The primary trophozoites of Malpighamoeba locustae excyst in the crop and midgut of the Desert Locust (Schistocerca gregaria) and then penetrate the epithelial cells of the midgut and caeca where they grow and multiply slowly. After about 10–12 days they leave the gut epithelium passively when the cells in which they have grown degenerate and are extruded. From the lumen of the gut they make their way into the lumen of the Malpighian tubules where they feed upon the brush border as extracellular parasites. No primary or secondary trophozoites were found in the haemocoele of the host.

During the first few days in the Malpighian tubules the secondary trophozoites undergo a rapid series of divisions which enables them to double their numbers every 24 h so that by day 20–22 the lumen of the tubules is packed with cysts and trophozoites. The trophozoites phagocy-tose small pieces of brush border and numerous food vacuoles are present in their cytoplasm. The cytoplasm of the primary trophozoite contains the normal complement of cell organelles, a notable feature of which are the large, numerous mitochondria with their tubular cristae. When the trophozoites are ready to encyst they round up and begin to lay down a series of membranes which totally cover the trophozoite. Numerous storage granules are found in mature trophozoites which are about to encyst and these may be utilized in cyst wall production.

The behaviour of four species of Eimeria was studied in lambs which were given either monospecific or multispecific infections. In the presence of other species the patency of oocyst production of E. ovina and E. weybridgensis was extended and the total number of oocysts produced by all species except E. ninakohlyakimovae was increased. Clinical symptoms were observed only in lambs which received E. ninakohlyakimovae.

Plasmodium falciparum parasites infecting Aotus trivirgatus erythrocytes were cultured in media (Harvard and TC199) augmented with human, foetal calf, or other sera. Conditions were established which supported growth of parasites and allowed cyclical multiplication when fresh erythrocytes (from Aotus or Homo) were added in sub-culture (mean multiplication rate: x 3). Immunoglobulin G pools, prepared from plasma collected in endemic malarious areas in Africa and from unexposed Britons, were tested for effects on the in vitro growth (measured by incorporation of tritiated leucine) and multiplication of parasites. Whilst non-immune IgG was without effect, IgG from both East and West Africa inhibited the multiplication of East African (Uganda-Palo Alto strain) parasites.

A number of common freshwater molluscs were exposed to Fasciola hepatica miracidia labelled in vivo with radioselenium. Radioactivity was rapidly incorporated in all lymnaeid species tested (L. auricularia, L. columella, L. glabra, L. natalensis, L. palustris, L. pereger, L. stagnalis, L. tomentosa and L. truncatula) whereas no radioactivity could be demonstrated in non-lymnaeid pulmonate species (Aplexa hypnorum, Physa acuta, Physafontinalis, Anisus vortex, Gyraulus albus and Planorbis planorbis) or in the prosobranchs Valvata cristata and Valvata piscinalis. However, the prosobranchs Bithynia leachii, Bithynia tentaculata and Potamopyrgus jenkinsi showed a slow but significant uptake of radioactivity which was presumably explained by uptake of labelled miracidia through a ‘filter-feeding] mechanism. Sphaerium corneum, a true filter-feeder, showed a similar course of uptake of radioactivity.

In young (6- to 8-week-old) NTH strain inbred mice expulsion of a primary infection of Trichinella spiralis began on day 8 and was virtually complete by day 11·5. In older mice expulsion occurred 1 or 2 days earlier. Experience of a primary infection elicited strong immunity to challenge, whether the challenge was given immediately after worm expulsion (day 14) or delayed (day 42). Challenge infections were expelled rapidly, the majority of worms being lost during the first day. Immunity to challenge was elicited by low-level primary infections and was effective against large challenge infections. These results are discussed in relation to conventionally accepted parameters of immunity to T. spiralis in mice which, it is considered, are applicable only to mice with a genetically-determined low-level of responsiveness to the parasite.

The genetic basis of virulence in a line (YM) of Plasmodium yoelii yoelii was investigated in a cross with a mild line (A/C). The blood forms of the virulent line developed extensively in mature erythrocytes of mice, causing death of the host within 7 days; infections with the mild line were normally restricted to reticulocytes, infected animals recovering after three weeks. Lines YM and A/C differed additionally in enzyme and drug-sensitivity markers. Studies on infections established from each line alone from sporozoite mixtures of the two lines and from the cross between the lines showed that the appearance of virulence had been caused by a genetic change in the parasite, and not by other factors such as a concurrent infection with another organism. An analysis of the characters of 56 clones derived from the cross showed that the virulence character had undergone recombination with the other markers, and appeared to be inherited in Mendelian fashion. Three clones exhibited atypical virulence, although it was not clear whether this had been produced by genetic recombination.

The distribution of the acanthocephalan Pomphorhynchus laevis along the alimentary tract of several species of freshwater fish was studied in both natural and experimental infections. The parasite exhibits a clear preference for a particular region of the alimentary canal, which differs from host species to host species, but it is capable of surviving in all regions of the intestine. In some host species, but not in all, its growth rate may be reduced in regions outside of the preferred site. The parasite remains in the same site throughout the period of infection, emigrations occurring only preparatory to complete loss of the parasite from the host. The presence of cestodes in the region of the preferred site has no effect upon the distribution of the parasite. At high levels of infection the range of the parasite's distribution is extended. The feeding of larval parasites to fish by stomach tube also leads to an extension of range, whereas when fish are allowed to feed on cystacanths removed from their intermediate host the parasite establishes in a more anterior position than usual and in a site that it does not occupy to any extent in natural infections. It is concluded that the distribution of P. laevis in the alimentary canal offish is determined primarily by the process of liberation, activation and establishment of the parasite, and that it normally attaches in the first available space and remains there. Unsuitable physico-chemical or feeding conditions affect only its growth, not the site that it occupies. It is suggested that P. laevis may be atypical in this respect.