24 SCIENCE BULLETIN, No. 21. 



Later on it was shown that they were agonal or post-mortem invaders, as 

 proved by their absence from blood, tissues, &c., when such were removed 

 immediately the animal had been seen to die. On reading Gilruth's articles 

 one cannot avoid the conclusion that the same thing happened in the case 

 of the Victorian and Tasmanian investigations, viz., that the bacteria 

 claimed to be the causal organisms were obtained from animals from which, 

 the possibilities of post-mortem invasion could not be excluded. 



Regarding the identity of the Australian disease with European braxy or 

 bradsot, the matter is more difficult to approach. The bacteriological find- 

 ings of a number of writers afford little aid in the solution of the question. 

 Some were undoubtedly dealing with post-mortem invaders, whilst others 

 had not eliminated that possibility. As regards the disease seen on the 

 continent of Europe, there is still dispute as to the etiological factor. Here 

 again some of the writers were undoubtedly working with cadaver 

 bacilli. It would greatly simplify matters if it could be shown that what- 

 ever bacilli were isolated, they were obtained from animals immediately 

 they were dead, and that means were taken to prevent any secondary con- 

 tamination of the fluids or tissues, this being an important considera- 

 tion. In spite of these uncertainties it would appear that braxy or bradsot 

 has a number of features in common as regards climatology and morbid' 

 anatomy, if one disregards the obvious post-mortem phenomena in connec- 

 tion with the latter; but (and this I consider to be an important difference) 

 I have not been able to discover any reference to the presence of liver 

 lesions in descriptions of the disease either in Great Britain or on the 

 Continent. If these are really absent, then one must conclude that either 

 the disease is not identical with that seen in Australia, or that the port of 

 entrance of the bacilli is not the same, and that the carrier can therefore- 

 hardly be the liver fluke. On the other hand it may be that the liver lesion 

 or lesions have been overlooked by those making the examination, or they 

 have been viewed as merely of secondary importance, and attention has been 

 directed elsewhere, as, for example, to the abomasum. It will be evident 

 that microscopical examination of, or cultures made from, any portion of 

 the liver, save from the necrotic foci themselves, would be entirely negative 

 if means were taken to avoid agonal or post-mortem invasion. The fact 

 that a bacillus, which has been isolated from blood, exudates, or organs of 

 sheep found dead, is very fatal to experimental animals upon parenteral 

 inoculation, is no proof that it was the causal agent of the disease, because 

 it is well known that quite a number of anaerobic cadaver bacilli are highly 

 pathogenic when so injected. 



It is rather strange that, although investigators have known of the- 

 fallacies introduced by working with cadaver bacilli, yet until the writer 

 pointed it out, no one working on braxy or its allies appears to have realised 

 the primary importance of the fact that in research work on diseases of this 

 nature in sheep, one should always be assured that the organisms isolated!; 

 were present in the body (in the strict sense of the word) before death, 

 unless it can be shown that invasion of the body itself is not necessary for 

 the organism to produce its pathogenic effects. Of course, it has te be. 



