Macrogametogony and the formation of the oocyst wall has been examined in Eimeria acervulina. Macrogametes develop within a parasitophorous vacuole. Within the cytoplasm can be observed wall-forming bodies of Type I (WFBI). and Type II (WFBII), a nucleus, mitochondria, canaliculi and polysaccharide granules. WFBII are unusual in possessing a membrane internal to the granular endoplasmic reticulum. Formation of the outer layer of the oocyst wall is preceded by the separation of a veil membrane, and accompanied by morphological changes in the WFBI. WFBI material is deposited between the veil-forming membrane and the two cytoplasmic membranes. A newly formed membrane divides this outer layer during its early development. The inner layer of the oocyst wall is formed from WFBII material which is deposited between the cytoplasmic limiting membranes. The outer layer of the oocyst wall consists of granular and osmiophilic parts, but the inner layer of the wall is homogenous.

The development of resistance by the Houghton strain of Eimeria tenella (H) to monensin has been studied by serially passaging the strain in groups of 30 birds, each inoculated with 106 oocysts and given 100 p.p.m. of drug in the food. After 16 passages a line partially resistant to this concentration of monensin was produced. Passage of the line in birds medicated with 200 or 300 p.p.m. of monensin did not result in the acquisition of a greater degree of resistance. A further reduction in sensitivity to 100 p.p.m. monensin was obtained, however, when the line was serially passaged in 15 groups of 6 birds each given 3 × 106 oocysts. Five passages in the absence of monensin resulted in restoration of sensitivity, suggesting that the resistance developed was not stable. The pathogenic effects of the line that had been passaged in chickens given 300 p.p.m. of monensin were less than those of the parent line.

Antigens of three lines of the rodent malaria parasite Plasmodium yoelii have been studied using crossed immunoelectrophoresis. P. y. yoelii line A1 is a mild line which is restricted to reticulocytes. P. y. yoelii line YM and P. y. nigeriensis line D1 are virulent infections which multiply in both immature and mature erythrocytes. One antigen, designated Py-1, was found to differ in its electrophoretic mobility between the lines, being fast (F) in lines A1 and YM and slow (S) in line D1. Antigen Py-1 also varied in quantity among the three lines; greater amounts were detected in parasites inhabiting mature erythrocytes than in those in reticulocytes. These characters were stable during blood and mosquito passage.

The inheritance of an antigen designated Py-1 in the rodent malaria parasite Plasmodium yoelii has been investigated. A cross was made between 2 lines differing in the electrophoretic mobility and quantity of Py-1 detected by crossed immunoelectrophoresis. In 10 clones isolated from the progeny of the cross the level of Py-1 always correlated with the virulence of the infection and it was concluded that these characters were different phenotypic effects of the same gene mutation. The electrophoretic mobility of Py-1 segregated independently of the virulence character and was therefore controlled by a different gene. These two antigenic markers also recombined with isoenzyme and drug-sensitivity characters distinguishing the parent lines.

The germinal layer of sterile 9-month-old murine peritoneal cysts of Echinococcus granulosus equinus shows interrelated variation in depth, tissue integrity, metabolic reserves and the number of autophagic lamellar bodies present. These features are similar in large and medium-sized cysts from the same host, whether occurring singly or within cyst masses. Deep germinal layers (> 16 μm) are lipid- and glycogen-rich and possess numerous autophagic vacuoles with 6 nm period lamellar stacks asymmetrically disposed peripherally; shallow layers (< 12 μm), with indications of degeneration, have depleted metabolic reserves and fewer lamellar bodies. These bodies are formed by smooth endoplasmic reticulum encirclement of small glycogen masses followed by further sequestration, and eventually definition of glycogen particles may be lost. Autophagy of mitochondria and cytoplasmic vesicles also occurs. The presence of lysosomal enzymes within the layer suggests autolysosomal compartmentalization of excess substrate and effete material. Mucopolysaccharide bodies, containing material similar to that exocytosed to form the laminated layer matrix, occur and are formed from fusion and autophagy of Golgi-derived vesicles. These bodies may also develop peripheral 6 nm period lamellar stacks, but of limited depth. Mucopolysaccharide bodies are the dominant feature of the germinal layer of very small cyst-mass cysts in which laminated layer production is considered to be arrested. They thus represent a repository for the unreleased mucopolysaccharide material.

Studies of antigenic variation in Trypanosoma vivax have been hindered by its low infectivity to laboratory hosts and difficulties in obtaining defined cloned populations. The recent isolation of mouse-infective T. vivax has partially overcome the first problem. We have developed a highly efficient cloning technique which has been applied to the isolation of a collection of 71 clones, representing 31 distinct variable antigen types, of mouse-infective T. vivax from Nigeria. This serodeme showed no cross-reaction with several T. brucei-group serodemes, but some cross-reaction with naturally occurring Kenyan T. vivax.

The cellular reactions to the migration of challenge schistosomula of Schistosoma mansoni through the cheek pouch skin in Chinese hamsters immunized 20 weeks previously via the abdomen has been investigated at the ultrastructural level. The composition of the leucocytic infiltrate into the dermis and epidermis changed with time after infection. At 24 and 48 h the infiltrate was composed mainly of neutrophils and mononuclear cells. At 72 h fewer neutrophils but more eosinophils were present. The interaction of the leucocytes with the challenge schistosomula is described. Degranulation of eosinophils at the cell-parasite interface has been observed. Despite the fact that approximately 30% of 48 h schistosomula and 50% of 72 h schistosomula examined had adherent leucocytes only a few of the parasites exhibited signs of damage, consisting of tegumental vacuolation and changes in the electron opacity of the tegumental cytoplasm. There was no strong evidence of increased attrition of challenge schistosomula in the cheek pouch skin relative to the primary infection, although some dead challenge parasites were observed. It is concluded that a substantial proportion of the attrition of challenge infections in the Chinese hamster occurs at a post-dermal location.

The ultrastructure of the tegument of Schistosoma haematobium was examined using scanning and transmission electron microscopy. The surface of the male worm is characterized by numerous raised tubercles bearing apically directed spines. The female in contrast to the male is cylindrical and relatively smooth. Details of oral and ventral suckers are given. The use of uranyl acetate as a tertiary fixative and en bloc stain has revealed the heptalaminate nature of the outer membrane. Tegumental mitochondria are shown to be morphologically more complex than those of S. mansoni. Spherical and elliptical inclusion bodies are also described. The ultrastructure of the oesophageal tegument of S. haematobium is described for the first time and corresponds with earlier observations of S. mansoni.

We report the results of experimental studies of the generation of age-prevalence curves for Schistosoma mansoni infections in laboratory populations of Biomphalaria glabrata. Within snail populations of varying sizes and age structures, the net force of infection is shown to be linearly dependent on the rate at which miracidia are introduced into the aquatic habitat of the host. For individual snails, the per capita force of infection is shown to be related to snail age and size, and the death rate of shedding snails is demonstrated to be dependent on the period of time during which a snail has been releasing cercariae. Both factors are important determinants of the proportion of infected snails within populations of hosts and may generate convex age-prevalence curves. Comparisons of snail abundance in populations either exposed, or not exposed, to infection suggest that S. mansoni can act to significantly depress the population growth of its intermediate host. Mathematical models are developed, encorporating the age structure of snail populations, to aid in the interpretation of experimental results.

The morphology of the post-hatch moulting and developmental sequence of an amphimictic population of Rotylenchulus reniformis has been examined in living and fixed material. Under suitable conditions of temperature and in a moist environment the 2nd-stage larva (L2) undergoes a series of 3 moults and developmental changes which result in the formation of males and immature females. After hatching and prior to the start of the first of these moults (the second moult), there is a pre-moult period, usually of 3–5 days duration. The morphology of the entire moulting and developmental sequences, from L2 to just after the final moult, has been followed in single living specimens of a parasitic nematode using differential interference contrast optics, and sections cut through different stages have been observed under the transmission electron microscope. These moulting sequences (at 24 °C) take place at similar times in developing males and females. The second moult takes place on the second day after commencement of moulting, the third on the third or fourth days and the fourth and final moult on the sixth or seventh days, followed by further development over several days to give rise to the adult male and the immature female. The ultrastructure associated with some of the more obvious of these developmental changes is described and includes the morphology of the head region and cuticles of L2, L4, adult males and immature females, the oesophageal glands of the immature female and the copulatory spicules and spermatozoa of the male.

Circulating antigen has been detected in the serum of rabbits experimentally infected with Taenia pisiformis. A rabbit antiserum against an antigen preparation derived from the in vitro maintenance of living metacestodes of T. pisiformis was used in a double-antibody enzyme-linked immunosorbent assay (ELISA). Antigen was detected in infected rabbit serum 48 h after infection and peak levels were recorded at 2 weeks post-infection or post-challenge. The pattern of circulating immune complex formation followed closely that of circulating antigen, and infected rabbit serum contained both anti-metacestode and anti-oncospheral antibodies. Serum antigen levels were just detectable (0·4–0·8 μg protein/ml) over the period (> 2 weeks post-infection) of peritoneal cyst development. The circulating antigen probably has antigenic determinants in common with the oncosphere, juvenile and mature metacestode stages. Possible reasons for the temporal variation in serum antigen levels are discussed.

In a series of in vitro experiments, adult male and female Moniliformis dubius were incubated at pH 6·88 and 37 °C for 3 h in a 2·5 mM solution of 18 amino acids. Fifteen of these were absorbed slightly from the medium, but L-serine was almost completely absorbed while the concentrations of glycine and alanine in the medium increased during the course of the incubation. By using L-[U-14C]serine, it was found that labelled ethanol and CO2 were the main end-products of metabolism excreted into the medium, with smaller amounts of labelled alanine, lactate and acetate. Small amounts of cystathionine with high specific radioactivity were found in extracts of the worms at the end of incubation, together with other radioactive metabolites including glucose, ethanol, lactate, succinate, malate, serine, glycine and alanine. Ammonia was found to be an excretory product of the amino acid metabolism of M. dubius. Possible metabolic pathways and suggestions for the significance of serine metabolism in this parasite are discussed.

Intestinal and faecal IgA responses against different developmental stages of Nippostrongylus brasiliensis were studied in Hooded Lister rats vaccinated subcutaneously with infective larvae or intragastrically with 4th-stage larvae, adult nematodes, adult worm somatic and metabolic antigens. It was found that intragastric administration of L4 or adult worms produced as high resistance to challenge as normal infection. Oral vaccination with adult nematode excretory–secretory (ES) and somatic antigens produced 69 and 17% protection respectively. All vaccination regimes induced a considerable IgA response against somatic and metabolic antigens of the intestinal stages. However, no correlation could be seen between the IgA levels and degree of protection. Analysis of intestinal mucosal, intestinal contents and faecal IgA specific to larval or adult antigens suggests that the IgA is probably induced by antigen(s) common to all intestinal stages. Also secretory IgA responses against surface antigens of intestinal L4 did not show stage specificity, although this was detected in sera.

Experiments were undertaken to investigate the factors which influence the transmission dynamics of Gyrodactylus bullatarudis within populations of laboratory guppies. The parasites possess a number of biological attributes which are almost unique amongst helminth parasites of vertebrates. These include the ability to reproduce viviparously and directly on the surface of the host, the ability to survive death of the host (for a short period of time) and the ability to transfer between hosts (despite the absence of a specialized transmission stage in the parasite's life-cycle). Long-term laboratory experiments demonstrated the inability of the parasite to persist within populations of the host in the absence of the continual introduction of naive susceptible fish. With regular addition of susceptible fish, the parasite population exhibited recurrent epidemic behaviour. The magnitudes of the epidemics and the time interval between them, were dependent on the rate at which fish were added to the populations. The parasite was over-dispersed in its distribution within the experimental fish populations and was a significant cause of host mortality (in a manner related to parasite burden). The experimental results suggest that acquired resistance to infection is an important factor determining epidemic behaviour.

Simple mathematical models are developed to examine the influence of variability in host susceptibility to infection, on the dynamics of host–parasite population interactions. When hosts differ in their innate susceptibility (at birth), to infection by a specific parasite, the average susceptibility of the host population as a whole may show systematic changes through time. Such patterns may arise as a result of demographic factors associated with the interaction between host and parasite populations, in the absence of inheritance mechanisms (a genetic component) or acquired resistance (an immunological component). The general significance of this observation is discussed in terms of the coevolution of host–parasite associations.