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 COLLEGE OF PHYSICIANS 
 AND SURGEONS 
 
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 1920 
 
 COLUMBIA UNIVERSITY 
 
 EDWARD G. JANEWAY 
 MEMORIAL LIBRARY 
 
Digitized by the Internet Archive 
 
 in 2010 with funding from 
 
 Open Knowledge Commons 
 
 http://www.archive.org/details/bacterialfoodpoiOOdieu 
 
FOOD POISONING 
 
WORKS BY 
 CHARLES P. BOLDUAN, M.D. 
 
 Immune Sera. 
 
 Antitoxins, Agglutinins, Hemolysins, Bacterio- 
 lysins, Precipitins, Cytotoxins, and Opsonins, 
 Anaphylaxis, and Serum Diagnosis of Syphilis. 
 Third edition, rewritten. By Charles F. Bolduan, 
 M.D. i2mo, 194 pages. Cloth, $1,50, 
 
 Bacterial Pood Poisoning. 
 
 A Concise Exposition of the Etiology, Bacteri- 
 ology, Pathology, Symptomatology, Prophylaxis, 
 and Treatment of so-called Ptomaine Poisoning. 
 By Professor Dr. A. Dieudonne, Munich, Trans- 
 lated and Edited, with additions, by Dr. Charles 
 F. Bolduan. 8vo, 127 pages. Cloth, $1 ,00. 
 
 The Suppression of Tuberculosis. 
 
 "With Observations concerning Phthisiogenesis 
 in Man and Animals, and Suggestions concerning 
 the Hygiene of Cow Stables and the Production 
 of Milk for Infant Feeding, with Special Refer- 
 ence to Tuberculosis. By Professor E. von 
 Behring, University of Marburg. Authorized 
 Translation by Charles F. Bolduan, M.D. i2mo, 
 91 pages. $1,00. 
 
 Manual of Serum Diagnosis. 
 
 By Doctor O. Rostoski, University of Wurzburg. 
 Authorized Translation by Charles F. Bolduan, 
 M.D. i2mo, 92 pages. Cloth, $1,00. 
 
 Collected Studies on Immunity. 
 
 By Professor Paul Ehrlich. Translated by 
 Charles F. Bolduan, M.D. 8vo, 597 pages. $6,00, 
 
 E. B, TREAT & CO. - NEW YORK 
 
BACTERIAL 
 
 FOOD POISONING 
 
 A CONCISE EXPOSITION OF THE ETIOLOGY, BACTERI- 
 OLOGY, PATHOLOGY, SYMPTOMATOLOGY, 
 PROPHYLAXIS, AND TREATMENT OF 
 
 SO-CALLED PTOMAINE POISONING 
 
 PROF. DR. A. DIEUDONNE 
 
 MUNICH 
 
 Translated and Edited, with Additions, by 
 DR. CHARLES FREDERICK BOLDUAN 
 Bacteriologist, Research Laboratory, Department of Health, 
 City of Ne<w York 
 
 AUTHORIZED TRANSLATION 
 
 NEW YORK 
 
 E. B. TREAT & COMPANY 
 
 1909 
 
Copyright, 1909, 
 By E. B. TREAT & COMPANY 
 
 Entered at Stationers' Hall, 
 London, England 
 
NOTE BY THE AMERICAN AUTHOR 
 
 Published less than a year ago, Professor Dieu- 
 donne's manual on " Bacterial Food Poisoning " has 
 already become favorably known as one of the best 
 presentations of the subject. In the present transla- 
 tion, the editor has incorporated descriptions of a 
 number of additional outbreaks of food poisoning, 
 elaborating upon the prophylaxis applicable to Ameri- 
 can conditions, and going more fully into the details 
 of treatment. Paragraph headings have also been 
 inserted, and the material slightly rearranged, so that 
 the same natural sequence is followed in the different 
 chapters. It is believed that these changes, together 
 with the index which has been added, will facilitate 
 reference and still further enhance the value of the 
 book. 
 
 Charles Bolduan. 
 
 New York, January, 1909. 
 
CONTENTS 
 
 PAGE 
 
 INTRODUCTORY ......... ^ 
 
 I. MEAT POISONING. Poisoning Through 
 
 Diseased Meat J 5 
 
 Historical 15 
 
 Etiology 20 
 
 Bacteriology 22 
 
 Occurrence of the Bacilli in Nature ... 29 
 
 Biology of the Bacilli 35 
 
 Technique of the Bacteriological Examina- 
 tions .■ 37 
 
 Clinical Types of Cases. Symptoms ... 41 
 
 Diagnosis 44 
 
 Serum Diagnosis .» 45 
 
 Prophylaxis 46 
 
 Treatment 47 
 
 II. MEAT POISONING (Continued). Poison- 
 
 ing Due to Eating of Decayed Meat . . 48 
 
 Etiology 48 
 
 Symptoms 49 
 
 Bacteria Found in Various Outbreaks . . 50 
 
 Diagnosis 58 
 
 Evidences of Putrefaction 59 
 
 Prophylaxis 60 
 
 Treatment 61 
 
 9 
 
io CONTENTS 
 
 PAGE 
 
 III. MEAT POISONING (Concluded). Sau- 
 
 sage Poisoning 62 
 
 Historical 62 
 
 Symptoms 63 
 
 Etiology 66 
 
 Bacteriology 67 
 
 Diagnosis 70 
 
 Prophylaxis 70 
 
 Treatment 71 
 
 IV. POISONING THROUGH FISH AND MOL- 
 
 LUSCS 72 
 
 Fish Poisoning 72 
 
 Clinical Types of Cases. Symptoms ... 73 
 
 Mussel Poisoning 76 
 
 Snail Poisoning 77 
 
 Poisoning through Oysters 78 
 
 Treatment 79 
 
 V. POISONING THROUGH CHEESE ... 80 
 
 Clinical Types of Cases 80 
 
 Other Bacteria Associated with Cheese Poi- 
 soning 82 
 
 Treatment 83 
 
 VI. POISONING THROUGH ICE CREAM 
 
 AND PUDDINGS . . 
 
 Historical ....... - M 
 
 Bacteriology . ., ,., . m 
 Prophylaxis .., L « .« ,1 ... 
 Treatment . -. w M ... ... 
 
CONTENTS ii 
 
 PAGE 
 
 VII. POTATO POISONING 91 
 
 Historical 91 
 
 Solanin Poisoning 92 
 
 Bacteria Associated with Potato Poisoning . 95 
 
 Prophylaxis 97 
 
 Treatment 98 
 
 VIII. POISONING THROUGH CANNED 
 GOODS 99 
 
 Canning and the Destruction of Bacteria . 99 
 
 Canned Meats; Clinical Types of Cases . . 99 
 
 Canned Vegetables 100 
 
 Clinical Types of Cases . 104 
 
 Bacteriological Examination 105 
 
 Prophylaxis 106 
 
 Treatment 107 
 
 IX. METALLIC POISONS ........ 108 
 
 Historical . 108 
 
 BIBLIOGRAPHY 113 
 
 General Articles 115 
 
 Meat Poisoning 116 
 
 Fish Poisoning 118 
 
 Cheese Poisoning 119 
 
 Poisoning through Ice Cream and Puddings . 119 
 
 Potato Poisoning 119 
 
 Poisoning through Canned Goods .... 120 
 
 INDEX ....... ;.. . . ,. ,., t .. ... 121 
 
INTRODUCTORY 
 
 Illness due to the eating of infected foods is very 
 frequent, in fact far more so than is generally believed, 
 for usually it is only when a large number of such cases 
 occur that the matter receives public notice. There is 
 little doubt that many indefinite infections and dis- 
 turbances of the intestinal tract, ordinarily termed 
 errors in diet, are due to the ingestion of decayed or 
 infected foods. 
 
 At one time most cases of poisoning through food- 
 stuffs, especially meat poisonings, were thought to be 
 true intoxications through putrefactive substances, 
 ptomaines, etc. Recent investigations, however, have 
 shown that they are mostly due to certain specific bac- 
 teria, and then either following the introduction of the 
 specific pathogenic bacteria themselves (infection), or 
 following the introduction of the specific poisons pro- 
 duced by the bacteria (intoxication). 
 
 It is often a difficult matter to establish the true 
 cause of a case of food poisoning, though, of course, 
 it is easier when the cases occur in large numbers, 
 especially among the inmates of barracks, prisons, 
 boarding schools, etc., where the conditions of life are 
 uniform and readily controlled. When but one or two 
 cases occur in a private family, it is much more diffi- 
 cult to ascertain the true cause, and then only by means 
 
14 INTRODUCTORY 
 
 of most painstaking investigation. Such an investiga- 
 tion, moreover, requires an exact knowledge of the 
 mode of origin of these poisonings, for otherwise the 
 subsequent investigation will be directed into entirely 
 false directions. Besides, the bacteriological examina- 
 tion which is necessary in most instances, can yield suc- 
 cessful results only if the suspected material (remains 
 of the suspected food, stool or vomit of the patient, 
 etc.) is at once sent, properly packed, to the laboratory. 
 The more important of the food poisonings due to 
 bacteria, often occurring in extensive outbreaks, are the 
 following: meat poisoning, fish and shell fish poison- 
 ing, and poisoning through cheese, ice cream, pud- 
 dings, potatoes, and canned goods. 
 
Bacterial Food Poisoning 
 
 MEAT POISONING 
 
 In studying the poisonings due to the eating of meat 
 it is well to divide these into three varieties : 
 
 1. Poisoning due to the eating of meat from dis- 
 eased animals. (This form is usually associated with 
 the bacillus enteritidis or bacillus paratyphi.) 
 
 2. Poisoning due to the eating of putrefied meat. 
 (This is usually associated with bacillus proteus and 
 bacillus coli.) 
 
 3. Poisoning due to " sausage poison." (This is 
 produced by the anaerobic bacillus botulinus.) 
 
 In the first variety, poisoning is produced even by 
 freshly-killed meat ; in the other two varieties, the meat 
 acquires poisonous properties only after the animal 
 has been slaughtered. Clinically the first two varieties 
 of poisoning manifest themselves largely by gastro- 
 intestinal symptoms, while the third variety is asso- 
 ciated especially with symptoms referable to the central 
 nervous system. 
 
 POISONING THROUGH DISEASED MEAT 
 
 Sepsis Intestinalis (Bollinger.) Infectious Enteritis 
 
 (Gaffky.) 
 
 This is the most common of the meat poisonings, 
 
16 BACTERIAL FOOD POISONING 
 
 and is due to bacteria of the typhoid-colon group 
 (bacillus enteritidis and bacillus paratyphi B) which 
 infect the animal during life. Although these germs 
 in no way alter the meat, they multiply and give rise 
 to poisonous metabolic products, so that the clinical 
 symptoms usually set in after a brief period of incu- 
 bation. 
 
 HISTORICAL 
 
 One of the first to draw attention to this variety of 
 poisoning was Bollinger, who described such cases in 
 1876. Five years later, this author 1 was able to report 
 on eleven large outbreaks, embracing over 1,600 cases. 
 The symptoms were chiefly gastro-intestinal, but varied 
 considerably according to the quantity of meat in- 
 gested, and on the individual susceptibility of the 
 patients. In fact, according to Bollinger, the symp- 
 toms ranged in a complete scale from simple digestive 
 disturbances, such as a little gastric catarrh, or per- 
 haps a diarrhoea with vomiting, to severe febrile dis- 
 turbances, such as those of enteritis, gastric fever, 
 typhoid fever, dysentery, etc. Dividing the cases 
 symptomatically, he distinguishes three groups, which, 
 however, are not sharply defined one from the other. 
 These are: — 1, choleraic cases with profuse diarrhoeas, 
 2, cases running more of a typhoid course, with a 
 longer incubation than the preceding and with marked 
 cerebral disturbances of various kinds, and, 3, cases be- 
 ginning with choleraic symptoms but soon presenting 
 more the symptoms of typhoid fever. If the disease 
 
MEAT POISONING 17 
 
 is severe, convalescence is slow, and the patient is left 
 weak and emaciated. The duration of the illness in 
 these cases is several weeks. In the milder cases, on 
 the other hand, the disease only lasts a few days. In the 
 fatal cases death usually occurs from the fourth or 
 fifth to the tenth or eleventh day, rarely after that 
 time. The autopsy findings are usually those of a 
 gastro-enteritis. The lymph nodules of the intestine 
 are very prone to involvement, ulceration of the intes- 
 tine being of frequent occurrence. The mesenteric 
 glands may be swollen, and so also the spleen, and 
 there may be haemorrhages into various organs. Oc- 
 casionally the entire anatomical picture resembles that 
 found in typhoid fever. The period of incubation de- 
 pends on the amount of infected meat ingested, and 
 may vary from 6 to 24 hours, to as much as a week or 
 more. Two epidemic outbreaks of this form of meat 
 poisoning are described by Bollinger as being especially 
 interesting, as the symptoms resembled those of ty- 
 phoid fever. 
 
 One of the outbreaks occurred in Andelfingen in 
 1 84 1, and embraced about 450 patients who had come 
 together at a musical festival. Ten of the patients died. 
 In all probability the direct cause of the poisoning was 
 some roast veal which had been eaten in large quantity. 
 The symptoms were nausea, vomiting, foul-smelling 
 diarrhoeas which exhausted the patients, dysphagia, 
 dilatation of the pupils, disturbances of vision, delir- 
 ium, and slow convalescence with great prostration. It 
 was found that persons who had not attended the 
 
18 BACTERIAL FOOD POISONING 
 
 festival, but who had eaten beef supplied by the same 
 butcher, also were affected, so that it is probable that 
 the infecting virus had been communicated from one 
 meat to the other while lying in the butcher's shop. 
 Cooking the meat did not destroy the poison. The 
 period of incubation varied from three to ten days. 
 
 The other interesting outbreak described by Bol- 
 linger occurred in Kloten in 1878. Like the preceding, 
 this was associated with the eating of meat at a musical 
 festival. Five hundred and ninety-one of those who 
 took part in the festival, numerous persons who had 
 eaten meat supplied by the same butcher, and finally, 
 also, a number of persons in whom the source of in- 
 fection could not be traced, a total of 657 persons, were 
 thus poisoned. Of these six died. The direct cause 
 was found to have been the eating of the meat of a 
 seven-day-old calf which had been slaughtered either 
 after death or while moribund. In several of the cases 
 the symptoms set in as early as the first day; in most, 
 however, there was an incubation period of from four 
 to six days. It is interesting to note that those who 
 drank wine freely either were not affected, or suffered 
 only a mild attack. The symptoms began with de- 
 pression, headache, pains in the limbs, constipation 
 followed by diarrhoea. Toward the end of the first 
 week the cerebral symptoms became less prominent, 
 stools assumed more of a typhoid character, and in the 
 severe cases there was often a roseola and a small 
 papular rash. At the height of the disease there was 
 quite constantly an enlargement of the spleen, and the 
 
MEAT POISONING 19 
 
 superficial lymph nodes, especially those of the groin, 
 were frequently swollen. A point of considerable in- 
 terest is the fact that the outbreak gave rise to 55 sec- 
 ondary cases. The autopsy findings were enlarged 
 spleen, infiltration of Peyer's patches and of the soli- 
 tary lymph follicles, also ulcers in the small intestine 
 either in a state of granulation or already cicatrized. 
 On the basis of the clinical symptoms, as well as of 
 the anatomical findings, and in view of the fact that 
 secondary cases occurred, most of the observers re- 
 garded the disease as typhoid fever. This opinion was 
 shared by Eberth, who had the opportunity of exam- 
 ining a number of the cases post mortem. For a con- 
 siderable time there was quite a difference of opinion 
 as to the real nature of the outbreak. One set of ob- 
 servers held that it was a true typhoid epidemic; the 
 other regarded it as an epidemic of meat poisoning. 
 Bollinger believed that the outbreak was due to a pe- 
 culiar infection which closely resembled and in fact was 
 closely related to typhoid fever. He thought it might 
 be regarded as a variety of that disease, and proposed 
 the terms sepsis intestinalis, or septiform gastroen- 
 teritis. (See page 15.) 
 
 Numerous outbreaks of meat poisoning have been 
 reported in the last twenty years. Ostertag 2 was able 
 to collect accounts of 85 epidemics in the period 1880- 
 1900, the larger part of which were reported from 
 Germany. The total number of cases was over 4,000. 
 There is no doubt, however, that the actual number is 
 much greater, since not all cases, even when they occur 
 
20 BACTERIAL FOOD POISONING 
 
 in considerable groups, find their way into the litera- 
 ture. Bollinger believes that many cases of disease 
 giving the clinical picture of febrile jaundice (Weil's 
 Disease) belong to the group of meat poisonings. 
 
 ETIOLOGY 
 
 Most of the outbreaks of this kind of meat poisoning 
 have been traced to the meat of calves which had 
 become septic from navel infection, or to the meat of 
 cows which were slaughtered because they had been 
 infected after calving, or were suffering from some 
 peculiar intestinal or udder infection. Schneidemiihl 4 
 has analyzed 61 large outbreaks reported from 1868 to 
 1898, with the following result. The total number of 
 cases was about 5,000, of which 76 died. In 38 of the 
 outbreaks the disease was traced to the meat of cows, 
 in 15 to that of calves, in 3 to that of steers, in 3 to 
 that of hogs, and in two outbreaks to horse meat. In 
 the case of the cows, in 16 instances the animals were 
 killed because of gastric and intestinal disease; in 12 
 instances, because of disease of the organs of parturi- 
 tion; in 3 instances because of disease of the udder; 
 and in 3 instances because of foot and mouth disease. 
 In the case of the calves, intestinal and joint disease 
 were the main reasons for slaughtering the animals. 
 According to these figures, therefore, the chief source 
 of this form of meat poisoning is the meat of cows 
 which have been slaughtered because of disease of the 
 gastrointestinal tract, because of septic infection after 
 calving, and septic infection of the udder. Next most 
 
MEAT POISONING 21 
 
 dangerous is the meat of calves which soon after birth 
 manifest signs of gastrointestinal disease, or pysemic in- 
 fection of the joints (polyarthritis, phlebitis of the 
 umbilical vein). In a case of this form of meat poison- 
 ing recently reported by Bryson, 55 a Scotch shepherd 
 became ill three hours after eating some mutton. In- 
 vestigation showed that the sheep had been ill for sev- 
 eral days, and had therefore been slaughtered. This 
 method of disposing of sick animals is said to be com- 
 mon practice among the Scotch shepherds, the meat 
 being known as " braxy." The patient vomited re- 
 peatedly, had severe abdominal pain, cramps in the 
 extremities and some retraction of the head. There 
 was also a slight rise of temperature the following day. 
 Within a week the patient had completely recovered. 
 
 From the above analysis it is apparent that the ma- 
 jority of these outbreaks of epidemic meat poisoning 
 thus far reported have been due to what may be called 
 " forced slaughtering," or " emergency slaughtering " 
 of diseased animals, and allowing the meat to be mar- 
 keted without proper medical control. It has been 
 found that usually the severest attacks followed the 
 eating of the raw meat, cooking destroying the in- 
 fecting bacteria. As a rule, however, cooking does 
 not destroy the toxin produced by these germs, though 
 there seem to be some exceptions to this. Cases have 
 occurred in which the severest attacks were associated 
 with the eating of the cooked meat and of the resulting 
 broth. 
 
 Most of the outbreaks occur in the summer, and in 
 
22 BACTERIAL FOOD POISONING 
 
 many instances following the eating of sausages, 
 pates, chopped meat, etc. These forms of meat are 
 especially dangerous because in their manufacture 
 viscera, such as lung, liver and spleen, are often em- 
 ployed, and it is well known that the infecting bacteria 
 often localize in these in large numbers. Furthermore, 
 in consequence of the long period which often elapses 
 from the time of manufacture to that of consumption, 
 the bacteria may have abundant opportunity to multiply 
 and produce their toxin. (Van Ermengem.) As a 
 rule, in contrast to what is observed in " sausage 
 poisoning" (page 62) all of the meat from these in- 
 fected animals is poisonous immediately after slaugh- 
 tering; it may, to be sure, increase in toxicity as the~ 
 result of further development of bacteria and conse- 
 quent further toxin production. It is usually impossi- 
 ble to distinguish the meat of such diseased animals 
 from that of normal animals either by appearance, 
 smell, taste, or consistency. The same is true of the 
 dishes prepared from such infected meat; they appear 
 quite normal. For this reason the meat is usually pur- 
 chased and consumed without question. In the very 
 acute septic infections, the meat often shows such slight 
 changes that unless one is very familiar with the course 
 of the disease and with all its symptoms, very little is 
 found by macroscopic examination. 
 
 BACTERIOLOGY 
 
 Our knowledge of the etiology of the above- 
 described form of meat poisoning has been aided 
 
MEAT POISONING 23 
 
 greatly by the bacteriological investigations of the past 
 twenty years. In all probability the exciting cause is 
 the bacillus discovered by Gartner, the so-called B. en- 
 teritidis, which is a member of the typhoid-colon 
 group. 
 
 In 1888 Gartner 5 investigated an outbreak of meat 
 poisoning in Frankenhausen, in which, two to thirty 
 hours after eating the meat of an infected cow, 57 
 persons became ill with symptoms of gastroenteritis. 
 One of the persons died. The cow from which the 
 meat was derived was found to have been slaughtered 
 because of an intestinal catarrh. Gartner was able to 
 isolate B. enteritidis in pure culture not only from the 
 infected meat, but also from the spleen of the fatal 
 case. This organism is a freely-motile bacillus, not 
 stained according to Gram, produces no indol in pep- 
 tone solution, and ferments dextrose with the forma- 
 tion of gas. By feeding, and by subcutaneous as well 
 as intraperitoneal inoculations of pure cultures, Gartner 
 was able to infect mice, guinea-pigs, rabbits, sheep and 
 goats. Cats, dogs, and chickens proved refractory. 
 The susceptible animals had fluid evacuations, and on 
 post-mortem examination showed a marked inflamma- 
 tory hyperemia in the intestines and abdominal viscera. 
 Frequently this was hemorrhagic in character. The 
 lungs showed lobular pneumonic areas, and there were 
 haemorrhages into the organs. The bacilli could be 
 demonstrated both microscopically and culturally in 
 the blood and internal organs. The B. enteritidis 
 forms a poison which is not destroyed by heat ; guinea- 
 
24 BACTERIAL FOOD POISONING 
 
 pigs and rabbits inoculated subcutaneously or by mouth 
 with cultures which had been sterilized by heat, showed 
 the same symptoms of gastroenteritis as those inocu- 
 lated with living cultures. In addition they showed 
 various nervous disturbances, paralyses of the lower 
 extremities alternating with spasmodic twitchings, 
 symptoms which are to be regarded as signs of toxic 
 action. An interesting point in connection with this 
 case is the fact that the mother of the dead boy, who 
 had nursed him, subsequently developed the same dis- 
 ease, although she had not partaken either of the meat 
 or the soup of the infected cow. In other words, she 
 had become infected from the discharges from her son. 
 
 An interesting outbreak is that reported by G. Ar- 
 buckle Brown, 56 of Partick, Scotland, in which twelve 
 persons became ill after eating canned meat. Al- 
 though no bacilli were found in the meat, the poisoning 
 was probably due to Gartner's bacillus, as the serum of 
 the patients agglutinated known cultures of this organ- 
 ism in dilutions of 1-30 and 1-60. The poisoning in 
 this case would appear to have been caused only by a 
 toxin produced by the bacilli in the meat, the organ- 
 isms themselves having been killed during the canning 
 process, but the toxin remaining intact. 
 
 Gaffky and Paak 6 in 1885, i.e., three years before 
 Gartner's discovery, had studied an epidemic of meat 
 poisoning in Rohrsdorf, which was traced to the meat 
 from a horse suffering from abscesses. Eighty per- 
 sons were taken ill, one of whom died. The meat had 
 been eaten in the form of sausage made from the flesh 
 
MEAT POISONING 25 
 
 and liver of the animal. The authors were able to 
 cultivate a bacillus from the organs of animals inocu- 
 lated with the sausage. This organism was subse- 
 quently found to agree in its important characteristics 
 with the bacillus later described by Gartner, and was 
 pathogenic for animals in feeding experiments. Un- 
 like Gartner's bacillus, however, the boiled cultures 
 proved innocuous. 
 
 In 1889 Neelson, Johne and Gartner 7 studied an 
 outbreak of meat poisoning in Cotta, near Dresden, 
 which was traced to a cow slaughtered because suffer- 
 ing from a purulent inflammation of the udder. There 
 were 126 cases, with four deaths. The authors were 
 able to isolate a bacillus identical morphologically and 
 culturally with the B. fenteritidis, not only from the 
 suspected meat, and the bone marrow of the cow, but 
 also from the intestinal tract, blood, and spleen of two 
 of the fatal cases. The bacillus was pathogenic for 
 mice and guinea-pigs. The cultures, however, were 
 rendered innocuous by boiling, and the same was true 
 for the meat and the soup made from the same. In 
 passing it may be said that the toxin from B. en- 
 teritidis does not always withstand boiling. 
 
 Very careful examinations were conducted by van 
 Ermengem 8 in connection with an epidemic of meat 
 poisoning which occurred at Moorseele in Flanders, in 
 1 89 1. Eighty persons were affected, of whom four 
 died. The outbreak was traced to the eating of 
 roasted and boiled meat derived from two calves suffer- 
 ing from enteritis. In most instances the symptoms 
 
26 BACTERIAL FOOD POISONING 
 
 commenced within a few hours after partaking of the 
 infected meat, although in one of the fatal cases the 
 interval was four days. Cultures made from the bone 
 marrow of the tibia of one of the calves, and from the 
 liver, spleen, and intestinal contents of one of the fatal 
 cases revealed the presence of a bacillus which agreed 
 in all particulars with Gartner's bacillus. Cultures 
 sterilized at ioo° C. and even at 120 C. were still 
 toxic and produced marked inflammatory changes of 
 a hsemorrhagic character. Van Ermengem called at- 
 tention to the similarity which B. enteritidis bore to the 
 bacillus of swine plague and the bacillus of hog cholera. 
 
 Hoist 9 studied an epidemic occurring in Gaustad, 
 near Christiania, in 1891. This outbreak was associ- 
 ated with the eating of meat from a calf suffering from 
 enteritis. There were 81 cases, with 4 deaths. Cul- 
 tures from the spleen yielded a bacillus which was 
 identical in character with that isolated at the Moor- 
 seele outbreak and with known cultures of B. en- 
 teritidis. The Gaustad bacillus produced toxins which 
 withstood heating, but it was found that this property 
 was rapidly lost with artificial cultivation. 
 
 An interesting outbreak of meat poisoning occurred 
 in Rotterdam in 1892. This was traced to the meat of 
 a cow which had been slaughtered in accordance with 
 the regulations at the municipal abattoir, and which 
 had passed the prescribed inspection as normal. Poels 
 and Dhont 10 were able to isolate a bacterium from the 
 meat, and found that the organism was pathogenic for 
 mice, guinea-pigs and rabbits, giving rise to intestinal 
 
MEAT POISONING 27 
 
 catarrh, and paralysis of the lower extremities. Even 
 the sterilized cultures were toxic. When small 
 amounts of the bacillus were injected intravenously 
 into cows transient fever, muscular twitchings, loss of 
 appetite and fluid evacuations were produced. The 
 meat from these animals, slaughtered four days later, 
 contained no bacilli and was eaten without any in- 
 jurious results whatever. Another cow was killed 20 
 minutes after such an inoculation. Small numbers of 
 the bacilli were found in the spleen, liver and blood. 
 After the meat had been kept for three days at 20 C, 
 however, the number of bacilli present was much 
 greater. Some of the meat had been kept in the re- 
 frigerator, and contained but few bacilli. Fifty-three 
 persons ate of this, and 15 were attacked 12 to 18 hours 
 after with headache, colicky pains, and diarrhoea. 
 
 Basenau 1X examined the meat of a cow which had 
 been slaughtered because of illness after calving. He 
 isolated a bacillus which he termed B. bovis mor- 
 bificans, which resembled the typhoid bacillus, was 
 pathogenic in feeding experiments, and was killed by 
 exposure to 70 ° C. 
 
 A small epidemic of meat poisoning occurred in 
 Rumfleth in 1893. This was traced to the meat of a 
 cow which had been ill for eight days after calving. 
 The cooked meat as well as the broth seem to have been 
 responsible for the poisoning. Fischer, 12 who studied 
 the outbreak, isolated a bacillus from the meat and 
 found it identical with B. enteritidis. Injected into 
 animals it produced intestinal disturbances. Steril- 
 
28 BACTERIAL FOOD POISONING 
 
 ized cultures also killed animals and produced similar 
 disturbances. It was found, however, that the toxicity 
 rapidly decreased with artificial cultivation of the or- 
 ganism. In 1895, in Haustedt, Fischer isolated the 
 same organism from the meat of an ox which had been 
 slaughtered because suffering from diarrhoea. The 
 meat of this animal produced symptoms of poisoning 
 in 50 persons. 
 
 In 1894 an outbreak of meat poisoning occurred in 
 Bischofswerde, Saxony, almost 100 persons being 
 affected. The cause of the poisoning was traced to 
 sausages and chopped meat, composed of pork and 
 beef. There were no deaths. Johne 13 examined the 
 meat and isolated a bacillus closely related to the B. 
 enteritidis. 
 
 In Ghent, in 1894, twelve persons became ill after 
 eating a species of cervelat sausage which is eaten raw. 
 The inspector having charge of the abattoir was asked 
 to have an examination of the sausage made, but, say- 
 ing that there was nothing wrong with it, cut off and 
 himself ate a few slices and gave several to his as- 
 sistants. The latter soon showed signs of a more or 
 less marked enteritis; the inspector himself was at- 
 tacked with severe choleraic symptoms, accompanied 
 by albuminuria, diarrhoea, vomiting, and collapse, and 
 died on the fifth day. Autopsy showed a very severe 
 hemorrhagic and gangrenous gastroenteritis, fatty 
 degeneration of the liver, acute interstitial nephritis, 
 etc. Van Ermengem 14 examined the sausages bac- 
 teriologically, and found, especially in the uneaten 
 
MEAT POISONING 29 
 
 part of the sausage cut up by the inspector, a very 
 virulent and toxic bacillus which proved to be identical 
 with B. enteritidis. The same organism was isolated 
 from the blood, intestine, and other organs of the 
 inspector. In this outbreak an instance of direct trans- 
 mission of the disease was encountered. The husband 
 of a woman who had become ill after eating some of 
 the sausage, himself became affected with the same 
 symptoms, although he had not eaten any of the 
 sausage. 
 
 In recent years a number of observers have reported 
 cases of epidemic meat poisoning in which bacilli were 
 found identical with B. enteritidis, or at least closely 
 related to that organism. The more important of 
 these are given in Table I. (See page 30.) 
 
 In the majority of these instances the infected or 
 suspected meat was derived from diseased animals after 
 " forced slaughtering." Furthermore, it was repeat- 
 edly found that the bacteria were present not merely 
 in certain particular organs, but also in the entire 
 muscular tissue, and especially in the glandular organs. 
 It was not always possible to demonstrate the bacilli 
 in the suspected meat, for often there was no material 
 left to examine. However, the bacilli were isolated 
 from the stools of the patients and from various organs 
 in the fatal cases. In the latter, they seemed to be 
 especially plentiful in the spleen. 
 
 OCCURRENCE OF THE BACILLI IN NATURE 
 
 But little is thus far known concerning the occur- 
 
30 
 
 BACTERIAL FOOD POISONING 
 
 
 
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MEAT POISONING 31 
 
 rence of B. enteritidis and B. paratyphi* outside of the 
 infected organism. They do not appear to be widely 
 distributed. We also know nothing as to how these 
 bacilli get into the animal. Levy and Jakobsthal 39 
 demonstrated the presence of true typhoid bacilli in a 
 splenic abscess of a steer, so that true typhoid bacilli 
 may perhaps also have some relation to meat poisoning. 
 In a number of instances, the exciting organism was 
 found in the organs of the slaughtered animals 
 (Aertryk, Meirelbeck), or in their flesh (Breslau, 
 Neunkirchen, Berlin, Giessen), showing that the ani- 
 mals had already been infected during life. In other 
 instances, however, the meat was originally sound and 
 was infected subsequently. Sound meat is easily in- 
 fected by contact with meat containing these bacilli, 
 especially if the pieces are laid one on the other. In- 
 fection may also result from infected persons handling 
 or preparing the meat, for now we know that " bacilli 
 carriers " are not at all uncommon. In studying out- 
 breaks of meat poisoning connected with restaurants, 
 canteens, and the like, the existence of such carriers 
 must not be forgotten, and bacteriological examina- 
 tions of the stools of such suspected carriers should 
 be undertaken. 
 
 In order to gain some idea as to the occurrence of 
 paratyphoid and enteritidis bacilli, Dieudonne recently 
 made some examinations among the cattle, calves, and 
 hogs killed in the Munich municipal abattoir. He se- 
 lected those which, for one reason or another, had been 
 sent to the sanitary division for further examination, 
 * For the relation of paratyphoid to enteritidis see p. 35. 
 
32 BACTERIAL FOOD POISONING 
 
 especially animals with septic processes, such as endo- 
 metritis, purulent peritonitis, suppurative inflammation 
 of joints in calves, etc. Recent investigations having 
 shown that typhoid and typhoid-like bacilli often are 
 especially numerous in the bile, cultures of this were 
 made at once and after enriching for 24 hours in the 
 incubator. The cultures were made on malachite- 
 green agar and on Drigalski's medium. In only a few 
 instances was there any growth in the cultures made 
 at once, and this was due to B. coli, with here and 
 there a streptococcus. In the cultures made after 
 enriching the bile, a profuse growth was always ob- 
 tained. Forty-two cases were examined; in thirty-six 
 instances the growth was mainly streptococcus, which 
 produced marked acidity in the medium, a few staphy- 
 lococci, and bacillus coli. In four instances bacillus 
 coli alone was present, and in two instances bacilli were 
 obtained which culturally and biologically were identi- 
 cal with paratyphoid bacilli. In one of these the cul- 
 ture was obtained from a calf which had become sep- 
 tic from navel infection. Pericarditis and joint inflam- 
 mation were marked. In the other case the animal 
 was a cow showing a suppurative peritonitis, abscesses 
 in the liver and spleen, and general sepsis. The bile of 
 both these animals was mucoid in character, yellow, 
 and quite thick, whereas in most of the other animals 
 it was normal in color. Evidently we are here dealing 
 with inflammatory phenomena with increased produc- 
 tion of mucus. According to Pies 40 this favors the 
 growth of typhoid bacilli. Cultures made from the 
 
MEAT POISONING 33 
 
 abscesses in the liver and spleen also yielded paraty- 
 phoid bacilli, but no bacilli were found in the flesh or 
 blood of these animals. In abscesses in the' other 
 animals streptococci were constantly present. 
 
 Uhlenhuth * 2 examined the intestines of apparently 
 sound hogs killed in the Berlin abattoir. In 6% of 
 his cases he isolated bacilli which it was impossible to 
 differentiate either from paratyphoid type B, or from 
 bacillus suipestifer. These bacilli, it should be said, 
 are evidently very closely related, as can be seen from 
 their serum reactions. Bacillus paratyphoid B. is also 
 a near relative of the bacillus of mouse typhoid. 
 
 Similar investigations were undertaken by Morgan 57 
 in 1905. This author concludes: " 1. There exist 
 in the intestines of healthy animals organisms con- 
 forming morphologically and biologically to the en- 
 teritidis and paratyphoid A types. 2. These organ- 
 isms, as regards their agglutination reactions, fall into 
 three groups, namely, those of the B. enteritidis, 
 Aertryk, or hog cholera type, those of the B. en- 
 teritidis, psittacosis * type, and those of the B. para- 
 typhoid A, unknown type. 3. The nomenclature 
 adopted by different observers is unsatisfactory, but 
 is based on the principal differentiating criterion we at 
 present possess, namely, specific virulence." 
 
 Hiibener 61 has recently reported on the occurrence 
 of paratyphoid and related bacilli and finds that not 
 
 * Psittacosis is a contagious disease of parrots, communicable 
 to man, marked by pulmonary disorder and high fever. The 
 organism is fully described by Nocard and Leclainche, 1898, 
 
34 BACTERIAL FOOD POISONING 
 
 only do these occur in the intestines of normal hogs, 
 but also occasionally in perfectly sound sausages, and 
 in the excreta of healthy human beings. Rimpau 62 ex- 
 amined 50 healthy school children and 50 healthy 
 orphans and found paratyphoid bacilli, type B., in three 
 of the former and one of the latter. No infections 
 were produced by any of these bacilli carriers. 
 
 These results are very interesting, for they show, 
 as Kutscher and Uhlenhuth emphasize, that we must 
 bear these diseases of animals in mind when consid- 
 ering the etiology and prophylaxis of human paraty- 
 phoid infection. Further investigations are very much 
 desired concerning the relations existing between these 
 diseases and human paratyphoid infections. Attention 
 will also have to be paid to the milk of such infected 
 animals, as has recently been demonstrated by 
 Fischer. 41 Investigating an epidemic of some 50 cases 
 exhibiting the clinical picture of a severe gastro- 
 enteritis, this author was able to isolate a paratyphoid 
 bacillus from the stools of two of the patients, and from 
 the meat, internal organs, and milk of two cows which 
 had died of gastroenteritis. Since none of the meat 
 had been eaten by the persons affected, the epidemic 
 was ascribed to the drinking of the milk from the 
 infected cows. 
 
 Muhlens 25a has recently studied the occurrence of 
 bacillus enteritidis, seeking especially to learn whether 
 this organism was commonly present in food. Fifty- 
 seven samples of different kinds of meat were ex- 
 amined — pickled goose breast, raw ham, pork, ox 
 
MEAT POISONING 35 
 
 tongue, corned beef, smoked sausage, smoked salmon, 
 smoked herring, etc. — the samples were examined 
 culturally, but no bacteria of this group were found. 
 At the same time each of the samples was fed to two 
 or three white mice, the greatest care being taken to 
 prevent the animals from infecting one another. 
 Forty out of the fifty-seven samples killed one or more 
 of the animals fed. From seventy out of seventy-four 
 such mice bacteria belonging to the " enteritis " group 
 were isolated either from the spleen, the blood, or the 
 intestines. It would seem that such bacteria may be 
 present in very small quantity so as to be overlooked 
 by cultural examinations. Under favorable circum- 
 stances the bacteria may multiply in the meat to a 
 sufficient degree to become pathogenic for man, thus 
 causing the disease known as " food poisoning." 
 
 BIOLOGY OF THE BACILLI 
 
 The cultural characteristics of the bacilli isolated in 
 the various outbreaks are quite regularly similar, and 
 correspond to those of the bacillus enteritidis and of 
 the bacillus first described by Schottmiiller 3I as paraty- 
 phoid, type B. These bacilli can be distinguished from 
 typhoid bacilli and colon bacilli in a number of ways, 
 but especially by their behavior to various sugars. 
 This is well shown in Table II 
 
 From this it will be seen that B. enteritidis and B. 
 paratyphi B. ferment glucose but not lactose; B. coli 
 ferments both ; B. typhi ferments neither. 
 
 An instructive table showing the biological charac- 
 
36 
 
 BACTERIAL FOOD POISONING 
 
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MEAT POISONING 37 
 
 teristics of the bacteria belonging to this group has also 
 been prepared by Morgan. 57 
 
 The best medium for isolating these bacilli is the 
 malachite-green agar of Lentz and Tietz. On this B. 
 coli grows little or not at all, B. typhi shows delicate 
 green colonies without discoloring the medium, while 
 B. enteritidis and B. paratyphi B. grow abundantly and 
 change the color to yellow. This medium might 
 therefore be called a selective one. 
 
 An important means of differentiation is afforded by 
 the tests on animals, especially on mice and guinea- 
 pigs. Typhoid and colon bacilli are but slightly path- 
 ogenic for these animals, whereas both enteritidis and 
 paratyphoid are markedly pathogenic. In fact, the 
 latter two organisms produce a toxin which when given 
 per mouth kills susceptible animals with symptoms of 
 gastroenteritis. This toxin, moreover, is generally 
 quite resistant to the action of heat, though here there 
 is some individual variation in the different cultures. 
 This explains what has already been said, that infected 
 meat, whether roasted or boiled, and even the broth 
 made from such meat, may cause severe toxic symp- 
 toms. When the bacilli are cultivated for some time 
 on artificial media, the virulence rapidly decreases, and 
 so does the production of the resistant toxin. 
 
 TECHNIQUE OF THE BACTERIOLOGICAL EXAMINATION 
 
 The isolation and identification of the exciting cause 
 of an outbreak of meat poisoning is quite a difficult 
 matter, and can be successfully performed only by 
 
38 BACTERIAL FOOD POISONING 
 
 trained laboratory workers. It is extremely impor- 
 tant, therefore, that the required material be properly 
 collected, be as fresh as possible, and then be properly 
 sent to the laboratory. The material to be examined 
 will include the suspected meat (sausage, pate, etc.), 
 vomit and stool from the patient, the patient's blood, 
 and in case of autopsy, pieces of the intestine, spleen, 
 and liver.* 
 
 According to Basenau 11 it is well to wait with the 
 bacteriological examination of the meat until 24 hours 
 after slaughtering. In that time the bacilli have mul- 
 tiplied, even at the low temperature at which the meat 
 is kept, so that the bacteriological examination is sim- 
 plified. It is well to select a piece of meat rich in loose 
 areolar tissue. The surface is seared with a hot iron, 
 and then an incision is made through the seared area 
 with a sterile scalpel. Smears and cultures are thus 
 made from the inside of the meat. The cultures are 
 made by smearing some of the material with a fine 
 platinum loop over the surface of gelatine and agar 
 plates, over plates made after the method of Conradi- 
 Drigalski, and over malachite-green plates. In pre- 
 paring these plates it is well to plate various quantities 
 of a suspension made from the inside of the suspected 
 meat. Another portion of the suspected meat may be 
 
 *The various materials should be placed each in a wide- 
 mouthed sterile bottle tightly corked, the bottles packed with 
 ice and saw-dust, and sent at once, by special messenger if pos- 
 sible, to the nearest laboratory. All the bottles should be care- 
 fully labeled as to their contents, the date of collection, and 
 a complete clinical account should be sent to the bacteriologist 
 for his guidance. 
 
MEAT POISONING & 
 
 kept for 24 hours at room temperature so as to 
 " enrich " it, i.e., in order to give the bacteria time to 
 multiply. After this, smears and cultures are made 
 as with the original specimen. In addition to this it 
 will be well to feed some of the meat to mice. Base- 
 nau " advises that two mice be fed with the meat raw, 
 and two mice with meat which has been heated for one 
 hour to ioo° C. Mice are particularly well suited to 
 such feeding experiments because of their extreme and 
 uniform susceptibility. The vomited material and stool 
 are sown on plain agar, on Drigalski medium, and on 
 malachite-green plates. The last named is very highly 
 spoken of for these examinations, as it also in- 
 hibits the growth of B. coli. Some of the stool is 
 used for inoculating mice subcutaneously. The exam- 
 ination of the patient's blood is of considerable diag- 
 nostic significance. The most convenient method is to 
 draw from 5 to 8 cc. by means of a sterile glass syringe 
 and needle from a vein at the bend of the elbow. It 
 is unnecessary to make any incision. The skin is to be 
 cleansed, compression of the upper arm is made by an 
 assistant, and the needle is thrust directly into the dis- 
 tended vein. The blood is distributed among a number 
 of tubes of melted agar, and also planted into broth. 
 Inoculation into bile medium has given good results 
 in the hands of several observers. A small quantity of 
 blood may be left to clot in the syringe, the serum 
 which separates being subsequently used to make ag- 
 glutination tests. 
 
 The bacteria isolated from the infected meat, from 
 the faeces of the patients, and from the body of the 
 
4 o BACTERIAL FOOD POISONING 
 
 fatal cases must be tested by all known methods of 
 differentiation, including biological properties, patho- 
 genicity, and serum reactions. Of these the last named 
 is the most delicate. The bacilli should be tested with 
 the serum of an animal immunized against known cul- 
 ture of B. enteritidis or B. paratyphi B. In this way 
 it is possible to differentiate these organisms from ty- 
 phoid or colon bacilli. Absorption tests should also 
 be undertaken.* 
 
 Extensive investigations made by de Nobele, 21 
 Trautmann, 33 Uhlenhuth, and others have shown that 
 the bacteria of meat poisoning may be divided into two 
 types. According to Uhlenhuth 26 these are as follows : 
 
 GROUP I. 
 
 i 
 
 B. enteritidis (Gartner) 
 
 B. Moorseele (v. Ermengem) 
 
 B. Ghent (v. Ermengem) [ B. enteritidis, Gartner, 
 
 B. Brugge (v. Ermengem) r group 
 
 B. Rumfleth (Fischer) 
 
 B. Haustedt (Fischer) 
 
 J 
 
 GROUP II. 
 
 Paratyphoid B. group 
 
 Paratyphoid B. 
 B. Breslau (Fliigge-Kansche) 
 B. Meirelbeck (de Nobele) 
 B. Diisseldorf (Trautmann) 
 B. Sirault (Hermann & v. Ermen- 
 gem) 
 B. Aertryk (de Nobele) 
 B. Neunkirchen (v. Drigalski) 
 B. Greifswald (Uhlenhuth) 
 
 *The principle of these is discussed in Bolduan, "Immune 
 Sera," Wiley & Sons, N. Y. 
 
MEAT POISONING 41 
 
 Bacilli of the paratyphoid B. type were also found in 
 meat poisonings in Alsfeld (Curschmann), in Berlin 
 (Kutscher), in Bern (Heller), and in Giessen 
 (Fromme). 
 
 CLINICAL TYPES OF CASES 
 
 According to van Ermengem 3 the clinical course of 
 the disease seen in most of the reported outbreaks 
 varied considerably. Gastrointestinal symptoms, how- 
 ever, were almost always prominent. The attack usu- 
 ally manifested itself like one of cholerine, or cholera 
 nostras, or of inflammatory gastroenteritis. In addition 
 to the main symptoms, offensive, yellow, diarrhceal 
 evacuations, colicky pains, vomiting, and muscular 
 weakness, there are frequently albuminuria, catarrhal 
 pneumonia, and various cutaneous lesions, such as 
 herpes, polymorphous erythema, roseola, urticaria, 
 scurvy-like haemorrhages into the skin, or petechia. 
 Dilatation of the pupils, and photophobia have been ob- 
 served in some cases, and occasionally there has been 
 marked scaling of the epidermis on the inner aspect of 
 the hands and soles of the feet. In most instances, 
 symptoms began in from six to twelve hours after the 
 meat was eaten ; occasionally, however, the interval was 
 much longer. In a few cases, the vomiting and diar- 
 rhoea began immediately after the meal, just as in an 
 ordinary indigestion. In general it may be said that 
 the severity of the attack depends on the amount of 
 meat eaten. The mortality varies from 2 to '5%. 
 At the autopsy one usually finds more or less well- 
 marked signs of gastroenteritis, often hemorrhagic in 
 
42 BACTERIAL FOOD POISONING 
 
 character. The solitary lymph follicles and Peyer's 
 patches are swollen and prominent; frequently there 
 are ulcers both in the small and the large intestine. 
 The spleen is enlarged, and the kidneys and liver are 
 congested. In cases which have run a rapidly fatal 
 course, there are usually no distinct anatomical 
 changes. 
 
 Trautmann, 33 struck by the close biological relation- 
 ship evidently existing between B. enteritidis and the 
 paratyphoid bacillus, called attention to the relation ex- 
 isting between the respective diseases produced by these 
 organisms, i.e., between epidemic meat poisoning and 
 paratyphoid fever. In meat poisoning, as we have 
 seen, certain clinical as well as pathological features are 
 distinctly typhoidal in character. Since both diseases 
 are produced by the same organism, Trautmann re- 
 gards meat poisoning as a highly acute, and paraty- 
 phoid fever as a more subacute form of a common in- 
 fectious disease. His explanation for the occurrence 
 of these two forms is as follows : In meat poisoning 
 the slaughtered animal is infected, and when the meat 
 is eaten both the disease germs and their toxic products 
 poison the patient. The short period of incubation in 
 meat poisoning, as compared with that in typhoid and 
 paratyphoid, is therefore due to the large number of 
 germs introduced, and to the fact that these are ac- 
 companied by their toxic products. If the amount of 
 poison is too much for the body and if the bacteria in- 
 vade the body juices, illness and death follow. In para- 
 typhoid the period of incubation, i.e., the time during 
 
MEAT POISONING 43 
 
 which the bacilli multiply sufficiently to produce toxic 
 symptoms, proceeds in the body of the infected human. 
 The bacilli develop slowly, and gradually give rise to 
 symptoms of illness. Even in meat poisoning the dis- 
 ease may take a typhoidal course. This will occur when 
 but few bacteria and little toxin have been ingested. In 
 the pathological findings there is considerable similarity 
 between paratyphoid fever and cases of meat poisoning 
 running a prolonged course. Both exhibit the same 
 lack of strict localization of the intestinal changes, both 
 the same hsemorrhagic character, and the same main 
 symptoms. Another point of agreement is the remark- 
 ably low mortality despite the severity of the clinical 
 symptoms. According to Kayser 34 the reason for the 
 short incubation period in meat poisoning as compared 
 to paratyphoid is to be found not only in the introduc- 
 tion of preformed toxins, but in the fact that the path 
 of infection differs. Typhoid and paratyphoid fever 
 he regards as primarily a lymph and blood infection; 
 the intestine is affected secondarily. In meat poison- 
 ing, on the other hand, the bacilli reach the intestine 
 at once, and multiply there. 
 
 Kutscher, 38 moreover, calls attention to the fact that 
 in paratyphoid infections not due to meat poisoning one 
 often sees cases exhibiting entirely the clinical picture 
 of a severe cholera nostras. Cases of this kind have 
 been described by Schottmuller, 31 and by Hetsch. 35 
 The latter observed a large epidemic of paratyphoid in 
 Kottbus in 1905, and noted that most of the cases ran 
 a choleraic course. Roily 36 divides the paratyphoid 
 
44 BACTERIAL FOOD POISONING 
 
 infections according to their clinical course, and recog- 
 nizes two groups of cases, namely, cases presenting the 
 symptoms of an ordinary typhoid fever, and cases of 
 a gastric type, in which gastrointestinal symptoms are 
 prominent. He describes a case of the latter type 
 which ended fatally, and exhibited the clinical picture 
 of cholera nostras. This division of the cases corre- 
 sponds, as can be seen, with that made by Bollinger in 
 his meat poisonings in 1881. Trautmann states that 
 many of the cases of meat poisoning seen in the epi- 
 demics in Andelfingen and in Kloten corresponded 
 entirely to cases of paratyphoid infection. The sim- 
 ilarity is still more striking when it is recalled that in 
 these epidemics instances of secondary infection oc- 
 curred in persons who had not eaten any of the infected 
 meat. These were probably due to contact infection. 
 In the Kloten epidemic the number of secondary cases 
 was 55. We see, therefore, that these more recent 
 etiological and bacteriological investigations confirm 
 the view expressed by Bollinger 1 in 1881, namely, that 
 these forms of epidemic meat poisoning are closely 
 related to typhoid fever. Zupnik 37 speaks of those 
 varieties of meat poisoning which run a more or less 
 marked typhoid course as " typhoidal meat poisoning." 
 
 DIAGNOSIS 
 
 As a" rule the diagnosis of this form of meat 
 poisoning is extremely difficult unless a number of 
 cases develop almost simultaneously. The cases with 
 a long period of incubation are especially liable to be 
 
MEAT POISONING 45 
 
 overlooked. In any event the diagnosis will rest mainly 
 on the history of the case. 
 
 SERUM DIAGNOSIS 
 
 The first to employ serum diagnosis in cases of epi- 
 demic meat poisoning was Durham, 32 who investigated 
 an outbreak in Hatton. From the body of a person 
 who had died after eating a meat pate Durham isolated 
 a bacillus resembling the B. enteritidis, and found that 
 it was agglutinated by the serum of the other per- 
 sons affected and of the convalescents in dilutions of 
 I : ioo to i : iooo. In subsequent outbreaks similar ob- 
 servations were made. The bacillus isolated from the 
 suspected meat or from the organs of the fatal cases 
 was agglutinated by the serum of the convalescents in 
 dilutions of i : 500 to I : 1000. The technique of the 
 serum test is exactly the same as that employed in the 
 Widal test for typhoid.* Whenever possible the serum 
 of the patients and of the convalescents should be 
 tested with a reliable laboratory culture of B. enter- 
 itidis or of B. paratyphi B. 
 
 It is possible in this way to establish a diagnosis of 
 epidemic meat poisoning even after the outbreak has 
 passed, for the agglutinating property persists in the 
 blood of the patients for several weeks. 
 
 It may be well to say that the bacillus isolated is not 
 always agglutinated in as high a dilution as a heterol- 
 ogous organism of a closely related species. Thus, in 
 
 *See in Rostoski-Bolduan "Serum Diagnosis," Wiley & 
 Sons, New York. 
 
46 BACTERIAL FOOD POISONING 
 
 a careful investigation of this question in connection 
 with an outbreak due to B. enteritidis, Liefmann 58 
 found that the sera of the patients agglutinated typhoid 
 bacilli in a higher dilution than the enteritidis organ- 
 ism isolated from the stools of the patients. There was 
 conclusive evidence, however, that the latter was the 
 cause of the infection. 
 
 PROPHYLAXIS 
 
 The prevention, or at least diminution, of this form 
 of meat poisoning can only be effected by a properly 
 organized system of meat inspection, especially in all 
 cases of " forced " or " emergency slaughtering." 
 Such an inspection must embrace a careful and thor- 
 ough examination of all the organs by a competent 
 veterinarian. It is essential that all meat which might 
 give rise to disease be excluded from sale for human 
 consumption. This will include especially the meat of 
 calves and cows which have been slaughtered because 
 of septic infection, and meat in which abscesses are 
 found in the interior of muscles. Moreover, since the 
 meat often shows no macroscopical changes, it will 
 be well to adopt the suggestions of Basenau, Ostertag, 
 v. Drigalski, and others, and resort to bacteriological 
 examinations in all cases where there is any suspicion 
 that the meat may be infected. Such examinations 
 could be made either in a special laboratory connected 
 with the abattoir, or in one of the regular hygienic 
 laboratories. In case infection were demonstrated by 
 this examination, the meat would of course be con- 
 
MEAT POISONING 47 
 
 demned and destroyed. Ostertag believes that such 
 a laboratory, would prove an economic advantage, for 
 if the suspected meat proved free from infection, it 
 could be passed for market, whereas at the present 
 time it is customary to order it condemned, in order to 
 be on the safe side. 
 
 TREATMENT 
 
 The treatment of these meat poisonings will natu- 
 rally depend on the type of case one is dealing with. 
 In the acute cases, with a short period of incubation, 
 it is well to wash out the patient's stomach, and this 
 plan should be followed even though the patient has 
 vomited. During the onset a brisk cathartic, such as 
 castor oil or calomel, should be administered. Later, 
 the administration of stimulants, especially alcohol, is 
 indicated. Alcohol seems to exert an inhibitory action 
 on the poison, and has given good results in a number 
 of reported cases. Gastric irritability is treated with 
 sedatives, mucilaginous drinks, cracked ice, heat to the 
 epigastrium, etc. The diarrhoea is best treated with 
 the initial dose of castor oil, followed by opium, rectal 
 infusions, etc. The typhoidal cases are treated exactly 
 like cases of typhoid fever, and the same precautions 
 should be observed to prevent infection of others. 
 
II 
 
 MEAT POISONING— (Continued) 
 POISONING DUE TO EATING DECAYED MEAT 
 
 ETIOLOGY 
 
 This variety of poisoning is due to the eating - of meat 
 from healthy animals, which originally was sound, but 
 which subsequently acquired toxic properties, owing 
 to the introduction of putrefactive organisms. This 
 form of decomposition may be due to any of the nu- 
 merous putrefactive bacteria; as a rule, however, the 
 majority of cases are due to the members of the proteus 
 group of organisms and to the colon bacillus. The 
 latter was isolated by Fischer 12 in cases of meat pois- 
 oning, once from a liver pate, and once from some liver 
 sausage. The colon bacillus produces a strong toxin 
 which withstands heat. 
 
 This form of meat poisoning is observed chiefly after 
 the ingestion of chopped meat, for this, almost in- 
 variably, is rich in germs. Sausages and game are 
 also responsible for a large number of cases. Putre- 
 factive decomposition of meat, however, does not in- 
 variably give rise to symptoms of poisoning. This is 
 shown, for example, by the extensive consumption of 
 game which is a little " high." Which of the putre- 
 factive products is especially poisonous, is impossible 
 to say. Further researches in this direction are much 
 
 48 
 
MEAT POISONING 49 
 
 desired. In all probability the poisoning is due to 
 specific toxins produced by members of the proteus 
 group of organisms. These toxins are destroyed by 
 heat. 
 
 Van Ermengem 3 states that these meat poisonings 
 are much less common after the ingestion of meat from 
 healthy animals which has become infected after kill- 
 ing than after meat from diseased animals similarly in- 
 fected. Most of these poisonings are observed in sum- 
 mer, probably because the bacteria can more readily 
 multiply in the temperature then prevailing outdoors. 
 In many instances the cases were due to the eating of 
 chopped meat. This is often mixed with water for 
 purposes of deceit, and this admixture favors the 
 multiplication of the bacteria. 
 
 SYMPTOMS 
 
 Clinically this form of poisoning exhibits usually the 
 picture of an acute gastroenteritis running a rapid 
 course, and, as a rule, without fever. The severity of 
 the symptoms depends on the amount of meat eaten, 
 and on the age and resistance of the patient. In most 
 instances the symptoms appear in from 4 to 20 hours 
 after eating the meat, and consist in vomiting, head- 
 ache, dysenteric, foul-smelling stools, colicky pains, 
 weakness, etc. In more severe cases there may be 
 convulsions, pains in the back and neck, and great de- 
 pression. Most of the cases, even the severe ones, 
 terminate favorably, though a feeling of weakness may 
 persist for some time. Deaths are infrequent. 
 
SO BACTERIAL FOOD POISONING 
 
 BACTERIA FOUND IN VARIOUS OUTBREAKS 
 
 According to statistics compiled by Schneidemiihl, 4 
 outbreaks of this form of meat poisoning were ob- 
 served in 1879 m Chemnitz, where 241 persons became 
 ill after eating raw meat and sausage. Some of the 
 cases ended fatally. In 1886, 160 persons became ill 
 in the same city after eating raw chopped meat. The 
 meat was prepared during a spell of very hot weather, 
 and had been kept for some time. It had, however, 
 been derived from healthy animals. The same meat 
 eaten roasted or boiled was either entirely innocuous 
 or at the most produced only transient malaise. Haupt 
 found that this outbreak was due to a variety of the 
 bacillus proteus. 
 
 In 1887, 20 persons became ill in Plauen after 
 having eaten raw chopped meat which had been 
 prepared six days previously and was in a state of be- 
 ginning decomposition. A similar outbreak is reported 
 from Gerbstadt in which 50 persons became ill after 
 eating raw chopped meat, and several kinds of bologna 
 sausage. 
 
 An interesting outbreak is described by Levy, 44 who 
 observed bloody diarrhoea and vomiting in 18 persons 
 frequenting a certain saloon. It was the custom here 
 to keep the meat from day to day in a refrigerator 
 which was found to be covered with a slimy brown 
 crust having a disagreeable sour smell. From the 
 bottom of the ice box proteus bacillus was isolated in 
 pure culture. The meat stored in the box had become 
 
MEAT POISONING Si 
 
 infected with proteus and had been the cause of the 
 outbreak. One of the cases ended fatally. At the 
 autopsy the bacteria were readily found in the intes- 
 tinal contents, but not in the blood of the individual. 
 When pure cultures of this organism were injected into 
 animals, the clinical symptoms produced resembled 
 closely those seen in the persons attacked during the 
 outbreak. The organisms apparently did not multiply 
 in the animal body. Levy therefore believes that the 
 pathogenic action is not an infection, but an intoxica- 
 tion, the proteus splitting the albumins and thus pro- 
 ducing a poison. 
 
 In 1897 Wesenberg 45 observed an outbreak of meat 
 poisoning in Mansfield, in which 63 persons were af- 
 fected after eating chopped meat. The meat was de- 
 rived from a cow slaughtered in an emergency. All 
 who had eaten the meat boiled or roasted remained 
 well. The persons affected had eaten the meat raw. 
 There were no deaths. Examination of the meat 
 showed the presence of proteus bacillus which was 
 highly virulent for test animals. It was shown that 
 the meat became infected after killing; it had been 
 stored in a damp close cellar, and instead of hanging 
 free on hooks, had been piled together, piece on piece. 
 
 Gliicksmann 46 reports the case of father and son who 
 became ill after eating from a piece of half-smoked 
 pork. The father died. Other persons, who had 
 eaten the same meat, but boiled or roasted, remained 
 unaffected. Examination of the smoked meat showed 
 the presence of proteus vulgaris. 
 
52 BACTERIAL FOOD POISONING 
 
 Silberschmidt 4T described an outbreak of meat 
 poisoning affecting 44 persons, one of whom died. 
 The outbreak was traced to the eating of smoked 
 sausages in which large numbers of proteus bacilli 
 were found. While the smoking had not killed the 
 bacilli, it sufficed to hide the disagreeable odor and 
 taste produced by these organisms. Mice and guinea- 
 pigs were killed by feeding the infected sausage; 
 proteus could not be isolated from the organs of these 
 animals, but was found in the intestinal contents. 
 
 In 1900 an outbreak of meat poisoning occurred 
 among the troops in Hannover. According to A. 
 Pfuhl, 48 who observed this outbreak, 81 soldiers were 
 attacked with symptoms of acute gastroenteritis, 
 which, however, soon subsided. The poisoning was 
 caused by a peculiar kind of sausage which, instead of 
 being filled in sausage cases, is packed into jars, making 
 a kind of head cheese. In color, taste, and odor the 
 sausage appeared perfectly normal. The bacteriolog- 
 ical examination, however, disclosed the presence of 
 bacillus proteus. 
 
 In the following year in the same city 34 persons be- 
 came ill several hours after eating this same kind of 
 sausage. The chief symptoms were nausea, profuse 
 diarrhoea, repeated vomiting, and considerable depres- 
 sion. In most of the cases the symptoms subsided 
 within 12 hours. The sausage was examined by 
 Schumburg, 49 who isolated a variety of proteus. When 
 the sausage was fed to mice and rats, the animals died 
 after 24 hours with severe intestinal disturbances. 
 
MEAT POISONING 53 
 
 Proteus bacilli could also be isolated from the organs 
 of these animals. Mice and rats fed with pure cultures 
 of the organism died with symptoms of severe enteritis. 
 
 All observers agree in believing that the meat in- 
 volved in these outbreaks was originally sound, and 
 was derived from sound animals. The proteus infection 
 takes place afterwards, probably because the meat is 
 not properly kept. According to the investigations of 
 Gliicksmann, Silberschmidt, and others, the disease is 
 not merely an infection with proteus bacilli, but also 
 an intoxication with the metabolic products of these 
 organisms. The proteus bacilli ingested with the 
 food multiply in the intestinal tract and produce 
 poisons which give rise to the constitutional symptoms. 
 The intoxication is thus an accompaniment of the in- 
 fection. A general infection, i.e., a flooding of the 
 body with bacteria, is probably very rare. This is 
 indicated by the results of animal experiments. As 
 was stated above, animals infected with proteus die 
 with symptoms of severe enteritis, yet the bacilli are 
 usually not found in the organs. Occasionally the 
 proteus may already have developed its poisonous 
 products in the meat. This, however, is not often the 
 case, for the odor of these putrefactive products would 
 at once excite suspicion (ammonia, hydrogen sulphide, 
 indol, etc.). In most of the outbreaks of meat poison- 
 ing belonging to this group, we are expressly informed 
 that the infected meat or sausage showed nothing ab- 
 normal in taste, odor, or appearance. 
 
 While smoking does not kill the proteus bacillus, as 
 
54 BACTERIAL FOOD POISONING 
 
 can be seen from the case reported by Silberschmidt, it 
 may occasionally hide some little disagreeable odor or 
 taste. Heating for half an hour, to 80 ° C, on the 
 other hand, not only kills the bacillus, but also destroys 
 the poison which it produces. In this respect the 
 proteus poison differs from that produced by B. en- 
 teritidis and B. paratyphi. 
 
 An epidemic of meat poisoning following the eating 
 of potted tongues has recently been reported by 
 Berry. 62a The outbreak occurred not far from Liver- 
 pool in the middle of January, 1908, and affected about 
 170 persons. The symptoms came on 36 hours after 
 eating. In preparing "potted tongue" the tongues 
 were first kept in brine for three or four days, then 
 cooked, and canned while hot. Some of the cooked 
 tongue in question was found to be in a bad state of 
 preservation, and smelled badly. Bacteriological ex- 
 amination disclosed the presence of B. enteritidis and 
 of an organism similar to B. coli. There was some 
 evidence to show that infection of the tongues had oc- 
 curred in the brine. 
 
 It may be mentioned, in passing, that Ohlmacher 59 
 investigated some cases of poisoning due to eating oat- 
 meal, and isolated the bacillus proteus as the cause of 
 the outbreak. 
 
 In addition to the colon and proteus organisms, meat 
 poisoning may occasionally be produced by the hay 
 bacillus (B. subtilis). An instance of this is reported 
 by Lubenau, 50 who observed an outbreak among the 
 inmates of the sanatorium Beelitz, in 1906. About 
 
MEAT POISONING 55 
 
 three-quarters of the 400 inmates and a large part of 
 the help were affected shortly after eating a dish known 
 as " Konigsberger Klops," a kind of meat croquette. 
 This had been served at the noon meal; at about 11 
 o'clock in the evening a large number of persons were 
 suddenly seized with profuse diarrhoea, persistent vom- 
 iting, severe headache, and great prostration. In two 
 or three individuals fever was also present. Most of 
 the cases recovered within three or four days. In a 
 few patients the diarrhoea persisted for several weeks. 
 Bacteriological examination of the meat balls revealed 
 the presence of a bacillus belonging to the hay bacillus 
 group. Grown in milk, this organism produced a 
 strong poison which was pathogenic for young dogs. 
 The dogs suffered from bloody diarrhoea and vomit- 
 ing, and showed a marked loss of weight. The or- 
 ganism, called B. peptonificans, belongs to that group 
 of hay bacilli which produces peptone in milk, and 
 which has been held to be associated with the intestinal 
 disturbances of infants. Investigation showed that 
 the meat balls had been prepared from meat which had 
 been kept in the refrigerator for four days. Then, 
 since it was still fresh, it had beeen parboiled and kept 
 for two more days before using. The boiling had not 
 sufficed to kill the resistant spores of the bacilli, and 
 the temperature in the refrigerator during the last two 
 days had been sufficiently high to allow the spores to 
 develop. 
 
 In view of the extensive distribution of the proteus 
 bacilli, it is curious that this variety of meat poison- 
 
56 BACTERIAL FOOD POISONING 
 
 ing is relatively infrequent. Very likely, however, it 
 is much more frequent than the reports indicate, the 
 rapid course of the poisoning often causing the attack 
 to pass without its nature being recognized. It is cer- 
 tain that the meat of animals slaughtered in an emer- 
 gency is much more to be feared than the meat of sound 
 animals. According to Bollinger four-fifths of the 
 meat poisonings are due to the former. The meat of 
 diseased, especially of septic animals, decomposes very 
 readily, and is dangerous even when only a slight de- 
 gree of putrefaction has taken place. It is probable 
 that the formation of poisonous products which has 
 begun during life, continues after the meat has been 
 dressed. As a rule the more rapid its putrefaction, 
 the more poisonous is the meat. 
 
 Owen 60 has recently reported on an interesting out- 
 break of meat poisoning which occurred in Kalamazoo, 
 Michigan, in 1906, and which embraced nineteen cases. 
 Within a few hours after eating the meat, the pa- 
 tients complained of rapid pulse, fever, and severe 
 abdominal pains, with vomiting and purging. Several 
 had muscular cramps in the legs ; one had convulsions. 
 All the patients made a good recovery in a few days. 
 The suspected meat was dried beef, all obtained from 
 the same butcher, and probably infected in his shop. 
 The meat had a normal odor and appearance, except 
 for a slight greenish tinge often seen in sound meat of 
 this character. Emulsions of the meat were fatal when 
 injected into rats. Careful bacteriological examination 
 revealed a staphylococcus as the probable cause of the 
 
MEAT POISONING 57 
 
 poisoning. This organism was isolated, practically in 
 pure culture, from along the fasciae, but not in the rest 
 of the meat. 
 
 Although no bacteriological examinations were 
 made, the following recent outbreak is reported be- 
 cause it suggests still another source of bacterial in- 
 fections. In a hospital in New York, fourteen out of 
 thirty-eight nurses suddenly became ill three or four 
 hours after eating some minced chicken. The symp- 
 toms were nausea, vomiting, prostration, diarrhoea. 
 All of the patients recovered by morning and were 
 able to attend to their regular duties. The chickens 
 used for preparing the minced chicken had been bought 
 as fresh-killed, though it is probable that some, at 
 least, were cold-storage fowls. They were cooked on 
 Saturday, and the resulting soup was eaten by patients 
 and others without producing any symptoms. Taken 
 out of the soup caldron, they were kept, whole, in the 
 refrigerator until Sunday afternoon, when they were 
 cut up, minced, mixed with chicken " stock " and 
 spices, and served as minced chicken for the evening 
 meal. 
 
 The rapidity with which the symptoms developed 
 point to a preformed poison as the cause of the out- 
 break. It is possible that chickens kept in cold stor- 
 age for some time become poisonous owing to the 
 bacterial changes going on even at that temperature.* 
 
 * The extent of bacterial growth which can take place at 
 o° C. is but little appreciated. This phase of the subject has 
 recently been studied by Pennington, who finds, for ex- 
 
58 BACTERIAL FOOD POISONING 
 
 We know from the investigations conducted in the 
 U. S. Department of Agriculture by Pennington 56a that 
 macroscopically visible degeneration does occur under 
 these conditions. Few bacteriological investigations 
 have been made in this direction,* so that at the pres- 
 ent time it is impossible to say just what role, if any, 
 cold-storage chickens play in the causation of food 
 poisoning. It may not be out of place to call attention 
 to the fact that the cold storage of undrawn chickens, 
 game, etc., is not at all comparable to the keeping of 
 dressed meats, such as beef, veal, pork, mutton, etc., 
 under similar conditions. 
 
 DIAGNOSIS 
 
 The diagnosis can only be definitely established by 
 means of bacteriological examination. For this pur- 
 pose plates should be made from the suspected meat, 
 and animals, preferably mice, infected by feeding. 
 When the poisoning is caused by bacillus proteus, the 
 animals usually die in twenty-four hours with symp- 
 toms of gastroenteritis. The germ can then be isolated 
 from the intestinal contents. It is useless to examine 
 the meat chemically for the presence of ptomains, 
 
 ample, that very clean milk containing originally 300 germs 
 per cc. when kept for 5 or 6 weeks at a temperature slightly 
 less than o° C, contains several hundred million germs per 
 cc. The taste and odor of the milk is not changed by this 
 enormous bacterial development, nor does the milk coagu- 
 late on heating. (See Journal of Biological Chemistry, Vol. 
 IV, 1908, page 353.) 
 * Brown, H. R., 39th Annual Report, Mass- St. Bd. Health. 
 
MEAT POISONING 59 
 
 putrefactive alkaloids, etc., as such an examination 
 yields no conclusive information. The only one compe- 
 tent to properly deal with this material is a trained 
 bacteriologist. 
 
 EVIDENCES OF PUTREFACTION 
 
 It is sometimes difficult to recognize beginning 
 putrefaction. The process commences at the surface 
 and then spreads to the deeper portions. At first the 
 connective tissue is affected, and extension is usually 
 along the fibrous tissue, especially in the neighborhood 
 of a bone or a large vessel. (Schneidemuhl. 4 ) As 
 the process continues, a thick greasy-looking layer is 
 formed and a gradually increasing foul odor is given 
 off. When this has continued for some time, and con- 
 nective tissue and muscle have completely disinte- 
 grated, putrefaction is complete. The cut surface of 
 such meat appears porous, indentations made by the 
 finger persist, the fat, originally yellow, is greenish, 
 the bone marrow is soft, or even fluid, and has a 
 greenish or brownish tint. The foul odor is most 
 marked about the bones and in the fat. This odor is 
 not lost by boiling or roasting the meat. 
 
 In examining meat for evidences of putrefaction it 
 is well to first examine the reaction of the meat to 
 litmus, and so seek to discover the presence of some of 
 the products of putrefaction, such as ammonia. For 
 this purpose it suffices to lay a piece of litmus paper 
 on a freshly cut section of the meat. This test is not 
 always reliable, for corned beef and smoked ham give 
 
6o BACTERIAL FOOD POISONING 
 
 an alkaline reaction even when perfectly sound. Fur- 
 thermore, the alkaline reaction of putrefaction may be 
 masked by the acid products of a fermentation going 
 on at the same time. It is better, therefore, to test for 
 the presence of free ammonia according to the method 
 devised by Eber. Into a test tube about five inches in 
 length, pour about half an inch of a mixture composed 
 of one part pure hydrochloric acid, three parts alcohol, 
 and one part ether. The mixture is shaken and then 
 a clean glass rod, rubbed into the suspected meat, is 
 quickly thrust into the test tube, so that the lower end 
 of the rod is about half an inch from the surface of 
 the fluid. In the presence of ammonia one at once 
 sees gray, bluish, or whitish fumes form about the end 
 of the rod and sink to the surface of the reagent. This 
 test is also not entirely free from objections, for sound 
 corned meat may give a positive reaction owing to the 
 frequent presence of trimethylamin. However, in the 
 presence of other signs of putrefaction, this test serves 
 to confirm the diagnosis. In important cases a bac- 
 teriological examination should always be made. 
 
 PROPHYLAXIS 
 
 In the prophylaxis of this form of meat poisoning, 
 particular attention must be paid to the manner of 
 keeping the meat. When proper facilities for cooling 
 are not available, it is important to eat the meat as 
 fresh as possible. Chopped meat is especially danger- 
 ous. Meat showing evidences of putrefaction should 
 not be eaten. Boiling and roasting or frying the meat 
 
MEAT POISONING 61 
 
 lessens the danger. Special care should be exercised 
 in summer, when most of these outbreaks have been 
 observed. In badly constructed refrigerators putrefac- 
 tion may readily occur. Owing to the lack of venti- 
 lation and the high degree of moisture, the putrefac- 
 tive bacteria may develop in large numbers. It will 
 be recalled that in the outbreak reported by Levy, the 
 B. proteus was isolated from the bottom of the re- 
 frigerator. In order to prevent putrefaction, the re- 
 frigerators should frequently be thoroughly cleansed 
 with hot soda solution. Keeping meat in refrigerators 
 poorly or not at all iced is highly dangerous. Edu- 
 cation of the public on this subject, and rigid inspec- 
 tions of the meat markets by the health authorities 
 are necessary to prevent this form of meat poisoning. 
 Chopped meat should be especially well scrutinized. 
 In view of what has been said above, it would appear 
 advisable to establish a maximum time limit beyond 
 which undrawn poultry could not be kept, even in cold 
 storage. 
 
 TREATMENT 
 
 The treatment of this poisoning is symptomatic, and 
 consists in washing out the stomach, securing free 
 evacuation of the bowels by means of cathartics, and 
 administering stimulants if necessary. Alcohol ap- 
 pears to be especially useful. In general the treatment 
 is that outlined on page 47. 
 
Ill 
 
 MEAT POISONING— (Concluded) 
 SAUSAGE POISONING (Botulism, Allantiasis) 
 
 HISTORICAL, 
 
 This group of meat poisonings, characterized by 
 severe nervous symptoms, is usually spoken of as 
 " sausage poisoning," because most of the cases re- 
 ported followed the eating of sausages. Other forms 
 of food have, however, been implicated, and the causa- 
 tive bacterium, the B. botulinus, was isolated during an 
 outbreak due to poisoning by ham. This bacillus is 
 a strict anaerobe, and the poisonings are therefore ob- 
 served in connection with foods which have been kept 
 hermetically sealed or at least closed so that air is 
 mostly excluded. Furthermore, it is usually found that 
 the implicated articles have been eaten without previous 
 cooking. This includes particularly sausages con- 
 tained in thick sausage skins, to meat pates thickly 
 embedded in fat, to pork insufficiently corned, etc. In 
 most cases the meat used in the preparation of these 
 dishes has been found to have come from perfectly 
 sound animals. Other cases of this form of poisoning 
 have been traced to the eating of canned fish and 
 canned beans. 
 
 The first definite account of sausage poisoning was 
 published by the poet and physician Justinius Kerner 
 
 62 
 
MEAT POISONING 63 
 
 in 1820, who reported on a case occurring in 1793 
 near Wildbad, and on a number of epidemics in various 
 parts of Wurttemberg. The total number of cases in- 
 volved was seventy-six, of which thirty-seven were 
 fatal. (See Ostertag. 2 ) In a second publication in 
 1822, the author reports ninety-eight additional cases 
 with thirty-four deaths. Since that time a considerable 
 number of poisonings have occurred in Wurttemberg 
 after the eating of liver sausage, and a sausage known 
 as " Schwartemagen," although in other countries, 
 particularly in the northern part of Germany, such 
 poisonings are rare. According to Ostertag the reason 
 for this is primarily because of the enormous extent 
 of the sausage industry and of sausage consumption 
 in Wurttemberg (especially as regards these varieties), 
 secondly because of the poor material used, and finally 
 because of the primitive mode of manufacture in vogue 
 at that time. The sausages were usually large in cali- 
 ber, having been filled into pig stomach instead of into 
 small gut. The smoking was therefore usually insuf- 
 ficient. The sausages also contained too much water. 
 Since the methods of manufacture have been improved 
 this form of meat poisoning has been of rare occur- 
 rence in Wurttemberg. 
 
 SYMPTOMS 
 
 The symptoms are very characteristic, and contrast 
 sharply with those seen in the other forms of meat 
 poisoning. Whereas, in the latter the symptoms are 
 mainly gastrointestinal, in botulism they are almost 
 
64 BACTERIAL FOOD POISONING 
 
 wholly referable to the central nervous system (v. 
 Ermengem), and consist of secretory disturbances and 
 symmetrical motor paralyses. The latter, either total 
 or partial, affect especially the muscles supplied by the 
 cranial nerves, hence one sees disturbances of accom- 
 modation, ptosis, double vision, dysphagia, dryness in 
 the mouth and throat due to inhibition of salivary se- 
 cretion, aphonia, obstinate constipation, and reten- 
 tion of urine. In addition there are disturbances in 
 the heart action and in respiration. Fever is absent. 
 Aside from this there are no motor or sensory paraly- 
 ses, and consciousness is unimpaired. Altogether the 
 symptoms remind one strongly of atropine poisoning. 
 As a rule they appear in from twenty-four to thirty- 
 six hours after the infected meal, though sometimes 
 the onset has been within four hours, or again not 
 until the fourth day. Death is not uncommon, and is 
 due to asphyxia of bulbar origin. Many of the other 
 cases take a long course, of weeks or months. Even 
 when the case terminates favorably, disturbances of 
 vision and muscular weakness persist for some time. 
 According to some statistics collected by Senkpiehl, 
 out of 412 cases which occurred from 1789 to 1886, 
 there were 165 deaths, making a mortality of about 
 40%. Autopsy findings are almost entirely negative; 
 usually all that can be seen is some hyperemia of the 
 organs. 
 
 Although no bacteriological examination was made, 
 the following is probably an instance of this form of 
 poisoning. It was reported by Sheppard, 97 in 1907, 
 
MEAT POISONING 65 
 
 and relates to three fatal cases. A party of three went 
 on a camping trip and took with them as part of their 
 rations two cans of pork and beans. About eighteen 
 hours after eating of these beans, all three became ill, 
 the symptoms in all being much the same. " There 
 was," says Sheppard, " an entire absence of the usual 
 gastrointestinal symptoms from first to last, no pain 
 or sensory disturbance and no elevation of tempera- 
 ture. The first complaint was disturbance of vision, 
 diplopia or a mistiness while looking in certain di- 
 rections. Ptosis was present in two of the cases. 
 Thickness of speech and difficulty in swallowing, which 
 later became impossible, were present in all. Difficult 
 breathing was also a constant and common symptom, 
 and a general failure of muscular power; the whole 
 picture being one of a gradually developing motor 
 paralysis. A profuse secretion of mucus in the throat 
 was a source of great distress, as owing to the para- 
 lyzed condition of the throat muscles it was impossible 
 to get rid of it. The pulse until near the end was but 
 little altered, except for a marked quickening on any 
 movement of the body. Temperature was normal or 
 subnormal. Free purgation could not be secured, ow- 
 ing presumably to the paralyzed condition of the in- 
 testines in common with the rest of the body. The 
 kidneys secreted freely an apparently normal urine, 
 but no examination of it was made. The mental con- 
 dition was clear and undisturbed to the last, except 
 for an unnatural irritability shown at times when the 
 patients were making an effort to say something which 
 
66 BACTERIAL FOOD POISONING 
 
 could not be understood." Death occurred on the 
 fourth day. 
 
 Investigation showed that the beans had been pur- 
 chased four months previously, and had been kept, for 
 a time at least, in rather a warm place. This would 
 give infecting bacteria opportunity to develop and pro- 
 duce abundant toxin. That such was the case was 
 shown by feeding what was left of the beans to twelve 
 chickens. Nine of these died, and the other three were 
 made ill. 
 
 ETIOLOGY, 
 
 The cause of sausage poisonings was found by v.' 
 Ermengem 51 to be an anaerobic bacterium which he 
 termed B. botulinus, and which produces a highly pois- 
 onous specific toxin. This organism was discovered 
 in a ham which had caused fifty cases of " sausage 
 poisoning " in Ellezelles in 1895, three of the cases end- 
 ing fatally. The bacillus was found in the intermuscu- 
 lar connective tissue in the form of spores, but was ab- 
 sent in the fat. The same organism were found in the 
 spleen and gastric contents of the fatal cases, though 
 here their number was much smaller. The ham was 
 derived from a hog which appeared perfectly sound; 
 and that this was the case was indicated by the fact 
 that the rest of the pork (eaten fresh), as well as the 
 other ham of the same animal, were eaten without pro- 
 ducing any toxic symptoms whatever. Further inves- 
 tigation showed that the poisonous ham had been 
 corned and had lain on the bottom of the cask covered 
 with brine ; the unaffected ham had been placed on top 
 
MEAT POISONING 67 
 
 of this, but had not been covered. In the latter, there- 
 fore, conditions for anaerobic growth were not fav- 
 orable. The poisonous ham was not putrid, but gave 
 off a marked rancid odor not unlike that of rancid 
 butter. It was also a little discolored, and somewhat 
 softened. Watery extracts of the ham were injected 
 into a number of animals and produced typical symp- 
 toms of botulism. In cats the symptoms consisted of 
 marked mydriasis, disturbances of salivary secretion, 
 various kinds of pareses, drooping of the tongue, 
 aphonia, dysphagia, retention of urine, faeces, and bile. 
 In pigeons there was paralysis of the wings, ptosis, 
 unequally dilated pupils ; in monkeys, guinea-pigs, rab- 
 bits, and mice there were symptoms of general or par- 
 tial paralysis. 
 
 BACTERIOLOGY 
 
 Bacillus botulinus is quite a large organism, having 
 rounded ends, and producing oval spores situated in 
 the end of the bacillus. Motility is slight, and is ac- 
 complished by four to eight very fine peritrichous 
 flagella. The bacillus stains according to Gram, i.e., 
 is Gram positive. It is a strict anaerobe, and grows 
 luxuriantly in glucose agar and bouillon with the de- 
 velopment of gas. The cultures have a rancid smell 
 strongly resembling the odor of butyric acid. The 
 resistance of the spores is relatively slight; cultures 
 containing spores are certainly killed by heating for 
 one hour to 80 ° C. The bacillus does not develop in 
 media containing over 5 to 6% salt; hence it should 
 not develop in properly corned meat, where the brine 
 
68 BACTERIAL FOOD POISONING 
 
 contains 10% salt. Bacillus botulinus produces a 
 strong toxin. Filtered cultures injected into suscep- 
 tible animals such as rabbits, guinea-pigs, mice, cats, 
 and monkeys in doses even as small as o.oooi cc, pro- 
 duce symptoms of paralysis. Larger doses o.i to 0.5 
 cc. are rapidly and intensely poisonous. After an in- 
 cubation period of several hours, the animals are often 
 seized with dyspncea and convulsions, they fall on their 
 sides paralyzed, and die as a result of rapid respiratory 
 paralysis in from one-quarter to half an hour. The 
 greater the dose of toxin, the more rapid and severe 
 the development of the symptoms. There is, however, 
 a minimum beyond which the period of incubation is 
 not affected. No matter how large the dose, this is 
 never less than from six to twelve hours. The symp- 
 toms have the character of a pure intoxication, with- 
 out any multiplication of the bacilli in the body taking 
 place. In contrast to what is seen in most other 
 toxins, the toxin of this bacillus produces its symp- 
 toms not merely after subcutaneous or intravenous 
 injections, but also and especially after feeding per os. 
 In the animals dead after such poisoning, degenera- 
 tion of the ganglion cells of the anterior horn, and of 
 the bulbar centers (motor oculi) are observed. These 
 are the organs which the clinical course of the disease 
 would show were implicated. 
 
 Kempner 52 immunized animals with botulism toxin 
 and succeeded in preparing an antitoxic serum which 
 possessed protective and also some curative power in 
 animal experiments. 
 
MEAT POISONING 69 
 
 Roemer 53 confirms all the above observations. In 
 an investigation in 1900 he isolated B. botulinus from 
 a ham which had given rise to typical symptoms of 
 botulism poisoning in four persons. This ham came 
 from a sound hog, and had been corned. So far as 
 could be learned the ham lay on top, but was covered 
 with brine. After five weeks it was noticed that bub- 
 bles of gas appeared in the brine. The fleshy part of 
 the ham for the most part was normal in color; here 
 and there, however, there were a few bluish-gray 
 areas, softer in consistency and moist. The odor was 
 not putrid, but rather sharply rancid, resembling the 
 odor of butyric acid. No bacilli were found in the 
 fat or in the healthy tissue, either by microscopical or 
 cultural examination. From the discolored areas, 
 however, B. botulinus was isolated, and also two aero- 
 bic bacteria. One of these was a large coccus, the 
 other a bacillus belonging to the hay bacillus group. 
 
 Van Ermengem also found aerobic bacteria associated 
 with the bacillus botulinus, and it is likely that it is 
 this association which enables the latter organism to 
 develop anserobically in the brine. Roemer found that 
 the bacillus does not produce its poison in the living 
 animal body, and that it does not multiply either at 
 the site of injection or in the internal organs, or in 
 the intestine. In other words, it is a saprophyte, and 
 produces the symptoms entirely through the toxin 
 which it produced in the infected meat. Man is poi- 
 soned because the toxin is absorbed from the gastroin- 
 testinal tract. Van Ermengem classes bacillus botu- 
 
70 BACTERIAL FOOD POISONING 
 
 linus with the " pathogenic saprophytes," in order to 
 show that although it cannot develop in the living 
 animal body, it is still pathogenic through the poison 
 which it produces in the infected food. 
 
 DIAGNOSIS, 
 
 The diagnosis of botulism can only be established 
 bacteriologically through miscroscopical examinations 
 of the suspected meat, through anaerobic cultures on 
 glucose agar plates or glucose gelatine, and through 
 animal experiments. The latter will include feeding 
 of the meat to mice, feeding and inoculating watery 
 extracts into rabbits and guinea-pigs, and testing the 
 toxicity of a several days' bouillon culture and of the 
 filtrate from such a culture on these animals. 
 
 PROPHYLAXIS. 
 
 In discussing the prophylaxis of this variety of poi- 
 soning, v. Ermengem advises that such foods as are 
 especially liable to botulinus infection, such as sausages, 
 salt pork, preserved meats, etc., should never be eaten 
 uncooked. In addition to this it is important that all 
 decayed foods whose greasy appearance, rancid or 
 butyric acid-like odor, consistency, or other abnormal 
 constitution excites suspicion, should be destroyed. In 
 corning meat the brine should always contain sufficient 
 salt, at least 10%, for bacillus botulinus cannot de- 
 velop in brine of this concentration. In the manufac- 
 ture of sausages and bologna, only sound meat and 
 organs should be used which have been thoroughly 
 cooked. The gut used for sausage casing should be 
 
MEAT POISONING 71 
 
 carefully cleansed, if necessary, with the addition of a 
 harmless antiseptic. Schilling 5i reports finding pieces 
 of fecal masses, straw, and hairs in such sausage cas- 
 ing. In one meter of gut he found what was equal 
 to 2 to 16 grams fluid faeces. It it well to avoid 
 sausage casing of very large caliber (beef or hog 
 stomach), for then it is difficult to thoroughly smoke 
 the sausages. Attention should be paid to proper 
 smoking. This should be carried out in suitably con- 
 structed chambers, and continuously until the sausages 
 are sufficiently firm and dry. The sausages should not 
 contain more than 30 to 35% water. In countries 
 where sausages are much eaten good results have been 
 achieved by issuing proper instructions to the public 
 concerning the dangers from this form of poisoning, 
 and formulating suitable laws to carry into effect the 
 above recommendations. 
 
 TREATMENT 
 
 The treatment of botulism is essentially sympto- 
 matic, and consists in washing out the patient's 
 stomach, administering stimulants subcutaneously, and 
 employing artificial respiration if necessary. The 
 bowels may be irrigated with hot saline infusions. If 
 available, one may also employ an antitoxic serum. 
 Such a serum possesses some curative value in animal 
 experiments, and it can therefore be employed even 
 after the onset of symptoms. Wassermann has re- 
 cently begun to supply such a serum from the Institute 
 for Infectious Diseases in Berlin. 
 
IV 
 
 POISONING THROUGH FISH AND 
 MOLLUSCS 
 
 FISH POISONING 
 
 These poisonings, too, must be divided into such in 
 which the poison exists in the living animal and such 
 in which the poison develops subsequently. 
 
 True poisonous fish are rare here, and are mostly- 
 observed in tropical countries. Poisoning occurs only 
 when the fish is used for food. In many species, e.g., 
 in the Japanese fish " Fugu," the roe is poisonous, and 
 when eaten by man give rise to choleraic symptoms, 
 paralyses, and convulsions which are rapidly fatal. It 
 is said that if the roe and all ovarian tissue is carefully 
 removed from the fresh fish, no harm follows the 
 eating of the fish itself. The poison is usually not 
 destroyed by boiling. In Germany the roe of barbs 
 (Cyprinus barba) is poisonous when eaten, especially 
 in the month of May, but the symptoms usually ter- 
 minate favorably. It is said that the roe of pike, and 
 the meat of sturgeon {acipenser huso and acipenser 
 Ruthenus), are also poisonous during the spawning 
 season. According to Robert 63 the liver, and espe- 
 cially the bile, of a number of fish is poisonous. 
 
 72 
 
FISH AND MOLLUSC POISONING 73 
 
 CLINICAL TYPES OF CASES 
 
 The greater number of fish poisonings, however, are 
 due to bacterial infection or to intoxication following 
 the eating of diseased fish or of fish whose meat has 
 undergone post-mortem putrefaction. Ulrich 64 de- 
 scribes an outbreak of fish poisoning in Zurich in 1904 
 that of healthy fish. Ulrich found that raw fish, es- 
 the coast. The transportation of the fish had taken 
 some days, and they were kept from twenty-four to 
 thirty-six hours and longer after cooking. The symp- 
 toms were gastroenteric and typhoidal in character, 
 and varied in intensity according to the interval elap- 
 sing from the time of catching the fish until they were 
 eaten. The longer the interval, the severer the symp- 
 toms. Furthermore, it was noticed that some sound 
 fish kept on the same platter as the poisonous ones 
 also become infected, and were fully as dangerous 
 as the latter. Wyss and Silberschmidt were able 
 to isolate the paratyphoid bacillus B. from the blood 
 of two of the persons who died. The blood of 
 the other patients agglutinated this bacillus. It was 
 impossible to determine whether the living fish had 
 been infected with the organism. It may be assumed, 
 however, that the flesh of diseased fish is more suitable 
 for the development of pathogenic bacteria than is 
 which was probably caused by some pike shipped from 
 pecially in summer, contains a large number of bac- 
 teria, particularly members of the colon and proteus 
 groups. Ordinary boiling does not suffice to kill all 
 
74 BACTERIAL FOOD POISONING 
 
 the bacteria, and if the fish is kept for some time after 
 cooking, especially in summer, bacterial multiplication 
 is rapid. When large numbers of bacteria are thus 
 taken with the food, severe gastric disturbances may 
 be produced. In this respect colon infection is much 
 more dangerous than proteus, for with the latter, pu- 
 trefactive changes (putrid odor) soon manifest them- 
 selves, which is not the case in colon infections. The 
 paratyphoid bacillus isolated from the fish grows luxu- 
 riantly in fish meat. Owing to the rapid multiplication 
 of bacteria in cooked fish at warm temperatures, Ulrich 
 regards the eating of fish in summer as dangerous 
 when more than twenty-four hours have elapsed since 
 the cooking. 
 
 In 1906 an outbreak of fish poisoning was reported 
 by Abraham. 65 This embraced twenty-eight cases 
 which developed eighteen hours after eating some 
 pike. The symptoms were fever, intestinal colic, 
 mild diarrhoea, and nausea. After two to three days 
 the fever subsided, the colic and diarrhoea ceased, and 
 the patients were entirely well at the end of a week. 
 The piece of fish that was left over showed nothing 
 abnormal either in color, odor, or taste. The bac- 
 teriological examination made by Neisser disclosed the 
 presence of a bacillus belonging to the paratyphoid 
 group, type Aertryk. This organism produces a toxin 
 which withstands considerable heating. Serum exam- 
 inations conducted on the blood of a number of the pa- 
 tients gave positive results with this bacillus. No 
 such bacilli could be found in the stools of the pa- 
 
FISH AND MOLLUSC POISONING 75 
 
 tients. In this case it was believed that the fish had 
 become infected during life, the bacilli lodging in the 
 flesh, and thus causing the infection in the persons who 
 ate of the meat. In view of the fact that the pike is a 
 voracious feeder, spends considerable time about the 
 mouth of sewers, and also feeds on other cadavers, it 
 is quite conceivable that pathogenic bacteria such as 
 the paratyphoid bacilli may gain entrance into his 
 body. 
 
 In addition to these two forms of poisoning, one 
 meets with cases of fish poisoning whose course is much 
 like that described under botulism. Such cases usu- 
 ally follow the eating of canned fish or lobster when 
 the can has remained standing open for some time. 
 In some instances it is probable that the poison was 
 contained in the mayonnaise dressing. It is not un- 
 likely that the numerous attacks of indigestion follow- 
 ing the eating of lobster salad are in part due to such 
 poisons. 
 
 Severe illness has often followed the eating of crabs. 
 It has been found that poisonous substances sometimes 
 develop in boiled crabs, on standing, even before the 
 appearance of a putrid odor. This is especially true 
 when the animals have been boiled after death 
 (Schneidemuhl 4 ). The symptoms which have been 
 observed with this form of poisoning were lassitude, 
 dragging pains in the back, and painful stiffness in 
 the limbs. 
 
 Convalescence was protracted, sometimes lasting 
 months. 
 
76 BACTERIAL FOOD POISONING 
 
 MUSSEL POISONING 
 
 In 1885 an outbreak of poisoning occurred in Wil- 
 helmshaven following the eating of common mussels 
 (Mytilus edulis) . There was no evidence of putrefac- 
 tion. In most of the cases, the symptoms appeared in 
 from one-quarter to one-half an hour after the meal, 
 and consisted in a feeling of constriction in the throat, 
 itching of the extremities, dizziness, marked weakness. 
 In the fatal cases death occurred in from two to five 
 hours. At the autopsy Virchow constantly found an 
 enlarged spleen, and fatty degeneration of the kidney 
 and liver. Fatal cases of this form of poisoning have 
 been reported by other observers. Brieger succeeded 
 in isolating a poisonous alkaloid which he termed 
 mytilotoxin, and whose action was very similar to 
 that of curare. He found that the poison could be 
 destroyed by boiling with water containing three to 
 five grams of sodium carbonate per liter. It is not 
 known how this poison originates. In most instances 
 it is said that the poisonous mussels came from stag- 
 nant water. Schmidtmann found that sound, non- 
 poisonous mussels placed in the water of the canal from 
 which the poisonous mussels had been derived, acquired 
 toxic properties; and conversely, when the poisonous 
 mussels were kept in the clean water of the bay, they 
 rapidly lost all trace of poison. He therefore as- 
 sumed that bacteria present in the canal water gave 
 rise to the poison in the mussels. Schmidtmann states 
 that poisonous mussels possess a sweetish, nauseating, 
 
FISH AND MOLLUSC POISONING 77 
 
 bouillon odor, while sound mussels have the odor of 
 fresh sea water. Lustig and Zardo isolated two dif- 
 ferent varieties of bacteria from mussels, and found 
 the cultures virulent for animals. They did not es- 
 tablish the identity of these organisms. 
 
 SNAIL POISONING. 
 
 A kind of marine snail, Murex bradatus, has also 
 been the cause of poisonings of this kind. Such an 
 outbreak was reported in 1900, in Isola, by Galeotti 
 and Zardo. 66 Forty-three persons were affected, the 
 symptoms being severe vomiting, hematuria, convul- 
 sions, paralyses, and diarrhoea. In some of the severest 
 cases constipation was observed. Five of the persons 
 died, and the autopsy revealed the presence of nu- 
 erous haemorrhages scattered through the subcutane- 
 ous connective tissue, the muscles, serous membranes, 
 and heart. There was also fatty degeneration of the 
 liver, heart, and kidneys. From a number of the other 
 snails captured in the same locality the observers iso- 
 lated a bacillus related to the bacillus of hemorrhagic 
 septicaemia. This organism was highly virulent and 
 was toxic even in feeding experiments. Animals 
 killed in this way exhibited pathological changes very 
 like those found in the human autopsies. Investiga- 
 tion showed that this bacillus was probably a common 
 normal inhabitant of the molluscs in those waters, 
 and that it in some way acquired pathogenic properties 
 for humans. 
 
 It must not be forgotten, however, that many of 
 
78 BACTERIAL FOOD POISONING 
 
 these mussel and sea snail intoxications are due to 
 changes caused by proteus and other putrefactive bac- 
 teria. 
 
 POISONING THROUGH OYSTERS 
 
 Oysters have also frequently been the cause of in- 
 toxications, especially when the oyster beds are located 
 near the mouths of sewers, or when the oysters are 
 fattened in such waters. According to Bardet, prac- 
 tically all oysters are diseased during the summer 
 months. Furthermore, oysters very readily spoil, and 
 the eating of such oysters is very dangerous. The 
 symptoms produced vary considerably. Sometimes the 
 poisoning takes the form of an urticaria, sometimes 
 that of a severe gastroenteritis, and fatal cases running 
 a course like that of botulism have been described. The 
 bacteriological investigations which have been made 
 in these cases have not yielded definite results. Ty- 
 phoid fever and cholera may also be spread by the eat- 
 ing of infected oysters, especially when the waters 
 from which the oysters come are polluted by sewage. 
 A number of outbreaks of typhoid fever, or a disease 
 resembling this, have been traced to the eating of 
 oysters, but in only very few instances was the typhoid 
 bacillus really demonstrated. On the other hand, 
 bacillus coli has repeatedly been found in oysters, and 
 this has been taken as indicating fecal pollution. Other 
 authors have interpreted this quite differently, saying 
 that colon bacilli are a common normal inhabitant of 
 these shell fish. Bacilli belonging to the proteus group 
 have also been demonstrated in oysters, and Vivaldi 
 
FISH AND MOLLUSC POISONING 79 
 
 and Rodella 67 isolated a bacillus resembling B. coli, 
 and belonging to the group of capsule bacilli. This 
 was pathogenic for humans. It is absolutely necessary 
 that oyster beds be located only where fecal contami- 
 nation from sewers, etc., can be excluded. Furthermore, 
 it is important that oysters, clams, and other shell fish 
 be eaten only when fresh. Travelers should be par- 
 ticularly careful, especially in southern countries, for 
 many a person has become infected with typhoid fever 
 or suffered from some grave intestinal disorder by the 
 indiscriminate eating of shell fish while traveling. 
 One should always hesitate when the oysters are of- 
 fered at especially low prices, for this is often merely 
 a means of disposing of stale or otherwise undesirable 
 wares. Attention should be paid to signs indicating 
 dead oysters (gaping shell), and to indications of 
 putrefaction (discoloration and softening, with a black 
 ring on the inner side of the shell. Vagedes 68 ). 
 Poisoning through oysters is especially frequent dur- 
 ing the summer months, whence comes the custom of 
 eating them only during months whose names con- 
 tain an R. 
 
 TREATMENT 
 
 The treatment of these poisonings does not differ 
 in general from that outlined under meat poisoning 
 on page 47, and under botulism on page 71. Cases 
 running a typhoidal course should be treated exactly 
 like typhoid fever, and the same precautions should be 
 observed. 
 
V 
 
 POISONING THROUGH CHEESE 
 
 CLINICAL TYPES OF CASES 
 
 Poisoning due to the eating of infected cheese has 
 been reported repeatedly. The ordinary symptoms are 
 diarrhoea and vomiting, and in severe cases vomiting 
 of blood, rectal tenesmus, collapse. In some instances 
 there were disturbances of vision, or taste, dryness in 
 the throat, obstinate constipation, etc., symptoms, in 
 other words, much like those of botulism. As a rule 
 nothing peculiar was noted about the taste of the 
 cheese, except that it was sometimes somewhat bitter. 
 The cause of this form of poisoning was formerly 
 believed to be a poisonous alkaloid discovered by 
 Vaughan, and termed by him tyrotoxicon. But re- 
 cent investigations have repeatedly shown bacteria to 
 be the cause of such poisonings. In an outbreak de- 
 scribed by Vaughan and Perkins, 69 twelve persons 
 became ill three to six hours after eating, with nausea, 
 vomiting, pains in the abdomen, and threatened heart 
 failure. Some of the patients had dilated pupils and 
 some even were delirious. The authors were able 
 to isolate a bacillus from the suspected samples, and 
 found this to be pathogenic for the ordinary laboratory 
 
 animals. The bacillus produced a strong toxin. By 
 
 80 
 
POISONING THROUGH CHEESE 81 
 
 mistake a patient was injected with ten drops of a steril- 
 ized culture of the bacillus in milk. Within thirty- 
 minutes the patient complained of dizziness, vomited 
 freely, and had severe diarrhoea. Two hours after the 
 injection he was almost entirely deaf, and delirious; 
 and after another hour the patient became stuporous, 
 with cold feet and hands, and imperceptible pulse. 
 After injections of strychnine the patient gradually 
 recovered, so that within twelve hours after the onset 
 all threatening symptoms had passed. It was two days, 
 however, before the patient was again able to move 
 about the room. Curiously, guinea-pigs withstood 
 much larger doses of this poison than ten drops. In 
 fact, it required I to 2 cc. of the poison to produce 
 toxic symptoms. The poison resisted heating to some 
 extent. Fifteen minutes' heating to ioo° C. did not 
 entirely destroy its toxicity. The bacillus, on the other 
 hand, was easily killed at much lower temperatures, 
 and sterilization of the milk therefore inhibits further 
 production of the poison. 
 
 According to Hoist, 70 a cheese known as " Knet- 
 kase," often produces attacks of acute gastroenteritis. 
 The cause of this illness was found to be a bacillus 
 related to the colon bacillus. This organism is very 
 highly virulent for rabbits and calves, and seems to be 
 similar to the bacillus of calf dysentery, described by 
 Jensen. The cheese may become infected in a number 
 of ways. The organism may reach the cheese through 
 uncleanliness of the persons engaged in its manufac- 
 ture, especially during the kneading process, or during 
 
82 BACTERIAL FOOD POISONING 
 
 the handling in transportation, or the bacillus may have 
 gotten into the milk by being derived from a cow suf- 
 fering from some diarrhceal infection. Gaffky, for 
 example, has shown that diarrhceal disease in man may 
 be due to the drinking of milk from a cow suffering 
 from diarrhoea. 
 
 Pfliiger 71 described an outbreak of poisoning in 
 which intense colicky pains, vomiting, diarrhoea with 
 great prostration, etc., developed suddenly twelve 
 hours after the persons had eaten some sour cheese. 
 In some of the cases there were also disturbances of 
 vision, diplopia, dryness of the mouth, dysphagia, and 
 other symptoms resembling those of botulism. It is 
 possible that anaerobic bacteria similar to the B. botu- 
 linus are concerned in this form of cheese poisoning, 
 but so far no investigations in this direction have been 
 reported. 
 
 OTHER BACTERIA ASSOCIATED WITH CHEESE POISONING. 
 
 In an outbreak of suspected cheese poisoning, Pep- 
 pier 72 isolated organisms identical with the bacilli of 
 swine erysipelas. According to recent investigations, 
 these bacilli can give rise to serious intestinal dis- 
 turbances in man. Furthermore, tubercle bacilli have 
 repeatedly been found in cheese, though their signifi- 
 cance in the etiology of human infections is still open 
 to question. According to Heim, 73 other pathogenic 
 bacteria, such as cholera or typhoid, which may chance 
 to get into cheese, usually die off within a few days. 
 
 In order to emphasize the importance of bacterio- 
 
POISONING THROUGH CHEESE 83 
 
 logical examinations in all these poisonings, the fol- 
 lowing account of a careful but disappointing chemical 
 examination may not be amiss. 74 A piece of cheese to 
 which decided toxic symptoms were correctly ascribed 
 by Dr. Lartigau, was sent to Professor Gies for exam- 
 ination. The symptoms were similar to those given 
 by Vaughan and Novy for poisonous cheese. A por- 
 tion of the cheese was therefore extracted and ex- 
 amined for tyrotoxicon by Vaughan's method, with 
 negative results. A portion of the extract was ex- 
 amined for proteins. The greater portion of the solu- 
 ble protein in the extract was found to consist of 
 deuteroproteose, with some peptone. After precipitat- 
 ing the proteose with alcohol, the filtrate yielded on 
 evaporation relatively large amounts of leucin and 
 tyrosin. It also contained some tryptophan. The un- 
 used residues, solid and liquid, were combined and 
 examined by the Stas-Otto method for alkaloidal sub- 
 stances, with negative results. The authors conclude 
 that " in all probability the poisonous matter in this 
 particular case consisted of toxic proteose, although 
 this was not suspected until practically all of the ma- 
 terial had been used up. The seeming certainty that 
 ptomaines were responsible for the symptoms noted 
 had been entirely misleading." 
 
 TREATMENT 
 
 The treatment of these poisonings is entirely symp- 
 tomatic, and depends on the clinical type of case. (See 
 pages 47 and 71.) 
 
VI 
 
 POISONING THROUGH ICE CREAM AND 
 PUDDINGS 
 
 HISTORICAL. 
 
 Poisoning due to the eating of vanilla sauce or va- 
 nilla ice cream is remarkably frequent. The symptoms 
 usually come on within one and one-half or two hours, 
 and consist in severe vomiting, pains in the stomach 
 and abdomen, diarrhoea, and signs of collapse. At one 
 time pharmacologists ascribed the poisonous action to 
 the vanilla used for flavoring, but during an outbreak 
 of this form of poisoning in 1898, M. Wassermann 75 
 was able to demonstrate that a bacterial intoxication 
 was involved. The poisonous dish contained milk, 
 eggs, sugar, and vanilla-sugar (10 grams sugar con- 
 taining 20'% vanilla). The dish was prepared in the 
 evening, and was then kept, uncovered and at room 
 temperature, in the pantry until the following noon. 
 Neither the vanilla nor the vanillin produced any 
 symptoms when tested in animals. It was found, how- 
 ever, that vanillin, the active principle in the vanilla 
 sugar, through its reducing action, favors the growth 
 of anaerobic bacteria. We know that milk often con- 
 tains bacteria which require anaerobic conditions, are 
 pathogenic for man, and withstand considerable heat- 
 
POISONING THROUGH ICE CREAM 85 
 
 ing. Under these circumstances we can understand 
 that in the preparation of a pudding such as that de- 
 scribed, we have conditions altogether favorable for 
 the development of these bacteria and the production 
 of their poisons. 
 
 Vaughan, 70 in studying an outbreak of poisoning 
 due to the eating of vanilla ice cream, also proved that 
 the vanilla employed was harmless. The milk used 
 for making the ice cream was fresh, and some lemon 
 ice cream made from the same lot of milk was abso- 
 lutely harmless. The custard mixture used for both 
 kinds of ice cream was prepared in one lot, and then 
 divided into two portions. One was flavored with 
 vanilla, the other with lemon. According to the in- 
 vestigations of Wassermann, the different behavior 
 of the two kinds of cream is to be explained by the 
 fact that vanillin favors the growth of anaerobic bac- 
 teria, while lemon extract even acts as an antiseptic. 
 
 In studying an outbreak of poisoning in 1895, fol- 
 lowing the eating of ice cream, Vaughan isolated the 
 same colon-like bacillus already mentioned in the out- 
 break of cheese poisoning. 
 
 BACTERIOLOGY 
 
 In recent years paratyphoid bacilli have been demon- 
 strated as the cause of poisoning through farinaceous 
 puddings. As already stated, Fischer 25 pointed out 
 the role played by milk in spreading paratyphoid in- 
 fection. In 1904, Vagedes " observed an outbreak of 
 poisoning in Berlin, which he traced to the eating of 
 
86 BACTERIAL FOOD POISONING 
 
 farina pudding. There were seven cases in all, and 
 the symptoms, which came on within a few hours after 
 eating the pudding, consisted of intestinal catarrh ac- 
 companied by fever and copious diarrhoeas. One of the 
 cases ended fatally, and showed merely a distinct 
 swelling of Peyer's patches. The bacteriological ex- 
 amination of the blood-tinged stools and mucus 
 showed the presence of paratyphoid bacilli type B. 
 The same organism was isolated from the spleen, liver, 
 and kidney of the fatal case. In cultures this organ- 
 ism produced a strong poison which was quite resist- 
 ant to heat. The serum of the patients agglutinated 
 this bacillus ; in fact, seven months after the attack the 
 serum of one of the patients still showed agglutinating 
 power. Typhoid bacilli were also agglutinated by the 
 serum of these cases, but only in much more concen- 
 trated dilutions. It was impossible to find these para- 
 typhoid bacilli in the food because nothing was left to 
 examine. Nevertheless all the clinical, epidemiolog- 
 ical, and bacteriological data pointed strongly to the 
 farina pudding as the cause of the poisoning. The 
 pudding was prepared with farina, zwieback, apples, 
 milk, sugar, vanilla powder, and three duck eggs. 
 How the bacilli got into the pudding could not be as- 
 certained. It was shown that neither the milk, vanilla 
 powder, nor the zwieback were infected. Perhaps the 
 duck eggs were to blame, for an examination of a num- 
 ber of other duck eggs shows that some of them con- 
 tained a considerable number of bacteria. It is prob- 
 able that decomposed eggs may also lead to poisoning, 
 
POISONING THROUGH ICE CREAM 87 
 
 for eggs constitute an admirable medium for the 
 growth of bacteria, and of course for typhoid and para- 
 typhoid bacilli. Moreover, Lange 78 has pointed out 
 that bacteria are able to penetrate the intact shell and 
 so reach the egg yolk. Naturally this is still more 
 liable to occur when the shell is cracked. It is well to 
 bear in mind that eggs may be the carriers of infection 
 in these cream and pudding poisonings. 
 
 An outbreak of poisoning is reported by Cursch- 
 mann 2T in which twenty-two persons were taken ill 
 after eating a pudding composed of milk, eggs, sugar, 
 gelatine and vanilla, and served with raspberry sauce. 
 The milk had previously been boiled ; the pudding had 
 been prepared the evening preceding the meal, and had 
 been kept in a cool place. When eaten there was noth- 
 ing whatever about taste or odor to excite suspicion. 
 All those who ate of the pudding were attacked in five 
 to six hours with severe abdominal pains, vomiting, 
 and diarrhoea; usually there was also high fever and 
 rapid pulse. Some of the patients were drowsy. There 
 was no enlargement of the spleen. One of the cases 
 ended fatally in collapse, and came to autopsy. Marked 
 inflammatory changes were found in the stomach, and 
 to some extent also in the intestine. There was also 
 some change in the kidney parenchyma. 
 
 From the remains of the pudding, and from the 
 stools of several of the patients, as well as from the 
 liver of the fatal case, Curschmann was able to isolate 
 a bacillus belonging to the enteritidis group; this or- 
 ganism was virulent for mice. It was impossible to 
 
88 BACTERIAL FOOD POISONING 
 
 learn how the bacillus had gotten into the pudding, 
 or which ingredient had carried the infection. The 
 vanilla was free from such bacteria ; there was no more 
 of the milk left to examine ; Curschmann believed that 
 in some unknown way the pudding had become in- 
 fected between the time of making and of eating. 
 Since we know practically nothing concerning the oc- 
 currence of enteritidis bacilli in nature outside of the 
 animal body, it is impossible to say anything more 
 concerning the spread of such infections. 
 
 In 1905 Levy and Fornet 79 studied an outbreak of 
 illness affecting seven persons in Strassburg. The pa- 
 tients were attacked with vomiting and severe diar- 
 rhoea, in some there were also a typhoid roseola and 
 enlargement of the spleen. The authors were able 
 to isolate paratyphoid bacilli, type B., from the stools 
 of all the patients. The symptoms appeared almost 
 simultaneously in all the members of the family, and 
 there is no doubt that the infection was due to food. 
 Investigation showed that only two articles of food 
 could be implicated, namely, some liver sausage and 
 some vanilla farina pudding. Examination of the liver 
 sausage failed to show any paratyphoid bacilli, and 
 there was nothing left of the pudding to examine. Ex- 
 amination of the farina itself and of the vanilla beans 
 yielded negative results. 
 
 It thus appears that the paratyphoid bacillus B. 
 plays an important part not only in meat poisonings, 
 but also in other food poisonings. Thus far, however, 
 we have absolutely no information concerning the man- 
 
POISONING THROUGH ICE CREAM 89 
 
 ner in which the bacilli get into the foods. It is sug- 
 gestive that almost always the suspected foods have 
 contained milk and vanilla. We may recall that 
 Fischer 41 in studying an outbreak of paratyphoid in- 
 fection in Futterkamp found that this was due to the 
 drinking of milk from cows suffering from gastroen- 
 teritis. He also isolated the paratyphoid bacillus from 
 the milk of these animals. In the paratyphoid infec- 
 tions associated with the eating of farina puddings, 
 we may therefore assume that the milk was probably 
 the carrier of the infection. E. Klein 80 inoculated 
 thirty-nine specimens of milk into guinea-pigs, using 
 the sediment from 300 cc. of milk. In ten of the 
 specimens the inoculation produced little foci of pus 
 in the spleen of the animals, and further examination 
 revealed the presence of bacillus enteritidis in these 
 foci. Feeding a milk culture of these bacteria to 
 guinea-pigs killed half of the animals in five days. As 
 far as could be ascertained none of the cows yielding 
 this milk were ill. 
 
 We have already called attention to the occurrence 
 of bacilli of the paratyphoid group in the intestines of 
 normal animals. It is obvious that such bacilli, when 
 they are discharged in the faeces, especially about a 
 dairy barn, can quite readily find access to the milk. 
 (See also Cheese Poisoning, page 85.) 
 
 PROPHYLAXIS 
 
 So far as the prophylaxis against this form of food 
 poisoning is concerned, very few positive statements 
 
go BACTERIAL FOOD POISONING 
 
 can be made. Certainly all such puddings, etc., should 
 be thoroughly boiled, and, after rapid cooling, should 
 be eaten soon after cooking. If they are to be kept 
 over for some time, they should be carefully covered, 
 and then placed in a cool place, preferably on ice. 
 
 TREATMENT 
 
 (See remarks on page 83.) 
 
VII 
 POTATO POISONING 
 
 HISTORICAL 
 
 Large outbreaks of poisoning through potatoes and 
 potato salad seem to be of frequent occurrence among 
 troops. Schmiedeberg 81 reports on an outbreak which 
 occurred in 1892, in which 357 members of one bat- 
 talion were attacked with frontal headache, severe 
 colicky pains in the stomach and abdomen, vomiting, 
 diarrhoea, prostration, and slight delirium. In a few 
 of the cases the symptoms were quite threatening, 
 cyanosis of the lips, markedly dilated pupils, syncope, 
 rapid pulse, etc. In the severe cases there was some 
 rise in temperature. Investigation pointed to new po- 
 tatoes as the cause of the outbreak. 
 
 About the same time a similar outbreak occurred in 
 a battalion belonging to an entirely different garrison. 
 Ninety men were suddenly attacked with frontal head- 
 ache, abdominal pains, diarrhoea, prostration, and diz- 
 ziness. Some of the patients had a little rise in tem- 
 perature, but none had any dilatation of the pupils 
 or increased frequency of the pulse. The probable 
 cause of the outbreak was believed to be potatoes. 
 Although somewhat soft and watery, the potatoes 
 were generally quite ripe. 
 
 91 
 
92 BACTERIAL FOOD POISONING 
 
 In 1893 a third outbreak of this form of poisoning 
 was reported from still another garrison, in which 
 125 men were affected with symptoms like those just 
 enumerated. All the persons made a good recovery. 
 
 Schmiedeberg also cites an outbreak described by 
 Cortial, occurring in Lyons, in July, 1888. This like- 
 wise occurred among the soldiers and affected 101 
 individuals. The main symptoms were prostration, 
 colicky pains, diarrhoea, fever, and headache. Some 
 of the cases had dilated pupils. The outbreak was 
 ascribed to the eating of potatoes, both new and old 
 sprouting ones. After the delivery of new potatoes 
 was stopped, no more cases occurred. A dog that had 
 eaten three times of these potatoes suffered from diar- 
 rhoea for a week. None of the cases in this outbreak 
 ended fatally. 
 
 In 1898, E. Pfuhl 82 reported an outbreak of poison- 
 ing among some soldiers. There were fifty-six cases, 
 and in almost all of them the symptoms began a few 
 hours after dinner. Most of the patients had chills, 
 fever, headache, severe abdominal pains, diarrhoea, 
 nausea, drowsiness, lassitude, and some complained of 
 a scratchy feeling in the throat. The pupils were not 
 dilated, and the fever lasted only for about three days, 
 dropping by crisis. The outbreak was ascribed to the 
 eating of salted potatoes. 
 
 SOLANIN POISONING 
 
 At one time all these cases were regarded as in- 
 stances of solanin poisoning. Schmiedeberg, however, 
 
POTATO POISONING 93 
 
 pointed out that this could be accepted only when the 
 potatoes could be shown to contain sufficient solanin 
 to produce symptoms of intoxication. According to 
 the investigations of Meyer 83 the solanin content of 
 potatoes in December and January is 0.04 g. per kilo 
 of unpeeled potatoes, in March and April it rises to 
 0.08 to 0.096 g., and in May, June and July to 0.100 
 to 0.1 16 g. The amount of solanin, however, which 
 is necessary to produce poisoning is stated by Clarus 
 to be 0.2 to 0.4 g., so that the amount contained even 
 in a whole kilogram of potatoes is insufficient to pro- 
 duce the symptoms described. 
 
 This question has been carefully studied by Wint- 
 gen. 84 In his extensive investigations he found large 
 fluctuations in the solanin content of sound potatoes 
 (0.017 to 0.08, g. per kilo), but the quantity was 
 always small. When the potatoes were stored for some 
 time, even when they sprouted, no increase in solanin 
 was observed provided the sprouts were carefully re- 
 moved. On the other hand, in diseased potatoes and 
 such as are vigorously sprouting, the solanin content 
 may be considerably higher. Thus Meyer found 0.58 
 g. per kilo, in the little dwarf potatoes which had de- 
 veloped from the sprouts of old potatoes, and in old 
 potatoes which were much shrunken and discolored 
 near the margins, he found as high as 1.34 g. solanin 
 per kilo. Wintgen was unable to discover any marked 
 difference in the solanin content of sound and diseased 
 potatoes. The distribution of solanin in the potatoes is 
 not at all regular; in the peel the amount is very 
 
94 BACTERIAL FOOD POISONING 
 
 high, and toward the center of the potato the amount 
 constantly decreases. Weil 85 stated that the quantity 
 of solanin in the potato increases under the action of 
 bacteria, and claimed to have isolated from diseased 
 potatoes, two species of bacteria which possessed this 
 power. Wintgen, however, was unable to confirm this 
 statement. 
 
 Poisoning with potatoes rich in solanin differs some- 
 what from poisoning with pure solanin. In the former 
 there are acute gastrointestinal symptoms and fever, 
 in addition to the symptoms observed in pure solanin 
 poisoning. The reason for the occurrence of these 
 symptoms in the former condition is because the swol- 
 len starch hinders the rapid absorption of the poison, 
 giving the alkaloid time to reach the lower part of the 
 intestinal tract, where it causes more or less marked 
 diarrhoea in addition to the vomiting. 
 
 In the outbreak described by Pfuhl, 82 the peeled, raw 
 potatoes contained 0.38 g. solanin per kilo, and the 
 peeled boiled ones, 0.24 g. The soldiers eating a large 
 portion (1 kilo) of potatoes thus took up 0.30 g. sola- 
 nin, a quantity which is sufficient to produce consider- 
 able toxic disturbances. These quantities of solanin, 
 however, are very unusual, and one is not justified in 
 charging an outbreak of potato poisoning to the solanin 
 unless careful examination shows that the solanin con- 
 tent was actually very high. As a matter of fact, these 
 examinations have hardly ever been carried out. 
 
POTATO POISONING 95 
 
 BACTERIA ASSOCIATED WITH POTATO POISONING 
 
 It is extremely probable that bacterial decomposi- 
 tion of potatoes by proteus bacilli, an observation first 
 made by Dieudonne, 89 is a much more frequent cause 
 of potato poisoning. During an encampment at Ham- 
 melburg, in August, 1903, 150 to 180 soldiers suddenly 
 became ill two hours after dinner with severe and re- 
 peated vomiting, headache, intense diarrhoea, more or 
 less marked symptoms of collapse, slight cramps in 
 the legs, etc. There was no fever. The symptoms be- 
 gan to subside after seven hours, except in a few cases, 
 where there was slight delirium, symptoms of collapse, 
 and convulsions. All of the cases, however, recovered. 
 The outbreak was ascribed to potato salad, and this 
 was accordingly examined bacteriologically, disclosing 
 the presence of numerous proteus bacilli. Mice fed 
 with the salad died in twenty-four hours with severe 
 gastrointestinal symptoms ; when examined at autopsy, 
 only a few bacilli were found in the organs. Bouillon 
 cultures of the bacilli thus isolated were not virulent 
 for test animals ; but when sterile potatoes were inoc- 
 ulated with the organisms, and grown for twenty-four 
 hours at 37 C, a highly poisonous culture was ob- 
 tained. Mice fed with this culture died in twenty-four 
 to forty-eight hours. If the potato cultures were grown 
 at 10 to 12 C, the resulting culture was unable to 
 kill mice. This shows that this proteus bacillus pro- 
 duced poisons on the potato, but only at high temper- 
 atures. Furthermore, the bacillus was not directly in- 
 
96 BACTERIAL FOOD POISONING 
 
 factious or toxic, but only indirectly through the toxic 
 substances produced from the potato. 
 
 It was impossible to learn how the bacilli got into 
 the potatoes, though it was perhaps from the hands of 
 the persons who did the peeling. The potatoes used 
 for the salad were new and tender, but they had been 
 boiled the night preceding the meal, then peeled, and 
 kept until the next day in two large baskets in a room 
 adjoining the camp kitchen. The weather during the 
 night and on the next morning was sultry, a fact which 
 favored the growth and development of the germs. 
 The potatoes used in making the salad were examined 
 for solanin content, but this was found to be low, 
 0.021 g. per kilo. The potatoes did, however, contain 
 considerable water, and this favored their decomposi- 
 tion. 
 
 It is interesting to know that such poisonings have 
 been rather frequent when the potatoes have been 
 cooked and peeled on one day and then kept in large 
 containers until made into salad on the next. In the 
 summer this poisonous decomposition can take place 
 with great rapidity, as is shown by the following in- 
 teresting outbreak. In a certain battalion of troops 
 the members of one company became ill after eating 
 potato salad which had been standing for two hours, 
 while several other companies, two hours previously, 
 had eaten from the same lot of salad without any 
 injurious effect whatever. These two hours, therefore, 
 sufficed for the formation of the poisonous products. 
 
 It is very probable that many of the potato poison- 
 
POTATO POISONING 97 
 
 ings formerly described were not due to solanin, but 
 to bacterial decomposition. As has already been 
 pointed out, solanin poisoning can only then be as- 
 sumed to have occurred when large quantities of this 
 alkaloid can be demonstrated in the potatoes. Be- 
 sides proteus other bacterial infections are probably 
 carried by potatoes. Both typhoid and paratyphoid 
 bacilli are known to grow very well on potato. These 
 bacilli may get into the potatoes on the farm, or the 
 potatoes may subsequently be infected by the infected 
 hands of a bacillus carrier. In studying an outbreak 
 of potato poisoning, therefore, the bacteriological ex- 
 amination should include a careful search for typhoid 
 and paratyphoid bacilli. The technique of this exam- 
 ination has already been outlined on page 38. 
 
 PROPHYLAXIS 
 
 Prophylaxis against this form of poisoning consists 
 in using the potatoes as soon as possible after cook- 
 ing, and not to keep them over from one day to the 
 next, especially in summer. Almost all the outbreaks 
 of potato poisoning reported have occurred in July 
 and August, and usually after the use of new potatoes. 
 Owing to their larger content of water, these potatoes 
 decompose much more readily than old ones. In order 
 to guard against solanin poisoning, it is wise to cut out 
 all sprouts, and to carefully peel the potatoes. It is im- 
 portant that the kitchen help in all large institutions 
 (barracks, hospitals, hotels, etc.) be frequently ex- 
 amined by physicians in order to exclude bacillus car- 
 
98 BACTERIAL FOOD POISONING 
 
 riers from this work. Furthermore, it is essential to 
 insist on absolute cleanliness on the part of all who 
 have the handling of the food. Since the typhoid and 
 paratyphoid bacilli thrive readily on potato, infection 
 with these germs, in the way just indicated, may not 
 be at all uncommon. 
 
 TREATMENT 
 
 Treatment of potato poisoning is symptomatic, and 
 consists in administering cathartics and stimulants, and 
 in washing out the stomach. (See page 47.) 
 
VIII 
 POISONING THROUGH CANNED GOODS 
 
 CANNING AND THE DESTRUCTION OF BACTERIA, 
 
 As the use of canned goods becomes more and more 
 extensive, poisonings of this kind are increasingly fre- 
 quent. This is especially true of canned meat, fish, and 
 vegetables. In the process of canning, the can with its 
 contents is heated in an autoclave for one-half to one 
 hour at 112 to 120 C. The cans are made of thin 
 sheet iron coated with tin. The seams are pressed, 
 and soldered with a thin coating of solder. The cans 
 are filled with the cooked meat or vegetables, the cover 
 is put on and then the whole is sterilized in the auto- 
 clave. It is true that practically all bacteria are killed 
 by the temperature employed, but sometimes the appa- 
 ratus does not work properly, or there is some other 
 slip, and then bacteria subsequently develop. With 
 this, of course, comes the development of putrefactive 
 products. When this is accompanied by the formation 
 of gas, the top of the can presents a convex appear- 
 ance (technically called a "blown" can), a sign of 
 warning to the consumer. On opening such a can a 
 foul-smelling gas escapes. 
 
 CANNED MEATS : CLINICAL TYPES OF CASES 
 
 Poisonings due to canned meats have been reported 
 quite frequently. Thus Bochereau 88 reports a number 
 
 99 
 
ioo BACTERIAL FOOD POISONING 
 
 of such instances occurring among the troops of the 
 French army. The nature of these is rendered very 
 probable by the statement that of 21,151 cans examined, 
 more than fifty were more or less " blown " and de- 
 composed. Canned fish is also frequently the cause of 
 poisoning, and this seems to occur especially with 
 canned salmon, particularly when the fish is not eaten 
 directly after the can is opened. We have already 
 pointed that fish constitute a splendid medium for the 
 development of bacteria, and so may easily become 
 the carriers of bacterial poisons. The symptoms ob- 
 served with poisoning by canned meat or fish are the 
 same as have already been described under meat poi- 
 soning, and are either gastrointestinal or nervous 
 (botulism) in character. 
 
 An instance in which canned pork and beans pro- 
 duced three fatal cases of poisoning of the botulism 
 type has been reported by Sheppard. 97 (See page 64.) 
 
 CANNED VEGETABLES 
 
 In recent years a number of outbreaks of poisoning 
 have been reported following the eating of canned 
 vegetables. In Darmstadt, in 1904, such an instance 
 occurred in a cooking school, twenty-one persons be- 
 coming ill after eating bean salad. Eleven of these 
 died. According to A. Fischer 89 the symptoms ap- 
 peared twenty-four to forty-eight hours after the meal, 
 and showed the typical characteristics of botulism. (See 
 page 64.) Thus there were disturbances of vision, 
 ptosis but no mydriasis, dysphagia, various motor 
 
POISONING THROUGH CANNED GOODS 101 
 
 paralyses, mostly bilateral, increased frequency of 
 pulse, etc. On the other hand, gastrointestinal dis- 
 turbances, fever, sensory and mental disturbances were 
 entirely absent. Death occurred with symptoms de- 
 noting bulbar paralysis, in two to fourteen days after 
 the poisoning. The autopsy disclosed the usual signs 
 of asphyxia, and hypersemia and submucous hsemor- 
 rhages of the lower part of the intestines. Otherwise 
 there was nothing peculiar. The cases which recovered 
 had a very slow convalescence. The beans used for the 
 salad had been canned by one of the cooks of the school, 
 who herself was one of those poisoned. On opening 
 the can a peculiar rancid odor, somewhat resembling 
 that of Parmesan cheese, had been noticed, but as there 
 were no signs of decomposition, nothing more was 
 thought of this. The beans were very tender, " soft 
 as butter," and were therefore not further cooked, the 
 salad being prepared after merely rinsing the beans 
 under the faucet. It was remarked that the rancid 
 odor increased after the salad had stood a while. Only 
 those who ate of the salad were poisoned. 
 
 In studying the cause of this outbreak, Landmann 90 
 examined some of the salad left over, and extracted 
 this with physiological salt solution. After passing 
 the extract through a Berkfeld filter the sterile filtrate 
 was found to be highly toxic, 0.5 cc. injected subcu- 
 taneously into mice killing the animals with symptoms 
 of general paralysis in twenty-four hours. Boiling 
 the extract destroyed the poison. This harmonizes 
 well with the fact that several persons who ate some 
 
102 BACTERIAL FOOD POISONING 
 
 of the salad which, through an oversight, had been 
 placed on the stove and allowed to boil, were not poi- 
 soned. So also in another case, where some of the 
 salad was eaten after moderate heating ; the toxic symp- 
 toms developed very slowly, with, however, a fatal 
 ending. Bacteriological examination of the salad re- 
 vealed the presence of an anaerobic bacillus which was 
 identical with bacillus botulinus. This organism pro- 
 duced a strong poison in cultures, especially when 
 grown at 24 C, so that white mice were killed with 
 O.000003 cc. and guinea-pigs with 0.0003. When 
 grown at 37 C, on the other hand, the fatal dose for 
 mice was 0.01 cc, and for guinea-pigs 0.1 cc. Gaffky 
 also isolated the bacillus botulinus from this salad. 
 
 It was impossible to learn how the string beans had 
 become infected. Landmann believed that the bacilli 
 had been carried into the can along with some little 
 piece of left-over meat such as might readily be found 
 in any kitchen. He bases this view on the fact that 
 thus far the bacillus botulinus has been found only in 
 meats or dishes prepared from meat. It is also possible, 
 however, that the spores of this bacillus were carried 
 in on the beans from the field. In the canning as 
 carried out in the cooking school the sterilization ap- 
 pears to have been incomplete; it is probable that in a 
 regular canning factory where sterilization is carried 
 out at 112 C, all of the spores would have been 
 killed. It follows from what has been said that canned 
 vegetables having the least rancid odor should be de- 
 stroyed, and that even those appearing normal in every 
 
POISONING THROUGH CANNED GOODS 103 
 
 way should always be boiled before serving. If this 
 had been done in the case just described, the catas- 
 trophe would have been averted. 
 
 An extensive outbreak of poisoning due to the eat- 
 ing of string beans occurred in Leipzig in 1906, among 
 the employees of a large department store. About 250 
 persons were affected, a few hours after the meal, the 
 chief symptoms being abdominal pains, chills, nausea, 
 headache, and dizziness. In some of the patients the 
 symptoms were at once accompanied by diarrhoea; in 
 others the diarrhoea came on during the evening or the 
 following morning. The symptoms lasted two to four 
 days, all the cases making a good recovery. The 
 string beans were delicious, and showed nothing ab- 
 normal in taste or odor. They had been packed in sev- 
 eral cans, which had been opened just before the meal, 
 and then placed for a time in hot water (about 80 ° C). 
 Boiling was purposely omitted because the beans were 
 so tender that they would have made a soft mush. The 
 bacteriological examination made by Roily 91 disclosed 
 the presence of two species of bacteria, bacillus coli, and 
 bacillus paratyphi, type B, both in large numbers. No 
 anaerobic organisms were isolated. The paratyphoid 
 bacilli were pathogenic for mice and guinea-pigs when 
 inoculated subcutaneously ; in cultures the bacilli pro- 
 duced a toxin which was resistant to heat. The poi- 
 soning in his case was due to the toxin and not to the 
 bacteria themselves, for otherwise the symptoms would 
 not have appeared so suddenly, but would have re- 
 quired a period of incubation. Furthermore, in none 
 
104 BACTERIAL FOOD POISONING 
 
 of the cases could paratyphoid bacilli be found in the 
 stools. 
 
 LINICAL TYPES OF CASES, 
 
 We see, then, that in poisoning due to canned vege- 
 tables the same two types of bacteria occur as are found 
 in outbreaks of meat poisoning, namely, bacillus botu- 
 linus, which produces a poison readily decomposed by 
 heat, and bacillus paratyphi, B, whose poison with- 
 stands heating. The first variety of poisoning can be 
 guarded against by heating the food to boiling just 
 before serving, although it is better not to eat any food 
 about whose condition there is the least question. 
 The second variety of poisoning cannot be safeguarded 
 against even by prolonged boiling. 
 
 Belser 92 made careful bacteriological examinations 
 of canned vegetables which had undergone decompo- 
 sition, as was shown by the ballooned tops of the cans. 
 He found that the change was due to a number of 
 bacteria which were more or less resistant to heat, such 
 as bacillus acidi lactici, and bacillus amylobacter. In 
 almost every case the decomposed vegetables showed 
 an increased acidity, though sometimes this was but 
 slight. The bacilli were not virulent for mice. Ba- 
 cillus proteus was also encountered; this organism 
 grows especially well in the broth of peas and beans, 
 and produces a toxin highly virulent for mice. Bac- 
 teria ordinarily occurring in water and soil have also 
 been found in canned vegetables ; among these are ba- 
 cillus mesentericus vulgatus, and bacillus megatherium. 
 
POISONING THROUGH CANNED GOODS 105 
 
 BACTERIOLOGICAL EXAMINATION 
 
 It is impossible to determine the absolute sterility of 
 canned goods without a careful bacteriological ex- 
 amination. According to E. Pfuhl, 8T canned goods 
 often contain bacteria without showing any ballooning 
 of the top. The reason for this is that the bacteria in- 
 fecting the can do not all produce gas. Furthermore, 
 the appearance of the contents on opening the can may 
 also give no hint of the presence of bacteria. Fre- 
 quently all that is noticed is that the contents have a 
 slightly sour odor, or one abnormally pungent. Where 
 large purchases are made, it is therefore necessary al- 
 ways to have several cans, selected at random, exam- 
 ined bacteriologically. The goods should not be ac- 
 cepted if this examination discloses the presence of any 
 bacteria. Pfuhl gives the following method to be fol- 
 lowed in making the examination: The can is kept 
 unopened in the incubator for eight to fourteen days. 
 This gives the obligate and faculative anaerobic bacteria 
 opportunity to develop. Then the lid is carefully ster- 
 ilized by flaming with alcohol, and a hole made with a 
 sterile ice pick or other sharp instrument. Through 
 this hole some of the meat juice and liquefied gelatine 
 is sucked up with a sterile pipette and planted into dif- 
 ferent media both for aerobic and anaerobic growth. 
 The hole is then covered with a bit of sterile cotton, 
 and the can returned to the incubator for another two 
 or three days. This gives the aerobic bacteria time to 
 develop. Then another set of cultures is made. The 
 
106 BACTERIAL FOOD POISONING 
 
 second test may be omitted if bacteria develop with 
 the first test. 
 
 PROPHYLAXIS 
 
 Schottelius 83 has repeatedly warned against the 
 ever-increasing use of canned foods in the household, 
 and we believe the warning fully justified. There is 
 a distinct field of usefulness for this form of food, for 
 example, in the feeding of armies in war, or in expe- 
 ditions of various kinds. On the other hand, in tem- 
 perate climates, as for example in Germany or in the 
 United States, there is really no reason, aside from con- 
 venience, why canned foods should be used in the 
 household. It seems not to be appreciated that canned 
 goods are always inferior to fresh vegetables, fruits, 
 etc.* Furthermore, just the fact that certain fruits or 
 vegetables are out of season for part of the time each 
 year, makes our appetite and appreciation of them all 
 the keener when the season returns. If we had straw- 
 berries and cream every day of the year, we should 
 soon be disgusted by the mere sight of them. Another 
 disquieting fact is that at the present time we have no 
 way of determining the age of the goods we are buy- 
 ing. It will be recalled that the proposal to date all 
 canned goods met with determined opposition on the 
 
 ♦While the superiority of fresh foods is unquestioned, 
 there is probably very little danger of food poisoning from 
 fruits or vegetables properly canned by a reputable firm. 
 In fact, it is likely that the " canning " as done in such an 
 establishment (in steam sterilizers under pressure), is more 
 efficacious than that done at home. 
 
POISONING THROUGH CANNED GOODS 107 
 
 part of the large packers. Yet there is no doubt what- 
 ever that the danger of decomposition increases with 
 age, and there is also a loss of flavor. Under no cir- 
 cumstances should the contents of a " blown " can be 
 eaten. It is said that unscrupulous packers have taken 
 " blown " cans which had been returned to them, 
 punched a small hole in the cover to let out the gas, 
 reheated the whole in the autoclave, resoldered the 
 punch hole, and then resold such goods at a reduced 
 price. It will be well, therefore, to refuse canned 
 goods showing more than one soldered opening. 
 
 TREATMENT 
 
 (See pages 47 and 71.) 
 
IX 
 METALLIC POISONS 
 
 HISTORICAL 
 
 There is still a widespread belief among the laity 
 that epidemic outbreaks of food poisoning are often 
 due to metallic poisons. As a matter of fact, this is 
 rarely the case. Nevertheless, notable outbreaks of 
 this nature have been known even in recent years. 
 Thus the famous " beer epidemic " of Manchester and 
 other English cities, in 1900, was due to the accidental 
 presence of arsenic. At one time, too, the chief cause 
 of poisoning through canned foods was thought to be 
 metallic poisons, especially lead and tin, but K. B. 
 Lehmann 94 declares that this is not true at the present 
 time. In Germany the law prescribes that the tin used 
 for tinning the cans shall not contain over 1% lead, 
 and the solder not over 10%. Lead poisoning from 
 this source is unknown in that country since the enact- 
 ment of this law. Poisoning from tin is probably also 
 very infrequent. According to Lehmann acute diges- 
 tive disturbances may be caused by foods which con- 
 tain large amounts of tin (100 to several hundred 
 milligrams), but the symptoms are usually not severe. 
 Freshly canned goods contain but little tin; the 
 amount, however, gradually increases in time, so that 
 
 108 
 
METALLIC POISONS 109 
 
 canned vegetables were found with from fifty or sixty 
 mg. to 200 mg. per kilo. Canned meats contained all 
 the way from fifty to 325 mg. The largest amounts 
 were found in decomposed canned foods, for in these 
 the acid which was formed in the decomposition dis- 
 solved the tin. Large amounts were also found in 
 acid preserves, such as pickled herring. In one such 
 instance 156 mg. of tin were found in 150 grams of the 
 pickled fish. It is important, therefore, to insist that 
 preserves containing considerable quantities of acetic, 
 tartaric, or malic acid be packed only in glass or por- 
 celain, and not in tin. 
 
 According to Lehmann the ordinary vegetable or 
 meat preserves, which are not highly acid, do not ap- 
 pear to give rise to any metallic poisoning. What 
 poisoning does occur is almost always of bacterial 
 origin. 
 
 Copper poisoning was also formerly believed to play 
 an important role in food poisoning. Lehmann 96 
 states that about 200 mg. copper must be swallowed be- 
 fore symptoms are produced in man, and 1200 mg. are 
 needed to produce really threatening symptoms. It 
 is difficult to see how such quantities of copper could 
 be present in the food under ordinary conditions, and 
 there is little doubt that most of the poisonings ascribed 
 to verdigris and copper are really due to bacterial de- 
 composition of the food. In fact, the symptoms re- 
 ported in these cases are very much like those of the 
 latter condition. 
 
 There is reason to believe that under certain condi- 
 
110 BACTERIAL FOOD POISONING 
 
 tions, lead poisoning may occur quite readily. Thus 
 earthen ware is sometimes coated with a cheap glaze 
 containing large quantities of lead. On boiling fluids 
 containing vinegar in such pots, considerable amounts 
 of lead pass into solution. Thus, in some tests made in 
 this direction, ioo to 700 mg. lead were extracted with 
 the first boiling. Lehmann 96 believes that attention 
 should be directed to this pottery, because the lead is 
 given off for a long time. Perhaps these lead glazes 
 are responsible for some hitherto unexplained cases of 
 lead poisoning. Lehmann cites a case of lead poison- 
 ing observed by Halenke. Two women had cooked 
 cranberries in an earthen pot, and had then made a 
 cranberry tart. Soon after eating the tart both be- 
 came ill, one very severely. Investigation showed that 
 the glaze had been completely dissolved from the inside 
 of the pot, and that a piece of tart contained about 160 
 mg. lead. Each woman had therefore consumed about 
 400 to 600 mg. lead in the form of lead malate. Ap- 
 proximately 1000 mg. lead had been given off by the 
 glaze in the one boiling. It will be well, when investi- 
 gating chronic lead poisonings whose origin cannot be 
 traced, to think of cheap pottery with a lead glaze. The 
 determination of the lead content can easily be under- 
 taken by any physician by merely boiling the pot with 
 4% acetic acid for half an hour, and then passing sul- 
 phureted hydrogen through the fluid. A black dis- 
 coloration or a black precipitate denotes the presence 
 of lead. 
 
 It is well to remember, however, that metallic poi- 
 
METALLIC POISONS in 
 
 sonings through cooking utensils, etc., are quite rare, 
 and one is justified in ascribing poisoning to this cause 
 only if a chemical examination has really demonstrated 
 large quantities of such a poison. The mere fact that 
 the food was prepared, for example, in a damaged cop- 
 per vessel, by no means justifies the diagnosis of cop- 
 per poisoning. In fact, one should first think of bac- 
 terial poisoning, for this is much more likely to have 
 occurred. 
 
BIBLIOGRAPHY 
 
BIBLIOGRAPHY 
 
 GENERAL ARTICLES 
 
 Novy, F. G. — Article on Food Poisons, in Modem Med- 
 icine, Osier, Vol. I., 1907. 
 
 Vaughan and Novy. — " Cellular Toxins," Fourth Edi- 
 tion, N. Y., 1902. 
 
 Vaughan, V. C. — " Protein Poisons," Science, N. Y., 
 1907. 
 
 Thresh and Porter. — " Preservatives and Food Exam- 
 ination/' Blakiston's Son & Co., Phila., 1906. 
 
 MEAT POISONINGS 
 
 1. Bollinger. — Arztl. Intelligenzblatt. Milnchener med. 
 
 Wochenschr., Vol. 28, 1881. 
 
 2. Ostertag. — Handbuch der Fleischbeschau. 4. Aufl. 
 
 1902. (Review of the older literature.) There is 
 an English translation of this. 
 
 3. van Ermengem. — Handbuch von Kolle-W asser- 
 
 mann. Vol. 2, 1903. 
 
 4. Schneidemuhl. — Die animalischen Nahrungsmittel, 
 
 1903. (Review of the older literature.) 
 
 5. Gartner. — Korresp.-Blatt des arztl. Vereins von 
 
 Thiiringen, 1888. 
 
 6. Gaffky und Paak. — Arb. a. K. Gesnndh. A., Vol. 
 
 6, 1890. 
 
 "5 
 
Ii6 BACTERIAL FOOD POISONING 
 
 7. Neelson, Johne und Gartner. — Cited by Ostertag 
 
 (2). 
 
 8. Van Ermengem. — 'Bull. acad. de med. de Belgique, 
 
 1892. 
 
 9. Holst. — Ref. Centralblatt f. Bakter., Vol. 17, 1895. 
 
 10. Poels und Dhont. — Holland. Zeitschr. f. Tierheil- 
 
 kunde, Vol. 24, 1894. 
 
 11. Basenau. — Archiv. f. Hyg., Vol. 20, and Vol. 32. 
 
 12. Fischer, B. — Zeitschr. f. Hyg., Vol. 39, 1902. (Re- 
 
 view of literature.) 
 
 13. Johne. — Cited by Ostertag, Handbuch der Fleisch- 
 
 beschau (2). 
 
 14. Van Ermengem. — Revue d'hyg., 1896. 
 
 15. Kaensche. — Zeitschr. f. Hyg., Vol. 22, 1896. 
 
 16. Scheef. — Med. Korrespondenzblatt des Wurtt. arztl. 
 
 Landesvereins, 1896. 
 
 17. Gijnther. — Arch. f. Hyg., Vol. 28, 1896. 
 
 18. Silberschmidt. — Korrespondenzblatt fur Schweizer 
 
 Arztl, 1896. 
 
 19. Pouchet. — Annates d' Hygiene, 1897. 
 
 20. Durham. — British med. Journal, 1898, 1899. 
 
 21. De Noble. — Ann. soc. med. Gand., 1899, 1901. 
 
 22. Hermann and Van Ermengem. — Arch, de medic. 
 
 ex per., 1899. 
 
 23. Trautmann. — Zeitschr. f. Hyg., Vol. 45, 1903. 
 
 24. Van Drigalski. — Festschrift fur R. Koch. Jena, 
 
 1903. 
 
 25. Fischer, B. — Ibid. 
 
 25 a . Muhlens, Dahm, and Furst. — Abstracted in Jour- 
 nal of the Royal Institute of Public Health, Vol. 
 XVI, 1908. 
 
 26. Uhlenhuth. — Gedenkschrift fur Leuthold. Berlin, 
 
 1906. 
 
BIBLIOGRAPHY 117 
 
 27. Curschmann. — Zeitschr. f. Hyg., Vol. 55, 1906. 
 
 (Review of recent literature.) 
 
 28. Kutscher. — Ibid. 
 
 29. Heller. — Centralbl. f. Bakt. Orig., Vol. 43. 
 
 30. Fromme. — Ibid. 
 
 31. Schottmuller. — Deutsche med. Wochenschr., 1900. 
 
 Zeitschr. f. Hyg., Vol. 36, 1901. 
 
 32. Durham. — The Lancet, 1898. 
 
 2,Z- Trautmann. — Zeitschr. f. Hyg., Vol. 46, 1904. 
 
 34. Kayser. — Centralbl. f. Bakt., Vol. 35, 1903. v. 
 
 Krehl imd Kayser,, Deutsche med. Wochenschr., 
 1906. 
 
 35. Hetsch. — Klin. Jahrbuch., Vol. 16, 1906. 
 
 36. Rolly. — Deutsches Arch. f. klin. Medizin., Vol. 87, 
 
 1906. 
 2,y. Zupnik. — Zeitschr. f. Hyg., Vol. 40. 
 
 38. Kutscher. — Paratyphus in: Kolle-Wassermann 
 
 Handbuch. 1. Erg'dnzungsband, 1907. 
 
 39. Levy und Jakobstal. — Arch. f. Hyg., Vol. 44, 1903. 
 
 40. Pies. — Archiv f. Hyg., Vol. 62, 1907. 
 
 41. Fischer, B. — Zeitschr. f. Hyg., Vol. 39, and Fest- 
 
 schrift fur R. Koch. 
 
 42. Uhlenhuth. — Deutsche med. Wochenschr., Nr. 11, 
 
 1907. 
 
 43. Basenau. — Arch. f. Hygiene, Vol. 32, 1898. 
 
 44. Levy. — Arch. f. experiment. Pathol, 1894; Vol. 34. 
 
 45. Wesenberg. — Zeitschr. f. Hyg., Vol. 28, 1898. 
 
 46. Glucksmann. — Centralbl. f. Bakt., Vol. 25, 1899. 
 
 47. Silberschmidt. — Zeitschr. f. Hyg., Vol. 30, 1899. 
 
 48. Pfuhl, A. — Zeitschr. f. Hyg., Vol. 35, 1900. 
 
 49. Schumburg. — Zeitschr. f. Hyg., Vol. 41, 1902. 
 
 50. Lubenau. — Centralbl. f. Bakt. Orig., Vol. 40, 1906. 
 
n8 BACTERIAL FOOD POISONING 
 
 51. Van Ermengem. — Zeitschr. f. Hyg., Vol. 26, 1897; 
 
 and Kolle-Wassermann, Handbuch d. pathog. 
 Mikroor ganismen, Vol. 2. 
 
 52. Kempner. — Zeitschr. f. Hyg., Vol. 26, 1897. 
 
 53. Roemer. — Centralbl. f. Bakt., Vol. 27, 1900. 
 
 54. Schilling. — Deutsche med. Wochenschr., 1900. 
 
 55. Bryson, M. — British Medical Journal, 1907, II., 
 
 page 1710. 
 
 56. Brown, G. A. — Lancet, 1907, I., page 1029. 
 
 56*. Pennington, Mary E. — Yearbook, U. S. Depart- 
 ment of Agriculture, 1907. 
 
 57. Morgan, H. deR. — British Medical Journal, 1905, I., 
 
 page 1257. 
 
 58. Liefmann, H. — Munchener medizin. Wochenschrift, 
 
 Vol. 55, 1908, page 157. 
 
 59. Ohlmacher. — Journal Medical Research, 1902, Vol. 
 
 VII., page 411. 
 
 60. Owen, R. — The Physician and Surgeon, Detroit, 
 
 1907, Vol. 29, page 289. 
 
 61. Hubener. — Deutsche med. Wochenschrift, 1908, No. 
 
 24. 
 
 62. Rimpau, W. — Ibid. 
 
 62a. Berry, W. — Public Health, Vol. XXII, 1908, page 
 
 FISH POISONINGS 
 
 6^. Kobert. — Uber GiftHsche und Fischgifte, Stuttgart, 
 1905. 
 
 64. Ulrich. — Zeitschr. f. Hyg., Vol. 53, 1906. 
 
 65. Abraham. — Munch, med. Wochenschr., 1906, Nr. 
 
 50, Vol. 2466. 
 
 66. Galeotti und Zardo. — Centralbl. f. Bakt. Orig., Vol. 
 
 31, 1902. 
 
BIBLIOGRAPHY 119 
 
 67. Vivaldi and Rodella. — Hygien. Rundschau, 1905. 
 
 68. Vagedes. — Vierteljahrschr. f. gerichtl. Medizin., 
 
 Vol. 30. I905- 
 
 CHEESE POISONING 
 
 69. Vaughan and Perkins.— Arch. f. 'Hyg., Vol. 27, 
 
 1896. 
 
 70. Holst, A.— Centralbl. f. Baku, Vol. 20, 1896. 
 
 71. Pfluger. — Zeitschr. f. Medizinalbeamte, 1894. 
 
 72. Peppler.— Cited by Heim, Lehrbuch der Hygiene, 
 
 page 26, 1903. 
 
 73. Heim. — Arb. aus dem K. Gesundheitsamt., Vol. 5. 
 
 74. Taltavall and Gies.— New York Medical Journal, 
 
 1907, Vol. 86, 726. 
 
 poisonings through ice cream and puddings 
 
 75. Wassermann, M.— Zeitschr. f. diatei. u. phys. 
 
 Therapie., Vol. 3, 1896. 
 
 76. Vaughan.— Arch. f. Hyg., Vol. 7. 
 
 yy. Vagedes. — Klin. Jahrbuch., Vol. 14, 1905. 
 
 78. Lange.— Arch. f. Hygiene, Vol. 62, H. 3. 
 
 79. Levy und Fornet.— Centralbl. f. Bakt. Orig., Vol. 
 
 41, 1906. 
 
 80. Klein, E.— Centralbl. f. Bakt. Orig., Vol. 38, 1905. 
 
 POTATO POISONINGS 
 
 81. Schmiedeberg.— Arch. f. exper. Pathologie u. 
 
 Pharm., Vol. 36, 1895. 
 
 82. Pfuhl, E. — Deutsche med. Wochenschr., 1899. 
 
 83. Meyer.— Arch. f. exper. Path. u. Pharm., Vol. 36, 
 
 1895. 
 
120 BACTERIAL FOOD POISONING 
 
 84. Wintgen. — Zeitschr. fur Untersuchung der Nah- 
 
 rungs- und Genussmittel., Vol. 12, 1906. 
 
 85. Weil. — Arch. f. Hyg., Vol. 38, 1900. 
 
 86. Dieudonne. — Deutsche militararztl. Zeitschr., 1904. 
 
 POISONINGS THROUGH CANNED GOODS 
 
 87. Pfuhl, E. — Zeitschr. f. Hygiene., Vol. 48, 1904. 
 
 88. Cited by Bischoff und Wintgen. — Zeitschr. f. 
 
 Hyg., Vol. 34, 1900. 
 
 89. Fischer, A. — Zeitschr. f. klin. Medizin., Vol. 59, 
 
 1906. 
 
 90. Landmann. — Hygien. Rundschau., Vol. 14, 1904. 
 
 91. Rolly. — Munch, med. Wochenschr., 1906. 
 
 92. Belser. — Arch. f. Hyg., Vol. 54, 1905. 
 
 93. Schottelius. — Blatter filr VolksgesundheitspHege, 
 
 Vol. 7, 1907. 
 
 94. Lehmann. — Arch. f. Hyg., Vol. 45, 1902. 
 
 95. Lehmann. — Deutsche Vierteljahrsschr. f. offentlliche 
 
 Gesundheitspiiege, Vol. 34, 1902. 
 
 96. Lehmann. — Hygienische Rundschau., 1902. 
 
 97. Sheppard, C. — Southern California Practitioner, 
 
 1907, Vol. 22, page 370. 
 
INDEX 
 
 PAGE 
 
 Abraham, studies on fish poisoning •.•••: 74 
 
 Abscesses in meat, their relation to meat poisoning 24 
 
 Acids of fruits, in relation to canned goods 109 
 
 Aertryck, bacillus of 3°> 74 
 
 outbreak of food poisoning in...._. 3° 
 
 Agglutination reaction in food poisoning. ._ 24, 40, 45, 73, 74 
 
 Alcohol, clinical application in food poisoning 18, 47 
 
 Allantiasis 62 
 
 Alsfeld, outbreak of food poisoning _ in. . 3° 
 
 Andelfinger, outbreak of meat poisoning in 17 
 
 Antitoxin for botulism 68, 71 
 
 Arsenic, cause of beer epidemic 108 
 
 Bacillus acidi lactici in canned vegetables 104 
 
 Bacillus Aertryck, occurrence in fish poisoning 74 
 
 occurrence in healthy animals 33 
 
 amylobacter 104 
 
 botulinus 62, 67, 101 
 
 growth as affected by salt 7° 
 
 growth in symbiosis 69 
 
 bovis morbificans 27 
 
 carriers 3 1 , 34 
 
 coli in canned vegetables 103 
 
 in cheese poisoning 81 
 
 in meat poisoning 48, 54 
 
 in oysters 78 
 
 toxin of 48 
 
 enteritidis, Gartner agglutination of 24 
 
 biological characteristics 35 
 
 in meat poisoning 40, 54 
 
 in pudding 87 
 
 occurrence in nature 31, 34 
 
 relation to other organisms 26 
 
 of calf dysentery, in cheese poisoning 81 
 
 of hemorrhagic septicaemia 77 
 
 of swine erysipelas 82 
 
 of tuberculosis in cheese 82 
 
 paratyphi, biological characteristics 35 
 
 in canned goods 103 
 
 in ice cream and pudding poisonings 85, 86, 88 
 
 occurrence _ in nature 31, 33, 34, 73, 74 
 
 pathogenicity 37 
 
 peptonificans, in meat poisoning 55 
 
 121 
 
122 INDEX 
 
 _ .„ . PAGE 
 
 Bacillus proteus, action of 51 
 
 in blown cans 48, 104 
 
 in meat poisoning 48, 50, 51, 52 
 
 in mussel poisoning 78 
 
 in oysters 78 
 
 in potato poisoning 95 
 
 pathogenicity 52 
 
 toxin of 49, 51, 95 
 
 subtilis, in meat poisoning 54, 69 
 
 suipestifer, occurrence in nature 33 
 
 typhi, biological characteristics 35 
 
 in oysters 78 
 
 viability in cheese 82 
 
 Bacteria in bile of slaughtered animals 32 
 
 Bacteriological examination, of canned goods, technique. . . 105 
 
 of meat, technique 38 
 
 Barbs (poisonous fish) 72 
 
 Basenau, studies on meat poisoning 27 
 
 technique of bacteriological examination 38 
 
 Beelitz, outbreak of meat poisoning in 54 
 
 Beer epidemic, in England 108 
 
 Belser, bacteriology of blown cans 104 
 
 Berlin, outbreak of meat poisoning 30 
 
 Bern, outbreak of meat poisoning 30 
 
 Berry, studies on meat poisoning 54 
 
 Bischofswerde, outbreak of meat poisoning in 28 
 
 "Blown cans," bacteria associated with 104 
 
 as evidence of putrefaction 99, 106 
 
 Bollinger, studies on meat poisoning 15, 16 
 
 Botulism, antitoxin for 68 
 
 diagnosis 70 
 
 etiology 62, 66 
 
 mortality in 64 
 
 prophylaxis 70 
 
 symptoms 64, 65 
 
 treatment 71 
 
 Boucherau, poisoning through canned goods 99 
 
 " Braxy," relation to meat poisoning 21 
 
 Breslau, outbreak of meat poisoning in 30 
 
 Brieger, studies on mussel poisoning 76 
 
 Brown, G. A., studies on meat poisoning 24 
 
 Brown, H. R., cold storage of poultry 58 
 
 Brugge, outbreak of meat poisoning in 30 
 
 Canned beans, bacillus botulinus in 101 
 
 goods, poisoning through, clinical types 104 
 
 poisoning through, etiology 99 
 
 poisoning through, prophylaxis 106 
 
 vegetables, bacteria associated with poisoning from..ioi, 103 
 
 Cans, " blown " 99> 106 
 
 Carriers of typhoid and other bacilli 31 
 
 Chadderton, outbreak of meat poisoning in 30 
 
INDEX 123 
 
 PAGE 
 
 Chemnitz, outbreak of meat poisoning in 50 
 
 Cheese poisoning, bacteria associated with 80, 82 
 
 chemical examination of 83 
 
 clinical types 80 
 
 treatment ■ 83 
 
 Cholera nostras, due to paratyphoid bacilli 43 
 
 spirilla, in cheese, viability of 82 
 
 spread by oysters 78 
 
 Cold-storage poultry in meat poisoning 57 
 
 influence of, on bacterial multiplication 57,58 
 
 Colon bacillus in meat poisoning 48- 54 
 
 in oysters 78 
 
 in canned vegetables i°3 
 
 in cheese poisoning 81 
 
 toxin of 48 
 
 Communicability of epidemic meat poisoning 19, 24, 29, 44 
 
 Cooking, effect on bacterial poisons 21, 27, 51, 54, 67, 74, 104 
 
 Copper, in food poisoning 109 
 
 Cortial, on potato poisoning 9 2 
 
 Cotta, outbreak of meat poisoning. . . . 25 
 
 Curschmann, poisoning due to pudding 87 
 
 Darmstadt, outbreak of food poisoning in 100 
 
 de Nobele, studies on food poisoning 30 
 
 Dhont, studies on meat poisoning . . . .3°> 45 
 
 Dieudonne, studies on enteritidis and paratyphoid bacilli. . 31 
 
 Diseased meat, poisoning due to, bacteriology 22 
 
 etiology 20 
 
 historical 16 
 
 v. Drigalski, studies on meat poisoning 30 
 
 Durham, studies on meat poisoning 30, 45 
 
 Diisseldorf, outbreak of meat poisoning in 30 
 
 Eber, test for putrefaction 60 
 
 Eberth, studies on meat poisoning 19 
 
 Eggs, bacterial infection of 86 
 
 Enteritidis bacillus, poisoning by, clinical types 4 1 
 
 diagnosis 44 
 
 prophylaxis 4° 
 
 relation to paratyphoid fever 4 2 
 
 treatment 47 
 
 Enteritis, infectious J 5 
 
 v. Ermengem, studies on meat poisoning 25, 28, 30, 70 
 
 Exanthem, in food poisoning 18, 78, 87 
 
 Fish, canned, as a cause of poisoning 99 
 
 poisoning, bacteria associated with 73, 74 
 
 symptoms 73, 74 
 
 treatment of _ 79 
 
 roe, in food poisoning 7 2 
 
124 INDEX 
 
 PAGE 
 
 Fischer, studies on food poisoning 27,30, 48, 100 
 
 Fliigge, studies on meat poisoning 30 
 
 Foot and mouth disease, relation to food poisoning 20 
 
 Forced slaughtering, relation to meat poisoning 21 
 
 see also "braxy" 21 
 
 Fornet, studies on pudding poisoning 88 
 
 Fromme, studies on meat poisoning 30 
 
 Fruit acids and canned goods 109 
 
 Fuga, Japanese poisonous fish 72 
 
 Gaffky, studies on food poisoning 15, 24, 82, 101 
 
 Galeotti, studies on snail poisoning 77 
 
 Gartner, studies on epidemic meat poisoning 23, 25 
 
 Gartner's bacillus enteritidis (see under Bacillus) 23 
 
 Gaustad, outbreak of meat poisoning in 26 
 
 Gerbstadt, outbreak of meat poisoning in 50 
 
 Ghent, outbreak of meat poisoning in 28 
 
 Giessen, outbreak of meat poisoning in 30 
 
 Gliicksmann, studies on meat poisoning 51 
 
 Greifswald, outbreak of meat poisoning in 30 
 
 Giinther, studies on meat poisoning 30 
 
 Ffalenke, lead in food poisoning no 
 
 Hannover, outbreak of meat poisoning in 52 
 
 Hatton, outbreak of meat poisoning in 30, 45 
 
 Haupt, studies on meat poisoning 50 
 
 Haustedt, outbreak of poisoning in 28 
 
 Hay bacillus, in meat poisoning 54, 69 
 
 Heat, effect on cheese poison 81 
 
 effect on fish poison 7 2 
 
 effect on mussel poison 76 
 
 effect on poison of B. Aertryck 74 
 
 effect on poison of B. botulinus 67 
 
 effect on poison of B. enteritidis 23, 24, 25, 26 
 
 effect on poison of B. proteus 51, 54 
 
 Heim, studies on bacteria in cheese 82 
 
 Heller, studies on meat poisoning 30 
 
 Hermann, studies on meat poisoning 30 
 
 Hetsch, studies on paratyphoid infections 43 
 
 Hoist, studies on food poisoning 26,81 
 
 Horb, outbreak of meat poisoning in 30 
 
 Hiibener, paratyphoid and related bacilli in healthy animals. 33 
 
 Ice cream poisoning 84 
 
 Incubation period in meat poisoning and in paratyphoid fever, 43 
 
 in botulism 68 
 
 Infection, bacterial 13 
 
 Infectious enteritis IS 
 
 Intoxication, bacterial 13 
 
 Isola, outbreak of snail poisoning 77 
 
INDEX 125 
 
 PAGE 
 
 Johne, studies on meat poisoning 25, 28 
 
 Kaensche, studies on meat poisoning 30 
 
 Kalamazoo, outbreak of meat poisoning in 56 
 
 Kayser, incubation period of meat poisoning 43 
 
 Kempner, studies on botulism antitoxin 68 
 
 Kerner, studies on sausage poison 62 
 
 Kiel, outbreak of meat poisoning in 30 
 
 Kloten, outbreak of meat poisoning in , 18 
 
 Kobert, on fish poisoning .., 72 
 
 Kutscher, on meat poisoning < 1 . 30 
 
 Lange, bacterial infection of eggs 87 
 
 Lead, as a cause of food poisoning 108, no 
 
 in cans and solder 108 
 
 in glaze on earthenware no 
 
 Lehmann, metallic poisons in food poisoning 108 
 
 Leipzig, outbreak of food poisoning 103 
 
 Levy, studies on food poisoning 50, 88 
 
 Liefmann, serum diagnosis of meat poisoning 46 
 
 Lubenau, on meat poisoning 54 
 
 Lustig, on mussel poisoning yy 
 
 Lyons, outbreak of potato poisoning in 92 
 
 Malachite green agar 37 
 
 Manchester beer epidemic 108 
 
 Mansfield, outbreak of meat poisoning in 51 
 
 Meat poisoning, enteritidis and paratyphoid, diagnosis 44 
 
 prophylaxis 46 
 
 serum diagnosis 45 
 
 treatment 47 
 
 from bacillus botulinus (see Botulism) 62 
 
 from decayed meat, diagnosis 58 
 
 frequency 55 
 
 historical 48 
 
 prophylaxis 60 
 
 symptoms 49 
 
 treatment 61 
 
 Meirelbeck, outbreak of meat poisoning in 30 
 
 Metallic poisons, historical 108 
 
 Meyer, solanin content of potatoes 93 
 
 Milk, in spread of paratyphoid infections 34, 85 
 
 Molluscs, poisoning through eating of 72 
 
 Moorseele, outbreak of meat poisoning in 25 
 
 Morgan, bacteriology of intestinal tract in animals 33 
 
 Mortality, in enteritidis poisoning 41 
 
 in putrefactive meat poisoning 49 
 
 in potato poisoning 92 
 
 in sausage poisoning 63, 64 
 
 Mouse typhoid, bacillus of 33 
 
126 INDEX 
 
 PAGE 
 
 Muhlens, occurrence of B. enteritidis in meat 34 
 
 Murex bradatus (marine snail) 77 
 
 Mussel poisoning 76 
 
 Mytilotoxin, action of 76 
 
 Mytilus edulis (mussels) 76 
 
 Neelson, studies on meat poisoning 25 
 
 Neisser, studies on fish poisoning 74 
 
 Neunkirchen, outbreak of meat poisoning in 30 
 
 de Nobele, studies on meat poisoning 30 
 
 Oatmeal, poisoning through 54 
 
 Ohlmacher, food poisoning through oatmeal 54 
 
 Ostertag, history of epidemic meat poisoning 19 
 
 Owen, studies on food poison 56 
 
 Oysters, colon bacilli in 78 
 
 capsule bacilli in 78 
 
 cholera transmitted by 78 
 
 relation to food poisoning 78 
 
 typhoid transmitted by 78 
 
 sewage pollution of 78, 79 
 
 Paak, studies on meat poisoning 24 
 
 Partick, outbreak of meat poisoning in 24 
 
 Paratyphoid bacillus (see Bacillus paratyphi) 31, 34, 73 
 
 fever, relation to enteritidis infections 42 
 
 Pathogenicity of typhoid, paratyphoid and enteritidis bacilli. 37 
 
 of bacillus botulinus 67 
 
 of bacillus proteus 52 
 
 Pennington, cold storage and bacterial multiplication 57 
 
 Peppier, studies on cheese poisoning 82 
 
 Perkins, studies on cheese poisoning 80 
 
 Peyer's patches, in meat poisoning 19, 42 
 
 Pfliiger, studies on cheese poisoning 82 
 
 Pfluhl, on examination of canned goods 105 
 
 on potato poisoning 94 
 
 on proteus poisoning 52 
 
 Phlebitis in calves, relation to meat poisoning 21 
 
 Pies, growth of typhoid bacillus 32 
 
 Pike, as cause of food poisoning 72, 73, 74 
 
 Plauen, outbreak of meat poisoning in 50 
 
 Poels, studies on meat poisoning 26 
 
 Poisoning through decayed meat • 48 
 
 through diseased meat 15 
 
 through molluscs 72 
 
 Poisonous fish 72 
 
 Polyarthritis in calves, relation to meat poisoning... 21 
 
 Posen, outbreak of meat poisoning in 30 
 
 Pouchet, studies on meat poisoning 30 
 
INDEX 127 
 
 PAGE 
 
 Potato poisoning, bacteria associated with > 95 
 
 historical 91 
 
 prophylaxis 97 
 
 relation to solanin content 92 
 
 treatment 98 
 
 Proteus bacillus (see under Bacillus proteus) 48, 51, 95 
 
 Psittacosis, bacillus 33 
 
 Pudding, poisoning through, bacteriology 85, 86 
 
 prophylaxis 89 
 
 treatment 90 
 
 Putrefaction of meat 48 
 
 test for 59 
 
 Pyaemia in calves, relation to meat poisoning 21 
 
 Rancid odor, in canned vegetables 102 
 
 Rimpau, paratyphoid bacilli in healthy humans 34 
 
 Rodella, studies on bacteria in oysters 78 
 
 Roe of fish in food poisoning 72 
 
 Roemer, studies on botulism 69 
 
 Roily, on food poisoning 103 
 
 on paratyphoid infections 44 
 
 Roseola, typhoidal, in meat poisoning 18, 88 
 
 Rotterdam, outbreak of meat poisoning in 26 
 
 Rumfleth, outbreak of meat poisoning in 27 
 
 Salt, effect on growth of B. botulinus 70 
 
 Sausage poison (see Botulism) - 62 
 
 Sausages, relation to meat poisoning 22 
 
 Scheef, studies on meat poisoning 30 
 
 Schmiedeberg, on potato poisoning 91 
 
 Schmidtmann, on mussel poisoning 76 
 
 Schneidemuhl, on meat poisoning 20, 50, 75 
 
 Schottelius, on canned goods 106 
 
 Schottmiiller, on paratyphoid infections 43 
 
 Schumburg, on meat poisoning 52 
 
 Secondary infections in epidemic meat poisoning. . . 19, 24, 29, 44 
 
 Senkpiehl, on sausage poisoning 64 
 
 Septic infection of cows, relation to meat poisoning 20 
 
 Sepsis intestinalis 15 
 
 Serum diagnosis in epidemic meat poisoning 24,45 
 
 in fish poisoning 73, 74 
 
 in food poisoning 86 
 
 treatment for botulism 68, 71 
 
 Sheppard, on botulism 64 
 
 Silberschmidt, on food poisoning 30, 73 
 
 Sirault, outbreak of meat poisoning in 30 
 
 Snail poisoning yy 
 
 Solanin content of potatoes 93 
 
 poisoning 92 
 
 Staphylococcus in meat poisoning 56 
 
 Sturgeon, as a cause of food poisoning 72 
 
128 INDEX 
 
 PAGE 
 
 Subtilis bacillus in meat poisoning 54 
 
 Swine erysipelas, bacillus of, in cheese poisoning 82 
 
 Temperature, effect of, on production of botulinus toxin. . 102 
 
 on proteus toxin 95 
 
 Tin, in food poisoning 108 
 
 Toxin of bacillus Aertryck 74 
 
 botulinus 67, 68 
 
 coli 48 
 
 enteritidis 23 
 
 proteus 49, 95 
 
 cheese poisoning 81 
 
 Trautmann, studies on meat poisoning 30, 41 
 
 Tubercle bacilli in cheese 82 
 
 Typhoid bacillus, biological characteristics of 35 
 
 in cheese, viability of 82 
 
 resemblance to enteritidis bacillus 27 
 
 Typhoid fever, and oysters 78 
 
 resemblance of meat poisoning to 19 
 
 Tyrotoxicon, in cheese poisoning 80 
 
 Uhlenhuth, on meat poisoning 30 
 
 on paratyphoid bacilli in intestines of hogs 33 
 
 Ulrich, on fish poisoning 73 
 
 Urticaria, in food poisoning 18, 78 
 
 Vagedes, detection of bad oysters 79 
 
 on paratyphoid poisoning through pudding 85 
 
 van Ermengem, on meat poisoning 25, 26, 28, 40, 70 
 
 Vanilla, in ice cream and pudding poisonings 84 
 
 Vegetables, canned, in food poisoning 100 
 
 Virchow, on mussel poisoning j6 
 
 Vivaldi, bacteria in oysters 78 
 
 von Drigalski, on meat poisoning 30 
 
 Wassermann, antitoxin for botulism 71 
 
 Weil, on solanin content of potatoes 93 
 
 Weil's disease 20 
 
 Wesenberg, on meat poisoning 51 
 
 Widal test (see Serum diagnosis) 45 
 
 Wildbad, sausage poisoning in 63 
 
 Wilhelmshaven, outbreak of mussel poisoning in j6 
 
 Wintgen, on potato poisoning 93 
 
 Wiirttemberg, sausage poisoning in 63 
 
 Wyss, on fish poisoning 73 
 
 Zardo, on mussel poisoning 77 
 
 on snail poisoning yy 
 
 Zupnik, typhoidal meat poisoning 44 
 
 Zurich, outbreak of fish poisoning in J2 
 
RA1260 
 DieudonnS 
 
 D56