Ill 



there results a necrosis of the tissues in their immediate 

 vicinity, giving rise to the typical caseous areas. 



These changes represent the characteristic appearances 

 of the granuloma, and, apart from bacterial infection of the 

 ulcerated surface, there is no reaction present which would not 

 be produced by the presence and degeneration of the larval 

 Nematode. 



This evidence is almost sufficient to prove that the larvae 

 are the essential cause of the granuloma, and that they cannot 

 be regarded as an epi-phenomenon. Added to this evidence 

 is the failure to demonstrate by any conceivable method the 

 presence of any bacterium, mould, or protozoon, except a 

 mixed variety of bacteria on the ulcerated surface. 



Experimentally it has been shown that larvae of 

 Habronema are capable of producing a granuloma very similar 

 to that found under natural conditions. This fact, taken with 

 the above evidence, is sufficient to prove that the presence of 

 the larvae in the cutaneous, subcutaneous, or submucous 

 tissues is the essential cause of the lesion. 



It is interesting to note that there is no essential difference 

 between the tissue reactions seen in these tumours and those 

 seen about many of the caseous areas to be found commonly 

 in the internal organs of most herbiverous animals. 



The fact that, although the larvae die out soon after the 

 first appearance of the lesion, the tumour goes on enlarging, 

 and vmay exist for some considerable time, is of ' extreme 

 interest. 



This gradual enlargement of the tumour consists of an 

 enlargement of the necrotic areas and an increased tissue 

 production. There is no increase in the number of foci as, 

 for example, occurs in actinomycotic granulomata, except in 

 the case of re-infection or super-infection. 



The growth of the tumour is due mainly to the fact that 

 the substances which originate in the degenerating or autolys- 

 ing larvae, and which apparently causes the death of the 

 tissue cells, very slowly penetrate to the outside of the 

 necrotic tissue, and thus cause a slow but gradual enlargement 

 or extension of the necrosis. This, of course, is limited, and 

 the maximum amount of necrosis is produced in a certain time, 

 according to various conditions which are difficult to measure. 



Once the larva becomes surrounded by necrotic tissue, the 

 diffusion outwards of the autolytic products is impeded. The 

 autolytic products would, therefore, become concentrated 

 towards the centre of the necrotic area, and their slow diffu- 

 sion to the outside would tend to produce a gradual extension 

 of the necrosis, even" after the complete disappearance of the 

 larva. The continued presence and enlargement of the 



