Emergency Preparedness

Kern Medical Bioterrorism Response Guide Section 2-A-3 – Botulism

The typical incubation period following the ingestion of contaminated food is 12 – 72 hours but may be as short as 6 hours or as long as 10 days depending on the size of the inoculum ingested. Recent primate studies indicate the symptoms may not appear for several days when a low dose of toxin is inhaled. Clinical Presentation Botulism is an acute, afebrile, symmetric, descending flaccid paralysis that always begins in the bulbar musculature. It is not possible to have botulism without having multiple cranial nerve palsies. Disease manifestations are similar regardless of botulinum toxin type. However, the extent and pace of paralysis may vary considerably among patients. Some patients may be mildly affected. Patients with botulism typically present with difficulty seeing, speaking, and/or swallowing. Eye symptoms such as blurred vision are due to mydriasis, diplopia, ptosis, and photophobia. Other cranial nerve symptoms include dysarthria, dysphonia, and dysphagia. Flaccid skeletal muscle paralysis follows in a symmetrical, descending, and progressive manner. Collapse of the upper airway may occur due to weakness of the oropharyngeal muscles. As the descending motor weakness progresses, the diaphragm and accessory muscles lead to respiratory failure. The autonomic effects of botulism are manifested by typical anticholinergic signs and symptoms. These include dry mouth, ileus, constipation, and urinary retention. Nausea and vomiting may occur as nonspecific sequelae of an ileus. Dilated pupils (mydriasis) are seen in approximately 50% of cases. Sensory symptoms do not occur with the exception of circumoral and peripheral paresthesias from hyperventilation as the patient becomes frightened by onset of paralysis. The toxins do not cross the blood/brain barrier and do not cause central nervous system disease. However, patients often appear lethargic and have communication difficulties because of bulbar palsies. The psychological sequelae of botulism may be severe and require specific intervention. On physical examination, the patient is generally afebrile, alert, and oriented. Postural hypotension may be present. The mucous membranes may be dry and crusted and the patient may complain of a sore throat, difficulty swallowing and speaking. The gag reflex may be absent and the pupils may be dilated and even fixed. Ptosis and extraocular muscle palsies may be present. Variable degrees of skeletal muscle weakness may be observed depending on the degree of progression in the individual patient. Deep reflexes may be present or absent. Cyanosis or narcosis from CO 2 retention may be evident as the respiratory muscles become paralyzed. Individual cases might be confused clinically with other neuromuscular disorders such as Guillian-Barré syndrome, myasthenia gravis, or tick paralysis. The edrophonium or Tensilon® test may be transiently positive in botulism so it may not distinguish botulism

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