As mice recover from infection with Babesia microti, abnormal forms of the parasite are present in some red cells. These forms are non-infective, indistinguishable by light microscopy from those present after treatment with amicarbalide, a babesicidal drug, and persist in splenectomized mice.

Electron microscopy confirmed that these abnormal forms are degenerating intra-erythrocytic parasites. In the absence of evidence for death of B. microti elsewhere in the body, it appears that infections of mice with this parasite are normally terminated by their death within circulating red cells. This has important implications for the mechanism of immunity to both this parasite and those Plasmodium spp. with which it cross-protects in this host.

A dark-ground photographic technique was used to analyse the reactions of Schistosoma mansoni miracidia to homogeneous solutions of snail–conditioned water (SCW). The most significant effect of this water was to increase miracidial turning. This effect was maintained under both acid and alkaline conditions, after passage of the SCW through a mixed bed resin and after chelation of either calcium or both calcium and magnesium ions. The stimulant in the water was unaffected by trypsin but was protease–sensitive, suggesting its possible identity as a peptide. The importance of ‘active spaces’ rather than concentration gradients in miracidial host–location was emphasized.

Infection with the avirulent piroplasm Babesia microti in mice is accompanied by a marked depression in the ability of the mice to mount an immune response to sheep red blood cells. The period of immunodepression begins 3 days after peak parasitaemia and is maximal 4 days later. There-after, there is a slow return to normal immune responsiveness, correlated with the gradual disappearance of the parasites from the blood. Both IgM and IgG responses are depressed. Cell-mediated responses as determined by contact sensitivity to oxazolone and allograft survival are apparently unaffected. Phagocytic activity as measured by carbon clearance tests is increased, and is correlated with the parasitaemia.

A simple technique for the maintenance in vitro of mature Schistosoma mansoni is described and critically assessed at the ultrastructural level. Females were cultured for 4–6 days with no apparent ultrastructural change, but after this period changes appeared in the cells of the ovary and vitelline gland. At a later stage (10–12 days) lipid bodies appeared in the parenchyma cells. These changes occurred in worms which were active, paired with males and were egg–laying. Thus the activity, pairing behaviour and egg–laying characteristics are not adequate to reveal the true morphological condition and presumably the physiological and biochemical status of cultured worms.

This technique was used to study the effect of Astiban on females and the results were compared with worms treated in vivo. Astiban concentrations greater than 30 µg/ml killed worms within 7–20 h and acted non–selectively. Astiban at low concentrations (10µg/ml) during short–term culture (1–3 h) resulted in a selective action of the drug on maturing vitelline cells. Thus, although the degree of cell damage caused by drug treatment was more severe and occurred earlier than the effects observed in worms cultured in vitro without drugs, both treatments resulted in differential cell death.

Metacercarial cysts of Bucephalus haimeanus occur throughout the liver of Pomatoschistus microps, greater concentrations being found around the gall bladder, blood vessels and periphery of the liver. The cyst wall is composed of three layers, an inner granular, middle vacuolated and outer nucleated layer. The inner layer consists of three zones, an inner zone of irregularly compacted, granular material; a middle densely compacted zone and an outer moderately compacted zone. Vacuoles of the middle layer vary in appearance and appear to be discharging their contents into the cyst cavity. The cells of the outer layer are flattened and elongated with elongate nuclei but no other distinct organelles. Occasionally at the outer edge of the cyst are electron-dense cells which are in the process of degeneration. Only small amounts of collagen and very few leucocytes are associated with the cysts.

The cyst wall is carbohydrate in nature containing some free aldehyde groups, galactogen and neutral mucosubstances. The inner layer appears to consist of mainly acidic mucopolysubstances and weakly acidic sulphomucins. Large amounts of protein, carbohydrate-protein complexes and DNA are also present within the cyst wall. Alkaline and acid phosphatases, ATPase, β-glucuronidase and N-acetyl-β-glucosaminidase were detected. The origin and function of the cyst wall is discussed.

The protein composition of Schistosoma mansoni was analysed by electrophoresis in polyacrylamide slab gels in the presence of sodium dodecyl sulphate. A high degree of identity existed between protein patterns obtained from immature and adult parasites of the two sexes. Some stage-and sex-specific components were identified and their possible origin discussed.

The uptake and retention of drug-related material by Schistosoma mansoni was studied in the mouse host following a single oral or intramuscular does (50 mg/kg) of [14C]oxamniquine. Male worms took up more labelled material than did female worms but the amount in each particular sex of worm was found to be similar after both routes of administration. Exposure of worms was therefore independent of the route of administration. Six days after drug administration, at the time of an hepatic shift, significantly more drug-related material* was present in male worms than in female worms. Examination of worms recovered from mice 4 h after treatment showed that metabolites of oxamniquine constituted 70–90% of the drug-related material present in the worms. Both sexes of worms were able to take up matebolites of oxamniquine win vitro.

The desiccation survival of 4th-stage larvae of Ditylenchus dipsaci revived from dry worm aggregations (‘wool’ larvae) was compared with that of larvae extracted from narcissus bulbs (‘bulb’ larvae). Both sorts survived desiccation well, but ‘wool’ larvae survived desiccation at various humidities somewhat better than ‘bulb’ larvae. The rate of drying of the former was more rapid than that of the latter; the ability to control water loss, therefore, does not of itself ensure survival. The number of larvae reviving decreased with repeated cycles of desiccation and hydration, and also with the increase in the period during which the nematodes were kept dry. However, this was not associated with any loss of ability to control drying. The rate of drying of ‘wool’ larvae remained unaltered irrespective of previous desiccation treatment. In contrast, the rate of drying of ‘bulb’ larvae was more rapid after an initial desiccation with the result that ‘bulb’ larvae dried at the same rate as ‘wool’ larvae. While ‘wool’ and ‘bull’ larvae differed initially in both the rate of water loss and survival, a period of desiccation eliminated only the difference in water loss.

The results suggest that the rate of drying is dependent largely on physical factors. It was shown, however, that the cuticle of dead larvae was completely permeable to water in both directions. Therefore the ability to control water loss must, in some as yet unknown way, be connected with the nematode as a living system.

Hepatic granulomas from mice infected with Schistosoma mansoni for periods of 8 weeks to 1 year were studied by electron microscopy. The different cell types present in the granulomas suggested that whilst a delayed hypersensitivity response predominated during early stages of infection an Arthus-type reaction associated with delayed hypersensi-tivity occurred at later stages of infection.

The number of adult Strongyloides ratti which developed in the guts of lactating rats after subcutaneous injection of 4000 L3 on day 18–20 post partum was taken to be a measure of the relative importance of alternative larval routes. When injection was carried out at different times before and after weaning, larvae were diverted from a route bypassing the gut in nursing mothers to one leading to the gut (‘migration reversal’) in mothers without young in a period of less than 10 h. Migration reversal was mostly completed in lactating females injected at the time of weaning when compared with nulliparous controls. A stimulus-sensitive period shortly after injection, predicted from these dynamics, was demonstrated. Worms injected into lactating females 10 h after removal from their pups showed complete migration reversal. In similarly treated rats, given 1 h suckling 3 h after injection, migration reversal was practically abolished. These inter-relationships, in conjunction with earlier findings, are used to deduce the possible humoral mechanisms involved and to develop a working hypothesis to account for larval orientation based on features of the mammalian pulmonary microvasculature.

The ultrastructure of penetrating stages of Babesia major merozoites responsible for causing trans–ovarian infection of the tick Haemaphysalis punctala was studied. These merozoites were different from forms of other Babesia species previously described in the tick in that they were highly pleomorphic. Most of the organelles found in these forms were similar to those found in other stages: however, the apical complex was found to be very active. Micronemes were found to the apical complex was found to be very active. Micronemes were found to be predominant in the cytoplasm of these merozoites and a cytoplasmic projection anterior to the polar ring and bounded by concentric rings was visible. A polar ring with radiating ribs, and microtubules was present. It is thought that the apical complex of these merozoites plays an important role in assisting the parasite to infect the ovary of the tick.

Hymenolepis microstoma from secondary infections in mice were found to grow initially more slowly than H. microstoma from primary infections. Eventually a similar rate of growth was attained by both kinds of worm. After transplantation, young worms (≤4 days old) grew more slowly in previously infected than in naive mice. In contrast, 10-day-old worms grew equally well in naive or resistant mice. The administration of cortisone to mice during a secondary infection of H. microstoma inhibited the stunting of growth in young worms which were able to grow as well as those in a primary infection. The effects of the cortisone persisted for less than 4 days. Worms in a secondary infection given 4days after cortisone treatment were stunted in growth. These experiments suggest that the susceptibility of the worms to the resistance of the mouse applies to the first 4 days within the host. The loss or reduction of this susceptibility might be associated with the worms' entry into the bile duct which occurs 3–4 days after infection.

Filaroides hirthi lungworm infection was diagnosed by the recovery of 1st-stage larvae from the faeces of dogs with heavy, artificially induced infections using zinc sulphate flotation. Diagnosis of low-grade natural infections was infrequently achieved. Zinc sulphate flotation was demonstrated to be about 100 times as efficient as the Baermann technique in concentrating F. hirthi larvae from dog faeces. Larvae recovered from faeces proved to be infective when fed to a pup and it was concluded that F. hirthi infection can be transmitted directly and immediately by fresh faecal contamination. Mongrel dogs of diverse ancestry were readily infected by feeding 1st-stage larvae from lung tissue. This, F. hirthi infection was shown not to be limited to the Beagle breed by biological restrictions. The observations that 1st-stage larvae pass through the alimentary tract on their way out of the body and that larvae are found in the mesenteric lymph modes long after a single exposure to infection support the hypothesis that there is an autogenous re-infection of the host by a proportion of these larvae.