Until such information is forthcoming we do well to err on the side of caution. The desirability of adopting this attitude is especially borne in upon us by the facts already instanced (pp.2-4) concerning the increased death-rates in the higher-age groups in this country. For aught we now know to the contrary, the relatively high death-rates from degenerative changes in the kidneys, blood vessels, and other organs may be in part caused by the use of irritating chemical substances in food. Although no one chemical by itself and in the quantities in which it is commonly present in food can perhaps be reasonably accused of producing serious and permanent injury, yet when to its effect is superadded the effect of still other poisonous ingredients in spiced, smoked, and preserved foods of all kinds the total burden laid upon the excretory and other organs may be distinctly too great. There can be no escape from the conclusion that the more extensive and widespread the use of preservatives in food the greater the likelihood of injurious consequences to the public health.
The use of spoiled or decomposed food falls under the same head. It cannot be assumed that the irritating substances produced in food by certain kinds of decompositioncan be continually consumed with impunity. We do not even know whether these decomposition products may not be more fundamentally injurious than preservatives that might be added to prevent decomposition!
So far as our present knowledge indicates, therefore, effort should be directed (1) to the purveying of food as far as possible in a fresh condition; (2) to the avoidance of chemical preservatives of all kinds except those unequivocally demonstrated to be harmless. The methods of preserving food by drying, by refrigeration, and by heating and sealing are justified by experience as well as on theoretical grounds, and the same statement can be made regarding the use of salt and sugar solutions. But the use of sulphites in sausage and chopped meat, the addition of formaldehyde to milk, and of boric acid or sodium fluoride to butter are practices altogether objectionable from the standpoint of public health.
The remedy is obvious and has been frequently suggested—namely, laws prohibiting the addition of any chemical to food except in certain definitely specified cases. The presumption then would be—as in truth it is—that such chemicals are more or less dangerous, and proof of innocuousness must be brought forward before any one substance can be listed as an exception to the general rule. Such laws would include not only the use of chemicals or preservatives, but the employment of substances to "improve the appearance" of foodstuffs. As already pointed out, the childish practice of artificially coloring foods involves waste and sometimes danger. It rests on no deep-seatedhuman need; food that is natural and untampered with may be made the fashion just as easily as the color and cut of clothing are altered by the fashion-monger. The incorporation of any chemical substance into food for preservative or cosmetic purposes could wisely be subject to a general prohibition, and the necessary list of exceptions (substances such as sugar and salt) should be passed on by a national board of experts or by some authoritative organization like the American Public Health Association.
On grounds of economy or convenience familiar and natural articles of food are sometimes replaced or supplemented by artificial chemical products, or by substances whose food value is not so definitely established. I need refer only briefly to those notorious instances of adulteration in which chicory is added to coffee, or ground olive stones to pepper, or glucose to candy. On hygienic grounds alone some such practices are not open to criticism, however fraudulent they may be from the standpoint of public morals. It might be argued with some plausibility that chicory is not so likely to harm the human organism as caffeine and that sprinklings of ground cocoanut shell are more wholesome than pepper. But there is another group of cases in which the artificial substitute is strictly objectionable. The use of the coal-tar product saccharin for sweetening purposes is an example. This substance, whose sweetening power is five hundred times as great as that of cane sugar, has no nutritive value in the quantities in which it would be consumed, and in not very large quantities(over 0.3 gram per day) is likely to induce disturbance of digestion. As a substitute for sugar in ordinary foodstuffs it is undesirable.[48]
The use of cheap chemically prepared flavors such as "fruit ethers" in "soft drinks," fruit syrups, and the like in place of the more expensive natural fruit extracts affords another well-known instance of substitution. Probably more important hygienically is the production of "foam" in "soda water" by saponin, a substance known to be injurious for red blood corpuscles.
Among the many other familiar examples of food substitution, sophistication, and adulteration there are some of demonstrable hygienic disadvantage and others whose chief demerit lies in simple deception. Of practically all it may be said that they are indefensible from the standpoint of public policy since they are based on the intent to make foodstuffs appear other than what they really are.
It is the opinion of some who have closely followed the course of food adulteration that, while the amount of general sophistication—legally permissible and otherwise—has greatly increased in recent years, the proportion of really injurious adulteration has fallen off. Be that as it may, it is plain that the opportunity for wholesale experimentation with new substances should not be allowed to rest without control in the hands of manufacturers and dealers largely impelled by commercial motives. So long as the motive of gain is allowed free scope, so long will a small minority of unscrupulous persons add cheap, inferior, and sometimes dangerous ingredients to foodstuffs. The net of restriction mustbe drawn tighter and tighter. The motives leading to the tampering with food fall mainly under three heads: (1) a desire to preserve food from spoiling or deterioration; (2) a puerile fancy—often skilfully fostered for mercenary reasons—for a conventional appearance, as for polished rice, bleached flour, and grass-green peas; and (3) intent to make the less valuable appear more valuable—deliberate fraud. Only the first-named motive can claim any legitimate justification, and its gratification by the use of chemical preservatives is surrounded with hygienic difficulties and uncertainty, as already set forth. From the unbiased view of human physiology the dangers of slow poisoning from chemically treated foods must be regarded as no less real because they are insidious and not easily traced.
Many cases of so-called food poisoning are due to the presence of pathogenic bacteria in the food. In some instances, as in the typical meat poisoning epidemics, symptoms develop so soon after eating that the particular food involved is immediately suspected and laid hands on. In other cases the guilty article of food is difficult to trace. Certain cases of tuberculosis are undoubtedly caused by swallowing tubercle bacilli in the food, but the precise source and date of infection can be rarely, if ever, certainly established.
The presence of pathogenic bacteria in food is usually due either to the contamination of the food by infected human beings during the process of preparation or serving, or to an infection of the animal from which the food is derived. The relative importance of these two factors is quite different in the various infections.
The typhoid bacillus does not attack any of the domestic animals; consequently all food-borne typhoid is caused more or less directly by human contamination. A remarkable instance of typhoid infection due to food was reported in 1914 in Hanford, California, where ninety-three typhoid cases were caused by eating Spanish spaghetti served at a public dinner.[49]Investigation showed that this dish was prepared by a womantyphoid-carrier who was harboring living typhoid bacilli at the time she mixed the sauce for the spaghetti before baking. Further laboratory experiments indicated that the ordinary baking temperature at which the spaghetti was cooked was not only not sufficient to sterilize the food, but afforded a favorable opportunity for the bacteria in the interior of the mass to multiply. The infection of the food was consequently heavy and involved a very large proportion (57 per cent) of those present at the dinner.
Merited celebrity attaches to the exploits of the typhoid-carrier, Mary Malloy, who, in pursuing her career as cook in and about New York City, is known to have caused at least seven typhoid outbreaks in various families in which she worked and one extensive hospital epidemic. Similar cases of typhoid food infection by employees in restaurants and public institutions are by no means uncommon, and show the necessity of protecting food from contamination during the whole process of preparation and serving. Acting on this principle, the Department of Health of New York City has inaugurated a comprehensive examination of the cooks and waiters (approximately 90,000) employed in the public restaurants and dining-rooms in that city. Results have been obtained in the discovery of typhoid-carriers and of cases of communicable disease that amply justify this procedure as an important measure for protecting the community against the dissemination of infection.
Some foods by their origin are exposed more than others to typhoid contamination. Such vegetables as lettuce, celery, radishes, and watercress, which arecommonly eaten without cooking, are more likely to convey typhoid than peas, beans, and potatoes. A typhoid outbreak apparently due to watercress has been reported from Philadelphia.[50]At a wedding breakfast to forty-three guests on June 24, 1913, watercress sandwiches were served, and subsequent inquiry showed that nineteen of the guests partook of these sandwiches. Eighteen of this number became ill with typhoid fever within a month, the illness developing in most cases after the guests had scattered to their summer homes. Those who did not eat watercress sandwiches were not affected. Typhoid infection by uncooked celery has also been reported.[51]
The practice of using human excreta as fertilizer in truck gardens is sometimes responsible for a dangerous contamination of the soil, which is communicated to the growing plants and persists for a long time.[52]Even scrupulous washing of vegetables is not sufficient to render them bacterially clean. In the future the danger to the community from this source is likely to become increasingly serious unless the growing use of this method of soil enrichment is definitely checked.
In 1915 an increasing number of typhoid cases in South Philadelphia led to an investigation by the state health department.[53]This disclosed the fact that the majority of the cases were clustered in and about three public markets.
These are all curb markets—fruits, vegetables, pastry, clothing, and miscellaneous merchandise of every description are dumped on push-carts and pavements without regard for any sanitary precautions. The patrons of these markets handle and pick over the exposed foodstuffs, thus giving every opportunity for the transmission of disease....
The greatest number of cases occurred in the immediate vicinity of the Christian Street Market. This market is largely patronized by the inhabitants of the section known as "Little Italy." The patrons of the South Street Market are principally Hebrews, while the Seventh Street Market is patronized in the main by Hebrews and Poles.
The following conclusion was reached regarding the particularly large number of cases among persons of one nationality:
Our inspectors have found that the different methods used by the Italians and Hebrews in the preparation of their food are responsible for the larger number of cases being found in the vicinity of the Christian Street Market in Little Italy. It is the custom of the Italians to eat many of the fruits and vegetables raw, while the Hebrews cook the greater portion of their food. It is presumably due to this custom that the members of the Italian colony have suffered to a greater extent than the other residents of the district.
A bacterial examination of various kinds of vegetables obtained from push-carts and curb markets led to the finding of the typhoid bacillus upon some of the celery. It would naturally be difficult to determine in such cases whether the typhoid bacilli were derived from infected soil in which the celery was grown or whether the contamination occurred through improper handling.
Bread, when marketed unwrapped, is subject to contamination from flies and from uncleanly handling.Katherine Howell[54]has shown that unwrapped loaves of bread sold in Chicago were more or less thickly smeared with bacteria and were coated on the average with a much larger number than wrapped loaves. In some cases typhoid fever has been directly traced to bread. Hinton[55]has recorded the occurrence of seven typhoid cases in the Elgin (Illinois) State Hospital, which were apparently due to a typhoid-carrier whose duty it was as attendant to slice the bread before serving. When this typhoid-bearing attendant was transferred to another department where she handled no uncooked food, cases of typhoid ceased to appear.[56]
Food such as milk that is not only eaten customarily without cooking, but is also suitable for the growth of typhoid bacilli, needs to be particularly safeguarded. It is noteworthy that the compulsory pasteurization of milk in New York, Chicago, and other large American cities has been accompanied by a great diminution in the prevalence of typhoid fever. Until recent years milk-borne typhoid in the United States has been common and hundreds of typhoid epidemics have been traced to this source.
Fig. 5.Fig. 5.—Bacteria left by fly passing over gelatin plate. (By courtesy of Doubleday, Page & Company.)
Fig. 5.—Bacteria left by fly passing over gelatin plate. (By courtesy of Doubleday, Page & Company.)
One food animal, the oyster, frequently eaten raw, has been connected on good evidence with certain typhoid outbreaks.[57]The number of well-establishedoyster typhoid epidemics is not great, however, and the danger from this source has sometimes been exaggerated. The source of oyster contamination is in sewage pollution either of the shellfish beds or of the brackish water in which the oyster is sometimes placed to "fatten" before it is marketed. State and federal supervision of the oyster industry in the United States in recent years has largely done away with the taking of oysters from infected waters, and although oysters—andclams and mussels as well—must be steadily safeguarded against sewage contamination, the actual occurrence of oyster infection at the present time is believed to be relatively rare.
Probably the most effective method of preventing typhoid food infection is to investigate every case of typhoid fever and trace it, so far as practicable, to its origin. In this way typhoid-carriers may be discovered and other foci of infection brought to light. Carriers, once found, may be given proper advice and warned that they constitute a danger to others; the complete control of typhoid-carriers who are not disposed to act as advised is a difficult problem and one not yet solved by public health authorities.
With Asiatic cholera, just as with typhoid fever, domestic animals are not susceptible to the disease, all cases of infection having a direct human origin. Drinking-water is the usual vehicle of cholera infection, and even in countries where the disease is endemic, food-borne outbreaks of this disease are far less common than those of typhoid fever. Occasional instances of Asiatic cholera due to milk supply and to contaminated fruits or lettuce are on record, but these are exceptional and cannot be regarded as exemplifying a common mode of spread of this disease. The extent, however, to which dwellers in tropical countries—and indeed in all lands—are at the mercy of their household helpers is illustrated by the following experience of the English bacteriologist, Hankin. "I have seen," he says, "a cook cooling a jelly by standing it in a small irrigationditch that ran in front of his cookhouse. The water running in this drain came from a well in which I had detected the cholera microbe. He cleaned a spoon by dipping it in the drain and rubbing it with his fingers; then he used it to stir the jelly."[58]
Animal experiments have shown that both meat and milk derived from tuberculous cattle are capable of conveying infection. The precise degree of danger to human beings from the use of these foods under modern conditions is still in dispute. Since the tubercle bacillus of bovine origin differs from the tubercle bacillus of human origin in certain well-defined particulars, it is possible by careful study to distinguish the human infections caused by the bovine bacillus from those caused by the so-called human tubercle bacillus. Additional comparative investigations are needed in this field, and these may enable us to estimate eventually more fully than is possible at present the extent of human tuberculous infection derived from bovine sources.
Meat is a less likely source of infection than milk, chiefly because it is rarely eaten without cooking. Opinion regarding the actual frequency of the transmission of tuberculosis by means of the meat of tuberculous cattle has been widely at variance in the past, and must even now be based on indirect evidence. There is no well-established instance of human infection from the use of the flesh of tuberculous cattle. The significance of this fact, however, is diminished by the observation that tubercle bacilli can pass through the intestinalwall without leaving any trace of their passage and can make their way to the lungs or to other distant organs where they find opportunity for growth. This, together with the long period which usually elapses between the actual occurrence of infection and the discovery of the existence of infection, makes the difficulty of securing valid evidence peculiarly great. Opposed to any very frequent occurrence of meat-borne tuberculosis are the facts that the tubercle bacillus is not commonly or abundantly present in the masses of muscle usually marketed as "meat," that the tubercle germ itself is not a spore-bearer and is killed by ordinary cooking, and that the reported cases of the finding of tubercle bacilli of bovine origin in adults over sixteen years of age are extremely rare. This latter fact is perhaps the strongest evidence indicating that tuberculous meat infection, although theoretically possible, is at least not of common occurrence.
Most of the commissions and official agencies that have considered the precautions to be taken against possible tuberculous meat infection are agreed that the entire carcass of an animal should be condemned when the tuberculous lesions are generalized or when the lesions are extensive in one or both body cavities as well as when the lesions are "multiple, acute, and actively progressive." Any organ showing evidence of tuberculous lesions is obviously not to be passed as food. On the other hand, it is considered that portions of properly inspected animals may be put on the market if the tuberculous lesion is local and limited and the main part of the body is unaffected; in such cases contamination of the meat in dressing must be avoided. It is thegeneral belief that when such precautionary measures are taken the danger of tuberculous infection through properly cooked meat is so slight as to be negligible.
Milk is a much more likely vehicle than meat for the transmission of tuberculosis. Freshly drawn raw milk from tuberculous cattle may contain enormous numbers of tubercle bacilli, especially if the udder is diseased. Contamination of milk by the manure of tuberculous cows can also occur. Observers in England, Germany, France, and the United States have found tubercle bacilli in varying numbers in market milk, and have proved that such milk is infectious for laboratory animals. Although, as pointed out with reference to meat infection, the difficulties of tracing any particular case of tuberculosis to its source are very great, there are a number of instances on record in which the circumstantial evidence strongly indicates that milk was the vehicle of infection. Especially convincing are the observations on the relative frequency of infection with bovine and human tubercle bacilli at different ages as shown in the following tabulation:[59]
The large proportion of bovine tubercle bacillus infections in children stands in all probability in causal relation to the relatively extensive use of raw milk in the child's dietary.
The proper pasteurization of milk affords a safe and reasonably satisfactory means of preventing tuberculous infection from this source. The general introduction of the pasteurizing process in most American cities has ample justification from the standpoint of the prevention of infection.
The facts related in the foregoing pages indicate that of all foods milk is the most likely to convey disease germs into the human body. This is partly due to the fact that milk is sometimes obtained from diseased animals, and partly to the fact that unless great care is taken it may readily become contaminated during the process of collection and transportation; if milk is once seeded with dangerous bacteria these can multiply in the excellent culture medium it affords. It is also partly because milk is commonly taken into the alimentary tract without being cooked. For these reasons the amount of illness traceable to raw milk far exceeds that ascribable to any other food.
There are several infections that may be communicated by milk, but are rarely if ever due to other foodstuffs. Diphtheria and scarlet fever are perhaps the best known of these. Both diseases have been repeatedly traced to the use of particular milk supplies, although various forms of individual contact also play a large rôle in their dissemination. Milk-borne scarlet fever and diphtheria seem to be generally, if not always, due to the direct contamination of the milk from human sources. It is considered possible, however, by some investigators that the cow may sometimes becomeinfected from human sources with the virus of scarlet fever or diphtheria and may herself occasionally contribute directly to the infection of the milk.
A serious milk-borne disease, which has lately been conspicuous in Boston, Chicago, Baltimore, and other American cities under the name of "septic sore throat" or "streptococcus sore throat," originates apparently in some cases from infection of the udder of the cow by an infected milker; in other cases the milk has seemingly been directly infected by a human "carrier." The specific germ is thought to have been isolated and its connection with the disease demonstrated in the laboratory. This disease, like diphtheria and scarlet fever, is sometimes due to contact. It is not known to be caused by any food except milk.
Foot-and-mouth disease of cattle is transmissible to man through the milk of infected cattle, but this infection in man is not very common or as a rule very serious. So far as known, it is not communicated to man in any other way except through the use of uncooked milk.
Such cases of infection or "poisoning" by milk may be prevented, as already stated, by the exclusive use of heated milk. The possible occurrence of nutritional disturbances (e.g., scurvy) in a small proportion of the children fed on pasteurized or boiled milk is considered by many physicians to be easily remedied and to possess much less practical importance than the avoidance of infection.
One widely distributed organism known asBacillus proteushas been several times held responsible for foodpoisoning outbreaks, but it is not yet certain how far this accusation is justified.B. proteusis related toB. coli, but most varieties do not ferment lactose and are much more actively proteolytic than the latter organism, as shown by their ability to liquefy gelatin and casein. LikeB. coli, they form indol and ferment dextrose with gas production. Varieties ofB. proteusare found widely distributed in decomposing organic matter of all sorts.
The evidence upon which this bacillus is regarded as the cause of food poisoning is not altogether convincing. The outbreak described by Pfuhl[60]is typical. Eighty-one soldiers in a garrison at Hanover were suddenly attacked with acute gastro-enteritis four to twelve hours after eating sausage meat. The meat was found to containB. proteusin large numbers, although it was prepared with ordinary care and was entirely normal in appearance, taste, and smell. Rats and mice fed with the sausage became ill andB. proteuswas isolated from the blood and internal organs. But these animals sometimes die when fed with quite normal meat, andB. proteusand other common intestinal bacteria are often isolated from the body after death.B. proteus, in fact, is found in many animal foods and in the apparently normal human intestine. LikeB. coli, it frequently invades the internal organs after or shortly before death. FindingB. proteusin food or in the internal organs does not therefore constitute definite proof of any causal relationship. The evidence attributing other outbreaks to infection withB. proteusis similarly inconclusive.
It is equally uncertain whether the production of a poison in food by this species can in any degree be held responsible for meat poisoning.B. proteusis common enough in decomposing food material and under certain circumstances is known to generate substances that are toxic for man. It is possibly true that toxic substances are produced in the early stages of decomposition by this organism. In the opinion of Mandel[61]and others, if any injurious effect at all is to be attributed toB. proteus, it is in the nature of an intoxication and not an infection (seechapter viii). So far as the existing evidence goes, the question of the responsibility of this organism for food poisoning is still an open one.
The most characteristic examples of "food poisoning," popularly speaking, are those in which the symptoms appear shortly after eating and in which gastro-intestinal disturbances predominate. In the typical group-outbreaks of this sort all grades of severity are manifested, but as a rule recovery takes place. The great majority of such cases that have been investigated by modern bacteriological methods show the presence of bacilli belonging to the so-called paratyphoid group (B. paratyphosusorB. enteritidis). Especially is it true of meat poisoning epidemics that paratyphoid bacilli are found in causal relation with them. Hübener[62]enumerates forty-two meat poisoning outbreaks in Germany in which bacilli of this group were shown to be implicated, and Savage[63]gives a list of twenty-seven similar outbreaks in Great Britain. In the United States relatively few outbreaks of this character have been placed on record, but it cannot be assumed that this is due to their rarity, since no adequate investigation of food poisoning cases is generally carried out in our American communities.
Typical paratyphoid outbreaks.—Kaensche[64]describes an outbreak at Breslau involving over eighty personsin which chopped beef was apparently the bearer of infection. The animal from which the meat came had been ill with severe diarrhea and high fever and was slaughtered as an emergency measure (notgeschlachtet). On examination a pathological condition of the liver and other organs was noted by a veterinarian who declared the meat unfit for use and ordered it destroyed. It was, however, stolen, carried secretly to Breslau, and portions of it were distributed to different sausage-makers, who sold it for the most part as hamburger steak (Hackfleisch). The meat itself presented nothing abnormal in color, odor, or consistency. Nevertheless, illness followed in some cases after the use of very small portions. With some of those affected the symptoms were very severe, but there were no deaths. Bacilli of theBacillus enteritidistype were isolated from the meat.
A large and unusually severe outbreak reported by McWeeney[65]occurred in November, 1908, among the inmates of an industrial school for girls at Limerick, Ireland. There were 73 cases with 9 deaths out of the total number of 197 pupils. The brunt of the attack fell on the first or Senior class comprising 67 girls between the ages of thirteen and seventeen. Out of 55 girls belonging to this class who partook of beef stew for dinner 53 sickened, and 8 of these died. One of the two who were not affected ate the gravy and potatoes but not the beef. Some of the implicated beef was also eaten as cold meat by girls in some of the other classes, and also caused illness. Part of the meat had been eaten previously without producing any ill effects. "The escape of those who partook of portions of thesame carcass on October 27 and 29 [five days earlier] may be accounted for either by unequal distribution of the virus, or by thorough cooking which destroyed it. Some of the infective material must, however, have escaped the roasting of the 29th, and, multiplying rapidly, have rendered the whole piece intensely toxic and infective during the five days that elapsed before the fatal Tuesday when it was finally consumed." The animal from which the fore quarter of the beef was taken had been privately slaughtered by a local butcher. No reliable information could be obtained about the condition of the calf at, or slightly prior to, slaughter. The meat, however, was sold at so low a price that it was evidently not regarded as of prime quality. In this outbreak the agglutination reactions of the blood of the patients and the characteristics of the bacilli isolated showed the infection to be due to a typical strain ofBacillus enteritidis.
An epidemic of food poisoning occurred in July, 1915, at and near Westerly, Rhode Island.[66]The outbreak was characterized by the usual symptoms of acute gastro-enteritis, and followed the eating of pie which was obtained at a restaurant in Westerly. All the circumstances of the outbreak showed that a particular batch of pies was responsible. About sixty persons were made seriously ill and four died. There was no unusual taste or odor to the pies to excite suspicion. The symptoms followed the eating of various kinds of pie: custard, squash, lemon, chocolate, apple, etc., that had been made with the same pie-crust mixture.Bacillus paratyphosusB was isolated from samples ofpie that were examined. No definite clue was obtained as to the exact source of infection of the pie mixture. It is possible that the pie became infected in the restaurant through the agency of a paratyphoid-carrier, but since there had been no change in the personnel of the restaurant for several months, this explanation is largely conjectural. Possibly some ingredient of animal origin was primarily infected.
General characters of paratyphoid infection.—The symptoms of paratyphoid food infection are varied. As a rule the first signs of trouble appear within six to twelve hours after eating, but sometimes they may come on within half an hour, or they may not appear until after twenty-four to forty-eight hours. Gastro-intestinal irritation is practically always present, and may take the form of a mild "indigestion" or slight diarrhea or may be of great severity accompanied with agonizing abdominal pain. Fever is usual, but is generally not very high. Recovery may occur quickly, so that within two or three days the patient regains his normal state, or it may be very slow, so that the effects of the attack linger for weeks or months.
Investigators have noted the occurrence of at least two clinical types of paratyphoid infection, the commoner gastro-intestinal type just described and a second type resembling typhoid fever very closely, and occasionally not to be distinguished from it except by careful bacterial examination. It is not yet clear how these two clinical varieties are related to the amount and nature of the infecting food material. No difference in the type of paratyphoid bacillus has been observed to be associated with the difference in clinical manifestation.Possibly the amount of toxin present in the food eaten as well as the number of bacilli may exercise some influence. The individual idiosyncrasy of the patient doubtless plays a part.
While there is still some uncertainty about particular features of paratyphoid infection, a few significant facts have been clearly established: (1) Certain articles of diet are much more commonly associated than others with this type of food poisoning. The majority of recorded outbreaks are connected with the use of meat, milk, fish, and other protein foods. Vegetables and cereals have been less commonly implicated, fruits rarely. (2) In many, though not all, of the cases of paratyphoid meat poisoning it has been demonstrated that the meat concerned has been derived from an animal slaughtered while ailing (notgeschlachtet, to use the expressive German term). There seems reason to believe that in such an animal, "killed to save its life," the specific paratyphoid germ is present as an infection before death. Milk also has caused paratyphoid poisoning and in certain of these cases has been found to be derived from a cow suffering from enteritis or some other disorder. (3) There is evidence that originally wholesome food may become infected with paratyphoid bacilli during the process of preparation or serving in precisely the same way that it may become infected with typhoid bacilli; the handling of the food by a paratyphoid-carrier is commonly responsible for this. In a few instances the disease is passed on from case to case, but this mode of infection seems exceedingly rare and is not nearly so frequent as "contact" infection in typhoid. (4) The majority of paratyphoid outbreaksare associated with the use of uncooked or partly cooked food. A selective action is often manifested, those persons who have eaten the incriminated food substance raw or imperfectly cooked being most seriously affected, while those who have partaken of the same food after cooking remain exempt.
Fig. 6.Fig. 6.—Bacillus enteritidis, Gärtner; pure culture; Van Ermengem preparation. (Kolle and Wassermann.)
Fig. 6.—Bacillus enteritidis, Gärtner; pure culture; Van Ermengem preparation. (Kolle and Wassermann.)
The discovery of the connection of paratyphoid bacilli with meat poisoning dates from the investigation by Gärtner,[67]in 1888, of a meat poisoning outbreak in Frankenhausen, a small town in Germany. This epidemic was traced to the use of meat from a cow that was slaughtered because she was ill with a severe enteritis. Fifty-eight persons were affected in varying grades of severity; the attack resulted fatally in one young workman who ate about eight hundred grams of raw meat. Gärtner isolated from the spleen of the fatal case and also from the flesh and intestines of the cow a bacillus to which he gave the nameB. enteritidis. Inoculation experiments showed it to be pathogenic for a number of animal species. Bacilli with similar characters have since been isolated in a number of other meat poisoning epidemics in Germany, Belgium, France, and England. One well-studied instance offood poisoning due to the paratyphoid bacillus has been reported in the United States.[68]
The bacteria of the paratyphoid group are closely related to the true typhoid bacillus, but differ from the latter organism in being able to ferment glucose with gas production. They are more highly pathogenic for the lower animals than is the typhoid bacillus, but apparently somewhat less pathogenic for man. Most types of paratyphoid bacilli found in food poisoning produce more or less rapidly a considerable amount of alkali, and, if they are inoculated into milk containing a few drops of litmus, the milk after a time becomes a deep blue color. Several distinct varieties of paratyphoid bacilli have been discovered. The main differences shown by these varieties are agglutinative differences. That is, the blood serum of an animal that has been inoculated with a particular culture or strain will agglutinate that strain and also other strains isolated from certain other meat poisoning epidemics, but will not agglutinate certain culturally similar paratyphoid bacteria found in connection with yet other outbreaks. Except in this single matter of agglutination reaction, no constant distinction between these varieties has been demonstrated. The clinical features of the infections produced in man and in the higher animals by the different varieties seem to be very similar if not identical.
The bacillus discovered by Gärtner (loc. cit.) and known asB. enteritidisor Gärtner's bacillus is commonly taken as the type of one of the agglutinative varieties. Bacilli with all the characters of Gärtner's bacillus have been found in meat poisoning epidemics in variousplaces in Belgium and Germany. Mayer[69]has compiled a list of forty-eight food poisoning outbreaks occurring between 1888 and 1911 and attributed toB. enteritidisGärtner. These outbreaks comprised approximately two thousand cases and twenty deaths. In twenty-three of the forty-eight outbreaks the meat was derived from animals known to be ill at the time, or shortly before, they were slaughtered. Sausage and chopped meat of undetermined origin were responsible for eleven of the remaining twenty-five outbreaks. Two of theB. enteritidisoutbreaks were attributed toVanille Pudding; one, to potato salad.
In other food poisoning outbreaks a bacillus is found which is culturally similar to the Gärtner bacillus, but refuses to agglutinate with the Gärtner bacillus serum. Its cultural and agglutination reactions are almost, if not quite, identical with those of the bacilli found in human cases of paratyphoid fever which have no known connection with food poisoning. Mayer[70]gives a list of seventy-seven outbreaks of food poisoning (1893-1911) in which organisms variously designated as "B. paratyphosusB" or as "B. suipestifer" were held to be responsible. The total number of cases (two thousand) and deaths (twenty) is about the same as ascribed toB. enteritidis. According to Mayer's tabulation meat from animals definitely known to be ailing is less commonly implicated in this type (ten in seventy-seven) than inB. enteritidisoutbreaks (twenty-three in forty-eight). Sausage and chopped meat of unknown origin, however, were connected with eighteen outbreaks.
The bacillus namedB. suipestiferwas formerly believed to be the cause of hog cholera, but it is now thought to be merely a secondary invader in this disease; it is identical with the bacillus calledB. paratyphosusB in its cultural and to a large extent in its agglutinative behavior, but is regarded by some investigators as separable from the latter on the basis of particularly delicate discriminatory tests. Bainbridge, Savage, and other English investigators consider indeed that the true food poisoning cases should be ascribed toB. suipestiferand would restrict the termB. paratyphosusto those bacteria causing "an illness clinically indistinguishable from typhoid fever." German investigators, on the other hand, regardB. suipestiferandB. paratyphosusB as identical. My own investigations[71]indicate that there is a real distinction between these two types.
Bearing directly on this question is the discussion concerning the distribution of the food poisoning bacilli in nature. Most investigators in Germany, where the majority of food poisoning outbreaks have occurred, or at least have been bacteriologically studied, are of the opinion thatB. suipestifer(the same in their opinion asB. paratyphosusB) is much more widely distributed thanB. enteritidisand that it occurs, especially in certain regions, as in the southern part of the German Empire, quite commonly in the intestinal tract of healthy human beings. Such paratyphoid-carriers, it is supposed, may contaminate food through handling or preparation just as typhoid-carriers are known to do. A number of outbreaks in which contamination of food during preparation is thought to have occurred have beenreported by Jacobitz and Kayser[72](vermicelli), Reinhold[73](fish), and others. Reinhold notes that in one outbreak several persons who had nursed those who were ill became ill themselves, indicating possible contact infection. In another outbreak also reported by Reinhold it was observed that those who partook of the infected food, in this case dried codfish, on the first day were not so severely affected as those who ate what was left over on the second day. A bacillus belonging to the paratyphoid group was isolated from the stools of patients, but not from the dried codfish. These facts were interpreted as signifying that the fish had become infected in the process of preparation and that the bacilli multiplied in the food while it was standing.
There seems no doubt that certain cases of paratyphoid food poisoning are caused by contamination of the food during preparation and are, sometimes at least, due to infection by human carriers. The bacilli in such cases are usually (according to many German investigators) or always (according to most English bacteriologists) of theB. suipestifertype. Other cases are due to pathogenic bacteria derived from diseased animals, and these bacteria are often, possibly always, of a slightly different character (B. enteritidisGärtner). It is still unsettled whether both types of food poisoning bacteria are always associated with disease processes of man or animals, or whether they are organisms of wide distribution which may at times acquire pathogenic properties. In certain regions, as in North Germany and England, such bacteria are rarely, if ever, foundexcept in connection with definite cases of disease. In parts of Southwest Germany, on the other hand, they are said to occur with extraordinary frequency in the intestines of healthy men and animals. Savage[74]believes that there is some confusion on this subject owing to the existence of saprophytic bacteria which he calls "Paragaertner" forms and which bear a close resemblance to the "true" Gärtner bacilli. They can be distinguished from the latter only by an extended series of tests. The bacilli of this group show remarkable variability, and in the opinion of some investigators "mutations" sometimes occur which lead to the transformation of one type into another.[75]
In spite of the present uncertainty regarding the relationship and significance of the varieties observed, a few facts emerge plainly from the confusion: (1) The majority of meat poisoning outbreaks that have been bacterially studied in recent years have been traceable to one or another member of this group and not to "ptomain poisoning." (2) Bacteria of theparatyphoid enteritidisgroup that are culturally alike but agglutinatively dissimilar can, when taken in with the food, give rise to identical clinical symptoms in man. (3) Food poisoning bacteria of this group, when derived directly from diseased animals, seem more likely to be of the Gärtner type (B. enteritidis) than of theB. suipestifertype.
Toxin production.—The problem of the production of toxin by the bacteria of this group and the possible relation of the toxin to food poisoning has been muchdiscussed. Broth cultures in which the living bacilli have been destroyed by heat or from which they have been removed by filtration contain a soluble poison. When this germ-free broth is injected into mice, guinea-pigs, or rabbits, the animals die from the effects. Practically nothing is known about the nature of the poisonous substances concerned, except that they are heat-resistant. They are probably not to be classed with the so-called true toxins generated by the diphtheria and tetanus bacilli, since there is no evidence that they give rise to antibodies when injected into susceptible animals. In the opinion of some investigators the formation of these toxic bodies by theparatyphoid-enteritidisbacilli in meat and other protein foodstuffs is responsible for certain outbreaks and also for some of the phenomena of food poisoning, the rapid development of symptoms being regarded as due to the ingested poisons, whereas the later manifestations are considered those of a true infection. Opposed to this view is the fact that well-cooked food has proved distinctly less liable to cause food poisoning than raw or imperfectly cooked food.
A large proportion of the recorded meat poisoning outbreaks are significantly due to sausages made from raw meat and to meat pies, puddings, and jellies. This is most likely because the heat used in cooking such foods is insufficient to produce germicidal results. In milk-borne epidemics also it is noteworthy that the users of raw milk are the ones affected. For example, respecting an extensiveB. enteritidisoutbreak in and about Newcastle, England, it is stated:
In no instance was a person who had used only boiled milk known to have been affected. Thus in one family, consisting ofhusband, wife, and wife's mother, the two women drank a small quantity of raw milk from the farm, at the most a tumblerful, and both were taken ill about twelve hours later. The husband, on the other hand, habitually drank a pint a day, but always boiled. He followed his usual custom on this occasion, and was unaffected.[76]
When in addition it is taken into consideration that the ordinary roasting or broiling of a piece of meat is often not sufficient to produce a germicidal temperature throughout, the argument that a heat-resistant toxin is present in such cases is not conclusive. It must be remembered also that in some outbreaks those persons consuming raw or partly cooked meat have been affected while at the same time others eating well-cooked meat from the same animal have remained exempt; this would seem to indicate the destruction of living bacilli by heat, since the toxic substances formed by these organisms are heat-resistant. The view that a definite infection occurs, is favored, too, by the fact that the blood-serum of affected persons so frequently has an agglutinative action upon the paratyphoid bacillus. This would not be the case if the symptoms were due to toxic substances alone. Altogether the rôle of toxins formed byB. enteritidisand its allies in food outside the body cannot be said to be established. The available evidence points to infection as the main, if not the sole, way in which the bacilli of this group are harmful.
Sources of infection.—The main sources ofenteritidis-suipestiferinfection are: (1) diseased domestic animals, the infected flesh or milk of which is used for food; (2) infection of food by human carriers during the processof preparation or serving. To these may be added a third possibility: (3) contamination of food with bacteria of this group which are inhabitants of the normal animal intestine. Considering these in order:
1. Diseased animals: The majority of the meat poisoning outbreaks are caused by meat derived from pigs or cattle.Table IIIgives the figures for a number of British[77]and German[78]epidemics.
TABLE III[79]
Occasional outbreaks have also been attributed to infection through eating rabbit, sheep, goose, fish, shrimp, and oysters. Especially noteworthy is the relative rarity of infection from the meat of the sheep.
More definite information is needed respecting the pathological conditions caused by these bacteria in animals and the relation of such conditions to subsequent human infection. A rather remarkable problem is presented by the relation ofB. suipestiferto hog cholera. This bacillus, although not now consideredthe causal agent of hog cholera, is very commonly associated with the disease as an accessory or secondary invader, and is frequently found in the internal organs of swine after death. It might be supposed that in regions where hog cholera is prevalent human infections would be more common than in other districts, but this seems not to be the case. No connection has ever been demonstrated between outbreaks of hog cholera—in whichB. suipestiferis known to be abundantly distributed—and so-calledB. suipestiferinfections in man.
Suppurative processes in cattle, and especially in calves, have given rise to poisoning from the use of the meat or milk of the infected animals. It has been often demonstrated that bacteria of theenteritidis-suipestifergroup are associated with inflammation of the udder in cows and with a variety of septicemic conditions in cattle and other domestic animals as well as with manifestations of intestinal disturbances ("calf diarrhea," etc.).[80]The frequency with which poisoning has occurred through the use of the meat of "emergency-slaughtered" animals has been already mentioned. K. F. Meyer[81]has reported an instance of accidental infection in a laboratory worker caused by handling a bottle of sterilized milk that had been artificially contaminated with a pure culture ofB. enteritidisfor experimental purposes. The strain responsible for theinfection had been isolated from the heart blood of a calf that had succumbed to infectious diarrhea.
2. Human contamination: In a certain number of paratyphoid food infections there is some evidence that the food was originally derived from a healthy animal and became infected from human sources during the process of preparation. In addition to the instances already mentioned (Reinholdet al., p. 67) the Wareham (England, 1910) epidemic[82]was considered by the investigators to be due to infection of meat pies by a cook who was later proved to be a carrier of paratyphoid bacilli. The evidence in this case, however, is not altogether conclusive. Söderbaum[83]mentions a milk-borne paratyphoid epidemic occurring in Kristiania which was ascribed to infection of the milk by a woman milker. Sacquépée and Bellot[84]report an interesting paratyphoid outbreak involving nineteen out of two hundred and fifty men in a military corps. The patients fell ill on different dates between June 14 and June 21.
It was found that an assistant cook who had been in the kitchen for several months had been attacked a little before the epidemic explosion by some slight malady which was not definitely diagnosed. He had been admitted to the hospital and was discharged convalescent. The cook, on being recalled and quarantined, stated that some days before June 10 he was indisposed with headache and anorexia. He had nevertheless continued his service in the kitchen....B. paratyphosusB (B. suipestifer) was repeatedly found in his stools in August, September, and October.... In all probability, therefore, theoutbreak was due to food contaminated by a paratyphoid-carrier who had passed through an abortive attack of the fever.[85]
Bainbridge and Dudfield[86]describe an outbreak of acute gastro-enteritis occurring in a boarding-house; it was found that no one article of food had been eaten by all the persons affected, and there were other reasons for supposing the outbreak to be due to miscellaneous food contamination by a servant who was a carrier.
There is, therefore, ground for believing that occasional contamination of food may be brought about by bacteria of this group derived from human sources. It is not clear, however, how frequent this source of infection is, compared to infection originating in diseased animals. It must be admitted, too, that English investigators are disposed to look upon outbreaks similar to those just described as infections withB. paratyphosusB, an organism which they would distinguish from the "true" food poisoning bacilli,B. enteritidisandB. suipestifer.
3. Miscellaneous contaminations: Some investigators, especially certain German writers, regard the bacilli of the paratyphoid group as so widely distributed in nature that any attempt to control the spread of infection is like fighting windmills. According to this view the bacilli occur commonly in our everyday surroundings and thence make their way rather frequently into a variety of foodstuffs. Various German investigators have reported the presence of paratyphoid bacilli in the intestinal contents of apparently normal swine, cattle, rats, and mice and more rarely of other animals,in water and ice, in German sausage and chopped meat, and in the bodies of apparently healthy men. To what extent their alleged ubiquity is due to mistaken bacterial identification, as claimed by some English investigators, remains to be proved. There is no doubt that in some quarters exaggerated notions have prevailed respecting a wide distribution of the true paratyphoid bacteria. Savage and others believe that the hypothesis that food poisoning outbreaks are derived from ordinary fecal infection of food is quite unfounded. It is pointed out that there is good evidence of the frequent occurrence of intestinal bacteria in such food as sausages and chopped meat, and that consequently, if paratyphoid infections could occur through ordinary contamination with intestinal bacteria not connected with any specific animal infection, food poisoning outbreaks should be exceedingly common instead of—as is the case—comparatively rare.
At the present time even those who maintain that these bacilli are of common occurrence admit that their abundance is more marked in some regions than in others. Southwest Germany, for example, seems to harbor paratyphoid bacilli in relatively large numbers. Possibly local differences in distribution may account for the discrepancies in the published findings of German and British investigators.
A special case is presented by the relation of these bacilli to rats and mice. Among the large number of bacteria of the paratyphoid group is the so-called Danysz bacillus, an organism quite pathogenic for rodents, and now and again used in various forms as a "rat virus" for purposes of rodent extermination. Several outbreaks of food poisoning in man have beenattributed on more or less cogent evidence to food contamination by one of these viruses either directly by accident, as in the case described by Shibayama,[87]in which cakes prepared for rats were eaten by men, or indirectly through food contaminated by mice or rats that had been infected with the virus.[88]The use of such viruses has not proved of very great practical value in the destruction of rodents, and is open to serious sanitary objections, since the animals after apparent recovery can continue to carry the bacilli of the virus and to distribute them on or near food substances.
It seems possible that rats and mice may become infected with certain bacteria of this group without human intervention, and that these infected animals may be the means of contaminating foodstuffs and so causing outbreaks of food poisoning. Proof of the frequency with which this actually occurs is naturally difficult to obtain.
There is no escape from the conclusion that in any given case of food poisoning the exact source of infection is often largely conjectural. Even when suspicion falls strongly on a particular article of food, it may not be possible to establish beyond a reasonable doubt whether the material (meat or milk) came from a diseased animal or whether it was infected from other sources (man or other animals) at some stage during the process of preparation and serving. The most definitely attested cases yet put on record are those in which it is possible to trace the infection to food derived from an ailing animal.
Means of prevention.—The most obvious and probably the most important method of preventing infection with paratyphoid bacilli is the adoption of a system of inspection which will exclude from the market as far as possible material from infected animals. To be most effective such inspection must be directed to examination of the living animal. The milk or the meat from diseased animals may give no visible sign of abnormality. In the Ghent outbreak of 1895 the slaughter-house inspector, a veterinary surgeon, was so firmly convinced that the meat which he had passed could have had no connection with the outbreak, that he ate several pieces to demonstrate its wholesomeness. The experiment had a tragic ending, as the inspector was shortly attacked with severe choleraic symptoms and died five days later, paratyphoid bacilli being found at the autopsy. Müller[89]also has described a case in which paratyphoid bacilli were found in meat that had given rise to a meat poisoning outbreak although the meat was normal in appearance and the organs of the animal showed no evidence of disease to the naked eye. It is evident that inspection of the live animal will often reveal evidence of disease which might be missed in the ordinary examination of slaughter-house products.
Although inspection of cows used for milking and of food animals before slaughter is highly important, it does not constitute an absolute protection. Emphasis must be repeatedly laid on the fact that meat, and especially milk that is derived from seemingly healthy animals, may nevertheless contain paratyphoid bacilli. To meet this difficulty in part the direct bacterialexamination of the carcasses of slaughtered food animals has been proposed, but this seems hardly practicable as a general measure. In spite of all precautions taken at the time of slaughtering it seems probable that occasionally paratyphoid-infected meat will pass the first line of defense and be placed on the market.
This danger, which is probably not a very grave one under a reasonably good system of inspection of live animals, may be met by thoroughly cooking all foods of animal origin. It is worth noting that some of the internal organs, as the liver and kidneys, are more likely to contain bacteria than the masses of muscle commonly eaten as "meat." Sausages, from their composition and mode of preparation, and chopped meat ("hamburger steak") are also to be treated with especial care. Consumption of such foods as raw sausage or diseased goose liver (paté de foie gras) involves a relatively high risk. It is true of paratyphoid infection as of most other forms of food poisoning that thorough cooking of food greatly diminishes the likelihood of trouble.
Whatever be the precise degree of danger from food infection by healthy paratyphoid-carriers (man or domestic animals), it is obvious that general measures of care and cleanliness will be more or less of a safeguard. As with typhoid fever so all outbreaks of paratyphoid should be thoroughly investigated in order that the sources of infection may be found and eliminated. The possible connection of rats and mice with these outbreaks should furnish an additional incentive to lessen the number of such vermin as well as to adopt measures of protecting food against their visits.