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PubMed1996

Influence of host and parasite genotypes on immunological control of Theileria parasites.

Infections with Theileria parva in the African buffalo are invariably asymptomatic, whereas infections in cattle usually result in clinical disease, the severity of which varies in different populations of cattle. The parasite exhibits antigenic heterogeneity, which in cattle manifests as differences between parasite strains in their cross-protective properties. A series of studies on T cell responses to T. parva in cattle have demonstrated that class I MHC-restricted cytotoxic T lymphocytes (CTL), specific for parasitized lymphoblasts, are important mediators of immunity. Cytotoxic T cell responses frequently display parasite strain-restricted specificities which appear to correlate with the capacity of strains to cross-protect. The strain specificity of CTL responses varies in animals immunized with the same parasite strain and is influenced by both host and parasite genotype. Recent studies have provided evidence that there is competition between epitopes for induction of CTL responses, which can result in a bias to strain-specific epitopes. These properties of the CTL response have important implications for vaccination. Thus, in designing a vaccine, it may be possible, by selecting parasite proteins containing appropriate CTL epitopes, to generate CTL responses that protect against a wide range of parasite strains. Although there are no comparable data on CTL responses in the buffalo, it is considered that the features of the immune response described for cattle would be advantageous for survival of parasite populations in the buffalo. Specifically, a bias in the immune responses to strain-specific determinants should favor establishment of infection in buffalo already carrying the parasite and allow fluctuation in the levels of different parasite strains during the course of persistent infection.

Animals↗
PubMedDate not supplied

[Parasitic systems under the conditions of human pressures (the problems of parasitic contamination)].

Foundations of the Parasitic Contamination (PC) conception being considered as an element of biological contamination and manifested itself in urbanized ecosystems under an influence of diversiform ecological (amenable to anthropopressure) and socio-economical factors are presented. PC is regarded as the "superthreshold" contamination exceeding the "natural background" (i.e. the parasitological situation outside urbanized ecosystems). As a rule, PC is accompanied with events as follow: an increase (often explosive in character) of hosts' number of all ranks, of vectors numbers and finally of parasites' numbers (parasitic expression); a partial replacement of parasite faunas (parasitic succession); a capture of new territories and hosts (parasitic expansion). As a rule, all processes run synchronously. They lead to disturbances of evolutionary generated relations (quantitative and qualitative ones) in parasitic systems and thereafter to changes in a tension of epidemic, epizootic and epiphytotic processes. It is assumed, that rates of evolutionary processes going in parasitic systems is increased at the recent historical stage. Their entropy character is being changed: they often transform from more of less regulated (balanced) processes, which were achieved in a long course of component coevolution, into chaotic (unbalanced) ones. It is stimulated with a powerful and at the same time differently vectored anthropogenic pressure onto parasitic system components. It promotes inhibition processes involved in generating of a natural parasite-host mutual adaptation.

Animals↗
PubMed2003

Intracellular parasitism: cell biological adaptations of parasitic protozoa to a life inside cells.

Several protozoan parasites evade the host's immune defence because most of their development takes place inside specific host cells. Only a few of these protozoa live within the host cell cytosol. Most parasites are sequestered within membrane-bound compartments, collectively called 'vacuoles'. Recent advances in the cell biology of intracellular parasites have revealed fundamental differences in the strategies whereby such organisms gain entry into their respective host cells. These differences have important implications for host-parasite interaction and for nutrient acquisition by the parasite. Leishmania spp. take advantage of the phagocytic properties of their host cells and presumably contribute little to the uptake process. In contrast, apicomplexan parasites have developed highly specialised organelles, called micronemes and rhoptries, to actively invade a variety of nucleated cells and, in the case of Plasmodium falciparum, human erythrocytes. Following invasion, parasites use a multitude of strategies to protect themselves from the defence mechanisms of the parasitized cells. In addition, they induce novel pathways within the infected cell that allow a most efficient nutrient acquisition both from the host cell cytoplasm and from the extracellular environment. Parasite-induced changes of host cells are most apparent in erythrocytes infected with Plasmodium spp. Mammalian erythrocytes are deficient in de novo protein and lipid biosynthesis and, consequently, pathways which allow the transport of macromolecules and small solutes are established by metabolic activities of the parasite. Research into the cell biology of intracellular parasitism has identified fascinating phenomena some of which we are beginning to understand at a molecular level. They are fascinating because they allow insights into a very intimate interaction between two eukaryotic cells of entirely different phylogenetic origins.

Journal Article↗
PubMed2002

The evolution of parasites from their hosts: intra- and interspecific parasitism and Emery's rule.

In some taxa of Hymenoptera, fungi, red algae and mistletoe, parasites and their hosts are either sibling species or at least closely related (Emery's rule). Three evolutionary mechanisms have been proposed for this phenomenon: (i) intraspecific parasitism is followed by sympatric speciation; (ii) allopatric speciation is followed by secondary sympatry and the subsequent parasitism of one sibling species by the other; and (iii) allopatric speciation of a species with intraspecific parasitism is followed by secondary sympatry, in which one species becomes an obligate parasite of the other. Mechanisms (i) and (ii) are problematic, while mechanism (iii) has not, to our knowledge, been analysed quantitatively. In this paper, we develop a model for single- and two-species evolutionary stable strategies (ESSs) to examine the basis for Emery's rule and to determine whether mechanism (iii) is consistent with ESS reasoning. In secondary sympatry after allopatric speciation, the system's evolution depends on the relative abundances of the two sibling species and on the proportional damage wrought by parasites of each species on non-parasitic members of the other. Depending on these interspecific effects, either the rarer or the commoner species may become the parasite and the levels of within-species parasitism need not determine which evolves to obligate parasitism.

Animals↗
PubMedDate not supplied

[Parasitic systems and the population structure of parasitic organisms].

The analysis of population systems is carried out on the basis of the classification of spatial and functional structure of populations developed by V. N. Beklemishev. Two aspects of the structure of population systems are established. Firstly, population systems are composed of the smaller groups characterised by different self-maintenance ability. Secondly, different functional parts are included into these systems in accordance with different stages (phases) of a life cycle. Peculiarities of the population systems are discussed from these points of view. The population system is a functional part of a particular community. Steady interrelationships between population systems in the community ("community links") are the basis on which the complexes of population systems in different species are formed. A prominent example of this is the parasitic systems, that is the population system of a parasite and all connected populations of its hosts. The structure of a parasitic system is examined. In general, it is characterised by a) peculiarities of the life cycle of the parasite, since its population systems are the organising component of the parasitic system; b) subdivision of the environment for parasites. The first trait is discussed from the standpoint of phase structure of populations which is could be clearly seen in parasites, and the second one-from the viewpoint of the availability of distinct microbiotopes connected with different parts of the population system of parasites. It is the subdivision of the parasites' environment and its organisation according to the scale (interspecies, interpopulation or intrapopulation) variability of the hosts, that make it possible to recognise spatial and functional parts in the framework of the parasitic system. The critical review of the terminology used in the population parasitology is presented.

Animals↗
PubMed1982

Processes influencing the distribution of parasite numbers within host populations with special emphasis on parasite-induced host mortalities.

The paper examines the factors which generate various patterns of dispersion in the distribution of parasites within their host populations. Particular emphasis is placed on the role played by chance elements in the growth and decay of parasite populations and on the influence of different types of demographic processes. It is argued that observed distributions are dynamic, rather than static, entities generated by opposing forces, some acting to create over-dispersion and others acting to generate under-dispersion. Monte Carlo simulation experiments, based on probability models of the growth and decay of host and parasite populations, are used to study the dynamics of parasite dispersion. Attention is specifically focused on the role played by parasite-induced host mortality. It is shown that, for certain types of host-parasite associations, convex curves of mean parasite abundance in relation to age (age-intensity curves), concomitant with a decline in the degree of dispersion in the older age, classes of hosts, may be evidence of the induction in host mortality by parasite infection. Empirical evidence is examined in light of this prediction. In general, however, simulation studies highlight the technical difficulties inherent in establishing clear evidence of parasite-induced host mortality from ecological studies of hosts and parasites in their natural habitats.

Aging↗
PubMed2000

Eicosanoids in parasites and parasitic infections.

Eicosanoids are lipid mediators with multiple functions in vertebrate tissues and invertebrate organisms. In this review the roles of eicosanoids--mostly prostaglandins (PGs), thromboxanes and leukotrienes--in parasite physiology and host-parasite interactions are discussed. PGs are present in the saliva of blood-sucking arthropods facilitating feeding by increasing local blood flow and prolonged attachment of ticks by immune suppression. Release of various eicosanoids has also been demonstrated for a number of protozoan and metazoan endoparasites. These substances appear to play a role in penetration, immune suppression, inflammation or modulation of haemostasis, enabling parasite invasion and establishment. Moreover, endogenous eicosanoids serve various functions in parasite metabolism and physiology. In many parasitic infections eicosanoids are involved in host pathology, e.g. granuloma formation, coagulopathy, secretory diarrhoea, or fever. Immune suppression by induction of PG release, in particular PGE2, by host defence cells appears to be a common feature of many parasitic infections and is though to be important for parasite establishment. Contradictory results have been obtained for gastrointestinal nematode infections, which probably reflect the considerable differences between the various models employed. Although most of the available studies indicate an important role for eicosanoids in parasites and parasitic infections, our current knowledge is still fragmentary and more data are urgently needed.

Animals↗
PubMed1984

Intracellular parasite killing induced by electron carriers. II. Correlation between parasite killing and the induction of oxidative events in macrophages.

Mouse peritoneal macrophages infected with Leishmania parasites were exposed in vitro to the electron carriers methylene blue (MB), toluidine blue 0 (TB), phenazine methosulfate (PMS) and crystal violet (CV). This led to parasite destruction without harm to the macrophages. The kinetics of intracellular killing depended on both the drug concentration and the duration of exposure; over 80% of the microorganisms were inactivated within 2.5 min of incubation of the parasitized cells with 10(-4) M MB. On a molar basis, the drugs were considerably more active against intracellular compared to free parasites, suggesting that the macrophages themselves play a role in the observed anti-parasite toxicity. Intracellular killing by macrophages exposed to MB, TB and PMS correlated with the stimulation of oxygen uptake and hexose monophosphate shunt activity in the cells. Cytochrome c markedly inhibited MB-induced intracellular parasite destruction as well as completely blocking parasite killing in macrophages activated by lymphokines, pointing to O-2, H2O2 or products derived therefrom as possible mediators of macrophage toxic activity in both instances. Cytochrome c did not protect free parasites from the direct toxicity of the drug, however. Lipopolysaccharide promoted parasite destruction by lymphokine-activated macrophages, but failed to do so for electron carrier-stimulated cells. These observations suggest that intracellular killing induced by electron carriers results from a direct interaction of the drugs with cellular redox systems, leading to the generation of oxygen metabolites toxic for the parasites.

Animals↗
PubMed2000

Vacuolar H(+)-ATPase localized in plasma membranes of malaria parasite cells, Plasmodium falciparum, is involved in regional acidification of parasitized erythrocytes.

Recent biochemical studies involving 2',7'-bis-(2-carboxyethyl)-5, 6-carboxylfluorescein (BCECF)-labeled saponin-permeabilized and parasitized erythrocytes indicated that malaria parasite cells maintain the resting cytoplasmic pH at about 7.3, and treatment with vacuolar proton-pump inhibitors reduces the resting pH to 6.7, suggesting proton extrusion from the parasite cells via vacuolar H(+)-ATPase (Saliba, K. J., and Kirk, K. (1999) J. Biol. Chem. 274, 33213-33219). In the present study, we investigated the localization of vacuolar H(+)-ATPase in Plasmodium falciparum cells infecting erythrocytes. Antibodies against vacuolar H(+)-ATPase subunit A and B specifically immunostained the infecting parasite cells and recognized a single 67- and 55-kDa polypeptide, respectively. Immunoelectron microscopy indicated that the immunological counterpart of V-ATPase subunits A and B is localized at the plasma membrane, small clear vesicles, and food vacuoles, a lower extent being detected at the parasitophorus vacuolar membrane of the parasite cells. We measured the cytoplasmic pH of both infected erythrocytes and invading malaria parasite cells by microfluorimetry using BCECF fluorescence. It was found that a restricted area of the erythrocyte cytoplasm near a parasite cell is slightly acidic, being about pH 6.9. The pH increased to pH 7.3 upon the addition of either concanamycin B or bafilomycin A(1), specific inhibitors of vacuolar H(+)-ATPase. Simultaneously, the cytoplasmic pH of the infecting parasite cell decreased from pH 7.3 to 7.1. Neither vanadate at 0.5 mm, an inhibitor of P-type H(+)-ATPase, nor ethylisopropylamiloride at 0.2 mm, an inhibitor of Na(+)/H(+)-exchanger, affected the cytoplasmic pH of erythrocytes or infecting parasite cells. These results constitute direct evidence that plasma membrane vacuolar H(+)-ATPase is responsible for active extrusion of protons from the parasite cells.

Acids↗
PubMed1995

Fate of Parasite and Host Organelle DNA during Cellular Transformation of Red Algae by Their Parasites.

The transfer of a nucleus into a cytoplasm of a genetically foreign cell and its subsequent multiplication in the cytoplasm of this cell characterize most parasitic red algal species and their interactions with specific red algal hosts. Nuclei enter the host's cytoplasm upon cell fusion of parasite and host cell; here, they replicate, are spread to contiguous host cells, and ultimately are packaged into spores that reinfect other host thalli. In this study, we examined whether the proplastids and mitochondria that occur in these red algal adelphoparasites are acquired from their host or whether they are unique to the parasite and are brought into the host along with the parasite nucleus. To establish their origins and fates, plastid and mitochondrial restriction fragment length polymorphisms (RFLPs) of parasite cells were compared with those of their host plastid and mitochondrial DNA in three host and parasite pairs. For plastids, no RFLP differences were found between hosts and parasites, supporting an earlier conclusion, based on microscopic studies, that the proplastids of parasites are acquired from their hosts. For mitochondria, characteristic RFLP differences were detected between host and parasite for two of the pairs of species but not for the third. Evidence of the evolutionary difference between hosts and their parasites was shown by RFLP differences between nuclear ribosomal repeat regions.

Journal Article↗
PubMed2001

Recognition of social parasites as nest-mates: adoption of colony-specific host cuticular odours by the paper wasp parasite Polistes sulcifer.

Colonies of the polistine wasp Polistes dominulus are parasitized by the permanent worker-less social parasite Polistes sulcifer. After usurpation of the host colony, parasite females are characterized by a change in the relative proportions of their cuticular hydrocarbons to match those of the host species. In this paper we present evidence from field data and laboratory experiments that P. sulcifer females adopt a colony-specific host odour that facilitates their acceptance by host females of the usurped colony. Presentation experiments demonstrate that parasite females are recognized as foreign individuals by workers of other parasitized nests. We show that the modification of parasite cuticular compounds is sufficient for this recognition. This provides evidence that, after invasion, P. sulcifer queens do not require appeasement or propaganda substances for their acceptance by host colonies. Furthermore, multivariate discriminant analysis of the cuticular hydrocarbon proportions of the parasites after usurpation assigns the parasites together with P. dominulus females of their own host colony. To the authors' knowledge, this is the first confirmation that social parasites adopt colony-specific host odours.

Animals↗
PubMed2002

The bittersweet interface of parasite and host: lectin-carbohydrate interactions during human invasion by the parasite Entamoeba histolytica.

Entamoeba histolytica, as its name suggests, is an enteric parasite with a remarkable ability to lyse host tissues. However, the interaction of the parasite with the host is more complex than solely destruction and invasion. It is at the host-parasite interface that cell-signaling events commit the parasite to (a) commensal, noninvasive infection, (b) developmental change from trophozoite to cyst, or (c) invasion and potential death of the human host. The molecule central to these processes is an amebic cell surface protein that recognizes the sugars galactose (Gal) and N-acetylgalactosamine (GalNAc) on the surface of host cells. Engagement of the Gal/GalNAc lectin to the host results in cytoskeletal reorganization in the parasite. The parasite cytoskeleton regulates the extracellular adhesive activity of the lectin and recruits to the host-parasite interface factors required for parasite survival within its host. If the parasite lectin attaches to the host mucin glycoproteins lining the intestine, the result is commensal infection. In contrast, attachment of the lectin to a host cell surface glycoprotein leads to lectin-induced host cell calcium transients, caspase activation, and destruction via apoptosis. Finally, trophozoite quorum sensing via the lectin initiates the developmental pathway resulting in encystment. The structure and function of the lectin that controls these divergent cell biologic processes are the subject of this review.

Amebiasis↗
PubMed1994

[Parasitic specificity and development of stray parasites of animal origin in man].

As on introduction to the selected topic, the author, after conjuring up the problem of parasite specificity, describes the various biological behaviour of parasites of animal origin having got into man. So doing, he quotes two main types of parasitic zoonoses (1) holozoonoses, in which the parasites are able to pass from animals to man and back; (2) hemi-zoonoses, in which parasites cannot go back from man to animals. The latter are due: (a) either to the inability for the parasite to reach, in man, the stage which would enable it to follow on its life cycle; this is a biological phenomenon: man is a dead-lock for the parasite; (b) or to the necessity for a parasite having reached a suitable stage in man, to go back-to animal through predation of man by the animal; this is an ethological phenomenon: man is a cul-de-sac for the parasite.

Animals↗
PubMed1997

[Implications of spatial aggregation of parasites for the population dynamics in host-parasite interaction].

Some aspects of the widely observed over-dispersed pattern of the distribution of parasites within the host population are examined. It has been established in the parasitological literature that most hosts usually harbour few parasites, while only few hosts harbour a large proportion of the parasite population. Factors that may influence the pattern of distribution of parasites, the relation between the level of parasite aggregation and the prevalence of infection, and changes in this level of aggregation as a function of host age are analysed. Factors which determine the diversity of species in parasite communities are presented, and aspects of exploitative and interference competition among parasites and their relations with biological control procedures are also considered. Attention is also focused on the regulatory and destabilizing processes influencing the dynamic behaviour of host-parasite population interactions.

Age Factors↗