A comparison was made between the early events (a sexual stages) in the life-cycle of Eimeria tenella in specifically immunized and control chickens. Particular attention was paid to the quantitative aspects and to the transport of sporozoites within intra-epithelial lymphocytes (IEL) from the enterocytes of the surface epithelium to the enterocytes of the crypts. There was a moderate decrease in the number of parasites initially seen in the mucosa of the immune birds, suggesting that some of the effects of immunity are exerted before penetration of the surface enterocytes, but the reduction in the numbers of developing parasites was more marked. This latter effect was due, at least partly, to failure of transfer of sporozoites from IELs to crypt enterocytes. These findings are discussed in relation to the efficacy of the immunity induced.

A 230000 molecular weight Plasmodium yoelii protective antigen was characterized. Two monoclonal antibodies against P. yoelii immunoprecipitated the 230000 mol. wt protein and a number of lower molecular weight polypeptides. These polypeptides were shown by peptide mapping and specific antibody binding to be fragments of the large protein. Iodination experiments suggested that the lower molecular weight species may be present on the surface of the merozoite. The protein was found not to be glycosylated. By serology, related antigens were shown to be associated with blood-stage schizonts of P. vinckei subspp., P. chabaudi subspp. and P. falciparum.

Mature asexual stages of the malaria parasite Plasmodium knowlesi synthesize proteins of Mr 180 000–225 000 that are expressed on the outer membrane of infected erythrocytes and which vary antigenically such that different parasite clones are specifically agglutinated with homologous antibody. Other non-agglutinable clones have been prepared which fail to express variant antigen on infected cells. Two agglutinable clones of different variant antigen phenotypes and a non-agglutinable clone were examined to determine the proportion of total malarial proteins represented by variant antigens. Malarial proteins were labelled with various radioactive amino acids and the sodium dodecyl sulphate—polyacrylamide gel patterns for the three clones compared by fluorography. The patterns were indistinguishable, the variant antigens being undetectable in analyses of total malarial proteins. Furthermore, these antigens were not detected by Coomassie Blue-staining of total cellular proteins after electrophoresis. Sodium dodecyl sulphate and Triton X-100 extracts of labelled cells were immunoprecipitated using a panel of sera of defined agglutination specificity. The variant antigens could not be detected in the fluorographic patterns of total malarial antigens immuno-precipitated by these sera. In contrast, after lactoperoxidase catalysed radio-iodination of intact schizont-infected cells, the 125 I-variant antigens on the cell surface were identified by demonstrating their accessibility both to antibody and to trypsin with intact cells. Thus, the variant antigens are quantitatively very minor malarial proteins that can only be detected by methods which selectively analyse the subset of proteins on the erythrocyte surface.

A technique is described for the growth of pure gametocyte cultures of Plasmodium falciparum. Using the classification of Hawking, Wilson & Gammage (1971) these cultures contain gametocytes of stages III, IV and V alone. Routine sexual cultures, varying from 0·35 ml static cultures to 500 ml shaking cultures, are exposed to an inhibitor of DNA synthesis (mitomycin C at 10 μg/ml) on the 11th day of culture, and the culture is harvested on the 14th day when capacitated stage V gametocytes are present. All other stages are killed by the drug and are morphologically degenerate within 2 days of the addition of the inhibitor.

The migration in mice of 20, 50 and 90 krad. 60Co-irradiated Schistosoma mansoni larvae, biosynthetically radio-isotope labelled with [75Se]-selenomethionine, was evaluated by autoradiography of compressed tissues and compared to the migration of non-irradiated 75Se-labelled larvae. The migration of 20 krad. -irradiated schistosomula between skin and lungs was slightly delayed but otherwise paralleled the migration of normal, non-irradiated schistosomula during the first 8 days following exposure. By day 8 over 90% of both non-irradiated and 20 krad. -irradiated organises were located in the lungs. In contrast to non-irradiated organisms, however, only a small proportion of 20 krad. organisms migrated to the liver. The delay in migration between skin and lungs was more pronounced with 50 krad. -irradiated schistosomula. Nevertheless, 45–93% of 50 krad. -irradiated organisms migrated to the lungs by 8 days post-exposure. Over 90% of the 50 krad. larvae detected in the mouse on day 21 were in the lungs; no more than an occasional 50 krad.-irradiated organism was ever detected in the liver. In three experiments, over 85% of the 90 krad. -irradiated organisms were retained in the skin; in a fourth experiment about half of the 90 krad. -irradiated organisms migrated as far as the lungs. As with 50 krad. organisms, only an occasional 90 krad. organism was ever detected in the liver. Removal of the skin exposure site within the first 4 days of immunization with either 50 or 90 krad. -irradiated cercariae completely blocked the induction of resistance. Removal between the 4th and 6th days gave variable results. Mice had to be in contact with the irradiated larvae for a minimum of 8–11 days to stimulate a level of resistance comparable to that of mice whose immunization site was not removed.

The parasitic protozoan Trypanosoma diemyctyli has a life-cycle that involves a vertebrate host, the red-spotted newt Notophthalmus viridescens, and an invertebrate host, the amphibian leech Batrachobdella picta. A study of the distribution and dynamics of this parasite in newts of known adult age and history of breeding in montane ponds in Virginia revealed a pattern of: (1) moderate prevalences of infection in post-metamorphic juvenile and adult stages, (2) rapid increases in numbers of trypanosomes in newts during their first year of maturity, (3) significant differences in the numbers of trypanosomes in male and female newts in mid-summer, (4) sustained high levels of infection in the first two years of newt adulthood, (5) significantly lower levels of infection in newts by the fourth and subsequent years of adulthood and (6) annual oscillations in the intensity of infection in older adult newts from spring and autumn lows to mid-summer peak levels. Newts with a history of skipping breeding seasons had higher levels of infection than those newts which returned to the pond for every breeding season. Newts brought to the laboratory and maintained under leech-free conditions failed to develop infection levels comparable to those in the field. The dynamics of infrapopulation sizes of trypanosomes in newts depend on multi plication rates of the trypanosomes, variable transmission rates from the invertebrate host and the development of resistance in older adult newts.

Y strain parasites (Wellcome stock) were cloned as epimastigotes by limiting dilution and one clone, Wel Tryp A2 was used to infect cell cultures and irradiated mice. The fibrosarcoma line, M4, was susceptible to infection with Wel Tryp A2 trypomastigotes but, after the first round of intracellular infection, proliferation and differentiation, failed to support parasite growth in long-term continuous culture. In contrast, a muscle-derived cell line, S2, produced regular waves of extracellular trypomastigotes and amastigotes during 80 days of continuous culture reported here. These infected S2 cultures have remained in continuous culture for up to 18 months over a 5-year period and have yielded in excess of 108 parasites/20 ml culture at 4–6 day intervals. Extracellular amastigotes produced in these cultures have a close morphological, immunological and biochemical analogy to intracellular parasites derived from rodents, and have maintained an absolute dependence on host cells for their growth and proliferation. These amastigotes produced low-grade chronic infections in normal CBA/T6 mice but produced acute, fatal infections with high parasitaemia in mice of the same inbred strain given 900 rad. whole-body irradiation prior to infection. Although present findings relate to a single parasite clone, the parent stock from which the clone was derived showed similar growth characteristics when co-cultured with S2 cells.

When jirds were infected with a single inoculum of 25–50 infective larvae of Brugia pahangi an overall mean recovery of adult worms of 44·5% (n = 41) was obtained. There was no difference in recoveries between male and female jirds. If jirds were repeatedly inoculated with larvae into the peritoneal cavity yields were only slightly reduced. Yields were 30·5% for 5 infections (n = 10), 26·7% for 10 infections (n = 8), 34·4% for 15 infections (n = 10) and 28·5% for 20 infections (n = 7). Twice as many worms were recovered from intraperitoneally inoculated jirds than from subcutaneously inoculated jirds.

Rats harbouring a 35-day-old primary infection of Moniliformis dubius were inoculated with constant doses of Nippostrongylus brasiliensis and 10 days later, after post mortem examination, rats with concurrent infections harboured significantly fewer Nippostrongylus than rats with single infections. Similar infections of Moniliformis were carried out, but with post mortem taking place on days 8,9, 12 and 14 of the Nippostrongylus infections. On days 8 and 9 of infection, rats with concurrent infections did not harbour significantly fewer Nippostrongylus compared with single infections. Both single and concurrent infections of 12-and 14-day-old Nippostrongylus were found to harbour lower numbers of worms. In the single infection this corresponds to the timing of the typical immune expulsion of a primary single infection which takes place on approximately day 12 of infection. The Moniliformis population was not significantly affected, in terms of numbers, dry weight and length, although each parasite population did show a slight shift in site in the presence of the other. A significant reduction in egg production by Nippostrongylus was detected throughout concurrent infection. The possible role of non-reciprocal cross-immunity is discussed as an explanation for the apparent early expulsion of the Nippostrongylus population in the presence of Moniliformis.

An analysis of the frequency distribution of numbers of Moniliformis dubius in rats of an outbred strain of Wistar origin (CFHB) and feeding ad libitum on Oxoid 41B diet, showed that over-dispersion occurred regardless of the age and sex of the rats and the infective dose given (12, 20 or 40 cystacanths/rat). Over-dispersion was also shown to be independent of variability in the age and sex of the cystacanths given. The analysis demonstrated that the over-dispersion declined as the course of the infection proceeded. As expected, parasite survival was found to be age-dependent with female worms living longer, on average, than males, and both male and female worms living longer in rats given 12 as opposed to 20 cystacanths. Possible mechanisms for generating the over-dispersion observed during this work are discussed and a tentative hypothesis, invoking host heterogeneity with regard to carbohydrate availability in the small intestine, is proposed for further experimental investigation.

The morphology of the mucosal surface of samples from the small intestine of young protein-deficient pigs was examined by scanning electron microscopy. Three pigs had been infected with Ascaris suum for at least 58 days while 1 had remained uninfected; all pigs were housed and maintained under the same conditions, at the same time. The tissue samples collected at post mortem examination from pigs which contained A. suum showed varying degrees of villous atrophy and fusion. In addition, unusual small craters and as yet unidentified objects were observed at the surfaces of the enterocytes of Ascaris-infected pigs. These changes in mucosal morphology were not seen in the tissue taken from the uninfected pig. The possible association between the mucosal lesions and lactose maldigestion in young, protein-deficient pigs infeceted with A. suum is discussed.

The entire surface of the early developmental stages of the cysticercoid of Hymenolepis diminuta bears microvilli. Posteriad differentiation produces a microthrix-bearing surface on the presumptive scolex region, commencing before scolex retraction in cysticercoids in Tenebrio molitor kept at 26°C. During sucker development, the scolex syncytial cytoplasm possesses electron-dense discoidal bodies, aligned parallel to the surface. They become associated with the apical membrane, domes are formed and electron-dense spine-like profiles become apparent. Elevation on short shafts follows, and multilaminate baseplates are then discernible. Fewer microvilli are now present and vesicles with asymmetric membranes (denser inner leaflet) occur within the syncytial cytoplasm. Before scolex retraction, this differentiation extends to the level of the suckers; thus the neck, which becomes reflected on retraction, still possesses only microvilli. After retraction, differentiation proceeds rapidly with increased growth of existing microtriches, discoidal bodies possibly contributing to the shaft support material; the reflected neck develops microtriches and the microvilli are shed into the scolex retraction cavity. The ‘asymmetric’ vesicles increase numerically, some fusing with the apical membrane and releasing their contents. Concurrently, apical membrane asymmetry (denser outer leaflet) becomes apparent. The adult-type surface is formed by 3 days post-scolex retraction, coinciding with the earliest time that the metacestode is infective to the final host.

Incorporation of four amino acids into protein by stage V cysticercoids of Hymenolepis diminuta occurred in the order leucine > phenylalanine > alanine > proline. Leucine incorporation was apparently linear over a 5 h period in contrast to uptake which was non-linear over the same time. Pre-incubation in sugars did not affect protein synthesis but incorporation was inhibited by cycloheximide. Uptake and incorporation of leucine by stage III cysticercoids exceeded that of stage V metacestodes and the 10-day-old adult worm.

Mice were infected per os with Trichinella spiralis and their lymphocytes were removed and fused with mouse myeloma cell line P3 × 63Ag8653P3 for the selection of monoclonal antibodies to biochemically defined, stage-specific surface antigens of 3 parasite developmental stages: muscle larvae, adults and newborn larvae. Two separate antibodies against a defined single surface antigen of each stage were isolated. In each separate case the pair of monoclonal antibodies precipitated the same component from detergent-solubilized surface antigen preparations, but only one was able to bind to the surface of the living worm. The other must therefore be directed against an antigenic epitope which is obscured in the intact worm surface. The latter type of antibody is unlikely to be involved in the initial phase of parasite rejection and hence is another example of a non-protective host antibody response. The stimulus for its synthesis may be release of surface antigen, which does occur in vitro. One surface antigen of the newborn larvae is only detected by antibody in the first 6 h after birth; thereafter its presence is obscured as other antigens appear. The major surface antigen of the infective larvae contains carbohydrate determinants which are not available at the parasite surface. In addition, it displays great molecular heterogeneity but all variants appear to be derived from a common polypeptide structure.

Trichinella spiralis infections may lead to the loss of behavioural dominance among male mice. Reversals of dominance order first appear at the time when newborn larvae are released into the circulation of the host. The duration of dominance reversals bears no relationship to the number of muscle larvae harboured.

The response of the plant parasitic nematode, Meloidogyne incognita (J2 stage) to avermectin B2a-23-one is triphasic, comprising an initial loss of locomotor activity where the juveniles remain sensitive to touch, a recovery phase and a final loss of activity where the juveniles are relatively insensitive to touch. In contrast, the acetylcholinesterase inhibitor, oxamyl, causes initial hyperactivity of juveniles followed by a progressive decline in movement. The addition of bicuculline and to a lesser extent picrotoxin, both antagonists of γ-aminobutyric acid (GABA), blocks the action of avermectin on M. incognita.