The Blood Flagellates 583 



host. T. equiperdum, possibly evolved through a similar accident of 

 distribution, is now transmitted through direct contact in coitus. 



Current differentiation of species is based, in some cases, upon host 

 relationships instead of conventional morphological features. For ex- 

 ample, T. briicei, T. gambiense, and T. rhodesiense are morphologically 

 indistinguishable. The same is true for T. equiperdum and T. evansi. In 

 such cases, the homologues could be, and probably should be, considered 

 specialized strains of a single species (31). 



The range in pathogenicity of trypanosomes has interested various 

 workers in possible explanations for pathological effects. The sugar con- 

 sumption theory (58) assumed that the consumption of sugar by trypano- 

 somes might reduce the blood sugar of the host too rapidly for the liver 

 to maintain a normal blood level. The resultant strain was supposed to 

 cause a breakdown of liver function, leading to fatal intoxication. In 

 spite of a few cases in which blood sugar levels have been low consistently 

 (56), marked reduction in sugar levels generally occurs only in the last 

 days or hours of a lethal infection. 



Another theory (7) holds that death of the host is caused by asphyxia- 

 tion, supposedly the result of a pulmonary oedema following partial ob- 

 struction of capillaries by agglutinated trypanosomes. A third suggestion 

 (35) is that lactic acid, produced from sugars by trypanosomes, interferes 

 with normal tissue oxidations. The lactic acid concentration of the blood 

 usually does show an increase during the terminal stages of a fatal in- 

 fection, but the concentrations reported are considered too low for 

 appreciable injury to the host. Approximate doubling of the serum potas- 

 sium level has been reported before death of rats infected with T. 

 equiperdum (78), while in other cases no correlation has been observed 

 between the time of survival and the tolerance to potassium (57a). Tryp- 

 anosomal toxins also have been suggested as an explanation for patho- 

 genicity. Although there is no evidence that trypanosomes produce true 

 exotoxins, it is possible that endotoxins (in the bacteriological sense) 

 might harm the host. 



African sleeping sickness 



Distribution. There are two varieties of this disease, Gambian and 

 Rhodesian. The Gambian variety has ranged from about 15° N. to 

 15° S. latitude but is more common in the western than in the eastern 

 part of this zone in Africa. Within its range, the disease occurs primarily 

 along rivers and near lakes, in correlation with the distribution of its 

 major vector, Glossina palpalis. In the eastern part of its range, Gambian 

 sleeping sickness extends into the territory of the Rhodesian variety. 

 The latter, which is less widely distributed, has been known in North 

 and South Rhodesia, Portugese East Africa, Nyasaland, Tanganyika Ter- 

 ritory, northeastern Mozambique, Uganda Protectorate, and the southern 



