有效期間：民國 99年06月01日 至 99年06月30日 止
< Presentation of case > The 41-year-old woman, previously healthy, was admitted because of progressive dysarthria, dysphagia, and bilateral ptosis. Five days prior to this admission, she went to Tainan and Chiayi County with her husband, brothers, and mother for graveside rituals and went back to Tao-yuan on the second day. She, her mother and husband ate some processed bean products (素豆乾) and 潤餅 during the stay in Chiayi County. Two days prior to this admission, she felt dizziness with diarrhea, nausea, vomiting, and abdominal pain. Meanwhile, her mother also had same illness on the same day. They went to a local hospital, where acute gastroenteritis was considered and prokinetics agents were used for symptomatic relief. However, both of them started to develop dysarthria, dysphagia, and bilateral ptosis at that night with progressive proximal muscle weakness and respiratory distress. In addition, her husband also started to have dizziness and diplopia on the same day. Due to worsening neurologic symptoms, she was referred to this hospital. The patient was an accountant and lived in Tao-yuan County with her husband and two children. The patient didn't drink alcohol or smoke. She also denied use of illicit drugs or a history of animal contact. On examination, she was conscious and orientated. The temperature was 37.3℃, the pulse rate 99 beats per minute, blood pressure 117/68 mmHg, and the respiratory rate 17 breaths per minutes. On neurologic examination, bilateral ptosis, facial diplegia, dysarthria, dysphagia, and poor bilateral palate elevation were noted. Gag reflex was present. No tongue deviation on protrusion was noted. Muscle strength examination disclosed neck muscle weakness and quadriparesis with more prominent weakness at the proximal part. Deep tendon reflex was hyporeflexia. Plantar reflex was flexor response. The other physical examinations were unremarkable. At emergency room (ER), the nerve conduction velocity (NCV) showed no abnormality. A neurologist was consulted and botulism was suspected according to her clinical presentation and the history of case clustering in the family. An infection specialist was consulted, who contacted with Taiwan Centers for Diseases Control to obtain botulism antitoxin. She was admitted to neurology intensive care unit due to impending respiratory failure six hours after arriving at ER. In addition, patient’s mother and husband were also hospitalized. One hour after admission, infusion of 250 ml of equine botulism antitoxin was begun and there were no symptoms or signs of anaphylaxis during the infusion. Another 250-ml antitoxin was given. However, muscle weakness continued to progress and endotracheal intubation for mechanical ventilation was performed due to hypercapnic respiratory failure 14 hours after hospitalization. Another 250-ml antitoxin was given after intubation. The repetitive stimulation study showed incremental changes on 30Hz stimulation, which was compatible with pre-synaptic neuromuscular junction lesion, such as botulism. She had gradually neurologic improvement five days after hospitalization. Both she and her mother were tested for botulism toxin A, which was reported as positive according to the mouse bioassay, in which blood specimens were injected into the peritoneal cavity of the mice. She was weaned from the ventilator successfully 22 days and was discharged 47 days after hospitalization. Swallowing rehabilitation was performed at the outpatient clinic. < Discussion > In this case, we described a case cluster of food-borne botulism in 3 patients who presented with nausea and vomiting followed by neurologic deficits. Botulism was first described in 1820 when hundreds of patients with sausage poisoning were found. It was caused by Clostridium botulism, a Gram-positive spore-forming anaerobic bacilli. The spores will germinate and grow to toxin-producing bacteria in certain conditions such as anaerobic condition, with a low acidity, or a temperature ranging from 25 to 37°C. The botulism toxins are designated from A to G according to antigenic differences and types A, B and E are the most common in causing human disease. All toxins can be inactivated by heating to 85°C over 5 minutes. Commercially canned food was commonly the source of botulism. In our case, though there was no identified source of botulism toxin, processed bean products have been identified the leading source in Taiwan and, by history, the three case patients shared the same processed bean products. The toxin acts on the cholinergic system at the presynaptic motor-neuron terminal by blocking acetylcholine transmission across the neuromuscular junction, which, therefore, results in flaccid paralysis. There was a classic triad for clinical manifestations: symmetric descending flaccid paralysis with prominent bulbar palsy (diplopia, dysarthria, dysphonia, and dysphagia), afebrile, and clear sensorium. The patients may also have autonomic symptoms, such as postural hypotension or urinary retention. Food-borne botulism often develops between 12 and 36 hours after toxin ingestion with the initial presentations of nausea, vomiting, dry mouth and diarrhea, as is seen in our patients. Respiratory failure may occur due to upper airway obstruction or respiratory muscles weakness. Botulism should be differentiated from Guillain-Barre syndrome, myasthenia gravis and Lambert-Eaton syndrome. Though Guillain-Barre syndrome may share similar preceding constitutional symptoms with botulism before the onset of neurologic illness, it predominantly presents with ascending paralysis and paresthesias. In addition, a cluster history should alert the physicians to the higher possibility of botulism. Diagnosis of botulism relies on a careful history taking and physical examination. In patients with suspected botulism, mouse bioassay for serum toxin analysis can be performed in special laboratories by contacting with Taiwan CDC. In our case, though there was no identified source of botulism, processed bean products would be the most possible source of botulism when the types of food were compared among the family members who travelled together. Treatment for botulism includes supportive care and botulism antitoxin; the latter should be started as soon as possible when botulism is suspected. One 250-ml bottle equine botulism antitoxin contains type A, B and E antitoxin. Initial dosage is 500 ml and infusion of additional 250 ml may be advised according to clinical conditions. Aminoglycosides should be avoided due to possibility of neuromuscular adverse events. Prognosis depends on the amount of toxin ingested and the time to antitoxin use. Mean ventilator dependent time is around 56 days for type A toxin botulism. Early ventilator weaning in our patient may be due to early initiation of antitoxin use. The key point for prevention is proper food handling and preparation by heating since the spores will be killed by this process. < References >
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Case Discussion
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| 1. (B) |
下列有關肉毒桿菌的描述，何者為非？ | ||
| A | 肉毒桿菌易在厭氧的環境下生長 | ||
| B | 肉毒桿菌之孢子無法藉由高溫加熱去活化 | ||
| C | 肉毒桿菌造成人類中毒以Toxin A, B, E為主 | ||
| D | 肉毒桿菌的毒素會阻止乙醯膽鹼(acetylcholine)在neuromuscular junction的傳遞 | ||
| 2. (D) |
有關肉毒桿菌中毒的描述，何者為非？ | ||
| A | 肉毒桿菌中毒的臨床症狀常常以噁心、嘔吐來表現 | ||
| B | 肉毒桿菌中毒時會造成對稱性的肌肉無力 | ||
| C | 大部分肉毒桿菌中毒的病患不會發燒 | ||
| D | 肉毒桿菌的治療必須要確定診斷後才能給予 | ||
| 3. (B) |
下列何項描述不符合肉毒桿菌中毒之表現？ | ||
| A | 四肢無力 | ||
| B | 意識不清 | ||
| C | 複視 | ||
| D | 自主神經失調 | ||
| 4. (A) |
有關肉毒桿菌之鑑別診斷，下列敘述何者為非？ | ||
| A | 肉毒桿菌中毒之臨床表現以ascending paralysis為主，可以此與Guillain-Barre Syndrome作區分 | ||
| B | 肉毒桿菌中毒不會侵犯感覺神經，可以此與Guillain-Barre syndrome作區分 | ||
| C | 肉毒桿菌中毒之臨床表現與重症肌無力極為相似，需將其列為鑑別診斷 | ||
| D | 有群聚發生的病史時需高度懷疑肉毒桿菌中毒 | ||
| 5. (C) |
下列何項治療不適用於肉毒桿菌中毒？ | ||
| A | 抗毒素 (Botulism antitoxin) | ||
| B | 呼吸器支持 | ||
| C | Aminoglycoside | ||
| D | 以上皆非 | ||
| 6. (B) |
有關肉毒桿菌中毒之預防，下列何者為非？ | ||
| A | 肉毒桿菌中毒為法定傳染病，有疑似病例須在24小時內通報 | ||
| B | 肉毒桿菌中毒之病患需採取空氣隔離 | ||
| C | 疑似病例需進一步進行接觸者及感染源檢查 | ||
| D | 以上皆非 | ||
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