Foodborne Neurotoxins

Botulism is a rare life-threatening neuroparalytic syndrome caused by an anaerobic organism, Clostridium botulinum, that produces an extremely potent neurotoxin. C. botulinum spores are heat resistant; when they germinate, these spores become toxin-producing bacilli. The spores are extremely hardy; in contrast, their toxins are denatured at greater than 80° C. The heat-resistant properties of Clostridium botulinum permit home-processed foods to provide a culture medium for spore growth and subsequent neurotoxin production. There are eight distinct C. botulinum toxin types (A, B, C1, C2, D, E, F, and G); only types A, B, and E may lead to clinical botulism. There are five acquired forms of botulism, namely foodborne, infantile, wound, adult enteric infectious, and inhalational. In the United States infantile botulism is the most common form (72%); the foodborne form comprises 25% of cases. Wound and adult infectious botulism are very uncommon (comprising 3% of cases).

Symptom onset in foodborne botulism begins 12 to 36 hours after toxin ingestion, characterized by nausea, vomiting, abdominal pain, diarrhea, and dry mouth. Neurologic manifestations develop rapidly, with pronounced cranial nerve paresis and extremity weakness. Pupils are sluggish or fixed. Ptosis, diplopia, dysphagia, dysarthria, and facial weakness develop. A descending muscle paralysis occurs; this initially affects arms, then legs, and subsequently there is diaphragmatic involvement.

Diagnosis is primarily a clinical, later confirmed by demonstration of toxin in the serum. This is a mouse bioassay performed by specialized laboratories. The toxin sometimes occurs in stool, vomitus, and contaminated food. This finding is diagnostic, with a classic clinical presentation. Electromyography/nerve conduction studies (EMG/NCS) demonstrate a classic presynaptic neuromuscular junction (NMJ) disorder with low-amplitude motor responses and postactivation facilitation.

When the clinical setting is highly suspicious, emergent antitoxin therapy is indicated. Equine serum heptavalent antitoxin, available through the Centers for Disease Control and Prevention (CDC, Atlanta), contains antibodies to botulism types (A through G). Utilizing expert respiratory/supportive care keeps mortality very low. Most patients have excellent recoveries within 3 months.

Trichinosis is an acute parasitic infection acquired by ingesting undercooked pork infested with roundworm Trichinella spiralis larvae. Typically, acute systemic infectious symptoms develop, that is, fever, headache, and severe muscle pain/tenderness; periorbital edema occurs early and is a good clue to diagnosis. Other manifestations include encephalitis, myocarditis, and subconjunctival hemorrhages. Leukocytosis with marked eosinophilia is present. Serum creatine kinase is elevated. Cerebrospinal fluid analysis demonstrates a lymphocyte pleocytosis and increased protein. Primary treatment is with mebendazole or albendazole; prednisone will blunt systemic responses to dying trichinella.

Ciguatera is the most common fish food poisoning in tropical coastal regions, accounting for the majority of fish-related foodborne disease outbreaks in the United States. There are several distinct ciguatera toxins; ciguatoxin is the best known. It is a heat-stable neurotoxin that opens voltage-dependent cell membrane sodium channels triggering depolarization. Dinoflagellates, algae-like organisms, form these toxins. These are later consumed by large reef fish, including grouper, red snapper, amberjack, and barracuda, which, when ingested by humans, leads to clinical poisoning.

Gastrointestinal symptoms develop acutely (3-6 hours) after eating contaminated fish. Neurologic symptoms may begin within 3 to 72 hours. These include paresthesias, nerve palsies, weakness, and hot/cold temperature reversal. Cardiovascular abnormalities occur within 2 to 5 days, including hypotension, bradycardia, and heart block.

There is no commercially available serum test for ciguatera toxin; diagnosis depends on clinical suspicion. Supportive care is the primary treatment modality when available; mortality is low. After an attack of ciguatoxin, patients are instructed to avoid all fish for at least 6 months because a second attack of ciguatera on the heels of the first may be much worse than the initial episode.

Shellfish poisoning relates to blooms of algae known as “red tides.” There are several toxins, with saxitoxin the best known. Bivalve mollusks, including clams, mussels, scallops, oysters, crabs, and snails preferentially take up saxitoxin. In humans, saxitoxin blocks sodium ion channels, leading to rapid evolution of neurologic symptoms, ranging from mild perioral tingling to severe paralysis with respiratory failure that leads to death within hours when ventilatory support is lacking. Treatment is supportive—primarily mechanical ventilation for severely affected patients. Patients improve gradually over 12 to 72 hours.

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