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.

Asexual stages and mature gametocytes of Plasmodium falciparum have been produced in a 500 ml suspension culture system containing 6–10% red cells. Medium change was automated and was accomplished using a tangential flow filtration unit. The rate of multiplication of the parasite (isolate NF 54) was consistently high when compared with static cultures and ranged from 6·4 × to 15·3 × per cycle in 8 experiments. Mature gametocytes were present in up to 2% of red cells in 14-day-old cultures. Only minor modifications would be required to further scale-up the volume of the culture.

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.

Living Schistosoma mansoni of various developmental stages were studied with respect to their ability to activate the complement system in sera of humans, mice and rats. Immunofluorescence assays demonstrated that binding of human C3 occurred on fresh schistosomula as well as on schistosomula prepared from mouse lymph-nodes or lungs and on adult schistosomes. However, rodent C3 was deposited only on fresh schistosomula. Deposition of human C3 on the worms' surface required activation of the complement system. The alternative pathway was shown to be involved in deposition of human C3 on schistosomes of all ages, whereas activation of the classical pathway was demonstrable only with fresh schistosomula. Immunoelectrophoretic studies demonstrated a dose-dependent cleavage of human C3 and conversion of factor B by living adult schistosomes. The results demonstrate that the ability of living schistosomes to activate complement in vitro is dependent not only on their developmental stage but also on the species of the serum.

The fate of irradiated, immunizing cercariae and challenge schistosomula was investigated in mice using a quantitative, histological technique which would appear to be more efficient in estimating parasite numbers in skin and lungs than does the tissue mincing and incubation recovery technique used previously by other workers. There was evidence for slight retardation of irradiated (20 krad.) parasite migration in skin, but death of schistosomula in the skin appeared negligible. It was observed that the majority of irradiated parasites remained in the lungs until at least day 21 after infection, and that most schistosomula observed at this time were dead. In mice immunized with irradiated cercariae there was no evidence of attrition of the challenge infection in the skin. The migration profile of challenge parasites in the lungs of immunized animals was not significantly different from that of normal parasites in the lungs of naive animals. Dead challenge parasites were observed in the lungs but their numbers were not considered great enough to account for the final attrition measured by perfusion. It is suggested that the remainder of the attrition of challenge schistosomula may occur in the systemic and/or hepatic portal circulation.

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.

Snell normal and dwarf mice were infected with Spirometra erinacei plerocercoids collected in Japan, to investigate the relationship between the growth-promoting effects of plerocercoids and the growth hormone releasing factor and the somatostatin – growth hormone – somatomedin axis in the host. Infection with plerocercoids caused increases in body weight and weights of muscle, liver, spleen and heart in the normal male mice, and increases in the head–body length, body weight and weights of muscle, liver, spleen, kidney and heart in the normal female mice, but did not increase the weight of the fat pad. Infection with plerocercoids caused increases in body weights and weights of muscle, liver and spleen in the male dwarf mice, and increases in the head–body length, body weight and weights of muscle, liver, spleen and kidney in the female dwarf mice. These observations suggest that plerocercoids promote the growth of dwarf mice as well as normal mice. As the dwarfism of Snell mice is due to a defective anterior pituitary gland, it seems that plerocercoids do not stimulate secretion of growth hormone from the pituitary. Accordingly, it seems to be more probable that the larvae secrete a growth hormone-like substance.

The guinea-pig has been reassessed as a potential laboratory host for Schistosoma mansoni. Twenty-six per cent of an infective cercarial population survive to maturity in this rodent and there are no gross fluctuations in worm burden subsequent to pairing of male and female parasites. Five day, 4-week and 6-week-old schistosomes grown in guinea-pigs have topographical features that are identical to those exhibited by similarly aged mouse worms, but different from those exhibited by rat worms. Schistosome eggs are never detected in the faeces of infected guinea-pigs, but they can be observed in the pulmonary, hepatic and intestinal tissues. Only 55% of the eggs that can be recovered from the intestinal tissues are viable, and some of these can be hatched to release miracidia that penetrate the intermediate snail host. Cercariae are sometimes liberated from infected snails, but in insufficient numbers to permit infection of naive guinea-pigs. The schistosome cycle cannot, therefore, be completed in this host. Collaterals are sometimes observed in the vasculature serving the rectum and kidneys of infected guinea-pigs and the fact that schistosome eggs are deposited in the lungs of these animals indicates that portal systemic anastomosis is a feature of the model. Pathology associated with cercarial invasion or egg deposition is not dissimilar to that described for other laboratory animals infected with S. mansoni, except that basophils participate in the inflammatory response observed in the skin and intestine.

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.

The anthelmintic effect of an alcoholic extract from a shrub, Diospyros mollis, popularly known as Ma-Klua in Thailand, on the adults and larvae of the dwarf tapeworm, Hymenolepis nana, in mice was studied in comparison with that of flubendazole. The experimentally infected mice were given a single oral dose of 10–1000 mg of Ma-Klua extract or flu-bendazole/kg body wt 1, 2, 3, 4, or 12 days post-infection and autopsied 14 days post-infection. Ma-Klua extract was effective in the elimination of adults (ED50 = 79 mg/kg) but not larvae. Drastic effects of Ma-Klua extract on the motility and structure of adults were observed and the number of the adults in mice decreased with time after administration of the drug 12 days post-infection. The small numbers of adults remaining in the host intestine 2 days after the drug administration showed severe damage in the gravid segments. These facts were thought to be responsible for the significant reduction in egg output observed 1 and 2 days after medication. Fresh eggs exposed to Ma-Klua extract in vitro and in vivo, or in vivo alone showed reduced infectivity. The effect of flubendazole on adults and larvae was minimal.

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.

In vivo and in vitro parameters of immunity have been assessed in guinea-pigs sensitized with 500 normal or 500 radiation-attenuated cercariae of Schistosoma mansoni. High levels of resistance to a challenge infection developed in both the chronic and irradiated vaccine model, but immunity was expressed earlier (week 4) and reached higher levels (90%) in the latter case. Vaccinated guinea-pigs have thus been shown to achieve greater resistance than the more commonly used rodent hosts. In vitro cytotoxicity assays have demonstrated that antibodies capable of participating in complement-dependent (lethal antibody) or eosinophil-mediated schistosomular killing, develop in the serum of guinea-pigs immunized with either normal or irradiated cercariae. The time course of development of the eosinophil adherence promoting antibody approximated in both models, the development of immunity in vivo, but the lethal antibody response paralleled the immune status of the animal only in the irradiated vaccine model

Mice selected as liable (L) and refractory (R) over 10 generations voided significantly more and less Nematospiroides dubius eggs compared with randomly mated (Rd) mice after primary infection with 100 larvae. Strong positive correlation was found between the numbers of N. dubius eggs in mouse faeces and the numbers of adult N. dubius recovered from mice culled from the R, Rd and L colonies. Selection limit based on a faecal e.p.g. was reached in the L mice after 9 generations whereas the faecal N. dubius e.p.g. voided by the R mice continued to decline throughout selection. In contrast, no change in worm numbers was found in L or R mice after 6 generations. The refractory state of the trait, liability to infection with N. dubius, was inherited as a dominant character with a realized heritability value of ~ 0∣2. Differential correlated responses from N. dubius infectivity compared with N. dubius fecundity and growth indicated murine genetic control of this trait by 2 major genetic units. In general, there were negative phenotypic and genetic correlations between the faecal N. dubius e.p.g. of mice and murine morphological conformation, but positive correlations between the faecal N. dubius e.p.g. of selected mice and establishment, growth and fecundity of N. dubius populations in these mice. There was little correlation between the faecal N. dubius e.p.g. after primary infection and anti-N. dubius antibody titres and parasite female/male sex-ratio.

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.

The ability of the cercariae of Schistosoma mansoni to penetrate the tails of mice was shown to remain constant throughout their lives. However, their capacity to establish themselves and then reach maturity decreased as they aged. The abdominal route of penetration produced consistently higher maturation rates than the tail route. Significantly different maturation rates were obtained by modifying the standard tail infection technique. Evidence is presented that age-related mortality of schisto-somula occurs within 24 h of penetration and may be associated with the exhaustion of energy reserves during the penetration of the stratum corneum. The relationship of this age-related mortality to ‘mass mortality’ is discussed.

A procedure for the blunt dissection of the syncytial intestine of Haemonchus contortus to separate the endotube–brush border complex is described. A similar complex can be obtained from the partially cellular intestine of Ancylostoma caninum. The structural features of the complexes from the two sources are compared. The main differences are in the retention of terminal bars by the endotube from A. caninum and in the extent and organization of the microfilaments associated with the basal side of the endotubes.

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.

With the exception of gudgeon (Gobio gobio) infection of cyprinid fish with the plerocercoid of Ligula intestinalis is associated with a host-tissue response. The nature and specificity of this response has been investigated using transplantation techniques. In roach there is an intense cellular response to implanted Sepharose, Spurr's resin and L. intestinalis, irrespective of donor host species. However, tegument damage only occurs in gudgeon-Ligula and cultured ro&ch-Ligula which has been exposed to gudgeon-plasma. L1 and L2 cell types predominate within the cellular response. Once the host leucocytes have breached the tegument, they migrate over the basal lamina and penetrate into the sub-tegumental region. In gudgeon an intense cellular attack occurs against Sepharose, Spurr's resin, ro&ch-Ligula and cultured gudgeon-Ligula which had been implanted directly or exposed to roach plasma. Tegument damage only occurs in the latter. In contrast, neither direct implantation of gudgeon-Ligula nor cultured roach-Ligula which has been exposed to gudgeon plasma evokes a cellular response. It is suggested that in these two instances, as in natural infections of gudgeon, protective host proteins may be absorbed onto the surface of the parasite.

The larvae of Brugia pahangi recovered from the jird have been shown to grow continuously between moults, their length increasing at least 5-fold during the 4th instar. This intermoult growth is achieved without an increase in the surface area of larvae. The cuticle of very early 4th and 5th-stage worms is highly folded and intermoult growth is accommodated by an expansion of surface annular folds. The major increases in the surface area of larvae occur only through ecdysis, with an 8-fold increase in the surface area being achieved at the 3rd moult. The growth curve of these worms is therefore sigmoidal but the surface area curve is stepped. The relationship between the cuticles of nematodes and insects is discussed

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.