Hobmaier (1932) added evidence connecting the toxin to the wild- 
demonstrating the toxin of Clostridium botulinun, type C, in ee by 
diseased birds. His findings were confirmed and elaborated by Quortrup and Sudheimer 
(1943) in a series of experiments which completed the chain of evidence concerning 
the cause of this malady. 
Gunnison and Coleman (1932) reported the first extensive, detailed laboratory 
atudy on Clostridium botulinum, type C, in relation to its toxicity to ducks. In 
addition, data on typeC were given in regard to morphology and cultural character- 
j{atics of the organism, toxicological and serological tests, and toxicity for laborsa- 
tory animals. — 
Kalmbach and Gunderson (193h) published their original observations and presented 
a complete analysis and review of the current information available on botulism among 
wild birds. 
Twomey and Twomey (1936) and later Twomey, Twomey, and Williams (1939) published 
data from their observations and experiments which they believed indicated that the 
symptoms scen in duck sickness were caused by the effects of a selenium build-up in 
the tissues of the bird, especially the liver. The findings of subsequent investiga- 
tors (Lakin, Quortrup, and Hotchkiss, 19l) gave direct evidence contrary to this view. 
Batson (190), working in South Dakota, reported experiments on avian botulism in 
which he was ‘able without fail to intoxicate ducks by penning them in locations thought 
to be toxic. Under conditions prevailing at Bear River Refuge, Utah, the consistence 
of these results has not been duplicated, even after extensive trial. 

Hotchkiss et al. (191) developed the theory of "cycles of organic decay" as the 
crucial factor in furnishing nutrient conditions conducive to the growth of Clostridium 
botulinum, type C, with consequent extensive toxin production. Later experiences ab 
Pear River have failed to confirm this idea as it was originally presented. 
An extensive and sustained investigation of avian botulism and the circumstances 
surrounding it was carried on at the Bear River Migratory Bird Refuge from 1937 through} 
1948. Both field and laboratory studies were undertaken at this location, the site of 
the great duck die-offs of previous years which first called attention to the sickness. 
The workers there were Coburn, Hervey, Holt, Jensen, Kalmbach, Quortrup, Sperry, 
Sudheimer, and Williams. Reports and publications made by this group during the 
1937-48 period are in the files of the Fish and Wildlife Service, and in several 
scientific journals. 

The most significant result of this work at the Bear River Refuge was the water- 
manipulation concept developed by Sperry and Williams. The results (Sperry, 197) 
indicate that reflooding of partially dried lake-bottom mud produces conditions 
leading to the disease, if ducks are present and normally active in the area. Further, 
it was shown that prevention of the usual wind reflooding of such water-edge soils by 
rapid lowering of water levels away from the damp, marginal mud resulted in great 
reductions of duck mortality from botulism. 
Sperry also pointed out that "an abundance of water coming into and going out of 
alake (at Bear River Refuge the impoundments embrace 5,000 acres) has little benefi- 
cial effect on sickness trends if extensive shore lines remain on flat terrain of an 
exposed lake bottom." 
ipa 
