A total of 480 snails were collected from 3 habitats on the Mau Escarpment, Kenya, and were identified as Bulinus tropicus. Of the 351 snails examined alive in London, 75 were infected with Calicophoron microbothrium, 39 with C. microbothrium and Schistosoma bovis, 1 with S. bovis, 24 with other species of trematodes and 212 were uninfected. Examination of digestive glands of B. tropicus either uninfected or infected with both C. microbothrium and S. bovis demonstrated that it is possible to differentiate between parasite and host enzyme activity using glucose phosphate isomerase. However, malate dehydrogenase enables a much clearer differentiation between the enzyme activity of the schistosome and that of the amphistome. Laboratory snail infection experiments demonstrated that it is possible successfully to infect B. tropicus with S. bovis if the snails have previously been exposed to miracidia of C. microbothrium.

Enzyme variation has been investigated in eight populations of Bulinus cernicus from Mauritius using isoelectric focusing and starch gel electrophoresis. Of 11 loci examined for 10 enzyme systems, seven were found to be polymorphic. These were malate dehydrogenase, glucose phosphate isomerase, acid phosphatase (A and B), 3‐hydroxybutyrate dehydrogenase, 6‐phosphogluconate dehydrogenase and NADH‐dependent diaphorase. Invariant loci were phosphoglucomutase, xanthine oxidase, fructokinase and αaL‐glycerophosphate dehydrogenase. The percentage of polymorphic loci within the populations ranged from 9.1% to 54.5%. The average heterozygosity per population for all loci ranged from 0,009 to 0.203. Genetic distance values ranged from 0.01 to 0.3 with the higher values associated with comparisons of populations from the north‐west and south‐east of the island. A comparison of data sets for 1980 and 1986 revealed the allelic frequencies at five enzyme loci to be remarkably consistent.

Blood samples from the Waskia and Takia populations of Karkar Island, Papua New Guinea, and other nearby mainland populations, were tested for genetic variation in blood group, serum protein and red cell enzyme systems. Polymorphic variation was present in the ABO, P, MNS, Rh, Lewis, Duffy, Kidd and Gerbich blood group systems, in the Hp and Tf serum protein systems, and in the acid phosphatase, 6-PGD, ADA, PGM, MDH, and G-6-PD enzyme systems. A small number of variants was found in other systems: there were 4 Lu(a+), 1 Kp(a+), 2 C variants in the acid phosphatase system, 6 LDH variants, 1 ADA3–1 and 1 AK2–1 sample. All samples were negative for the red cell antigens C^w, Vw, He, K, Js^a, Di^a, Wr^a, Rd and Marriott, and no variation was observed in the PHI enzyme system. The results are discussed in relation to those obtained on other Papua New Guinea populations.

Bjarnason, Bjarnason, Edwards, Fridriksson, Magnusson, Mourant and Tills (1973) published preliminary data on a study of Iceland. The present paper gives the complete data of the study and extends the sample size for most of the genetic systems to over 1500 individuals, approximately 1/130 of the population. The sample was divided into seven subpopulations and these were compared using a genetic distance matrix. Considerable internal variation was revealed with two groups appearing very different. The seven regions were then compared with possible founding populations and no close relationships were found. The possible mechanism for the internal variation and the differences between Icelandic gene frequencies and those from other N.W. European populations are discussed.

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