A 12-year-old case of botulism with acute flaccid paralysis, August 1999 - Chiba
(IASR 1999; 20: 272-273 & 301-302)

A 12 year old girl complained nausea to a nearby physician in the morning of August 1999. She was given IV fluid, however she developed difficulty in speech, gait and stand up, then she visited the University Hospital in the evening. Upon admission, she had no edema, no eruption with body temperature 36.7C, heart rate 135/min., respiratory rate 42/min., blood pressure 172/104mmHg, and paO₂ 94%. Her consciousness level was normal. Neurological examination revealed normal light reflex, remarkably decreased muscular tension, negative deep tendon reflex, and negative neck stiffness. On auscultation respiratory sound diminished and abdomen was soft and flat. She presented progressive quadriplesia. Blood chemistry resulted, when O₂ was given by 3 litter/sec; pH 7.183, pCO₂ 67.9mmHg, pO₂ 346.0mmHg, HCO₃ 25.5mmol/L, BE-4.4, WBC 9,900/mm³, RBC 5.02million/mm³, HB 14.3g/dL, Ht 41.2%, PLT 183,000/mm³, PT 91%, APTT 32.4sec, Fbg 313mg/dL, GOT 14IU/L, GPT 10IU/L, LDH 202IU/L, CRP 1.2mg/dL, CPK 65 IU/L IgG 1,565mg/dL, IgA 128mg/dL, and IgM 66mg/dL.

Chest x-ray showed the normal cardio-pulmonary ratio and atelectasis in the right upper lobe. Abdominal X-ray presented remarkable reduced abdominal gas suspecting paralytic ileus.

She was born with low body weight, but she grew up without any retardation. She had asthma, but it was well-controlled.

Paralysis deteriorated progressively, and she was intubated when respiratory failure was observed. Communication was possible by slight movement of her fingers.

We initially suspected Guillan-Barre Symdrome (GBS) and we gave her large dose of gamma-globulin. However, her symptoms did not improve. She could not move her fingers and light reflex became negative on Day 4. Motor nerve pulse was not observed in the peripheral nerve. Auditory brainstem response (ABR) was almost normal. Tensiron test was negative. We suspected botulism, then her stool and serum was submitted to the Tokyo Metropolitan Institute of Public Health on Day 8. Following day botulismotoxin A was detected. Clostridium botulinum serotype A was isolated from her stool. Multi-valent anti-botulism sera were given immediately, but her illness did not improve quickly. On Day 16 she responded to the light reflex, and she started to move her fingers. She needs respiratory support by Day 60.

Epidemiological investigation was conducted by the local health center, and hashed curry was suspected as implicated food. It was shipped as boil-in-the-bag food under refrigerated temperature, but the patient stored it under room temperature at home. Because notification of the incidence delayed more than one week, it was difficult to collect food items she left or abandoned. Thus, 25 samples which were delivered on the same day to other community market members, as well as remained food in the refrigerator of the patient's home, were examined(Table).

Botulinus toxin A was detected from one of the vacuumed hashed curry pack samples. Clostridium botulinum type A was also isolated by yolk-added CW agar. Using Takara and Takeshi's primers for polymerase chain reaction, this isolate was turned out to have genes for both type A and type B toxins. We understand that this isolate is "silent B", which has the gene but do not produce enough amount of type B toxin. Two isolates from the patient and food showed the same DNA patterns by pulsed-field gel electrophoresis (PFGE) using Sma I, Nur I, and Ksp I enzymes (Figure).

Reported by Hiroshi Kobayashi, Naokiyo Kurokawa, Masahisa Kobayashi, Yoshihiro Saito, Naokaki Kobayashi, Takashi Tsuda, Koji Fujisawa, Masakatsu Kubo, and Yoshikatsu Eto, Dept. Pediatrics, Jikei Univerisity Kashiwa Hospital; Chie Monma, Yoshitoki Yanagawa, and Satoshi Morozumi, Tokyo Metropolitan Research Laboratory of Public Health; Masako Uchimura and Kenji Koiwai, Public Health Laboratory of Chiba Prefecture.

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