Food poisoning book pdf

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Browse the color drawing book or download a copy of the PDF below. To adjust the PDF size, just use the plus and minus keys. Examples of foods that are shown to treat food poisoning are made only from The Ingredients recommended by McDougall. See our free recipes and detailed instructions (no gimmicks). Dr McDougall Colour Picture Book: Food Poisoning Translate Dr. McDougall Colour Picture Book to another Please follow these instructions. Translations are now available: Start your review of food poisoning and foodborne diseases This book examines the problems of foodborne diseases and reviews of the various microbes and toxins in foods that make us sick. Project Gutenberg EBook Food Poisoning, Edwin Oaks Jordan This e-book is for use by anyone anywhere at all costs and with virtually no restrictions what it may be. You can copy it, give it away or reuse it under the terms of the Gutenberg License project included in this e-book or online on www.gutenberg.net Title: Food Poisoning Author: Author: Oakes Jordan Release Date: November 1, 2010 Language Book #34189 Language: English Character Coding Set: ISO-8859-1 - START THIS PROJECT GUTENBERG EBOOK FOOD POISONING - Produced by Brian Ness, Iris Schroeder-Goering and an online distributed adjustment team (This file was prepared from images, (P.i) UNIVERSITY OF CHICAGO SCIENCE SERIES Editorial Committee ELIAKIM HASTINGS MOORE, Chairman of JOHN MERLE COULTER ROBERT ANDREWS MILLIKAN created by the University's trustees, owes its origins to the sense that there should be a publishing environment, taking a stand between technical journals with their short articles and complex treatises that try to cover several aspects of the wide area. The volumes of the series will differ from the discussions usually found in technical journals in that they will present the full results of an experiment or a series of studies that previously appeared only in disparate articles, if they were published at all. On the other hand, they will differ from detailed treatises, confining to specific problems of current interest and presenting the issue as a summary and with as few technical details as is consistent with a sound method. P.IV UNIVERSITY OF CHICAGO PRESS CHICAGO, ILLINOIS THE BAKER - TAYLOR COMPANY NEW YORK THE CUNNINGHAM, CURTISS - WELCH COMPANY LOS ANGELES THE CAMBRIDGE UNIVERSITY PRESS LONDON AND EDINBURGH THE MARUZEN-KABUSHIKI-KAISHA TOKYO, OSAKA, KYOTO, FUKUOSA, SENDAI MISSION BOOK COMPANY SHANGHAI BY EDWIN OAKES JORDAN Chair of Hygiene and Bacteriology university UNIVERSITY OF CHICAGO OF CHICAGO PRESS CHICAGO, ILLINOIS (p.vi) Copyright 1917 University of Chicago All Rights Protected Published May 1917 Compiled and Printed by the University of Chicago Press Chicago, Illinois, USA 1 Degree of Food Poisoning the most commonly associated with food poisoning sensitization protein products 9 poisonous plants and animals 13 poisonous plants poisonous animals mineral or organic poisons added to the food 26 Arsenic Lead Lead Tin Copper Various Dyes Of Food Preservatives Food Substitutes Food Pathogens 44 Typhoid Food Infection Asia Possible Infection B. proteus Food Pathogen Bacteria (Continued) 58 Paratyroid Infection Typical Paratythypoid Outbreak Common Characters of Paratyphoid Infection Toxins Sources Produced Infectious Prevention Agents p.viiiAnimal 79 Trichiniyaz Teniasis Uncinariasis Other parasites Poisonous foods formed in food Microorganisms 85 Ergaultism Botulism Symptoms of Anatomical Lesions Bacteriology Epidemiology Prevention and Treatment Other bacterial poisons spoiled and decomposing food poisoning Obscure or unknown nature 100 Dairy disease or tremor Disease Deficiency Beriberie Pellagra Lathyrism Favyrism Scurvy Rachitis Foods Most commonly poisonous index 109 How often food poisoning occurs is not necessary. Everyone knows that some foods are now and again responsible for more or less serious attacks of indigestion or other physiological disorders that followed their consumption, but in many cases the evidence for making a causal relationship is of the slightest importance. This convenient refuge from the etiological uncertainty, ptomain poisoning, is a diagnosis that has undoubtedly been made to cover a wide variety of different conditions, from appendicitis and pain caused by gallstones to simple abdominal scattering as a result of reckless devouring. No doubt it is possible to entertain, however, that intestinal and other disorders due to specific foods occur much more often than they are recorded. There are several people who have not experienced moderate gastrointestinal seizures, which may be reasonably attributed to something eaten shortly before. It is often possible to point out offensive food with a sufficient degree of certainty. The vast majority of such attacks are mild, recover quickly and are never heard outside the immediate circle of relatives. Only when the attack is more serious than average, or when a large number of people are involved at the same time, is knowledge of the incident becoming more widespread. A small proportion of food poisoning cases are notified in the public press, and an even smaller proportion are reported in medical journals. Very few have really ever fully researched their origins. While most cases of food poisoning tend to be minor and appear to be temporary, this does not mean that they are considered minor or trivial from a public health point of view. The human body is always more or less weakened by such attacks, many of which, we shall see, are genuine infections; and as is known, in the case of many infectious diseases, some permanent harmful impression can be left on the body of the affected person. Under certain conditions, degenerative changes or acceleration in the kidneys or blood vessels in acute poisoning are possible, which manifests itself in a short time even in lighter cases. To an even greater extent, these changes may follow those insidious forms of food poisoning due to frequent intake of small mineral or organic poisons, which in each dose can cause little or no measurable physiological changes, changes, whose cumulative effect can be perverse. In view of the severe situation, as evidenced by the increase in degenerative diseases affecting early middle life in the United States, the extent, causes and means of food poisoning prevention appear to be relevant subjects for research. (p.3) EXTENT OF FOOD POISONING Since cases of food poisoning, ptomain poisoning and the like are not required by law, public health authorities generally do not have the information to respect their occurrence. Very indirect and imperfect signs of the prevalence of certain types of food poisoning are random reports in the press. Such as they are, these accounts are the only available material. Tables I and II summarize data collected from the Press Circumcision Bureau and from other sources between October 1913 and October 1915. They serve, at least, to show the versatility and complexity of the problem. A total of 5,238 people participated in 375 group and family outbreaks. While it is unlikely that all cases of food poisoning may be properly dealt with, there is no doubt that the number recorded in the tables is far from the actual cases. Over the past few years, the writer has investigated several major outbreaks of food poisoning that have never been reported to the press or received any public notification. There is reason to believe that in most cases avoid notice. It is likely that several thousand outbreaks of food poisoning in families and larger groups, affecting at least 15,000 to 20,000 people, occur in the United States within a year. The purpose of the reasons mentioned in Table I has limited value. There is a tendency to incriminate canned food. A proper investigation into the origin of the outbreak is so rare that articles about food are usually blamed for being chosen more by popular prejudices and traditions than by any thorough investigation. TABLE I Food Poisoning in the United States, October 1913, October 1915 Appointed Cause Group and Family Outbreaks Individual Cases Total Meat 40 35 75 Canned Fish 29 35 64 Canned Vegetables 27 34 61 Ice Cream 31 22 53 Fish, Oysters 17 31 48 Cheese 31 9 40 Sausage and Canned Meat 18 36 Milk 14 13 27 Mushrooms 12 7 19 Fruits 8 11 19 Vegetables 11 7 18 Fowl 12 4 16 Salad 9 5 14 Contact Food or Beverages with Metal 12 1 13 Different 29 55 84 No Reason Assigned 300 287 587 357 88 445 657 375 1032 TABLE II Seasonal distribution of food poisoning cases, 1914-15 (Group, Family, and Individual) January 90 May 63 September 76 February 66 June 108 October 75 July 99 November 96 April 79 August 96 December 88 There is not very striking seasonal incidence in numbers here gathered (Table II). The warmer months seem to have a slight preponderance of cases, but the common common such data is hardly justified. VARIOUS KINDS OF FOOD POISONING Cases of food poisoning can be identified as: (1) those that are caused by some harmful components in the food itself, and (2) those caused by the peculiar state of the person consuming food, so that essentially useful food substances are able to produce physiological disorders in some people. The latter group includes persons who appear to be normal in other ways who are more or less harmfully affected by any particular article diet, such as eggs or milk, which are eaten with impunity by all normal people. This is the so-called food sensitization or food allergy. Food poisoning is more commonly understood to be associated with the composition, content or contamination of the food itself. It is not within this book to consider any of those cases in which certain poisonous substances are added to food with criminal intent. The term food poisoning here is common to include occasional cases of poisoning from organic poisons present in normal animals or plant tissues, more or less harmful effects after consumption of food in which mineral or organic poisons have been introduced accidentally or with the intention of improving the appearance or maintenance of quality, cases of infection due to the swallowing of bacteria and other parasites that infect or contaminate certain products, and poisons certain products, and poisonings due to harmful substances. produced in food by the growth of bacteria, mold and similar organisms. As noted, little is known about the relative frequency of these various causes or the extent to which they are separate and collective operational. ARTICLE FOOD MOST USUALLY CONNECTED WITH FOOD POISONING In addition to particularly poisonous plants or animals, some everyday foods have often been associated with more serious outbreaks of food poisoning. Meat in particular has been involved so often that the term meat poisoning is used about as often as the term food poisoning in general discussions on the subject. In some cases, the vast majority of the most studied and most severe outbreaks of food poisoning are due to the use of meat or meat products. Other animal products, and especially milk and its derivatives, cheese and ice cream, have also been held accountable for extensive and notable outbreaks. Perhaps the most important feature of food poisoning attacks is the frequency at which they have been traced using raw or imperfectly cooked food. The likely interpretation of this fact will be discussed in later chapters. Especially eating the use of raw milk, either by itself or mixed with other foods, and eating raw sausage brought into their train symptoms Disproportionately in a number of cases. Canned food has also been repeatedly accused of causing harmful effects, but the evidence presented is not always conclusive. The actual degree of danger from this source is far from being determined. The National Canner Association publishes in the secretary's annual report a short list of defamations against industry or cases where canned goods of various kinds were considered as the cause of the disease. The 1916 report contained 51 such casees, none of which, according to the Association's investigator, were based on conclusive evidence. It would seem appropriate to search all such cases even more not for the purpose of incriminating or stealing a particular product, but simply for the purpose of establishing and establishing all the facts. Chapter II SENSITIZATION TO PROTEIN FOODS The first introduction of a minute's egg-white or other seemingly harmless protein substance under the skin of a guinea pig without apparent harmful effect, but if this is followed by a second injection of the same substance at intervals of about ten days, the animal will die in a few minutes with symptoms of violent poisoning. Whatever the physiological explanation for the remarkable change, which is thus the result of the inclusion of a foreign protein in the body, there can be no doubt that a phenomenon known as protein sensitization or anaphylaxis is relatively common. For the first time, sensitization of proteins became known as a result of the study of therapeutic serum, and it was found that they have unexpectedly wide bearings. It is now known that not only are rashes and other symptoms that sometimes follow the administration of a horse serum containing antitoxin diphtheria, but the reaction to tuberculosis and similar accompaniment to bacterial infection is likely to be explained by the principle of anaphylactic changes. The sensitivity of some individuals to plant-specific pollen (hay fever) is also considered as a typical case of anaphylaxis, accompanied by both asthma and other characteristic manifestations of anaphylactic condition. Among the reactions usually classified as anaphylactic are random cases of sensitivity to specific foods. It is a familiar fact that some foods that can be eaten with impunity by most people prove more or less acutely poisonous to others. Strawberries and some other fruits and some types of shellfish are among the articles of food more often implicated. There are also unpleasant reactions to the consumption of eggs and cow's milk. The severity of seizures can range from mild rash to violent gastrointestinal, circulatory and nervous disorders. Kues described a fairly typical case in a child of twenty-one old and apparently healthy, except for some eczema. When the child was a little more than a year old, he was given egg white, and immediately followed by nausea and vomiting. About eight months later another feeding with egg white was followed by sneezing and all symptoms of acute coriander. Extensive hives covering most of the body also appeared, and the eyelids became edematosis. The temperature remained normal and there was no noticeable prostration. Symptoms of such attacks vary greatly in people, but usually include expressed hives along with nausea, vomiting and diarrhea. The speed with which symptoms appear after eating is quite characteristic. Schloss reported an incident where an eight-year-old boy was a stare with a sensitivity to eggs, almonds and oatmeal. Experiments in this case showed that the reaction was produced only by the proteins of these few products, and that protein-free extracts and drugs were completely inert. It has also been found that by injecting a patient's serum of guinea pigs can be passively sensitized against the substances in question, thereby showing the condition to be one of real anaphylaxis. Idiosyncrasy of cow's milk, which is sometimes observed in infants, is anaphylactic. The replacement of goat's milk with cow's milk in such cases was followed by favorable results. In very troublesome cases, protein features have been promoted a method of treatment based on experiments on animals. This is to produce a state of anti-anaphylaxis by systematically feeding the smallest doses of a particular protein substance. S.R. Miller describes a case involving a child in which a constitutional response followed the administration of one teaspoon of a mixture consisting of one pint of water plus one drop of egg white, while a similar amount of albumen diluted with one quart of water was perfectly tolerated. Starting with dilution, which could not produce a reaction, the child was given a gradual increase in the number of decisions to increase strength. The dosage has always been one teaspoon given three times during the day; as a result, for about three months the child was desensitized to such an extent that one of the dramas of pure egg white is now taken with impunity. Many other cases of albumen egg anaphylaxis are on record. In some of these cases, the amount of specific protein sufficient to produce a reaction is extremely small. One doctor writes about a patient who was unable to take the slightest amount of eggs in any form. If a spoon was used to beat the eggs and then stir the coffee, it became very nauseating and vomiting violently. The dependence of many asthma cases on specific products is an established fact. Various skin rashes and are also associated with sensitization of certain foods. McBride and Shorer believe that each particular type of food (like tomatoes or cereals) produces a permanent and characteristic set of symptoms. Perhaps some are definitely characterized by skin diseases because of this form of food poisoning. Blackfan found that of forty- three patients without eczema, only one showed any evidence of susceptibility to protein through capacious and intracutaneous tests, while twenty-two of the twenty-seven patients with eczema testified to the susceptibility to proteins. Chapter III POISONOUS PLANTS AND ANIMALS Some normal plant and animal tissues contain substances that are poisonous to humans, and are sometimes eaten by mistake for healthy foods. POISONOUS plants are sometimes curly noticeably in human affairs. Every reader of ancient history knows how Socrates drunk the hem and how cunning imperial killers most likely replaced poisonous mushrooms with edible in dishes prepared for guests that were not in favor. Nowadays, the use of poisonous plants is usually an accident, and poisoning from this cause occurs mainly among the young and ignorant. According to Chesnut, the catalog of North American Heller plants includes 16,673 leaf-bearing plants, and of these almost five hundred, one way or another, were poisonous. Some are relatively rare or for other reasons unlikely to be eaten by man or beast; others contain poison only in a particular part, or are only poisonous in certain seasons of the year; in some poison is not dangerous when taken in the mouth, but only when in contact with the skin or injected under the skin or in circulation. There are large differences in individual susceptibility to some p.14 of these plant poisons. One familiar plant, the so-called poison ivy, is not harmful to many people, even if it is handled recklessly; It can be eaten with impunity by most pets. The actual number of poisonous plants that can be inadvertently eaten by humans is not large. Chesnut has listed about thirty important poisonous plants originating in the United States, and some of them are not known to be poisonous, except for pets. Many cases of human poisoning are classified as extremely rare accidents and are of little importance in this discussion. Such are the use of the leaves of the American false hellebore (Veratrum viride) by mistake for those of the swamp-calendulas, the use of the fruit pulp of the Coffee Tree of Kentucky (Gymnocladus dioica) by mistake, that of honey locusts, the accidental use of daffoded bulbs for food, and the confusion of children's young shoots from the broadleaf laurel (Kalmiaif) One of the most serious cases of poisoning of this kind is that of the use of spindle-shaped roots of deadly water hemlock (Cicuta maculata) in alliance with the more famous, but not more deadly poisonous hem. These underground parts of the plant are sometimes exposed to vision by washing or freezing, and are mistaken for horseradish, artichokes, parsnips, and other edible roots. Water spray poisoning is undoubtedly more common than shown in any record. It is known that in one year alone, the State of New Jersey has had eight cases and two deaths from this cause. Figure 1.-Konium macula. Konium's fresh maculatum juice was used in the preparation of the famous hem potion, which the Greeks used to execute their criminals. (From applied and economic botany, courtesy of Professor Kremer (after Holm).) An example of food poisoning to be included under this head is an outbreak in Hamburg and about thirty other German cities in 1911 due to the use of poisonous vegetable fat in the preparation of a commercial butter substitute. In an attempt to make margarita preparation as cheap as possible, various vegetable oils have been added by the producers. During the outbreak in Hamburg, which involved more than two hundred cases, the poisoning appears to have been caused by the replacement of the so-called maratti oil derived from a tropical plant (Hydrocarpus). This fat is said to be identical to cardamom oil, and its toxic nature in the quantities used in margaritas has been proven by an experiment in animals. Increased economic pressures on cheap food can lead to recurrence of such accidents unless appropriate precautions are taken when testing new fats and other untested substances for use in cooking. Fig. 2.-Cicuta maculata (water gemlock); A, top of the stem with leaves and composite umbels; B, stem base and thick tubular roots; C, cross section of the stem; D, flower; E, fruit; F, fruit in the longitudinal section; G, cross-section of mericarp. (From applied and economic botany, courtesy of Professor Kremer (after Holm).) Investigators from the New York City Department of Health found that some cases of suspected ptomain poisoning were actually caused by acid herb soup. This soup is made from the leaves of the species of sorrel, rich in sorrel. One restaurant found that the soup contained up to ten grains of sorrel acid per pint! Fig. 3.-Fly Amanita (poisonous). (Amanita Muskariya L.) (After Marshall, Mushroom Book, courtesy of Doubleday, Page and Company.) To date, the most famous example of this form of poisoning, which is the result of mixing poisonous The food is that because of the poisonous fungi. There is reason to believe that the mushroom (or greedy rack) intoxication in the in recent years has been increasingly occurring, partly because of the general increase in the use of mushrooms as food and therefore greater responsibility for the error, and partly because of the increase in immigration from the mushroom-eating communities of southern Europe. Many cases have become known in which immigrants mistakenly venomous varieties in this country for edibles with which they were familiar at home. In the New York area, 22 people died in torrential rains in a single ten-day period (September 1911). The Flying Amanita (Amanita muscaria) in this country, apparently, is often mistaken for a European variety of Royal Amanita (A. caesaria). Such a mistake seems to have caused the death of Count de Vecchi in Washington, D.C., in 1897. Graf, an attache of Italian heritage, cultivated by a gentleman for almost sixty years, was considered something of an expert on mycology, bought near one of the markets in Washington, the number of mushrooms recognized by him as an edible mushroom. The plants were harvested in Virginia about seven miles from Washington. The next Sunday morning, the Count and his doctor, a warm personal friend, had breakfast together on these mushrooms, commenting on their pleasant and even delicious taste. Breakfast was concluded in half after eight and within fifteen minutes the count felt symptoms of a serious illness. So quickly it was early that by nine o'clock he was found prostrate on his bed, oppressed by the feeling of impending doom. He quickly developed blindness, trismus, difficulty swallowing, and soon lost consciousness. The stunning convulsions then faded, so cruel a character as to break the bed on which he was placed. Despite the strict treatment and administration of morphine and atropine, the count never regained consciousness and died the day after the accident. The Earl's doctor was also attacked on his return to his office, dizziness and eye symptoms, warning him of the nature of the troubles. Energetic treatment with apomorphine and atropine was immediately initiated by his colleagues and for five hours he was in a coma with rare periods of clarity. Serious symptoms were improved and recovery set around about seven o'clock in the evening. His recovery was without complications, his recovery is complete, and he is, I believe, still alive. In this case, the graph probably identified the fungi as cesaria or aurantiaca. From the symptoms and cessation of species eating were to muscaria. A. muscaria contains an alkaloid substance, which has a characteristic effect on nerve centers and which is given the name muscarin and the temporary chemical formula C5H15NO3. Drug atropine is a more or less perfect physiological antidote to muscarin and has been introduced with success in cases of muscarin poisoning. It is said that farmers in the Caucasus have a habit of preparing a drink from Amanita fly, which they use to produce intoxication. Deaths, as they say, occur frequently from the overuse of this drink. Deadly Amanita or Lethal Cup (A. phalloides) are probably responsible for most cases of mushroom poisoning. Ford estimates that between twelve and fifteen deaths occur annually in this country from this species alone. This fungus is usually eaten by sheer ignorance of individuals who have gathered and eaten everything they accidentally find in the forest. Some of these poisonous mushrooms mixed with edible varieties may be sufficient to cause the death of the family. Ford thus describes the symptoms of A. phalloides poisoning: After consumption of mushrooms there is a period of six to fifteen hours during which no symptoms of poisoning are shown by the victims. This corresponds to the incubation period of other intoxications or infections. The first sign of trouble is the sudden pain of the greatest intensity, localized in the abdominal cavity, accompanied by vomiting, thirst and cholera diarrhoea with mucous and bloody stools. The last symptom is by no means permanent. The pain continues in paroxysms often so severe as to cause a peculiar Hippocratic facies, la face vultueuse of the French, and although sometimes improved in nature, usually repeated with greater severity. Patients quickly lose strength and flesh, their complexion takes a peculiar yellow tone. After three or four days in children and six to eight adults, the victims are immersed in a deep coma from which they cannot be separated, and death soon ends in a terrible and useless tragedy. Convulsions rarely, if ever occur, and when the present is indicated, I tend to believe, mixed intoxication, samples of Amanite muscaria eaten with falloids. Most people poisoned by deadly Amanite die, mortality varies from 60 to 100 percent in various accidents, but recovery is not impossible when a small amount of fungus is eaten, especially if the stomach will be very quickly emptied, naturally or artificially. A number of other closely related species of Amanite (e.g. A. verna, destroy angel, probably a small form of A. phalloides) have a poisonous effect similar to A. phalloides. All of them are different from muscrine. Fig. 4.-Death-cup; Destroy the angel (Amanita falloids fries); Shortened; Natural size: cover, 31/2 inches; stalk, 71/2 inch. (After Marshall, Mushroom Book, courtesy of Doubleday, Page and Company.) The nature of the poison was first thoroughly researched by Cobert, who showed that Amanita extract has the power of laking dissolving the coloration of the substance from the red blood cells. This hemolytic action is so powerful that it turns on the red bull's blood cells even when diluted by 1:125,000. Ford has since shown that in addition to the hemolytic substance in this type of Amanite there is another substance, much more toxic, and it concludes that the poisonous effect of the fungus is primarily caused by the latter (Amanita toxin). The juice of cooked Amanita is devoid of hemolytic force, but is poisonous to animals in small doses, which agrees with the observation that these mushrooms, after cooking, remain strongly poisonous to humans. Extensive fat degeneration in the liver, kidneys and heart muscle is produced by the true toxin Amanite. In the Baltimore cases studied by Clark, Marshall and Rowntree, the kidney, not the liver, was the site of the most interesting functional changes. These authors conclude that nervous and mental symptoms, instead of due to some peculiar neurotoxin, are probably uremic. A successful treatment is not known. Antibodies for hemolysine have been produced, but antitoxin for another poisonous substance seems to be formed in very small amounts. Attempts to immunize small animals with Amanite toxin will succeed only to a limited extent. POISONOUS ANIMALS While the muscles or internal organs of many animals are not acceptable due to unpleasant taste or strength, there do not seem to be many cases where normal animal tissues are poisonous when eaten. As indicated elsewhere (chapter vi), most outbreaks of meat and fish poisoning should be associated with the presence of pathogenic bacteria or poisons formed after the death of the animal. This was especially true for many poisoning outbreaks attributed to oysters and other molluscs; in most cases, if not all, vaccinated molluscs were obtained from water contaminated with human waste and either infected or partially decomposed. In some animals, however, in particular, some fish, living and healthy organs are definitely poisonous. The Tetrodontidae family (poufs, balloon-fish, globe-fish) consists of a number of venomous species, including the famous Japanese Fugu, which has many hundreds of deaths scored against it and is often used for suicide. Poisonous fish varieties seem more abundant in tropical waters than in temperate waters, but this may be due to the more general and indiscriminate use of fish as food in places such as the Japanese and southern sea islands. It is known that some fish with cool water are poisonous. The flesh of the Greenland shark has poisonous qualities for dogs and produces a kind of intoxication in these animals. There is a great deal of uncertainty about the conditions under which different forms of fish Occur. One type is thought to be associated with spawning season, and being caused by the poison present in reproductive tissues. The caviar of the European barbel is said to cause frequent poisoning, usually not of a serious kind. The flesh or caviar of sturgeon, pike and other fish is also considered poisonous during spawning. Some fish are said to be poisonous only when they feed on certain marine plants. There is little definite knowledge about poisons interested. They are, of course, not homogeneous in nature. Yad Fugu causes symptoms of cholera, convulsions and paralysis. It doesn't break down by boiling. The effect of the Greenland shark flesh on dogs is described as alcohol. It is said that dogs that feed on gradually increasing amounts of poisonous shark flesh become somewhat immune. Various symptoms are described in other cases of fish poisoning. Chapter IV MINERAL OR ORGANIC POISONS ADDED TO FOOD Known mineral or organic poisons - chemical poisons - sometimes they know their way into food, being either accidentally introduced in the process of production or cooking, or added intentionally with the intention to improve the appearance or preserve the quality of food. ARSENIC Is as powerful a poison as arsenic, sometimes injected into food by stupidity or negligence. It was found that arsenic was found to be commonly found in food materials dried or fried with gases resulting from coal burning, as well as in materials treated with sulphuric acid during preparation. In both cases, the source is the same: iron pyrites, almost always arsenic contained in coal or used in the manufacture of sulphuric acid. The famous epidemic of peripheral neuritis in the English Midlands in 1900 was associated with the presence of dangerous amounts of arsenic in beer. About 6,000 people have been affected by the outbreak and the death toll is about seventy. Beer produced at prospective breweries was made using brewing sugars derived from a single source, and it was found that these sugars were impregnated with arsenic sulphuric acid used in their preparation, some acid samples containing up to 2.6 percent arsenic. The use of glucose not only in beer, but also as impurities or adultery in jams, syrups, and the like, is open to serious objections, unless glucose is known to have been cooked with sulphuric acid released from arsenic. In fact, the use of any food material prepared with sulphuric acid is only permissible if arsenic-free acid is used. ANTIMONY Cheaper varieties of enamelled kitchen utensils used in this country contain antimonium, and this dissolves in remarkable quantities when cooked Products. (34) (34) nipples used for infant milk bottles also sometimes contain antimony. Although the poisonous properties of antimonia are well known, there is little information about the toxic effect of repetitive very minute doses. Recognized cases of chronic anti-disease poisoning are very rare. Further investigation is needed. LEAD The known poisonousness of lead and its compounds prevents the usually deliberate addition of lead salts to food substances, although it is true that lead chromat is sometimes used to give yellow color to candies and flavor sugars. However, products wrapped in foil, such as chocolate and soft cheese, contain traces of lead, as do the contents of cans with metal caps and soft drinks jammed in bottles with patent metal corks. Sometimes taking tiny amounts of lead is probably a matter of little physiological importance, but since lead is a cumulative poison, frequent intake of even very small amounts entails danger. Severe lead poisoning is known as a result of the usual use of acid drinks contained in bottled lead corks. Investigations conducted to determine the possible risk of lead poisoning taken from glazed and pottery indicate that damage to this source is unlikely. The enamelled utensils used in this country have no lead. Objections to possible contamination were raised in connection with the use of solder to seal food cans. Such objections have less weight than before, due to changes in the design of the container, so any solder contact with food is being minimized and largely understood overall. As many natural waters attack lead, the use of lead pipes for wells, tanks and public water sources has led to numerous outbreaks of lead poisoning. It is now generally accepted that drinking water should not pass through lead pipes. There is a special responsibility to keep lead in the stomach in artists and other professions related to contact with lead and its salts. It has been shown that eating food treated with smeared hands leads to a significant amount of lead and, when it continues, leads to lead poisoning. The risk of food contamination with lead in this way can be greatly reduced by carefully cleansing hands with soap and hot water before eating. TIN's particular interest in the possibility of tin poisoning was associated with the widespread use of canned food. Chemically established that the tin is attacked not only acid fruits and berries, but also some vegetables, which have only a slightly acidic reaction. More tin in drained solids than in liquor, and metal metal in an insoluble way. There was a general consensus, based on the experiments of Lehmann and others, that the amount of tin usually present in canned food does not merit serious attention and this view has found expression in leading hygiene textbooks. Of course, there was no noticeable amount of tin poisoning observed to coincide with the huge increase in the use of canned foods. An example of canned asparagus poisoning observed by Friedman, however, is attributed to his tin content, and this view is likely as a result of his bacteriological and serological examinations. Canned asparagus seems to contain an unusually large number of soluble tin compounds. There seems to be some reason to believe that some people are particularly susceptible to small amounts of tin and that the relative rarity of such cases, as cited by Friedman, can be best explained in this way. Lacquered or enamelled jars are increasingly used for fruits and vegetables, which can especially attack tin. Deliberate addition of tin salts to food substances does not appear to be common, although tin protochloride is said to sometimes be added to molasses in order to reduce color. Chlorides are considered more definitely poisonous than other tin compounds, and for this and other reasons the practice is undesirable. Sanitarists insist that chemicals that can irritate human tissue when digested or eliminated should not be used in food. Each new irritant, even in small quantities, can add to the burden of organs already weakened by age or previous severe treatment. COPPER Danger is popularly supposed to be involved in cooking and especially the long position of some foods in copper vessels due to verdigris or copper acetate, which is sometimes formed, but Professor Long, of the Judicial Council of Consulting Scientific Experts, 45 points out that this substance is much less toxic than it once imagined to be, and he considers it likely that cases of the disease related to Verdigri poisoning, as reported in the old literature, had to be explained in some other way. The use of copper sulfate to green some vegetables, such as peas, beans and asparagus, is a relatively modern practice that began in France around 1850. Since natural green vegetables partially destroyed or altered the heat, the restoration of color appealed to the color sense of some consumers. Admittedly, this aesthetic satisfaction is fraught with a certain degree of health risk. Long's experiments show that copper is absorbed and preserved in certain tissues, and that even small gets in at short intervals of time can have a detrimental detrimental He concludes that the use of copper salts to stain products should be considered highly undesirable. Currently, the United States Government prohibits the import of copper-stained products as well as the interstate trade in these substances. VARIOUS COLORING SUBSTANCES Copper sulfate is just one of the host chemicals used to different foods to change the color that products would otherwise possess. In some cases, there may be a general consensus that the attractiveness of the food increases when treated, as when the flour of dark color is bleached white with nitrogen peroxide, but in many cases the change of color is based on ridiculously artificial standards. The use of poisonous aniline dyes to stain the brushes of all colors of the rainbow must be protected, if at all, on aesthetic, and not on sanitary grounds. Some coloring issues in general use, such as annatto, commonly used in oil coloring, are thought to have no harmful effect, but others should be treated with suspicion, while others, like copper sulfate, are undoubtedly dangerous. All food coloring practices at best include waste and can pose a serious health risk. In general, all changes in the natural color of food are based on idle convention and should be banned in the interest of public welfare. Bleached flour, dyed oil, dyed jelly and ice cream are no more desirable as products than natural unprocessed substances; in fact, they are essentially less desirable. If the whole process of food coloring was known to the public, artificially colored products would not be particularly appetizing. Economically, this practice is extremely useless. Artificial bleaching of flour with high-venomous nitrous oxide is hardly worth an additional tax of fifty cents per dollar per barrel. Such bleaching by poisonous gas, of course, does not improve the nutritional or digestive properties of flour; it can be insidiously harmful. The solution to the problem of food coloring seems to be an education education policy that should make natural products more desirable than those sold under false colors. The custom, however, backed by skilful advertising, offers a difficult barrier to reform in this area. FOOD PRESERVATIVES It is not only legal, but in every way the most desirable to keep food from the season of excess to season deficit. Since time immemorial, food is preserved by drying, smoking or salting, and nowadays - by cooling and heat (canning). These latter methods have come to play a big role in the food habits of civilized communities. Since food deteriorates due to microbial action, all conservations are based on the destruction of germs or restraint of restraint their growth by various physical and chemical institutions. The use of some chemical preservatives, such as strong solutions of sugar and salt, salt brine and sour pickles have long been known and such. Recently, the use of chemical preservatives has taken on a new dimension due to the growing tendency of manufacturers to add antiseptic chemicals to food products in a wide variety of and questionable physiological effects. It is not as easy and easy as it may seem to declare that no poisonous substance should be added to food. The scientific concept of poison is one involving quantity as well as the kind of substance. Ordinary salt itself is poisonous in large doses, but as everyone knows, small amounts are not only not harmful, but also absolutely necessary for health. Known and very powerful protoplasmic poisons, such as strychnine and quinine, are often injected in minute doses for medicinal purposes without causing serious results. How difficult the use of food preservatives really is in the case of smoked meat and fish, which owe their compliance to the qualities of creosote and other substances by which they are impregnated with smoke. Although these substances are much more poisonous than chemical preservatives such as benzoic acid, there has been much concern, but little if any objections have been made to the use of smoked foods. The use of benzoic acid (benzoate soda) as a food preservative illustrates several phases of controversy. Wiley's observations in 1908 on so-called poisonous detachments were thought to indicate, in his opinion, that benzoate soda injected with food led to a very serious metabolic dysfunction present with digestive and health trauma. On the other hand, the experiments of the Judicial Council of Scientific Experts (1909), conducted at least with equal care and care, were considered justified conclusions that: (1) sodium benzoate in small doses (less than five tenths of a gram per day), mixed with food, has no harmful or poisonous effect and is not harmful to health. (2) Sodium benzoate in high doses (up to four grams per day), mixed with food, has had no detrimental effect on overall health, nor act as a poison in the general acceptance of the term. In some areas there have been small changes in some physiological processes, the exact value of which the modification is unknown. (3) Sodium benzoate impurities with food in small or large doses have not been found to adversely affect or impair the quality or nutritional value of such food. Even more recent experiments under the auspices of the German government (1913) showed that in the case of dogs and rabbits relatively large doses of benzoic acid (appropriate to sixty to a hundred per day for a person weighing one hundred and fifty pounds) were necessary in order to produce obvious effects of any kind. This conclusion can be considered to confirm in general the conclusion of the Judicial Council that four grams per day are harmless. Probably, evidence supporting the effects of benzoic acids and benzoates when used as food preservatives is a favorable case that can now be made for the use of any chemical. Benzoic acid is present in remarkable quantities in many fruits and berries, especially cranberries, and its presence in these natural products has never been associated with any harmful effects. In fact, the substances present in many ordinary foods are converted into the human body first into benzoic acid and then into hypuric acid. The virtuoso summing up of Folin is worth quoting: We know that the human body is willing to care for and render harmless those small amounts of benzoic acid and benzoic acid compounds that occur in foods or that are formed in the body; we know how this is achieved, and we are fairly sure of which body is doing it. We also know that the mechanism by which poisonous benzoic acid is converted into harmless hypuric acid is extremely effective and that it is able to take care of relatively large amounts of benzoic acid. In this case, as in many others, the normal animal organism in abundance is able to perform functions that it must regularly perform in order to survive. From this point of view it can be argued, and it has been proven with considerable force, that the human body in abundance is capable of making harmless reasonable amounts of benzoic acid or benzoate that are added for the purposes of preserving certain articles of our food. In my opinion, this view will prevail, and the fight will resolve itself into a controversy over how much benzoic acid should be allowed to go into our daily meals. But we have to be extremely careful in taking any particular figure, of course, any big figure, as representing the allowable amount of added benzoic acid in our food. The very fact that we are in possession of an effective process of converting poisonous benzoic acid into harmless hypuric acid points to the need for this. This suggests that even a small amount of benzoic acid that we get from pure food, or produce within ourselves, can be harmful to health, except to maintain the process of forming hypuric acid. And since this safety factor is large in relation to the normal content of benzoic acid in our food, it does not follow that we can encroach on it with impunity. will effect a general, regular encroachment on it, there can be no several relatively short feeding experiments. It is known that while some chemicals may be taken in significant quantities for a month or a year without apparently harmful effects, further use of the same substances, even in smaller amounts, will ultimately undermine health. Perhaps the ultimate solution to the problem of benzoic acid is best obtained directly from people in general. If they consumed benzoic acid as consciously as they consume, such as soda carbonate in soda cookies, or caffeine and theobromine in coffee and tea, it would not take more than ten or two years before we should have a clear and informed public opinion on the subject, at least in the medical profession. As for other familiar and more or less poisonous substances used to preserve food, protection against their harmlessness is much more difficult. Formaldehyde, salicylic acid, sulphuric acid and sulfite are compounds that are particularly poisonous in relatively small amounts, their harmful effects in minute successive doses in animal experiments are quite noticeable, and their use in human food is almost without explanation. Boric acid and borax may be on a slightly different basis, but are never present in natural foods, and there is no hard evidence that they are long-term use in small doses without harmful effects. It should not be forgotten that all such substances owe their preservative or antiseptic force to the poisonous effect they have on bacterial protoplasm. It is fair to assume that, in general, bacterial protoplasm is not easier to get injured than a person's protoplasm, and this raises the immediate decency of re-exposure to human tissues of substances that can lead to injury, even if such an injury is minor and recovery from it is usually easy. In any case, the burden of proof must be properly placed on those who advocate the addition of bacterial deterrents to human-made food. It is for them to show that the substances are powerful enough to control the development of bacteria, but are not able to seriously interfere in the vital processes of the cells of the human body. At the same time, the opinion about the situation, not only the chemicals mentioned earlier fall under some suspicions, but also some household preservatives have long been sanctioned by customs. Spices such as cinnamon, clove oil, and the like, as far as we know, are likely to have harmful physiological effects when used in small repetitive amounts, like some of the chemical preservatives whose use is devoid of law. Chemicals stored in wood smoke in meat (p.38) particularly undesirable, and their continuous use can well lead to serious injury. One fact persistently comes to the front in comprehensive study of the food-preservative issue, namely the need for further experimentation and observation. At present, we do not know what effect people of different ages and varying degrees of force produce as a result of prolonged consumption of food stored by specific chemicals. There is, I think, only one way to get at the facts regarding the various chemicals that have been used to preserve food, and that's by trying them out and tracking the results. However, their proper and quite wide and long enough time is more of a task than can be carried out by private investigators; for it is only through their continuous use for many years under competent control and control that we can hope to obtain adequate information for the final conclusions. This type of work must be carried out and could well be carried out in large public institutions, such as certain categories of prisoners. I don't know how many life-long-term prisoners or long-term prisoners can be available, but there must be many. They will do better subjects than students on which to try a substance like boric acid. This is not because they are prisoners whose fate or health is relatively small, but because they represent the body of persons whose lifestyle is essentially homogeneous and whose health can be easily preserved for a long period of years. I am well aware that this proposal will impress many people as heartless and cruel, but such an experiment would be mild and humane compared to the unaccounted-for boric acid experiments that were made by manufacturers on all kinds and conditions of people. Unfortunately, prisoners are not in a position to provide any useful service to society. Probably not many of them would be willing to cooperate in long- term feeding experiments such as the short p.39 conducted by Dr. Wylie and the Judicial Council. An acceptable reward in the way of well-cooked food with sufficient variety will attract volunteers. If additional stimulation is required, the shortened lifespan is likely to appeal to many. And in the face of the fact that every civilized country is willing to sacrifice thousands of its most courageous citizens for the sake of honoring its flag (and its foreign trade), the mood against the threat to the health of a handful of people in the interests of all mankind is not particularly smart. Until such information is received, we should also make a mistake on the side of caution. The desirability of adopting such a position is particularly evidenced by the already stated facts (p. 2-4) regarding the increase in mortality rates in older groups in that country. For aught we now know, on the contrary, relatively high rates from degenerative changes in the kidneys, blood vessels, and organs can be partly caused by the use of irritant chemicals in food. Although no chemical in itself and in the quantities in which it is usually present in food may be reasonably blamed for producing serious and permanent injuries, but when its effect superadded the effect of even other poisonous ingredients in spicy, smoked and canned foods of all kinds the overall burden placed on excremental and other organs may be clearly too great. It cannot be concluded that the wider and wider use of preservatives in food, the greater the likelihood of serious public health consequences. The use of spoiled or decomposed food falls under the same head. It cannot be assumed that irritants produced in food by certain types of decomposition, p.40, can be constantly consumed with impunity. We don't even know if these decomposition products can be no more fundamentally harmful than preservatives that can be added to prevent decomposition! Therefore, as far as our current knowledge shows, efforts should be made (1) to ensure that, as far as possible, as fresh as possible; (2) to avoid chemical preservatives of all kinds except those uniquely shown to be harmless. The methods of preserving food by drying, cooling, heating and sealing are justified by experience as well as theoretical considerations, and the same statement can be made with regard to the use of salt and sugar solutions. But the use of sulfites in sausage and sliced meat, the addition of formaldehyde to milk, as well as boric acid or sodium fluoride in butter are a practice completely undesirable from a public health point of view. The remedy is obvious and is often proposed, namely, laws prohibiting the addition of any chemical to food, except in certain specific cases. Then the presumption will be, as in fact, that such chemicals are more or less dangerous, and evidence of innocence must be put forward before any single substance can be listed as an exception to the general rule. Such laws would include not only the use of chemicals or preservatives, but also the use of substances to improve the appearance of food. As noted, children's practice of artificial coloring of products includes waste and sometimes danger. It relies on the absence of deep-rooted p.41 human needs; Food that is natural and unbridled with can be made fashion as easily as color and cut clothes changed fashion monger. Incorporating any chemical into foods for conservative or cosmetic purposes may be subject to a blanket ban, and the necessary list of exceptions (substances such as sugar and salt) should be referred to the National Council of Experts or some organization, like the American Public Health Association. FOOD SUBSTITUTES Based on savings or convenience, familiar and natural foods are sometimes replaced or supplemented with artificial chemicals, or substances whose nutritional value is not so clearly established. I need to refer only briefly to those notorious cases of tampering in which chicory is added to coffee, or ground olive stones for pepper, or glucose in candy. Only for hygienic reasons are some practices open to criticism, however fraudulent they may be from the point of view of public morality. It can be argued with some plausibility that chicory is not as likely to harm the human body as caffeine, and that spraying ground cocoa nut shells are more beneficial than pepper. But there is another group of cases where artificial replacement is categorically undesirable. An example would be the use of sugar-drying coal-resin product for sweetening. This substance, whose sweetening power is five hundred times larger than that of cane sugar, has no nutritional value in the quantities in which it will be consumed, and in not very large quantities (more than 0.3 grams per day) is likely to cause digestive disorders. As a sugar substitute in conventional foods, this is undesirable. The use of cheap chemically prepared flavors such as fruit esters in soft drinks, fruit syrups and the like instead of more expensive natural fruit extracts provides another well-known example of replacement. Probably more important hygienically is the production of foam in soda water saponin, a substance that is known to be harmful to red blood cells. Among many other familiar examples of food substitution, complexity and falsification there are some of the obvious hygienic deficiencies, while others, the main drawback of which is simple deception. From almost anything it can be said that they are unjustified in terms of public policy because they are based on the intention of making food appear, except that they are actually. According to some who closely followed the course of food falsification, in recent years the share of really harmful falsification has increased significantly. However, it is obvious that the possibility of wholesale experiments with new substances should not be allowed for recreation without control in the hands of manufacturers and dealers, largely fueled by commercial motives. As long as the motives of getting are allowed a loose framework, for so long will a small minority of unscrupulous individuals add cheap, low and sometimes dangerous ingredients to food. The network of restrictions should be tighter and tighter. Motives to the falsification of food, fall basically under three three (1) the desire to keep food from spoiling or worsening; (2) puerile fantasies - often expertly promoted for mercenary reasons-for the usual appearance, such as for polished rice, bleached flour, and grass-green peas; and (3) the intention to make intentional fraud less valuable. Only the first named motive can claim any legitimate justification, and its satisfaction with chemical preservatives is surrounded by hygienic difficulties and uncertainty, as already outlined. From an objective point of view of human physiology, the dangers of slow poisoning by chemically processed foods should be considered as no less real, as they are insidious and not easily traces. Chapter V FOOD-BORNE PATHOGENIC BACTERIA Many cases of so-called food poisoning are associated with the presence of pathogenic bacteria in food. In some cases, as in typical meat poisoning epidemics, symptoms develop so soon after eating that a particular diet involved is immediately suspected and put your hands on. In other cases, the culprit is difficult to trace. Some cases of tuberculosis are undoubtedly caused by swallowing bacilli tubers in food, but the exact source and date of infection may be rare, if ever, certainly established. The presence of pathogenic bacteria in food is usually associated with either contamination of food by infected people during cooking or feeding, or with an infection of the animal from which the food is derived. The relative importance of these two factors is very different in different infections. TYPHOID FOOD INFECTION Belly bacillus does not attack any of the pets; consequently, the entire typhoid of foodborne origin is caused more or less directly by human contamination. A remarkable case of typhoid due to food was reported in 1914 in Hanford, California, where ninety-three cases of typhoid were caused by the consumption of Spanish spaghetti served at a public dinner. The study found that the dish was prepared by a woman, p.45) of the typhoid carrier, who harboured live abdominal bacilli while she mixed spaghetti sauce before baking. Further laboratory experiments showed that the usual baking temperature at which spaghetti was cooked was not only insufficient to sterilize food, but also provided an opportunity for bacteria to multiply within the mass. Thus, the food contamination was severe and concerned a very large proportion (57 per cent) of those present at the dinner. A well-deserved celebrity lends the exploits of a typhoid carrier, Mary Malloy, who, while continuing her career as a cook in and around New York, is known to have caused at least seven outbreaks of typhoid in the various families in which she worked and one extensive hospital epidemic. Similar cases of typhoid food infection restaurants and public institutions are categorized, and show the need to protect food from pollution throughout the preparation and maintenance process. On the basis of this principle, the New York City Department of Health has opened a comprehensive examination of the chefs and waiters (approximately 90,000 people) employed in public restaurants and canteens in the city. The results were obtained in connection with the detection of typhoid carriers and cases of infectious diseases, which strongly justify this procedure as an important measure to protect society from the spread of infection. Some products by their origin are exposed to more typhoid pollution than other typhoid. Vegetables such as lettuce, celery, radishes and watercress, which are usually eaten without cooking, are more likely to transmit typhoid fever than peas, beans and potatoes. An outbreak of typhoid apparently due to a watercress has been reported from Philadelphia. At the wedding breakfast for forty-three guests on June 24, 1913, sandwiches with watercress were served, and a subsequent investigation revealed that nineteen guests took part in these sandwiches. Eighteen of this number contracted typhoid fever within a month, the disease developing in most cases after guests dispersed into their summer homes. Those who did not eat watercress sandwiches were not affected. There were also reports of abdominal infection with raw celery. The practice of using human excrement as fertilizer in cargo gardens sometimes causes dangerous soil pollution, which is transmitted to growing plants and persists for a long time. Even scrupulous washing of vegetables is not enough to make them bacterial clean. In the future, the danger to society from this source is likely to become increasingly serious unless the increasing use of this method of soil enrichment is finally verified. In 1915, an increasing number of cases of typhoid in South Philadelphia led to an investigation by the state health department. This revealed the fact that most of the cases were grouped in and around three public markets. These are all kerb markets - fruits, vegetables, confectionery, clothing and various goods of any description are dumped on trolleys and sidewalks without taking into account any sanitary precautions. Patrons of these markets handle and pick up more exposed food, thereby giving every opportunity for disease transmission.... The largest 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 mostly Jews, while the Seventh Street market is under the patronage of Jews and Poles. The following was made relatively relatively particularly high number of cases among persons of the same nationality: Our inspectors have found that the various methods used by Italians and Jews in cooking are responsible for the greater number of cases that have been detected in the vicinity of the Christian street market in Little Italy. It is customary for Italians to eat many fruits and vegetables raw, while Jews cook most of their food. Presumably, it is because of this custom that the members of the Italian colony suffered more than other residents of the area. Bacterial studies of different types of vegetables derived from trolleys and curb markets have led to the finding of typhoid bacillus on some of the celery. Naturally, in such cases it will be difficult to determine whether the abdominal bacilli were derived from the contaminated soil in which celery was grown, or whether the contamination occurred as a result of mishandling. Bread, when the market is deployed, is subject to contamination from flies and from unclean processing. Katherine Howell testified that the unpacked loaf of bread sold in Chicago was more or less thickly smeared with bacteria and was covered on average by much larger amounts than wrapped loaves. In some cases, typhoid fever was directly related to bread. Hinton recorded seven cases of typhoid at Elgin State Hospital, Illinois, which were apparently caused by typhoid, which was used to chop bread before serving. When this typhoid fever was transferred to another department where it was not processed raw food, cases of typhoid fever ceased to appear. Foods such as milk, which is not only eaten normally without cooking but also suitable for the growth of typhoid bacillus, should be especially protected. It is noteworthy that the mandatory pasteurization of milk in New York, Chicago and other major American cities was accompanied by a large decrease in the prevalence of typhoid. Until recent years, typhoid milk was common in the United States, and hundreds of typhoid epidemics had been traced to that source. Fig. 5.-Bacteria left by a fly passing over a gelatin plate. (Courtesy of Doubleday, Page and Company.) One food animal, oysters, often eaten raw, has been linked to good evidence with certain outbreaks of typhoid. However, the number of established typhoid epidemics is not high, and the danger of this source is sometimes exaggerated. The source of oyster contamination is sewage contamination either from clam beds or brackish water, in which oysters are sometimes placed on fat before it is marketed. State and federal oversight of the oyster industry in the United States in recent years has largely oysters are from contaminated waters, and although oysters as well as molluscs and mussels must be permanently protected from wastewater contamination, the actual occurrence of oyster infection is now considered relatively rare. Perhaps the most effective method of preventing typhoid food infection is to investigate each case of typhoid and trace it as far as possible to its origin. Thus, typhoid carriers can be detected and other pockets of infection are brought to light. Carriers, once found, can receive appropriate advice and be warned that they pose a danger to others; full control over typhoid carriers, which are not inclined to act in accordance with the urgent task, is complex and not yet resolved by public health authorities. ASIATIC CHOLERA With Asian cholera, as with typhoid, pets are not susceptible to this disease, all cases of infection are of direct human origin. Drinking water is a common means of cholera infection, and even in countries where the disease is endemic, food-borne outbreaks are much less common than typhoid outbreaks. Cases of Asian cholera are sometimes caused by milk supplies and contaminated fruit or lettuce, but they are exceptional and cannot be considered as an example of the general way in which the disease spreads. However, the extent to which the inhabitants of tropical countries, and in all lands, are at the mercy of their home assistants, is evidenced by the following experience of the English bacteriologist Hankin. I saw, he says, a chef cooling jelly while standing in a small irrigation ditch that ran in front of his cook. The water, the fun in this drain, came from a well where I found a cholera microbe. He cleaned the spoon, dipping it down the drain and rubbing his fingers; He then used it to stir the jelly. TUBERCULOSIS Animal experiments have shown that both meat and milk derived from tuberculosis cattle are capable of transmitting infection. The exact extent of the danger to humans from the use of these products in modern conditions is still being challenged. Since tuber bacillus of bovine origin differs from tubers bacillus of human origin in some clearly defined particular particulars, it is possible by careful study to distinguish human infections caused by cattle bacillus from those caused by the so-called human tbula bacillus. More comparative research is needed in this area, and they may allow us to ultimately assess more fully than is currently possible, the extent of the infection from cattle sources. Meat is a less likely source than milk, mainly because it is rarely eaten without cooking. Opinion on the actual incidence of TB transmission by tb meat in the past, in broad differences, and even now they must be based on circumstantial evidence. There are no well-established human infections as a result of the use of tubular cattle flesh. The significance of this fact, however, is diminished by the observation that bacillus tubers can pass through the intestinal wall, leaving no trace of their passage and can make their way to the lungs or other distant organs where they find room for growth. This, along with the long period that usually passes between the actual occurrence of infection and the discovery of the existence of infection, makes the difficulty of providing valid evidence particularly great. Against any very common occurrence of tuberculosis transmitted through meat, there are facts that bacillus tubers are usually or abundantly present in muscle masses, usually on the market as meat, that the tuber embryo itself is not a spore and killed by conventional cooking, and that reported cases of finding tubers of bullish bascill in adults over sixteen years of age are extremely rare. This latter fact is perhaps the strongest evidence that tubular meat infection, although theoretically possible, is at least not common. Most commissions and official agencies that have considered precautions to be taken regarding possible tuberculous meat infections agree that the entire carcass of an animal should be condemned when tuberculous lesions are generalized or when lesions are extensive in one or both body cavities, and when lesions are somewhat, acute, and actively progressive. Any body showing evidence of tuberculous lesions obviously should not be passed on as food. On the other hand, it is believed that parts of properly tested animals can be put on the market if the tubular lesion is local and limited and the main part of the body is not affected; in such cases, you should avoid contaminating the meat in the sauce. It is a common belief that when such precautions are taken the risk of tubular infection through properly cooked meat is so small as to be insignificant. Milk is a much more likely means than meat for tuberculosis transmission. Freshly prepared raw milk from tubular cattle can contain a huge amount of tuber bacilli, especially if the quenching is sick. Contamination of milk by tubular cow manure can also occur. Observers in England, Germany, France and the United States found bacillus tubers in varying quantities in market milk, and proved that such milk is infectious to laboratory animals. Although, as indicated in reference to meat infection, the difficulty in tracking any particular case of tuberculosis with its source is very high, evidence strongly suggests that milk was a means of infection. Particularly convincing are the observations of the relative incidence of infection with bull and human bacillus tubers at different ages, As shown in the following table: 59 Adults sixteen years old or more children aged five to sixteen children under five years of age, human tuber bacilli found 677 99 161 bull tubers bacilli found 9 33 59 Large proportion of bullish bacillus tubers in children is likely to be causal with the relatively widespread use of raw milk in a child's diet. Proper milk pasteurization provides safe and satisfactory means of preventing TUBercuous infection from this source. The overall introduction of pasteurization in most American cities is well-founded in terms of infection prevention. VARIOUS MILK-BORNE INFECTIONS Facts associated with the above pages indicate that of all foods, milk is most likely to transmit disease microbes to the human body. This is partly due to the fact that milk is sometimes produced by sick animals and partly by the fact that, unless care is taken, it can easily become contaminated during collection and transportation; If milk is once sown with dangerous bacteria they can multiply in the excellent culture environment it gives. This is also partly because milk is usually taken in a child support tract without cooking. For these reasons, the amount of disease traced to raw milk far exceeds what is attributed to any other food. There are several infections that can be transmitted by milk, but rarely if ever because of other foods. Diphtheria and scarlet fever are perhaps the most famous of them. Both diseases have been repeatedly linked to the use of specific milk supplies, although different forms of individual contact also play a large role in their distribution. Dairy scarlet fever and diphtheria seem to tend, if not always, due to direct contamination of milk from human sources. However, some researchers believe it is possible that a cow can sometimes contract scarlet fever or diphtheria virus and can sometimes directly contribute to milk infection. A serious disease transmitted by milk, which has recently been ingested in Boston, Chicago, Baltimore and other American cities under the name septic sore throat or streptococcus sore throat, appears to be occurring in some cases from a cow wiped infection by an infected milkmaid; in other cases, the milk appears to have been directly contaminated by the human carrier. The specific microbe is believed to have been isolated and its link to the disease was demonstrated in the laboratory. It is a disease like diphtheria and scarlet sometimes because of contact. It is known that this is not caused by any food other than milk. The man-of-the-tongue is passed on to humans through the milk of infected cattle, but this infection in humans is not very common or usually very serious. As far as is known, it is not transmitted to a person in any other way than with raw milk. Such cases of infection or milk poisoning can be prevented, as mentioned, by the exclusive use of heated milk. According to many doctors, the possible occurrence of eating disorders (e.g. scurvy) in a small proportion of children fed pasteurized or boiled milk is easily corrected and has much less practical value than preventing infection. POSSIBLE INFECTION WITH B. PROTEUS One widespread organism known as Bacillus proteus has been prosecuted several times for food poisoning outbreaks, but it is not yet clear how justified this charge is. B. proteus is associated with E. coli, but most varieties do not ferment lactose and are much more actively proteolytic than the last organism, as evidenced by their ability to liquefy and kasin. Like b. coli, they form an ingol and enzyme dextrose with gas extraction. B. proteus varieties are widespread in decomposing organic matter of all kinds. The evidence on which this bacillus is seen as the cause of food poisoning is not entirely conclusive. The flash described by Ptuul is typical. Eighty-one soldiers in a garrison in Hanover were suddenly attacked with acute gastroenteritis four to twelve hours after eating sausage meat. It was found that meat contains B. proteus in large quantities, although it was prepared with the usual caution and was perfectly normal in appearance, taste and smell. Rats and mice fed on sausage became ill, and B. proteus was isolated from blood and internal organs. But these animals sometimes die when fed perfectly normal meat, and B. proteus and other common intestinal bacteria are often isolated from the body after death. B. proteus is, in fact, found in many animal products and in the clearly normal human gut. Like b. coli, it often invades internal organs after or shortly before death. Therefore, the detection of B. proteus in food or internal organs is not a definite proof of any causal relationship. The data attributed to other outbreaks of B. proteus infection are also inconclusive. Equally uncertain is whether the production of poison in food by this species can be in any way responsible for meat poisoning. B. proteus is quite common in food material decomposition and under certain circumstances is known to generate substances that are For a man. It may be true that toxic substances are produced in the early stages of decomposition by this organism. In B the opinion of Mandel and others, if any harmful effect at all should be attributed to B. proteus, it is in nature intoxication, not infection (see chapter viii). As for the existing evidence, the question of the responsibility of this organism for food poisoning remains open. Chapter VI FOOD-BORNE PATHOGENIC BACTERIA (Continued) PARATYPHOID INFECTION The most common examples of food poisoning, popularly speaking, are those in which symptoms appear shortly after eating and in which gastrointestinal disorders predominate. Typical group outbreaks of this kind show all degrees of severity, but are usually recovered. The vast majority of such cases studied by modern bacteriological methods indicate the presence of bacilli belonging to the so-called parathyroid group (B. paratyphosus or B. enteritidis). This is especially true of meat poisoning epidemics that paratyphoid bacilli are causal to them. Heubener lists forty-two outbreaks of meat poisoning in Germany that showed the group's bacilli, and Savage gives a list of twenty-seven similar outbreaks in the UK. There have been relatively few outbreaks of this nature in the United States, but it cannot be assumed that this is due to their rarity, as food poisoning is generally not properly investigated in our American communities. Typical paratyphoid outbreaks.-Kaensche 64 describes an outbreak in Breslau involving more than eighty people (p.59), in which sliced beef appears to have been a carrier of infection. The beast from which the meat came was sick with severe diarrhoea and high fever and was slaughtered as an emergency measure (notgeschlachtet). During the examination, the pathological condition of the liver and other organs was noted by a veterinarian, who declared the meat unusable and ordered it to be destroyed. It was, however, stolen, secretly delivered to Breslau, and some of it was distributed to various sausage producers, who sold it for the most part as a hamburger steak (Hackfleisch). The meat itself did not present anything abnormal in color, smell or consistency. However, the disease followed in some cases after the use of very small portions. Some of the victims had very severe symptoms, but there were no deaths. Bacillus enteritidis-type bacilli were isolated from meat. A large and unusually severe outbreak reported by McVini occurred in November 1908 among prisoners at the Industrial School for Girls in Limerick, Ireland. Seven cases were reported, 9 out of a total of 197. The main brunt of the attack was in the first or senior class, consisting of 67 girls between the ages of thirteen and seventeen. Of the 55 girls class that partook of beef beef 53 people fell ill for dinner, 8 of them died. One of the two that were not affected ate sauce and potatoes, but not beef. Some of the beef mixed up were also eaten as cold meat by girls in some other classes, and also caused illness. Some of the meat was eaten earlier without any negative effects. The flight of those who parted with parts of the same carcass on 27 and 29 October (five days ago) can be caused either by the unequal spread of the virus or by the careful preparation of the food that destroyed it. Some of the infectious materials, however, escaped the roasting of the 29th, and, rapidly multiplying, made the whole piece intensely toxic and infectious within five days that expired before the fateful Tuesday, when it was finally consumed . The beast from which the first quarter of beef was taken was killed by a local butcher privately. Reliable information about the condition of the calf for slaughter or a little before it could not get. The meat, however, was sold at such a low price that it was obviously not regarded as a mere quality. In this outbreak of agglutination of the blood reaction of patients and characteristics of bacillus isolated showed the infection to be due to the typical strain of Bacillus enteritidis. The food poisoning epidemic occurred in July 1915 in and around Westerly, Rhode Island. The outbreak was characterized by the usual symptoms of acute gastroenteritis, followed by the use of a pie, which was obtained in a restaurant in Westerly. All the circumstances of the outbreak showed that a certain batch of pies was responsible for this. About sixty people became seriously ill and four died. There was no unusual taste or smell to the pies to arouse suspicion. Symptoms followed the consumption of different types of pie: custard, pumpkin, lemon, chocolate, apple, etc., which were made with the same mixture of pie crust. Bacillus paratyphosus B was isolated from pie samples that were researched. No exact data was available on the exact source of the pie mixture infection. It is possible that the pie became infected in the restaurant through the agency paratyphoid-carrier, but since the restaurant staff has not changed for several months, this explanation is in many ways speculation. It is possible that some animal ingredient was first infected. The general natures of parathyroid infection.- Symptoms of parathyroid food infection are varied. Typically, the first signs of trouble appear within six to twelve hours after eating, but sometimes they can come within half an hour, or they may not appear until after twenty-four to forty-eight hours. Irritation of the gastrointestinal tract is almost always present, and can take the form of mild indigestion or small diarrhea or can be of great severity with excruciating abdominal pain. Fever is common, but usually not very high. Recovery can occur quickly, so within two to three days the patient regains his normal condition, or it can be very slow, so the effects of the attack linger for weeks or months. Researchers noted the occurrence of at least two clinical types of parathyroid infection, a common gastrointestinal type of newly described and the second type resembling typhoid very close, and sometimes not distinguishable from it, except for a thorough bacterial study. It is not yet clear how these two clinical varieties relate to the quantity and nature of contaminating food materials. No difference in the type of bacilli parathyroids was observed to be associated with a difference in clinical manifestations. Perhaps the amount of toxin present in the food eaten, as well as the amount of bacilli may have some effect. The individual feature of the patient undoubtedly plays a role. While there is still some uncertainty regarding the specifics of parathyroid infection, several significant facts have been clearly established: (1) Some diet articles are much more common than others with this type of food poisoning. Most of the reported outbreaks are related to the consumption of meat, milk, fish and other protein products. Vegetables and cereals were less involved, fruits are rare. (2) In many, though not all cases of parathyroid meat poisoning, it has been demonstrated that the meat was derived from an animal slaughtered during illness (notgeschlachtet, to use the expressive German term). There seems to be reason to believe that in such an animal being killed to save his life, a specific parathyroid microbe is present as an infection before death. Milk also caused parathyroid poisoning and in some of these cases it has been found to be derived from a cow suffering from enteritis or some other disorder. (3) There is evidence that initially healthy food may become infected with parathypoid bacilli in preparation or serve in the same way as it can contract typhoid fever; the processing of the food of the paratyphoid carrier is usually responsible for this. In some cases, the disease is transmitted from case to case, but this method of infection seems extremely rare and not as common as a contact infection in typhoid. (4) Most parathyroid outbreaks (p.63) are associated with the use of raw or partially cooked food. Often there is selective action, those who have eaten the accused food raw or imperfectly cooked, most seriously suffer, while those who took part in the same food after cooking, remain released. Fig. 6.-Bacillus enteritidis, Gurtner; Pure culture Van Emengem's preparation. and Wasserman.) The discovery of a link between paratyphoid bacillus and meat poisoning was the result of an investigation initiated by Geertner in 1888 during a meat poisoning outbreak in Frankenhausen, a small town in Germany. This epidemic was associated with the consumption of meat from a cow that was slaughtered because it was sick with severe enteritis. Fifty-eight people of varying degrees of severity were injured; as a result of the attack, a young worker ate about eight hundred grams of raw meat. Gurtner is isolated from the spleen of the deadly case, as well as from the flesh and intestines of the bacillus cow, to which he gave the name B. enteritidis. Vaccination experiments have shown that it is pathogenic to 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. In the United States, there has been one well-studied case of food poisoning due to bacilli paratyphoids. Bacteria of the paratyphoid group are closely related to the true abdominal bacillus, but differ from the last organism in that they are able to ferment glucose during gas production. They are more highly pathogenic to lower animals than typhoid fever, but apparently slightly less pathogenic to humans. Most types of paratyphoid bacilli found in food poisoning produce more or less rapidly a significant amount of alkaline, and if they are inoculated into milk containing a few drops of litmus test, the milk becomes dark blue after a while. Several different varieties of bacilli of parathyroids have been found. The main differences shown by these varieties are agglutinative differences. That is, the serum of an animal, grafted by a particular culture or strain, will agglutinate this strain, as well as other strains isolated from some other meat poisoning epidemics, but will not agglutinate some culturally similar parathyroid bacteria detected in connection with other outbreaks. With the exception of this single question of agglutination of the reaction, no permanent distinction between these varieties has been demonstrated. Clinical features of infections produced in humans and in higher animals of different varieties seem very similar, if not identical. Bacillus, discovered by Ertner (loc. cit.) and known as B. enteritidis or Ertner bacillus, is generally regarded as a type of agglutinative varieties. Bacilli with all the characters of Guartner bacillus have been found in meat poisoning epidemics in various places in Belgium and Germany. Mayer compiled a list of forty-eight food poisoning outbreaks that occurred between 1888 and 1911 and were attributed to B. Enteritisys Geurtner. These outbreaks accounted for about two thousand cases and twenty deaths. Twenty-three of the forty-eight outbreaks meat was obtained from animals that were known to be ill at the time, or shortly before, they were killed. Sausage and chopped meat of unknown origin were the cause of eleven of the remaining twenty- five outbreaks. Two B. enteritidis outbreaks were attributed to Vanilla Pudding; one, potato salad. Other outbreaks of food poisoning have found bacillus, which is culturally similar to Gurtner's bacillus, but refuses to agglutinate the serum of Guartner's bacillus. Its cultural and agglutination reactions are almost, if not quite, identical to those of bacilli found in human cases of parathyroid fever, which have no known association with food poisoning. Mayer cites a list of seventy-seven outbreaks of food poisoning (1893-1911), in which organisms differently designated as B. paratyphosus B or B. suipestifer were prosecuted. The total number of cases (two thousand) and deaths (twenty) is about the same as attributed to B. enteritidis. According to the tabulation of Mayer Meat from animals known to be sick, less often implicated in this type (ten out of seventy-seven) than in outbreaks B. enteritidis (twenty-three out of forty-eight). Sausage and sliced meat of unknown origin, however, were associated with eighteen outbreaks. Bacillus named B. suipestifer was previously thought to be the cause of swine cholera, but is now considered only a secondary invader in the disease; it is identical to a bacilli called B. paratyphosus B in its cultural and largely agglutinative behavior, but is regarded by some investigators as separating from the latter on the basis of particularly sensitive discriminatory tests. Bainbridge, Savage, and other English investigators believe, indeed, that true cases of food poisoning should be attributed to B. suipestifer and will limit the term B. paratyphosus for those bacteria causing the disease clinically indistinguishable from typhoid. German investigators, on the other hand, consider B. suipestifer and B. paratyphosus B identical. My own research shows that there is a real difference between the two types. This issue is directly influenced by the discussion of the spread of food poisoning bacteria by nature. Most researchers in Germany, where most food poisoning outbreaks have occurred, or at least have been bacteriologically studied, believe that B. suipestifer (the same, in their opinion, as B. paratyphosus B) is much more widespread than B. enteritidis and that this happens, especially in some regions, as in the southern part of the German Empire, quite often in the gastrointestinal tract of people. It is assumed that such carrier paratyphoids can contaminate food by processing or preparing just like abdominal typhoid carriers, as Do. A number of flare-ups in the Food contamination during cooking is believed to have occurred were p.67 reported by Jacobitz and Kaiser (vermicelli), Reinhold (fish), and others. Reinhold notes that in one outbreak, several people who cared for the sick became ill themselves, indicating a possible contact infection. Another outbreak also reported Reinhold was noted that those who partook infected food, in this case dried cod, on the first day were not as seriously affected as those who ate what was left on the second day. Bacilli belonging to the paratyphoid group were isolated from the stools of patients, but not from dried cod. These facts were interpreted to mean that the fish became infected in preparation and that the bacilli multiplied into food while it stood. There seems to be no doubt that some cases of parathyroid food poisoning are caused by food contamination during preparation and, sometimes at least, due to infection by human carriers. Bacilli in such cases are usually (in the opinion of many German researchers) or always (according to most English bacteriologists) type B. suipestifer. Other cases are associated with pathogenic bacteria derived from sick animals, and these bacteria are often, perhaps always, of a slightly different nature (B. enteritidis Guertner). It is not yet known whether both types of food poisoning bacteria are related to human or animal disease processes, or whether they are widespread organisms that can sometimes acquire pathogenic properties. In some regions, as in northern Germany and England, such bacteria are rare, if in life, found p.68, except in cases. In some parts of southwestern Germany, on the other hand, they are said to occur with extreme frequency in the intestines of healthy men and animals. Savage believes that there is some confusion in this matter because of the existence of saprophytic bacteria, which he calls the forms Paragertner and which bear a close resemblance to the true bacillus of Gertner. They can be distinguished from the last only in an extended series of tests. The bacilli of this group show remarkable variability, and according to some researchers, sometimes there are mutations that lead to the transformation of one type into another. Despite the current uncertainty about the relationship and significance of the observed varieties, some facts stem from confusion: (1) Most meat poisoning outbreaks that have been studied in recent years have been traced by a member of this group, rather than by ptomain poisoning. (2) Bacteria paratythoid enteritidis group, which are culturally but agglutinatively dissimilar can, when taken in with food, lead to clinical symptoms in humans. (3) The food bacteria poisoning of this group, when obtained directly from sick animals, seems to be more likely to type with Guertner (B. enteritidis) than B. suipestifer type. The production of toxins.- The problem of the production of the toxin by bacteria of this group and the possible connection of the toxin with food poisoning has been much p.69 discussed. The culture of broth, in which live bacilli have been destroyed by heat or from which they have been removed by filtration, contain soluble poison. When this broth without germs is injected into mice, guinea pigs or rabbits, the animals die from the effects. The nature of poisonous substances is virtually unknown, except that they are heat-resistant. They probably should not be classified with the so-called true toxins generated by diphtheria and bacillus tetanus, as there is no evidence that they give to antibodies when injected into susceptible animals. According to some researchers, the formation of these toxic organs of paratyroid-enteritis bacillus in meat and other protein foods is responsible for certain outbreaks, and for some food poisoning events, the rapid development of symptoms is seen as due to ingested poisons, while later manifestations are considered those of true infection. This view is opposed by the fact that well-cooked food has been clearly less prone to food poisoning than raw or imperfectly cooked food. A large proportion of the reported outbreaks of meat poisoning are largely related to raw meat sausages and meat pies, puddings and jelly. This is most likely because the heat used in the preparation of such foods is not enough to produce bactericide results. It is also noteworthy that consumers of raw milk also suffer in milk-transmitted epidemics. For example, respecting the extensive outbreak of B. enteritidis in Newcastle and near Newcastle, England, states: in no case was there a person who used only boiled milk known to have been affected. Thus, in one family consisting of a husband, wife and mother of the wife, two women drank a small amount of raw milk from the farm, mostly tumblers, and both fell ill about twelve hours later. Husband, on the other hand, usually drank a pint a day, but always cooked. He followed his usual custom on this occasion, and was not hurt. Considering that conventional roasting or roasting a piece of meat is often not enough to increase the temperature of the germ worldwide, the argument that a heat-resistant toxin is present in such cases is not convincing. It should also be remembered that in some outbreaks these individuals consuming raw or partially cooked meat have been affected, while others eat well-cooked meat from The animals remained released; this seems to indicate the destruction of living bacilli by heat, since the toxic substances produced by these organisms are heat-resistant. The view that a certain infection occurs is favourable, too, to the fact that the blood serum affected individuals so often has an agglutinative effect on bacilli paratyphoids. This would not be the case if the symptoms were due to toxic substances alone. In total, it cannot be said that the roar of toxins formed by B. enteritidis and its allies in food outside the body cannot be established. The available evidence points to infection as the main, if not the only, way in which this group's bacilli are harmful. Sources of infection.- The main sources of infection of enteritidis-sufestifer are: (1) sick pets infected with flesh or milk which is used in food; (2) infestation of food by human carriers during cooking or serving. To these can be added a third possibility: (3) the contamination of food by bacteria of this group, which are the inhabitants of the normal intestine of animals. Given their order: 1. Sick animals: Most outbreaks of meat poisoning are caused by meat derived from pigs or cattle. Table III provides figures for a number of British and German epidemics. TABLE III (B. enteritidis B. suipestifer Belonged to this group, but Undifferentiate British German Total British Pig 1 1 2 3 5 8 4 Bull or Cow 3 9 12 2 3 5 5 Calf 0 7 2 2 0 Horse 0 1 1 0 1 1 1 ... Chickens 1 0 1 0 1 1 ... Accidental outbreaks are also attributed to infection from the consumption of rabbits, sheep, geese, fish, shrimp and oysters. The relative rarity of infection from sheep meat is particularly remarkable. More information is needed if we know the pathological conditions caused by these bacteria in animals and the relationship of such conditions with subsequent human infection. A rather notable problem is related to the connection of B. suipestifer with cholera pigs. This bacillus, although not currently considered p.72 by the cause agent of the pig's cholera, is very often associated with the disease as an accomplice or secondary invader, and is often found in the internal organs of pigs after death. One might have suggested that in regions where cholera pigs are common human infections will be more common than in other areas, but this does not seem to be the case. No link has ever been demonstrated between outbreaks of swine cholera, in which B. suipestifer is known to be abundantly distributed, and so-called B. suipestifer infections in humans. Superpurative processes in cattle, and especially in calves, have led to poisoning from the consumption of meat or milk of infected animals. It has often been demonstrated that the bacteria enteridis-sufestifer groups are associated with washed out in cows and with various septic conditions in cattle and other pets, as well as with manifestations of intestinal disorders (calf diarrhoea, etc.). The frequency with which poisoning occurred as a result of the use of meat of emergency killed animals has already been mentioned. K. F. Meyer reported an accidental infection in a laboratory employee caused by the treatment of a bottle of sterilized milk artificially contaminated with pure B. enteritidis culture for experimental purposes. The strain responsible for the p.73 infection was isolated from the heart blood of a calf that succumbed to infectious diarrhoea. 2. Human Pollution: In a certain number of parathyroid food infections, there is some evidence that food was originally obtained from a healthy animal and contracted from human sources in preparation. In addition to the already mentioned cases (Reinhold et al., p. 67) the Wareham epidemic (England, 1910) was considered by investigators to be due to an infection of meat pies by a cook who was later proven to be the carrier of the paratyphoid bacilli. The evidence in this case, however, is not entirely convincing. Soderbaum mentions the milk-transmitted parathifoid epidemic that occurred in Christiania, which was attributed to a milk infection by a thrush woman. Sakkap and Bello report an interesting outbreak of parathyroids involving nineteen of the two hundred and fifty people in the military corps. Patients became ill on different dates between 14 and 21 June. It was found that an assistant chef who had been in the kitchen for several months was attacked shortly before the epidemic explosion had some minor illness that definitely had not been diagnosed. He was hospitalized and discharged to a recovering state. The cook, at the time of the recall and quarantine, said that in the days before June 10 he was unwell with headache and anorexia. However, he continued his service in the kitchen.... B. paratyphosus B (B. suipestifer) was repeatedly found in his chairs in August, September and October.... Thus, in all likelihood, the outbreak was caused by food contaminated with parathyroid carriers, which went through a failed fever attack. Bainbridge and Dadfield describe an outbreak of acute gastroenteritis occurring in the guesthouse; it was found that no food articles had been eaten by all the affected persons, and there were other reasons to believe that the outbreak was caused by different food contamination by the employee who was the carrier. Thus, there is reason to believe that sometimes food contamination can be caused by bacteria in this group derived from human sources. It is not clear, however, how often this source of infection infections occur in sick animals. It should also be recognized that British researchers tend to look at outbreaks similar to those just described as B. paratyphosus B infections, an organism that they will distinguish from true food poisoning bacilli, B. enteritidis and B. suipestifer. 3. Different Pollution: Some researchers, especially some German writers, consider the bacilli parathyroid group so widespread in nature that any attempt to control the spread of infection is similar to fighting windmills. According to this point of view bacilli occur usually in our daily environment and from there make their way quite often in different foods. Various German researchers reported the presence of parathyroid bacilli in intestinal contents, apparently normal pigs, cattle, rats and mice and less frequently other animals, p.75 in water and ice, in German sausage and sliced meat, as well as in the bodies of apparently healthy men. The extent to which their perceived ubiquity is due to erroneous bacterial identification, as some British investigators claim, has yet to be proved. There is no doubt that in some quarters exaggerated concepts prevailed while respecting the widespread spread of true parathyroid bacteria. Savage and others believe that the hypothesis that food poisoning outbreaks are derived from the usual fecal food infection is completely unfounded. It is noted that there is strong evidence of frequent appearance of intestinal bacteria in foods such as sausages and sliced meat, and that, therefore, if parathyroid infections may occur as a result of normal contamination by intestinal bacteria not associated with any particular animal infection, food poisoning outbreaks should be extremely common and not, as is the case, relatively rare. Nowadays even those who claim that these bacilli are commonplace recognize that their abundance is more noticeable in some regions than in others. For example, in south-western Germany, there seems to be a relatively large number of parathyroid bacilli. Local differences in distribution may explain discrepancies in the published findings of German and British investigators. A special case is represented by the attitude of these bacilli to rats and mice. Among the large number of bacteria in the parathiroid group there is the so-called Danysz bacillus, an organism quite pathogenic to rodents, and now and then used in various forms as a rat virus for the destruction of rodents. Several outbreaks of food poisoning in humans have been linked to more or less conclusive evidence of food contamination by one of these viruses either directly by accident, as in the case described in which cakes made for rats were eaten by men, or indirectly through food contaminated by mice or rats have been infected with the virus. The use of such viruses has not proven to be very practical in the destruction of rodents, and is open to serious sanitary objections, as animals after an apparent recovery can continue to carry the bacilli virus and spread them on or near food substances. It is possible that rats and mice may become infected with certain bacteria in this group without human intervention, and that these infected animals may be a means of contaminating food and thus causing food poisoning outbreaks. Proof of the frequency with which this actually occurs is naturally difficult to obtain. There is no avoiding the conclusion that in any particular case of food poisoning the exact source of infection is often largely conjecture. Even when suspicion falls heavily on a particular article of food, it may not be possible to establish beyond any reasonable doubt whether the material (meat or milk) came from a sick animal or whether it has been infected from other sources (man or other animals) at some point in the preparation and feeding process. The most definitely tested cases yet put on record are those in which it is possible to trace the infections of food received from the sick animal. Prevention-- The most obvious and probably the most important method of preventing infection with paratyphoid bacillus is the adoption of an inspection system that excludes from the market as far as possible, material from infected animals. To be most effective, such a check should be aimed at inspecting a live animal. Milk or meat of sick animals cannot give any visible signs of anomaly. During the ghent outbreak in 1895, the homicide ward inspector, a veterinary surgeon, was so firmly convinced that the meat he had passed could have nothing to do with the outbreak, that he ate several pieces to demonstrate its usefulness. The experiment had a tragic end, as the inspector was soon attacked with severe cholera symptoms and died five days later, paratyphoid bacilli were found during autopsy. Mueller also described a case in which paratyphoid bacilli were found in meat, leading to an outbreak of meat poisoning, although the meat was normal in appearance and the animal's organs showed no signs of disease to the naked eye. It is obvious that the examination of a live animal often reveals signs of a disease that can be missed during a routine examination of slaughter products. Although the inspection of cows used for milking and food animals before slaughter is important, it is not an absolute protection. The emphasis should be repeatedly placed on the fact that meat, and especially milk, which is derived from seemingly healthy animals, can nevertheless contain paratyroid To meet this difficulty of difficulty part of a direct bacterial study of carcasses of slaughtered food animals has been proposed, but this seems unlikely as a general measure. Despite all the precautions taken during the slaughter, it seems likely that sometimes parathyroid-infected meat will pass the first line of defense and be placed on the market. This danger, which is probably not very serious with a good enough system of inspection of live animals, can be solved by carefully preparing all animal products. It is worth noting that some internal organs, like the liver and kidneys, are more likely to contain bacteria than muscle masses are commonly eaten as meat. Sausages, of their composition and method of cooking, and sliced meat (hamburger steak) should also be treated with extreme caution. Consumption of foods such as raw sausage or diseased goose liver (pate de foie gras) involves a relatively high risk. This refers to a parathyroid infection, like most other forms of food poisoning, that careful cooking greatly reduces the likelihood of trouble. Whatever the exact degree of danger from food infection by healthy parathifoids (humans or pets), it is clear that general care and cleanliness measures will be more or less a guarantee. As with typhoid fever, all outbreaks of parathyroids must therefore be thoroughly investigated so that sources of infection can be found and eliminated. The possible link between rats and mice with these outbreaks should provide an additional incentive to reduce the number of such pests, as well as take measures to protect food from their visits. Chapter VII ANIMAL PARASITES not only pathogenic bacteria, but also some types of animal parasites sometimes enter the human body in food products or on them. One of the most important of these is the parasite that causes trichiniasis. TRICHINIASIS Trichiniosis or trichinosis is a disease characterized by fever, muscle pain, a huge increase in eosinophilic blood cells and other more or less clearly defined symptoms; in the beginning sometimes mistaken doctors for typhoid fever. The responsible parasite is the roundworm (Trichinella spiralis, formerly known as Trichina), which is swallowed while in its ensed larval stages in raw or imperfectly cooked pork. Cysts or envelopes in which parasites live are dissolved by digestive fluids, and young larvae that are released develop in the small intestine of an adult worm, usually within two days. Young embryos, which are produced in large numbers of mature worms, gain entry into the lymphatic channels and bloodstream, and after about ten days begin to invade the muscle-procedure that generates many of the most characteristic symptoms of infection. In severe cases, it is estimated that fifty million embryos can enter the bloodstream. Parasites finally calm down and become encysted in muscle tissue and symptoms tend to gradually subside. The use of a large number of parasites at one time is often fatal, mortality from trichiniasis is on average slightly over 5 percent and the increase in some outbreaks to a much higher rate (30 percent). On the other hand, many infections are so mild that they go unnoticed. Williams found that Trichinella embryos are present in 5.4 percent of the bodies of people dying from other causes. Such findings are thought to indicate that sometimes minor Trichinella infections, even in the United States, are quite common. This really could be expected from frequent infection of pigs, about 6 percent of these animals are found to harbor a parasite. Fig. 7.-Trichinae encysted in the pig's inter-rib muscle. (About 35×1.) (After Neumann and Mayer.) Specific symptoms (such as muscle pain) trichiniasis may be partly related to mechanical damage to muscle tissue, but they are also likely to be partly due to toxic foods depleted by worms, and partly to the introduction of an alien protein material, the worm protein, into the tissue. A secondary bacterial infection is also a possibility, but there is p.81 with little evidence to prove that this is an important factor in most cases of trichiniase. The different stages observed during the disease are clearly associated with different phases of the worm's development - initial localization in the intestines, muscle intrusion and final bone. Pigs become infected with this parasite by eating scraps of contaminated meat, or pro-salt their own species, or by eating infected rats. The rat, through its cannibalistic tendencies, is frequently infected, and is a major factor in the widespread spread of the disease. Human infection is almost accidental and self-justified; biologically speaking, a person as a host is not included in the calculations of the parasite. Treatment of the established trichiniasis infection is palliative, not truly restorative. Parasites, once in the body, can not significantly affect the administration of any drug. Although the treatment of trichiniasis is thus difficult, if not impossible, prevention is very simple. Careful cooking throughout the food is enough to rule out infection. This relatively simple means of killing larvae is a more defined and less costly method of preventing infection than a time-consuming microscopic examination of the tissues of each slaughtered pig. In Germany, between 1881 and 1898, more than 32 percent of the 6,329 cases studied were related to meat, which was microscopically researched and passed as trichin-free. On the other hand Careful cooking eliminates all hazard opportunities. TENIASIS Various tapeworm or cystods infections are infected by eating meat containing the parasite. Special types of tapeworms usually infect the flesh of specific hosts like Tenia saginata in beef and Tenia solium in pigs. The dwarf tapeworm, Hymenolepis nana, develops in rats, and human infections with this parasite are sometimes observed, probably caused by food contamination by these animals. Fig. 8.-Cysticercus pulp in pig tongue. (After Neumann and Mayer.) Sometimes the existence of tapeworms in a person is limited to alimony tract and symptoms range from trivial to severe, but sometimes (Shadow Salt) larvae stage tapeworms invade the tissues and become encysted in various organs (brain, eye, etc.) where, as in the case of cerebral infection, it can lead to death. Enzisted larvae Tenia solium (p.83) was once considered an independent species of animal and was called Cysticercus cellulosae. A condition known as pork pulp is produced as a result of the emergence of this ensstead parasite. The so-called hydatide disease is associated with cystic growth produced by the larvae of the type of tapeworms (Echinococca) inhabiting the intestines of the dog. Human infection can be caused by contaminated food as well as more directly by hands contaminated by the caress of infected dogs. Several varieties of tapeworms that infect fish, especially some freshwater species, can be injected into the human body in raw or partially cooked fish. Methods for preventing tapeworm infection include the destruction of larvae with heat, i.e. the careful preparation of all meat and fish, and minimizing close contact with animals like the dog and cat that can harbor parasites. Cleanliness in cooking and serving food, as well as attention to hand washing before eating, and especially after touching pets, are a necessary consequence. Infection UNCINARIASIS Hookworm (neciniosis, ankylostomyosis) is usually caused by infection through the skin of the feet, but the possibility of oral infection cannot be ignored, and in regions where nematode disease there are methods of protection against food contamination should be practiced as well as other precautions. Billings and Hickey believe that the disease of nematodes behind the infected unconscious coprophagia (from raw vegetables) is much more common than is usually assumed. OTHER PARASITES A number of other parasitic worms (e.g. Strongyloides, Ascaris or eelworm, and Oxyuria or pinworms) may presumably enter the human body in contaminated food, and while, as in nematode disease, other types of infection are probably more important, the responsibility for accidental raw food infections should not be overlooked. Fig. 9.-Lamblia intestinal. (After Neumann and Mayer.) forms of dysentery or diarrhea have been attributed to infection with Giardia (Lamblia) intestinal. Observations made by Fantam and Porter on business, having stopped in Gallipoli and Flanders, supported this view. Strains of this parasite of human origin have been shown to be pathogenic to mice and kittens. It is believed that these animals may act as reservoirs of infection and the spread of the disease by contaminating human food. Chapter VIII POISONOUS PRODUCTS FORMED IN FOOD BY BACTERIA AND OTHER MICRO-ORGANISMS In direct association with cases of animal or plant parasite infection that have been discussed, there are certain well-established cases of poisoning substances that have been created in food while it is still outside the body. This is a common type of food poisoning in popular evaluation, but in fact proven cases of this class are much less common than cases of true infection by the bacteria paratyroid-enteridis group (chapter vi). Until now, botulism and ergothism are the most well-known examples of poisoning by microorganisms. Ergotism ergotism or ergot poisoning is associated with the use of rye, which became sick as a result of the fungus attack, Claviceps purpurea. This often happened in the Middle Ages, when during the famine of spores or spurred rye (O.Fr. argo, rooster spur) is often used in non-less than food. In Limoges, 922, it is said that 40,000 people died from this cause. Improving the conditions for transporting food to regions where crops have not been successful, as well as the use of special methods to separate sick grains from useful foods have significantly reduced the prevalence of ergotism. In Western Europe, poisoning has virtually ceased, although Hirsch recorded about twenty-eight outbreaks in the nineteenth century; in some parts of Russia, the disease is said to still occur during years of poor harvest. The poison itself has long been used as a drug in obstetrics, but its composition is complex and still not fully understood. Several components of ergot have been extracted and they have been shown to have different physiological effects. Symptoms observed in medieval ergism outbreaks are not fully replicated experimentally by the drug and are believed to have been partly caused by a half-head generated by the use of rye, from which the nutrient parts were largely removed by the fungus's growth. BOTULISM The best established case of poisoning using bacterial foods taken into account is a serious disease known somewhat inappropriately as botulism (botulus, sausage). This type of food poisoning, which has a characteristic set of symptoms, seems to have been first recognized and described in 1820 German poet and medical writer Justin Kerner. In two articles (1820-22) he lists 174 cases, 71 of which occurred in Wurttemberg between 1793 and 1822 and appear to be most associated with the consumption of insufficiently smoked sausage. Mayer reports 600 additional cases reported in various parts of Germany by the end of 1908, with a total mortality rate of 800 cases of about 25 per cent. In France, botulism is said to be very rare. In the UK, Savage says he has not been able to track the occurrence of a single outbreak. In the United States, several cases of botulism poisoning (Sheppard, 1907, 3 deaths, 3 deaths, canned pork and beans; Peck, 1910, 12 cases, 11 deaths; Wilbur and Ofels, 1914, canned string beans, 12 cases, 1 death; Frost, 1915, 3 deaths, 3 deaths). Professor Stiles gave a graphic description of his own attack of probable botulism due to, in all likelihood, minced chicken. Fig. 10.-Claviceps purpurea: 1, ergot on rye grass; 2, ergot on rye; 3, section of the conidial portion of the fruit form, ×300; 4, sclerion or ergot; 5, head ascigerous fruit forms; 6, Ascus, ×300; 7, one dispute, ×300. (After Massey, Plant Disease, courtesy of Macmillan Company.) Symptoms -- The description of the case seen by Wilbur and Ofels is so typical that it can be cited: A girl, aged 23, ate dinner on Tuesday night, November 23, 1913, including canned light green beans along with a small rare roast beef. The next day she felt perfectly fine, except that at 10:00 pm her eyes felt tense after some sewing. On Thursday morning, thirty-six hours after the meal, when the patient woke up, her eyes were out of focus, her appetite was not very good, and she felt very tired. At night she still had no appetite, nausea, and vomiting at noon eating apparently undigested. On Friday morning, two and a half days after the meal, the eyes were worse, the objects were seen twice on rapid traffic, and it was noticed that they tended to be crossed. Special Nebula vision also complained. She was in bed until late at night when she visited Dr. Black. She had some irregularities in swallowing up to this time and stated that it felt as if something had come up from below that was hindering deglutition. On the fourth day she stayed in bed, had a lot of constipation, and noticed a noticeable decrease in the amount of urine annulled. There was never a pain, except for occasional mild cramps in the abdomen, no headache, subnormal temperature and normal pulse. The fourth and fifth days of breathing became difficult at times and swallowing was almost impossible. The patient complained of dry throat with irritating thirst. On the sixth day there were periods vague sense of excitement and, as if there might be difficulties in getting the next breath. The upper lids started to fall. The voice was nasal. When an attempt was made to swallow the fluids, they went back through the nose. The patient felt visibly weak. Physical examination at this time showed ptosis of both upper eyelids, enlargement of the right pupil, sluggish reaction to the light of both pupils, apparent paralysis of the inner directness of the left eye, normal retina, inability to lift the head, control, apparently loss of neck muscles, inability to swallow, lack of taste. The tongue was heavily covered and the throat was covered with viscous whitish mucus clinging to the mucous membrane. The soft sky could be lifted, but it was sluggish, especially on the right side. The exsudate on the right amygdala was so marked that it resembled several diphthetic membranes. On the seventh day there was some change in the condition; random periods occurred when swallowing was more effective, and there was less tendency to suffocation. On the eleventh day there was some improvement in the eyes, still smothering when swallowing, the taste sensation was sharper, and the overall condition improved. On the twelfth day, the patient was able to move her head, but was unable to lift her, except when she took the pigtails of her hair and pulled her head forward. The eyes could be slightly opened, the speech was less nasal and p.90 more distinct, and an improvement in swallowing was noted. At the end of two weeks the patient was able to freely take a soft diet, and at four weeks she was in the chair for several hours, complaining only about general weakness and inability to use the eyes. At the end of five weeks she was able to leave the hospital and return home and then resume her normal work. In all cases, the nervous system affects in this form of food poisoning. Dizziness, double vision, difficulty chewing and swallowing, as well as other symptoms of nervous intervention occur with varying intensity and can persist for a long time after the first signs of an attack. Temperature, pulse and breathing remain almost normal. Unlike the traditional type of food poisoning, gastrointestinal symptoms may be mild or non-existent. Freedom from abdominal pain is usually noted; Diarrhea is the exception and constipation rule; vomiting sometimes occurs but may be absent. In the cases described by Sheppard, there was a complete absence of the usual gastrointestinal symptoms from the first to the last, no pain or sensory abnormalities and no fever. Visual disturbances are very characteristic. Stiles recounts his own experiences as follows: Vertigo and Nystagmus designed a few hours after eating to an astounding degree, the car in which he was taken to his home seemed to be bubbling endless spiral, the stars made circles in the sky, and the house on the side of the road staggered. The ignited doorway of my house seemed to approach and surrounded me as I was being carried. My bed at the moment presented itself as a vertical surface that I could not imagine to be a resting place.... Whenever I opened my eyes that day (the next day), the room gyration... To turn your head even very slowly from one side to the other brought joining the irresistible vertigo .... (eight days after the attack began). Nistagm has now become limited to momentary beginnings, but in its place I became aware of a kind of diplopia. The image of one retina was not just displaced from the position of his fellow, but was tilted about 15 degrees from the parallel.... This fantastic diplopia gradually gave way to a familiar variety, and it happened less and less often, as my recovery continued. From that date, my recovery continued a course that was woefully slow but free from any setbacks. Among the persistent symptoms were ... visual difficulties mentioned. The left pupil tended to be smaller than the right, and I thought I found a slight inability to relax housing with my left eye. Reading has been difficult for several weeks, and the ability to write, both requiring closer fixation, is still greater in return. In cases reported by Sheppard visual symptoms were initial signs of trouble, double vision, nebula, and inability to hit the target in the shooting is the first complaint. The time elapsed between eating the food involved and the onset of the earliest symptoms is usually twelve to forty-eight hours, but can be much less. In Stiles' case, the interval appeared to have been less than three hours. Anatomical lesions.- In fatal cases, there are no characteristic gross changes in different organs. It has been stated by some writers that microscopic degenerative changes occur in ganglion cells, including especially so-called Nissl pellets, but in a carefully studied case the reported Oph'ls'107 Nissl pellets were quite normal in sizes, arrangements, and coloring qualities. In fact, there was no evidence to support the hypothesis of a specific toxin effect on nerve cells. On the other hand, Ophels found numerous brain hemorrhages and multiple thrombosis in both arteries and veins. Therefore, he believes that the signs of serious cerebral circulatory disorders associated with hemorrhage and thrombosis in the medull and pones are sufficient to explain the symptoms of botulism poisoning without resorting to the assumption that the poison has a specific effect on certain ganglion cells. Bacteriology.- The cause of botulism poisoning was Van Ermengem as a toxin produced by the bacillus he B. Botulin. This organism was isolated from parts of ham that caused fifty cases of poisoning (1895) in Ellezelles (Belgium), as well as from the spleen and gastric contents of one of the three deaths. Bacillus grows only in the absence of oxygen (strict anaorobe), spots according to the Graham method, forms the spores of the terminal and develops best at 22 degrees Celsius. Unlike most human-threatening bacteria, it is unable to grow in the human body, and its harmful effect is limited by the action of a toxin produced in foods outside the body. Botulism is intoxication, not infection. The fact that bacillus can grow naturally only when the free oxygen supply is cut off partially explains at least the relatively rare occurrence of botulism, since all the conditions necessary for the production of botulism toxin usually do not coincide. Virtually nothing is known about how widely B. botulinus spreads. Except cases of poisoning have been reported, but once in nature. Botulism venom (p.93) is a true bacterial toxin, chemically unstable, destroyed by heating at 80 degrees Celsius for 30 minutes, capable of provoking violent symptoms in minute doses and possessing a property characteristic of all true antitoxin-generating toxins when administered in small, non-life doses in the bodies of susceptible animals. In animal experiments, a toxin formed by B. botulinus was found to reproduce a typical clinical picture of this form of food poisoning. Symptoms of paralysis are produced in rabbits, guinea pigs and other animals by injecting such a small dose as 0.0001 c.c. filtered broth culture. Fig. 11.-Bacillus botulinus with disputes. Pure culture on gelatin sugar. Van Emengem's preparation. (Coll and Wasserman.) Epidemiology.- The conditions under which B. botulinus occurs and is given the opportunity for multiplication are not fully known. It is possible that there are settlements where this bacillus is particularly abundant in the soil or in the intestinal contents of pigs or other pets, but in general it seems more likely that the body is widespread, but that it does not often find suitable conditions to enter in, and multiply into human food. Virtually all reported cases of botulism were caused by food that was given a kind of pre-treatment like smoking, pickiness, or canning, the p.94 allowed to stand for a while and eat before cooking. Since both the bacilli, including the spores stage, and its toxin are destroyed with relatively little heating, it is clear that in order for botulism poisoning to occur, a rather unusual set of factors must be collaborated. This is obvious: (1) the presence of bacillus in sufficient quantities in suitable foods; (2) preparing food by a method that Do not destroy B. botulinus -inadequate smoking, too weak brine, or insufficient cooking; (3) carrying out this underserved food for a sufficient period of time under the right temperature and lack of oxygen; (4) the use of this food, in which the conditions conspired in favor of the production of the B. botulinus toxin, without the final adequate cooking. It seems reasonable to assume that the infrequentness with which these multiple factors coincide is the cause of the relative rarity of botulism, as suggested, due to the rarity of a particular bacillus. During the Belgian outbreak studied by Van Hermengem, the poisonous ham lay at the bottom of a barrel of brine (anaorial conditions), while another ham of the same animal lay on it, but was not covered with brine and was eaten without any poisonous effect. In this case, the decisive factor seems to be the availability or absence of favourable conditions for anaerobic growth. Prevention and treatment.- The food in which B. botulinus grew does not seem to change in a way that necessarily arouses suspicion. In the case described by Rumer, the incriminating ham showed bluish-gray areas from which B. botulinus could be isolated, but this condition did not appear to have attracted attention before the poisoning and was observed only after the event. As far as you can know the meat that caused botulism has always come from the utter sound of animals. In some cases the accused article about food is said to have a rancid or caustic taste (because of butic acid?), but there is nothing definitely characteristic about it, since most anorobes produce butyric acid. If, as in the epidemics of Darmstadt and Stanford University, food (canned beans) is served with dressing for salads, sour taste can pass without notice or even add to the enjoyment. In the case reported Sheppard canned beans were good in appearance, taste and smell. The obvious precaution to combat poisoning of this kind is primarily the use of adequate methods of food conservation. Judging by the reported outbreaks, vegetables and meat of domestic production are more likely to bring botulism than those that are prepared on a large scale on a commercial basis. The general use of steam under pressure in large canning plants provides a high degree of protection against anorobic bacteria and their resistant spores. Regardless of the treatment method, all canned or canned foods with an unnatural appearance, taste or smell should be rejected. Heating all finished products just before use is an additional guarantee. Foods such as salads, p.96, which are entirely or partially made up of raw materials, should not stand the night before the serve. If symptoms of botulism, such as visual impairment, become The stomach should be emptied by the gastric pump, cathartics injected, and strychnine and other stimulants, given as needed. Since one of the notable features of this disease is the paralysis of the gastrointestinal tract toxin, the absorbed, guilty food can lie for a long time in the stomach (cf. Stiles, loc. cit.). Consequently, measures to empty the stomach should be taken even if the patient is not monitored until a few days after the poisonous food has been eaten. The antitoxic serum was prepared at the Koch Institute in Berlin. This serum has produced successful results in animal experiments, but has not been used, as far as I can learn, in any human outbreak. It is not available at any time in this country. OTHER BACTERIAL POISONS An interesting case reported by Barber shows that there are other possibilities of food poisoning formed by bacterial poisons. Acute bouts of gastroenteritis were produced in several individuals using milk containing a poisonous substance developed by white staphylococcus. This staphylococcus occurred almost in pure culture in the queaming of the cow from which the milk was derived. Milk when using fresh was harmless, and the poison was created in effective quantities only when the milk stood for several hours at room temperature (p.97) before being used. The symptoms were similar to those commonly attributed to ptomaine poisoning. SPOILED AND DECOMPOSED FOOD There is a general belief that food is unhealthy whenever evidence of feelings shows that it more or less decomposes. This view is expressed in civilized countries in many laws prohibiting the movement of decomposed meat, vegetables and fruits. Unfortunately, there is no evidence of which species or degree of visible decomposition are most dangerous. In fact, some foods with high nutritional value, particularly cheeses, are eaten only after a few extensive decomposition processes (the term maturation) have taken place. The characteristic aromas or aromas of various hard and soft cheeses are caused by substances produced by certain types of mold and bacteria, and should also be properly treated as decomposition products, as unpleasant walls generated by decaying eggs or meat. Indeed, some decomposition products shaped at the ripening of Bree, Camembert or Limburger are similar, if not identical, to those associated with spoiled products. Sour milk, again, is recommended and commonly used as a food or drink for people with tender health, and yet sour milk contains many millions of bacteria and their decomposition products. Some bacteria, usually associated with natural milk oxide, are closely related to pathogenic types. Partial meat and blinker birds are often considered profitable rather than otherwise. Even eggs, eggs, whose freshness is overshadowed for most people by the initial stages of decomposition, mature differently by the Chinese and is eaten as a delicacy after the expiration of several months or years. Preserved duck eggs, known as pedane, are stored for months in a pasted mixture of tea, lime, salt and wood ash. They are very different from fresh eggs. The slightly darkened shell has numerous dark green dots on the inner membrane. Both white and yolk are coagulated; white brown, more or less similar to coffee jelly.... The increase in ammonia nitrogen occurred to an extraordinary extent in these eggs, indicating a significant decomposition of the egg protein. Ammonium nitrogen in pidan is much higher than in eggs known by egg candles as black rot. Therefore, it is obvious that the growth of bacteria in substances used as food is not necessarily harmful and in some cases can increase the taste of food without destroying its usefulness. Little or nothing is known about the correlation of visible signs of decomposition with the presence of poisonous products, and at present it is impossible to say at what point in the process of decomposition food becomes unusable due to the accumulation of poisonous substances in it. There seems to be no link between the natural ejedation to the use of food and its unwholesomeness. Under normal circumstances, the sickening nature of very stale eggs is notorious, and yet few nitrogen products have so clearly that health records like eggs have been so rarely associated with outbreaks of food poisoning. It may seem tempting to conclude on the basis of the available evidence that spoiled or decomposed foods have poisonous properties only when certain specific bacteria, such as the already discussed B. botulinus, accidentally invaded them and formed certain and specific poisons. But we are not entitled to believe that everyday products of decomposition of banal bacteria in all cases have no harmful consequences. Despite the fact that no sharply defined form of poisoning can be laid at their doors, it does not follow that the irritating or perhaps slightly toxic effect of conventional decomposition products is not at all. Our current knowledge of the nature and degree of danger that should be apprehended as a result of the use of tainted food is imperfect and unsatisfactory. However, this fact does not absolve us from the obligation to continue protection measures based even on experience to a limited extent. Chapter IX POISONING OF OBSCURE OR UNKNOWN NATURE While many and varied causes of food poisoning have been discussed on the above pages, there remain certain attachments, definitely related to food, that are still unclear or questionable causality. MILKSICKNESS OR TREMBLES Is a disease common to humans and some of the higher characterized by a a certain symptom-complex, the main features of excessive vomiting and stubborn constipation is accompanied by usually subnormal temperature. Many cases are fatal. It is now known that in some of the southern and central western states of the country this is rare, but during the pioneer settlement it is quite common in areas that are now rarely affected. Very many references to milksickness are found in the writings of early travelers and doctors in the Midwest, one observer predicts that some of the fairest parts of the West as a result of the prevalence of this disgusting disease should never remain uninhabitable waste if cause and remedies can be discovered. In some regions, it is estimated that almost a quarter of the pioneers and first settlers died of the disease. Abraham Lincoln's mother was the victim of the disease in 1818 in southern Indiana. The disease appears to have been contracted primarily by grazing cattle or sheep, who have access to specific plots of land; The pastures of milk disease are generally well known at the local level for their dangerous qualities. Milksickness is reported to a person through an environment of raw milk, or butter and possibly meat. While some of the earlier observers make the statement that the disease spreads independently and can be transmitted without restriction from one animal to another, later experiments have called into question this view. Many different theories have been put forward to explain the origin of the disease. The belief that mineral poisons such as arsenic or copper can be used by grazing animals and eliminated in milk is not justified in analytical or clinical data. Many plants, known or suspected of poisonous substances, have been accused of providing a substance that gives a poisonous quality to milk to animals suffering from tremors, but there is no agreement on responsible species. Experiments on feeding suspicious plants in the event did not give unambiguous results. While some facts are thought to indicate that living microorganisms are the cause of breast disease, other facts are the opposite of this view, and recent experiments in this direction have not produced definitive results. The true cause of breast disease is currently completely unknown. DEFICIENCY DISEASES Although sick conditions due to absence rather than the presence of certain ingredients in food may not need to be properly classified as food poisoning, they can be mentioned here to illustrate the complexity of the food problem. Some observers attribute at least one disease: pellagra to the presence of a harmful substance in food or others lack certain ingredients to sustain life properly. Life. of the best established cases due to a one-sided or defective beriberi diet. This attachment is common among those peoples, subarmism mainly or completely on a diet of rice prepared in a certain way. As for the trade convention, shredded white rice has long been considered above unpolished cereals. The process of polishing rice by machines removes red husk or pericar grain, and a diet based almost exclusively on polished rice causes this well-designated disease - beriberi, which has long been considered infectious. It has been shown that if the husk is restored to the polished grain and the mixture used as food, the disease will not develop. Experiments on chickens and pigeons show that an exclusive diet of white rice causes these animals disease (polyneurorite birds), similar to beriberi, which can also be arrested or prevented by a change in diet. Such observations concluded that rice grain pericarpes contain certain substances necessary to maintain health and that their withdrawal from the diet leads to eating disorders. The name vitamin was given to these substances, but little is known about their chemical or physiological nature. In a varied diet vitamins are presumably present in the p.103 variety of foods, but if the diet is significantly limited, some apparently trivial food treatments can lead to their elimination. It is unclear how much and how different substances that have been classified by some writers under the designation of vitamin. It is believed that at least two determinants are interested in growth nutrition, fat-soluble and water-soluble substance. Pellagra is one of the diseases associated with an unbalanced diet, and it has been suggested that the increased use of highly shredded corn and wheat flour, from which vitamins are missing, may be the cause of the spread of the disease in recent years. Other observers, while acknowledging that a faulty diet may predispose to pellagra in relation to tuberculosis and other diseases, do not suggest that it is a major factor. Lathyrism.- The name of satirism has been given to a disease that is supposed to be associated with the use of pulse and chicken peas. Nervous symptoms are noticeable and sometimes severe, although love has a milder type than pellagra. The disease is said to be associated with the exclusive or almost exclusive use of legal foods and generally miserable living conditions. It is not yet clear whether latirism is a deficient disease, such as beriberi and possibly pellagra, or whether it is due to a mixture of foreign and poisonous seeds with specific legumes consumed, or whether, under certain conditions, legumes alone may contain poisonous substances. Some unknown fungus on the growth. Favism (from fava, bob) is an acute feverish anemia with jaundice and hemoglobinuria, which occurs in Italy and has been attributed to the use of beans as food or even the smell of flowering plant beans. It is said that there is a marked individual predisposition to the disease. Although the symptoms are very severe and seem to indicate acute poisoning, no toxic substance has been isolated from the sacrament beans. It has been suggested that some that bacterial infection, and others that fungal growth on the beans, is responsible, but no evidence has been put forward to support either assumption. Tsinga in some forms is undoubtedly associated with the lack of certain necessary components of normal nutrition. The development of scurvy on the ship's board in the absence of fresh milk, fresh vegetables, fruit juice and the like has long been familiar. Guinean pigs feed on milk, raw and heated, and milk and grain have developed typical symptoms of scurvy. On the other hand, a form of experimental scurvy was produced in guinea pigs and rabbits, which were kept on a normal diet of green vegetables, hay and oats by intravenous injection of some streptococcus. The relative proportion of diet and infection in the production of human scurvy is therefore seen by some investigators as uncertain. Rachit or rickets are a pathological condition, in one way or another associated with a long-term digestive disorder, which, in turn, leads to a faulty calcium metabolism. It doesn't seem likely that rickets are caused by too little calcium in food, but the inability of bone tissue to use calcium brought to it in body fluids. Experiments on the causal link of the disease have not produced uniform results, and it is not currently possible to place responsibility for this condition on any specific form of diet, such as fat deficiency or excess carbohydrates or protein. It seems true that prolonged use of any food leading to eating disorders causes the inability of bone cells to take calcium salts as usual. While there are many obscure points regarding the origin of both scurvy and rickets, there is no doubt that some dietary flaw lies at their base and that they can be cured or generally avoided by maintaining suitable dietary conditions. FOODS MOST MOST COMMONLY POISONOUS Some articles of food figure with a particular frequency in reports of food poisoning outbreaks. In all cases, it is not clear why there is a particular responsibility for causing harm. For example, vanilla ice cream and vanilla puddings were so often implicated that some researchers did not hesitate to attribute the poisonous quality of vanilla itself. But there is no hard evidence that this is the case, and has been suggested Reducing the action of vanilla contributes to the growth of anoric bacteria that produce poisonous substances, an explanation of the very hypothesis. The noticeable frequency with which the consumption of raw meat provokes food poisoning has already been established and is largely due to the accidental withdrawal of meat from parasites harmful to humans. Even greater culpability of raw milk is due to the fact that milk is not only like meat, sometimes obtained from an infected animal, but that it is a particularly good culture environment for bacteria, and in the process of collecting or distributing can become infected through the agency of the human carrier. Foods such as ice cream, which are made with milk, are also often associated with food poisoning. It seems likely that the disease caused by ice cream is much more common due to a bacterial infection than metal poisoning or flavoring extracts. Responsibility for these latter substances is quite problematic. Cases of cheese poisoning, which appear to be relatively numerous, have rather vague cause-and-effect reports. Whether such poisoning is more often associated with some original milk contamination, or with the invasion of cheese by pathogenic bacteria during cooking, or with the formation of toxic substances by bacteria or mold in the process of maturation, which passes the cheese, remains uncertain in most cases. Poisoning of molluscs from eating oysters, mussels or molluscs is undoubtedly caused in some cases by contamination of sewage with water from which bivalve water is taken, and in such cases usually concerned about typhoid bacilli or parathyroid groups. The contentious question is whether some of the reported outbreaks of mussel poisoning were caused by a bacterial infection or whether sometimes healthy or p.107 patients with mussels taken from uncontaminated water contain a poisonous substance. Similarly, it is not clear whether a particular sea snail (Murex bradatus), sometimes used in food under certain conditions, contains a naturally poisonous substance for humans, or whether it is poisonous only when it is infected or when toxic bacteria have grown in it. Potato poisoning in some cases is due to bacterial decomposition of potato proteus-bacillus; in other cases, the poisonous alkaloid, soline, is said to be present in excessive quantities in patients and in potato germination. It should be noted that many cases of potato poisoning have been associated with the use of potato salad, which stood for some time after mixing, so the possibility of contracting bacillus with paratyphoids or other pathogens cannot be ruled out. The fact that Sozanin is always really responsible for potato poisoning, many investigators consider doubtful. These examples are sufficient to show that the proportion of suspected food poisoning is largely due to uncertainty about the real source of the troubles. While the trend towards opinion has been towards a broader recognition of the proportion of some bacteria, especially the parathioid group, there is an important residue of unexplained food poisoning that needs further qualified research. One of the objects of this book is to point out this need and draw attention to the many problems that are waiting to be resolved. The first step is to regularly and thoroughly investigate every outbreak of food poisoning. INDEX Acid Pickles, 33 Falsified cucumbers, food, 41 Agglutination, 60, 64, 70 Alkaloid, 107 Allergies, Food, 6 Almonds, 11 Amanita: aurantiaca, 20; Caesar, 18, 20; Muskaria, 18, 19, 20, 22; phalloids, 21, 22, 23; Verna, 22 Amanita toxin, 22, 24 Anaphylaxis, 9, 10, 11 Anilin Dyes, 32 animal parasites, 79 animals, 13, 14, 24, 44, 50, 67, 68, 70, 71, 72, 78, 93, 95, 100, 106; 59, 62, 63, 65, 72 Ankylostomyosis, 83 Anantto, 32 Antianaphylaxis, 11 Antimonium, 27 Antiseptic Chemicals, 33, 40 Antitoxin, 24; diphtheria, 9 Appendicitis, 1 arsenic, 26, 101 arteries, 3 artichokes, 16 ascaris, 84 Asian cholera, 50 asparagus, 30, 31 Asthma, 10, 12 Atropine, 20 B Bacillus: 92-96; E. coli, 56; Danish, 75; diphtheria, 69; enteritidis, 58, 59, 60, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 74; enterididis sufestifer, 70, 72; paratyphoid enteritidis, 68, 69, 85; paratyphos, 58, 66; paratyphos b, 60, 65, 66, 73, 74; proteus, 55, 56, 57, 107; 65, 66, 67, 68, 71, 72, 73, 74; tetanus, 69; 44, 51, 52, 53; typhoid fever, 44-47, 64, 106 Bacteria: food, 44, 58; pathogens, 44, 58 Bacterial products, 85 Balloon Fish, 24 Barbel, 25 beans, 14, 31, 46, 86, 88, 95, 104 beef stew, 59 Beer, 26, 27 Benzoate soda, 34 benzoic acid, 34, 35, 36 Beriberi, 102 berries, 29, 35 birds, game, 97 Biscuits, soda, 36 blood vessels, 2, 39 Borax, 37 borax, 37, 38, 40 botulism, 86; Anatomical lesions, 91; Bacteriology, 92; cases, 87; Epidemiology, 93; Prevention and Treatment, 94; Symptoms, 88 (p.110) Bread, 47, 48 Butter, 16, 32, 40, 101 Butyric acid, 95 C Caffeine, 36, 41 Cakes, 76 Calf Diarrhea, 72 Cady, 27, 28, 32, 41 Canning, 4, 5, 7, 8, 29, 30, 95 Canning, 33, 93 Cap, Metal, 28 Cardamom, Oil, 16 Carriers, 55; paratyphus, 61, 62, 66, 67, 70, 73, 78; typhoid fever, 45, 48, 50, 66 cases: botulism, 87, listed by Mayer, 88, in the United States, 88-91; dysentery, 84; Food sensitization, 10, 11, 12; Dairy disease, 100; mushroom poisoning, 20, 21, 22; Plant poisoning, 14; asparagus poisoning, 30; trichiniyaz, 80, 81; Tuberculosis, 53 Cat, 83 Cathartic, 96 cattle, 10, 51, 53, 54, 55, 62, 63, 71, 72, 74, 82, 86, 96, 100 Celery, 45, 46, 47 12, 62 Cestode Infection, 82 Cheese, 5, 7, 28, 97, 106 Chemicals, Antiseptic, Antiseptic, 40 Chicken, 71, 88 Chicken peas, 103 Chicory, 41 Chocolate, 28 cholera germ, 51 sliced beef, 59 Cicuta maculata, 14, 16, 17 Cinnamon, 37 clams, 50, 106 Claepvics: paspali, 86; Purpleea, 85, 87 Codfish, 67 Coffee, 36, 41 Coffee Tree, 14 Coloring, Artificial, 40 Coloring Substances, 31 Conium maculatum, 15 Contact Infection, 62, 67 Cook, 44, 45, 50, 73, 74 Copper, 30, 101 Copper: Acet, 31; Salt, 31; sulfate, 31, 32 Cranberries, 35 Creosote, 34 Cysticercus pulp, 82, 83 D Narcissus bulbs, 14 Danysz bacillus, 75 Death Camas, 14 Death-cup, 21, 23 Death-rates, 2, 3, 4, 39 Delphinium, 14 Diarrhea, 84 Diet, Defective, 102, 103, 104, 105 Diphtheria, 54 Diseases: Deficit, 101; degenerative, 2; Dairy, 54; leather, 12 Dog, 25, 83 Drying, 33, 40 dyes, aniline, 32 Dysentery, 84 E Echinococcus, 83 Eczema, 10, 12 Eelworm, 84 Eggs, 6, 10, 11, 12, 97, 98 Egg White, 9, 10, 11, 12 .111 Epidemics. See The Flashes of Ergoth, 85 Ergothism, 85-86 Waiting for Life, 2 extracts, flavors, 106 F Favism, 104 Fish, 5, 24, 25, 34, 62, 67, 71, 83 Flies, 47 Flour, 32, 43, 103 Fly Amanita, 18, 19, 21 Fly poison, 18 Food: Falsification, 41; Allergy, 6; Colouring, 32; intoxication, 18, 57, 92; preservatives, 33; substitutes, 16, 41 Foods: canned food, 4, 5, 7, 8, 29, 30, 95; cooked, 47, 51, 52, 53, 54, 60, 63, 69, 70, 78, 81, 94; decomposed, 39, 97; most commonly poisonous, 105; protein, sensitization up, 9; Smoked, 34, 39; 39, 97; raw, 7, 46, 47, 48, 55, 63, 69, 70, 79, 84, 94, 96 feet and mouth disease, 55 Formaldehyde, 36, 40 foul, 5 fruits, 5, 10, 29, 30, 35, 47, 50, 62, 97, 104 Fruit esters, 42 Fruit syrups, 42 Fugu, 25 Mushroom, 85 G gallstones, 1 Bird Game, 97 gastroenteritis, 56, 60, 74, 96 Giardia (Lamblia) intestinal, 84 Globe-fish , 24 Glucose, 277 41 Goose, 71; liver, 78 grain, 85, 104 Grass, Wild, 86 Gymnocladus dioica, 14 H Hackfleisch, 59 Ham, 86, 92, 94, 95 Hamburger Steak, 59, 78 Hay, 104 Hay Fever, 9 Heart, 3, 22 Heating, 40 Hellebore, 14 Hemlock, 13, 15; poison, 16; water, 14, 16, 17 Gipuric acid, 35, 36 Hog cholera, 66, 71 Honey Locust, 14 Hookworm Infection, 83 Horse, 71, 86 horseradish, 16 Hydatid disease, 83 Hydrocarpus, 16 Gimenolepis Nana, 82 I Ice, 75 Ice Cream, 5, 7, 32, 105, 106 Infection: accidental, 72; Asian cholera, 50; Bacillus proteus (?), 55; bacterial poisons, 86, 96; carrier, 44, 45, 48, 50, 55, 61, 62, 66, 67, 70, 73, 78; cerstode, 82; Giardia (Lamblia) Kishetis, 84; Nematode, 83; Laboratory, 72; Dairy, 54; Parasitic, 79; paratyphoid, 58; zing, 104; Secondary bacterial, 80; Soil, 46; Tapeworm, 82; meat tube, 51; tubular milk, 53; typhoid fever, 44 Intoxication, nutrition, 18, 57, 92 iron pirites, 26 (p.112) J Jams, 27 Japanese Fugu, 25 Jars, Save, 28 Jelly, 32, 50 K Kalmia latifolia, 14 kidneys, 2, 3, 22, 24, 39 kittens, 84 L Larkspur, 14 Lathyrism, 103 Loel, 14 lead, 27 lead: chrome, 28; 28; Pipes, 28; salts, 29 Legumes, 104 Salad, 45, 50 Liver, 22, 24; Goose, 78 Loko-Uz, 14 Lupins, 14 M Corn, 103 Maratti Oil, 16 Margaritin, 16 Swamp Marigolds, 14 Maria Malloy, 45 Pork Meat, 83 Meat, 5, 7, 24, 33, 37, 40, 44, 51, 52, 53, 57, 58, 59, 62, 63, 64, 65, 68, 69, 70, 71, 72, 75, 76, 77, 78, 79, 83, 95, 97, 101, 106; jelly, 69; pies, 69, 73; puddings, 69 Meat Inspection, 77, 81 Metals, 5, 106 mice, 56, 74, 75, 78, 84 Milk, 5, 6, 7, 10, 11, 40, 48, 50, 51, 53, 54, 55, 62, 69, 70, 72, 73, 76, 77, 96, 97, 101, 104, 106 Milksickness, 100-101 Molasses, 30 Murex bradatus, 107 Muscarin, 22 Mushrooms, 5, 13, 13 18-24 Mussels, 50, 106 Mutations, 68 N Neurit, 26 Neurotoxin , 24 nipple, rubber, 27 pellets of nisla, 91 nitrogen peroxide, 32 O oatmeal, 11 oats, 104 Cardamom oil, 16; cloves, 37 olive stones, 41 Flashes from behind: Beans, Darmstadt, 95, Stanford University, 95; beef, Breslau, 58; beef stew, Limerick, 59; Beer, England, 26; bread, Elgin, 48; cod, 67; Sick animals, 71; Ergoth, Limoges, 85; gastroenteritis, 74; Groups and families in the U.S., 4, 5; ham, Ellesells, 92; Human pollution, 73; List: Hirsch, 85, Hibeneer, 58, Mayer, 65, Savage, 58; Margarine, Hamburg, 16; meat, 65, 69; Frankenhausen, 63, Gent, 77; Meat Pies, Wareham, 73; Milk, 96; Christiania, 73, Newcastle, 69; Different pollution, 74; Mushrooms, New York City, 18; oysters, 48; paratyphoid carrier, 73; Pie, Westerly, 60; potato salad, 65; Public Markets, South Philadelphia, 46; rat virus, 75; sausage, 65, Hanover, 56, Wurttemberg, 86; Sour Herbal Soup (p.113), New York, 18 years old; spaghetti, Hanford, 44; typhoid fever, New York, 45; Vanilla Pudding, 65; Vermichel, 67; watercress, Philadelphia, 46; water hemlock, New Jersey, 16 oxaline acid, 18 Oxyuria, 84 oysters, 5, 24, 48, 49, 50, 71, 106 P Palmolin, 16 Panaluseo papilionaceus, 21 Paragaertner forms, 68 parasites, 79, 84 Paratyroid fever, 58-78; carriers, 61, 62, 66, 67, 70, 73, 78; Sick animals, 67, 71; gastrointestinal tract, 61; Common Characters, 61; Human pollution, 73; Prevention, 77; Different pollution, 74; Sources of infection, 71; Symptoms, 61; Toxin production, 68; typhoid fever, 61; typical flash, 58 parrots, 72 Pasternak, 16 Pasteurization, 48, 54 Confectionery, 47 Pate de foie gras, 78 Peas, 31, 43, 46 Pellagra, 102, 103 Pepper, 41 Pericarp rice, 102 Peripheral Nevrit, 26 Pickling, 93 Pidan, 98 pie, 60 pigs, 71 pike, 25 Pinworm, 84 vegetable oils, 16 plants, 9, 13-24, 25, 101 Poisons: bacterial, 96; Chemical, 26; Mineral, 26; Organic, 26; protoplasm, 33 Poisoning: aniline dyes, 32; Animals, 24; Antimonia, 27; arsenic, 26; Asian cholera infection, 50; Bacillus Proteus (?) infection, 55; Botulism intoxication, 86; Coloring of substances, 31; copper, 30; defective diet: Beribery, 102, Favizm, 104, Latirus, 103, 103, rickets, rickets, zing, 104; Egg white, 9; Ergault, 85; fish, 25; Food preservatives, 33; Food substitutes, 41; lead, 27; Milk-borne infections: diphtheria, 54 years old, foot-and-mouth disease, 55; Dairy disease, 100; scarlet fever, 54, and septic sore throat, 55; mushrooms, 18; parasites, animals: tenase, 82, trichiniyaz, 79, others, 84; paratyphoid infection, 58; Plants, 13; clams, 24; Tin, 29; Tuberculosis infection, 51; typhoid fever, 44 Poisoning, food: food, most commonly associated with, 7; Effects, 2; Degree, 3; Frequency, 1; Species, 6; Prevention, 2; Unclear, 100; outbreaks, in the United States, 3, 4, 5; 3, 4, 8; Scope of the book, 6; Seasonal morbidity 5; unknown, 100 Poison Ivy, 14 Poisonous Squads, 34 Pollen, 9 Polyneirot Birds, 102 Pork, 79 Pork and Beans, 88 Potatoes, 46, 107 Potato Salad, 65 Preservatives: Chemical, 33; Food, 33; Household, 37 Protein, 9, 11, 12, 62, 69, 80 (p.114) Protochloride Tin, 30 Ptomain Poisoning, 1, 3, 18, 68, 97 Puffers, 24 Pulse, 103 Pirita, Iron, 26 Kwinin, 33 R Rabbit, 71 Rahitis, 105 Radishes, 45 Rush, 10, 12 Rats, 56, 74, 75, 78, 81, 82 Rat Virus, 75 Cooling, 33, 40 Rice, 43, 102 Ricin, 14 Ricketts, 105 Maturation , 97 Roundworm, 79 Royal Amanita, 18 Rai, 85 S Saharin, 41 Salad, 5, 95, 107; dressing, 95 Salicylic acid, 36 Salt, 33, 41, 94 Salt Solution, 33, 40 Salt, 33 Salts, 33 Sandwiches, 46 Saponin, 42 Sausage, 5, 7, 40, 56, 65, 69, 75, 78, 79, 86, 88 Scarletina, 54 Singi, 55, 104 Sensibilization, Nutrition, 6, 9 Sept. blood, 11, 64, 65, 70; Therapeutic, 9 Shark, 25 Sheep, 71, 100 clams, 10, 24, 106 Shrimp, 71 Smoking, 33, 93, 94 Snail, 107 Soda Water, 42 Soda Carbonate, 36 Sodium benzoate, 34 sodium fluoride, 40 Soft drinks, 28, 42 Soil, Infected, 46, 47 Solinen, 107 Solder, 28 Sorrell, 18 Sour Herb Soup, 18 Sour Milk, 97 Spaghetti, 44 Spices, 37 Staphylococcus, 96 Traffic, Patent Metal , 28 Strawberries, 10 Streptococcus sore throat, 55 Strongyloides, 84 Strychnine, 33, 96 sturgeon, 25 substances, coloring, 31 Substitutes, food, 16, 41 Sugar, 26, 28, 41, 42 Sugar Solution, 33, 40 Sulfite, 36, 40 Sulphuric Acid, 26, 27, 36 Pigs, 74, 80, 81, 82, 93 Symptoms: Cholera-like, 25, 77; circulation, 10; coma, 22; constipation, 89, 90, 100; convulsions, 20, 22, 25; Coriza, 10; diarrhea, 10, 21, 61, 90; difficulty swallowing, 20; Digestive, 1, 61, 105; dizziness, 20, 90; eyelids, edematose, 10; Febrile anemia, 104; fever, 61, 79; gastrointestinal, 1, 10, 58, 61, 90; haemoglobinuria, 104; jaundice, 104; Mental, 24; nausea, 10, 12, 88; nervous, 10, 24, 90, 103; abdominal pain: 21, 61, 89, muscle, 79, 80; paralysis, 25, 96; Speed, 10, 44, 58, 61, 91; rash, 10, 12; sneezing, 10; Temperature, subnormal, 89, 100; thirst, 21, 89; 20; visual, 20, 88, 89, 90, 90, 96; vomit, 10, 12, 21, 88, 90, 100 Syrups, 27, 42 T Tapeworm, 82, 83 Tea, 36 Tenia Saginata, 82 Teniaaz, 82 Shadow Salts, 82 Tetrodontidae, 24 Theominbro, 36 Tin, 29-30 Tin Salt, 30 Toadstools, 18 Tomatoes, 12 Toxins, 68 Shiver, 100 Trichin, 79 Trichinella spiralis, 79 3 80 Trichiniaz, 79 Trichinosis, 79 Tuberculin, 9 Tuberculosis, 44, 51 Tifoid fever: 44-50, 78, 79; carriers, 45, 48, 50, 66; Dairy, 48 U Uncinariasis, 83 Urticaria, 10 Utensils, cooking, 27, 28, 30 v Vanilla: 105; ice cream, 105; pudding, 65, 105 Vegetables, 5, 29, 30, 31, 45, 46, 47, 62, 83, 95, 97, 104 Veratrum viride, 14 Poisoning Verdigri, 31 Vermicelli, 67 Vitamin, 102, 103 Water, 28, 50, 75 Cress Salad, 45, 46 Wintergreen, 14 Sigadenus, 14 FOOTNOTES: Transcriber Notes: Illustrations were moved from the middle of the point to the nearest break point. Missing page numbers connect to blank pages and move illustrations. The following illustrations have been moved to other pages: pic. 1 was moved from page 15 to page 16 of Reece. 3 was moved from page 19 to page 18 Ofe. 4 was moved from page 23 to page 22 Ofes. 5 was moved from page 49 to page 48 Ofes. 10 was moved from page 87 to page 88 Punctuation in the index was inconsistent, all the colonies in the lists for page numbers were changed to commas, they are not specifically mentioned/marked in the list of changes. The intakes are usually separated by semi-colonized intestines, they have been added or altered from other punctuation in silence. Subcharging is usually separated by commas, they have been added or altered with other punctuation in silence. Atropine and atropine have been preserved in both versions of this project. Table A in footnote 1 contains a potential mathematical error, 2nd column (Waiting for Life 1879-81), Line (Ages) 40 shows a value of 23.0, it should be 23.9 to fold correctly in the 4th column (Gain or Loss). The original value (23.0) is saved. Footnote 2 is also Doerr, Allergy and Anaphylaxis, in Coll often cited as also Doerr , allergy and anaphylaxis, in Coll. It was preserved in a version printed in the book for reasons of authenticity. Margaritin (pages 16 and 112) generally spelled margarine, it was preserved in this book for reasons of authenticity. Maratti oil (pages 16 and 112) is generally known as moratti oil, it was preserved in this book for reasons of authenticity. Hydrocarpus (pages 16 and 111) in general known as Hydnocarpus, it was preserved in this book for reasons of authenticity. Amanita Caesar (pages 18, 20 and 109) is also known as Caesar Amanita, but has kept for this project in its first form. Muskarin (pages 20, 21, 22 and 112) generally spelled muskarin, it was preserved in this book for reasons of authenticity. Sigadenus (pages 25 and 115) is generally known as Sigadenus, was preserved in this book for reasons of authenticity. The typhoid carrier of New York's Mary Mallon (aka Typhoid Mary) mentioned on page 45, and on page 112 written in this book as Mary Malloy, the original book was saved. In addition to the corrections listed below, the printer's spelling, punctuation, hyphenation, and ligature inconsistencies have been preserved. Fixed the following typos: added from 0 to 0.89 in the footnote of table B 1, the second to the last value in the 4th column. changed la face vulteuse to page 21 Paneolus papilionaceus to Panaeolus papilionaceus 21 Italian markup for XLV in f. ffentl. Ges., XLV was removed, footnote 69 altered by R. Trommsdorf, L. Reichmann, and A.E. Porter, at R. Trommsdorff, L. Rajchman, and A.E. 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