Introduction

Botulism is caused by neurotoxins elaborated by Clostridium botulinum, an anaerobic gram- positive organism with sub-terminal spores. Human botulism occurs worldwide. Food borne botulism is acquired by ingestion of food contaminated with preformed toxin most commonly, home canned food (₁).

Clostridium botulinum toxin blocks acetylcholine in a dose-dependent fashion, resulting in acute symmetric diplopia, dysarthria, dysphonia, dysphagia and possible neurological sequela despite the route exposure (i.e. food-borne, wound, intestinal, inhalation). Disease secondary to genetically engineered C. botulinum may differ from that of inadvertence exposure.

Clostridium botulinum commonly found in food poisoning: poorly preserved meat, sausage, fruit or vegetables (type A or B), marine products (type E), liver pate, venison jerky (type F). An anaerobic, spore-forming, gram-positive bacteria; ingestion of the toxin or wound contamination are likely routes of exposure; a heat labile neurotoxin which causes irreversible neuromuscular blockade and prevents acetylcholine release; the spores are heat-resistant (₂).

Case report

A forty years old male patient admitted to emergency department of our hospital complaining of stomachache, nausea and vomiting for two days. The patient's medical history revealed an inguinal hernia operation three years ago. Surgery clinic thought that the patient's clinical situation was brid ileus, since he had been operated three years ago. The patient was operated and no surgical pathology was obtained to explain his ileus.

In postoperative second day, the patient was admitted to ICU from the general surgery department for diplopia, dysphagia and ptosis followed by descending paralysis and respiratory failure. He had confused consciousness, normo-isocoric pupils, bilateral positive light reflexes, Hb: 11 gr/dl, Htc: 32%, white blood cell count: 8700 mm3, platelet: 315 000 mm3, Na: 140 mEq/dl K: 3.63 mEq/dl, Cl: 103 mEq/dl, Ca: 8 mEq/dl, pH: 7.40, pO2: 50 mmHg, pCO2, 54 mmHg, HCO3: 32 mEq/dl, Sat O2: 84%. The patient was intubated awake and ventilated by mechanic ventilator.

According to the information taken from his parents, he had eaten canned green bean which has been made by him, 3 days before he came to the hospital. The clinical situation was thought that it might be botulism. Although laboratory tests for botulism cannot be conducted in our hospital, botulinum antitoxin (Trivalent A, B, and E) (250 mg two times) administered as soon as possible and also pridostigmin bromure (60 mg 4x1), antibiotics and supportive therapy. On the 7th day of mechanical ventilation patient was extubated.

The patient was transferred from ICU to neurology department as conscious and with bilateral light ptosis, well soft palate, without any paresthesia, light weakness, absent gag reflex, hypophonic voice, usual cranial nerves, absent motor lateralization signs, usual cerebellum, absent pathologic reflexes. The patient was discharged from the hospital two days later.

Discussion

An anaerobic, spore-forming, gram-positive bacteria; ingestion of the toxin or wound contamination are likely routes of exposure; a heat labile neurotoxin which causes irreversible neuromuscular blockade and prevents acetylcholine release; the spores are heat-resistant (₂). Signs and symptoms of acute overdose may be delayed up to 36 hours. Because the incubation period for botulism is usually 18-36 hours after ingestion of food containing toxin. Cranial nerve involvement marks the onset of symptoms, which usually consist of diplopia, dysarthria and/or dysphagia. Paralysis is symmetrical and descending and can lead to respiratory failure and death. Nausea, vomiting, and abdominal pain may precede or follow the onset of paralysis. Dizziness, blurred vision, dry mouth and dry sore throat are common. Fever is not documented usually. Ptosis is common; fixed or dilated pupils are noted in 50% of cases. The gag reflex can be suppressed and deep tendon reflexes can be either normal or decreased. Paralytic ileus, severe constipation and urinary retention are common. Gastrointestinal symptoms are usually absent in wound botulism (₂).

The diagnosis of botulism must be suspected on clinical grounds in the context of an approximate history. Conditions are often confused with botulism include Myasthenia Gravis and Guillain- Barre Syndrome. Definitive diagnosis is made by demonstration of toxin in the serum; however, the test may be negative despite of infection and cannot be conducted in all laboratories. Other fluids that may yield toxin are vomits, gastric fluid, and stool. Isolation of the organism from food is not diagnostic (₁). In our case, due to no necessary laboratory tests for botulism can be conducted in our hospital setting, we could not support our diagnosis with laboratory tests. We diagnosed the case relying on the neurological examination and history of the patient. As the administration of trivalent botulism antitoxin and supportive care are essential when botulism diagnosed, the patient was transferred to the ICU where the necessary treatment is available. Clinical improvement was observed after the administration of botulism antitoxin.

The patient with neurological toxicity or respiratory failure should be admitted into intensive care unit. In food-borne Botulism trivalent equine antitoxin (types A, B, and E) should be administered as soon as possible after laboratory specimens are collected. A repeat dose is probably not necessary but may be given after 2- 4 hours. Cathartics may be used unless there is ileus. Antibiotics are of unproven value. Early initiation of antitoxin limits the extent of paralysis, but does not reverse it.

Botulinum toxin is the most potent toxin known to humans and as little as 100 ng can be lethal. The toxin blocks peripheral cholinergic neurotransmission at the neuromuscular junction and cholinergic autonomic nervous system by introducing an endopeptidase enzyme into the presynaptic side of the synapse. The endopeptidase cleaves acetylcholine vesicle docking proteins that are required for the synapse to release acetylcholine into the synaptic cleft. Botulism occurs due to consumption, inhalation of preformed botulinum toxin or growth of C. botulinum bacteria in the infant gastrointestinal tract or within a wound. Growth of botulinum in the immature gut or wound will release botulinum toxin that reaches circulation. All forms of botulism cause progressive weakness, bulbar signs (blurred vision, diplopia, mydriasis, dysphagia, and dysarthria) and respiratory failure with normal sensation and mentation. Treatment is aimed at 1) maintaining respiration via intubation and mechanical ventilation, 2) stopping progression of weakness by administration of botulinum antitoxin (equine trivalent botulinum antitoxin for adults and botulism immune-globulin intravenous-human for infant botulism), and 3) prevent complications from weeks of paralysis with good supportive care. The source of the botulinum toxin should be identified to prevent additional cases. Patients can recover normal muscle strength within weeks to months but usually with complaint of fatigue for years (₃). In our case, the patient was mechanically ventilated for 7 days and discharged from ICU to neurology clinic in a good general condition.

Changes in dietary habits, improvements in food preservation techniques in industrial food processing and awareness of risk of botulism have made botulism a rare disease. Nevertheless, following several outbreaks of botulism in various European Union (EU) countries (cases of botulism associated with the consumption of mushrooms and vegetable soup in Italy, shrimps in France, fermented fish in Norway, and cases in the United Kingdom), Euro surveillance has taken the opportunity of surveying the current epidemiology of botulism and its surveillance in the countries of the EU (₄).

In food borne botulism, classically clinical signs and symptoms occurs 12-36 hours after eating toxin contaminated foods and cranial nerve involvement marks the onset of symptoms (₅). In our patient abdominal pain, nausea and vomiting occurred 12 hours after ingesting home canned green beans, he was brought to the hospital and observed for his symptoms and operated with the diagnosis of brid ileus. In our case, the preceding symptoms were abdominal pain, nausea and vomiting. All complaints of the patient at the admission to the emergency ward were related to ileus clinic. Atypically, neurological symptoms had taken place on postoperative second day and the patient was transferred to ICU for his respiratory failure. At literature; Kothare et al reported a case of infant botulism beginning with colonic ileus symptoms (₆).

In our case, preceding symptoms were related to gastrointestinal system and neurological symptoms occurred 5 days after ingestion of food containing Clostridium botulinum toxin. The diagnosis of food borne botulism could be made on postoperative second day, after determining neurological symptoms and having been informed about his history of eating home canned green beans. The late occurrence of neurological symptoms in food borne botulism may confuse the clinical diagnose and even can cause unnecessary operations.

Correspondence to

TAYFUN ADANIR M.D. Address: P.B: 12 HATAY 35370 IZMIR TURKEY E-mail: tadanir@tnn.net Phone : +90 232 2444444-2380 FAX : +90 232 2434848