A microsporidium, isolated from echinostome and strigeid larval trematodes in Lymnaea peregra, is described as a new species Unikaryon slaptonleyi sp.nov. The nuclei isolated at all stages of development, the disporoblastic sporogony and development in contact with host cell cytoplasm are used to assign the species to the genus Unikaryon. The absence of a vacuolar membrane to isolate the meronts and stages of sporulation from the host cell cytoplasm differentiates this genus from Encephalitozoon. Spores are uninucleate, have 17–21 turns of the polar filament coil and measure 5·0 × 2·8/μm fresh. U. slaptonleyi was isolated from rediae and metacercariae of Echinoparyphium recurvatum and sporo-cysts and cercariae of an unidentified strigeid trematode in L. peregra. It was transmitted in the laboratory to unidentified echinostomes in L. peregra and to unidentified strigeids in Planorbis planorbis by feeding the spores to field-collected snails from which cercariae were already emerging. In these natural and experimental hyperinfections the snail tissues were lightly infected but, in the helminths, much of the parenchyma and germinal tissue was destroyed, so that few cercariae were released and most of those were distorted. Similar heavy infections were produced in Fasciola hepatica in Lymnaea truncatula, when spores were fed to the snails 14 days after miracidial penetration, but even high doses (106 spores/snail) produced only light infections in Schistosoma mansoni in Biomphalaria glabrata, in only 2 out of 9 snails. No infections were obtained in larvae producing xiphidiocercariae in P. planorbis although echinostomes became infected under the same conditions. Of a number of aquatic and terrestrial arthropods tested for susceptibility by feeding or by inoculation of spores into the haemocoele, only Pieris brassicae became infected. In a small proportion of pupae surviving from larvae which had been inoculated with spores at 3rd or 4th instar, there was clear evidence of spore replication.

We have examined several taxonomic features of a number of strains of Eimeria from many sources world wide. The strains were isolated on the basis of their small spherical (or sub-spherical) oocysts. From a study of mean oocyst dimensions, electrophoretic variation of enzymes, ability to develop in embryonated eggs, absence of gross lesions in heavily infected chickens, and cross-immunity, all the strains were found to belong to one species. For convenience, the parasites when isolated, were referred to as strains of E. mitis/mivati-type, but after characterization they were clearly found to be E. mitis. In contrast, a laboratory strain of E. mivati supplied to one of us (M.W.S.) was found to be a mixture of E. acervulina and E. mitis. Evidence from these and other studies supports the notion that E. mivati is a nomina dubia.

Recent studies on the motility of coccidian sporozoites have demonstrated a membrane-associated contractile system capable of moving certain intramembraneous components down the parasite surface propelling it forwards. The properties of this system resemble recorded observations on host cell invasion. In this study the invasive behaviour of Eimeria tenella and E. acervulina has been examined, with reference to the above findings, by light microscope and scanning and transmission electron microscopes. Known inhibitors of motility prevent invasion, though attachment appears unaffected. Invasion itself consists of 3 phases; attachment and orientation, induction of a parasitophorous vacuole and translocation of the parasite into the vacuole. Ultrastructural examination reveals a close membrane/membrane association maintained throughout invasion. From these results it is suggested that the parasite enters the parasitophorous vacuole by ‘capping’ the host/parasite junction down its body, so locomoting into the host cell. Such a model has two main advantages; it requires no additional modifications to either cell, and the specificity of membrane receptors would enable the one membrane-associated contractile system to be responsible for locomotion, antibody capping and host cell invasion.

We have previously shown the presence of various purine salvage enzymes in Trypanosoma cruzi, including phosphoribosyltransferase, aminohydrolase, kinase, phosphorylase and hydrolase activities. We now report that a similar situation occurs in Leishmania mexicana amazonensis and Trypanosoma brucei brucei. In all three organisms we found higher levels of activity for the phosphoribosyltransferase enzymes than for the nucleoside kinases, suggesting a preference for the salvage of purine bases rather than nucleosides. Similarly, absence of inosine phosphorylase activity suggests that only one route for the salvage of hypoxanthine is available to the three organisms. The most striking difference was that whereas T. cruzi and T. brucei possessed adenosine aminohydrolase activity, this was not detected in L. mexicana; instead adenine amino-hydrolase activity was found. The overall similarity, as judged by the distribution of enzyme activities, of purine salvage in these three members of the kinetoplastida suggest a broad spectrum of activity for any inhibitor acting in this area; the plethora of alternative salvage pathways, however, suggests that in no case would such inhibition be cidal.

Trypanosoma cruzi trypomastigotes occur as a mixture of morphologically distinct forms in natural and experimental infections. We have been able to separate mixed populations into slender and broad forms using a continuous gradient composed of 12·5–25·0% hypaque in culture media. Previously, comparisons could only be made by using various strains of T. cruzi which show a predominance of either form. This separation procedure gave recoveries of 88–98% and had no effect on the viability of the parasites. Infectivity studies showed that slender forms were much more infectious to cultured muscle cells than were broad forms. However, studies with macrophages from CFW mice showed both forms to be equally capable of infection. It is concluded that the mechanism by which each form infects host cells is different; slender forms being capable of infecting both by penetration and by phagocytosis, while broad forms are only capable of infecting through phagocytosis.

The course of infection with a Malaysian dog strain of Ancylostoma ceylanicum was investigated in 15 inbred strains of mice, in outbred and inbred mice immunosuppressed with prednisolone, and in immuno-deficient hypothymic mice. Oral, percutaneous and subcutaneous routes of infection, in both sexes of mice, were assessed. In only one instance was a single small adult male worm found. Following oral infection, larvae migrated from the stomach to the large bowel and then a proportion of worms penetrated the perianal skin. This was followed by the appearance of larvae in the lungs. Living 3rd-stage larvae were seen in the anterior small intestine, perianal skin and lungs for the 6 weeks of the study, with peak recoveries being at 12 h, 8 days and 3 weeks, respectively. It is clear that systemic migration of larvae occurs after oral infection, and it is possible that recirculation may occur. Only a small percentage of larvae penetrated the abdominal skin after being administered percutaneously. In subcutaneous infections, a small proportion of larvae moved rapidly from the site of injection and were recovered from the lungs 2 h after infection. Most larvae, however, migrated from the injection site over the ensuing few days. Living 3rd-stage larvae were seen in the lungs and in the small intestine for the 4 weeks of observation. The strain of A. ceylanicum employed does not complete its development in mice. Nevertheless, this model offers significant potential for studying the immune responses, as well as investigating the means by which these parasites evade host defences.

The migration, growth and development of Cyclocoelum oculeum Kossack, 1911 was studied in orally and parenterally exposed coots, Fulica americana (Gm.). Young flukes injected into the body cavity migrate to the sinuses from the body cavity via the air sacs and air passages. Young flukes were first found in the trachea on day 18 post-infection and in the sinuses on day 21. Migration was not synchronous and some flukes were found in the air sacs and trachea of parenterally exposed coots up to 45 days post-infection. Exponential growth and organogenesis began between days 9 and 12. Flukes in the sinuses were consistently larger than flukes of the same age in either the air sacs or trachea. Growth and organogenesis proceeded in the latter flukes but at a slower rate than those in the sinuses.

Surface antigens of three stages of three species of the filarial nematode genus Brugia have been analysed by radio-iodination and immunoprecipitation. These surface antigens have been shown to be characteristic for each stage by polyacrylamide gel electrophoresis. For example, infective larvae and adult worms have relatively complex patterns while microfilariae have few bands which are not found when other stages are radio-isotope labelled by the same technique. The surface antigens of Brugia malayi, B. timori and B. pahangi adult worms are all closely homologous, as are the surface antigens of infective larvae of the same three species, and of microfilariae of B. malayi and B. pahangi. Immunoprecipitation revealed that antibody raised in mice against one stage or species reacted with surface antigens from other stages and species. For example, sera raised against B. pahangi male adults reacted strongly with surface antigens from all three species. This cross-reactivity was dominant despite the apparent stage-specificity of the surface pattern seen on SDS-PAGE analysis. Moreover, in cross-immunization experiments, infective larvae were able to stimulate a secondary antibody response in mice previously primed with microfilarial surface antigens. The major microfilarial surface antigens (of mol. wt 65−70000 Daltons) were recognized by serum antibody from microfilariae-, infective larvae- or adult-infected animals. Thus, although the dominant antigens from each stage are of different molecular weight, cross-reactions with stage-specific antisera suggest that there must be shared epitopes on Brugia surface antigens from each stage. Such shared antigenic determinants dominate the immune response, although other evidence, including the differences in molecular weight, indicates the existence of stage-and species-specific components.

Experiments were carried out to investigate the possible influence of host-dietary fructose concentration on the relationship between worm burden and the fecundity of Moniliformis dubius. Worm length was found to be dependent both on the fructose concentration of the host's diet and on worm burden. The number of free ovaries/female worm was found to increase linearly with increasing dietary fructose concentration but was independent of worm burden. The length of the ovaries increased with increasing dietary fructose concentration and decreased in response to increases in worm density. The magnitude of the density-dependent reduction in the volume of ovarian tissue/female was decreased in worms from rats fed on diets containing low concentrations of fructose. The numbers of eggs present in the body cavities of the female worms was found to be positively correlated with dietary fructose concentration. At 5 weeks post-infection, mature eggs (containing fully developed acanthor larvae) were found in the body cavities of female worms from rats whose diets contained 3 and 12% fructose, but not in those from rats whose diets contained 1 and 2% fructose (w/w). The experimental results are discussed in the wider context of the influence of host nutrition on parasite population biology.

Sprague–Dawley rats were infected by intraperitoneal injection with either the cysticerci of Taenia crassiceps or the tetrathyridia of Mesocestoides corti. Both species of metacestodes reproduce asexually in the peritoneal cavity. The effect of T. crassiceps upon the rats was to cause chronic inflammation of the peritoneum, fibrous adhesions between the visceral organs and hyperplasia of the gut mesenteries which became extended into a large sac-like structure. Dead parasites surrounded by white calcareous material were found free in the peritoneum and attached to the inner body wall and viscera. The histopathology of the hyperplastic mesenteries and fibrous membrane is described. The tetrathyridia of M. corti were found free in the peritoneal cavity as well as in the liver (mainly the left liver-lobe), gut mesenteries and in an outgrowth of the connective tissue associated with the pancreas. The connective tissue outgrowth comprised 2 layers; an inner reticular layer and a thickened marginal layer. Metacestodes were found in collagen—fibrin capsules within the connective tissue. A layer of mucopolysaccharide material was interposed between the parasite and the capsule wall. A possible method by which the parasites gain entry into the connective tissue is described. The connective tissues of rats harbouring either M. corti or T. crassiceps had increased numbers of mast cells compared to connective tissues from control rats. Younger mast cells containing biogenic amines predominated in infected tissues whereas older heparin-containing cells dominated control tissues.

A thymine–uracil transport system is present in the plasma membrane brush-border of the tapeworm, Hymenolepis diminuta. The relation between initial uptake and substrate concentration of either thymine or uracil was sigmoidal when 2-14C-labelled substrates were used. In contrast, absorption kinetics of methy 1-14C- and 3H-labelled substrates were hyperbolic. Since there was no metabolism of the labelled substrates during the incubation period, these differences indicate that the sigmoidal kinetics of pyrimidine transport in this organism is an isotope effect associated with the presence of the 14C label at the 2 position in the pyrimidine ring.

The inner cyst tissue development is anteriad and centripetal. The cells produce lamellar extensions which assume parallel alignment. The first contact points (approximately 4 days post-infection) establish heptalaminar (gap) junctions. Lamellar attenuation results in a decreased intercellular space, and at 5–6 days pentalaminar junctions (with fused outer plasmalemma leaflets to give an electron-dense, approximately 3 nm wide O–O line) occur. This is the first maturation (Ml) stage. The O–O lines are permeable to lanthanum, and evidence of their possible transformation from heptalaminar junctions is presented. Continued lamellar attenuation, associated with scolex retraction and subsequent growth, results in cytoplasmic occlusion and contact between the inner leaflets of the same lamella. The resultant electron-dense I–I line is approximately 3 nm wide; the O–O line is now less electron-dense and thinner (approximately 2 nm). This final maturation (M2) stage, resembling vertebrate myelin, occurs over limited areas; closely adjacent regions either remaining at the M1 stage, or not displaying junctional complexes. Since in vivo and in vitro excystment can occur before the M2 stage, the inner cyst tissue is not considered to be protective against the definitive host. That the tissue may function in limiting nutrient flow, thus regulating the size of the presumptive adult, is discussed.

During its life-cycle, the cestode Schistocephalus solidus is parasitic in both an ectotherm (Gasterosteus aculeatus) and an endotherm (Gallus domesticus) host, and so provides an excellent model with which to study temperature adaptation in parasites. A mitochondrial fraction was prepared from the adults and plerocercoids of S. solidus and from their respective hosts; the activities of the mitochondrial adenosine triphosphatase (ATPase) were then measured over the temperature range 1–45 °C. The plerocercoids of S. solidus show evidence of immediate temperature compensation; this would provide a mechanism for withstanding the abrupt temperature change experienced during infection of the final host. Analysis of the Michaelis constant data suggests that variation of Km, a with temperature may be a major factor in this immediate temperature compensation. In response to acclimation at 5 and 19°C, plerocercoid ATPase showed inverse or paradoxical rate compensation, as did the enzyme from the fish host. Acclimation at the two temperatures had no effect on the Q10 or on the linearity of the Arrhenius plots for the plerocercoid mitochondrial ATPase and only a small effect on the Km a. Acclimation of the fish host again had only a small effect on the Km, a of the fish mitochondrial ATPase but, in contrast to the plerocercoid, there was also a significant effect on the Q10 and the Arrhenius plots. Adult S. solidus ATPase showed partial rate compensation and had a biphasic Arrhenius plot, suggesting that after infection there had been a change in the enzyme or its micro-environment. In terms of the effect of temperature on the Q10 amd Km, a and in the biphasic nature of the Arrhenius plot, the mitochondrial ATPase of adult S. solidus showed similarities with the enzyme from its bird host.

The host–parasite relationship of the Chinese mainland strain of Schistosoma japonicum in CBA mice is described and compared to previous reports on this parasite in mice. S. japonicum took under 2 weeks to complete its migration to the portal system of mice, and peak passage of schistosomula through the lungs occurred 5–6 days after infection. The mean percentage establishment of worms, which was independent of the infecting inoculum, was 46%. The adult worm burdens remained constant over a 28-week period of infection. Male and female worms reached maximum mean lengths of 13 and 19 mm, respectively. Egg laying commenced 30 days after infection. The number of ova deposited in the liver stabilized at some 55000 by 12 weeks of infection with 30 cercariae, but the intestinal egg burden rose from 132000 at 12 weeks to 430000 at 28 weeks. Faecal eggs were first observed 6 weeks after mice were exposed to 100 cercariae and 7 weeks after lighter exposures. Faecal egg output also stabilized 12 weeks after infection. The formation of granulomas in the liver occurred within 2 weeks of egg deposition and encompassed a maximum area 14 weeks after infection. Fifty per cent mortality occurred 15 weeks after exposure, but only in hosts infected with 100 cercariae.

Available data in the literature pertaining to the life-history characteristics of all known species of mammalian schistosomes have been gathered, and correlations between such variables as length of pre-patent period, adult worm size, rate of progeny production and progeny size have been explored. Accommodation of the schistosome life-cycle to the constraints imposed by certain host characteristics such as life-expectancy and size is discussed. Of the 23 known species of mammalian schistosomes, 20 species apparently rely to a major extent on relatively large-bodied and long-lived mammals such as primates, ungulates and proboscideans for their transmission. Only 1 species, Schistosomatium douthitti, is exclusively dependent on rodents for its transmission. S. douthitti attains maturity within its definitive host faster than any other mammalian schistosome, and is the only species known to be capable of producing viable eggs by facultative parthenogenesis. For all species of mammalian schistosomes, adult worm size, as estimated by female length, is positively correlated with the number of uterine eggs contained within the female (r = 0·682). For the 7 species for which data exist, rate of egg production/worm pair/day is positively correlated with uterine egg counts (r = 0·873) and inversely correlated with egg length (r = −0·787) and miracidium length (r = −0·953). Length of the pre-patent period is positively correlated with egg length (r = 0·503). With respect to the molluscan host, the number of cercariae produced by snails is positively correlated with the shell size of the snail (r = 0·657). For the 5 species for which data exist, the rate of egg production is inversely correlated with shell size of the intermediate host (r = −0·955) and the common logarithm of the number of cercariae produced (r = −0·893). Comparisons between species suggest that exceptionally low rates of cercariae production in the intermediate host may be compensated for by rapid rates of egg production in the definitive host, implying a degree of integration in the schistosome life-cycle not previously appreciated. Most species of mammalian schistosomes have long-lived definitive hosts, and snail hosts capable of producing many cercariae; compensatory relationships are therefore less obvious in such species. Additional quantitative data on all aspects of schistosome life-histories, particularly rate and duration of egg production, are needed to confirm or refute the relationships discussed above.