The Topic of This Month Vol.21 No.3(No.241)


Botulism, Japan

Botulism is a paralytic disease caused by the neurotoxin of Clostridium botulinum. Botulinum toxin comprises seven, A through G, immunologically distinct types. Human botulism is caused principally by Type A, B or E toxin and rarely by type F toxin. Clostridium botulinum is an anaerobe, forming heat-stable spores, which can be detected in soil samples throughout the world. There are three forms of botulism grouped according to the pathogenesis: foodborne, infant, and wound botulism (see p.51 of this issue). The following is a summary of epidemiological features of foodborne and infant botulism in Japan, based on the Japanese Statistics of Food Poisoning compiled by the Food Sanitation Division, the Ministry of Health and Welfare, and literature and personal communication, respectively.

Foodborne botulism: Various kinds of food, contaminated with C. botulinum spores and stored under anaerobic conditions, would support both growth and toxin production of C. botulinum. If such food containing preformed toxin is ingested, botulism will occur. Since the first episode of botulism in Hokkaido in 1951, a few outbreaks restrictedly in northern prefectures (Hokkaido and Aomori) have occurred almost annually, caused by eating home-prepared "izushi" or similar kinds of fermented fish products: these outbreaks implicated principally type E toxin. Such outbreaks, having recently decreased in number, still occur even at the present time in Japan.

Occurrence of foodborne botulism must be reported as food poisoning in compliance with the Food Sanitation Law. During 1955 through 1998, reports of foodborne botulism totaled at 86. The yearly incidence is shown in Fig. 1. Type A toxin was implicated in six outbreaks, type B in three, and unidentified type in one; type E toxin was implicated in all the other 76 outbreaks. Cases per outbreak of type E botulism have been rather few. The cumulative botulism cases have totaled at 351, of which 68 died, the case fatality rate being 19%. Type E cases counted at 263 (53 deaths), type A cases 45 (12 deaths), and type B cases 42 (three deaths). There was one case in which the toxin type was not identified (no death).

Table 1 and Fig. 2 show the outbreaks occurring during 1977 and 1998. The outbreaks occurring in other districts than Hokkaido and Tohoku were caused mainly by commercial foods and toxins of other types than E. The outbreak occurring in Miyazaki Prefecture in 1969 due to German-imported bottled caviar implicated 23 type B cases, of which three died. Another outbreak occurring in 1984 due to "karashi renkon" (deep-fried mustard-stuffed lotus root) from the same manufacturer was due to type A toxin implicating 36 cases spread out in 14 different prefectures , of which 11 died (see IASR, Vol. 5, No. 11). Another outbreak occurring in Tokyo in 1998 due to green olives in brine imported from Italy implicated 18 type B cases (see p.52-53 of this issue). These type A and B outbreaks are characterized by rather a large number of cases per outbreak in broad areas where the incriminated foodstuffs were distributed. Yet another incident occurring in Chiba Prefecture in 1999 was due to a vacuum-packaged ready-to-eat food (not pressure-cooked) implicating a single type A case (see IASR, Vol. 20, Nos. 11 & 12).

C. botulinum spores are distributed widely in soil, which may serve as a source of food contamination. Type E spores have often been detected in soil samples and marine sediments in the northern parts and type A spores have also been detected in some soil samples collected within the country. Attention must always be paid to the possibility of international trading of food materials as well as products that might be contaminated with C. botulinum spores.

Although occurrence is very rare nowadays, foodborne botulism entails very high fatality rates. Its treatment depends on antitoxin therapy with horse serum and symptomatolytic therapy. It is important to keep 'botulism' always in mind, actively carry out etiological diagnosis of patients showing symptoms resembling Guillain-Barre syndrome, rapidly identify the responsible food, and transfer the information to the public health and clinical personnel concerned to minimize patients and deaths associated with the same foodstuff.

Infant botulism: It is a form of the disease caused by botulinum toxin produced intraintestinally. Infant botulism was first recognized in 1976 in the USA as a result of adopting coproexamination of infants suspected of botulism. A decade later in 1986 in Japan, it was first diagnosed in Chiba Prefecture. In the following year, nine cases of infant botulism, all of which had been fed bee honey, were reported, reflecting the increased concern of clinicians. In October 1987, the Ministry of Health and Welfare issued a warning not to feed infants under 12 months old with honey and to set up botulism survey systems (see IASR, Vol. 8, No. 11). Ever after, reports of incidents of infant botulism have decreased in number.

All 17 cases diagnosed so far are listed in Table 2. No particular regional or seasonal trend nor sex difference in the occurrence has been seen. In many cases, type A C. botulinum and toxin were detected from stool samples and the spores of the same type occasionally from the honey fed to the cases. In three of the infant botulism cases (cases Nos. 3, 6 and 7), no organisms were detected from stools nor the honey, but they were ascribed from clinical symptoms and the honey feeding. Since 1990, honey has not been only the indispensable vehicle. In one case, home-prepared vegetable soup was incriminated (No. 16). Type C and B organisms were respectively incriminated in 1990 and 1995.

It has been reported that infant botulism cases may account for about 5% of cases of sudden infant death syndrome (SIDS) (Arnon, S. S., Rev. Infect. Dis., 6:S193-201, 1986); cases Nos. 12 and 13 showed a clinical course similar to that of SIDS but survived (near-miss cases). It seems legitimate to consider the possibility that some near-miss SIDS cases might actually be infant botulism cases.

Treatment of infant botulism is depending generally upon administration of penicillin-group antibiotics. Application of antitoxin therapy with horse serum to infants should be done very carefully.

Stools of infant botulism cases may contain C. botulinum and the toxin, sometimes attaining one million CFU/g and 100,000 MLD (to mice) /g, respectively. Stubborn constipation is a major sign of infant botulism; excretion of the toxin lasting for more than a month has been reported. Therefore, stools of infant botulism cases should carefully be disposed.

Infant botulism has been classified into the category IV notifiable infectious diseases in the Law Concerning the Prevention of Infectious Diseases and Medical Care of Patients of Infection enacted in April 1999. Only one case has been reported in compliance with the law as of February 2000 (Table 2, No. 17).


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