708 



ECOLOGY AND EVOLtJTION 



boscid flies transmit the Haemoproteus of 

 birds, while the vector for the reptile types 

 is unknown. The vertebrate host of Leu- 

 cocytozoon is always a bird, and the two 

 species for which the life cycle is known 

 are transmitted by blackflies (Simuliidae). 

 In all three genera, the asexual cycle is in 

 the vertebrate, most of the sexual cycle is in 

 the fly, and no free-living stage occurs 

 (see p. 686). Sporozoans {Lankesteria 

 culicis) related to malarial parasites infect 

 mosquitoes without an intermediate host. 



The evolutionary parallelism between the 

 original hosts and the parasites would be 

 expected to be greater than between the 

 more recent hosts. Also, one would expect 

 greater adjustment to the original hosts. 

 This adaptation would result from natural 

 selection, since the strains of parasites hav- 

 ing the greatest pathogenicity would prob- 

 ably be eliminated through the death of 

 the host (Disoperation, p. 699). Likewise, 

 the more susceptible of the hosts would 

 succumb to the eff'ects of the parasite. 

 Through the closer phylogenetic relation- 

 ship of the fly vectors compared with that 

 of the vertebrate hosts, one would assume 

 that malarial protozoans evolved primarily 

 with the Diptera. 



Huff (1938) found that infected and 

 noninfected mosquitoes showed no signifi- 

 cant differences in {a) ability to lay viable 

 eggs, (b) length of life after a blood meal, 

 (c) length of time between a blood meal 

 and oviposition, and {d) number of eggs 

 laid after a blood meal. He concludes that 

 there are no pathological effects in the 

 mosquitoes, although the vertebrate hosts 

 may suffer from the disease. Again, tolera- 

 tion in the older parasite-host adjustment 

 is indicated, while pathogenicity is char- 

 acteristic of the more recent parasite-host 

 relationship. 



Hoare (1943) states: 



"In a non-susceptible animal (or plant) 

 various factors may prevent a parasite from 

 setting up an infection. Thus, the character of 

 the digestive juices may not be suitable for 

 hatching the cysts of intestinal protozoa, or 

 the serum may possess natural parasiticidal 

 properties which affords protection against in- 

 fection with blood protozoa. It is known, for 

 instance, that the oocysts of coccidia, when 

 ingested by animals other than natural hosts, 

 pass unchanged through the alimentary tract. 

 The resistance of man to infection with Tryp- 

 anosoma hrucei is probably due to the fact 



that normal human serum kills this trypano- 

 scme, whereas it has no effect upon T. gam- 

 biense. The other race, T. rhodesiense, appears 

 to occupy an intermediate position— in the 

 human body it resists the action of serum, but 

 may lose this property after passages through 

 other animals." 



Huff and Coulston (1946) postulate 

 several barriers that may prevent an in- 

 fection by malarial parasites. First, phag- 

 ocytic cells or humoral substances may de- 

 stroy the sporozoites before they reach the 

 appropriate host cells. Secondly, there may 

 be cellular or humoral interference with the 

 change of parasites from tissue cells to 

 erythrocytes. Thirdly, the host may de- 

 velop immunity to the parasite in the eryth- 

 rocyte stages. These hazards to the para- 

 sites differ in different species of hosts. The 

 saurian malarial parasite, Plasmodium 

 mexicanum, produces gametocytes in its 

 normal host lizard, Scleroporiis ferrari- 

 perezi, but not in the lizard, Crotaphytiis 

 collaris. The ability to form gametocytes 

 was regained when the parasite was ex- 

 perimentally transferred to close relatives 

 of the normal host {Scleroporiis olivacetis 

 and S. tindulatus) . 



Physiological characteristics of parasites 

 in combination with ecological adjustment 

 of hosts may influence the evolution of the 

 parasite-host relationship. The ciliate pro- 

 tozoan, Balantidium coli, chiefly occurring 

 in domestic pigs, is nonpathogenic in the 

 pig and is often pathogenic in man. It feeds 

 mainly on starch, which is abundant in the 

 intestine of a pig, but is scarce in the in- 

 testine of man. Insufficiency of starch in 

 the human intestine may induce the ciliate 

 to attack the walls with consequent symp- 

 toms of balantidiosis (Hoare, 1943, p. 

 142). 



Ball (1943) takes exception to the ab- 

 solute rule that "a high degree of patho- 

 genicity of a parasite is prima facie evi- 

 dence of a recent and still imperfect devel- 

 opment of the host-parasite relation." He 

 states that "evolution may, in many cases, 

 have brought about a mutual adaptation 

 between host and parasite resulting in rel- 

 ative harmlessness of the relation, but in 

 other instances no such decrease in patho- 

 genicity seems to have occurred; and in 

 still others as the parasite becomes better 

 adapted for life in its host, it has become 

 rather more than less capable of producing 



