Meat Poisoning

MEAT POISONING, gastroenteritic diseases in humans following their consumption of meat and meat products containing toxins of certain bacteria. Such phenomena may be observed in the following cases: 1) upon infection of completely wholesome-looking meat by the so-called meat poisoning bacteria from the group paratyphi-enteritidis, namely Bacillus enteritidis Gartneri, Bacillus enteritidis Breslau (Bacillus aertrycke), and in rare cases Bacillus paratyphi B Schottmülleri. The infection of meat in the vast majority of cases occurs while the animal is still alive and only occasionally during storage or accidental contamination of the meat. 2) Upon the multiplication in putrefying meat of Bacillus proteus vulgaris, which produces a heat-stable poisonous toxin. In addition, some authors also point to Bact. coli commune, Bacillus prodigiosus, enterococci, and others as culprits in the acquisition of properties harmful to humans by putrefying meat; moreover, these microorganisms, in their opinion, acquire the ability to produce poisonous toxins only when growing on putrefying meat. Apart from bacterial toxins, poisonous ptomaines, which are also heat-stable, may sometimes form in decomposing meat. In human poisoning by toxins of the paratyphi-enteritidis bacterial group and toxins of putrefying meat bacteria, depending on the amount of secreted toxins and individual susceptibility, symptoms of gastroenteritis of varying degrees occur, ranging from milder to very severe, sometimes ending fatally. 3) Besides these cases, upon the multiplication of the anaerobe Bacillus botulinus in fatty sausages, fatty fish, canned preserves (meat, fish, vegetable, and fruit), a toxin is formed that causes human poisoning (see Botulism). The phenomena of meat poisoning have been known for a very long time. Until the end of the 19th century, their causes were sought in the formation within the meat of poisonous protein degradation products, ptomaines, assuming their appearance in the body of a sick animal during its lifetime. Bollinger in the 1870s established that meat becomes harmful in certain cases during septic-pyemic diseases of slaughter animals (blood poisoning); under the influence of this teaching, in many countries up to the present time, the slaughter for meat of animals with septic-pyemic processes is prohibited. The discovery in 1888 by Gaertner of one of the true causative agents of meat poisoning, Bacillus enteritidis Gartneri, and the introduction by Basenau of the bacteriological method of meat examination clarified the cause of meat poisoning. Over the past decade, the resolution of the question regarding the nature of meat poisoning has moved forward significantly thanks to the works of the Hygienic Institute of the University of Kiel (Kiel school). Based on the study of 466 cases of mass meat poisoning (26,780 cases of illness and 262 deaths) by this school, the true cause of such human diseases was established. The second causative agent, Bacillus enteritidis Breslau, was first isolated from meat poisoning in 1892 by de Nobele and then in 1893 by Flügge and Känsche. For a very long time, this bacterium was not distinguished by many researchers from Bacillus paratyphi B Schottmülleri, until the Kiel school proposed a methodology for its differentiation. Meat poisoning bacteria belong to the extensive genus of coli-typhus bacteria, which includes 1) species pathogenic to humans and causing epidemics: Bacillus typhi abdominalis hominis, Bacillus paratyphi B Schottmülleri, Bacillus paratyphi A, Bacillus Erzindjani; 2) a group of paratyphoid causative agents in animals: Bact. ratti Danysz's and Isachenko, Bact. typhi murium, Bact. abortus equi, and others; and 3) conditionally pathogenic species—the enteritidis-paratyphi group of bacteria causing meat poisoning, namely Bacillus enteritidis Gartneri and Bacillus enteritidis Breslau. Furthermore, non-pathogenic saprophytes belong to this same group, indistinguishable culturally from the meat poisoning bacilli, but not agglutinated by sera against them. (For the bacteriology of the enteritidis-paratyphi group, see Paratyphoid Fever.) Human disease is caused by poisoning with poisons produced by meat poisoning bacteria. These poisons (endotoxins) can form both in the meat and, apparently, in the human intestine. The disease occurs on the condition that meat poisoning bacteria or their toxins enter the human body with food in very large quantities and with a certain individual susceptibility of the person to the toxins of these bacteria. The passage of meat poisoning bacteria into human blood is observed only in very severe cases. The transmission (infection) of meat poisoning from one person to another is not observed. This circumstance imposes a peculiar stamp on the epidemiology of mass meat poisoning and helps to differentiate them from paratyphoid outbreaks (see Paratyphoid Fever). The infection of slaughter animals during their lifetime by bacteria of the enteritidis-paratyphi group can occur in the following cases: 1) Bacteria of this species can themselves cause disease in animals: a) gastrointestinal diseases in all slaughter animals (on average in 31.6% of all investigated cases of meat poisoning, the meat came from animals suffering from gastroenteritis); b) inflammation of the navel and umbilical vessels in calves; c) septic pyemia in calves; d) joint-ill in sucklings. 2) Meat poisoning bacteria, residing as saprophytes in the animal's intestine, can penetrate its blood during a temporary weakening of the body's defense mechanisms: a) in diseases associated with parturition (13.8% of all investigated meat poisoning cases); b) in septicemia and pyemia (Bollinger's "blood poisoning") (16.4%); c) in various other animal diseases (38.2%). The latter category includes the most diverse diseases: infectious, traumatic, local abscesses, pneumonias, and even severe overfatigue of the animal before slaughter. Throughout the animal's body, meat poisoning bacteria are distributed unevenly, accumulating more in the lymph nodes and internal organs and less in the muscles. Weak infection is frequently observed. In preserved meat, meat poisoning bacteria multiply very easily, growing especially luxuriantly in minced raw meat at room temperature; therefore, meat poisoning is more often encountered in the warm season upon the consumption of minced meat, especially raw and semi-raw. Some authors (e.g., Uhlenhuth and Seifert) believe that postmortem infection of meat by bacteria of the enteritidis-paratyphi group is observed in 90% of all meat poisoning cases. The Kiel school, conversely, while admitting the possibility of postmortem contamination of meat by these bacteria, asserts that in the majority of cases, meat infections are intravital, wherein at the time of slaughter a very insignificant amount of meat poisoning bacteria may be present in the meat, and such meat does not cause illness in humans, but depending on the conditions of storage and processing of the meat, greater or lesser multiplication of meat poisoning bacteria occurs in it, upon which its greater or lesser degree of toxicity depends. Regarding the question of which slaughter animals most frequently yield meat contaminated with meat poisoning bacteria, Standfuss cites the following statistical data: in all investigated cases of meat poisoning, the meat that caused the poisoning originated in 39.7% from cattle, in 29.1% from horses, in 18.1% from pigs, in 11.1% from calves, in 2% from sheep and goats; in 19.4% the poisoning was caused by meat products without indication of the animal species. For the bacteriological examination of meat for bacteria of the enteritidis-paratyphi group, one piece of meat with a volume of 7 cm³ is cut from the carcass out of the anterior and posterior quarters of one half of the carcass, and one large lymph node is taken from the quarters of the other half. The surface of the cut meat pieces is charred on a strong flame. Then pieces of the spleen, liver, and kidney are taken, and their cut surfaces are cauterized. All these parts are placed in a thermostat for 12–18 hours for enrichment. Then, cultures are made from each sample onto elective media, after which the bacterial species is determined. In case of weak infection (single colonies not in all Petri dishes), the meat is released for consumption, but only in a form sterilized by high temperature. In case of strong infection, the meat is destroyed, since the toxins (endotoxins) of meat poisoning bacteria are not destroyed at a temperature of 100°. The possibility of meat contamination by meat poisoning bacteria through contamination with intestinal contents during the dressing of the carcass at the slaughterhouse, sloppy storage, and dirty processing of meat, etc., is not excluded. For prophylaxis, see Meat, Sick Animals. If heavily decomposed meat is identified without difficulty, determining the initial stage of meat decomposition and distinguishing the latter from the adsorption of putrid odor by unspoiled meat when stored in the same place already presents certain difficulties. Until now, there has been no single universal method for determining the onset of meat decomposition, and for this it is necessary to perform several different reactions, from the results of which a conclusion should be drawn. The principal ones are: determining the reaction of the meat and establishing the hydrogen ion concentration of the meat. Meat at the moment of the animal's slaughter has an almost neutral reaction (at that, pH = 6.8–6.9). Twenty hours after slaughter, the meat acquires an acid reaction; the pH of beef and pork is then 6.0, horsemeat 5.8, mutton 6.2. During meat storage, the pH value remains unchanged until the onset of microbial decomposition of the meat, when under the influence of microorganisms NH₃ is formed, and the acid reaction of the meat changes to alkaline.

For beef, pH = 6.3 signifies the onset of spoilage (conditionally edible meat); at pH 6.6 the meat is unfit for consumption. For determining pH during meat examination, the colorimetric method is sufficient. - O t h e r methods for determining meat reaction. Litmus paper - see Meat. - L i t m u s tincture: aqueous extracts are prepared from the test meat and from knowingly wholesome meat. Three test tubes are taken and 10 cm³ of liquid are poured into each: into the 1st - Aq. destil., into the 2nd - extract from wholesome meat, and into the 3rd - the same from the test meat, and 2 drops of litmus tincture are added to each. The reaction of the meat is judged by the color change of the liquids. A new method for determining meat freshness has been proposed by Andriyevsky (Andrijevskyj; Prague, 1927), consisting of a whole series of tests: 1) M i c r o s c o p y. A small piece of meat is cut from the middle of the sample and applied to a microscope slide. The resulting smear is dried, stained, and examined with oil immersion. In a smear from fresh meat, microorganisms are either absent or single specimens fall into the field of view. In strongly spoiled meat, a mass of diverse microbes is visible in the field of view. - 2) Determination of the p h y s i c a l properties of the meat extract. An aqueous extract is prepared from the meat: 10.0 of minced meat is infused for 10 minutes in 100 cm³ of distilled water. This amount of extract from fresh meat filters through a smooth paper filter within 10 minutes, whereas that from decomposed meat takes 40-60 minutes and longer. The deeper the decomposition has gone, the slower the filtration proceeds. The extract from fresh meat is transparent and pink; from spoiled meat it is turbid and of a gray-muddy color. Meat that has yielded such an extract is unfit for consumption. - 3) Determination of pH - see above. - 4) Determination of ammonia - see Meat. - 5) Determination of p e r o x i d a s e: 20 hours after slaughter, the presence of peroxidase is always detected in wholesome meat. In the meat of animals that have died, been killed in agony or in a state of disease, as well as in rotting meat, peroxidase is absent. Determination of peroxidase: 5 drops of an alcoholic solution of benzidine or alpha-naphthol (1 : 500) and 2 drops of a 10% H₂O₂ solution are added to 2 cm³ of aqueous meat extract. In the case of peroxidase presence, adding benzidine produces a greenish-blue coloration that quickly turns to brown; with alpha-naphthol, a faint cherry color appears after 2-3 minutes. Reagents are valid for one month. - 6) D e t e r m i n a t i o n of g l o b u l i n s. When ammonia forms in meat, globulins, which are soluble in alkalis, pass into the aqueous extract and are detected by precipitation with acid solutions. To 2 cm³ of the extract, 2 drops of a 1% solution of one of the following acids are added: acetic, citric, or lactic. Upon heating to 70°, globulins precipitate. - 7) Determination of c h l o r i d e s appearing in rotting meat. To 1 cm³ of meat extract, 3 cm³ of Aq. destil. and 5 drops of a 2% AgNO₃ solution are added - a white precipitate is obtained. Sometimes meat decomposition proceeds toward acidic fermentation with the formation of H₂S. In these cases, the pH of beef is below 6.0. Determination of H₂S - see MEAT.

V. Volferts. The pathogenesis of meat poisoning is determined by the toxic and septic properties of the microbes causing these poisonings. The toxins produced by them are characterized by considerable heat resistance. Hence, upon consuming meat heated to a degree sufficient only to destroy microbes, the toxins, having retained their properties, can lead to a pure form of poisoning (intoxication). Upon consuming a product containing a significant amount of toxins and live microbes, the disease, having begun as acute intoxication, subsequently develops as an infectious disease. Forms of the disease in which septic phenomena predominate in the clinical picture are also possible (see Paratyphoid). The forms of diseases caused by the so-called meat poisoners (Bac. Breslau, or Flugge-Kansche, and Bac. Gartneri) can be divided into two main groups: 1) cholera-like, most acute gastroenteritis, cholera nostras paratyphosa, and 2) gastroenteritis proceeding in the form of an acute febrile disease (gastroenteritis paratyphosa). Usually, violent phenomena of the disease occur within a few hours after consuming the contaminated product. The onset of the disease is characterized by a feeling of general malaise, dizziness, nausea, weakness, the appearance of cold sweat, and pain in the epigastric region. Profuse vomiting and diarrhea develop rapidly. Such a form can pass as quickly as it developed. The entire disease can end within a day, leaving only general weakness. In severe cases, profuse vomiting and diarrhea (the stool loses its fecal coloration and takes on the appearance of rice water) lead to rapid dehydration of the body and disruption of its thermal balance. A picture fully corresponding to the algid stage of cholera develops: low temperature, rapid pulse drop (to a thready state), cyanosis, hoarse voice, sharpened facial features; skin gathered into a fold does not flatten out; hiccup; cramps occur in the extremities; urine output drops rapidly, down to complete anuria. In the sediment of scarce urine, there is protein, a lot of renal epithelium, various casts, erythrocytes, etc. Consciousness is preserved at the same time; patients complain of a feeling of anguish, insomnia, and dizziness. Such a severe state of the patients can change sharply for the better within a few hours or days, without any therapeutic intervention. In very 3!)

MEAT POISONING. In rare cases, it leads to rapid death. More often, death occurs on the 3rd to 4th day of the illness, when the phenomena of acute gastroenteritis and acute circulatory disorder are already subsiding and uremic phenomena begin to increase: facial flushing, conjunctivitis, deep infrequent breathing, nausea, painful vomiting, and stools acquiring the character of a colitic stool_; containing mucus and blood. Hence, the great prognostic significance of the degree of urinary output disturbance follows. The form of the disease depending predominantly not on toxins, but on infection, is characterized by an increase in temperature, headaches, aching, dryness in the mouth, the appearance of a cough, hoarseness, often the appearance of herpes; the tongue is coated, nausea, sparse vomiting, liquid foul-smelling stool, often mixed with blood and mucus. As a rule, within 1-2 days, the spleen enlarges. Yellowishness of the sclera and skin is often noted. The general appearance of the patient is febrile, sometimes there is a pronounced status typhosus. Erythematous rashes, urticaria, and hemorrhages are noted on the skin. Sometimes pain in the joints and neuralgic pain occur. The temperature curve is not characteristic. The disease lasts on average from 5 to 10 days and as a rule ends in recovery. Death usually depends on the outcome into sepsis. The most frequent complication of the disease is pneumonia. Diagnosis. The recognition of meat poisoning, i.e., establishing the connection of the disease with the consumption of contaminated meat, is facilitated in cases of group outbreaks. The paratyphoid nature of the disease is ascertained by bacteriological examination of duodenal contents, feces, urine, and blood. In infectious forms, along with bacteriological examination, serological methods (agglutination) must also be tested. In cases of pure intoxication, the diagnosis, not supported by laboratory examination, remains presumptive. Mild cases of meat poisoning are usually overlooked because they belong to the so-called vulgar gastroenterites of various etiologies. Forms of the cholera nostras type must be differentiated from cholera. Differentiation will be aided by taking into account the epidemiological situation, the initial rise in temperature usual for paratyphoid diseases, if only for the shortest period, significantly less than in cholera, and the success from the use of copious intravenous saline infusions. The question is resolved by bacteriological examination, i.e., the presence or absence of cholera vibrios. Confusion with arsenic poisoning is possible (anamnesis, severe abdominal cramps, and tenesmus). Mushroom poisoning is excluded or established by anamnesis. Acute febrile forms require differentiation from the onset of typhoid fever (acute onset, presence of vomiting, foul stool, temperature course) and from the so-called gastrointestinal form of influenza. The controversial nature of the existence of purely influenza-related gastroenterites, without the superposition of any secondary intestinal infection on the influenza infection, and the wide spread of paratyphoid infections gives reason to think that at least a significant part of the gastrointestinal forms of influenza so frequently diagnosed are essentially primary paratyphoid diseases. Part of them may be associated with the consumption of infected meat products. Supporting points for the clinical recognition of the paratyphoid nature of the diseases are enlargement of the spleen, jaundice, the appearance of rashes, and mucosanguineous stools. Treatment is symptomatic, there is no serotherapy, and vaccine therapy has not been developed. In forms of cholera nostras, the use of copious intravenous saline infusions, which restore the water, salt, and thermal balance and the blood circulation of the organism, acquires great importance. It is necessary to administer 2-3 liters of a 0.7% NaCl solution, warmed to 40°, in a single dose. In less severe and acute cases, subcutaneous administration of the saline solution can also be used. By supplying the organism with water and chlorides, one can safely intensify diarrhea for the purpose of the quickest elimination of the infectious agent and toxins. Sodium sulfate is prescribed at 20-30 g, dissolved in ¹/₂ a glass of hot water, along with abundant drinking. Vomiting can be alleviated by prescribing a 0.3 : 100.0 Cupri sulfurici solution, a tablespoon until effect. Gastric lavage is useful. Among cardiac remedies, 20% camphor oil at 2.0, 3-4 times a day. Hot baths, heating pads. For the purpose of toxin destruction, the use of potassium permanganate is recommended (Kali hyperm. 0.25 : 500.0 water, 1 glass every ¹/₂ hour). The use of animal charcoal (in tablespoons) or a suspension of white clay for the purpose of toxin adsorption is burdensome for patients and of little productivity. The prescription of binding agents in meat poisoning must be considered contraindicated.