A recent case of botulism in Hokkaido, Japan

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Background: Botulism is a rare, potentially severe illness, often fatal if not appropriately treated. Data on treatment are sparse. We systematically evaluated the literature on botulinum antitoxin and other treatments. Methods: We conducted a systematic literature review of published articles in PubMed via Medline, Web of Science, Embase, Ovid, and Cumulative Index to Nursing and Allied Health Literature, and included all studies that reported on the clinical course and treatment for foodborne botulism. Articles were reviewed by 2 independent reviewers and independently abstracted for treatment type and toxin exposure. We conducted a meta-analysis on the effect of timing of antitoxin administration, antitoxin type, and toxin exposure type. Results: We identified 235 articles that met the inclusion criteria, published between 1923 and 2016. Study quality was variable. Few (27%) case series reported sufficient data for inclusion in meta-analysis. Reduced mortality was associated with any antitoxin treatment (odds ratio [OR], 0.16; 95% confidence interval [CI], .09-.30) and antitoxin treatment within 48 hours of illness onset (OR, 0.12; 95% CI, .03-.41). Data did not allow assessment of critical care impact, including ventilator support, on survival. Therapeutic agents other than antitoxin offered no clear benefit. Patient characteristics did not predict poor outcomes. We did not identify an interval beyond which antitoxin was not beneficial. Conclusions: Published studies on botulism treatment are relatively sparse and of low quality. Timely administration of antitoxin reduces mortality; despite appropriate treatment with antitoxin, some patients suffer respiratory failure. Prompt antitoxin administration and meticulous intensive care are essential for optimal outcome.
Although outbreaks of human botulism in the UK are rare, the recent cases of botulism in Birmingham have provided a reminder that the potential hazards from foods contaminated with Clostridium botulinum cannot be ignored. Outbreaks of botulism in Europe and the USA are more frequent and have not always received the publicity given to the Birmingham outbreak. Data on outbreaks of botulism in Europe during the past 20 years have been collated and will be presented. Spores oj Cl.. botulinum are known to occur widely in soil, freshwater mud and marine muds in many parts of the world. Contamination of foods and subsequent growth by CI. botulinum is therefore possible unless foods are adequately preserved. Some data on natural contamination of food material by Cl. botulinum will be presented. Traditional preservation methods, including commercial sterilisation (e.g. in canning), use of low pH conditions (e.g. in acid fruits and pickles), restriction of available water (by drying or addition of humectants), and restriction of storage temperature (e.g. by chilling or freezing) are all used to prevent growth of both spoilage and foodpoisoning bacteria. Whilst the critical process conditions can be defined in some cases (e.g. the minimum botulinum cook (F0 3 min) for canned foods), in other situations insufficient data exist to quantify a ‘safe’ process with regard to CI. botulinum. This is particularly important where interactions of two or more preservation systems are required for safety and stability. Examples will be provided of the interactions between factors such as pH value and water activity (an.) in processed cheese and of those factors important in the safety and stability of pasteurised cured meats (e.g. salt, nitrite, other additives, thermal process value, pH value, storage temperature and time). The relative importance of these factors will be considered in relation to the establishment of a product risk evaluation system which could form the basis of a computer model.
There are seven known serotypes of botulism, designated A through G; almost all human cases of botulism are caused by types A, B, and E. Botulism type E is the predominant serotype causing disease associated with native Arctic foods. In the circumpolar regions of the world, the coastal soils are rich in botulism type E, and consumption of fish and marine animals in these areas are the sources of clusters of botulism. Unlike spores of type A and B, botulism type E can withstand freezing down to 3.5°C. Alaskan native fermentation of fish heads, fish eggs, and beaver tail allow proper anaerobic conditions for botulinum toxin to be elaborated from Clostridium botulinum. The consumption of whale meat, "muktuk" has also been associated with outbreaks of botulism in Alaska and the Canadian Arctic. Elsewhere in the Arctic regions, type E botulism has been associated with Norwegian "rakfisk" prepared by a process similar to fermented Alaskan foods. Outbreaks in Egypt with the salted gray mullet "faseikh", in Israel and New York linked to salted uneviscerated whitefish "kapchunka", in Iran from eating "ashbal" an uncooked salmon, and in Japan with "izushi" a traditional fermented fish preserved in rice have occurred. Importation of vacuum-packed whitefish from Alaska and Canada has also been associated with sporadic cases of botulism type E in Europe. In March 2010, the Center for Disease Control and Prevention released the heptavalent antitoxin (H-BAT) for use in the USA, under an Investigational New Drug program, as the preferred treatment for food-borne botulism, including type E, which had not been covered by the bivalent antitoxin, the prior approved antitoxin product in the USA.
Botulism is a neuroparalytic illness caused by botulinum toxin, a product of the Clostridium botulinum bacteria and characteristically presents as an acute, symmetrical, descending flaccid paralysis. Albeit it is the most poisonous substance known, which even poses a major threat as biological weapons, purified and highly diluted botulinum toxin can be used to treat a wide variety of conditions associated with muscular hyperactivity, glandular hypersecretions and pain. There are six clinical presentations associated with current occurring botulism, each results from absorption of botulinum toxin into the bloodstream. The aim of this review is to summarize the current knowledge on the microbiology, epidemiology, vaccine research and clinical management of human botulism. Early diagnosis and management rely on history and physical examination. Delay in treatment may allow progression of paralysis, protracted hospitalization and deaths of long-term mechanical ventilation and intensive care unit care. The clinicians must take this disease into consideration of a possible outbreak. Awaiting laboratory confirmation is an egregious error, while awareness of the clinical sign and symptoms of botulism is critical for early diagnosis. Rapid management and followed public health surveillance may greatly alleviate disease severity and decrease mortality rates.
Clostridium botulinum and its toxin were identified in the faeces of four infants, aged 6 to 13 weeks, who had symptoms consistent with botulism. Two cases had type-A toxin and two cases had type-B toxin present in their faeces. No toxin was detectable in sera C. botulinum and toxin could be recovered from faeces more than 8 weeks after admission to hospital. All four cases occurred within a 6-month period. The source of the toxin in these infants may have been in-vivo production from ingested organisms.
This chapter briefly explains Clostridium botulinum from a group of anaerobic bacteria which causes neuroparalytic disease affecting man and animals called botulism. A brief explanation of various studies on the incidents of Clostridium botulinum by which it can be distributed and classification and nomenclature is presented. The chapter discusses the methods for isolation and identification of toxins in Clostridium botulinum. Factors affecting germination, growth, sporulation, and toxin production are because of various environmental reasons. The inhibitory effects of temperature, pH, and salt have been recognized for many years. Inhibition of Clostridium botulinum in foods has been reviewed on a number of occasions. Fishery products can be preserved in various methods—such as— pasteurization, freezing, canning, and cooking. The chapter concludes with a brief summary of production, processing, preservation, and consumption of fishery products.
A 19-year-old woman presented with internal ophthalmoplegia, dryness of mouth, ileus, bladder paralysis and anhidrosis. She had an incomplete recovery in 28 months. Clinical and pharmacological examination showed impairment of peripheral autonomic functions governed by cholinergic parasympathetic and sympathetic nerves, probably caused by an impaired synthesis or release of acetylcholine in post-ganglionary autonomic nerves. Electron microscopy revealed no abnormality of skin nerve fibres. The site of the lesion resembles that seen in some cases of botulism, but the protracted course of the present case is unique. Its etiology remains obscure.
Botulism, a food-borne toxin-mediated disease caused by Clostridium botulinum is still a common disease, which is most frequent in the rural environment; 108 cases, 66 males and 42 females, average age 32 years, were recorded from 1965 to 1990 in the infectious disease department of the University Hospital of Poitiers (France). In 83% of patients, the food responsible was home-cured ham. Mean incubation time was 3.4 days; digestive symptoms were observed in 93% of cases, ocular symptoms in 92% and urinary tract dysfunction in 22%. A scale of severity was used to classify the patients into those suffering from severe (6), intermediate (50) and mild (52) forms of the disease. Botulinum toxin type B was found in 36 (52%) of 69 blood samples and in 41 (51%) of 81 samples of the suspected food. From 1965 to 1976, 44 patients were treated with both toxoid and heterologous equine serotherapy. Since 1976, 29 patients have been treated with guanidine hydrochloride (35 mg/kg daily) and 35 patients with guanidine hydrochloride plus heterologous serotherapy. All 108 patients recovered without any sequelae.
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Salmon, sole, cod, oysters, clams, and crabs from ocean waters along the coast of Oregon and Washington were examined for the presence of Clostridium botulinum type E. The organism was detected by identification of the type E toxin in enrichment cultures of the viscera of individual fish. Of 369 salmon specimens, 48 yielded cultures containing toxin lethal to mice, and almost half of the toxic cultures were shown to contain botulinal toxin, chiefly type E. Eighteen of 113 sole and cod specimens, 4 of 22 Dungeness crab specimens, 5 of 16 oyster specimens, and 27 of 115 clam specimens gave rise to cultures containing botulinal toxin which was usually type E, although types A and B were occasionally encountered.
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Bott, Thomas L. (University of Wisconsin, Madison), Janet S. Deffner, Elizabeth McCoy, and E. M. Foster. Clostridium botulinum type E in fish from the Great Lakes. J. Bacteriol. 91 919–924. 1966.—The intestinal contents of more than 3,000 fish from Lakes Erie, Superior, Huron, and Michigan were examined for Clostridium botulinum type E. Demonstration of the organism was accomplished by identifying its toxin in liquid cultures inoculated with material from the alimentary tract. Incidence figures, expressed as per cent of the fish tested, were: Lake Erie, 1%; Lake Superior, 1%; Lake Huron, 4%; the main body of Lake Michigan, 9%; and Green Bay (on Lake Michigan), 57%. Thus, C. botulinum type E appears to be widely but unevenly distributed in the Great Lakes, and fish from all areas are potential carriers of it.
Botulism, very rare disease as it is, has long been reported in Europe and America, although no report referring to occurrence of this disease had been presented in Japan prior to 1952, when Nakamura, Iida and Saeki reported an outbreak of type E botulism at Iwanai, Hokkaido, due to herring-izushi. In the following year, another two outbreaks of type E botulism due to izushi involving fish were reported by the same authors. Again, early in October, 1953, the authors learned of the fourth outbreak in Hokkaido. Incidentally, concurrently with the fouth outbreak in Hokkaido, four persons of a family at Tenno, a small town upon the coast near the Lagoon Hachiro, Akita, developed symptoms of botulism and two of them died. The incliminated foodstuff, gilthead-izushi, was shown to possess type E botulinal toxin and therefrom a strain of Cl, botulinum type E was isolated. This occurrence adds up the total outbreaks of botulism in Japan, all of which were due to izushi involving fish and type E organisms, to five with thirty-two cases and nine fatalities. The data relating to the known outbreaks of botulism in Japan are shown in the table.
A previous report concerning the high incidence of Clostridium botulinum type E in marine deposits in Swedish coastal waters has been confirmed. The organism was not found in the North Sea or in fish caught in the North Sea or the Skagerrak.
The first known occurrence of type E botulism took place in the late summer of 1932, in the eastern United states. At Cooperstown, N. Y., a 15-year old girl died, and her parents became ill, after eating uncooked salmon which had been caught and smoked in Labrador. The toxicity of portions of the fish for laboratory animals was demonstrated, but efforts to isolateClostridium botulinumwere initially unsuccessful (MacKenzie, 1934) . Two years later, a similar episode occurred in Westchester County, N. Y., in which canned sprats imported from Germany were implicated. From remnants of fish in the can, Hazen isolated at the New York Department of Health Laboratories, Albany, a strain ofCl. botulinumnot classifiable as type A, B or C; and the main characteristics of this apparently new type were described by her in 1937 (Hazen, 1937) . Meanwhile, in 1936, Gunnison, Cummings and Meyer (1936), at the University of California, San Francisco, had proposed the designation type E for 6 cultures ofCl. botulinumforwarded to Dr. Meyer for identification by Doctors Bier and Kushnir of the Bacteriological Institute at Dniepropetrovsk, in the Soviet Ukraine. These cultures had been isolated, in the course of microflora surveys, from the intestines and muscle of sturgeon caught in the Sea of Azov (Dolman and Chang, 1953) . Soon afterwards, Hazen was able to verify that her sprat strain, and likewise a strain eventually isolated from the Labrador salmon, shared the chief properties of the tvne E cultures from Russia (Hazen, 1938) . The findings of the past 20 years reinforce the earlier evidence, which already suggested a special liability of fish to serve as vehicle for type E botulism in widely separated parts of the world. But by now it is clear that the flesh of marine mammals must be grouped with fish and fish products as potential sources of type E botulism for man, and also that this rare disease has a relatively high incidence in certain areas. Moreover, many of the reasons for these peculiarities are becoming plain. To date there have been 36 known outbreaks of type E botulism, affecting a total of 158 persons, of whom 65, or 40 per cent, died. In 29 of these episodes, the flesh of raw or improperly cooked fish was implicated, on both epidemiological and bacteriological grounds; while raw fish eggs, and the meat of white whale (beluga) or seal, each caused 3 outbreaks. Geographically, type E botulism so far has been confined to the Northern Hemisphere, with a marked predilection for Japan and Canada. In Canada, since 1944 there have been 6 proven episodes, involving 20 persons, with 15 deaths, a case fatality rate of 75 per cent. Five of these occurrences were in British Columbia (4 on the Pacific coast, the other some 300 miles inland), and one on the coast of Labrador. At least 2 other type E outbreaks have occurred on the north-west coast of Alaska in the last 6 years. In the same period, no fewer than 23 outbreaks have been identified in Japan, 7 of which were in northern Honshu, and 16 in the most northerly and least inhabited island of Hokkaido. Altogether 31 outbreaks, or six-sevenths of the known total, have occurred in regions bordering the North Pacific Ocean and contiguous waters. This brief historical review may serve as introductory background to a consideration of some of the apparent mechanisms and unsolved problems in the epidemiology, pathogenesis and prevention of type E botulism.
In a previous paper (Nakamura, Iida, Saeki, Kanzawa and Karashimada, 1956) it was reported that nine outbreaks of proven type E human botulism had taken place in Hokkaido, Japan, since 1951. Eight additional episodes have been encountered subsequently, of which two were of particular interest from the epidemiological viewpoint. These two episodes form the chief subject of this communication.In addition, observations on the activation of type E toxin are described. As Duff, Wright and Yarinsky (1956) reported, type E toxin is activated by trypsin, and the present authors applied this phenomenon to the demonstration of type E toxin in foods. The toxicity of incriminated foods is evidently increased by treatment with trypsin, a fact which seems to be of some importance in considering the pathogenesis of type E botulism.
Clostridium botulinum in Sweden and the adjacent waters
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