E>3TAMOEBA HISTOLYTICA 59 



pathogenic strains — such as are seen in contact carriers — is, on a priori 

 grounds, ahiiost inconceivable. A ** highly virulent " strain of the 

 parasite, which always causes acute amoebic dysentery to its host, could 

 not come into existence unless it simultaneously underwent a radical 

 change in its life-cycle. Amoebic dysentery, as already noted, is disad- 

 vantageous to the parasite as much as to its host ; for during a dysenteric 

 attack the amoebae are cast out of the body and are unable to encyst. 

 The " virulent strain," if it ever arose, would therefore be unable, in 

 nature, to transmit itself beyond its first host. As I have elsewhere 

 pointed out: "If the dysentery amoeba were always to cause acute 

 dysentery in every human being it infected, it would become extinct 

 within a period of time immeasurably less than that necessary for its 

 extermination by any conceivable human agency" (Dobell, igiSa). It 

 thus seems clear that "virulent" and "non-virulent" races of the parasite 

 do not occur in nature. 



The clinical differences between a healthy contact carrier of E. his- 

 tolytica and a person suffering from acute amoebic dysentery are easily 

 and simply explained if they are referred to differences in the suscepti- 

 bility of the hosts. Some individuals are unable to tolerate the parasites, 

 and react to their presence by developing acute dysentery ; but such 

 individuals are the rare exceptions, and the disharmony which results 

 when they accidentally become infected is as disadvantageous for their 

 parasites as it is for themselves. The ordinary individual, when he 

 acquires an infection, becomes a carrier ; and an equiHbriiim is at 

 once established between his parasites and himself — a balance is struck 

 between the regenerative powers of the host, and the destructive powers 

 of the parasite, resulting in a condition which is not distinctly harmful 

 to either. 



That this explanation of the apparent differences in pathogenicity of 

 E. histolytica in different hosts is the correct one, there is abundant 

 evidence to show. We constantly see amoebic dysentery patients who 

 make a complete clinical recovery without losing their infections. They 

 become convalescent carriers indistinguishable clinically from contact 

 carriers who have never had dysentery, though remaining still infected 

 with the same strain of amoebae. But the cysts from the stools of such 

 convalescent carriers, who are not suffering from dysentery, will, if 

 swallowed by a susceptible host, again produce amoebae which cause 

 dysentery. This experiment has been made on man by Walker, and has 

 been frequently made with cats, which are so susceptible to the action 

 of the parasite that they invariably acquire dysentery if they become 

 infected. The cat never becomes a carrier, no matter what strain of 

 amoebae is used to infect it ; and consequently the infection in these 

 animals can only be maintained by artificial means. Such experiments 

 have been performed with the cat by many different workers, and there 

 can be no doubt as to the facts. I may cite as a particularly instruc- 

 tive instance, however, an experiment made by Wenyon and O'Connor 

 (1917), who gave a kitten a most acute and fatal dysentery by feeding 

 it with cysts from the stools of a perfectly healthy man who had never 

 himself had dysentery. Experiments such as this show clearly that it 

 is the susceptibility or resistance of the host, and not a difference in the 

 virulence of the parasite, which determines whether any given infected 

 individual does or does not suffer from amoebic dysentery. 



Equally conclusive experiments have been made upon man himself. 



