In its mammalian host, Trypanosoma brucei is able to change the antigenic character of its glycoprotein surface coat and so evade the host's immune response. This phenotypic change seems to occur spontaneously in 1 in 10,000 individuals but is not due to genetic mutation: host antibody is not necessary for its induction but plays a selective part in bringing about the gross changes in parasite numbers and antigenic character observed in the bloodstream by destroying the main component of what is actually a heterogeneous population. The infecting trypanosome population injected into the mammalian host by the tsetse fly vector may also be heterogeneous. Such heterogeneity complicates plans to vaccinate cattle and people against the African trypanosomes based on the premise that the metacyclic trypanosomes of a clone bear the same surface antigen.