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General Review


Early Descriptions

Botulism, or sausage poisoning as it was originally termed, was first seriously studied following an outbreak in Wildbad, Germany in 1793. The outbreak involved 13 people, 6 of whom died, and was associated with consumption of a locally produced blood sausage. Following this outbreak, the number of reported cases of sausage poisoning rapidly increased prompting a study of the disease by local health officer, Justinius Kerner (1829). He described 230 cases, most of which were attributed to the consumption of sausage. The illness became known as "botulism" after "botulus" the Latin word for sausage.

Many years later, Van Ermengem (1897) investigated an outbreak of botulism involving 34 individuals who had consumed raw, salted ham served at a gathering of amateur musicians in Ellezelles, Belgium. In the investigation of this outbreak, Van Ermengem established that botulism was an intoxication, not an infection, and that the toxin was produced by a spore-forming obligate anaerobic bacterium, Clostridium botulinum. He also found that toxin was rapidly inactivated by heating and was only toxic to certain animal species.

A later outbreak in Darmstadt, Germany associated with canned white beans established that there was a second type of botulism. The new strain was type A and the Van Ermengem strain was probably type B (Landmann 1904).

In 1922, type C botulism was identified as causing disease in chickens (Bengston 1922) and cattle (Seddon 1922). Robinson (1929) identified type D in cattle and type E was identified by Gunnison (1936-1937) as causing botulism in people after consuming fish. Type F was first described by Moller and Scheibel (1960) from a Danish outbreak of botulism involving homemade liver paste. Finally, type G botulism was identified in soil from cornfields in Argentina by Giménez and Ciccarelli (1978). The principal types of botulism involved in human disease are types A, B, and E.

The toxin of C. botulinum acts at cholinergic neuromuscular junctions by blocking the release of acetylcholine. The action only affects peripheral sites and is believed to be irreversible. Both autonomic and voluntary motor activities are affected and molecular differences in toxin types may result in somewhat different signs and symptoms for the three toxin types responsible for most human disease.

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Foodborne Botulism in the Arctic

a. Epidemiology

For many years, outbreaks of illness associated with traditionally prepared and preserved food have been described. Early explorers reported clusters of deaths in villages and among groups of northern Natives which the explorers attributed to "ptomaine" poisoning or trichinosis (Stefansson 1914). However, descriptions of many of these outbreaks resemble foodborne botulism. Later, ethnographers described food preparation and storage practices which could support the production of botulism toxin (Nelson 1971).

The first reported outbreaks of foodborne botulism in the Arctic occurred in the early 1900s and over 200 outbreaks have been recorded since. In Canada, the first reported outbreak was in 1919 and since then, over 100 outbreaks involving over 230 individuals have occurred (Dolman 1960 and 1974). The first reported outbreaks in Greenland (Muller and Thomsen 1968) occurred in 1967 and 25 additional outbreaks have been reported since. Rabeau (1959) recorded the first outbreak in Alaska in 1947 which involved beluga whale flipper consumed in the village of Kotzebue. Outbreaks among Siberian Eskimos in Russia are not well reported.

The overall case fatality rate in Arctic outbreaks is about 20%. Because not all northern Native groups consume traditionally prepared foods, it is difficult to determine true incidence rates of disease. However, using total population as the denominator, Canadian Inuit and Alaska residents had annual incidence rates of 30 cases/100,000 (Smith 1977) and 8.5 cases/100,000 (MacDonald et al. 1986), respectively. These rates compare to 0.43 cases/100,000 in Washington State, the highest rate in the United States other than Alaska (MacDonald et al. 1986). Most foodborne botulism in the Arctic is type E.

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Foodborne Botulism in the Arctic

b. The foods, their preparation and storage

There is an important difference between foodborne botulism in Alaska compared to the rest of the United States. All cases in Alaska have been associated with the preparation and storage of traditional Alaska Native foods. This includes "fermented" foods, dried foods, and traditionally prepared condiments such as seal oil. In other parts of the United States, foodborne botulism is usually associated with improperly canned foods or with improperly stored unrefrigerated foods.

Foods involved in northern Native botulism outbreaks are usually putrefied (fermented). These foods are either intentionally subjected to putrefaction or are unintentionally putrefied due to inadequate storage and preservation. In either case, most outbreaks involve traditional foods such as sea mammals or fish. Whale and seal are the most frequently involved sea mammals. Salmon, including salmon eggs, is the most frequently involved fish. Land mammals (beaver and caribou) account for a small proportion of outbreaks.

Conditions allowing the inadvertent putrefaction of food were described by the ethnographer Nelson (1971) when he observed: "Meat is frequently kept for a considerable length of time and sometimes until it becomes semiputrid. At Point Barrow, in the middle of August 1881, the people still had the carcasses of deer which had been killed the preceding winter and spring. This meat was kept in small underground pits, which the frozen subsoil rendered cold, but not cold enough to prevent the bluish fungus growth which completely covered the carcasses of the animals and the walls of the storerooms." Similar conditions and practices are still found in many areas of the Arctic.

Dried foods, particularly dried fish, have also been implicated in foodborne botulism outbreaks. Fish are dried either with or without a brine stage. However, even if fish are put in brine prior to drying, the salt concentration is rarely high enough to inhibit botulism toxin formation (Zottola and Zoltai 1981).

In addition to inadvertent spoilage, many traditional methods of food preparation lend themselves to botulism toxin formation. Traditional "stink" foods such as fermented salmon eggs (stink eggs) or salmon heads (stink heads) are prepared by burial in moss-lined pits or barrels in the ground. Nelson (1971) described the process he observed during a visit to the coastal villages of northwest Alaska in 1878-1881: "In the district between the Yukon and Kuskokwim, the heads of king salmon, taken in the summer, are placed in small pits in the ground surrounded by straw and covered with turf. They are kept there during the summer and in the autumn have decayed until even the bones have become the same consistency as the general mass. They are taken out and kneaded in a wooden tray until they form a pasty compound and are eaten as a favorite dish by some of the people."

The process described by Nelson has changed somewhat. Now, fermentation is usually carried out in either a barrel, a plastic or glass jar, or a plastic bag. These containers increase the risk of botulism toxin formation because most can be easily sealed, thereby increasing the likelihood of anaerobic conditions. Some foods are fermented in a seal skin or fish skin bag or "poke" which is either buried or hung up. If salmon eggs are fermented in this manner, they can be left until they dry out somewhat and form a "cheese" which is firm on the outside and soft in the center.

Toxin production is also temperature dependent, and is less likely to occur at the lower temperatures used during traditional fermentation. However, fermentation now may be done indoors, or in a container above ground and in the sun. These methods involve warmer temperatures which make fermentation more rapid and production of botulism toxin more likely.

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