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distal affection of the limbs to a rapidly evolving, ascending paralysis, like that of the Guillain-Barre syndrome; CSF ndings are similar as well (acellular uid with elevated protein) The neuropathic symptoms progress for a week or two, and if the patient does not succumb to respiratory paralysis or cardiac failure (cardiomyopathy), these conditions stabilize and then improve slowly and more or less completely The early oropharyngeal symptoms, the unique ciliary paralysis with relatively retained pupillary response to light, and the subacute evolution of a delayed symmetrical sensorimotor peripheral neuropathy distinguish diphtheria from all other forms of polyneuropathy The long latency between the initial infection and the involvement of the nervous system has no clear explanation In experimental animals, Waksman and colleagues demonstrated that the toxin reaches the Schwann cells in the most vascular parts of the peripheral nervous system within 24 to 48 h of infection, but its metabolic effect on cell membranes extends over a period of weeks As in humans, the toxin produces demyelination in the proximal parts of spinal nerves, in dorsal root ganglia, and in spinal roots The cardiac musculature and the conducting system of the heart undergoes mild focal necrosis The source of diphtheritic infection may be extrafaucial a penetrating wound, skin ulcer, or umbilicus The systemic and neurologic complications of faucial diphtheria can also be observed in the extrafaucial form of the disease, after a similar latent period It is probable, therefore, that the toxin reaches its neural site via the bloodstream; but, in addition, some action is exerted locally, as evidenced by palatal paralysis in faucial cases and by initial weakness and sensory impairment in the neighborhood of the infected wound There is no speci c treatment for any of the neurologic complications of diphtheria It is generally agreed that the administration of antitoxin within 48 h of the earliest symptoms of the primary diphtheritic infection lessens the incidence and severity of the peripheral nerve complications The polyneuropathy of diphtheria is discussed further in Chap 46 (page 1128).

Botulism is a rare form of food-borne illness caused by the exotoxin of C botulinum Outbreaks of poisoning are most often due to ingested bacteria contained in home-preserved than to commercially canned products, and vegetables and home-cured ham are incriminated more commonly than are other food products Very rarely, a contaminated wound is the source of infection Although the disease is ubiquitous, ve western states (California, Washington, Colorado, New Mexico, and Oregon) account for more than half of all reported outbreaks in the United States Neonatal and infantile forms of the disease have been reported These are due to absorption of the toxin formed by germination of ingested spores (rather than ingestion of preformed toxin), an important source of which is contaminated natural (raw) honey A few adult cases may have a similar source It is now well established, on the basis of observations in both animals and humans, that the primary site of action of botulinus toxin is at the neuromuscular junction, more speci cally on the presynaptic endings The toxin interferes with the release of acetylcholine from peripheral motor nerves by a mechanism like that of tetanus toxin on the spinal interneurons (see previous discussion) The physiologic defect is similar to the one that characterizes

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the myasthenic syndrome of Lambert-Eaton (page 1259) but different from that of myasthenia gravis Symptoms usually appear within 12 to 36 h of ingestion of the tainted food Anorexia, nausea, and vomiting occur in most patients As a rule, blurred vision and diplopia are the initial neural symptoms; their association with ptosis, strabismus, and extraocular muscle palsies, particularly of the sixth nerve, may at rst suggest a diagnosis of myasthenia gravis In botulism, however, the pupils are often unreactive Other symptoms of bulbar involvement nasality of the voice and hoarseness, dysarthria, dysphagia, and an inability to phonate follow in quick succession, and these, in turn, are followed by progressive weakness of muscles of the face, neck, trunk, and limbs and by respiratory insuf ciency Despite the oropharyngeal weakness, it is not unusual for the gag re ex to be retained Tendon re exes are lost in cases of severe generalized weakness These symptoms and signs evolve rapidly, over 2 to 4 days as a rule, and may be mistaken for those of the Guillain-Barre syndrome Sensation remains intact, however, and the spinal uid usually shows no abnormalities Severe constipation is characteristic of botulism, due perhaps to paresis of smooth muscle of the intestine Consciousness is retained throughout the illness unless severe degrees of anoxia develop In the past, the mortality was consistently above 60 percent, but it has declined in recent decades, with improvements in the intensive care of acute respiratory failure and the effectiveness of C botulinum antitoxins The clinical diagnosis can be con rmed by electrophysiologic studies Speci cally, there is reduced amplitude of evoked muscle potentials and an increase in amplitude with rapid repetitive nerve stimulation (the opposite of what is found in myasthenia gravis) In patients who recover, improvement begins within a few weeks, rst in ocular movement, then in other cranial nerve function Complete recovery of paralyzed limb and trunk musculature may take many months The three types of botulinus toxin, A, B, and E, cannot be distinguished by their clinical effects alone, so that the patient should receive the trivalent antiserum as soon as the clinical diagnosis is made This antitoxin can be obtained from the Centers for Disease Control and Prevention, Atlanta An initial dose of 10,000 U is given intravenously after intradermal testing for sensitivity to horse serum, followed by daily doses of 50,000 U intramuscularly until improvement begins Guanidine hydrochloride (50 mg/kg) has been somewhat useful in reversing the weakness of limb and extraocular muscles Antitoxin and guanidine probably change the course of the illness relatively little, and recovery, in the nal analysis, depends on the effectiveness of respiratory care, maintenance of uid and electrolyte balance, prevention of infection, and so on The skilled injection of small quantities of botulinus toxin into a muscle will weaken or paralyze it for weeks to months Advantage is taken of this phenomenon in the treatment of the localized dystonias (page 93).

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