Girl, aged 23, Tuesday evening, Nov. 23, 1913, ate the dinner including the canned string beans of the light green color together with a little rare roast beef. The following day she felt perfectly normal except that at 10:00 in the evening the eyes felt strained after some sewing. Thursday morning, thirty-six hours after the meal, when the patient awoke, the eyes were out of focus, appetite was not good, and she felt very tired. At night she had still no appetite, was nauseated, and vomited the noon meal apparently undigested. Friday morning, two and one-half days after the meal, the eyes were worse, objects being seen double on quick movement, and it was noticed that they had a tendency to be crossed. A peculiar mistiness of vision was also complained of. She was in bed until late in the afternoon, when she visited Dr. Black. She had had some disturbance in swallowing previous to this time and stated that it felt as if "something came up from below" that interfered with deglutition. The fourth day she remained in bed, was much constipated, and noticed a marked decrease in the amount of urine voided. There was at no time pain except for occasional mild abdominal cramps, no headache, subnormal temperature, and a normal pulse. The fourth and fifth days the breathing became difficult at times and swallowing was almost impossible. The patient complained of a dry throat with annoying thirst. The sixth day there were periods of a sense of suffocation with a vague feeling of unrest and as if there might be difficulty in getting the next breath. The upper lids had begun to droop. The voice was nasal. When the attempt was made to swallow liquids they passed back through the nose. The patient felt markedly weak.
Physical examination at this time showed ptosis of both upper eyelids, dilatation of the right pupil, sluggish reaction to light of both pupils, apparent paralysis of the internal rectus of the left eye, normal retina, inability to raise the head, control apparently having been lost of the muscles of the neck, inability to swallow, absence of taste. The tongue was heavily coated and the throat was covered with a viscid whitish mucus clinging to the mucous membrane. The soft palate could be raised but was sluggish, particularly on the right side. The exudate on the right tonsil was so marked that it resembled somewhat a diphtheritic membrane. The seventh day there was some change in the condition; occasional periods occurred when swallowing was more effective, and there was less tendency to strangle. On the eleventh day there was some improvement of the eyes, still strangling on swallowing, sensation of taste was keener, and the general condition improved. The twelfth day the patient was able to move her head, but was unable to lift it except when she took hold of the braids of her hair, and pulled the head forward. The eyes could be opened slightly, speech was less nasal and more distinct, and improvement in swallowing was marked. At the end of two weeks the patient was able to take soft diet freely, and at four weeks she was up in a chair for a couple of hours complaining only of general weakness and inability to use her eyes. At the end of five weeks she was able to leave the hospital and return to her home and later to resume her regular work.
In all cases the nervous system is strikingly affected in this form of food poisoning. Dizziness, double vision, difficulty in chewing and swallowing, and other symptoms of nervous involvement occur with varying intensity and may persist for a long time after the first signs of the attack. Temperature, pulse, and respiration remain practically normal. In contrast with the traditional type of food poisoning gastro-intestinal symptoms may be slight or altogether lacking. Freedom from abdominal pain is usually noted; diarrhea is the exception and constipation the rule; vomiting sometimes occurs, but may be absent. In the cases described by Sheppard there was "an entire absence of the usual gastro-intestinal symptoms from first to last, no pain or sensory disturbance and no elevation of temperature." The visual disturbances are very characteristic. Stiles relates his own experiences as follows:
Vertigo and nystagmus developed 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 Ophüls[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, Ophüls 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 associated with hemorrhages and thrombosis in medulla and pons are sufficient to explain the symptoms of botulism poisoning without having recourse to the assumption 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 anaërobe), stains by Gram's method, forms terminal spores, and develops best at 22°C. 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 80°C. for 30 minutes, capable of provoking violent symptoms in minute doses, and possessing the property characteristic of all true toxins of generating an antitoxin 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.
