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The role of parasites in acute appendicitis of pediatric patients.

There is little evidence regarding the relationship between parasites and acute appendicitis. In order to determine such a relationship, if any, 830 appendectomy specimens were studied. Age, sex, pathological findings and the presence and type of parasites and the type of parasite were analyzed. Parasites were present in 62 cases (7.46%). Ascaris lumbricoides and Trichuris trichiura were the most frequently encountered parasites. These were observed, alone or in combination, in 45 cases (72.5%). Appendix perforation, peritonitis, necrosis and flegmonous appearance, were more frequent in the cases of acute appendicitis without parasitic infestation (p < 0.05). There were no differences between the cases with or without parasitic infestation (p > 0.05) In cases of peritonitis. The low incidence of parasites among the appendectomy specimens and the failure to demonstrate its relationship with all events derived of appendicitis, do not support the hypothesis that parasites are a major cause of appendicitis in pediatric patients.

Acute Disease↗

Malaria parasite developmental analyses by the nested polymerase chain reaction method: an implication for the evaluation of mosquito infection rates in epidemiological studies.

A malaria mosquito vector, Anopheles saperoi, and a non-vector, Aedes albopictus, were allowed to feed on mice infected with murine malaria, Plasmodium yoelii nigeriensis, and were subsequently monitored for the development of parasites by the nested polymerase chain reaction (PCR) method, using Plasmodium genus-specific primer pairs. The mosquitos were divided into two parts, head/thorax and abdomen, for DNA analyses. The parasite DNA and murine DNA for each mosquito were examined in parallel. In both groups of mosquitos, murine DNA was detected up to 4 days post-blood meal in both the head/thorax and abdomen. After 4 days, the murine DNA fell below detectable limits. Murine DNA and parasite DNA remained undigested for the first 4 days post-blood meal. Parasite DNA was detected in the abdomen of 25% (3/12) of Ae. albopictus on day five and 10% (1/10) on day six, after murine DNA had fallen below detectable limits. Parasite DNA was not detected in the head/thorax of Ae. albopictus on those days or afterwards in either the head/thorax or abdomen, demonstrating that the parasite detected on days 5 and 6 in the abdomen degenerated and did not develop into mature oocysts or sporozoites. In the vector An. saperoi, parasite DNA was detected continuously in the head/thorax and abdomen for many days after the murine DNA had fallen below detectable limits. The detection rate of parasite DNA in the head/thorax of An. saperoi increased gradually from day 8 post blood meal until it reached a maximum level of 71.4% (15/21 12 days post-infection. Parasite DNA in abdomen reached its maximum level of 81% (17/21) 10 days post-blood meal. The implications of these results for the design and interpretation of epidemiological surveys is discussed.

Animals↗

[Metazoan parasites of the pearl cichlid, Geophagus brasiliensis (Quoy and Gaimard, 1824) (Osteichthyes: Cichlidae) from the Lajes Reservoir, Rio de Janeiro, Brazil].

During May 2002 and January 2003, 65 specimens of pearl cichlid, Geophagus brasiliensis (Quoy & Gaimard, 1824), collected from the Lajes Reservoir, Rio de Janeiro, Brazil (22 degrees 42'-22 degrees 50'S, 43 degrees 53' -44 degrees 05'W), were necropsied to study their infracommunities of metazoan parasites. Fifty three fishes (81.5%) were parasitized by one or more metazoan. Six species of parasites were collected. The hirudinean Glossiphonid not identified was the majority (60%) of the parasite specimens collected and was the dominant species, with highest abundance and prevalence. The parasites of G. brasiliensis showed the typical aggregated pattern of distribution. No species of parasites of the pearl cichlid had correlation between the host's total length and parasite prevalence and abundance. The sex of hosts did not influence prevalence and abundance of any parasite species. The mean of Berger- Parker's index of dominance was 0.77 +/- 0.38. The mean species diversity in the infracommunities of G. brasiliensis was H = 0.154 +/- 0.06, with no correlation with the host's total length. The parasite community of G. brasiliensis from Lajes Reservoir is characterized by the low species richness and diversity.

Animals↗

Minimal selfing, few clones, and no among-host genetic structure in a hermaphroditic parasite with asexual larval propagation.

Little is known about actual mating systems in natural populations of parasites or about what constitutes the limits of a parasite deme. These parameters are interesting because they affect levels of genetic diversity, opportunities for local adaptation, and other evolutionary processes. We expect that transmission dynamics and the distribution of parasites among hosts should have a large effect on mating systems and demic structure, but currently we have mostly speculation and very few data. For example, infrapopulations (all the parasites in a single host) should behave as demes if parasite offspring are transmitted as a clump from host to host over several generations. However, if offspring are well mixed, then the parasite component population (all the parasites among a host population) would function as the deme. Similarly, low mean intensities or a high proportion of worms in single infections should increase the selfing rate. For species having an asexual amplification stage, transmission between intermediate and definitive (final) hosts will control the variance in clonal reproductive success, which in turn could have a large influence on effective sizes and rates of inbreeding. We examined demic structure, selfing rates, and the variance in clonal reproductive success in natural populations of Plagioporus shawi, a hermaphroditic trematode that parasitizes salmon. Overall levels of genetic diversity were very high. An a posteriori inference of population structure overwhelmingly supports the component population as the deme, rather than individual infrapopulations. Only a single pair of 597 adult individuals was identified as clones. Thus, the variance in clonal reproductive success was almost zero. Despite being hermaphroditic, P. shawi appears to be almost entirely outcrossing. Genetic estimates of selfing (<5%) were in accordance with the proportion of parasites from single infections. Thus, it appears that individual flukes outcross whenever possible and only resort to selfing when alone. Finally, our data support the hypothesis that aquatic transmission and the use of several intermediate hosts promotes high genetic diversity and well-mixed infrapopulations.

Animals↗

Pathways for the reduction of oxidized glutathione in the Plasmodium falciparum-infected erythrocyte: can parasite enzymes replace host red cell glucose-6-phosphate dehydrogenase?

Plasmodium falciparum-infected human red cells possess at least two pathways for the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH): (1) the glucose-6-phosphate dehydrogenase (G6PD) pathway and (2) the glutamate dehydrogenase (GD) pathway using glutamate as a substrate. Uninfected erythrocytes lack the GD pathway. The NADPH generated can be used to reduce oxidized glutathione (GSSG), which accumulates in the presence of an oxidative stress. In red cell G6PD deficiency, this pathway is reduced or absent, and the host cells as well as the parasites within them are vulnerable to oxidant stress. In view of the presence of the GD pathway in parasitized red cells and the recent description of a parasite-derived G6PD enzyme, we have asked whether the pathways for the reduction of GSSG provided by the parasite can substitute for the host G6PD in red cells deficient in G6PD activity. We have devised a functional assay in which the reduction rate of GSSG is monitored in the presence of buffered infected or control red cell lysates and substrates. Infected G6PD-deficient erythrocytes were obtained from in vitro cultures after a single prior growth cycle of the parasites in G6PD deficient cells to eliminate contaminating normal red cells. The results show that only parasitized red cells can reduce GSSG via the GD pathway. In parasitized G6PD Mediterranean red cells (completely G6PD-deficient), there is a detectable GSSG reduction via the G6PD pathway, not found in uninfected lysates from the same individual. In G6PD A- (African type, featuring partial deficiency), a small increment in the G6PD-dependent reduction of GSSG can also be detected. However, when compared to G6PD normal red cells, the activities from the parasite-derived pathways are small and could not be considered substitutes for normal host enzyme activity. It is concluded that while the plasmodium provides additional pathways for the generation of NADPH that may serve its own metabolic needs, the host red cells and hence the parasite itself remain vulnerable to oxidant stress.

Erythrocytes↗

Invasion of erythrocytes by Plasmodium falciparum malaria parasites: evidence for receptor heterogeneity and two receptors.

Plasmodium falciparum malaria parasites with different capabilities of invading sialic acid-deficient erythrocytes were identified. Thai-2 parasites cultured in Tn erythrocytes invaded neuraminidase-treated and Tn erythrocytes twice as efficiently as Thai-2 parasites cultured in normal erythrocytes and seven to ten times more efficiently than a cloned line of Camp parasites cultured in normal erythrocytes. All three parasite lines required sialic acid for optimal invasion, but Thai-2 parasites cultured in Tn erythrocytes invaded neuraminidase-treated erythrocytes with 45% efficiency whereas Camp parasites invaded neuraminidase-treated erythrocytes with less than 10% efficiency. P falciparum malaria parasites probably possess two receptors: one that binds to a sialic acid-dependent ligand and another that binds to a sialic acid-independent ligand. Parasites may differ in the quantity or affinity of their receptors for the sialic acid-independent ligand.

Binding Sites↗

[Malaria plasmodia in the mouse. Parasitization of mature and immature erythrocytes by Plasmodium berghei, Plasmodium yoelii and Plasmodium chabaudi (author's transl)].

Plasmodium berghei parasites (strain K173) in mice with developing immunity changed to a variant type with increased resistance against antibodies and enhanced invasion of mature erythrocytes; on passages in normal mice this variant type retransformed to the normal type (Kretschmar 1964). On detailed study, parasites of the variant type showed a markedly decreased predilection for polychromatophilic erythrocytes, leading to slowed multiplication during prepatency, increased invasion of mature erythrocytes and rapidly fatal course of the infection. Avoidance of parasitized immature erythrocytes remained unaltered in the variant type. In presence of antibodies many parasites invaded mature erythrocytes even in blood with high concentrations of immature erythrocytes. --Plasmodium yoelii (strain 17X) showed very high predilection for polychromatophilic erythrocytes, only slight lowering of immature erythrocyte concentration and low parasitization of mature erythrocytes. Parasites with altered preference for polychromatophilic erythrocytes were not observed in animals with parasitemia relapsing after spontaneous disappearance of the primary parasitemia or after injection of antiserum. It is suggested that in a variant of Plasmodium yoelii with high invasion of mature erythrocytes (Yoeli et al. 1975), the decisive virulence factor might be a lowered predilection for polychromatophilic erythrocytes. Avoidance of parasitized immature erythrocytes is less marked in Plasmodium yoelii than in Plasmodium berghei. In presence of antibodies more parasites invade mature erythrocytes. --Plasmodium chabaudi showed an appreciable preference for invasion of immature erythrocytes. Moreover, significantly more multiply parasitized mature and immature erythrocytes were found than would have been produced by random invasion of erythrocytes.

Animals↗

Oxidative killing of the intraerythrocytic malaria parasite Plasmodium yoelii by activated macrophages.

The capacity of macrophages activated in vivo and in vitro to kill Plasmodium yoelii was investigated. Macrophages activated by BCG-, Con A-, or malaria-induced lymphokines (LK) were cultured with P. yoelii-parasitized erythrocytes (PE). In some experiments, effector and target cells were separated by a 0.45-micron filter. Parasite viability was assessed a) in vivo by injection of mice and quantitative detection of parasites by RIA or b) in vitro by the incorporation of 3H amino acids into parasite proteins. Activated macrophages killed target PE in a dose-dependent manner by elaborating a membrane-permeable soluble factor(s). The addition of small amounts of immune serum augmented the killing of the parasites. LK-activated macrophages underwent an oxidative burst upon the phagocytosis of PE as evidenced by the accumulation of reduced formazan in the NBT assay. The magnitude of the oxidative response corresponded to the number of parasites that were ingested. The phagocytosis-induced oxidative burst was necessary for subsequent killing of Plasmodium. Parasites incubated in microchambers separated from macrophages by a 0.45-micron filter were susceptible to H2O2 released by LK-activated macrophages incubated with PMA, opsonized zymosan, or P. yoelii antigen. Inhibition of protein synthesis by parasites exposed to products of activated macrophages was abrogated by preincubating macrophages with catalase but not with SOD, mannitol, or histidine. These results suggest that phagocytosis-associated oxidative mechanisms mediate the destruction of the malaria parasite. Hence, cell-mediated as well as antibody-dependent mechanisms cooperate in the immune response against malaria.

Amino Acids↗

Proliferation and lymphocyte stimulatory capacity of Theileria-infected lymphoblastoid cells before and after the elimination of intracellular parasites.

A prominent pathogenic facet of Theileria infections is that the parasite infects lymphocytes and 'transforms' them into parasitized lymphoblastoid cells which are highly proliferative and can be cultured indefinitely in vitro. To analyse the relationship between the intracellular parasite and lymphocyte transformation we have studied the effects of eliminating parasites from these lymphoblastoid cells using the naphthoquinone derivative 993.C. Treatment of Theileria-infected lymphoblastoid cells with 993.C gradually eliminates intracellular parasites but cell proliferation is not inhibited until several days after parasite elimination. The proliferating cells no longer contain schizont particles and are medium-sized lymphocytes and small blast cells. The surface phenotype of these cells, as defined by lectins and monoclonal antibodies, remains unchanged after parasite elimination. The division of non-parasitized cells, under the culture conditions examined, was not indefinite. The compound 993.C itself does not appear to be mitogenic and possible mechanisms for this continued division are discussed. It has been previously reported that co-cultivation of irradiated Theileria-infected lymphoblastoid cells with autologous lymphocytes induces marked DNA synthesis in the latter. We examined further the relevance of this observation for immunity to Theileria by using lymphoblastoid cells treated with 993.C. Elimination of intracellular parasites by this compound does not impair the ability of these cells to stimulate DNA synthesis in autologous lymphocytes. Furthermore, lymphocytes from Theileria-immune or non-immune cattle react similarly. The reaction differs from a classical mixed lymphocyte reaction induced by antigens encoded in the main histocompatibility complex since the stimulator cells are exclusively T lymphocyte-derived cells, the magnitude of response is greater and stimulated lymphocytes are able to act as 'stimulator cells' to fresh autologous lymphocytes. Thus we question the immunological relevance of the observed lymphocyte division. The possibility that Theileria-infected lymphoblastoid cells carry viral genomes or infectious virus particles is discussed. Preliminary electron microscopic studies have not revealed any virus particles.

Animals↗

Mode of action of iron (III) chelators as antimalarials: II. Evidence for differential effects on parasite iron-dependent nucleic acid synthesis.

Iron chelation treatment of red blood cells infected with Plasmodium falciparum selectively intervenes with iron-dependent metabolism of malaria parasites and inhibits their development. Highly permeant hydroxamate iron chelator RSFileum2 affects all parasite stages when cultures are continuously exposed to drug, but affects primarily ring stages when assessed for irreversible effects, ie, sustained inhibition remaining after drug removal. On the other hand, the hydrophilic and poorly permeant desferrioxamine (DFO) affects primarily trophozoite/schizont stages when tested either in the continuous mode or irreversible mode. Unlike parasites, mammalian cells subjected to similar drug treatment show complete growth recovery once drugs are removed. Our studies indicate that parasites display a limited capacity to recover from intracellular iron depletion evoked by iron chelators. Based on these findings we provide a working model in which the irreversible effects of RSFs on rings are explained by the absence of pathways for iron acquisition/utilization by early forms of parasites. Trophozoite/schizonts can partially recover from RSFileum2 treatments, but show no DNA synthesis following DFO treatment even after drug removal and iron replenishment by permeant iron carriers. At trophozoite stage, the parasite uses a limited pathway for refurnishing its iron-containing enzymes, thus overcoming iron deprivation caused by permeant RSFileum2, but not by DFO because this latter drug is not easily removable from parasites. Their DNA synthesis is blocked by the hydroxamate iron chelators probably by affecting synthesis of ribonucleotide reductase (RNRase). Presumably in parasites, prolonged repression of the enzyme leads also to irreversible loss of activity. The action profiles of RSFileum2 and DFO presented in this study have implications for improved chemotherapeutic performance by combined drug treatment and future drug design based on specific intervention at parasite DNA synthesis.

Adenosine Triphosphate↗

[Impairment of immune response in parasitic infections].

Parasite escape mechanisms may depend upon factors intrinsic to parasites (host antigen uptake, antigenic variation) and upon partial failure of host's immune mechanisms. Impairment of immune response in parasitic infections, analysed and discussed from literature (138 references), is characterized by a high prevalence of autoantibodies and the common observation of immunosuppression in human parasitic infections as well as in experimental models. The high prevalence of autoantibodies accompanying increased levels of immunoglobulins contrasts with the low prevalence of autoimmune diseases in parasitic endemic areas. Evidence for cell mediated autoimmune process has rarely been reported. This might be related to an impairment of T-helper cell function and to the direct role, on B cells, of mitogens from parasite origin. Immunosuppression has been described in many human parasitic infections and in numerous experimental models. The defect in host's immune response is expressed by an impairment of both humoral and cell mediated immune responses to various heterologous antigens, and increased susceptibility to tumorigenesis, prolonged survival of skin allografts and an increased susceptibility to bacterial or viral infections. Various mechanisms of immunosuppression have been described, including failure of macrophage function or release of soluble immunosuppressive factors by parasites. The authors report some of their recent experiments in experimental schistosomiasis, which have allowed the characterization of such factors. Parasites appear in general to play a role in the regulation of the immune response that they have themselves evoked.

Animals↗

The parasite connection in ecosystems and macroevolution.

In addition to their obvious negative effects ("pathogens"), endoparasites of various kinds play an important role in shaping and maintaining modern animal communities. In the long-term, parasites including pathogens are indispensable entities of any ecosystem. To understand this, it is essential that one changes the viewpoint from the host's interests to that of the parasite. Together with geographic isolation, trophic arms race, symbiosis, and niche partitioning, all parasites (including balance strategists, i.e. seemingly non-pathogenic ones) modulate their hosts' population densities. In addition, heteroxenic parasites control the balance between predator and prey species, particularly if final and intermediate hosts are vertebrates. Thereby, such parasites enhance the bonds in ecosystems and help maintain the status quo. As the links between eukaryotic parasites and their hosts are less flexible than trophic connections, parasite networks probably contributed to the observed stasis and incumbency of ecosystems over geologic time, in spite of continuous Darwinian innovation. Because heteroxenic parasites target taxonomic levels above that of the species (e.g. families), these taxa may have also become units of selection in global catastrophies. Macroevolutionary extrapolations, however, are difficult to verify because endoparasites cannot fossilize.

Animals↗

Metazoan parasites and feeding behaviour of four small-sized fish species from the central North Sea.

The metazoan parasites and stomach contents of the small-sized demersal fishes Agonus cataphractus, Buglossidium luteum, Callionymus lyra and Rhinonemus cimbrius were studied and analysed. The fishes were captured using various sampling gears at 12 stations in the central North Sea. A total of 16 metazoan parasite species were isolated: six adult Digenea, three larval and adult Cestoda, four larval and adult Nematoda and three larval and adult Crustacea. With nine parasites species each, A. cataphractus and R. cimbrius harboured the highest parasite diversity, while B. luteum and C. lyra hosted only six and five parasite species, respectively. Eighteen new hosts and four new locality records were established. No Myxozoa, Monogenea or Acanthocephala were found. Most of the detected parasites showed a wide geographical range and a low host-specificity. The composition of the parasite fauna differed between the fish species, in accordance with their different feeding behaviours. The diet of bentho-pelagic feeders ( A. cataphractus, R. cimbrius) was more diverse in comparison with the more specialised benthic feeders ( C. lyra, B. luteum). This correlated with the lower diversity of heteroxenic parasites within both small-sized benthic fish species.

Animals↗

Relationships between the parasites of some wild and cultured fishes in two lakes and a fish farm in central Finland.

A total of 526 Atlantic salmon and 500 brown trout from a fish farm were studied for parasites, as were 272 roach, 251 perch and 150 whitefish from the lake which formed the water source, and 196 roach and 136 perch from the effluent recipient lake. The cultured fish harboured 14 parasite species, of which most were protozoan generalist parasites. Nine species were found on salmon and 12 on brown trout. Epizootically the most important species were Ichthyobodo necator, Chilodonella cyprini and Ichthyophthirius multifiliis. The mean number of species per studied fish was 0.71 for salmon and 0.61 for brown trout. The seasonal occurrences of the ectoparasites were found to be irregular due to preventative bathing of the fish. The wild whitefish harboured 19 parasite species, roach 41 and perch 33. The proportions of the parasite species common to both wild and cultured fishes were 17% of the species from roach, 36% of those from perch and 47% of the species from whitefish. Jaccard's similarity index, indicating similarities between wild and farmed fish, was highest between whitefish and brown trout. It was concluded that the source of parasites in the fish farm is the water supplying lake, but the farm itself was unlikely to effect the fish parasite fauna of the water recipient lake, although some ectoparasites, which had high prevalences in this lake, could originate from the farm. The high standard of maintenance and hygiene in this farm kept problems caused by parasites under control.

Animals↗

Factors contributing to the public health and economic importance of waterborne zoonotic parasites.

This is the first of a series of review articles in a Special Issue publication on waterborne zoonotic parasites. A brief historical overview of the occurrence and importance of waterborne parasites, dating from early civilization is presented. The article considers the diversity of parasites including protozoa, nematodes, cestodes and trematodes and the related zoonotic organism microsporidia. Many of the life cycle stages and their characteristics, which make parasites environmentally resistant and suitable for waterborne transmission are discussed. Surfaces of transmission stages consist of multiple layers of proteins, lipids, chitin or other substances capable of withstanding a variety of physical and chemical treatments. Delivery of waterborne parasites is facilitated by various mass distribution systems to consumers, and by transport and intermediate hosts such as fish and filter-feeding invertebrates which are consumed by humans. The article discusses the trends in global warming and climate change and potential for concurrent rise in waterborne disease outbreaks due to parasites. Impacts of technological modernization and globalization on the transmission of zoonotic waterborne zoonotic parasites are considered, including the effects of large-scale agricultural practices, rapid transportation of goods, and widespread movement of individuals and animals. Finally, transmission features and parasite attributes which contribute to concerns about accidental or orchestrated waterborne disease outbreaks are discussed.

Animals↗

The vulnerability of animal and human health to parasites under global change.

The term 'global change' is used to encompass all of the significant drivers of environmental change as experienced by hosts, parasites and parasite managers. The term includes changes in climate and climate variability, atmospheric composition, land use and land cover including deforestation and urbanisation, bio-geochemistry, globalisation of trade and transport, the spread of alien species, human health and technology. A subset of land use issues relates to the management of protective technologies in relation to residues in food and the environment and the emergence of resistance. Another is the question of changing biodiversity of both parasites and their associated natural enemies, and the effects on the host--parasite relationship and on parasite management. A framework for studying impacts of global change is proposed and illustrated with field data, and CLIMEX and simulation modelling of the cattle tick Boophilus microplus in Australia. Parasitology suffers from the perception that the key impacts of global change will be driven by changes at lower trophic levels, with parasitic interactions being treated as secondary effects. This is incorrect because the environment mediates host-parasite interactions as much as it affects parasites directly. Parasitologists need to strive for holistic solutions to the management of animal and human health, within a wider context of overall management of those systems, if they are to make a meaningful contribution to global efforts aimed at coping with global change.

Africa, Northern↗

Aggregated parasite distributions on hosts in a homogeneous environment: examining the Poisson null model.

Parasites are typically aggregated on their hosts in nature. The null hypothesis is that parasites should follow a Poisson distribution if environment, parasites and hosts are homogeneous. From this starting point, models have shown that factors such as heterogeneity in host susceptibility and spatial aggregations of parasites may cause parasite aggregations on hosts. I used computer simulations to show that parasites typically become aggregated on their hosts even in a homogeneous environment where parasites do not differentially prefer any host, and hosts do not differ in susceptibility, provided that hosts are randomly distributed and spatial distance between host and parasite influences the likelihood of colonisation.

Animals↗

Parasites and behavior: an ethopharmacological analysis and biomedical implications.

Parasites and disease are increasingly recognized as agents of behavioral, ecological and evolutionary importance having a variety of influences on their hosts other than the more obvious pathological and immunological changes. Parasites can have significant behavioral effects even when parasitism is sub-clinical with these effects proposed to either benefit the parasite (parasite 'manipulation'), benefit the host, or to simply arise as side-effects of the infection (parasitic 'constraints'). However, until relatively recently little attention has been paid to the neuromodulatory substrates that mediate these behavioral changes. Ethopharmacology incorporates an evolutionary approach to the study of behavior with pharmacological analysis of neuromodulatory mechanisms. As such, this approach is appropriate for, and has been applied to, the analysis of the effects of ectoparasites (e.g. biting and blood-feeding flies) and endoparasites (e.g. protozoa, nematodes) on a number of behaviors (e.g. pain inhibition, learning and memory, responses to predators and anxiety, mate selection) in selected host-parasite systems. Ethopharmacology suggests a promising direction by which neuromodulatory mechanisms that underlie the effects of parasites on behavior, including that of humans, can be addressed.

Animals↗