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Molecular parasitism in the Escherichia coli-Bdellovibrio bacteriovorus system: translocation of the matrix protein from the host to the parasite outer membrane.

During the intracellular maturation in Escherichia coli of the parasite Bdellovibrio bacteriovorus the outer membrane, major protein I of E. coli (i.e., the matrix protein) becomes associated with the outer membrane of the emerging parasite cells. The binding properties of this protein with the outer membrane of the host and of the parasite are identical. An analogous phenomenon also occurs during Bdellovibrio parasitism on Klebsiella pneumoniae and on Salmonella typhimurium. Possible roles for this scavenging action of Bdellovibrio, and similar phenomena in other parasitic systems, are discussed.

Bacterial Outer Membrane Proteins↗

Quantification of parasite development in the host-parasite system Biomphalaria glabrata and Schistosoma mansoni.

The visceral mass of Biomphalaria glabrata uninfected or infected with Schistosoma mansoni was serially sectioned. The amount of hepatopancreas tissue and of parasite tissue was quantified. In pool-infected snails the volume of the whole visceral mass increased very significantly until week 6 and then decreased. Due to the growing parasites the volume of the visceral mass in infected snails was at most times higher when compared with uninfected snails of the same dimensions. Two weeks p.i. there was a permanent and significant increase of parasite tissue until week 6. During this time the amount of hepatopancreas tissue still increased. From this time onwards till week 12 the proportion of parasite tissue remained rather constant, indicating a kind of regulation, whereas the hepatopancreas tissue decreased to about one-third of the volume found in uninfected snails of the same shell diameter. Compared with infections by a single miracidium there was a significant increase in parasite tissue after infection with two miracidia. Infections with more miracidia (5, 10, and 20) gave no significant further increase. This also demonstrates a kind of regulation. Mortality rate, growth rate and egg production were studied during an infection period of 12 weeks.

Animals↗

On the evolutionary ecology of host-parasite interactions: addressing the question with regard to bumblebees and their parasites.

Over the last decade, there has been a major shift in the study of adaptive patterns and processes towards including the role of host-parasite interactions, informed by concepts from evolutionary ecology. As a consequence, a number of major questions have emerged. For example, how genetics affects host-parasite interactions, whether parasitism selects for offspring diversification, whether parasite virulence is an adaptive trait, and what constrains the use of the host's immune defences. Using bumblebees, Bombus spp, and their parasites as a model system, answers to some of these questions have been found, while at the same time the complexity of the interaction has led expectations away from simple theoretical models. In addition, the results have also led to the unexpected discovery of novel phenomena concerning, for instance, female mating strategies.

Animals↗

Niche breadth in parasites: an evolutionarily stable strategy model, with special reference to the protozoan parasite Leishmania.

A parasite's host range essentially defines its niche breadth, which, as foraging theory predicts, is influenced by resource availability. For parasites, the interaction of infection and transmission characteristics with host population dynamics determines host availability. An epidemiological model, involving two host types and describing competition between a "generalist" parasite strain and a related "specialist" strain, is used to examine the interplay among host range, relative host availabilities, and adaptational compromises engendered by increased host range. Results show that the generalist can predominate even when it cannot maintain itself in either host alone, but that the specialist can persist if its reproductive rate attains some threshold relative to either of the generalist's respective rates in its two hosts. The model is in rough, qualitative agreement with observed dynamics of two Leishmania parasite-host systems, and overall results suggest that infection of two species with a common parasite can lead to complex, indirect coevolutionary dynamics.

Adaptation, Biological↗

Peptidyl-prolyl cis-trans isomerases (immunophilins) and their roles in parasite biochemistry, host-parasite interaction and antiparasitic drug action.

Immunophilin is the collective name given to the cyclophilin and FK506-binding protein families. As the name suggests, these include the major binding proteins of certain immunosuppressive drugs: cyclophilins for the cyclic peptide cyclosporin A and FK506-binding proteins for the macrolactones FK506 and rapamycin. Both families, although dissimilar in sequence, possess peptidyl-prolyl cis-trans isomerase activity in vitro and can play roles in protein folding and transport, RNA splicing and the regulation of multi-protein complexes in cells. In addition to enzymic activity, many immunophilins act as molecular chaperones. This property may be conferred by the isomerase domain and/or by additional domains. Recent years have seen a great increase in the number of known immunophilin genes in parasitic protozoa and helminths and in many cases their products have been characterised biochemically and their temporal and spatial expression patterns have been examined. Some of these genes represent novel types: one example is a Toxoplasma gondii gene encoding a protein with both cyclophilin and FK506-binding protein domains. Likely roles in protein folding and oligomerisation, RNA splicing and sexual differentiation have been suggested for parasite immunophilins. In addition, unexpected roles in parasite virulence (Mip FK506-binding protein of Trypanosoma cruzi) and host immuno-modulation (e.g. 18-kDa cyclophilin of T. gondii) have been established. Furthermore, in view of the potent antiparasitic activities of cyclosporins, macrolactones and non-immunosuppressive derivatives of these compounds, immunophilins may mediate drug action and/or may themselves represent potential drug targets. Investigation of the mechanisms of action of these agents may lead to the design of potent and selective antimalarial and other antiparasitic drugs. This review discusses the properties of immunophilins in parasites and the 'animal model'Caenorhabditis elegans and relates these to our understanding of the roles of these proteins in cellular biochemistry, host-parasite interaction and the antiparasitic mechanisms of the drugs that bind to them.

Amino Acid Sequence↗

Sexual showiness and parasite load: correlations without parasite coevolutionary cycles.

Hamilton & Zuk (1982, Science 218, 384-387.) produced a model of sexual selection in which coevolutionary cycles of host and parasites generate consistently positive correlations between parent and offspring viability, and that animals choose mates for genetic disease resistance by scrutinizing characters whose full expression is dependent on health and vigour. They predicted a positive correlation between sexual showiness and parasite burden across species, and a negative correlation within a species. First, recent suggestions that interspecific correlations in the opposite direction to that indicated above are consistent with the mechanisms of Hamilton & Zuk's model are discussed. Second, it is shown that the model's predictions can be produced by heritable variation maintained by non-parasite fluctuating selection. In this case, the parasites associated with degree of sexual showiness are those able to amplify any initial heritable differences in vigour. Alternative sources of positive correlation between parent and offspring viability, which include the indirect effects of climatic change and exclude the need for host-parasite coevolutionary cycles, are also proposed.

Animals↗

Apoptosis and parasitism: from the parasite to the host immune response.

Apoptosis, a form of programmed cell death (PCD), plays a central role in normal tissue development as well as in the pathogenesis of different diseases. PCD is responsible for the non-inflammatory physiological elimination of potentially harmful or unnecessary cells during embryogenesis, and for the proper functioning of continuous cell renewal systems in adult organisms. Maturation of the immune system and the specific immune response are examples of situations where PCD plays important roles. This review discusses the importance of apoptosis in two fundamental elements of a host-parasite interaction: the parasite (Section 1), and the host's immune response (Section 2). Section 1 discusses questions raised by the description of apoptosis in unicellular eukaryotes, such as the evolutionary origin of the molecular components of PCD, its role in the emergence and maintenance of parasitism, and the constraints of a multicellular organization for the proper operation of a cell death programme. The proposal is that PCD can occur in any situation where living cells display features of an organized network which operates through interactions within themselves and/or with elements of their environment. The possibility is also discussed that evolutionary relics of a complete cell death system may operate in unicellular parasites with functions other than inducing cell death. Section 2 reviews data on the mechanisms of host-cell PCD and the consequences of this phenomenon in host defence and pathogenesis. Infectious agents, from viruses to parasites, can either delay or induce apoptosis of different types of host cells. Apoptosis following lymphocyte polyclonal activation and stimulation of peripheral T lymphocytes, as a result of the engagement of specific counter-receptor systems, is of special interest for defining host immunocompetence and mechanisms of immunopathology.

Animals↗

Intracellular protozoan parasites and apoptosis: diverse strategies to modulate parasite-host interactions.

Programmed cell death (apoptosis) is an important regulator of the host's response during infection with a variety of intracellular protozoan parasites. Parasitic pathogens have evolved diverse strategies to induce or inhibit host-cell apoptosis, thereby modulating the host's immune response, aiding dissemination within the host or facilitating intracellular survival. Here, we review the molecular and cell-biological mechanisms of the pathogen-induced modulation of host-cell apoptosis and its effects on the parasite-host interaction and the pathogenesis of parasitic diseases. We also discuss the previously unrecognized phenomenon of apoptotic cell death in (unicellular) protozoan parasites and its potential implications.

Animals↗

Rapid changes in the surface of parasitic nematodes during transition from pre- to post-parasitic forms.

All mammalian-parasitic stages of a range of nematode species investigated (Brugia pahangi, Acanthocheilonema viteae, Strongyloides ratti, Nippostrongylus brasiliensis, Trichinella spiralis and Ostertagia ostertagi) labelled in a surface-restricted manner with the fluorescent lipid analogues 5-N-(octadecanoyl)aminofluorescein (AF18) or nitrobenzoxadiazole-cholesterol (NBD-chol), but failed to bind other similar probes. In contrast, the surfaces of the 'pre-parasitic' infective stages of these species had affinity for neither AF18 nor NBD-chol. This exclusion of lipid analogues changed rapidly upon exposure of the larvae to tissue culture conditions which mimic the mammalian tissue environment (e.g. RPMI 1640/37 degrees C) such that the above probes could then insert into the surface layer of the larvae. The dauer larva of Caenorhabditis elegans also excluded the probes, but became permissive to labelling upon stimulation to emerge from the dauer state. The time taken for the surface transformation to occur ranged from less than 10 min in the vector-borne parasites to approximately 5 h in those which enter by the oral route, with direct skin-penetrators occupying an intermediate position. In all cases, the alteration proceeded too rapidly for it to have been associated with a moult. Fluorescence Recovery After Photobleaching (FRAP) studies of A. viteae larvae showed that approximately 50% of the AF18 probe was free to diffuse within the plane of the surface immediately after transformation. This is only a transitory state because AF18 was found to be highly restricted in its lateral diffusion on the surface of adult parasites. In the larvae of S. ratti, the change in affinity for AF18 was accompanied by the rapid shedding of an otherwise stable surface coat of polyanionic material, here visualized by labelling with fluorescein-conjugated cationized ferritin. Incubation of larvae in lipid-rich host serum during the induction of transformation inhibited subsequent labelling with AF18. This possibly reflects competition for insertion sites and an in vivo propensity towards the acquisition of host lipid by invading parasites.

Animals↗

Effects of host condition on susceptibility to infection, parasite developmental rate, and parasite transmission in a snail-trematode interaction.

Whether or not organisms become infected by parasites is likely to be a complex interplay between host and parasite genotypes, as well as the physiological condition of both species. Details of this interplay are very important because physiology-driven susceptibility has the potential to confound genetic coevolutionary responses. Here we concentrate on how physiological aspects of infection may interfere with genetic-based infectivity in a snail-trematode (Potamopyrgus antipodarum/Microphallus sp.) interaction by asking: (1) how does host condition affect susceptibility to infection? and (2) how does host condition affect the survival of infected individuals? We manipulated host condition by experimentally varying resources. Contrary to our expectation, host condition did not affect susceptibility to infection, suggesting that genetics are more important than physiology in this regard. However, hosts in poor condition had higher parasite-induced mortality than hosts in good condition. Taken together, these results suggest that coevolutionary interactions with parasites may depend on host condition, not by altering susceptibility, but rather by affecting the likelihood of parasite transmission.

Animals↗

Host-parasite relatedness shown by protein fingerprinting in a brood parasitic bird.

Brood parasitism as an alternative female breeding tactic is particularly common in ducks, where hosts often receive eggs laid by parasitic females of the same species and raise their offspring. Herein, we test several aspects of a kin selection explanation for this phenomenon in goldeneye ducks (Bucephala clangula) by using techniques of egg albumen sampling and statistical bandsharing analysis based on resampling. We find that host and primary parasite are indeed often related, with mean r = 0.13, about as high as between first cousins. Relatedness to the host is higher in nests where a parasite lays several eggs than in those where she lays only one. Returning young females parasitize their birth nestmates (social mothers or sisters, which are usually also their genetic mothers and sisters) more often than expected by chance. Such adult relatives are also observed together in the field more often than expected and for longer periods than other females. Relatedness and kin discrimination, which can be achieved by recognition of birth nestmates, therefore play a role in these tactics and probably influence their success.

Animals↗

Organization of ETRAMPs and EXP-1 at the parasite-host cell interface of malaria parasites.

The parasite-host cell interface is a key compartment of vacuolated intracellular pathogens but little is known about its molecular composition and architecture. We used in vivo cross-linking to analyse the parasite-host cell interface of asexual stages of the most virulent human malaria parasite Plasmodium falciparum. We show that the integral membrane protein members of the early transcribed membrane protein (ETRAMP) family and exported protein 1 (EXP-1), which are components of the parasite-host cell interface, form complexes of oligomeric arrays in this compartment. The most notable feature is that each ETRAMP member and EXP-1 define separate arrays, demonstrating that the protein distribution in this membrane is non-random. Each of three recombinant ETRAMPs readily oligomerized in bacterial membranes, confirming that these arrays can form independently of other Plasmodium proteins. We propose that the malaria parasite-host cell interface contains patches of integral membrane proteins forming a mosaic of different microdomains in this membrane.

Animals↗

Relationships between the parasitic mite Spinturnix andegavinus (Acari: Spinturnicidae) and its bat host, Myotis daubentonii (Chiroptera: Vespertilionidae): seasonal, sex- and age-related variation in infestation and possible impact of the parasite on the host condition and roosting behaviour.

Host-parasite relationships between the Daubenton's bat, Myotis daubentonii Kuhl, 1817 (Chiroptera: Vespertilionidae), and its haematophagous ectoparasite, the mite Spinturnix andegavinus Kolenati, 1857 (Acari: Spintumicidae), were subjected to analyses based on data gathered during a six-year study (1999-2004) within a single study area in South Bohemia, Czech Republic. Seven hundred and fifty-one Daubenton's bats were examined by screening wing membranes with an intensive light source, resulting in 4,690 recorded mites. Sex, age, weight and reproductive state were evaluated for each bat. A body condition index was calculated as a ratio of weight to forearm length. The seasonal course of mite infestation displayed distinct dynamics with the peak during the lactation and post-lactation periods coinciding with occurrence of the most numerous colonies of Daubenton's bats in the study area. Infestation rates differed between the two sexes, being higher in adult females than adult males. Juvenile bats of both sexes (with no differences between males and females) were the most infested group of all. Pregnant females had a significantly higher parasite load than non-pregnant ones, while no differences in infestation rates were found between lactating and non-lactating females. The analyses of the relationship between parasite load and body condition of bats revealed no common trends for all sex- and age-related groups. Two possible explanations are suggested and discussed: (1) There is no true relationship between the two tested variables and, thus, the significant results were attained due to a random statistical effect. (2) Different underlying causal mechanisms may exist that influence parasite load and, especially, body condition, with respect to the particular sex and age category of bats. The seasonal roosting dynamics of the Daubenton's bat are suggested to be the result not only of changing energetic demands of resident population members, but also of coevolutionary strategies within host-parasite relationships.

Acari↗

Regulatory networks induced by live parasites impair both Th1 and Th2 pathways in patent lymphatic filariasis: implications for parasite persistence.

Patent lymphatic filariasis is characterized by a profound down-regulation of immune responses with both parasite Ag-specific tolerance and bystander suppression. Although this down-regulation is confined to the Th1 arm of the immune system in response to parasite Ag, we hypothesized a more generalized suppression in response to live parasites. Indeed, when we examined the cytokine profile of a cohort of filaria-infected (n = 10) and uninfected (n = 10) individuals in response to live infective-stage larvae or microfilariae of Brugia malayi, we found significant impairment of both Th1 and Th2 cytokines characterized by diminished production of IFN-gamma, TNF-alpha, IL-4, IL-5, and IL-10 in infected patients. The molecular basis of this impaired Th1/Th2 response was examined, and we identified three major networks of immunoregulation and tolerance. First, impaired induction of T-bet and GATA-3 mRNA underlies the Th1/Th2 deficiency in infected individuals. Second, regulatory networks, as evidenced by significantly increased expression of Foxp3 (natural regulatory T cell marker) and regulatory effectors such as TGF-beta, CTLA-4, PD-1, ICOS, and indoleamine 2,3-dioxygenase play an important role in immunosuppression. Third, the compromise of effector T cell function is mediated by the enhanced induction of anergy-inducing factors cbl-b, c-cbl (cbl is abbreviation for Casitas B lymphoma), Itch, and Nedd4. Indeed, blocking CTLA-4 or neutralizing TGF-beta restored the ability to mount Th1/Th2 responses to live parasites and reversed the induction of anergy-inducing factors. Hence, we conclude that a profound impairment of live parasite-specific Th1 and Th2 immune responses occurs in lymphatic filariasis that is governed at the transcriptional level by a complex interplay of inhibitory mediators.

Animals↗

Occurrence of prostaglandins and other eicosanoids in parasites and their role in host-parasite interaction.

Prostaglandins have been already pretty well recognized as metabolic regulators in vertebebrata tissues mainly in mammals. I.ess reports concerned the occurrence of prostaglandins in invertebrates. In the present review we summarise literature data about the presence of prostaglandins and other eicosanoids in various groups of parasites and their possible role in host-parasite interaction. Prostaglandins have also been found in very primitive organisms as bacteria, varions plants and protozoa. We summarise that prostaglandins seem to be a very ancient group, going back to the roots of evolution. They are as universal in cell physiology as DNA in genetics. In host-parasiter eicosanoids also parasitic origin, play an important role as a modulators of hosts immune responsiveness.

Animals↗

Imprinting and the origin of parasite-host species associations in brood-parasitic indigobirds, Vidua chalybeata.

Brood-parasitic village indigobirds, Vidua chalybeata, were bred in captivity and foster-reared by their normal host species, the red-billed firefinch, Lagonosticta senegala, or by an experimental foster species, the Bengalese finch, Lonchura striata. Captive-reared female indigobirds were tested as adults for mate choice and for host choice. In tests of mate choice, female indigobirds responded preferentially towards mimicry songs of male indigobirds that were similar to those of the females' own foster parents. Females reared by Bengalese finches responded to male songs that mimicked Bengalese finch song rather than to male songs that mimicked their normal host species, the firefinch. In tests of host choice, females reared by Bengalese finches laid in the nests of Bengalese finches, and females reared by firefinches laid in the nests of firefinches. Wild-caught females showed the same behaviours as captive-bred females reared by firefinches. A female indigobird's social companions (firefinch or Bengalese) following her independence of her foster parents had no effect on her sexual response to male mimicry song or her choice of a host species in brood parasitism. The results support the predictions of a model of imprinting-like behaviour development in which young indigobirds focus their attention on their foster parents, rather than a model of innate bias for songs and nests of their normal host species, or a null model of nonspecific brood parasitism and differential survival. The results provide experimental support for the recent origin of brood parasite-host associations and the significance of imprinting in speciation in these brood parasites. Copyright 2000 The Association for the Study of Animal Behaviour.

Journal Article↗

Population biology of the parasitic phase of trichostrongylid nematode parasites of cattle and sheep.

This paper reviews the previous mathematical and conceptual models for the parasitic phase of a range of trichostrongylid nematode parasites of cattle and sheep. It reassesses the results of single and trickle infection experiments and suggests as a working hypothesis that the common trichostrongylids are essentially identical with respect to the processes that determine their survivorship in the host. Parasite abundance in the parasitic phase is explained in terms of immune exclusion, which acts on recently ingested third stage larvae, and mortality of established (fifth stage) parasites. The functional forms used to describe immune exclusion and the mortality of fifth stage worms are defined, respectively, as a declining sigmoid and an asymptotic curve.

Animals↗

Use of a DNA probe to analyse the dynamics of infection with rodent malaria parasites confirms that parasite clearance during crisis is predominantly strain- and species-specific.

A DNA probe, PCsv4.1, isolated from Plasmodium chabaudi chabaudi AS, generates in Southern blotting experiments restriction fragment length polymorphisms specific to a particular rodent malaria parasite line. It was used to develop an assay which allows identification and semi-quantitative compositional analysis of sample parasite populations in which one or more strains, subspecies or species were present. In experiments where mechanisms effecting parasite clearance during crisis were studied, the assay was used to determine the composition of parasite populations present in P. c. chabaudi AS infected mice challenged during crisis with homologous or heterologous parasites. It was thus confirmed that clearance mechanisms during crisis operate in a predominantly specific manner.

Animals↗