EVOLUTION OF INTERSPECIES INTEGRATION AND ECOSYSTEM 



707 



its winter food supply. The herd declined 

 from 100,000 to 40,000 in 1924-1925, and 

 from 30,000 to 20,000 in 1929 to 1931. 

 The normal carrying capacity of the Kaibab 

 plateau is estimated to be about 30,000 

 deer, and this number does not damage the 

 plant forage as do excessive population 

 eruptions. In 1939 the population stood at 

 about 10,000, with few pumas and a de- 

 pleted range (Leopold, 1943; Fig. 252). 



It would seem that an optimal number 

 of predators keeps the deer population in 

 better adjustment to its food supply, and 

 the plants are also indirectly benefited by 

 these predators in the community. The orig- 

 inal population of predators on the Kaibab 

 plateau kept the deer below the carrying 

 capacity of the range, but too many were 

 eliminated by man for benefit to either the 

 deer or the forage plants. Leopold (1943a) 

 suggests that wolves be allowed to increase 

 in overbrowsed areas of W^isconsin in order 

 to benefit the deer (see also Sears, 1937, 

 p. 261; Cartwright, 1944). 



The best illustrations of the evolution of 

 toleration are the host-parasite relations of 

 certain pathogenic organisms (p. 260). 

 Huff (1938) gives a summary discussion 

 and interpretation of the facts indicating 

 reciprocal evolution of hosts and parasites. 



The hemoflagellates of the family Tryp- 

 anosomidae were originally parasites of 

 invertebrates, particularly of insects. Many 

 species are found only in insect digestive 

 tracts and are transmitted through the 

 feces of the hosts. Tsetse flies (Glossina) 

 transmit African sleeping sickness of man 

 and nagana of animals; the sand fly 

 (Phlebotomus) transmits the oriental sore; 

 reduviid bugs transmit Chagas' disease; 

 and Trypanosoma lewisi of rats is transmit- 

 ted by rat fleas.* The pathogenicity of some 

 of these species— for example, the African 

 sleeping sickness of man— is great, while T. 

 lewisi of rats and T. duttoni of house mice 

 are nonpathogenic. T. lewisi increases in 

 numbers for about 4-7 days after the in- 

 fection of the rat. An antibody (ablastin) 

 then inhibits further reproduction of the 

 parasites, but does not kill them (Talia- 

 ferro, 1941). Also, specific trypanolysins 

 that kill many parasites are acquired on 

 about the tenth day of infection. The 



* Trypanosoma equiperdum, which causes a 

 venereal disease of equines (dourine), lacks an 

 insect vector and is an exception. 



course of infection for T. lewisi and T. dut- 

 toni in their respective hosts is similar, but 

 the T. duttoni population does not rise 

 parallel with that of T. lewisi, and the 

 mouse has a natural immunity through 

 macrophage function that is similar in ef- 

 fect to the acquired immunity through 

 macrophage function in the rat (Taliaferro 

 and Pavhnova, 1936; Taliaferro, 1938). 



The trypanosomes of the native game 

 animals of Africa are comparatively harm- 

 less to their natural hosts, but two (T. 

 gambiense and its close relative, T. rhode- 

 siense) are highly pathogenic to man, 

 while all attempts to infect man with T. 

 hrucei have failed, although morphologi- 

 cally it is indistinguishable from the other 

 two species and is probably the ancestral 

 species of the human parasites. Tn/pano- 

 soma gambiense in man produces chronic 

 sleeping sickness with well marked nervous 

 symptoms, while T. rhodesiense in man 

 causes a toxic disease without nervous 

 symptoms. Trypanosoma brucei produces 

 a disease in laboratory animals hke that 

 produced in man by T. rhodesiense. Hoare 

 (1943) thinks that T. brucei originally oc- 

 curred in antelopes and gave rise to the 

 two species in man, T. gambiense being 

 somewhat older in man than T. rhode- 

 siense. Trypanosoma brucei is nonpath- 

 ogenic in antelopes, but produces the 

 disease nagana in cattle (p. 476) . 



Huff concludes that there is a strong 

 likelihood that the trypanosomes have been 

 adapted to insect hosts much longer than 

 to vertebrates, to wild game animals of 

 Africa much longer than to man or cattle, 

 and that evolution toward toleration has 

 probably occurred in the older associations. 

 Natural immunity may have evolved in 

 some instances, while in others there has 

 been an evolution of mechanisms produc- 

 ing acquired immunity. Acquired im- 

 munity, however, is not always the result 

 of an evolutionary reaction to the specific 

 parasite. 



Malarial protozoans indicate that their 

 major phyletic evolution (megaevolution) 

 has been more closely tied to that of their 

 insect vectors than to their vertebrate hosts 

 (Huff, 1945). Plasmodium is found in the 

 blood of man, apes, monkeys, bats, birds, 

 and lizards, and is transmitted to these 

 hosts by mosquitoes. Haemoproteus occurs 

 in birds, turtles, and snakes. The hippo- 



