Parasitism often influences the phenotype of individuals. Many of the resulting changes are due to changes in resource allocation that come with infection. Here we examine the effect of a trematode parasite on the shape and defence morphology of a New Zealand freshwater snail, Potamopyrgus antipodarum. The trematode Microphallus sp. asexually produces hundreds of metacercarial cysts in the snail. The length, width and 2-dimensional area of each snail were measured. Snails were also assessed for their degree of spininess. Snails were dissected to determine gender, brooding condition and parasitism. Snails infected with Microphallus sp. were found to be significantly less spiny than uninfected snails. Microphallus-infected snails were also found to have a significantly greater width to length ratio at larger sizes than their uninfected counterparts. These trends could be explained in at least 3 ways. (1) Infection causes the snails to not produce spines and to become wider. (2) Spiny and narrower snails are more likely to die when they become infected. (3) Spiny and narrower snails are more resistant to infection. The changes in phenotype observed are unlikely to be adaptive for either the host or parasite and probably represent physiological by-products of the host-parasite relationship.

1. Factors controlling the distribution of the bird fleas Ceratophyllus styx, the sand-martin flea, C. gallinae, the hen flea, and Dasypsylla gallinulae, the blackbird flea, were investigated in the field.

2. Sand-martin fleas (C. styx) pass the winter as adults within cocoons in the old nests of their host. Observations indicate that the fleas are stimulated to emerge from the cocoons by the rise in temperature in the spring, and some of the adult fleas emigrate in the spring and invade new nest burrows. Observations and experiments showed that sand-martin fleas disperse from old burrows both laterally and vertically and that emigrating fleas could reach areas as far as 33·8 m. from the old nests. The detection of the new burrow entrances is not due to vision, or to the recognition of difference of humidity between the burrow and the cliff face, or to the reaction to air current differences between the burrow and the cliff face, but to recognition of the horizontal floor of the burrows and a tendency to congregate upon horizontal surfaces. How the fleas distinguish the horizontal burrow surface from the cliff top is still unknown. The colonization of new burrows by the fleas does not occur at night. It is suggested that, in addition to finding their hosts in the spring by invading new burrows, sand-martin fleas may jump on to the birds when they are hovering near the cliff face. Many adult fleas leave the burrows within 3 days of the fledging time of the young sand-martins but a small number remain within the nest. The fate of these specimens is not known.

3. C. gallinae, the hen flea, and D. gallinulae, the blackbird flea, pass the winter principally as adults enclosed in the cocoons in the old nest material. In the spring they emerge from the cocoons, emigrate away from the old nest and are free-living on the ground. Probably the adult C. gallinae and D. gallinulae jump on to birds when they are feeding on the ground in the spring.* Therefore the absence of hen fleas in nests situated on the ground or in open nests built in low vegetation, is not due to lack of opportunity of contact between the adult flea and the birds which construct such nests.

4. It is concluded that in host-seeking, adults of C. gallinae and D. gallinulae emigrate away from old nests in the spring and come in contact with the host birds on the ground in the birds' feeding area, whereas C. styx adults emigrate into the hosts' breeding area and come in contact with the birds in the new nesting burrows.

We have extracted RNA from Schistosoma mansoni using the lithium chloride–urea method which gives good yields of undegraded RNA. The results of agarose gel electrophoresis of RNA extracted by this procedure suggest that S. mansoni has an in vivo nick in the large rRNA sub-unit. Translation of the RNA in a rabbit reticulocyte lysate gave significant incorporation of [35S]methionine into synthesized proteins. Immuno-precipitation of these translation products using a hyperimmune monkey serum sedimented between 5 and 8% of the radioactivity, which appeared to be present in approximately 13 proteins of molecular weights 18, 20, 21, 22, 23, 35, 40, 54, 60, 70, 74, 78 and 105 K Daltons.

Two clones, totalling 8068 bp and spanning over half of the coding region of the mitochondrial genome of Schistosoma mansoni, have been sequenced. Complete sequences are presented of the large and small ribosomal RNA subunits, CO2, ND3, ND4, ND6 and ATPase 6 genes. Incomplete sequences were found for the CO1, ND2 and CytB genes. At least 10 tRNAs were also detected and alternative structures for some of these discussed. The gene order of S. mansoni is unique and differs from that of Fasciola hepatica, the only other trematode for which any information is available.

From three specimens of the Amazon Siluroid fish Platystomatichthys sturio (the “Lenha”) I have described (1) Othinoscolex lenha, representing not only a new genus and species but also a new subfamily (the Othinoscolecinae) of the Proteocephalidae, (2) Othinoscolex myzofer, a second species of the new genus, (3) a distinct new species of La Rue's genus Monticellia—Monticellia lenha, and (4) a new species of Proteocephalus, Proteocephalus lenha.

Leishmania (L.) amazonensis [L. (L.) amazonensis] is widely distributed in Brazil and its symptomatic infections usually lead to few localized lesions and sometimes to diffuse cutaneous form, with nodules throughout the body, anergy to parasite antigens and poor therapeutic response. The variability of these manifestations draws attention to the need for studies on the pathophysiology of infection by this species. In this study, we analysed the course and immunological aspects of L. (L.) amazonensis infection in BALB/c and C57BL/6 strains, both susceptible, but displaying different clinical courses, and athymic BALB/c nude, to illustrate the role of T cell dependent responses. We analysed footpad thickness and parasite burden by in vivo imaging. Furthermore, we evaluated the cellular profile and cytokine production in lymph nodes and the inflammatory infiltrates of lesions. Nude mice showed delayed lesion development and less inflammatory cells in lesions, but higher parasite burden than BALB/c and C57BL/6. BALB/c and C57BL/6 mice had similar parasite burdens, lesion sizes and infiltrates until 6 weeks after infection, and after that C57BL/6 mice controlled the infection. Small differences in parasite numbers were observed in C57BL/6 macrophages in vitro, indicating that in vivo milieu accounts for most differences in infection. We believe our results shed light on the role of host immune system in the course of L. (L.) amazonensis infection by comparing three mouse strains that differ in parasitaemia and inflammatory cells.

Strongyloidiasis can be perpetuated by autoinfection with the filariform larvae L3, causing asymptomatic chronic infections and creating a population of carriers, affecting not only developing countries. So far, very little is known about the proteins that interact with the human host, and few proteins from the infective Strongyloides stercoralis L3 have been characterized. Here, we report results obtained from a proteomic analysis of the proteins from S. stercoralis L3 larvae obtained from patients. Since the genome of S. stercoralis is not yet available, we used proteomic analysis to identify 26 different proteins, 13 of them released by short digestion with trypsin, which could represent surface-associated proteins. The present work extends our knowledge of host-parasite interactions by identifying proteins that could be of interest in the development of diagnostic tools, vaccines, or treatments for a neglected disease like strongyloidiasis.

The aim of this study was to develop, perfect and validate the PCR (polymerase chain reaction) technique using mitochondrial (mt) and ribosomal (ITS-2) DNA for the accurate identification of Dicrocoelium dendriticum in molluscs and ants, the first and second intermediate hosts, and their early detection. The first primers that were designed amplified a 169 pb mtDNA fragment of D. dendriticum permitted the detection of a single D. dendriticum metacercaria from the Formica rufibarbis and Formica pratensis abdomen, as well as the detection of the brainworm in the head of the ants collected in tetania. Although these primers did not amplify Dicrocoelium chinensis DNA and permitted detected D. dendriticum in the molluscs, they did not discriminate Brachylaimidae metacercariae found in the same mollusc. The PCR that was designed to amplify a 93 bp fragment of the ITS-2 is D. dendriticum specific as it did not amplify D. chinensis, Brachylaimidae and other trematodes. This technique is very sensitive since it permitted the detection of D. dendriticum in the molluscs from the first day post-infection, the brainworm in the head of the ants and only 1 D. dendriticum metacercaria from the abdomen of the ants. Both techniques are important, mainly the latter.

Homologous and heterologous resistance in Echinostoma revolutum infections was studied in mice. A high level of homologous resistance was demonstrated in mice harbouring a 13-day-old primary E. revolutum infection with 9–10 and 11–15 worms, corresponding to a 70·0 and 66·7% reduction in the size of the established worm burden as compared with that of the challenge control group. A 14- and 20-day-old primary infection with 3–4 worms induced a level of resistance of 61·7 and 81·8% respectively, while higher worm levels of 9–10 and 11–15 induced almost complete resistance corresponding to a 95·1–100% reduction in the size of the established worm burden. Complete resistance was also demonstrated in mice challenged 8 days after elimination of a 20-day-old primary infection with 11–15 worms by anthelmintic treatment. A primary 43-day-old Schistosoma mansoni infection induced a 73·1% reduction in the size of the established E. revolutum challenge infection while infections of an age of 79 and 99 days conferred complete resistance to heterologous challenge with E. revolutum. Primary pre-patent S. mansoni infections and a patent S. bovis infection of an age of 56 days did not induce any resistance to challenge with E. revolutum. A primary 14- and 21-day-old infection of E. revolutum did not stimulate any significant level of resistance to heterologous challenge with S. mansoni.

A single exposure to radiation-attenuated cercariae of Schistosoma mansoni induces a high level of protective immunity in C57BL/6 mice, which is mediated by Th1 responses. Events in the skin and/or draining lymph nodes early after exposure are crucial for the induction of protection, and we have investigated the interactions of vaccinating parasites with host leucocytes in these 2 locations. We observed extensive lateral spreading of cercarial secretions along layers of the stratum corneum but not between keratinocytes. There was little direct contact with host leucocytes during the first 1–2 days when the parasites lay at the base of the epidermis, but cells accumulated in the underlying dermis. In contrast to normal parasites, attenuated larvae persisted in the dermis for >10 days, often surrounded by aggregates of macrophages/dendritic cells. Whilst cells bearing MHC II, CD11b or CD11c markers were present in the lymph nodes, particularly in the periphery and paracortical areas, no obvious redistribution was seen as a result of parasite residence there for 5–15 days. However, ultrastructural observations revealed numerous cells with macrophage/dendritic morphology in the vicinity of parasites, in some instances closely adherent to the tegument. The observations strongly suggest that the tegument is a potent source of the antigens which prime the immune system in the lymph nodes of vaccinated mice for a protective response.

Different hydrogen peroxide (H2O2)-scavenging mechanisms, and the conditions under which they operate, have been examined in promastigotes and amastigotes of Leishmania donovani. For promastigotes, the ability of the parasite to remove H2O2 was completely ablated by sonication whereas for sonicated amastigotes substantial loss of H2O2 from the phagocyte-fre¸e test system still occurred. In direct contrast, the ability of amastigotes, but not promastigotes, to remove H2O2 was markedly inhibited by aminotriazole or sodium azide. This suggested a role for haem-containing enzymes, catalase or peroxidases, as a protective H2O2-scavenging mechanism and was consistent with detection of catalase in amastigotes but not promastigotes using a spectrophotometric assay. Both forms of the parasite did, however, show reduced ability to remove H2O2 at 5–7°C indicating that additional enzymatic scavenging mechanisms may operate. Glutathione peroxidase activity was undetectable in either form of the parasite. The total thiol sink, glutathione (GSH) plus protein thiols, was greater in promastigotes but the ability to regenerate GSH via glutathione reductase was equivalent for promastigotes and amastigotes. Less temperature-dependent non-enzymatic mechanisms (e.g. an unsaturated lipid sink) also appear to contribute to removal of H2O2 by both promastigotes and amastigotes. It seems likely, nevertheless, that the difference in H2O2 sensitivity between the two forms of the parasite relates to the activity of the direct H2O2-scavenging enzyme, catalase, which appears to operate more efficiently against a bolus of reagent H2O2.

Leishmania infantum and Leishmania donovani both pertain to the L. (L.) donovani complex and are responsible for visceral leishmaniasis. To explore the L. donovani complex, we focused our study on cysteine protease B (cpb) and especially on 2 cpb copies: cpbE and cpbF. We selected cpb genes because of their phylogenetic interest and host–parasite interaction involvement. Sequencing these 2 copies revealed (i) that cpbE is specific to L. infantum and cpbF is specific to L. donovani and (ii) that these 2 copies are different in length and sequence.Nucleotide sequence data reported in this paper are available in the GenBank database under Accession numbers AY896776 AY896777, AY896778, AY896779, AY896780, AY896781, AY896782, AY896783, AY896784, AY896785, AY896786, AY896787, AY896788, AY896789, AY896790, AY896791. Phylogenetic analysis and protein predictions were carried out in order to compare these copies (i) with other trypanosomatid cpb, especially L. mexicana, and (ii) within the L. donovani complex. Our results revealed patterns specific to the L. donovani complex such as the COOH-terminal extension, potential epitopes and N-glycosylation sites. Moreover, phylogenetic analysis revealed different levels of polymorphism between L. infantum and L. donovani and confirmed the ancestral status of the latter. L. infantum has a shorter sequence and a deleted sequence responsible for modifications in protein conformation and catalytic triad. Considering the clinical aspect, L. infantum dermotropic strains appeared more polymorphic than L. infantum viscerotropic strains.

Twenty-one monoclonal antibodies, obtained after immunization of mice with erythrocytic stages of Plasmodium falciparum, produced a double dot image in IFA. Immunoelectronmicroscopy indicated that the mAbs reacted with the rhoptries. Rhoptries are pear-shaped apical organelles, believed to be involved in invasion of the host cell by the parasite. The mAbs all immunoprecipitated the high molecular weight antigen complex. Some mAbs recognized on immunoblots only 1 protein of this complex, whereas others reacted with RhopH1 and RhopH3, or RhopH2 and RhopH3 or with the 3 proteins. An additional antigen of 52 kDa was also recognized by some of the mAbs. The epitopes defined by the mAbs were present in most of the 40 P. falciparum strains or isolates studied by IFA. Interestingly, the mAbs also reacted with high titres on P. vivax and P. ovale, but produced images that did not indicate an apical location. The mAbs failed to react on the non-human malaria parasites studied, P. cynomolgi and P. inui. On P. berghei or P. chabaudi parasites, only 5 mAbs gave a positive reaction, labelling a large network outside the parasite. Finally, the mAbs did not react with P. falciparum sporozoites, indicating that the rhoptries of merozoites and sporozoites, the two invasive stages of the malaria life-cycle are equipped with distinct sets of proteins.

The population dynamics of Ascaridia galli infections of poultry was studied under repeated doses of 10, 100 and 1000 eggs. Daily doses were continued for 6 weeks only. At low dose rates patency is noted by the fifth week. At higher dose rates there is an accumulation of larvae whose development has been arrested at a precise developmental stage, i.e. the third larval stage. Sporadic development of some of these larvae to adults occurs later. Arguments are produced to show that this inhibition of larval development is a resistance and not a density-dependent phenomenon. The epidemiological significance of this inhibition is discussed. This resistance phenomenon is shown to occur in single infection experiments where 1000 eggs were used. This gives rise to the development of a worm population of two facies. The whole finding is suggested to be related in some way to the phenomenon of ‘tissue phase’, which is accepted as a normal life-cycle behaviour of this parasite. A brief review of previous work on this is given and it is postulated that the ‘tissue phase’ phenomenon is not an obligatory part of the normal life-cycle of the parasite but represents a reaction to factors of resistance inherent in chickens and controlled to a large extent by a complex dynamic interplay of dose size and the chickens.

I wish to thank the Department of Technical Co-operation and the Federal Government of Nigeria for financing this project, Dr Boulton of the Poultry Research Centre, Edinburgh, for advice on nutrition, and the Department of Zoology, especially Dr J. A. Campbell, University of Edinburgh, for facilities and advice on the work. I am greatly indebted to the Ministry of Agriculture, Fisheries and Food, Poultry Research Laboratories, Lasswade, for the free supply of chickens used in this work.

The construction of the Diama dam on the Senegal River and the ensuing ecological changes have led to a massive outbreak of Schistosoma mansoni infection in Northern Senegal, associated with very high intensity of infections, due to extremely intense transmission. The vectorial capacity of Biomphalaria pfeifferi from Ndombo, near Richard-Toll was investigated in order to assess the role of the snail–parasite relationship in this particular epidemiological situation. The results revealed an unusually high compatibility between the Senegalese S. mansoni strain and its local snail intermediate host, B. pfeifferi. The snail infection rate after exposure to a single miracidium per snail was 87%. The cercarial production of infected snails was very high, with a mean total production of 50456 cercariae per snail. No significant difference was found in the total cercarial output between snails exposed to 1 miracidium and those exposed to 5 miracidia. The increase in the rate of cercarial output was significantly greater in snails exposed to 5 miracidia, but there was a higher mortality in this group. The chronobiological cercarial production pattern showed a peak around mid-day. The implications of these findings on the epidemiology of schistosomiasis in Northern Senegal are discussed.

Standard intracellular microelectrode techniques were used to determine the electrical properties of the tegument and sub-tegumental regions in male Schistosoma mansoni. Three distinct compartments of electrical potential were observed. The resting potentials recorded in these compartments of –45·9±2·5 mV (Eteg), –22·0±1·1 mV (E2) and – 4·7±0·3 mV (E3) corroborate those previously reported by Fetterer, Pax & Bennett (1980) and Bricker, Pax & Bennett (1981). Input resistance was measured in each compartment and was found to be 4·5 MΩ (tegument), 9·2 MΩ (E2) and 3·5 MΩ (E3). Time-constants for the tegument, E2 and E3 were 0·24±0·01 msec, 0·25±0·01 msec and 0·13±0·01 msec, respectively. Multiple electrode experiments revealed that the tegument and E2 compartment are electrical syncytia with similar current-spreading capabilities. Low resistance pathways also appear to connect the tegument and E2 region, since electrotonic signals initiated in either of those compartments experience only a 15–25% reduction upon passing into the other. Injecting large (> 200 nA) depolarizing current pulses into the tegument or E2 compartment often resulted in the initiation of active membrane responses. These spikes were highly variable, ranging from 4 to 75 mV in magnitude (occasionally overshooting zero potential by as much as 25 mV) and from 10–40 msec in duration. The responses were not actively propagated along the parasite, and their decay over distance was approximately equal to that predicted on the basis of length constant values obtained from electrotonic signals. The addition of a non-diffusible solute to the recording medium resulted in a significant reduction in the current-spreading capacity of both the tegument and E2 compartment. Coupling ratios between the tegument and E2 compartment were decreased, and the input resistance for both compartments increased, while resting potentials remained constant. Active responses could not be evoked in schistosomes exposed to the hyperosmotic medium.

Plasmodium and Theileria parasites are obligate intracellular protozoa of the phylum Apicomplexa. Theileria infection of bovine leukocytes induces transformation of host cells and infected leukocytes can be kept indefinitely in culture. Theileria-dependent host cell transformation has been the subject of interest for many years and the molecular basis of this unique phenomenon is quite well understood. The equivalent life cycle stage of Plasmodium is the infection of mammalian hepatocytes, where parasites reside for 2–7 days depending on the species. Some of the molecular details of parasite-host interactions in P. berghei-infected hepatocytes have emerged only very recently. Similar to what has been shown for Theileria-infected leukocytes these data suggest that malaria parasites within hepatocytes also protect their host cell from programmed cell death. However, the strategies employed to inhibit host cell apoptotic pathways appear to be different to those used by Theileria. This review discusses similarities and differences at the molecular level of Plasmodium- and Theileria-induced regulation of the host cell survival machinery.

A leptomonad parasite was found in the sap of the tomato and in one unidentified plant, but it has not yet been seen in several others on which the insect feeds.

Interesting characteristics of this Leptomonas are (a) its extreme polymorphism, (b) the development of metacyclic forms in the salivary glands of its insect host, and (c) its alternation between insect and plant host.

Helminth immunology is a field which has changed beyond recognition in the past 30 years, transformed not only by new technologies from cDNA cloning to flow cytometry, but also conceptually as our definition of host immune pathways has matured. The molecular revolution defined key nematode surface and secreted antigens, and identified candidate immunomodulators that are likely to underpin parasites' success in eluding immune attack. The immunological advances in defining cytokine networks, lymphocyte subsets and innate cell recognition have also made a huge impact on our understanding of helminth infections. Most recently, the ideas of regulatory immune cells, in particular the regulatory T cell, have again overturned older thinking, but also may explain immune hyporesponsiveness observed in chronic helminth diseases, as well as the link to reduced allergic reactions observed in human and animal infections. The review concludes with a forward look to where we may make future advances towards the final eradication of helminth diseases.

The present studies were designed to characterize the response of sheep infected with N. spathiger to challenge infection with the same species.

The results showed that: (1) the level of worm counts attained on secondary infection with the parasite was much reduced compared with the counts recorded following initial infection; (2) the relative fecundities of parasite populations which developed in individual hosts following challenge infection, ranked in magnitude in an order which was similar to that established following initial infection; (3) as fecundity was highly correlated with the number of egg-laying females and the number of males and females was nearly equal in individual specimens, it was concluded that worm burdens were also ranked for individual animals on primary infection and following challenge; and (4) the animals of the control group remained as susceptible as the animals of groups 1 and 3 at the time of their primary infection; consequently, in the absence of previous immunological experience due to infection, there was no apparent change in susceptibility of the animals due to an effect of age during the course of the 17 weeks of the experiment.

We are greatly indebted to Dr Michael Tallis, Division of Mathematical Statistics, C.S.I.R.O., for advice and assistance with the statistical analyses, and to Dr D. F. Stewart for his interest and constructive criticism during the course of these studies. Our thanks are also due to Mr E. Teleki and Misses Helen Giller and Lindy Stothart for their valuable technical assistance.