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PubMedDate not supplied

[Host-parasite interactions between Coccus hesperidum L. (Hom. Coccidae) and its parasite Coccophagus scutellaris Dalman (Hym. Aphelinidae)].

The eggs laid in the host gut will develop normally. The larva resulting from those eggs penetrate the hemocele through the gut wall. The structure of the cells near the entry point is not affected because of the continuous renewal of those cells. On the other hand, development of the ovaries is most seriously affected. In fact, ovogenesis is stopped and vitellogenesis slowed down. But this phenomenon is related to the initial level of ovary development. If the attack takes place when the host is young, the effect on the ovaries is more serious. In extreme cases gonad development is annihilated. Otherwise, the host will still be able to lay eggs, but its reproduction capacity is diminished. Factors reducing development of gonads or maintaining them at a juvenile stage are discussed.

Animals↗
PubMed1998

Skin problems and parasites in children: 2. Parasitic worms.

The skin is an organ which has many important functions for body maintenance and health. Infestation by a wide variety of worms is a worldwide public health problem. Threadworms are believed to infect up to 50% of London school children. Dogs and other pets have much to teach children but regular care of pets should include attention to hygiene. Nurses and midwives can help to educate the public about worms and their advice can help prevent toxocara infections.

Adult↗
PubMed2000

The diversity of parasites.

Parasitism is one of the most successful modes of life displayed by living organisms, as measured by how often it evolved and how many parasitic species are presently in existence. Studying the diversity of parasites is particularly relevant because sympatric diversification may be important in some parasite taxa, and because of the opportunity for independent tests of evolutionary hypotheses in the many separate lineages in which parasitism evolved. Our incomplete knowledge of existing parasite species--the result of a range of phenomena that includes inadequate sampling effort or the lumping of different cryptic species under one name--is not always a major obstacle for the study of parasite diversity. Patterns in the diversity of parasites may be associated with either host or parasite characteristics. The distribution of parasite diversity among host taxa does not simply reflect the species diversity of the host taxa themselves; life history and ecological traits of hosts appear to play important roles. These may determine the likelihood that hosts are colonized by parasite species over evolutionary time. It is not yet clear whether some host traits also favor intrahost speciation and diversification of parasites, and the formation of new parasite species. Certain features of parasites may also be associated with speciation and diversification. Only parasite body size has received much attention; the patterns observed are not greatly different from those of free-living species, with small-bodied parasite taxa being more speciose than related large-bodied taxa. Epidemiological parameters such as the basic reproductive rate of parasites, or R0, can also generate predictions regarding the distribution or evolution of parasite diversity. For instance, parasite taxa characterized by high R0 values may be more speciose than related taxa with lower values of R0; such predictions remain untested. Large-scale biogeographical patterns of diversity have only been well studied for metazoan parasites of marine fish; for these parasites, latitudinal patterns can be explained by effects of temperature on speciation rates and epidemiological variables, though other causes are possible. The emphasis for future research must shift from pattern description to the elucidation of the processes responsible for the structure and diversity of parasite faunas. A better integration of ecological and historical (or phylogenetic) approaches to the study of parasite diversity should make this objective possible.

Animals↗
PubMed1987

Host effector mechanisms against parasites.

The first part of this presentation considers some of the complexities of parasitic infections and parasite-specific effector mechanisms which have hampered the development of practical methods of immunisation against parasitic diseases. In the second part, an outline is given of the effector mechanisms involved in immunity of cattle to the protozoan parasite Theileria parva. Parasites are antigenically complex organisms which often have distinct developmental stages, sometimes with different predilection sites within the host. Antigenic polymorphism between strains is a common feature of parasites and sometimes results in strain-specific immunity. Certain parasites have also evolved mechanisms of modulating surface antigens which allow them to escape host effector mechanism. Effector mechanisms which control parasitic infections may operate by preventing establishment of the parasites, by eliminating the parasites once they have established or by affecting growth or fecundity of the parasites. In addition to specific antibody and cell-mediated immune responses, inflammatory or physiological responses play an important role in the control of some parasites. Current evidence suggests that effector mechanisms against T.parva parasites operate at two levels. First, antibodies produced against the infective stage of the parasite, the sporozoite, can, by neutralising infectivity, reduce the numbers of organisms which establish in the host. Second, cytotoxic T cells directed against parasitised lymphoblasts cause destruction of parasites following their establishment in the host. Moreover, in situations where immunity is parasite strain-specific, the cytotoxic T cell responses have also been found to be strain-specific. The elucidation of these effector mechanisms has indicated potential new strategies of immunisation against T.parva.

Animals↗
PubMed1997

The malaria parasite supplies glutathione to its host cell--investigation of glutathione transport and metabolism in human erythrocytes infected with Plasmodium falciparum.

Malaria-infected red blood cells are under a substantial oxidative stress. Glutathione metabolism may play an important role in antioxidant defense in these cells, as it does in other eukaryotes. In this work, we have determined the levels of reduced and oxidized glutathione (GSH and GSSG, respectively) and their distributions in the parasite, and in the host-cell compartments of human erythrocytes infected with the malaria parasite Plasmodium falciparum. In intact trophozoite-infected erythrocytes, [GSH] is low and [GSSG] is high, compared with the levels in normal erythrocytes. Normal erythrocytes and the parasite compartment display high GSH/GSSG ratios of 321.6 and 284.5, respectively, indicating adequate antioxidant defense. This ratio drops to 26.7 in the host-cell compartment, indicating a forceful oxidant challenge, the low ratios resulting from an increase in GSSG and a decline in GSH concentrations. On the other hand, the concentrations of GSH and GSSG in the parasite compartment remain physiological and comparable to their concentrations in normal red blood cells. This results from de novo glutathione synthesis and its recycling, assisted by the intensive activity of the hexose monophosphate shunt in the parasite. A large efflux of GSSG from infected cells has been observed, its rate being similar from free parasites and from intact infected cells. This result suggests that de novo synthesis by the parasite is the dominating process in infected cells. GSSG efflux from the intact infected cell is more than 60-fold higher than the rate observed in normal erythrocytes, and is mediated by permeability pathways that the parasite induces in the erythrocyte's membrane. The main route for GSSG efflux through the cytoplasmic membrane of the parasite seems to be due to a specific transport system and occurs against a concentration gradient. Gamma-glutamylcysteine [Glu(-Cys)] and GSH can penetrate through the pathways from the extracellular space into the host cytosol, but not into that of the parasite. This implies that the parasite membrane is impermeable to these peptides, and that the host cannot supply GSH to the parasite as suggested previously. Exogenous Glu(-Cys) is not converted into GSH in the host cell, arguing that GSH synthetase may not be functional. Compartment analysis of Mg2+ in infected erythrocytes revealed that the host compartment exhibits a low concentration of Mg2+ (0.5 mM) in comparison with the parasite compartment (4 mM) and the normal erythrocytes (1.5-3 mM). The drop in [Mg2+] results in cessation of Glu(-Cys) synthesis, and hence of GSH synthesis in the host-cell compartment. The decrease in [Mg2+] can affect other Mg2+-ATP-dependent functions, such as Na+ and Ca2+ active efflux. The present investigation confirms that the host-cell compartment is oxidatively distressed, whereas the parasite is efficiently equipped with anti-oxidant means that protect the parasite from the oxidative injury. The parasite has a huge capacity for de novo synthesis of GSH and for the reduction of GSSG. Part of the GSSG that is actively extruded from the parasite is reduced to GSH in the host cell whose own GSH synthesis is crippled.

Animals↗
PubMed1988

The population biology of parasite-induced changes in host behavior.

The ability of parasites to change the behavior of infected hosts has been documented and reviewed by a number of different authors (Holmes and Bethel, 1972; Moore, 1984a). This review attempts to quantify the population dynamic consequences of this behavior by developing simple mathematical models for the most frequently recorded of such parasite life cycles. Although changes in the behavior of infected hosts do occur for pathogens with direct life cycles, they are most commonly recorded in the intermediate hosts of parasites with complex life cycles. All the changes in host behavior serve to increase rates of transmission of the parasites between hosts. In the simplest case the changes in behavior increase rates of contact between infected and susceptible conspecific hosts, whereas in the more complex cases fairly sophisticated manipulations of the host's behavioral repertory are achieved. Three topics are dealt with in some detail: (1) the behavior of the insect vectors of such diseases as malaria and trypanosomiasis; (2) the intermediate hosts of helminths whose behavior is affected in such a way as to make them more susceptible to predation by the definitive host in the life cycle; and (3) the behavior and fecundity of molluscs infected with asexually reproducing parasitic flatworms. In each case an expression is derived for R0, the basic reproductive rate of the parasite when first introduced into the population. This is used to determine the threshold numbers of definitive and intermediate hosts needed to maintain a population of the pathogen. In all cases, parasite-induced changes in host behavior tend to increase R0 and reduce the threshold number of hosts required to sustain the infection. The population dynamics of the interaction between parasites and their hosts are then explored using phase plane analyses. This suggests that both the parasite and intermediate host populations may show oscillatory patterns of abundance. When the density of the latter is low, parasite-induced changes in host behavior increase this tendency to oscillate. When intermediate host population densities are high, parasite population density is determined principally by interactions between the parasites and their definitive hosts, and changes in the behavior of intermediate hosts are less important in determining parasite density. Analysis of these models also suggests that both asexual reproduction of the parasite within a host and parasite-induced reduction in host fecundity may be stabilizing mechanisms when they occur in the intermediate hosts of parasite species with indirect life cycles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

[Parasitic zoonoses in Japan, with special reference to the current topics].

The present situation of parasitic zoonoses in Japan is reviewed. A total of 51 species, i.e., 6 species of protozoan parasites, 14 species of trematode parasites, 11 species of cestode parasites, 18 species of nematode parasites and 2 species of acanthocephalan parasites are potential zoonotic parasites. Most (11 species) of the zoonotic nematodes provoke larva migrans. Habitats of zoonotic parasites vary greatly depending upon individual species. Some parasites cause heterotopic parasitism (e.g., Paragonimus westermani) and metastasis (Entamoeba histolytica). In larva migrans, parasites migrate through various parts of body tissues, affecting multiple organs (gnathostomiasis and sparganosis mansoni). The majority of parasitic zoonoses are food-borne infections. Some of them are an arthropod-borne (or -mediated) infection (dirofilariasis, thelaziasis and moniliformiasis), or acquired by percutaneous infection with cercariae (schistosome cercarial dermatitis) or 3rd-stage infective larvae (hookworm diseases). The diagnosis of parasitic zoonoses, especially larva migrans, is difficult; although some unique clinical symptoms and the presence of eosinophilia and/or increased level of serum IgE antibody are frequently seen in larva migrans, the application of various immunodiagnostic methods is usually required. For the prevention and control of parasitic zoonoses, the ingestion of not only strange food (e.g., snakes, frogs, slugs, etc.) but also raw fish and cuttlefish (sashimi) must be prohibited. Fishes and the meat of wild animals (e.g., bear and wild boar) should be frozen or thoroughly cooked before eating. Pets and domestic animals play an important role as a direct or indirect source of infection with various parasitic zoonoses. The treatment of those animals and/or the eradication of intermediate hosts (or vectors) of the parasites are thus required.

Animals↗
PubMed2001

Genetic variation in a host-parasite association: potential for coevolution and frequency-dependent selection.

Models of host-parasite coevolution assume the presence of genetic variation for host resistance and parasite infectivity, as well as genotype-specific interactions. We used the freshwater crustacean Daphnia magna and its bacterial microparasite Pasteuria ramosa to study genetic variation for host susceptibility and parasite infectivity within each of two populations. We sought to answer the following questions: Do host clones differ in their susceptibility to parasite isolates? Do parasite isolates differ in their ability to infect different host clones? Are there host clone-parasite isolate interactions? The analysis revealed considerable variation in both host resistance and parasite infectivity. There were significant host clone-parasite isolate interactions, such that there was no single host clone that was superior to all other clones in the resistance to every parasite isolate. Likewise, there was no parasite isolate that was superior to all other isolates in infectivity to every host clone. This form of host clone-parasite isolate interaction indicates the potential for coevolution based on frequency-dependent selection. Infection success of original host clone-parasite isolate combinations (i.e., those combinations that were isolated together) was significantly higher than infection success of novel host clone-parasite isolate combinations (i.e., those combinations that were created in the laboratory). This finding is consistent with the idea that parasites track specific host genotypes under natural conditions. In addition, correspondence analysis revealed that some host clones, although distinguishable with neutral genetic markers, were susceptible to the same set of parasite isolates and thus probably shared resistance genes.

Animals↗
PubMed1993

Effects of parasitism by the braconid wasp Cotesia congregata on host hemolymph proteins of the tobacco hornworm, Manduca sexta.

Parasitism by the braconid wasp Cotesia congregata causes major alterations in the hemolymph proteins of host tobacco hornworm larvae. Earlier studies showed that the total amount of hemolymph protein is reduced during parasitism, beginning almost immediately after the host is parasitized. Simultaneously, parasitism induces synthesis of large amounts of novel proteins that appear in the blood as early as 1-2 h post-parasitization. The present report confirms earlier studies describing the presence of novel proteins in last instar hosts, and also characterizes the effects of parasitism in altering the titers of several endogenous host hemolymph proteins normally produced by the fat body and other tissues. Analysis of hemolymph plasma using SDS-PAGE and densitometry, as well as immunodiffusion assays, showed that in terminal stage fifth instar host larvae, the titers of serpins and arylphorin were dramatically reduced relative to the levels of these proteins detected in nonparasitized gate II fifth instar larvae of the same age. The relative differences between parasitized and nonparasitized larvae increased with time following ecdysis to the fifth instar, so that the day 4 nonparasitized larvae had arylphorin titers of c. 30 mg/ml, whereas parasitized day 4 larvae with newly emerged wasps had only one sixth that amount of storage protein circulating in the hemolymph. Similarly, in nonparasitized larvae the hemolymph serpin concentration increased from c. 200 micrograms/ml (on day 0) to > 600 micrograms/ml (on day 4) in prewandering gate II larvae, but in parasitized larvae the hemolymph serpin concentration was maintained in the range of 100-200 micrograms per ml hemolymph until the pharate third instar parasites emerged from the host larva on day 4. In contrast, the level of hemolymph lipophorin was unaffected by parasitism, and lipophorin increased from c. 1.3 to > 3 mg/ml during the time interval between days 0 and 4 in both nonparasitized and parasitized larvae. Hemolymph titers of insecticyanin also were not significantly different in parasitized vs nonparasitized larvae, and in both types of larvae the concentration of this pigment decreased by c. 50% during the same time interval when lipophorin was increased significantly. Instead of causing a generalized inhibition of host hemolymph protein synthesis, parasitism causes a complex array of changes in the hemolymph protein profile of Manduca sexta, possibly via the mediation of hormonal modulators of host protein synthesis, or transcriptional or translational regulation of host gene expression by factors associated with the polydnavirus or molecules secreted by the parasites.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

The functional importance of parasites in animal communities: many roles at many levels?

Past research on parasites and community ecology has focussed on two distinct levels of the overall community. First, it has been shown that parasites can have a role in structuring host communities. They can have differential effects on the different hosts that they exploit, they can directly debilitate a host that itself is a key structuring force in the community, or they can indirectly alter the phenotype of their host and change the importance of the host for the community. Second, certain parasite species can be important in shaping parasite communities. Dominant parasite species can directly compete with other parasite species inside the host and reduce their abundance to some extent, and parasites that alter host phenotype can indirectly make the host more or less suitable for other parasite species. The possibility that a parasite species simultaneously affects the structure of all levels of the overall community, i.e. the parasite community and the community of free-living animals, is never considered. Given the many direct and indirect ways in which a parasite species can modulate the abundance of other species, it is conceivable that some parasite species have functionally important roles in a community, and that their removal would change the relative composition of the whole community. An example from a soft-sediment intertidal community is used to illustrate how the subtle, indirect effects of a parasite species on non-host species can be very important to the structure of the overall community. Future community studies addressing the many potential influences of parasites will no doubt identify other functionally important parasite species that serve to maintain biodiversity.

Animals↗
PubMed1995

Use of hydroethidine and flow cytometry to assess the effects of leukocytes on the malarial parasite Plasmodium falciparum.

Flow cytometry was evaluated as a method of assessing in vitro the effects of leukocytes on blood-stage Plasmodium falciparum. Hydroethidine is converted by metabolizing cells to ethidium, a nucleic acid fluorochrome. After incubation with hydroethidine, viable and dead leukocytes and parasitized and uninfected erthrocytes could all be identified on the basis of fluorescence intensity and size. Leukocytes can therefore be eliminated from further analysis; this allows assessment, at any parasite developmental stage, of the level of parasitemia within erythrocytes in the presence of any of several types of leukocytes. Whether leukocytes actually kill intraerythrocytic parasites can therefore be determined and the level of cytotoxicity can be assessed. The ability of leukocytes to prevent merozoites from invading new erythrocytes, i.e., inhibition of parasite invasion, can also be assessed by this method. When erythrocytes containing schizont-stage parasites were cocultured with different leukocyte populations and the level of parasitemia was determined after merozoite release and invasion, only cultures containing gamma delta T cells inhibited parasite invasion. The different blood-stage forms of the parasite vary in nucleic acid content, which allows each of the developmental stages to be distinguished by flow cytometry; this permits assessment of changes in parasite development in the presence of leukocytes. Monocyte-derived macrophages (MDMs) appeared to have an effect on parasite development. In this instance, when erythrocytes containing ring-form parasites were cocultured with MDMs and harvested 24 h later, the parasites in cultures containing MDMs were at the late schizont stage, whereas parasites in control cultures were early trophozoites; this finding suggests that MDMs accelerate parasite development. Together, these results indicate that flow cytometry is potentially useful for measuring the following effects mediated by leukocytes: (i) level of cytotoxicity, (ii) changes in parasite development, and (iii) inhibition of parasite invasion.

Animals↗
PubMed1994

Recognition and polymorphism in host-parasite genetics.

Genetic specificity occurs in many host-parasite systems. Each host can recognize and resist only a subset of parasites; each parasite can grow only on particular hosts. Biochemical recognition systems determine which matching host and parasite genotypes result in resistance or disease. Recognition systems are often associated with widespread genetic polymorphism in the host and parasite populations. I describe four systems with matching host-parasite polymorphisms: plant-pathogen interactions, nuclear-cytoplasmic conflict in plants, restriction enzymes in bacterial defence against viruses, and bacterial plasmids that compete by toxin production and toxin immunity. These systems highlight several inductive problems. For example, the observed patterns of resistance and susceptibility between samples of hosts and parasites are often used to study polymorphism. The detectable polymorphism by this method may be a poor guide to the actual polymorphism and to the underlying biochemistry of host-parasite recognition. The problem of using detectable polymorphism to infer the true nature of recognition and polymorphism is exacerbated by non-equilibrium fluctuations in allele frequencies that commonly occur in host-parasite systems. Another problem is that different matching systems may lead either to low frequencies of host resistance and common parasites, or to common resistance and rare parasites. Thus low levels of host resistance or rare parasites do not imply that parasitism is an unimportant evolutionary force on host diversity. Knowledge of biochemical recognition systems and dynamical analysis of models provide a framework for analysing the widespread polymorphisms in host-parasite genetics.

Animals↗
PubMed1993

Hemoglobin catabolism and host-parasite heme balance in chloroquine-sensitive and chloroquine-resistant Plasmodium berghei infections.

Catabolism of host hemoglobin by the malaria parasite liberates required amino acid precursors, but is also releases large amounts of potentially toxic heme that accumulates in parasite food vacuoles during intra-erythrocytic development. The schizonticidal drug chloroquine binds to free heme with high affinity and is concentrated in parasite food vacuoles. To better understand the disposition of heme within the host-parasite complex, we studied the balance of hemoglobin and heme in Plasmodium berghei-infected reticulocytes in the rat and compared this process in chloroquine-sensitive (CS) and chloroquine-resistant (CR) parasites. We found that CS P. berghei parasites have 1.5-fold more heme than CR parasites isolated from rats, and that CS P. berghei-infected reticulocytes accumulate more chloroquine than CR P. berghei-infected reticulocytes. Despite these differences in parasite heme content, the decrease in host cell hemoglobin content and the rate of free amino acid generation within the host-parasite complex is similar in CS and CR P. berghei-infected rat reticulocytes. The heme content of the infected reticulocyte-parasite complex decreases with increasing parasitemia but to a lesser extent than expected for the decrease in hemoglobin. Furthermore, the decrease in host-parasite heme is accelerated in the CR P. berghei infection compared with the CS P. berghei infection. Therefore, hemoglobin catabolism by malaria parasites is associated with the overall loss of heme from the host-parasite complex and with variable deposition of heme within parasites.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMedDate not supplied

[Is there a role for parasites in the etiology of inflammatory rheumatism?].

Parasitic rheumatism is a rare condition characterized by inflammatory joint manifestations due to a parasitic infestation without parasites into joint cavity, (but, with circulating immune complexes, in serum, and synovial fluid; and with immunoglobulins and complement deposits in synovium in some cases reported in the literature). The number of parasites (now 15) which can induce such an arthritis by immune mechanisms is steadily increasing. In all, but few cases of parasitic rheumatism, usual parasitic manifestations (diarrhea, abdominal pain, nausea...) are mild or absent; but, if present, they are a very good criteria to evoke the diagnosis. Clinical pictures of arthritis induced by parasitic infestation are very polymorphic, and non specific of the involved parasite; they seem to depend on genetic predisposition: the symptoms are monoarticular, pauciarticular, or polyarticular, involving small, medium, and or large joints. They can mimic the clinical picture of different inflammatory rheumatic diseases. The most striking feature of parasitic rheumatism is the failure of antirheumatic agents (especially non steroidal anti-inflammatory agents), contrasting with the dramatic efficacy of specific anti-parasitic treatment. The proof of the responsibility of parasitic infestation by indirect mechanism is given by an exceptional case report of a patient with arthritis, dramatically cured after removal of larvae from Anisakiasis gastric granuloma. To explain the uncommon occurrence of this variety of reactive arthritis, due to parasitic infestation, despite the high prevalence of parasitic infestation in the world, hypothesis of genetic predisposition seems valuable. Among 34 well documented reported cases of parasitic rheumatism in the literature, HLA B 27 antigen has been researched in 13; out of these 13, HLA B 27 is absent in 9; in 7 out of these 9, clinical picture is symmetrical polyarthritis. Out of the 13 cases, HLA B 27 is present in 4: In all these 4 cases, clinical picture is asymmetrical pauciarthritis, mimicking arthritis of Reiter's disease.

Animals↗