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Relation Of Food To The Public Health

( Originally Published 1939 )



Microbial infection. Microorganisms have quite definite nutritional requirements. They can grow only when they find themselves in an environment which furnishes the proper food and which at the same time does not inhibit their metabolism. An organism may lie dormant on a food until the environment becomes favorable for its growth. Many human foods furnish just the proper assortment of substances that meet these microbic requirements.

The metabolism of proliferating germs causes the breakdown of the constituents of foodstuffs, and produces the end-products which are characteristic of the life processes of particular organisms. Some of these changes are desirable, such as the fermentation of sugars to make vinegar. Other effects are only obnoxious, as the souring of milk or the molding of bread. A few are harmful, as the growth of pathogenic bacteria in milk or meat products. Microorganisms are dangerous, not only because their growth on the food may produce massive doses of infection, but also because their metabolism may elaborate toxins. Illness caused by toxic products formed by organ-isms in the food itself is called food poisoning or intoxication. If the food merely serves as a vehicle for conveying the microbes themselves into the body, the disease produced is termed a food-borne infection.

Autolytic deterioration. A foodstuff begins to undergo changes in composition very soon after it is removed from its natural habitat. These changes are caused to a large extent by the action of its enzymic system, and the process is known as autolysis. This effect is enhanced by exposure to oxygen, sunlight, moisture, and warmth, and is further accelerated by such contaminants as copper and iron. These changes are the causes of more or less loss of quality.

The deterioration may manifest itself in several ways, chief of which from the standpoint of our immediate interest is the decrease in the nutritive value. Enzymic effects may start with a loss of "freshness," possibly also of some color and flavor; next follow the more serious destruction of some of the vitamins, an oxidation and splitting of the fats with the development of rancidity, and then an attack on the proteins to form various decomposition products, such as ammonia, hydrogen sulphide, and other undesirable substances. These seldom develop to the degree of causing illness, because the food becomes obnoxious long before the concentration of these end-products is physiologically appreciable.

The old idea that the decomposition products of food (generally called by a misinformed public "ptomaines") were responsible for the ordinary gastrointestinal upset is no longer held (see pages 43, 198). Decomposition decreases nutritive value by a loss of nutrients, reduces gustatory appeal by the development of staleness, often makes the food repulsive, and opens the way for microbic invasion.

Composition. The composition of a given food determines to a large extent its significance to the public health. This manifests itself as nutritive value and as susceptibility to attack by disease-producing (pathogenic) organisms. In general, foods usually consist of a relatively large percentage of water; carbohydrates in the form of the soluble sugars like dextrose and insoluble ones like starch and fiber; proteins in relatively high proportion in meats, dairy products, and legumes; fats in meats and dairy products; minerals in cereal grains (especially when whole), dairy products, and fruits and vegetables; acids in fruits and fermented products; and vitamins in dairy products, egg, fruits, and vegetables. These constituents are scattered through all the common foods in varying proportions, giving to each its characteristic value as well as its degree of health hazard. For example, milk spoils very rapidly and is an excellent medium for the growth of disease germs; meat and bread spoil more slowly; and sugar and flour do not spoil appreciably during their commercial life.

Some types of microorganisms such as the molds will grow easily on acid products in the presence of air and moisture, whereas pathogenic organisms usually do not grow on such foods, unless some local condition has arisen to neutralize or remove the acidity. The amount of water present, the content of nitrogenous products, and the avail-ability of the carbohydrate individually contribute their effects to determine the type of deterioration to which the given food is subject. Knowledge of the composition of the food suspected of being incriminated in an outbreak of disease may help direct the investigation in the search for the etiologic agent.

SECTION I. NUTRITION

Older conception. For many years the nutritive worth of a food was thought to be adequately expressed when its percentage content of carbohydrate, protein, fat, and roughage was known. The amount of energy that the food would yield was expressed in calories. The protein content was thought to be adequately evaluated by determining the organic nitrogen and multiplying this figure by the factor 6.25. Roughage or "crude fiber" is the indigestible part of food. It was often calculated as comprising those residual constituents not included in direct determinations. The minerals were known to have value but not in the quantitative and qualitative degree now recognized as essential.

Newer knowledge. Nutritional research showed that animals could be given foods which were the same in composition as expressed by the above constituents but which were very different in their property of nourishing the body. This led Sir Frederick Gowland Hopkins in England to the idea that there must be unrecognized constituents in foods which were essential to nutrition. Some of these dietary necessities were later called vitamins. Moreover, the classic researches of Osborne and Mendel, McCollum, and others had shown that proteins could not be evaluated in terms of their nutritive quality by the old method because some proteins lacked amino acids which were essential in body building, whereas other proteins might possess these amino acids in large amount. With regard to minerals, the interest of the period in organic chemistry seemed to dominate the minds of the physiological or biological chemists so largely that it has been only since the discovery of the role of vitamin D in building skeletal tissue that the importance of these elements in the diet has received proper attention.

Essential dietary ingredients. As the technique of nutritional and biochemical research has become more refined, the list of products

found to be essential to life has increased; it is not static but grows as our knowledge advances. McCollum has pointed out that the list now is as follows:

Amino acids ... .10 of the 22 known ones.

Minerals Na, K, Ca, Mg, CI, I, P, S, Fe, Cu, Mn, Zn, Co.

Vitamins 6 established: A, B (B1), C, D, E, G(B2) 8 postulated but not well authenticated.

Fatty acids linoleic acid.

Carbohydrates ..a source other than that which can be formed from protein or fat since ordinarily not enough would be sup-plied from these sources.

Of course, water is necessary, and also air or more particularly oxygen. If we include these, consistency forces us to include carbon, hydrogen, nitrogen, and oxygen among the necessary minerals.

Amino acids. Some of the amino acids are synthesized in the body; some seem to have no particular nutritional value; but a few have been shown to be quite necessary and must be supplied in the diet, namely, lysine, tryptophane, methionine, histidine, phenylalanine, leucine, isoleucine, thrednine, and valine. Another amino acid, arginine, can be synthesized in the body but not fast enough to meet the demands for normal growth. If these two groups of amino acids are not ingested in adequate amount, the body will be undernourished regardless of how much of the other nutrients may be supplied. Complete proteins, when eaten in reduced amount, may act as incomplete ones by reason of the decrease in certain of their amino acids to sub-subsistence levels.

Minerals. Plants and, to a more limited degree, animal tissues contain varying amounts of minerals, reflecting to a large extent the mineral content of the environment. When these products are used as food, their minerals find their way into the body tissues. It is known that thirteen of these minerals are essential to physical well-being. The absence of calcium and phosphorus results in faulty bone and tooth structure, skeleton malformation, and impairment of nerve and tissue health, leading to rickets, osteomalacia, tetany, dental caries, and other disorders. Deprivation of iron leads to anemia by impairment of blood building and cell structure. Copper is necessary for the utilization of iron by the blood cells. The absence of sufficient iodine is reflected in faulty functioning of the thyroid gland with consequent development of goitrous conditions. Other minerals are known to be necessary, but their supply is usually adequate in the common diet. Five minerals—calcium, phosphorus, iron, copper, and iodine—are the only ones which are often insufficient in the dietary.

Vitamins. Research in the field of the vitamins is so active that the list of the recognized ones is changing rapidly. Most of those discovered in the early days have been found to be mixtures of several chemical entities. They are usually designed with subscript figures after the letter, as, for example, B1, B2, B3, etc., although a fraction from B is designated as G by the American workers and as B2 by the English.

Some of the vitamins have been identified as definitely known chemical compounds, and several have been synthesized in the laboratory. Among the better known ones. vitamin A has been synthesized as an alcohol derivative of the yellow pigment carotene. Among the several constituents of the vitamin B complex, B is known as thiamin, a compound formed by a union of a pyrimide and a thiazole group by a CH2 linkage. The vitamin B2 (also known as vitamin G) has been synthesized in the laboratory and given the name riboflavin on account of its relation to the sugar ribose. Vitamin C is known as ascorbic acid, a xylose sugar acid, earlier known as hexuronic and cevitamic acids. With regard to vitamin D, the most important of its eight or nine forms is the alcohol calciferol, a derivative of ergosterol. The anti-pellagric dietary factor has been identified as nicotinic acid and its derivatives.

The richest sources of vitamin A are eggs, dairy products, and the colored and leafy green vegetables. Vitamin B * is widely distributed among foods of animal and plant origin, and is found extensively in the outer coats of the cereals which have not been highly milled. An appreciable amount of vitamin C occurs in fresh milk and a larger amount in many fresh fruits and vegetables, especially those of the citrus group. Vitamin D is abundant in some fish oils, and less so in eggs and milk. Vitamin G * is prevalent in fresh fruits and vegetables, certain meats, milk, and eggs.

One of the important contributions which knowledge of nutrition has made to medicine is the increased resistance to infection which attends a proper diet. The evidence is not clearcut that the administration of any of the vitamins exerts special benefits unless the patients have been subsisting on diets which were partially deficient in these products. The administration of vitamin A is not anti-infective per se. There are conflicting reports as to the effectiveness of the other vitamins in the therapy of the various diseases on which they have been tried. An adequate diet, especially in the early months of life, may decrease the severity of infections. The evidence is positive that deficiencies of the vitamins A, C, and possibly B in the diet do entail a loss of resistance to various infections.

AVITAMINOSES. Each of the vitamins has a specific role in physical well-being. When any one of them is lacking in the diet, the body develops characteristic symptoms of disease. Such a condition is known as an avitaminosis. The absence of vitamin A results in the development of serious eye trouble, affections of the mucous membranes, and urinary calculi (kidney and bladder stones). Avitaminosis B produces the serious disease beriberi which involves a degeneration of the nervous system with cardiac weakness, atrophy of the muscles, and edema. Lack of vitamin C produces the painful disease scurvy, with soreness and hemorrhages of the joints, swollen bloody gums, loose teeth, skin hemorrhages, and poor calcification. When vitamin D is insufficient, the common disease that results is rickets, in which the calcium and phosphorus are not utilized effectively to form good bones and teeth, with resultant skeletal malformation. Vitamin E has not been shown to be important in human nutrition. Vitamin G deprivation produces in experimental animals a disease which at first was thought to be comparable to human pellagra, but this is now doubted. However, this disease is known to be caused by the lack of a dietary factor aptly called "P P" (pellagra-preventive), now recognized as nicotinic acid or its derivatives. When severe, pellagra is characterized by a skin rash, sore mouth, digestive and nervous disturbances, and anemia. A dietary deficiency of riboflavin, one of the constituents of the vitamin B group, has been reported recently by Sebrell and Butler [U. S. Pub. Health Repts., 53, 2282 (1938) ] to produce a clinical syndrome, prominent among which are lesions of the lips in the angles of the mouth. This condition has been successfully treated by dosage with synthetic riboflavin [ibid. 54, 790 (1939)].

SUBCLINICAL CONDITIONS. As refinements in diagnostic technic have been developed, threshold stages of these deficiency diseases are coming to light. The widespread prevalence of avitaminosis A is indicated by night-blindness in many Iowa children. Impaired health may result from a diet deficient in vitamin B but without signs of beriberi. Skeletal lesions and other pathological conditions, without signs of scurvy, may be attendant on subclinical avitaminosis C. Malformations of the skeleton, defective teeth, and other diseases seen in subclinical form have been traced to vitamin D deprivation without actual rickets. Eddy and Dalldorf point out that the vitamins act in as unique and characteristic a fashion to maintain bodily defenses against infectious elements as they do to maintain body structure.'

Carbohydrates. The carbohydrates are the chief sources of calorific energy. When they are not present in sufficient amount, the body weakens from insufficiency of this energy, and draws on its fat reserves in the tissues. This results in loss of weight and ordinary starvation, if continued long enough.

Carbohydrates possess what is called a "sparing" effect on the elimination of nitrogen. When food does not supply enough carbohydrates for the calorific requirements of the body, the proteins are drawn upon to supply the necessary energy. However, when carbohydrates, and to a less extent the fats, are ingested, they furnish the necessary fuel, and also contribute to some extent to protein synthesis. The limiting factor in the use of carbohydrate is the calorific requirement of the individual. The best practice has established the desirability of eating enough carbohydrate and fat to supply 90 percent of the food calories, and enough protein to supply about 10 percent.

The presence of carbohydrates in the diet also contributes to a safe metabolism of the fats. For the proper utilization of fat, there must be a simultaneous oxidation 9f carbohydrate; otherwise, the fat is incompletely oxidized, with the result that there is an accumulation of fatty-acid products which act as body poisons. The keto-antiketogenic ratio expresses the amount of fat that can be safely oxidized with the given amount of carbohydrate. There is not much agreement among workers in this field as to just what this ratio should be, and some give figures 1 : 1 and others 2 : 1. It is apparent that no fixed ratio is applicable to all individuals.

Nerve and brain tissue contains the sugar galactose, which is synthesized only in the mammary gland as a constituent of the lactose molecule. Galactose is formed in the body as a hydrolytic product of lactose. Accordingly, this important carbohydrate, lactose, must be supplied in the food. It is noteworthy that this sugar occurs in large degree in the only product which Nature made to be a food, namely, milk. Galactose also occurs in small amounts in some of the proteins of egg whites and is reported to be present in traces in scattered plant products. These considerations indicate that possibly this carbohydrate must now be included among specifically necessary nutrients.

Fats. Fats are nutritionally essential because of their content of linoleic acid. If this unsaturated fatty acid is lacking in the diet of experimental rats, they develop characteristic disease, entailing loss of hair, dermatitis, and hemorrhage, and die at an early age. Further-more, fats retard the gastric digestion of foods containing them, and thereby impart a feeling of satiety to the consumer.

Protective foods. When a diet lacks any of the nutritional requirements, the foodstuff which supplies this deficiency is called a protective food. Inasmuch as the dietary regimen differs with race, geographical area, climate, and economic level, a nutritional deficiency in one place, or even among groups in the same locality, may differ from that in another.' For example, in the United States where the diet is mostly based on white flour, sugar, and the muscle meats, these protective foods are milk, leafy vegetables, and fruits. In the Orient where the diet is chiefly polished rice or soy beans with a small quota of green vegetables, the protective food is meat because of the high quality of its protein value. In areas where the people subsist largely on dried or cooked foods, the fresh fruits and vegetables afford dietary adequacy.

Malnutrition. The technique employed by biochemists in evaluating the effects of the various elements and constituents of foodstuffs on health has been to reduce the concentration of the product being studied until it is supplied in amounts too small for normal health. In experimental animals, syndromes of certain dietary deficiency diseases can be clearly recognized. The same or similar symptoms are seen in human cases. These symptoms are relieved when the dietary deficiencies are corrected. The broad significance of malnutrition as a factor in morbidity and mortality is indicated, for example, by the tendency of decayed teeth and unhealthy gums to become abscessed, with attendant retardation of physical and mental development and the degeneration of the circulatory system.

The Final Report of the Mixed Committee of the League of Nations contains the following significant statement:

The health of the individual, in the majority of cases, is destroyed, not so often by severe attacks of illness (which are more in the nature of accidents), as by the gradual action of persistent but unrecognized causes, of which one of the most important is a badly composed dietary. This is one cause of inferior physical development and nervous instability, of lack of recuperative power and endurance, and consequently of cumulative fatigue and lack of resistance to tuberculosis and other infections. Moreover, the diet largely influences the rate at which the organism ages and consequently the duration of life.'

The recognized relation of undernourishment in children to their backwardness in school work and incorrigibility, the increased resistance to infection which attends a proper diet, and the marked improvement in development which is noticed in the modern youth attest the significance of proper nutrition.

Adequate versus optimum nutrition. When the amounts of the various nutrients that enter the body are equal to those that leave it, the body is in equilibrium with respect to these particular products. If there is an excess of input over output to provide for wastage and reproduction, and an addition as a margin of safety so that the body functions normally and produces healthy young, it may be considered as receiving adequate nutrition. However, Sherman has emphasized that it is possible to select food which can be added to a diet already adequately maintaining a normally healthy body to raise the vitality and vigor to a still higher level. He distinguishes between adequate and buoyant health, and shows the further possibility of actually in-creasing the span of life. On the basis of well-controlled animal experiments, he demonstrated that this increase can add about seven years to man's standard three-score-years-and-ten, making the reason-ably attainable age to be seventy-seven years.' This effect does not manifest itself solely by the addition of these years, but advances the age of normal development and raises the level of vitality and physical well-being over the whole life span. McCollum calls the application of this newer knowledge of nutrition the preservation of the characteristics of youth.'

SECTION II. FOOD POISONING

Prevalence. Any agent present in food which causes illness when taken into the body may be classed as a food poison. This condition may range all the way from mild digestive disturbances to severe prostration and even death. As a rule, food poisoning is characterized by a very low mortality. Most of this has been associated with botulism which has received notoriety out of all proportion to the number of cases involved. Inasmuch as food poisoning is generally not a report-able disease, it is impossible to give any reliable figures as to its extent. Jordan endeavored to arrive at some idea of this. In his opinion, the majority of cases escape notice. He points out that many of the re-corded cases are not chargeable to food poisoning at all but that nevertheless the number of real cases is large. Geiger studied more than 800 alleged food-poisoning outbreaks from 1910 to 1923 inclusive, and found that more than 80 percent did not actually incriminate food at all.' A later writer in the Journal of the American Medical Association made an epidemiological study of 425 alleged food-poisoning cases in the years 1923, 1924, and 1925, and pointed out that 43 necropsies on 145 fatal cases of "ptomaine poisoning" required a change of diagnosis. Many such causes of death as appendicitis, malaria, alcoholism, carbon monoxide poisoning, mercury poisoning, and others had been blamed on food poisoning. Savage 10 reported more carefully on 203 cases which were distributed as follows:

Canned meat 31

Canned marine products 27

Canned fruit 4

Milk 14

Milk products 16

Made-up meat 54

Manipulated meat 10

Fresh meat 33

Fruit and vegetables (notcanned) 8

Other foods 6

The U. S. Food and Drug Administration investigated 69 cases of alleged food poisoning during the year ending June 30, 1936, but in 40 out of the 47 samples examined in the laboratory no injurious ingredients or harmful microorganisms were found. In more than 100 cases of alleged food poisoning investigated in the city of Baltimore, less than 8 were found to have been caused by food purchased at public food establishments, and the majority of illnesses were found to be the result of improper care of food in the home. In the city of New York, only 19 out of 50 alleged food out-breaks were traced to food origin. Geiger points out, in a later paper, that the incidence of food poisoning is increasing, although its etiology, epidemiology, and control are better known than those of influenza, acute anterior poliomyelitis, and measles."

Foods may be poisonous in themselves, as certain mushrooms and plants, or they may contain added harmful substances such as lead, arsenic, bacterial toxins, or animal parasites. Hence, food is often merely the carrier of the toxic or infectious agent. In such diseases as botulism and several gastrointestinal disorders, food is the most common agent of transmission. In other diseases, food is only occasionally implicated. For practical purposes, water and beverages should be classed as foods. In general, most of the so-called water-borne diseases such as typhoid and dysentery are also transmitted by foods, but the reverse is not generally true. Thus, botulism, diphtheria, and Salmonella outbreaks are rarely carried by water. The microorganisms occurring in polluted water are mainly intestinal bacteria which have passed through the alimentary tract of men or some warm-blooded animal. Thus, food and water are closely allied and, for the most part, may be considered together.

Historically, food-poisoning outbreaks were commonly attributed to ptomaines, those bacterial decomposition products of bacteria. Since some of the compounds isolated from decomposing flesh were found to be toxic upon inoculation into the blood stream of laboratory animals, the conclusion was reached that ptomaines were the real cause of many food-poisoning cases. More recent investigations have shown that ptomaines are rarely involved as active agents in food poisoning, and that the true cause is usually a bacterial infection or intoxication. The ptomaine theory has fallen into disuse although even now physicians occasionally diagnose various forms of acute food intoxications as "ptomaine poisoning." A number of states have removed ptomaine poisoning from the approved list of causes of death on official death certificates.

Physiological disturbances. Overindulgence. Undoubtedly, over-eating causes at times certain acute symptoms of distress which may be diagnosed as food poisoning. Similarly, various food combinations may upset some people. Emotional stress has been shown markedly to influence digestion. The body organs or functions may be impaired and thus produce stomach, intestinal, or nervous disturbances. These disorders correctly cannot be considered true food poisoning.

Allergy. Hypersensitiveness to ingested foods has long been recognized as food idiosyncrasy. It is now known as alimentary anaphylaxis, gastrointestinal allergy, allergic toxemia, and also a variety of similar terms. Along with the usual gastrointestinal symptoms of food poisoning, persons suffering from allergy may exhibit urticaria (or hives), asthma, skin eruptions, and disorders of the gastrointestinal tract and nervous system, including eczema, abdominal pain, vomiting, diarrhea, chronic colitis, prostration, convulsions, and possibly epilepsy. Allergy is specific to the individual and reveals itself when he eats the incriminated food. Food-sensitivity is caused by many types of food, particularly the proteins. Sometimes the oils, fats, and carbohydrates possess this property. The allergic constituent or property may not be constant. Alvarez states that wheat may be harm-less to certain individuals in winter but not in summer when pollens are about. The condition may be diagnosed by the use of so-called elimination diets where the various suspected foods are fed with a previously established control. Sometimes the patient's history reveals his sensitiveness to certain foods. The scratch test may be used, in which a little of the suspected food, dissolved in a drop of dilute sodium hydroxide solution, is applied to a patch of the skin, and a scratch is made through the drop. A positive reaction consists of an urticarial wheal, surrounded by an area of erythema at the site of inoculation. The intradermal test is performed by injecting a small amount of the product under the superficial layer of skin. A positive reaction is similar to the above. The passive transfer test (also called the Prausnitz-Kustner reaction) depends on the presence in the patient's blood of sensitizing bodies. The serum from a drop of blood is injected into the superficial layers of another person's skin, and the second person is tested with the food by the intradermal test. None of these cutaneous tests are so reliable as the elimination diet.

A person's dislike for a food cannot be depended upon to indicate his allergic sensitization.

Harmful chemicals. The toxic property of a chemical is a relative matter. Numerous substances are listed as poisons even though, in proper concentration, they are useful remedies, and some are listed in the U. S. Pharmacopoeia as, for example, strychnine. The most common metals which have been incriminated in food poisoning are lead, arsenic, and thallium. Others, such as copper, zinc, nickel, and antimony, have not been clearly absolved. Aluminum, tin, and chromium are regarded as non-toxic. In any event, with the exception of the metals in the first group, it is clear that the amounts of these substances necessary to cause illness is much greater than those likely to get into foods through the use of utensils containing them.

Victims of chemical poisoning complain of cramps, nausea, vomiting, diarrhea, thirst, and headache, accompanied by shallow breathing, weak pulse, cyanosis, convulsions, or coma. There may be a metallic or sweetish taste if a heavy metal is involved.

Metals. Lead poisoning has been attributed to the use of lead tableware and utensils; lead dyes in foods; drinking of water which passed through lead pipes; beer and wine prepared in lead vessels, or carbonated beverages exposed to lead fittings; the eating of fruit covered with insecticide sprays containing lead or bakery products exposed to wood smoke from lead-painted wood; and to many other such contaminations. Arsenic has caused illness through utensils and reagents used in the handling or manufacture of certain foods, and also in insecticide sprays. Antimony and zinc have figured in several outbreaks from acid foods which had been in enamel-lined containers.

Other chemicals. There have been a number of cases of poisoning by silverware polish which contained cyanogen compounds. A shipment of 140 tons of raisins was recently condemned because of too high a content of hydrocyanic acid used as a liquid disinfectant which had failed to evaporate. The literature contains reports of many cases from miscellaneous and occasional, accidental poisonings, some of which do not lend themselves readily to control measures, whereas others do: the mistake, for instance, of selling tartar emetic to a food manufacturer who used tartaric acid regularly in his formulas could be guarded against.

Glass. From time to time there are more or less publicized reports of the finding of powdered glass in packaged foods. The more finely divided the glass, the less the harm because it becomes coated with food, mucus, and internal secretions which cause its elimination with no apparent harm. The British Ministry of Health 14 had 156 samples of food and beverages in glass analyzed, and 113 or 72.4 percent were found to contain some pieces. The largest portions were in jams, 3/8 inch by 5/16 inch. In another series of 79 samples, 31.6 percent were positive. Pieces of lead and barium glass, smaller than 2 mm. in diameter, can be located by roentgen rays in the soft tissues of the body, and "ordinary" glass might be expected to be seen in the abdomen. Glass has been thought by consumers to be present in canned crustaceans, but this has been shown to be crystals of harmless magnesium ammonium phosphate which is present in the flesh of the animals.

Poisonous plants. Certain plants contain definite chemical poisons. Since these are fairly well known, a history of the foods consumed is usually sufficient to determine whether inherently toxic foods were the cause of the poisoning.

Poisonous mushrooms are the cause of frequent poisoning out-breaks. Solanine poisoning from "greened, sunburned" potatoes has been repeatedly reported in literature, particularly from Europe. Rhubarb has been incriminated in a few rare cases where its oxalic acid content accounted for its toxicity. The milk from cows which have eaten white snakeroot and rayless goldenrod has caused "milk sickness."

The literature records numerous cases of illness from eating miscellaneous substances such as berries, leaves, bark, and roots. The roots of the deadly water hemlock have been mistaken for horseradish. Many of this class of poisonings may be classed as occasional happenings which scarcely lend themselves to any formal control. General education in matters of food identification and proper food handling is the only remedy.

Poisonous animal substances. The flesh of some animals may be poisonous. The Mosaic regulations in regard to foods forbidden to the Jews were undoubtedly designed in part to avoid foods either poisonous in themselves or subject to becoming toxic before use. Mussels are poisonous during the summer months and have caused repeated outbreaks of serious illness. The meat of the moose and sometimes the deer during the spring and summer has caused illness. Certain fishes, like the barracuda, have also been suspected of being poisonous under some conditions, but the possibility of bacterial infection of the fish cannot be disregarded. The subject of decomposed meats is more properly treated elsewhere (see pages 281 to 283).

Infestation by parasites. One of the most important types of food illness is trichinosis due to the parasitic nematode Trichinella spiralis. This small worm is communicated to man largely by the meat of the hog and bear, although other animals may occasionally act as reservoirs. In birds and in cold-blooded animals, the nemas are present largely in the intestinal tract rather than as encysted forms in the muscles. When pork containing encysted nemas reaches the human stomach, the cyst is dissolved and the parasite begins its life cycle in man, ending in the muscles. The illness is very painful, but the mortality is probably under 10 percent.

Taenia (tapeworm) infections occasionally occur as a result of eating "measly pork" containing the armed tapeworm, Taenia solium. Though normally confined to the intestinal tract, these worms may invade other tissues. The beef tapeworm, Taenia saginata, is of some-what lesser importance. Insufficiently cooked meat is the principal means of human infection.

Diphyllobothrium latum, the so-called broad or fish tapeworm, is gradually becoming established in the northwest lake region of the United States and Canada. The parasite must pass through two inter-mediate hosts, the cyclops and a fresh-water fish such as the pike or perch, before completing its life cycle. Uncooked or partially cooked fresh-water fish is the main vector of infection, which centers largely in the small intestine of man.

Amebic dysentery. The Entamoeba histolytica is a parasite which invades the gut wall of the large bowel. It secretes a thin wall about itself and forms cysts. These pass out in the bowel discharges. Their modes of entrance are through the ingestion of contaminated food and water from infected food handlers, from flies which have fed on contaminated material, and from human fertilizer on garden products. About 2 percent of the employees in public dining rooms and kitchens in San Francisco are infected, and the infestation of the public is much higher. Craig l' states that probably about 10 percent of the population of the United States harbors this parasite, that at least 50 percent of these persons exhibit symptoms caused by it, and that amebic abscess of the liver may occur in symptomless individuals. The first recorded explosive outbreak occurred in Chicago during the summer and fall of 1933, involving 1409 cases incompletely reported."

INFECTIONS AND INTOXICATIONS DUE TO BACTERIA

By far the most frequent and important types of food poisoning are those caused by bacteria. The important ones concerned are the Eberthella, Salmonella, Staphylococcus, Streptococcus, Brucella, Clostridium, and Mycobacterium groups. These will be considered individually.

Eberthella typhosa, the cause of typhoid fever, is perhaps the best known of all the food-poisoning bacteria. It is spread by contaminated foods, particularly milk and shellfish, by sewage-polluted water, and by typhoid carriers. Under favorable conditions of temperature, this organism is able to survive for a long time and even propagate itself in some non-acid foods. Normally, this organism affects man only, and thus man is either directly or indirectly the cause of its spread. It may continue to inhabit the intestinal tract and gall bladder and occasionally the urinary tract for years after the patient has fully recovered from the disease. There have been numerous cases where carriers have caused successive outbreaks of typhoid among their associates or contacts. Many cases are known where infection occurred ten or more years after the carrier had the disease. The Health Department of New York City constantly has several hundred known typhoid carriers under supervision. The importance of detection and after-supervision of carriers cannot be overestimated.

Carriers usually infect food by means of their hands. Naturally, carriers should never be allowed to handle food.

Sewage may contaminate oysters and clams, to which many out-breaks have been traced. Milk, of course, leads all foods as a carrier of typhoid. This is readily understood when we consider the intimate contact between the hands of the milker and the milk itself. Further-more, milk is a favorable medium for the growth of the typhoid bacillus.

Neither canned nor frozen fruits and vegetables have been implicated in typhoid outbreaks. The use of raw sewage in the irrigation of garden vegetables is a dangerous procedure and should not be practiced. The typhoid organism does not withstand desiccation well. In water, it may survive for more than a month.

Except in stool examinations, attempts are not often made to isolate the typhoid bacillus. Rather, it is taken for granted that the presence of fecal Escherichia coli, indicative of fecal or sewage pollution, is sufficient to show the possibility of the presence of Eberthella typhosa.

Ice cream, beef, cheese, chicken salad, spaghetti, lobster, and shell-fish have all been implicated in outbreaks.

Salmonella infections and intoxications. Although in Bergey's Manual of Determinative Bacteriology, the generic type Salmonella includes many species of closely similar organisms, the most important from a human food-poisoning viewpoint are S. enteritidis, S. suipestifer, S. aertrycke, S. schottmülleri, and S. paratyphi. Methods of differentiation are described by Bergey, by Jordan," and by Tanner. All the Salmonella and Eberthella typhosa are readily separated from the other members of the colon-typhoid group by their inability to ferment lactose. All are rather closely allied to the typhoid bacillus, from which they are differentiated by several different reactions on sugar media. Though they are cosmopolitan in occurrence, Jordan reports 22 that S. paratyphi are most often associated with man; S. suipestifer with pigs; S. aertrycke with rodents. S. enteritidis has been found associated with bovine, porcine, rodent, and human infections.

There has been much confusion and dispute in the literature concerning the organisms included in this group. Much of the older work must now be largely discredited because precise and accurate diagnostic and laboratory methods were not available. It is only in the past few years that order has been restored from a veritable chaos of contradiction and conflict.

Importance. There is no question but that a majority of the gastrointestinal type of food poisonings result from the Salmonella-infected foods. Although some members of the group can be separated and identified with some accuracy by means of cultural and biochemical tests, serological reactions are very important in establishing species identity beyond a doubt. Usually the clinical manifestations of the illness give a definite clew to the specific organism involved.

The mortality rate has been reported as between 1 and 4 percent, though higher in certain outbreaks. Geiger, reporting 705 epidemics in the United States involving 5038 persons, found a mortality of 4.1 percent. In England, Savage 24 reported 112 outbreaks involving 6190 persons, with a mortality of 1.5 percent. It seems certain that many outbreaks and cases of mild food poisoning from Salmonella have not been reported at all and thus escape notice. Almost every-body has experienced one or more personal attacks of gastrointestinal disturbance of a more or less serious nature. Laboratory examination of stools or of suspected foods are seldom made unless the illness is serious, so usually the actual cause of the attacks remains unproved.

Symptoms. Generally speaking, gastrointestinal symptoms occur within 4 to 12 hours after ingesting the causative food, although the incubation period may vary from 2 to more than 72 hours, even in the same outbreak. Usually, the incubation period is shortened and the severity of symptoms increased in proportion to the amount of food consumed. Often the onset of the intestinal irritation or poisoning is preceded by severe headache, prostration, and chills. Abdominal pain, nausea, vomiting, diarrhea, cramps, and involvements are present.

The period of the attack is from 1 to 3 or more days, followed by prompt recovery.

Epidemiology. Salmonella food-poisoning outbreaks are explosive and readily traced if a trained investigator is promptly called. Few persons are immune to this type of intoxication, and generally all who eat the contaminated food suffer illness. It is only necessary to find out which particular food was eaten in common by the sufferers in order to determine its identity. Treatment consists in an attempt to eliminate the toxic material from both the stomach and the intestinal tract (vomiting, purging, and enema).

Contaminated foods. Meat foods, especially comminuted ones, are most often incriminated, although many other products have been implicated. Among the more important are vegetable salads, milk products and custards, egg products, fish, and baking products. In England, Savage 24 reported that 68 percent of the outbreaks were due to meat products. Pork was implicated more often than other meats. Fruits and. acid foods are unfavorable media for the growth of Salmonella. Custards, eclairs, and cream puffs have been responsible for a number of outbreaks of Salmonella poisoning. These foods which serve as excellent culture media for the growth of bacteria often undergo an incubation period before being consumed. As demonstrated by Koser and others, the appearance, taste, and odor of foods infected with Salmonella or the typhoid and dysentery bacilli are unchanged or only slightly affected. Hence, there is no sure organoleptic means for determining in advance whether or not a food contains these bacteria. Geiger, Davis, and Benson 26 artificially inoculated canned foods and found that, whereas S. enteritidis did not produce noticeable changes in canned foods, S. schottmülleri, S. paratyphi, 'and Bacillus paratyphosum C did grow and produce marked changes in the food. Since canned foods are subjected to a heat process, and Salmonella and similar bacteria do not form spores, there is little chance that canned foods will carry the living bacteria. Even if there is some evidence of decomposition, it is more often than otherwise due to the presence of proteolytic saprophytic bacteria. Because of the more favorable temperatures, food-poisoning outbreaks are much more likely to occur in the warmer months. Many of the reported outbreaks have originated from food eaten at picnic lunches and community or church suppers.

Infection or intoxication. There has been much discussion as to whether Salmonella produce toxins only, or whether they actually cause infections. It seems patent that S. schottmülleri, S. enteritidis, and S. paratyphi have caused infections as well as intoxications in humans. One of the most important toxin formers is S. aertrycke. This organism has caused many food-poisoning out-breaks in Europe, England, and the United States. Culturally, it closely resembles S. schottmülleri, from which it is separated only by serological reactions. In the past, S. aertrycke has been much con-fused with both S. schottmülleri and S. suipestifer. Savage and White stated that S. aertrycke was responsible for 75 percent of the Salmonella food-poisoning outbreaks in England. Since it has been isolated from the blood stream and organs of some persons suffering from food poisoning, it is believed to cause infections as well as intoxications. S. enteritidis also seems to be among the most frequently involved.

The question of the formation of heat-stable toxins or gastro-intestinal irritants by Salmonella has long been a mooted one. Without entering into a long discussion, it seems safe to state that many species of Salmonella do elaborate them at certain times in their growth cycle and in certain foods. For example, Savage and White 27 reported the presence of thermostable toxic substances of S. aertrycke and S. enteritidis in canned and heated foods to which food-poisoning out-breaks were traced. Geiger and Myer 28 also found heat-resistant toxins in 3- to 4-day-old cultures of S. aertrycke. However, Dack, Cary, and Harmon 29 fed 24 persons 20 to 40 milliliters of cultures of filtrates of both S. aertrycke and S. enteritidis which had been heated at the boiling point for 20 minutes, with entirely negative results. Further data by Dack and Davison 2° indicate that infection is the cause of Salmonella food poisoning.

Streptococcus epidemicus, a highly pathogenic, beta hemolytic streptococcus, is the cause of milk-borne septic sore throat. This organism closely resembles ordinary hemolytic bovine streptococci, but the origin is probably always human. The organism may infect the udders of cows and thus pass into the milk. It must not be con-fused with the streptococci often encountered in mastitis, garget, or similar conditions. Non-pathogenic streptococci are often found in milk of good quality. All streptococci including Streptococcus epidemicus are readily destroyed by pasteurization.

Septic sore throat is always a serious illness with a mortality rate of about 10 percent. Epidemics have been relatively common. Many of these in the United States have involved several hundred persons each. The principal cause is raw milk or other dairy products which have been infected by persons acutely ill with or in the carrier stage of sore throat. Often the infection is secondary, that is, through an infected udder or quarter. The diagnosis is made both from the clinical symptoms and bacteriological examination of throat cultures. In many cases it is possible by means of careful udder examinations of the herds involved to find the cow producing the infected milk. Nearly always it will be found that a milker or milk handler was suffering from sore throat, which may not necessarily have been severe. The above statement holds also for scarlet-fever epidemics arising from milk. They are caused by Streptococcus scarlatinae.

Staphylococcus poisoning. Staphylococci, as agents of food poisoning, were not blamed until Jordan and Dack and colleagues demonstrated conclusively the causal relationship. Since that time, many explosive outbreaks due to staphylococci have been reported. The causative organism appears indistinguishable from the common yellow saprophyte Staphylococcus aureus, yet it forms in foods a powerful toxin or gastrointestinal irritant. The toxin is present in the filtered serum and is somewhat thermostable. Animal inoculations are of no value in diagnosis. Little is known as to the nature of the poison. The organism grows in the food and forms its toxin there. Some of the foods most often implicated are cream puffs, eclairs, cakes, "creamed" foods, and salads. In outbreaks, there is usually an incubation period of several hours at warm temperatures. Symptoms of staphylococcus poisoning appear in a few hours and consist of weakness, nausea, vomiting, diarrhea, and severe abdominal pains or cramps. Fever is usually present. Extreme exhaustion some-times lasts for several days. Recovery is complete, and the death rate is very low. An excellent summary on staphylococcus food poisoning has been prepared by Dack." Typical outbreaks are described by Denison.

Undulant fever (Malta fever). Undulant fever is characterized by a progressive rising temperature which reaches a maximum in about 5 days, and after one to six weeks gradually falls. This step-like rise and fall of body temperature continues for several months. Headaches, muscular pain, and often sore throat and bronchial involvement are other symptoms.

Human Mediterranean or Malta fever has long been endemic in southern Europe. Here, it is transmitted largely by goat's milk. Undulant fever is identical with or closely similar to Malta fever; Brucella melitensis or abortus is the cause of the infection. This organism also causes Bang's disease or contagious abortion in cattle. Various investigators have found 2 to 30 percent of raw American milks to contain the living organisms. Apparently, many cows not suffering from Bang's disease eliminate the organisms in their milk. There is also marked variation in pathogenicity among the different strains. Active control measures against Bang's disease in dairy herds is increasing rapidly in the more progressive areas. Infected. cows are detected by means of a blood agglutination test. Because of the general presence of Brucella abortus in raw milk, and the relatively small number of cases of undulant fever, it follows that only a small percentage of the users of raw milk are susceptible to the infection. Methods for the detection and isolation of the organism were first outlined by Miss Evans in 1915. A lactose agar containing blood serum is excellent for this purpose. The organism does not form spores and is readily destroyed by pasteurization temperatures. Unlike its action in cows, the infection in humans does not cause abortion.

Tuberculosis. Tuberculosis may be transmitted to man by means of such foods as infected milk and meat. Cattle, swine, sheep, and poultry are often tuberculous. True, these infections are due to bovine or avian types of Mycobacterium tuberculosis, but the former, at least, has been repeatedly demonstrated to be transmitted to man. Conversely, human strains have also been used in successful inoculation experiments in cows and guinea pigs. The "human" type infects man, but not swine or fowls. The "bovine" type infects man and swine but not fowls. The "avian" type infects swine and fowls but not man. Guinea pigs are quite susceptible to human and bovine but not to avian infection. Rabbits succumb to bovine and avian but not to the human type of tubercle bacillus infection. All three types produce tuberculosis in certain strains of mice.

Human pulmonary tuberculosis is probably always caused by Mycobacterium tuberculosis (hominis). In New York, Park and Krumwiede 37 reported data covering 1511 cases in which the type of bacillus was determined. From 3 to 5 percent of cases at the age levels of 0 to 16 years were of bovine origin. These same investigators state that 10 percent of the tuberculosis of the bones, joints, and lymph nodes of adults, and 25 percent of the same type in children, were caused by the bovine strain. Other extensive data show that much higher percentages of glandular tuberculosis have been attributable to the bovine strain, infants and young children being particularly susceptible.

It is only in tuberculosis of the udder that tubercle bacilli are freely eliminated in the milk. However, some experiments have shown that, in other types of tuberculosis, there may be occasional discharges in milk. Manure containing the organism is also a primary source of infection. Hence, it is unsafe to use raw milk from any animal suffering from tuberculosis.

Raw milk markets of the United States, Canada, England, and Germany have been carefully examined for the presence of tubercle bacilli by the guinea pig inoculation method. Tanner 19 has tabulated the data from 46 investigators involving 16,713 milk samples collected from many cities in several countries. The percentage of samples positive for Mycobacterium tuberculosis was 14.47.

Botulism. The toxemia known as botulism is caused by toxins of Clostridium botulinum. This was formerly confused with so-called ptomaine poisoning, but since 1920 much new information has been discovered concerning this form of food poisoning. Botulism has been known in Europe for many years, where the chief causative agent was improperly cooked sausage or meats. In America, the chief causative food is canned vegetables and meats, though animal botulism is frequently due to decayed forage and vegetables. Cl. botulinum, a strict anaerobe, grows in a variety of foods where air is excluded as by canning, fermentation, or associative action of saprophytic microorganisms. The organism is only moderately proteolytic, and normally it produces in foods a cheesy, butyric odor after several days' growth. Gas is usually formed if meats or carbohydrates are present.

The natural habitat of the organism is the soil, particularly that of the Pacific Coast and Rocky Mountain states. Unlike the tetanus bacillus, Cl. botulinum is as abundant in virgin as in cultivated and manured soils. It gains access to food through contact with soil, dust, and possibly water. The organism in itself is harmless and no doubt is regularly ingested with food and water. However, under proper conditions of anaerobiasis, temperature, and food, a powerful toxin is produced. As little as 1/1,000,000 milliliter is often fatal to guinea pigs. The author has personally investigated two cases of botulism where death ensued following the mere tasting of the toxic canned vegetable, and so far as could be determined none was swallowed. The toxin is heat labile, and toxic food is rendered harmless by heating to the boiling point of water for a few minutes. This is always a simple and safe precaution if there is any doubt whatever relative to the safety of the food. If in doubt, never taste food suspected of containing botulinus toxin.

Prevalence of symptomatology. Even though botulism is not commonly encountered in the United States, its characteristic symptoms should always be looked for in food-poisoning outbreaks. Geiger 8 reported 129 outbreaks involving 435 cases (mortality 67.1 percent) as occurring in this country prior to 1924. Tanner 19 summarized data on 134 outbreaks, and the reader is referred to this excellent book for a more detailed description of botulism. Most cases have occurred in the Pacific Coast and Rocky Mountain states, only a few having originated in the east and south. The most probable explanation of this is the greater prevalence of Type A, the most toxic to man, in the soils of the western states. Type B is much less toxic. Types C and D have been reported only in outbreaks among various animal species, and are of little importance to man. Two type E strains have recently been identified as incitants of two fatal cases of human botulism 38 one from canned sprats and the other from smoked salmon, both imported.

Only occasionally in botulism are there acute gastrointestinal symptoms. Primarily the toxin is a nerve poison. Typical symptoms occur about 12 to 48 hours following the eating of the toxic food. Dizziness,nausea, lassitude, diplopia, and loss of reflex to light stimulation are more common early symptoms. Later, swallowing becomes difficult, and there is extreme muscular weakness and difficulty in breathing.

Causative foods. Improperly home canned foods are by far the most important agents causing botulism. Canned vegetables such as string beans, asparagus, sweet corn, and spinach, as well as pork products have all been implicated many times. Insufficient heat processing to kill the resistant spores of Cl. botulinum allows bacterial growth to take place in the jar or can under anaerobic conditions with consequent toxin formation. Whereas commercially canned foods formerly caused several outbreaks, prompt corrective measures by the canners' associations and public-health officials have made this class of foods safe. Home canning methods have also been improved, but it is a difficult task to educate millions of home-makers, largely in rural districts, to learn to operate pressure cookers properly, and to pack and process non-acid canned foods so as to preclude danger of botulism. Again, the safe rule is: If in doubt, boil the canned food for several minutes as safety measure.

Cases of limberneck (botulism) in chickens, and forage poisoning in cattle sometimes accompany human cases and offer a clew as to the toxic agent.

Botulinus toxin is rather easily identified by either guinea pig or white mice inoculation. This is usually made intraperitoneally with graduated amounts administered to different animals. Symptoms develop in from 4 to 24 hours, and death usually ensues promptly. By means of anti-toxins administered at the time of inoculation, the type can be easily ascertained. If symptoms of botulism do not occur in inoculated animals, then it is probable that the toxin is not present. The organism itself is best isolated by heating the suspected food to boiling for 10 minutes to eliminate contaminating organisms, inoculating into brain or beef heart agar media, and incubating at 37° C. anaerobically.

Clostridium botulinum, grows best at a neutral or slightly alkaline reaction, though slight growth may occur at pH values of 5.0 or slightly less. Salt and alcohol both inhibit growth. Cold acts as a deterrent in toxin development, but as soon as the food containing spores is warmed up, toxin formation may occur. It has been shown that there is no danger from botulism in frozen foods, even if de-frosted, when eaten within a reasonable time. Of course, improperly handled foods of all kinds may become dangerous under especially favorable environmental conditions.

Canned food containing botulism toxin usually is swelled from car-bon dioxide gas formed by the organism. There is positive pressure in the can, and after it is opened the contents often froth or bubble from the escaping gases. The odor varies from only slightly abnormal to a decidedly obnoxious putrid odor. A cheesy or butyric odor is often encountered. Apparently toxin develops only slowly, even after some months, in foods which furnish a poor medium of growth. The rubbers of glass jars containing active Cl. botulinum may be pushed out and the jar itself leaky and foul-smelling. The contents are often soft, semi-liquefied, and gassy. Such materials should be destroyed and kept from poultry, swine, or other animals.

Tularemia. Tularemia is a plaguelike disease affecting both man and animals. It was first discovered and studied in the United States in 1910 by McCoy and Francis of the U. S. Public Health Service, though it has now been recognized in Europe and Asia. The disease is caused by Pasteurella tularensis, earlier known as Bacterium tularense. Man becomes infected by skinning or handling with bare hands such animals as rabbits, hares, muskrats, and foxes as well as by the bites of ticks and flies which have previously fed on warm-blooded animals infected with this organism. Most cases have been reported as due to fresh-killed and market rabbits. Hunters, trappers, house-wives, and marketmen who may handle the animals with the bare hands are most likely to become infected. Many laboratory workers have become infected as a result of working with the cultures. The eating of insufficiently cooked rabbit meat has also occasionally caused the disease. Recent summaries on this subject have been prepared by Francis and by Lillie, Francis, and Parker.

Diagnosis of tularemia should be considered if the patient shows skin ulcers, fever, and lymph-node enlargements, especially if he has been handling rabbits or has been bitten by ticks or flies. Positive agglutination of the patient's serum by P. tularensis confirms the diagnosis. The liver, lungs, and spleen of the infected rabbit usually show characteristic small round spots, which, however, may be too small to be easily recognized during the early stages of the disease.

Tularemia is a serious disease with a mortality of about 5 per-cent. Complicating pneumonia sometimes results. Convalescence is slow, but when complete recovery occurs, no after-effects have been noted.

Miscellaneous organisms. Poliomyelitis is not usually considered to be spread by foods, yet the New York State health department (1926) definitely traced 10 cases of the disease to market milk. The virus gained entry to the milk through a sick employee. Similar cases have recently been reported in England.

It is well known that. diphtheria may be transmitted by foods, particularly milk.

Bacillary dysentery, caused by Shigella dysenteriae in milk and in solid foods, has occasionally been implicated in food-poisoning out-breaks. Carriers usually are responsible for the food contamination.

Members of the Proteus group of bacteria have been incriminated from time to time as being responsible for food-poisoning outbreaks. Although toxins have been reported in foods inoculated with these organisms, other investigators believe the group to be non-toxic. Tanner 19 states "The evidence presented in many outbreaks has been so scant that we may seriously doubt whether Proteus organisms were the cause."

Similarly, Escherichia coli, Aerobacter cloacae, and other members of the coli-aerogenes group have been occasionally cited as the cause of food-poisoning outbreaks. Although these organisms, under specially favorable conditions, may produce weak toxins in foods, they cannot be considered important as food-poisoning agents.

DECOMPOSED FOODS IN THEIR RELATION TO FOOD POISONING

The term "ptomaine poisoning" has been used by physicians to characterize severe gastrointestinal upsets and infections of unknown origin. The term originated long before the development of modern bacteriology but it has outlived its usefulness. Ptomaines result from the action of bacteria on proteins, and they consist of various complex malodorous degradation products of proteins, such as neuridine, paraphenylenediamine, putrescine, and cadaverine. They vary in their toxicity to animals. Ptomaines are heat resistant. Hence, cooking or canning has no effect on them. At the present time, it is not believed that ptomaines play an important part in food poisoning be-cause experience has not demonstrated their etiological significance in food poisoning outbreaks. It is probably true that certain bacteria which do produce toxins also produce ptomaines, but it is the toxins that are the primary causes of illness. There is little doubt that food containing ptomaines would invariably be destroyed because of the offensive odor and unattractive appearance. Both experimental and human experience shows that putrid foods may usually be consumed with impunity. At least, the relationship between putridity of foods and food poisoning has not been proved. Many of the bacteria responsible for most food-poisoning outbreaks such as the salmonellas, typhoid bacilli, and staphylococci produce little outward change in the appearance or odor of foods on which they are growing. Long storage which allows the organisms to increase in numbers may in-crease the degree of decomposition as well as the food-poisoning bacteria, but the relationship is merely accidental. Decomposed foods should be rejected on esthetic grounds anyhow.

SUMMARY

The nutrients in foods make them susceptible to attack by micro-organisms. The metabolism of microorganisms, together with the autolytic changes in the foods caused by their natural enzymes, enhanced by favorable environmental conditions such as temperature and moisture, causes deterioration and ultimately spoilage.

The nutritive values of foods lie chiefly in their content of proteins, fats, carbohydrates, minerals, and vitamins. The proteins must be adequate in quantity and also in quality because certain amino acids must be supplied by the food, regardless of how much other protein is furnished, for proper growth and maintenance. There seems to be no specific requirement for any particular carbohydrate, al-though there is some evidence that galactose is necessary to the young for building nerve and brain tissue. The minerals calcium, phosphorus, iron, copper, and iodine are particularly necessary because they are so often present in inadequate amounts in the ordinary diet. The vitamins and linoleic acid are essential for health. The proper use of this newer knowledge of nutrition has operated to build better health and physique, and to increase resistance to infection.

Food poisoning is a very common ailment. It may be caused by the ingestion of too much food or of food which contains some constituent to which the body is sensitive. Various plant and animal tissues may be poisonous in themselves. Sometimes chemical substances contaminate the food and make it harmful. Among the greatest sources of food poisoning are the several types of pathogenic bacteria such as the typhoid bacteria, the salmonellas, some of the streptococci and staphylococci, the undulant-fever organisms, those causing tuberculosis, and the comparatively rare but spectacular microbes of botulism. The old idea that ptomaine poisoning was caused by protein decomposition products of microbic attack is seldom if ever now entertained as a factor in food poisoning.

Although the etiology and prophylaxis of food poisoning are in general well understood, in fact better so than those of such common diseases as measles and anterior poliomyelitis, yet our knowledge is very incomplete concerning the factors which determine the pathogenicity of different strains, especially of streptococci and staphylococci.

REFERENCES

1. W. H. EDDY and G. DALLDORF, The Avitaminoses, Williams and Wilkins Co., Baltimore, 1937.

2. TECHNICAL COMMISSION OF THE HEALTH COMMITTEE, The Problem of Nutrition, Vol. II, Report on the Physiological Bases of Nutrition. League of Nations Publication Department, Geneva, 1936.

3. Final Report of the Mixed Committee. The Relation of Nutrition to Health, League of Nations Publication Department, Geneva, 1937.

4. S. W. CLAUSEN, Physiol. Rev., 14, 309 (1934).

5. H. C. SHERMAN, Hui. N. Y. Acad. Med., 13, 311 (1937).

6. E. V. MCCoLLUM and N. SIMMONDS, The Newer Knowledge of Nutrition, Macmillan Co., New York, 4th ed., 1929.

7. E. O. JORDAN, Food Poisoning and Food-Borne Infection, University of Chicago Press, 1931.

8. J. C. GEIGER, Am. J. Pub. Health, 14, 302 (1924).

9. J. Am. Med. Assoc., 90, 459 (1928).

10. W. G. SAVAGE, Brit. Med. J., II, 560 (1925).

11. J. C. GEIGER and J. P. GRAY, Am. J. Pub. Health, 23, 1039 (1933).

12. M. A. RAMIREZ, J. Am. Diet. Assoc., 9, 286 (1933-4).

13. W. T. VAUGHAN and D. M. PIPES, J. Allergy, 8, 257 (1937).

14. G. C. HANCOCK, Ministry of Health Rept. on Pub. Health and Med. Subjects, No. 37, London, 1927.

15. R. K. LEwIs, Am. J. Roentgenol. Radium Therapy, 27, 853 (1932).

16. M. L. IVERSON and H. G. JOHNSTONE, J. Am. Med. Assoc., 108, 875 (1937).

17. C. F. CRAIG, Am. J. Pub. Health, 28, 187 (1939).

18. H. N. BUNDESEN, Pub. Health Repas., 49, 1266 (1934). See also ibid., 51, 845 (1936).

19. B. K. SPECTOR, J. W. FOSTER, and N. G. GLOVER, ibid., 50, 163 (1935).

20. F. W. TANNER, Food-Borne Infections and Intoxications, Twin City Printing Co., Champaign, Ill., 1933.

21. D. H. BERGEY, Manual of Determinative Bacteriology, Williams and Wilkins Co., Baltimore, 4th ed., 1934.

22. E. O. JORDAN, J. Infectious Diseases, 33, 567 (1923).

23. E. O. JORDAN and I. S. FALK, Newer Knowledge of Bacteriology and Immunology, University of Chicago Press, 1928.

24. J. C. GEIGER, J. Am. Med. Assoc., 81, 1275 (1923).

25. W. G. SAVAGE, Food Poisoning and Food Infections, Cambridge, 1920.

26. S. A. KosER, J. Infectious Diseases, 31, 79 (1922).

27. J. C. GEIGER, E. DAVIS, and H. BENSON, Am. J. Pub. Health, 14, 578 (1924).

28. W. G. SAVAGE and P. B. WHITE, Brit. Med. Research Council. Special Repu., Ser. 91 (1925).

29. J. C. GEIGER and K. F. MEYER, Proc. Soc. Exptl. Biol. Med., 26, 91 (1928-9).

30. G. M. DACK, W. E. CARY, and P. H. HARMON, J. Prevent. Med., 2, 479 (1928).

31. E. DAVISON, Food Research, 3, 347 (1938).

32. E. O. JORDAN, J. Am. Med. Assoc., 94, 1648 (1930) ; 97, 1704 (1931).

33. G. M. DACE, W. E. CARY, O. WOOLPERT, and H. WIGGERS, J. Prevent Med., 4, 167 (1930).

34. G. M. DACK, Am. J. Pub. Health, 27, 440 (1937).

35. G. A. DENISON, ibid., 26, 1168 (1936).

36. A. C. EVANS, Science, 42, 352 (1915).

37. E. R. LONG, ibid., 87, 23 (1938).

38. W. H. PARK and C. KRUMWEIDE, J. Med. Research, 23, 205 (1910) ; 25, 313 (1911-2); 27, 109 (1912-3).

39. E. L. HAZEN, Science, 87, 413 (1932).

40. E. FRANCIS, U. S. Pub. Health Repas., 52, 103 (1937).

41. R. D. LILLIE, E. FRANCIS, and R. R. PARKER, U. S. Natl. Inst. Health Bul., 167 (1937).

GENERAL REFERENCES

S. R. DAMON, Food Infections and Intoxications, Williams and Wilkins Co., Baltimore, 1928.

F. W. TANNER, Food-Borne Infections and Intoxications, Twin City Printing Co., Champaign, Ill., 1933.

E. O. JORDAN, Food Poisoning and Food-Borne Infections, University of Chicago Press, 1931.

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