The pathogenesis and pathology of animal trypanosomosis has been a subject of numerous investigations and anaemia has long been recognized as a significant pathological feature. It is the consensus that this anaemia is haemolytic in origin, occurring intravascularly in the acute phase and also extravascularly in the subacute and chronic stages of the disease. The cause of this anaemia is multifactorial and includes increase in erythrocyte destruction coupled with shortening of erythrocyte lifespan. The destruction of erythrocytes largely occurs in the liver by erythrophagocytosis. The other mechanism that has been suggested is that trypanosomes may exert a direct haemolytic action on erythrocytes by generating potentially haemolytic factors on autolysis, a phenomenon that was first described by Landsteiner & Raubitscheck (1901) who hypothesized that the haemolytic factor is lipid in nature. Other mechanisms that have been suggested are haemodilution, bone marrow dysfunction (dyshaemopoiesis) and immunologically-mediated destruction of erythrocytes. In this chapter, the roles of biochemical changes particularly the lipid sub-fraction, bone marrow dysfunction and haemodilution in Small East African goats experimentally infected with Trypanosoma congolense or T. brucei brucei shall be examined. The effect of T. congolense on the life span of erythrocytes in sheep, inferred from 51Cr-labelled erythrocytes, will be presented and discussed. An in-depth knowledge of development of anaemia during trypanosomosis in different animal species is pivotal in instituting appropriate treatment in clinically sick animals and during convalescence. Similarly, the same knowledge can be utilized by animal health workers to manage anaemia derived from causes other than trypanosomosis.