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[The parasite fauna of the chub mackerel (Scombridae: Scomber japonicus Houttuyn, 1782) in the central-eastern Atlantic (Atlantic coast of the Northern Africa and the Azores Archipelago banks)].

The parasite fauna of the chub mackerel Scomber japonicus Houtuym, 1782 was studied from the neritic areas of Morocco, Western Sahara, Mauritania and from the banks of the Azores Archipelago (the Great Meteor Bank, the Hyeres Bank and the Irving Bank) in 1994-2001. Twenty eight species of parasites of following group have been were found: Coccidia (1 species), Microsporidia (1), Myxosporea (4), Monogenea (4), Cestoda (5), Trematoda (5), Acanthocephala (1) and Nematoda (6). The differences between mackerel parasite fauna in the neritic areas and from of the Azores Archipelago banks were established. Peculiarities of the mackerel parasite fauna in two areas (Morocco--Western Sahara and Mauritania) corroborate the hypothesis that two populations of chub mackerel are available: "Sahara-Moroccan" and "Senegal-Mauritanian". Ontogenetic variability of parasite fauna was related to food demands of mackerel and its feeding habits in the areas Morocco and Mauritania. Kudoa histolytica has negative influence on the commercial value of S. japonicus. These parasites were localized in the muscles of mackerel from Mauritania (40%, TL = 20-25 cm). Parasites being dangerous for human health were presented by larvae of Bolbosoma sp. (occurred on the banks of the Azores Archipelago), Anisakis simplex and Contracaecum sp. (occurred in all areas investigated).

Acanthocephala↗

[Evaluation of the distribution of intestinal parasites in the Uludag University Medical Faculty during a period of eight years.].

The purpose of the present study was to investigate retrospectively the distribution and prevalence of intestinal parasites in patients who presented at the routine parasitology laboratory of the Uludag University Medical Faculty, Bursa, during the 8 years from January 1993-December 2000. A total of 32,346 stool specimens were examined for intestinal parasites using native- Lugol and formol ethyl ether methods. Also, 10,897 cellophane- tape preparations were studied directly. Parasites were found in 8.14% of the samples. Of the patients, 46.32% were females and 53.68%, male. G. intestinalis (3.63%) and Enterobius vermicularis (3.41%) were the most prevalent parasites. The distribution of the parasites according the species was as follows: 115 (0.35%) Entamoeba histolytica and/or dispar, 73 (0.22%) Ascaris lumbricoides, 29 (0.089%) Taenia spp., 7 (%0.021) Dicrocoelium dentriticum, 6 (0.018%) Trichuris trichiura, 4 (0.012%) Hymenolepis nana, and 2 (0.006%) Strongyloides stercoralis. At least one parasite was seen in 96.47% of samples. Two parasites were found in 3.53% of the stool specimens,. The results of our study were similar to the rates of the Marmara Region. Our laboratory findings were found to be lower than previous laboratory findings.

English Abstract↗

Rheological analysis of the adhesive interactions of red blood cells parasitized by Plasmodium falciparum.

Adhesion of parasitized red blood cells (RBCs) to vascular endothelium is thought to be a key factor in the pathology of falciparum malaria. However, quantitative analyses of the intercellular forces and of the effects of flow on adhesion have been lacking. We have characterized cytoadhesion of RBCs parasitized by the strains ITO4 (which can bind to receptors ICAM-1 or CD36) and FCR3A2 (which can bind to CD36 only) using micropipette manipulation and flow chamber techniques. Target cells were unfixed or glutaraldehyde-fixed human umbilical vein endothelial cells (HUVEC, bearing ICAM-1 only) or human amelanotic melanoma cells (C32, bearing CD36 and ICAM-1). In the static, micropipette assay, 60% to 70% of parasitized cells would adhere when tested at up to three successive sites. The percentage of cells adhering and the force required for their detachment (approximately 10(-10) N) were similar for each combination of parasite strain and adhesion target (ITO4/HUVEC, ITO4/C32, FCR3A2/C32). In the flow chamber, efficiency of initial adhesion of parasitized cells was essentially constant (at about 1%) up to a stress of 0.1 Pa, and then decreased rapidly with increasing stress. Either receptor (ICAM-1 or CD36) could immobilize flowing cells at a physiologic flow stress (0.1 Pa), but the numbers of cells adhering varied for the different combinations (ITO4/C32 greater than ITO4/HUVEC greater than FCR3A2/C32). When flow was increased in steps, adhered cells were gradually washed off but many could withstand stresses at which they would not initially adhere. The force for detachment estimated in this way was similar to the pipette value, and again, was similar for the different combinations of strains and targets. Adhesion from flow depends on the affinity between surfaces being above a critical level, and once adhesion is established, the fracture energy determines resistance to disruption of adhesion. The results show that the fracture energy is greater than the affinity (ie, that adhesion becomes stabilized after it is initially established) and that the ratio of affinity to fracture energy is different for different receptor/ligand pairs, with ICAM-1 appearing to be the more efficient immobilizing receptor. Also, static and flow-based assays of adhesion clearly differ; the affinity is less critical in the static situation, so that most parasitized cells were capable of adhering in a static assay, but fewer did so under flow. Adhesiveness varied markedly from cell to cell, both for targets and parasitized cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Isolation of Plasmodium berghei by hemolysin lysis of infected erythrocytes and evidence for a parasite hexokinase.

A rapid and simple procedure has been developed for the isolation of Plasmodium berghei parasites from infected-mouse erythrocytes employing the heat stable hemolysin produced by Pseudomonas aeruginosa. Using parasites isolated by this method, the presence of a parasite specific hexokinase has been demonstrated, providing an explanation for the increased glucose consumption observed with infected cells. Enzyme assays and serology were employed in determining the purity and yield of purified parasites. The enzyme assays showed that about 25% of the parasites in infected RBCs were recovered in the purified state. The purified parasites were not agglutinated by rabbit-anti-mouse RBC serum which indicated the purified parasites were not contaminated by RBC components.

Animals↗

Variability in parasite protein antigen structure and protective immunity to malaria.

Cloned lines of the rodent malaria parasite Plasmodium chabaudi (denoted AS and CB) have been used to investigate the strain specificity of immunity to malaria. One defined difference between these lines is their expression of serologically and structurally distinct forms of an Mr 250Kd parasite-encoded antigen. This antigen is a member of a family of schizont/merozoite-associated polypeptides which have been implicated in the induction of protective immunity to rodent, simian and human malaria parasites. CBA/Ca mice were immunized by either (a) purified P. chabaudi AS-250Kd antigen, (b) chronic AS infection or (c) irradiated nonreplicating AS-parasitized erythrocytes. Post-immunization sera were examined by immunoprecipitation of 35S-methionine-labelled parasites, and the mice challenged with either AS or CB parasites. On challenge, mice developed a parasitaemia, the level of which was determined in part by isolate specificity, but only mice in groups (b) and (c) later developed a response which transcended AS/CB differences. The implications of these findings for the nature of exposed parasite antigens and the induction of protective immunity to malaria is discussed.

Animals↗

Effect of salinomycin-Na on malaria parasites (Plasmodium falciparum and P. berghei).

In vitro exposure of Plasmodium falciparum and P. berghei to salinomycin-Na showed that 10 min incubation in RPMI 1640 medium containing 100 micrograms/ml of the polyether antibiotic led to complete destruction of most parasites; in media containing 10 or 1 microgram/ml salinomycin-Na some young developmental stages seemed to survive, apparently due to the protection of the mostly intact host cell. In vitro treatment of rats infected with P. berghei revealed that a single subcutaneous (oral) dose of 20 mg/kg (80 mg/kg salinomycin-Na caused complete destruction of parasites. Incipient degeneration of the parasites could be already observed 1 h after treatment. After 22 h parasites had disappeared from blood smears. Repeated subcutaneous doses of the polyether as low as 5 mg/kg (X3) completely destroyed the asexual stages of P. berghei. During the ultrastructural investigation of the action of salinomycin-Na it was found that initially the inner lacunes (such as endoplasmic reticulum and perinuclear space) and the mitochondrion were markedly swollen. This was followed by mitochondrial disruption with rupture of the parasites' pellicle. Since the infected host cells also ruptured, mainly extracellular parasites were seen in blood smears beginning 6 h after treatment. Salinomycin-Na seems to act similarly on the malarial parasites and on the free merozoites of chicken intestinal coccidia.

Animals↗

The use of 75-seleno-methionine labelled Trypanosoma brucei to measure parasite replication in vivo.

The suitability of 75-Se-labelled trypanosomes for the measurement of trypanosome replication rates in vivo was investigated. The principle used to estimate the doubling time of the circulating parasites was the decrease in specific activity of 10(-7) parasites and this was determined both for parasites contained in a whole blood sample and for parasites separated from the blood sample by DEAE-cellulose chromatography. When two stocks of T. brucei (TrEU 226, TrEU 667) were compared it was found that the parasitemic profiles of radio-labelled trypanosomes transfered into naive mice were essentially the same as those of unlabelled parasites of each stock. Furthermore it was found that in an acute infection (TrEU 226) there was a rapid and continuous fall in the specific activity implying a constant doubling time. However, in the more chronic relapsing infection (TrEU 667) a biphasic decrease in the specific activity occurred which although initially similar to that of the acute infection changed to a much slower rate of replication at the time of peak parasitemia. The results indicate that radiolabelled trypanosomes can be used to measure parasite replication rates in vivo, and may therefore be a valuable method for investigating the factors governing parasite growth in the circulation.

Acute Disease↗

Radical-mediated damage to parasites and erythrocytes in Plasmodium vinckei infected mice after injection of t-butyl hydroperoxide.

Intravenous injection of t-butyl hydroperoxide rapidly killed Plasmodium vinckei in mice, and caused haemolysis. The same dose seemed harmless to unparasitized mice. Many parasites disintegrated inside circulating erythrocytes, so parasite death was not simply a passive consequence of haemolysis. Injection of desferrioxamine, which removes the traces of free iron that promote the dissociation of t-butyl hydroperoxide into radical species, prevented both parasite death and haemolysis. Lipid peroxidation, as measured by accumulation of malonyldialdehyde over 2 h in vitro, occurred in erythrocytes exposed to t-butyl hydroperoxide, and was particularly marked in erythrocytes from parasitized mice. These erythrocytes accumulated appreciable malonyldialdehyde even without exposure to t-butyl hydroperoxide. Desferrioxamine inhibited the accumulation of malonyldialdehyde, but did not prevent depletion of reduced glutathione by t-butyl hydroperoxide. This suggests that t-butyl hydroperoxide damaged parasites and erythrocytes by dissociating into radical species, rather than by decreasing intraerythrocyte anti-oxidant capacity. In earlier experiments we suggested that intraerythrocytic parasite death and haemolysis caused by alloxan were mediated by radical species, and these experiments with t-butyl hydroperoxide add weight to this interpretation. We regard both of these systems as models for macrophage-induced parasite death and host pathology in acute malaria.

Animals↗

Membrane rigidity of red blood cells parasitized by different strains of Plasmodium falciparum.

Changes in the structure of parasitized red blood cells may influence their ability to circulate. We have used a micropipette technique to examine the effects of invasion and maturation of Plasmodium falciparum on the membrane rigidity of red blood cells. In the presence of immature, ring form parasites from different laboratory strains, membrane rigidity remained unchanged as compared with uninfected red cells. However, development of more mature pigmented trophozoites caused a marked increase in membrane rigidity. Parasites from knobless strains caused a less-pronounced increase than parasites from knob-positive strains. Using closely synchronized cultures, the dependence of membrane rigidity on parasite maturation was studied in more detail for selected knob-positive and knobless strains. Over a period of 12 hours, while trophozoites developed into schizonts, no further rigidification of the red cell membrane occurred. The increase in membrane rigidity, occurring with the initial development of pigmented trophozoites, may be related to insertion of neoantigens into the red cell surface or modification of native membrane proteins that also occur at this time. In contrast to others, we found no effect of parasite-culture supernatant, harvested at different stages, on the rigidity of uninfected cells exposed to it. Interstrain variation of membrane rigidity could influence pathophysiology in several ways: by promoting margination and cytoadherence of knob-positive strains in the microcirculation, by modulating clearance of parasitized cells by the reticuloendothelial system, and by influencing ischemic complications of severe falciparum malaria.

Animals↗

Comparative study of the adhesion of sickle cells and malarial-parasitized red cells to cultured endothelium.

Increased adhesion of red cells to vascular endothelium has been implicated in the pathogenesis of falciparum malaria and sickle cell disease. We have carried out a comparative study of the adhesiveness of normal (AA), sickle trait (AS), and homozygous sickle (SS) red cells, with and without parasitization by Plasmodium falciparum, with an in vitro flow system. Adhesion of nonparasitized red cells to cultured human umbilical vein endothelial cells (either glutaraldehyde fixed or untreated) was strongly dependent on the wall shear stress. Many AA and SS cells adhered at low stress (0.02 Pa), but far fewer did so when the stress was increased to a physiologic level (0.1 Pa). Compared with AA cells, SS adhered in greater number (about threefold) and required greater stress (about two-fold) for their subsequent removal. In contrast, the efficiency of adhesion of AA cells parasitized by Plasmodium falciparum was essentially constant up to 0.1 Pa, where it was about 1000 times greater than the efficiency for nonparasitized cells. The stress required to remove parasitized cells was about 6 times that for controls. When parasites were grown in SS cells, fewer cells adhered than when parasites were grown in AA cells. However, the adhesion of malarial-parasitised AS cells was only slightly less than that of parasitized AA cells, so that modulation of adhesion is unlikely to underlie the protective effect of sickle gene in malaria. Adhesion of red cells to endothelium may promote blockage of microvessels, and the interaction of parasitized cells appears strong enough to directly cause ischemic complications in falciparum malaria.

Anemia, Sickle Cell↗

In vivo removal of malaria parasites from red blood cells without their destruction in acute falciparum malaria.

During acute falciparum malaria infection, red blood cells (RBC) containing abundant ring-infected erythrocyte surface antigen (Pf 155 or RESA), but no intracellular parasites, are present in the circulation. These RESA-positive parasite negative RBC are not seen in parasite cultures in vitro. This indicates that in acute falciparum malaria there is active removal of intraerythrocytic parasites by a host mechanism in vivo (probably the spleen) without destruction of the parasitized RBC. This may explain the observed disparity between the drop in hematocrit and decrease in parasite count in some hyperparasitemic patients. The fate of these "once-parasitized" RBC in vivo is not known.

Acute Disease↗

Effect of gamma radiation on Brugia L3 development in vivo and the kinetics of granulomatous inflammation induced by these parasites.

Previous studies have shown that the downregulation of parasite-specific cellular immune response in Brugia-infected jirds requires viable worms but is not dependent on microfilariae (MF) for either induction or maintenance of this phenomenon. To clarify further which life cycle stages induce filarial hyporesponsiveness, jirds were infected intraperitoneally with third stage larvae (L3) exposed to 0, 15, 25, 35, 45, or 90 krad of gamma radiation to differentially alter L3 development. Necropsies were performed at 7, 14, 28, and 118 days postinoculation (DPI). The degree of parasite development, intraperitoneal inflammation, and pulmonary granulomatous inflammation (PGRN) to parasite antigen-coated beads embolized in the lungs were monitored at the time of necropsy. Parasite survival and worm lengths were inversely related to the irradiation dose. Gamma radiation at 35, 45, or 90 krad prevented larval molt to the adult stage. Some parasites irradiated with 15 or 25 krad developed beyond fourth stage larvae (L4) to infertile adult females. The PGRN peaked at 14 DPI in all infected groups. Downregulation of the PGRN occurred after 14 DPI in groups that received nonirradiated L3 or L3 irradiated with 15 krad. No significant decrease of the PGRN occurred in groups that received parasites irradiated with more than 15 krad. Significant peritoneal inflammation as indicated by an increase in macrophages occurred only in jirds that received nonirradiated L3. These data demonstrate the importance of the adult stages in inducing downmodulation in the absence of MF and suggest that the L4 may also play a role in the induction of this phenomenon. An alternate conclusion is that parasite burden and not developmental stage is important in the induction of this hyporesponsive state.

Animals↗

The contributions of host age and size to the aggregated distribution of parasites in yellow perch, Perca flavescens, from Garner Lake, Alberta, Canada.

The independent effects of host age and size on parasite abundance are examined in yellow perch from Garner Lake in east-central Alberta. Older, larger perch tend to have more species of parasites combined with larger parasite infrapopulations. Sexual size dimorphism in perch generates 2 different size classes within each age class >2+ yr, thus allowing the opportunity to separate the effects of age and size on the recruitment of parasites by perch. The abundances of Diplostomum adamsi and Bothriocephalus sp. both increase with host age, whereas the increased abundances of Crepidostomum isostomum and Raphidascaris acus in larger fish are, in part, suggestive of size-specific feeding behaviors of the host. A combination of parasites with size- and age-dependent infrapopulations results in a size-dependent increase in infracommunity size. A comparison of variance-to-mean ratios within age classes to overall variance-to-mean ratios shows that the effects of host age and size on parasite recruitment do contribute to parasite aggregation.

Age Factors↗

Metazoan parasites of the red rockfish Sebastes capensis off northern Chile.

The parasites of the red rockfish Sebastes capensis off northern Chile are described quantitatively for the first time and compared with those of congeneric species of the Northern Hemisphere as well as of other Chilean marine fishes. Sixteen species were recorded, including 8 ectoparasites (2 copepods, 2 isopods, 1 turbellarian, and 3 monogeneans) and 8 endoparasites (2 acanthocephalans, 3 digeneans, and 3 nematodes). The ectoparasites Lepeophtheirus chilensis and Caligus cheilodactylus, and the endoparasites Pseudopecoelus sp. and Corynosoma sp. were predominant. Eighty percent of the fishes harbored 3-6 parasite species. Four parasite genera new to the genus Sebastes were found in S. capensis, which also shares several parasite genera with its congeneric species from other geographic areas. However, in contrast to its congeners, S. capensis exhibits a lower helminth species richness, although when all the metazoan fauna is considered the species number and diversity are similar. When compared with other demersal fishes of the Chilean coast, S. capensis shows a high number of species and high parasite abundance. Diphtherostomum sp. and Gnathia sp. are new generic records for the parasite fauna of Chilean coast fishes and the finding of Paramicrocotyle sp., Neobenedenia melleni, and Interniloculus chilensis in this study represents a new geographical record for these parasites.

Acanthocephala↗

Intestinal parasitism in Peruvian children and molecular characterization of Cryptosporidium species.

Intestinal parasitism was studied in children of Trujillo (Peru) to create a prevention and control program. Fecal samples of 489 children were examined. The general prevalence of intestinal parasitosis was found to be 68%. The most frequent pathogenic enteroparasites were Giardia lamblia (26.4%), Cyclospora cayetanensis (13%), Hymenolepis nana (2%), Hymenolepis diminuta (1.6%), and Cryptosporidium spp. (1%). All these parasites appeared both in diarrheic and nondiarrheic children, except Cryptosporidium, which invariably caused diarrhea. Multiple parasitism was frequent, 45.6% of the children presenting two, three, or four intestinal parasites. Cryptosporidium was the only parasite that was not associated with the others. Only five children were affected of cryptosporidiosis, presenting explosive diarrhea, nausea, and vomiting. Cryptosporidium species and genotypes involved in the infantile cryptosporidiosis were determined by polymerase chain reaction-restriction fragment length polymorphism. Four children were parasitized by Cryptosporidium hominis and only one by Cryptosporidium parvum. Our results confirm that anthroponotic transmission of Cryptosporidium is predominant in Peru.

Animals↗

Causes of inter-individual variation in reproductive strategies of the parasitic nematode Graphidioides subterraneus.

Several factors capable of affecting the amount of resources available to an individual parasite, such as the number of other parasites in the host or host quality, may cause variability in reproductive success among parasites. Variation in egg output and mean egg volume was investigated among adult females of the nematode Graphidioides subterraneus, parasitic in the herbivorous subterranean rodent Ctenomys talarum (Octodontidae). Female nematode body size correlated strongly with the number of eggs produced. However, neither host body mass nor the number of other nematodes per host had any influence on the number or volume of eggs produced by the parasites. There was also no evidence for a trade-off between the number of eggs produced and mean egg volume among female nematodes. All these results suggest that resource supply to individual worms is not limited by host size or by the number of conspecific parasites vying for the same resources, despite the 30-fold variation in intensity of infection and the twofold variation in host body mass observed in the present study. Instead, resource availability does not appear to constrain reproduction in G. subterraneus, with its host providing a stable, predictable environment.

Animals↗

Vector-parasite interactions for vaccine development.

The ingestion of blood by arthropod vectors of disease can be exploited in order to either kill the vector or render it incapable of disease transmission. This paper examines some approaches to identifying target molecules of vector origin, against which immunisation could result in blocking parasite transmission. Manipulation of the blood meal of vectors through such techniques as membrane feeding can help identify true target sites for attack, but just as useful, can identify structures or molecules that play no significant role in parasite development. Examples, mostly derived from the interactions between the malaria parasite, Plasmodium, and the mosquito midgut, illustrate the real need to understand the multiple aspects of vector-parasite interactions before they can be exploited for control purposes. The approaches outlined are however applicable directly to any vector-borne disease. Careful examination of the parasite life cycle in the vector, and comparisons with other parasites, vectors, non-vector insects and analogous vertebrate systems (the latter being often relatively well advanced) can result in the identification of specific and definable interactions which can then be further developed for vaccine purposes.

Animals↗

"Adaptive" changes in the behaviour of parasitized animals: a critical review.

Changes in host behaviour following infection with parasites are frequently reported in the literature, and are often hypothesized to be adaptive for either host or parasite. However, investigators of such phenomena often use the "adaptation" label for host behavioural changes based on their intuition and not on rigorous criteria. Alterations in host behaviour following infection can only be considered adaptive if they satisfy certain conditions: (1) they must be complex; (2) they must show signs of a purposive design; (3) they are more likely to be adaptations if they have arisen independently in several lineages of hosts or parasites; and (4) they must be shown to increase the fitness of either the host or the parasite. A survey of published examples of host behavioural changes indicates that while some are spectacularly complex and are extremely well-fitted to their presumed function, most are simple increases or decreases in an activity performed prior to infection. There are some suggestions of convergent evolution in behavioural change in distantly related host or parasite groups but more evidence is needed. Finally, most known behavioural changes have not been demonstrated to lead to fitness gains in either hosts or parasites. Few known examples satisfy more than two of the above criteria, and, in general, the adaptive function of changes in host behaviour following infection is in need of more solid proof.

Adaptation, Psychological↗