Type B botulism in man

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      An outbreak of type B botulism occurring in four of eight family members consuming a meal of home-canned “pickled” beans is reported. With the exception of somnolence, which has not been emphasized previously, the symptoms and signs were virtually identical with those noted previously in an outbreak of type E disease studied by the same group.
      Routine laboratory studies were of no aid in establishing a diagnosis. Electromyographic and electroencephalographic studies were likewise unrevealing. However, electrocardiograms in three of the four patients showed changes in the T waves adding to the mounting evidence that botulinus toxins exert a direct cardiac action.
      The mouse inoculation test again proved to be a useful tool in confirming the diagnosis of botulism. Serum obtained from all four patients seven to nine days after toxin ingestion contained a mouse-toxic substance which in two cases could be definitely identified as type B toxin by neutralization tests. As noted in past outbreaks of botulism, the clinical disease did not develop in all who ate the toxin-contaminated food. Studies on those who escaped disease in this outbreak failed to demonstrate pre-existing botulinus antitoxin. The 50 per cent attack rate and the possible presence of toxin in the blood stream of one asymptomatic subject who consumed the contaminated beans suggest that certain individuals may possess inherent resistance mechanisms to botulinus toxins which are not yet defined.
      As with type E disease, type B botulism did not result in detectable antibody response. Type B antitoxin was found only in those subjects who received antitoxin therapy; it did not appear after recovery from clinical botulism and was not evoked by botulinus toxoid.
      All the patients in the present series recovered completely. Ophthalmologic abnormalities were the last to return to normal. Contrary to experience with type E disease, antitoxin therapy was not accompanied by dramatic clinical improvement. However, the demonstration of toxin in the blood stream of patients long after toxin ingestion suggests that all persons with moderate or severe clinical botulism should be treated with antitoxin when the diagnosis is made to neutralize toxin as yetunbound.
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