We have investigated the metabolic disturbances in 2 murine models of blood-stage malaria, Plasmodium chabaudi and Plasmodium yoelii. Blood glucose, plasma insulin and parasitaemia were measured in normal and infected mice before and after treatment with diazoxide, adrenaline, Sandostatin and quinine. Severe hypoglycaemia and marked hypersinsulinaemia developed during both infections. A single injection of diazoxide (25 mg/kg i.p.) or adrenaline (0·03 mg s.c.) lowered insulin concentrations in normal mice, reversed the hypoglycaemia in both infections and significantly reduced the hyperinsulinaemia in P. chabaudi-infected mice (P < 0·0001). Higher doses of Sandostatin (500 μg/kg s.c.) were required to reverse hypoglycaemia. Quinine (25 mg/kg i.p.) significantly increased blood glucose in normal and infected mice (P < 0·001) and no hypoglycaemia was observed in mice with normal blood glucose for more than 3 h. This study shows that the major cause of hypoglycaemia in murine malaria is hyperinsulinaemia rather than high consumption of glucose by host and parasites or chemotherapy with quinine, and that hypoglycaemia can be reversed by correcting the hyperinsulinaemia.

Two genetically defined parents of Eimeria tenella, each characterized by a selectable phenotype, were mated to provide ‘recombinant’ oocysts for an analysis of the inheritance of DNA markers into the sporocyst stage of the life-cycle. A total of 23 populations was established from infection with a putative single sporocyst and their inheritance of DNA markers provided compelling evidence that the 2 sporozoites within each sporocyst are genetically identical. Each of the 5 polymorphic DNA markers used segregated independently within the ‘recombinant’ parasites and only 1 of the parental forms was inherited in 22 of the populations aimed to have been established from a single sporocyst.

Soluble adult worm antigens (SWAP) of Schistosoma mansoni were fractionated by fast protein liquid chromatography (FPLC) system, using Q-Sepharose anion-exchange resin, in order to characterize antigenic fractions that may elicit cell responses in human schistosomiasis. SWAP fractions were eluted by 20 HIM Tris–HCl solution (pH 9·6) with an increasing gradient of 1 M NaCl. The FPLC system was able to resolve 6 fractions, enumerated I to VI, according to the NaCl gradient. The analysis of each fraction on SDS–PAGE showed that fractions I to IV were constituted by multiple protein bands with Mr ranging from 21 to > 200 kDa. Large amounts of nucleic acids were evidenced in fractions V and VI, as revealed by ethidium bromide staining of agarose electrophoresis gels. Using ELISA, it was shown that sera from chronic schistosomiasis patients contained antibodies that recognized antigens in practically all fractions. Studies were designed to investigate the capacity of these fractions to induce cell proliferation and granuloma formation. It was demonstrated that fraction III stimulated a significant proliferative response of peripheral blood mononuclear cells (PBMC) from chronic schistosomiasis patients. However, fraction III coupled to polyacrylamide beads induced small granuloma formation in vitro, whereas beads coated with fractions I, II and V were able to induce significant granuloma reactions.

The detection of egg-derived antigens in the serum and urine of Schistosoma mansoni-infected individuals and experimental animals would provide an alternative method to assess the tissue egg burden. The detected levels are, however, not only a function of the amounts of antigen produced, but also of the processing or clearance by the host. In the present study the immunolocalization pattern of antigens using 2 recently described monoclonal antibodies to repetitive carbohydrate epitopes of S. mansoni soluble egg antigen (114–5B1–A and 114–4D12–A) in various organs of the host was investigated. In the liver strong immunoreactivity could be detected around the entrapped eggs and in egg-shells, as well as in Kupffer cells accumulating both antigen and schistosomal pigment. In the spleen, immunohistochemistry revealed antigen in the plasma as well as in secondary lysosomes of macrophages. Strong labelling was found in the vesicles of the eosinophilic granulocytes: indirect evidence perhaps for the presence of antigen–antibody complexes. In conclusion, the secreted egg antigens were sequestered in the reticulo-endothelial macrophages of the liver and the spleen as already partly described for worm-derived antigens. The presence of large quantities of antigenic material in the spleen could suggest an important role of this organ in the clearance of antigen and might even provide an additional explanation for the hepatosplenomegaly mainly present in S. mansoni-infected children.

Based on the ability of bacterial associates of entomopathogenic nematodes to produce antibiotic compounds on artificial media, it has been commonly accepted that Xenorhabdus sp. and Photorhabdus sp. inhibit a wide range of invading microorganisms in insects infected with Steinernema spp. or Heterorhabditis spp. Therefore, the question of whether antibiotic compounds produced by the primary form of bacterial symbionts associated mutualistically with S. carpocapsae and H. bacteriophora explain why insect carcasses do not putrefy but provide nutritional requirements for insect parasitic rhabditoid nematodes to complete their life-cycle was examined. Laboratory bioassays of anti-bacterial activity on nutrient agar and during parasitism in larvae of Galleria mellonella have confirmed earlier observations that in vitro colonies of the primary form of X. nematophilus and P. luminescens produced agar-diffusible antibiotic compounds of a broad spectrum of anti-bacterial activity; their role in parasitism seems doubtful, however. This hypothesis is supported by a low antibiotic potency of a limited spectrum of anti-bacterial activity throughout the life-cycle of the parasites, principally in Galleria infected with S. carpocapsae. Since the lack of putrefaction cannot be explained simply by antibiotic inhibition of contaminating bacterial microflora, other competition mechanisms must be operating in parasitized insects. I postulated that a rapid and massive colonization of the insect body by nematophilic bacteria creates unfavourable conditions for the growth and multiplication of bacterial (proteolytic) contaminators making the insect carcass decay-resistant. In the case of H. bacteriophora, low antibiotic activity at an early stage of parasitism could support the colonization by P. luminescens of the host.

Pasteuria penetrans is a bacterium with the potential to control plant-parasitic nematode populations; the mechanism of spore adhesion, however, is poorly understood. Attachment assays were performed in media supplemented with various concentrations of fibronectin and in the presence and absence of KSCN which modulates hydrophobic interactions. A reduction in the strength of the hydrophobic effect prevented spores from binding to the cuticle as did 20 μg/ml fibronectin. It was also shown directly utilizing a newly-developed technique which utilizes 3-hexadecanoyl-7-hydro-coumarin as an indicator of the fibronectin binding to the spore surface that the presence of KSCN prohibited binding. This effect was interpreted to indicate that the reduction of binding was the direct result of the influence of hydrophobic interactions between the fibronectin and the spore surface. Western blot analysis of cuticle extracts of Meloidogyne incognita and Caenorhabditis elegans revealed small amounts of fibronectin to be present. Fibronectin, or a similar receptor, present in the cuticle could be responsible for the adhesion of P. penetrans by hydrophobic interactions.

Infection of intermediate hosts with eggs of taeniid parasites results in a larval infestation known as cysticercosis. A number of studies have indicated that cysticercosis is associated with immunosuppression, although little is known about the mechanisms involved. In the present study, mice infected with the larvae of Taenia crassiceps were found to exhibit a pronounced anergy, which preferentially affected T-cells located anatomically close to the parasite. This anergy was linked to late events in the T cell activation pathway; that is, stimulation through the T cell receptor(TCR)/CD complex by Concanavalin-A, or plate-bound monoclonal antibodies (mAb) to TCRαβ or CD3ε, or combinations of phorbol ester and ionomycin (all of which can bypass early membrane-related events), failed to fully activate T lymphocytes. The relative proximity of T cells to the parasite was directly related to upregulation of IL-4 and downregulation of IL-2 production. In addition, the profiles of parasite-specific Abs showed an exclusive increase of serum IgG1 during infection. Taken together, the data suggest that infection of mice with larvae of T. crassiceps alters the balance of CD4+ Th cells by upregulating Th2 and downregulating Th1 cells located in close proximity to the parasite.

We investigated the timing of seasonal activity of the seabird tick Ixodes uriae by examining engorgement rates of off-host ticks and the prevalence of infested common guillemots (Uria aalge) and kittiwakes (Rissa tridactyla) on the Isle of May, Scotland. More than 99% of I. uriae fed during the period late April to early August which coincided with the seabird breeding season. No ticks fed in the autumn and winter, and none over-wintered in the engorged state. Peak tick feeding activity was during the hosts' incubation period in May and early June, when over 70% of birds were parasitized. Few ticks were active when guillemot chicks were being brooded, or during the early part of kittiwake chick-rearing. Adult female tick feeding peaked in the first week of June, while nymphal and larval activity peaked in the third week of May. Adult female ticks fed later than nymphs on guillemots and larvae on both guillemots and kittiwakes; however, there was considerable temporal overlap in the feeding periods of the 3 stages on both hosts. All larvae and nymphs fed in May and early June, but up to 18% of adult females remained unengorged at this time, and probably deferred feeding by 1 year. A small proportion of individuals which fed as larvae in May appeared to feed again as nymphs in July of the same season, thereby shortening their life-cycle by 1 year. The duration of the life-cycle of I. uriae on the Isle of May is typically 3 years but varies from 2 to 4 years. Ticks feeding on guillemots did so significantly earlier than those feeding on kittiwakes, possibly because guillemots start breeding earlier in the year. Breeding of both guillemots and kittiwakes was later in 1994 than in 1993. This delayed the activity of all tick stages on kittiwakes and adult female ticks on guillemots, but did not affect the timing of activity of nymphs or larvae feeding on guillemots.

Parasites are generally found aggregated among hosts. In this paper we propose a method for measuring aggregation at different scales in the host population. We use the method to characterize the pattern of aggregation of the tick Ixodes uriae on chicks of its seabird host, the Kittiwake Rissa tridactyla. We found evidence of aggregation at the among-nest scale, but not among chicks within nests. This shows that the processes leading to aggregation occur at a higher scale than the nest. The methods we develop provide a way to compare parasite aggregation at different scales in a quantitative fashion and can be applied in a large number of epidemiological studies.