing rice by machinery removes the red husk or pericarp of the grain, and a diet based almost exclusively on polished rice causes this well-marked disease—beriberi—which was for long regarded as of an infectious nature.[116]It has been shown that if the husks are restored to the polished grain and the mixture used as food the disease fails to develop. Experiments upon chickens and pigeons show that an exclusive diet of white rice causes in these animals a disease (polyneuritis of fowls) similar to beriberi, which likewise can be arrested or prevented by a change in diet. From such observations the conclusion has been drawn that in the pericarp of the rice grain there are certain substances essential to the maintenance of health and that their withdrawal from the diet leads to nutritional disturbances. The name "vitamin" has been given to these substances, but little is known about their chemical or physiological nature. In a varied diet vitamins are presumably present in avariety of foodstuffs, but if the diet is greatly restricted, some apparently trivial treatment of the food may result in their elimination. It is uncertain how many and how various the substances are that have been classed by some writers under the designation vitamin. At least two "determinants" are thought to be concerned in the nutrition of growth, a fat-soluble and a water-soluble substance.[117]
Pellagrais one of the diseases attributed to an unbalanced diet,[118]and it has been suggested that the increased use of highly milled maize and wheat flour from which vitamins are absent may be responsible for the extension of this malady in recent years. Other observers, while admitting that a faulty diet may predispose to pellagra as to tuberculosis and other diseases, do not assent to the view that it is the primary factor.[119]
Lathyrism.—The name lathyrism has been given to a disease supposed to be connected with the use of the pulse and the chick pea. Nervous symptoms are conspicuous and sometimes severe, although the affection is of a milder type than pellagra. The disease is said to be associated with the exclusive or almost exclusive use of leguminous food and with generally miserable conditions of living. It is yet uncertain whether lathyrism is a deficiency disease like beriberi and possibly pellagra, or whether it is due to a mixture of foreign and poisonous seeds with the particularlegumes consumed, or whether under certain conditions the legumes themselves may contain poisonous substances generated by some unknown fungus growths.
Favism(fromfava, "bean") is an acute febrile anemia with jaundice and hemoglobinuria which occurs in Italy and has been attributed to the use of beans as food or even to smelling the blossom of the bean plant.[120]A marked individual predisposition to the malady is said to exist. Although the symptoms are very severe and seem to point to an acute poisoning, no toxic substance has been isolated from the implicated beans. It has been suggested by some that bacterial infection, and by others that a fungous growth on the bean, is responsible, but no evidence has been brought forward to support either assumption.
Scurvyin some forms is undoubtedly connected with the lack of certain necessary components of a normal diet. The development of scurvy on shipboard in the absence of fresh milk, fresh vegetables, fruit juice, and the like is a fact long familiar. Guinea-pigs fed on milk, raw and heated, and on milk and grain have developed typical symptoms of scurvy.[121]On the other hand, a form of experimental scurvy has been produced in guinea-pigs and rabbits kept on an ordinary diet of green vegetables, hay, and oats by the intravenous injection of certain streptococci.[122]The relative share of diet and infection in the production of human scurvy is consequently regarded by some investigators as uncertain.
Rachitisor rickets is a pathological condition in some way connected with a protracted disturbance of digestion which in turn leads to faulty calcium metabolism. It does not seem probable that rickets is caused by too little calcium in the food, but rather by the inability of the bone tissue to utilize the calcium brought to it in the body fluids. Experiments upon the causation of the disease have not given uniform results, and it does not seem possible at present to place responsibility for this condition upon any particular form of diet, such as deficiency of fat or excess of carbohydrates or protein. It appears to be true that the prolonged use of any food leading to nutritional disturbance causes an inability on the part of the bone cells to take up calcium salts in the normal manner.
While there are many obscure points with regard to the origin of both scurvy and rickets, there is no doubt that some dietary shortcoming lies at their base, and that they can be cured or altogether avoided by maintenance of suitable nutritional conditions.
Certain articles of food figure with special frequency in the reports of food poisoning outbreaks. It is not clear in all cases why this special liability to inflict injury exists. For an example, vanilla ice-cream and vanilla puddings have been so often implicated that some investigators have not hesitated to ascribe a poisonous quality to the vanilla itself. But there is no good evidence that this is the case, and it has been suggested that the reducing action of the vanilla favors the growth of anaërobic bacteria which produce poisonous substances, an explanation highly conjectural.
The conspicuous frequency with which the consumption of raw meat provokes food poisoning has already been set forth and in large part explained by the occasional derivation of meat from animals infected with parasites harmful to man. The even greater culpability of raw milk is due to the fact that milk is not only, like meat, sometimes obtained from an infected animal, but that it is a particularly good culture medium for bacteria, and in the process of collection or distribution may become infected through the agency of a human carrier. Foods such as ice-cream that are prepared with milk are also often connected with food poisoning. It seems probable that illness caused by ice-cream is much more commonly due to bacterial infection than to poisoning with metals or flavoring extracts. The responsibility of these latter substances is entirely problematic.
Cases of cheese poisoning, which apparently are relatively numerous, are of quite obscure causation. Whether such poisoning is due more commonly to some original contamination of the milk, or to an invasion of the cheese by pathogenic bacteria in the course of preparation, or to the formation of toxic substances by bacteria or molds during the process of ripening which the cheese undergoes, is left uncertain in the majority of cases.
Shellfish poisoning from eating oysters, mussels, or clams is unquestionably caused in some instances by sewage contamination of the water from which the bivalves are taken, and in such cases bacilli of the typhoid or paratyphoid groups are commonly concerned. It is a disputed question whether certain recorded outbreaks of mussel poisoning have been due to bacterial infection or whether sometimes healthy ordiseased mussels taken from unpolluted water contain a poisonous substance. In a similar way it is uncertain whether a certain marine snail (Murex bradatus), sometimes used for food, contains under certain conditions a substance naturally poisonous for man, or whether it is poisonous only when it is infected or when toxigenic bacteria have grown in it.
Potato poisoning has been attributed in some cases to bacterial decomposition of potatoes by proteus bacilli; in other cases, to a poisonous alkaloid, solanin, said to be present in excessive amounts in diseased and in sprouting potatoes. It is noteworthy that many instances of potato poisoning have been connected with the use of potato salad which had stood for some time after being mixed, so that the possibility of infection with the paratyphoid bacillus or other pathogenic organisms cannot be excluded. That solanin is ever really responsible for potato poisoning is considered doubtful by many investigators.
These examples are sufficient to show that in a considerable proportion of cases of alleged food poisoning there is a large measure of uncertainty about the real source of trouble. Although the trend of opinion has been in the direction of an increased recognition of the share of certain bacteria, especially those of the paratyphoid group, there is an important residue of unexplained food poisoning that needs further skilled investigation. It is one of the objects of this book to point out this need and to draw attention to the numerous problems that await settlement. The first step is the regular and thorough investigation of every food poisoning outbreak.