Karl Pearson 
91 
divergence. Only a month later than Stephen and Fantham's paper appeared 
another paper by Sir David Biuce and others* comparing human trypanosomes 
from Nyasaland with T. brucei and T. rhodesiense and T. gamhiense. But the 
curve for T. brucei is wholly different from that of a year earlier. Instead of a 
minimum at 24 microns there is now a maximum at 24 microns, and the "general 
resemblance " of T. brucei to 2\ evansi is much increased. We are now told that 
T. rhodesiense (Stephens and Fantham) is "a distinct species, nearly related to 
T. brucei and T. gamhiense!' and the conclusion drawn that " the human trypano- 
some disease of North-east Rhodesia and Nyasaland is not the disease known as 
Sleeping Sickness in Uganda and the West Coast of Africa f." But the divergence 
between the frequency distributions of T. brucei and the human trypanosome of 
Nyasaland when accurately measured is of exactly the same order as that which 
suffices to demonstrate the identity of the human Nyasaland trypanosome and 
T. rhodesiense. Thus the two cases in which divergence is asserted, i.e. (i) T. brucei 
and T. evansi, (ii) T. brucei and T. rhodesiense, seem to be differentiated largely on 
the base of unanalysed statistical evidence of a nature precisely like that which in 
other cases is interpreted to mean close " general resemblance " or " .sameness." 
We do not feel that we are in the possession of independent evidence of differen- 
tiation which would enable us to test how far statistical divergency corresponds to 
recognised morphological differences of strain, — a fundamental requisite if we are 
to interpret as " sameness " a statistical divergence of an extremely high order. 
In concluding these introductory remarks we must refer to the types of 
trypanosome in Nyasaland recognised by Sir David Bruce and his colleagues as 
distinct on other grounds than numerical measurements. They are : 
(i) T. brucei vel rhodesiense. This is said to be the cause of the human 
trypanosome disease of Nyasaland. The modal length appears to be 24 to 25 
microns J. According to Bruce and colleagues T. gambiense appears to have a 
mode of 20 microns, but there is evidence for a submode at 26. 
(ii) T. pecorum. This is said to be the cause of trypanosome diseases of 
domestic animals in both Uganda and Nyasaland. The modal length varies from 
13 to 14§. There is no statistical evidence of bimodality. 
(iii) T. simiae. This attacks monkey, goat and warthog. Oxen, dogs, white 
rats, etc., are said to be immune. The length distribution appears to be very 
homogeneous and with a single mode at 18 microns ||. 
* R. S. Proc. Vol. 8.3, B, p. 4.31, 1912. 
t R. S. Proc. Vol. 85, B, p. 433, 1912. In 1913, however, we find that " there is some reason for the 
belief that T. rhodesiense and T. brucei are one and the same species," see Sir David Bruce and others, 
R. S. Proc. Vol. 86, B, p. 407. 
t R. S. Proc. Vol. 84, B, p. 331. Stephens and Fantham's measurements on 2'. rhodesiense 
suggest modes at 20 and 26. Ibid. Vol. 85, B, p. 231. The double mode— roughly 18 to 20 and 
28 to 29— appears in the Zululand (1894) and Uganda (1909) strains of T. brucei. Ibid. Vol. 83, 
B, p. 12. 
§ R. S. Proc. Vol. 82, B, p. 468, and Vol. 87, B, p. 14. 
II R. S. Proc. Vol. 85, B, p. 477, and Vol. 87, B, p. 48. 
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