RESEARCH ON AVIAN BOTULISM 
Progress in avian-botulism investigations has been intermittent and slow, yet 
it is creditable that significant advance has been made. It must be borne in mind 
that some of the most important aspects of this complex disease could not be studied 
in well-equipped laboratories. Investigations had to be carried on with limited 
facilities and in the ooze of marshes, strewn with the bodies of sick and dying ducks, — 
Clarke (1913) appears to have been the first investigator to do experimental work 
on the disease then known as "duck sickness." The results of his field observations 
and experimental manipulations were thought to indicate that heavily mineralized 
waters were responsible for the death of the birds, presumably by intoxication. Betw 
1915 and 1918, Wetmore carried out in the Great Salt Lake region the most detailed and 
extensive early work on the disease. He recognized that the condition was the result 
of a toxic agent, associated with the reflooding of drying, alkaline mud flats. More 
specifically, Wetmore suspected that the sickness was caused by high concentrations of 
talkali" dissolved from crusted deposits on the mud surface. He assumed that ducks 
feeding and drinking in this shallow water took in sufficient salts to result in intox 
ication and death. From these findings came the idea that the sickness was "alkali 
poisoning." 
Some years later, Bengtson (1923, 192) studied and described for the first time 
the bacterial organism now known as Clostridium botulinum, type C, but she had at that 
time no knowledge of its role as a possible cause of botulism among wild ducks. Grah 
and Boughton (1923), however, associated the toxin of Clostridium botulinum, type 0, 
with a limberneck-like disease in chickens and domestic ducks, resembling botulism. 
Sperry (1927) fed tissues of ducks afflicted with the disease to other healthy 
ducks. These attempts to reproduce the sickness experimentally failed, with a single 
exception. In a healthy mallard, the feeding of a portion of a liver removed from a 
diseased bird resulted in the production of the characteristic symptoms of the duck 
sickness. This was the first experimental reproduction of the malady in wild birds. 
Sperry concluded that "Experiments substantiated the more advanced belief that the 
trouble was due to the toxic action of a chemical or a vegetable poison," and not to 
falkali"™ alone. 
Shaw (1929, 1930) found, in several instances, an apparent correlation between 
nitrate and nitrite content in marsh soils and duck sickness. He undertook feeding 
experiments on waterfowl, using mixed salts containing nitrates and nitrites. Shaw 
believed that by feeding these salts in certain proportions he could simulate closely 
the sumptoms of sick birds found under natural conditions. His ideas were thus along 
the lines of an inorganic~-chemical poisoning, but one dependent upon certain proportio 
of nitrogenous salts rather than upon "alkali He did not claim to be able to reprodu 
precisely the symptoms seen in the naturally occurring sickness. 
As a result of field work by E. R. Kalmback at Klamath Falls, Oreg., and Tule Lake 
Calif., in 1929 and consequent to submission of ducks by him to L. T. Giltner, Kalmbach 
(1930), and Giltner and Couch (1930), presented evidence strongly indicating that 
western duck sickness was not "alkali poisoning," but was in reality a form of botuli 
Subsequently, Kalmback (1932) revealed that toxin had been demonstrated in the field 
in materials used by ducks as food. This toxin was shown to be that of Clostridium 
botulinum, type C, thus tying the disease seen under natural field conditions to the 
toxin of a specific identifiable anaerobic organism. 
alk, 
