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.