190 Drs. Stephens and Blacklock. T. brucei, Plirnmer and [Dec. 7, 



impossible to match a typical Uganda slide by any slide from the Zululand 

 strain. 



We have stated in the above history of the Uganda strain that it was 

 recently returned to us by Prof. Mesnil, who remarked in his letter that he 

 had maintained it in mice (for nearly a year), and that it showed now very 

 few " trapues " forms. This we have been able to verify in the films made 

 from the infected mouse sent to us. But, as soon as we had re-inoculated it 

 into guinea-pigs, it again showed numerous stumpy forms. But the same 

 does not hold good for the Zululand strain ; in guinea-pigs, as in rats and 

 rabbits, the strain is typically monomorphic, i.e. it does not show stumpy forms. 

 We therefore conclude that the two strains, as we now possess them in the 

 laboratory, are different. 



How, then, are we to explain these facts ? There seem to us three 

 possibilities : — 



1. That the strain we now possess, which we have been designating 

 T. brucei, Zululand, is not this strain at all, but some other trypanosome 

 inoculated erroneously during the course of inoculations extending over 

 years. We think this view is untenable, for it would not explain the 

 monomorphic character of the old slides we have examined, nor would it 

 explain Laveran's monomorphic trypanosome. 



2. While Bruce may have been working with a dimorphic trypanosome in 

 Zululand, and still has slides showing these characters, it is quite possible 

 that the strain sent by him to England was something quite different. This 

 is all the more likely, as Bruce successfully infected dogs from a variety of 

 wild game, viz., wildebeeste, kudu, bushbuck, and buffalo, and, as Bruce 

 himself states, " when T. brucei was discovered in Zululand in 1894, it was 

 naturally thought to be the one and only trypanosome in Africa," and no 

 suspicion arose at that time of a multiplicity of trypanosomes in native game. 



This is the simplest explanation, and the fact that Plirnmer and Bradford 

 do not describe or figure stumpy forms, and our examination of Dr. Plimmer's 

 slides had the same result, makes it probable that this is the true one. 



3. That the strain originally sent to England was dimorphic, but that it 

 has now become monomorphic. This may have come about in two ways : — 



(a) The strain originally was a mixture of a long trypanosome and a 

 stumpy trypanosome, and the stumpy has now died out. If this explanation 

 were valid, it would probably imply that T. gambiense and other dimorphic 

 trypanosomes were also mixtures. This we regard as a not impossible view, 

 but one we cannot at present prove or disprove. 



(b) The strain was originally dimorphic (but not a mixture), and that it 

 has now become monomorphic. If this were so, it would modify materially 



