Food Poisoning Part 8

Vertigo and nystagmus developed [a few hours after eating] in a startling degree, the car [in which he was being taken to his house]

seemed to be ascending an endless spiral, the stars made circles in the sky, and the houses by the wayside reeled. The lighted doorway of my house seemed to approach and surround me as I was carried in.

My bed for the moment presented itself as a vertical surface which I could not conceive to be a resting place.... Whenever I opened my eyes on this day [the next day] the impression of gyration of the room was appalling.... To turn my head even very slowly from one side to the other brought an accession of the overpowering giddiness.... [eight days after the beginning of the attack]. The nystagmus now became limited to momentary onsets, but in its place I became aware of a peculiar diplopia. The image of one retina was not merely displaced from the position of its fellow but was tilted about 15 degrees from parallel.... This fantastic diplopia gradually gave place to the familiar variety and this occurred less and less often as my convalescence proceeded. From [this date] my recovery pursued a course which was dishearteningly slow but free from any setbacks. Among the persistent symptoms were ... the visual difficulties mentioned. The left pupil was usually smaller than the right and I thought I detected a slight failure to relax accommodation with the left eye. Reading was difficult for several weeks and the ability to write, as requiring closer fixation, was still longer in returning.

In the cases reported by Sheppard visual symptoms were the initial signs of trouble, double vision, mistiness, and inability to hit the mark in shooting being the first complaint.

The time elapsing between eating the implicated food and the onset of the earliest symptoms is usually between twelve and forty-eight hours, but may be much less. In Stiles's case the interval was apparently less than three hours.

_Anatomical lesions._--In fatal cases no characteristic gross changes are observed in the various organs. It has been stated by some writers that microscopic degenerative changes occur in the ganglion cells, involving especially the so-called Nissl granules, but in the carefully studied case reported by Ophuls[107] the Nissl granules were quite normal in size, arrangement, and staining qualities. There was, in fact, no evidence to substantiate the hypothesis of a specific action of the toxin on the nerve-cells. On the other hand, Ophuls found numerous hemorrhages in the brain-stem and multiple thromboses in both the arteries and veins. He holds, consequently, that the indications of severe disturbances of brain circulation a.s.sociated with hemorrhages and thrombosis in medulla and pons are sufficient to explain the symptoms of botulism poisoning without having recourse to the a.s.sumption that the poison has a specific action on certain ganglion cells.

_Bacteriology._--The cause of botulism poisoning was discovered by Van Ermengem to be the toxin produced by a bacillus which he named _B.

botulinus_. This organism was isolated from portions of a ham that had caused fifty cases of poisoning (1895) at Ellezelles (Belgium), and also from the spleen and gastric contents of one of the three fatal cases.

The bacillus grows only in the absence of oxygen (strict anaerobe), stains by Gram's method, forms terminal spores, and develops best at 22C. Unlike most bacteria dangerous to man, it appears unable to grow in the human body, and its injurious effect is limited to the action of the toxin produced in foodstuffs outside the body. Botulism is an intoxication--not an infection. The fact that the bacillus can grow in nature only when the free oxygen supply is cut off explains in part at least the relatively rare occurrence of botulism since all the conditions necessary for the production of the botulism toxin do not commonly concur. Next to nothing is known as to how widely _B.

botulinus_ is distributed. Except in connection with the cases of poisoning it has been reported but once in nature.[108] The botulism poison is a true bacterial toxin, chemically unstable, destroyed by heating at 80C. for 30 minutes, capable of provoking violent symptoms in minute doses, and possessing the property characteristic of all true toxins of generating an ant.i.toxin when injected in small, non-fatal doses into the bodies of susceptible animals. In animal experiments the toxin formed by _B. botulinus_ has been found capable of reproducing the typical clinical picture of this form of food poisoning. Symptoms of paralysis are produced in rabbits, guinea-pigs, and other animals by the injection of so small a dose as 0.0001 c.c. of a filtered broth culture.

[Ill.u.s.tration: FIG. 11.--_Bacillus botulinus_ with spores. Pure culture on sugar-gelatin. Van Ermengem preparation. (Kolle and Wa.s.sermann.)]

_Epidemiology._--The conditions under which _B. botulinus_ occurs and is given opportunities for multiplying are not completely known. It is possible that there are localities where this bacillus is particularly abundant in the soil or in the intestinal contents of swine or other domestic animals, but on the whole it seems more probable that the organism is widely distributed, but that it does not often find suitable conditions for entrance into, and multiplication in, human food.

Practically all the reported cases of botulism have been caused by food which has been given some sort of preliminary treatment, as smoking, pickling, or canning, then allowed to stand for a time, and _eaten before cooking_. Since both the bacillus, including the spore stage, and its toxin are destroyed by relatively slight heating, it is clear that a rather unusual set of factors must co-operate in order that botulism poisoning shall take place. These are evidently: (1) the presence of the bacilli in sufficient numbers in a suitable foodstuff; (2) the initial preparation of the food by a method that does not destroy the _B.

botulinus_--inadequate smoking, too weak brine,[109] or insufficient cooking; (3) the holding of this inadequately preserved food for a sufficient length of time under the right conditions of temperature and lack of oxygen; (4) the use of this food, in which conditions have conspired to favor the production of toxin by _B. botulinus_, without final adequate cooking. It seems as reasonable to suppose that the infrequency with which these several factors coincide is responsible for the relative uncommonness of botulism as to suppose it due to the rarity of the specific bacillus. In the Belgian outbreak studied by Van Ermengem the poisonous ham had lain at the bottom of a cask of brine (anaerobic conditions) while the other ham of the same animal lay on top of it but was not covered with brine, and was eaten without producing any poisonous effect. In this instance the presence or absence of favorable conditions for anaerobic growth seemed to be the decisive factor.

_Prevention and treatment._--The food in which _B. botulinus_ has grown does not seem to be altered in a way that necessarily arouses suspicion. In the case described by Romer the incriminated ham showed bluish-gray areas from which _B. botulinus_ could be isolated, but this condition does not seem to have attracted attention before the poisoning occurred and was an observation made only after the event. So far as can be learned the meat that has caused botulism has always come from perfectly sound animals. In some cases the accused article of food is said to have had a rancid or acrid taste (due to butyric acid?), but there is nothing definitely characteristic about this, as the majority of anaerobes produce butyric acid. If, as in the Darmstadt[110] and Stanford University[111] epidemics, the food (canned beans) is served with salad dressing, a sour taste might pa.s.s without notice or even add to the relish. In the instance reported by Sheppard the canned beans were good in appearance, taste, and smell.

The obvious precaution to take against poisoning of this sort is first the use of adequate methods of food preservation. To judge from the recorded outbreaks, domestically prepared vegetables and meats are more likely to give rise to botulism than those prepared commercially on a large scale. The general use of steam under pressure in the large canning factories affords a high degree of protection against the anaerobic bacteria and their resistant spores. Whatever the method of treatment, all canned or preserved food having an unnatural appearance, taste, or odor should be rejected. Reheating of all prepared foods immediately before use is an additional safeguard. Foods, such as salads, composed wholly or in part of uncooked materials should not be allowed to stand overnight before being served.

If symptoms of botulism, such as visual disturbances, become manifest, the stomach should be emptied with a stomach pump, cathartics administered, and strychnine and other stimulants given as required.

Since one of the noteworthy features of this disease is the paralysis of the intestinal tract by the toxin absorbed, the guilty food may lie for a long time in the stomach (cf. Stiles, _loc. cit._). Consequently, measures to empty the stomach should be taken even if the patient does not come under observation until several days after the poisonous food has been eaten.

An ant.i.toxic serum has been prepared at the Koch Inst.i.tute in Berlin.

This serum has given successful results in animal experimentation, but has not been used, so far as I can learn, in any human outbreak. It is not available at any point in this country.

OTHER BACTERIAL POISONS

The interesting case reported by Barber[112] shows that there are other possibilities of food poisoning by formed bacterial poisons. Acute attacks of gastro-enteritis were produced in several individuals by the use of milk containing a poisonous substance elaborated by a white staphylococcus. This staphylococcus occurred in almost pure culture in the udder of the cow from which the milk was derived. The milk when used fresh was harmless and the poison was generated in effective quant.i.ties only when the milk stood some hours at room temperature before being used. The symptoms were similar to those usually ascribed to "ptomain poisoning."

SPOILED AND DECOMPOSED FOOD

There is a general belief that food is unwholesome whenever the evidence of the senses shows it to be more or less decomposed. This opinion finds expression in civilized countries in many legal enactments forbidding traffic in decomposed meats, vegetables, and fruits. There is unfortunately lack of evidence as to what kinds or degree of visible decomposition are most dangerous. In fact, some foods of high nutrient value, notably cheeses, are eaten only after somewhat extensive decomposition processes (termed ripening) have taken place. The characteristic flavors or aromas of the various hard and soft cheeses are due to the substances formed by certain species of molds and bacteria and are just as properly to be regarded as decomposition products as the unpleasant stenches generated by decomposing eggs or meat. Indeed, some of the decomposition products formed in the ripening of Brie, Camembert, or Limburger are similar to, if not identical with, those which are a.s.sociated with spoiled foods. Sour milk, again, is recommended and commonly used as a food or beverage for persons in delicate health, and yet sour milk contains many millions of bacteria and their decomposition products. Some of the bacteria commonly concerned in the natural souring of milk are closely related to pathogenic types. The partial decomposition of meats and game birds is often considered to be advantageous rather than otherwise. Even eggs, a food whose "freshness" is marred for most persons by the initial stages of decomposition, are ripened in various ways by the Chinese and eaten as a delicacy after the lapse of months or years. The preserved ducks'

eggs known as pidan are stored for months in a pasty mixture of tea, lime, salt, and wood ashes. "They are very different from fresh eggs.

The somewhat darkened sh.e.l.l has numerous dark green dots on the inner membrane. Both the white and yolk are coagulated; the white is brown, more or less like coffee jelly...."[113] Increase of ammoniacal nitrogen has taken place to an extraordinary degree in these eggs, indicating much decomposition of the egg protein. The ammoniacal nitrogen in pidan is considerably higher than in the eggs known by egg candlers as black rots.

It is evident, therefore, that bacterial growth in substances used as food is not necessarily injurious and may in some cases increase the palatability of food without destroying its wholesomeness. Little or nothing is known about the correlation of visible signs of decomposition with the presence of poisonous products, and it is at present impossible to say at what point in the process of decomposition a food becomes unfit to use owing to the acc.u.mulation of poisonous substances within it. There seems to be no connection between the natural repugnance to the use of a food and its unwholesomeness. Under ordinary conditions the nauseous character of very stale eggs is proverbial, and yet few nitrogenous foods have so clear a health record as eggs or have been so infrequently connected with food poisoning outbreaks.

It might seem tempting to conclude on the basis of the available evidence that spoiled or decomposed foods possess poisonous qualities only when certain specific bacteria, like the _B. botulinus_ already discussed, have accidentally invaded them and formed definite and specific poisons. But we have no right to a.s.sume that the everyday decomposition products of the ba.n.a.l bacteria are in all cases without injurious effects. Even though no sharply defined acute form of poisoning may be laid at their door, it does not follow that an irritating or perhaps slightly toxic action of the ordinary decomposition products is altogether absent. Our present knowledge of the nature and degree of danger to be apprehended from the use of spoiled food is imperfect and unsatisfactory. That fact, however, does not release us from the obligation to continue measures of protection based even to a limited extent on experience.

FOOTNOTES:

[95] Another species of _Claviceps_ (_C. paspali_) which attacks the seeds of a wild gra.s.s is believed to be responsible for certain outbreaks of poisoning among cattle and horses (_Science_, XLIII [1916], 894).

[96] Barger (_Jour. Chem. Soc._, XCV [1909], 1123) has shown that parahydroxyphenylethylamine is present in ergot and is in some degree responsible for the physiological action of the drug.

[97] Although some of the early outbreaks were traced to the use of sausage, particularly in Wurttemberg, the proportion of recent botulism poisoning attributed to this food is no greater than of sausage-conveyed infections with the paratyphoid bacillus (chap. vi), and a number of the most completely studied outbreaks of botulism have been traced to ham, beans, and other foods.

[98] _Deutsche Viertelj. f. offentl. Ges._, XLV (1913), 8.

[99] E. Sacquepee, _Progres med._, XXVI (1910), 583.

[100] _Report to Local Govt. Board on Bacterial Food Poisoning and Food Inspection_, N.S. No. 77, 1913, p. 27.

[101] _Southern Cal. Pract._, XXII (1907), 370.

[102] _Ibid._, XXV (1910), 121.

[103] _Arch. of Int. Med._, XIV (1914), 589.

[104] _Amer. Med._, X (1915), 85.

[105] _Jour. Amer. Med. a.s.soc._, LXI (1913), 2301.

[106] _Loc. cit._

[107] _Loc. cit._

[108] In the feces of a healthy pig (Kempner and Pollock, _Deutsche med.

Wchnschr._, XXIII [1897], 505).

[109] _B. botulinus_ does not develop in media containing over 6 per cent of salt and should not be able to grow in meat properly covered in brine made with 10 per cent of salt (Romer, _Centralbl. f. Bakt._, XXVII [1900], 857).

[110] G. Landmann, _Hyg. Rundschau_, XIV (1904), 449.

[111] Wilbur and Ophuls, _Arch. of Int. Med._, XIV (1914), 589.

[112] _Phil. Jour. of Science_, IX (1914), B6, p. 515.

[113] K. Blunt and C. C. w.a.n.g, _Jour. Biol. Chem._, XXVIII (1916), 125.

CHAPTER IX

POISONING OF OBSCURE OR UNKNOWN NATURE

While many and diverse causes of food poisoning have been discussed in the foregoing pages, there remain certain affections definitely connected with food that are still of obscure or doubtful causation.