Parasitic amoebae of the genus Entamoeba are transmitted from one host to another as cysts. The active amoeboid forms are so adapted to life within their particular hosts that, outside the host, they soon die, but encysted stages survive conditions fatal to the unprotected amoebae. The cyst is an integral and critical phase in the life-cycle of Entamoeba; its attributes directly influence the dissemination of the organism, and are an important aspect in the epidemiology of amoebiasis. The following account of the morphology, formation and development of the cysts of Entamoeba is an assessment of present knowledge, and is not a comprehensive review of all available observations.

1. A thirty-two-fold increase in resistance to sulphadiazine has been induced in Plasmodium gallinaceum in chicks by treatment with that drug.2. No loss in resistance to sulphadiazine occurred in the resistant strain during cyclical passage through Aëdes aegypti.3. The sulphadiazine-resistant strain was resistant also to sulphathiazole, sulphanilamide and sulphapyridine, but not to mepacrine, quinine or pamaquin. An increase in sensitivity to pamaquin was observed.4. The sulphadiazine-resistant strain was resistant to paludrine and its methyl homologue M 4430.5. In strains maintained in a state of acute infection and treated with sulphadiazine, resistance to paludrine developed more rapidly than resistance to sulphadiazine, and in one strain a high degree of resistance to paludrine was obtained before any increase in resistance to sulphadiazine could be detected.6. Resistance to paludrine as induced by sulphadiazine, develops rapidly and extends at once over the full range of doses which the chick will tolerate, whereas resistance to paludrine as induced by that drug itself, develops more slowly and by stages.7. Whereas resistance to paludrine is induced readily by treatment with sulphadiazine, resistance to sulphadiazine is induced by paludrine only after treatment with high doses of the drug for a prolonged period.8. In latent infections of Plasmodium gallinaceum resistance to paludrine or sulphadiazine was not induced by sulphadiazine during the period of the experiment (49–75 days), though the aggregate dosage of drug used was much greater than that with which resistance was induced in strains maintained in an acute state.9. It is not considered probable that cross-resistance between sulphadiazine and paludrine is due to a similar mode of action of these drugs, as whereas sulphadiazine is antagonized by p-amino-benzoic acid paludrine is not.

1. Optimum growth of E. invadens occurred in HSre + S in the presence of Bact. coli, at 24–30° C. The amoebae could not be ‘trained’ to grow above 35° C.2. The amoebae ingested normal rat erythrocytes, but not those of chick or frog.3. Mass encystation occurred only under conditions which favoured the growth of the amoebae, but was not dependent on an acceleration in growth rate; in certain strains, an increased production of cysts was correlated with the depletion of starch in the medium.4. The amoebae were always killed by treatment with N/20-HCl for 1 hr. at room temperature, although usually they did not survive after treatment for only 10 min. At room temperature, the cysts survived treatment with N/10-HC1 for at least 6 days, and with 0·002% HgCl2 for at least 4 hr.5. The amoebae of E. invadens were adversely affected by aerobic conditions.6. The amoebae could survive for up to 35 days at 8° C. but for not more than 7 days at 37° C. The cysts survived for at least 14 days at 8° C., for 7, but not 11, days at 24° C., and for less than 7 days at 37° C.7. It is suggested that, in view of the morphological identity of E. aulastomi, E. invadens, E. moshkovskii and E. histolytica, and the fact that the amoebae of these groups form a series growing at increasingly higher temperatures, these four organisms constitute subspecies rather than full species. The taxonomic status of E. ranarum is still open to question.