The frequency distribution of an ectoparasitic mite, Gammaridacarus orchestoideae, on its amphipod host, Orchestoidea corniculata, was found to differ significantly from random for all monthly samples taken between October 1977 and October 1978. The negative binomial distribution provided a good fit to these aggregated distributions. The degree of aggregation was negatively correlated with the prevalence of infestation. Prevalence and intensity were highest in the winter, when the degree of aggregation was lowest, and vice-versa in the late summer. This seasonal pattern can be explained through changes in size and density of the host population, which are associated with changes in the size of the habitat of the hosts. Within each sample the host population was highly heterogeneous with regard to infestation by mites. Females carried heavier loads of mites than did males. Both prevalence and intensity were low in the post-moult stages of the moult cycle. Reproductive females showed lower prevalence and intensity of infestation than did either non-reproductive females or males. Analysis of the regression analysis of ‘mean crowding’ on mean density also indicated that aggregation stemmed from a non-random distribution of individual parasites, rather than from clumping of the infective stages of the parasite. Heterogeneity of the host population is suggested as an important cause of the aggregated distribution of the parasite population.

Infection of intact (nu/+) or hypothymic (nu/nu) BALB/c mice with the lethal intra-erythrocytic parasite, Babesia rodhaini, induced several changes in the surface proteins of red cells from infected blood. Lactoperoxidase-catalysed radio-iodination was used to compare the surface proteins on normal mouse erythrocytes and the total red cells from infected blood at different levels of parasitaemia. At very low parasitaemia, when only 2·5% of the red cells contained parasites, we observed significant changes in the profile of radio-iodinated proteins separated by SDS-polyacrylamide gel electrophoresis. These changes included the appearance of a group of high molecular weight proteins, and a protein with an apparent molecular weight (Mr) of 60 000, both of which were absent from normal erythrocytes. The major labelled band on the erythrocyte surface (Mr 92 000) also appeared to be less heavily labelled during infection. The magnitude of these differences in surface proteins increased as the parasitaemia rose, until the new bands dominated the radioactivity profile with blood of greater than 50% parasitaemia. Several control experiments established that the radio-iodinated proteins were surface molecules on intact cells and that artifactual proteolysis did not contribute to the observed differences. The results suggest that changes in the surface proteins occur on all red cells in the blood of infected mice. The results of labelling the surface glycoproteins by oxidation with periodate or galactose oxidase, followed by NaB3H4 reduction, have varied with the isolate of B. rodhaini. With the isolate currently in use, no significant differences were observed in the labelled surface glycoproteins of normal erythrocytes and red cells from infected blood of high parasitaemia, whereas an earlier isolate exhibited a marked decrease of glycoprotein labelling of both infected and uninfected red cells.

The surface proteins and glycoproteins of red cells from Plasmodium berghei-infected blood have been radio-isotope labelled and compared with those of normal mouse erythrocytes using the following protein labelling probes: lactoperoxidase-catalysed radio-iodination of tyrosyl residues, periodate oxidation and NaB3H4 reduction of sialic acid and oxidation of galactosyl/N-acetylgalactosaminyl residues by galactose oxidase with subsequent NaB3H4 reduction. During P. berghei infection, new tyrosyl-labelled proteins with apparent molecular weights (Mr) of 60000, 54000, 40000 and 27500 appeared on the surface of most, if not all, red cells in the blood. Purified multinucleate cells (mostly reticulocytes) differed only in that they also had a surface protein with Mr of 83000. However, this molecule is thought to be specific to mouse reticulocytes rather than derived from parasites. In contrast to the relatively minor changes detected with radio-iodination, striking changes in glycoprotein radio-isotope labelling resulted from infection. All of the red cells in infected blood of greater than 20% parasitaemia lost their periodate-sensitive glycoprotein sialic acid. With some samples there was little change in glycoprotein labelling by the galactose oxidase method, provided neuraminidase was also added. Modification of the exocyclic hydroxyls of sialic acid is postulated to account for this. Other blood samples exhibited a dramatic loss of galactose oxidase-dependent labelling. It is suggested that these observations may relate to the excessive red cell destruction of uninfected as well as infected cells which has been inferred in many haemosporidial infections, including malaria.

Lactoperoxidase-catalysed radio-iodination was used to compare the surface proteins on red cells from Plasmodium yoelii-infected and normal BALB/c mice. The profile of radio-iodinated proteins separated by SDS-polyacrylamide gel electrophoresis was different for infected blood of similar parasitaemia from mice inoculated with different doses of the parasite. Inoculation with the lower dose resulted in the appearance of a major radio-iodinated protein of apparent molecular weight (Mr) 76000 which was labelled to a similar extent on uninfected red cells from infected blood and purified multinucleate infected cells. Several minor radio-iodinated bands, with identical mobilities to the minor bands on normal BALB/c erythrocytes, were also present on red cells from this infected blood. In contrast, the higher inoculation dose produced changes in the minor labelled bands, and the band with Mr of 76000 was absent. In this case, the minor radio-iodinated proteins of the normal BALB/c erythrocyte (with Mr of 65000, 57000, 48000, 38000 and 32000) were replaced by a series of bands with Mr of 60000, 50000, 43000 and 28000 on both uninfected and infected red cells. These differences with inoculation dose may be related to the different duration of these infections, the development of anaemia and the extent of pathological changes at the erythrocyte surface. P. yoelii infection caused a marked loss in periodate-dependent labelling of sialoglycoproteins on most, if not all, red cells in infected blood. There was also a large decrease in galactose oxidase-dependent glycoprotein labelling with or without neuraminidase treatment. These changes in the carbohydrate groups on red cell membrane glycoproteins may be linked to the excessive loss of both uninfected and infected red cells during some malaria infections.

Pathogenic effects caused by graded doses of recent isolates of Eimeria acervulina, E. mivati and a new isolate, thought at first to be E. mitis, were compared. Cross-immunity studies were conducted with 3 strains of E. acervulina and 2 strains of E. mivati, together with the new isolate. The results showed marked similarities between E. mivati and the new isolate and clear distinctions between these and E. acervulina. E. mivati produced scattered petechiae but did not form discrete lesions in the intestine comparable to those seen with E. acervulina. Endogenous stages of E. mivati were most numerous in the lower small intestine and proximal caeca. The ratio of villus height to total mucosal thickness in the lower intestine was reduced. Similar changes caused by E. acervulina were seen in the anterior intestine only.

A variety of measurements was made on small samples of schistosomula recovered from the skin, lungs and hepatic portal system of percutaneously infected mice, on the basis of which development could be divided into a migration and a growth phase. The density of schistosomula, estimated using a Ficoll gradient, was found not to vary significantly between Day 0 and Day 24 post-infection, having a mean value of 1·077. The reduced weight was measured by means of a Cartesian diver balance and used in conjunction with density to estimate the change in wet weight of schistosomula. Wet weight was found to decline slightly during the migration phase and to increase exponentially following arrival of schistosomula in the hepatic portal system. No change in nitrogen content was detected during migration but there was a rapid increase after arrival in the hepatic portal system. The rate of oxygen consumption, measured by Cartesian diver respirometer, declined significantly during migration and then increased exponentially after arrival of worms in the hepatic portal system. No change was detected in the lactic dehydrogenase activity of migrating worms but again, an exponential increase occurred after entry into the hepatic portal system. It was concluded that the migrating schistosomulum is in a semi-quiescent metabolic state, although it possesses the ability to take up nutrients and undergoes morphological changes. Growth is triggered by an unknown mechanism after arrival in the hepatic portal system. Examination of the various sets of data suggests that it is initiated between 10 and 11 days post-infection in the most advanced schistosomula.

Survival curves for cercariae of Schistosoma mansoni maintained at different temperatures were determined. Between 15 and 35 °C the curves were of reverse sigmoid form and the probit transformation gave a statistically good fit. The slope of the regression lines fitted to the probit transformations increased exponentially as the temperature rose. Above 35 °C heat intolerance became important and increased exponentially as the temperature rose. Below 15 °C, cold intolerance caused an initial high level of mortality followed by an extended period with insignificant mortality. The glycogen content of whole cercariae and separated cercarial bodies and tails was measured during ageing. The glycogen content of whole cercariae declined exponentially during ageing. This was a product of exponential decreases in the glycogen content of both the body and the tail of the organism. The cercarial tail was shown to contain slightly over half of the total glycogen content. The rate of glycogen use was higher in the tail than in the body. A computer simulation model was used to demonstrate that the observed exponential use of glycogen could generate survival curves similar to those observed experimentally.

By transferring Schistosoma mansoni (12 to 14-day-old worms) from one host into the peritoneal cavity of a host of a different species, it was possible to demonstrate that worms grown in rats, hamsters, Mastomys natalensis and Cebus monkeys were rejected by recipient animals previously immunized against red blood cells of the donor hosts. These results suggest that host-like antigens are acquired by S. mansoni in all hosts. The transfer of worms into the peritoneal cavity has proved to be a simple and convenient method for studying the presence of host antigens in S. mansoni.

Mice given primary infections of Schistosoma mansoni by percutaneous or subcutaneous routes were found to acquire a higher degree of resistance against homologous challenge after 7–8 weeks than mice infected intraperitoneally. Mice infected by the intraperitoneal route tended to have smaller worm burdens than those infected with the same number of cercariae by the other two routes and this may, in part, have contributed to the relative lack of efficacy of intraperitoneal infections in inducing resistance to re-infection. The same degree of resistance was acquired after primary percutaneous infection irrespective of whether it was administered in 3 equivalent weekly doses, or the same total number of cercariae was administered as a single infection. The same degree of resistance was also observed when a percutaneous challenge was administered on the same or a different skin site to that which received the percutaneous primary infection. The degree of resistance to re-infection acquired after a percutaneous primary infection correlated well with the size of the primary worm burden and the number of eggs in the intestine and liver, but did not correlate with the number of eggs in the lungs.

Chicken macrophages, obtained by cultivation of blood monocytes, were infected with epimastigote and bloodstream trypomastigotes of the Y and the CL strains of Trypanosoma cruzi. The percentage of infected cells and the mean number of parasites per cell were determined after 2, 6, 12 and 24 h of parasite–cell contact. After 6 h of contact about 80% and 40% of the macrophages were infected by trypomastigotes of the Y and CL strains respectively. After longer periods of contact almost all macrophages were infected by Y trypomastigotes while only about 60% were infected by those of the CL strain. After 2 h of contact almost all macrophages were infected by CL epimastigotes while only about 50% were infected by Y epimastigotes. After 6 h of contact almost all macrophages were infected by epimastigotes of both strains. These results are discussed taking into consideration differences between parasites of the two strains and between the two developmental stages of the T. cruzi life-cycle.

Uptake of radioactively labelled purine bases and nucleosides by suspensions of Trypanosoma brucei and Trypanosoma congolense in bicine buffer was determined at 37 °C. With T. brucei, the rate of uptake of adenosine was much greater than that of the other compounds tested, the uptake of which decreased in the order adenine, inosine, guanosine and hypoxanthine. With T. brucei, adenosine uptake increased with concentration in a manner suggesting two mechanisms, one with high and the other with low affinity for adenosine. The uptake of adenine increased with concentration only up to about 1·5 µM while the uptake of guanosine increased little with concentration and that of inosine and hypoxanthine not at all. In both species adenosine strongly inhibited the uptake of both of the other nucleosides and of both purine bases. In T. brucei, guanosine and inosine caused small increases in adenosine uptake which was, however, inhibited by them in T. congolense. In T. brucei, each of the purine bases adenine and hypoxanthine inhibited its own uptake maximally but that of each other less effectively. Hypoxanthine was more effective than adenine in inhibiting the uptake of the nucleosides guanosine and inosine, but neither base effected marked inhibition of adenosine uptake. The uptake of adenosine by T. brucei was inhibited by dipyridamole and its analogue, compound RA–233, strongly at 100µM and slightly at 10 µM. The other dipyridamole analogues, VK–744 and VK–774, were ineffective.

Aromatic amino acids (phenylalanine, tryptophan and tyrosine) are absorbed by Hymenolepis diminuta through a combination of mediated (non-Na+-sensitive) transport and diffusion. All 3 amino acids are accumulated against an apparent concentration difference during a 30-min incubation of tapeworms in 0·1 mM 3H-labelled amino acid. Inhibitor studies demonstrate that phenylalanine, tryptophan and tyrosine are mutually competitive inhibitors of the uptake of each other, and the uptake of these amino acids is inhibited by aliphatic amino acids but not by basic or dicarboxylic amino acids. The D- and L-isomers of aromatic amino acids are equally effective in inhibiting aromatic amino acid uptake. The data indicate that at least 3 amino acid transport loci are involved in aromatic amino acid transport by H. diminuta.

An experimental study of the effects of parasitism by H. diminuta on the intermediate host, Tribolium confusum, is described. No density- dependent constraints on parasite establishment within individual hosts are evident, although a reduction in cysticercoid size at high parasite burdens is demonstrated. The relationship between parasite burden, host mortality and host fecundity is investigated. Host mortality is linearly related to parasite burden, whereas the relationship between parasite burden and host fecundity is non-linear. There is no difference in viability between eggs from infected and uninfected females. The generative causes of these effects are not investigated experimentally, although it is postulated that survival is related to the degree of damage to the midgut wall caused by parasite penetration, and fecundity to the biomass of parasites harboured by the host. The significance of these effects is discussed in relation to the overall dynamics of the host-parasite association.

The surface morphology of fixed ovarian balls from female Moniliformis dubius, aged 12, 18, 26, 28, 42, 77, 105 and 118 days, has been examined by means of scanning electron microscopy. The appearance of the surface has been found to be variable between ovarian balls from worms of the same and different ages. Some parts of the surface are seen to possess micro-projections, cavities and ridges while other parts have the appearance of an irregular meshwork of fibres. Various protruding features have been observed to extend from the surfaces of the ovarian balls taken from the inseminated female worms. In most cases, the surfaces of the protruding features differ in appearance from the surrounding surfaces of the ovarian balls. Some of these features have been assumed to represent growing zygotes and developing eggs covered by the supporting syncytium of the ovarian ball. Single or several thread-like structures have been observed in association with the surfaces of ovarian balls taken from the inseminated female worms. At present, the thread-like structures are believed to be portions of spermatozoa. By means of light microscopy, preliminary observations have been made on what is considered to be the division process of ovarian balls taken from uninseminated and inseminated worms varying in age from 7 to 98 days.

By means of light and electron microscopical techniques, the organization of the reproductive tract of female Moniliformis dubius is described. The tract consists of an efferent duct system associated with 2 ligament sacs present in the body cavity. The efferent duct system consists of uterine bell, uterus and vagina. The uterine bell contains a complex system of routes and is associated with the ligament sacs in a way that facilitates egg sorting. The dorsal and ventral ligament sacs exist with separate cavities at the posterior end, where they are attached to the efferent duct, but merge into a single sac at the anterior of the trunk.

The transmission of parasites often involves a high mortality of free-living stages in the environment outside the host. This may be offset by a high biotic potential. In addition, adaptations of nematode eggs and larvae that ensure their survival or increase their chances of infecting a host will reduce the potential wastage rate. Increasing transmission will have an effect equivalent to increasing the fecundity of the parasite and, energetically, may be the more favourable strategy.