PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “parasitism”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1983

[Argyrophilic structures of the larval forms of 2 strains of Paramphistomum microbothrium: 1 a parasite of Isidora guernei and Ovis aries, the other a parasite of Isidora truncata and Bos taurus].

The life cycle of a Paramphistome from North Senegal is completed starting from cercariae shed by naturally infected Isidora guernei: a sheep and then uninfected Isidora guernei were successively infected experimentally. Adults obtained were identifiable as P. phillerouxi or as P. microbothrium. Species determination cannot be made on the basis of argentophilic structures in the miracidium. Morphology of sporocysts and rediae differs from that observed in P. phillerouxi but is undistinguishable from that described in P. microbothrium. Cercarial chaetotaxy differs from that of P. phillerouxi. Mollusc host: Isidora guernei belongs to the same genus as Isidora truncata and I. alluaudi, reported hosts to P. microbothrium. Therefore the material is provisionally identified as P. microbothrium. To confirm this, a strain of P. microbothrium from naturally infected Bos taurus in Egypt was studied. Miracidia were used to experimentally infect Isidora truncata; cercariae obtained were identical to those previously described for this species from I. truncata and I. alluaudi. Cercarial chaetotaxy was not significantly different from that of material from North Senegal. They represent therefore two strains of Paramphistomum microbothrium.

Animals↗
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↗
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↗
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↗
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↗
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↗
PubMed1988

The use of enzymopathic human red cells in the study of malarial parasite glucose metabolism.

The in vitro growth of Plasmodium falciparum malaria parasites was assayed in mutant red cells deficient in either diphosphoglycerate mutase (DPGM) or phosphoglycerate kinase (PGK). In addition, cDNA probes developed for human DNA sequences coding for these enzymes were used to examine the parasite genome by means of restriction endonuclease digestion and Southern blot analysis of parasite DNA. In both types of enzymopathic red cells, parasite growth was normal. In infected DPGM deficient red cells, no DPGM activity could be detected, and in normal red cells, DPGM activity declined slightly in a manner suggestive of parasite catabolism of host protein. However, in infected PGK deficient red cells, there was a 100-fold increase in PGK activity, and in normal red cells, a threefold increase in PGK activity was observed. Parasite PGK could be recovered from isolated parasites, and a marked increase in heat instability of parasite PGK as compared with the host cell enzyme was noted. Neither cDNA probe was found to cross-react with DNA sequences in the parasite genome. It is concluded that the parasite has no requirement for DPGM, and probably has no gene for this enzyme. On the other hand, the parasite does require PGK, (an adenosine triphosphate [ATP] generating enzyme) and synthesizes its own enzyme, which must have been encoded in the parasite genome. The parasite PGK gene most likely lacks sufficient homology to be detected by a human cDNA probe. Enzymopathic red cells are useful tools for elucidating the glycolytic enzymology of parasites and their co-evolution with their human hosts.

Animals↗