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[Recent features of parasites detected from clinical specimens].

It is generally considered that we have already been through with problems caused by various kinds of parasites which had once raged throughout the country. On the contrary to our common concept, we occasionally encounter some kinds of parasites in a laboratory as well as in clinical fields, which have become unfamiliar to us in these days. Parasitic diseases are in the first place, proper and limited to certain local regions, but the present situation has been greatly changed. Nowadays, specific parasites are no longer limited to polluted areas, but also they can be detected in any part of the world owing to facilitated transportations and a promoted international exchange of people. A recent gourmet boom is also one of the causes of infection as seen in anisakiasis. This study was conducted on the investigation of parasites detected from clinical specimens in our laboratory during the period from 1989 to 1993. 1) The following parasites were detected : (1) Strongyloides stercoralis, (2) Giardia lamblia, (3) Diphyllobothrium latum, (4) Schistosoma mansoni, (5) Entamoeba histolytica, (6) Necator americanus, (7) Isospora belli. 2) Strongyloides stercoralis was detected at the highest frequency. This result gives an account of high prevalence of the parasite among the inhabitants in Okinawa. In addition, the agar plate medium method which has been newly adopted has definitely led to far-advanced results for detection of this parasite. 3) Schistosoma mansoni and Necator americanus were found from foreigners one of whom was a Tanzanian and the other was a Dominican. 4) Isospora belli was found from those compromised cases such as ATL and AIDS.

Animals↗

Prevalence and etiology of intestinal parasites in Lebanon.

As there are no studies done on the prevalence of intestinal parasites in Lebanon since 1967, this study was undertaken to reveal the current patterns of intestinal parasitic infestations in Lebanese patients from two geographic regions: Beirut and Tripoli. Analysis was based on 33,253 stool specimens examined at the American University of Beirut Medical Center (AUH) and 11,611 specimens examined at the Islamic Hospital (IH) in Tripoli over five and three years, respectively. The prevalence of intestinal parasites at AUH and IH were 8.47% and 45.35%, respectively (overall 18%). The prevalence in males vs females was almost the same; being 8.23% vs 8.74%, and 44.67% vs 45.88%, at AUH and IH, respectively. Multiple infections were noted in 8.8% and 3.5% of stool specimens at AUH and IH, respectively. Although 18 different types of parasites were encountered, the most common pathogenic parasites found at AUH vs IH were: Giardia lamblia (20.7% vs 10.5% of parasites found), Entamoeba histolytica (19.41% vs 1.25%), Taenia spp. (6.03% vs 4.08%) and Ascaris lumbricoides (2.09% vs 46.97%). The overall yearly or monthly prevalence of parasites recovered from both hospitals did not show clear seasonal patterns. Compared to developed countries, Lebanon still suffers from a high prevalence and a wide spectrum of intestinal parasites.

Animals↗

[Parasitic amoebae and amoebo-flagellates from the Lobosea and heterolobosea classes].

Different cited evidences on parasitic amoebae and amoebo-flagellates belonging to the Lobosea and Heterolobosea classes (Pages, 1987) have been reviewed. Special attention is paid to various degree of their adaptation to parasitic mode of life, which ranges from a parasitism on a border with commensalism to true parasitism (both facultative and obligatory ones). Besides the coprophilous and commensal species, the number of true parasites among the Lobosea and Heterolobosea classes is comparatively small. In many cases, both facultative and obligatory parasites cause the death of their hosts. Apparently this strongly pronounced pathogenicity of parasitic amoebae and amoebo-flagellates suggest a recent origin of such parasite-host systems. Pathogens of amoebic dysentry, primary amoebic meningoencephalitis and granulomatous amoebic encephalitis are specially considered. In the Russian text-books on a parasitology the information on most of them, except Entamoeba hystolytica, is either totally absent or very scare and out of date.

Amoeba↗

Modeling host-parasite coevolution: a nested approach based on mechanistic models.

In this study we introduce a mechanistic framework for modeling host-parasite coevolution using a nested modeling approach. The first step in this approach is to construct a mechanistic model of the parasite population dynamics within a host. The second step is to define an epidemiological model which is used to derive the fitness functions for both the host and the parasite. The within-host model is then nested within the epidemiological model by linking the epidemiological parameters such as the transmission rate of the infection or the additional host mortality rate to the dynamics of the within-host model. Nesting the within-host model into an epidemiological model allows us to evaluate the fitness functions for each interactor which in turn allows us to determine the coevolutionary dynamics of the system. This nested approach has the advantage over other approaches in that mechanistic descriptions of the host-parasite biology are used to derive, rather than impose, life-history trade-offs. We illustrate this framework by analysing a simple host-parasite system. In this particular system we find that the coevolutionary equilibrium is always stable and that host survivorship and parasite fitness vary greatly with the cost of the immune response and parasite growth.

Animals↗

Parasites, ecosystems and sustainability: an ecological and complex systems perspective.

Host-parasite relationships can be conceptualised either narrowly, where the parasite is metabolically dependent on the host, or more broadly, as suggested by an ecological-evolutionary and complex systems perspective. In this view Host-parasite relationships are part of a larger set of ecological and co-evolutionary interdependencies and a complex adaptive system. These interdependencies affect not just the hosts, vectors, parasites, the immediate agents, but also those indirectly or consequentially affected by the relationship. Host-parasite relationships also can be viewed as systems embedded within larger systems represented by ecological communities and ecosystems. So defined, it can be argued that Host-parasite relationships may often benefit their hosts and contribute significantly to the structuring of ecological communities. The broader, complex adaptive system view also contributes to understanding the phenomenon of disease emergence, the ecological and evolutionary mechanisms involved, and the role of parasitology in research and management of ecosystems in light of the apparently growing problem of emerging infectious diseases in wildlife and humans. An expanded set of principles for integrated parasite management is suggested by this perspective.

Animals↗

Emphasizing the ecology in parasite community ecology.

In natural systems, individuals are often co-infected by many species of parasites. However, the significance of interactions between species and the processes that shape within-host parasite communities remain unclear. Studies of parasite community ecology are often descriptive, focusing on patterns of parasite abundance across host populations rather than on the mechanisms that underlie interactions within a host. These within-host interactions are crucial for determining the fitness and transmissibility of co-infecting parasite species. Here, we highlight how techniques from community ecology can be used to restructure the approaches used to study parasite communities. We discuss insights offered by this mechanistic approach that will be crucial for predicting the impact on wildlife and human health of disease control measures, climate change or novel parasite species introductions.

Animals↗

Transmission modes and evolution of the parasitism-mutualism continuum.

An analysis of fitness costs and benefits associated with pathogenicity suggests that modes of transmission are key determinants of evolution toward severely pathogenic, benign, or mutualistic symbioses. Specifically, this approach suggests that symbionts with mobile life history stages should evolve toward extremely severe parasitism, vector-borne symbionts should evolve toward severe parasitism in vertebrate hosts and benign parasitism in the vectors, waterborne symbionts should evolve toward severe parasitism, symbionts transmitted by predation should evolve toward severe parasitism in prey hosts and benign parasitism in predator hosts, and vertically transmitted symbionts should evolve toward benign parasitism and mutualism. Detailed reviews of the literature on human diseases support the hypothesized severity of vector-borne and waterborne transmission. Evaluation of the other associations is less detailed, but each association appears to be present. This framework draws attention to the need for detailed reviews of relationships between transmission modes and the nature of symbiotic interactions, and experimental manipulations of transmission.

Animals↗

[Regulation of defence and allergic reaction in infections with parasites].

Cytokines regulate development, differentiation and expression of effector function of the immune system. The profile of immune reactions depends on cytokine contents at the recognition of parasite. However, parasites themselves can modify immunological events and favourite these, which allow them to survive. The host immune defence can be transformed into the chronic reaction. Inflammatory reactions result from the recruitment of different cells, to the site where worms are localised. The eosinophil and mast cell migration preferentially is induced. These cells play also a major role in immediate allergic responses. Mast cells can bind allergen-specific IgE to their FcepsilonRI, the high affinity receptor for IgE. Eosinophils, through their receptors for IgG1, IgG2, IgA and IgE are mainly involved in the cytotoxic reaction directed against parasites. Crosslinking of these receptors by antigen binding will lead to subsequent release of stored mediators and cytokines. Granular materials released from mast cell accelerate inflammatory reaction and in the case of intestinal worm parasites may be involved in the expulsion phenomenon. However these cells may also induce Th2 related immunological response because they produce and release of IL-4. Eosinophils are required into the tissue and release cytotoxic and stress proteins including reactive oxygen species. Parasites are destroyed but accelerated reaction results in the destruction of host proteins and cells. Antibodies, cytokines, chemokines and adhesion molecules are essential for elevation of defence against parasites. The role of cytokines, emphasizing IL-5, and function of eosinophils, mast cells and IgE are discussed in terms of induction and effector mechanisms during parasite infections.

Allergens↗

Research needs on internal parasites of horses.

The importance of the horse industry to the economy of the United States and the impact of parasitic infections on the industry are well documented. However, contemporary research activity on internal parasites of horses has not kept pace with growth of the horse population. Parasitic infections are a major facet of enteritis and colic in horses. Parasites are also associated with poor growth and development, respiratory tract disease, dermatitis, and CNS lesions. Babesia infections remain a threat to horses imported from some regions of the world. Most research activity has dealt with the development of new antiparasitic drugs. Efforts must be made to integrate these studies with observations on the bionomics of parasites in different regions and under different management conditions into more effective and less costly integrated parasite control programs. Increased research activity concerning the pathogenesis and immune response to equine parasitic infections is also necessary. A better understanding of these factors will lead to improved diagnostic, treatment, and preventative measures. Specific research objectives designed to produce short-term and long-term benefits are suggested.

Animals↗

[The ecological concept of parasitism].

Analysis of morpho-ecological adaptations of parasites showed that their necessary and sufficient characteristic is their inhabiting the host environment. Integration with the environment is achieved 1) by adaptations towards a particular habitat (first order environment) at certain phases of ontogenesis, and 2) by adaptations to the aggregate of hosts, their ecology and factors regulating the numbers of parasites (second order environment) at the level of their entire life cycle. The evolutionary progress of parasites is sustained by the increase in their independence from extrinsic factors not by means of general organization complication and integration (as in free-living animals), but by elimination of free-living developmental stages and by increase of integration with the host environment. The basis of the latter is formed by ecological adjusting of parasites to the environment. It is achieved by syncytial transformation of the covers and the use of communication means analogous to those of host cells. The consequence of host-parasite integration is the transition of parasites from resource consumption to the "management" of the environment. It is manifested by their influence on defensive reactions and other functions of the organism, as well as on its behavior and ecology. Parasitism may turn into other forms of coexistence (commensalism, mutualism) in the course of coevolution, as a result of dialectical overcoming of antagonistic interactions of the two partners.

Animals↗

Early parasite containment is decisive for resistance to Leishmania major infection.

We investigated the early spread of Leishmania major in various mouse strains. In BALB/c mice, which are extremely vulnerable to L. major infection, the parasites disseminated within 10-24 h from the site of subcutaneous footpad infection in to the popliteal lymph node, spleen, lung, liver and bone marrow. Application of recombinant (r)IL-12 prior to infection prevented the early dissemination of parasites into visceral organs and the animals healed the infection. In three mouse strains tested, C57BL/6, CBA/J and C3H/HeJ, which are all resistant to L. major infection, the parasites remained localized in the footpad and in the draining LN for 3 days without evidence of dissemination. In C57BL/6 mice, depletion of NK1.1+ cells or neutralization of interferon (IFN)-gamma prior to infection led to rapid parasite spreading with kinetics similar to those seen in susceptible animals. Depletion of either CD4+ or CD8+ T cells in vivo prior to infection did not alter the kinetics of dissemination in any mouse strain tested. Experiments with severe-combined immunodeficient mice provided further evidence that parasite containment depends on natural killer cells and IFN-gamma, but is independent of T cells. The finding that all resistant mouse strains restrict the spread of the parasites within the first 24 h after infection strongly suggests that early parasite containment is closely associated with a resistant phenotype. The data show that local restriction of parasites in the pre-T cell phase of the infection is mediated by the innate immune system and suggest that this function plays an important role in the development of a protective T cell response.

Animals↗

Characterization of permeation pathways in the plasma membrane of human erythrocytes infected with early stages of Plasmodium falciparum: association with parasite development.

Human intraerythrocytic malarial parasites (Plasmodium falciparum) induce permeability changes in the membrane of their host cells. The differential permeability of infected erythrocytes at various stages of parasite growth, in combination with density gradient centrifugation, was used to fractionate parasitized cells according to their developmental stage. By this method it was possible to obtain cell fractions consisting essentially of erythrocytes infected with the youngest parasite stage (i.e., rings). These preparations were used for the measurement of transport of various solutes. It is shown that permeabilization of host erythrocyte membrane appears as early as 6 h after parasite invasion of the erythrocyte and increases gradually with parasite maturation. Since the selectivity for several different solutes and the enthalpy of activation of transport remain unaltered with maturation-related increase of permeability, it is concluded that the number of transport agencies in the host cell membrane increases with parasite maturation. Evidence is presented to indicate the need for parasite protein synthesis as an essential factor for the generation of the new permeability pathways.

Alanine↗

An immigration-death model to estimate the duration of malaria infection when detectability of the parasite is imperfect.

Immigration-death models are proposed to analyse the infection dynamics in longitudinal studies of panels of heavily parasitized human hosts where parasites have been typed at regular intervals by PCR. Immigration refers to the acquisition of a new parasitic genotype, occurring at rate lambda, and death refers to the clearance of a parasitic genotype (with rate mu). The models assume that corresponding to each observed process which is the detection or failure to detect a parasitic genotype, is an underlying true process which is hidden as a result of imperfect detection. We consider: (i) a model in which no distinction is made between the different members of the human population, who collectively represent the habitat of the parasites, and (ii) a model that allows for the accrual of infections with age. The models are fitted to a panel data set of malaria genotype of parasites belonging to the msp2 FC27 and 3D7 allelic families from a study of the dynamics of Plasmodium falciparum in Northern Ghana. Maximum likelihood estimates suggest that on average any individual residing in this holo-endemic area will acquire 16 new infections per year (95 per cent CI, 15-18) (defined by their single locus genotypes) and that infection with any of these genotypes lasts on average 152 days (95 per cent CI, 138-169). We estimate that an average of 47 per cent (95 per cent CI, 42-51) of the parasite types present in the host are detected in a finger-prick blood sample. This model provides a basis for analyses of how these quantities vary with the age, and hence the immune status of the host.

Adolescent↗

American trypanosomosis: in situ and generalized features of parasitism and inflammation kinetics in a murine model.

American trypanosomiasis: In situ and generalized features of parasitism and inflammation kinetics in a murine model. Experimental Parasitology 83, 267-274. Mimicking the natural conditions of mammalian infection, metacyclic trypomastigote forms of a Mexican isolate (Ninoa) of Trypanosoma cruzi were inoculated into mice in order to study inflammation kinetics and parasite clearance at the inoculation site, parasite tropism to different organs, and local inflammatory cell infiltrates. Polymorphonuclear cells were detected at the inoculation site as early as 1 hr after inoculation. Peak cell infiltrate was observed at 24 hr; at 96 hr polymorphonuclear cells had disappeared. Mononuclear cell infiltrates began at 24 hr, peaking at Day 15, and then stared disappearing by Day 30. Antigens and parasites were detected by conventional techniques up to 15 min and thereafter became undetectable. Amplification of the hypervariable region of kinetoplast minicircle DNA by polymerase chain reaction was positive from 24 hr to Day 15, and the reaction became negative on Day 30. Myositis was observed in skeletal muscle from Days 7 to 180, it progressed from slight to severe, with an inflammation process which included macrophages, plasmatic cells, and a few eosinophils, the phenotype of the infiltrating cells included LyT2+ and LyT1+ on Day 30, and both cell populations decreased in parallel on Day 180. Antigen and parasite nests were present from Day 15 to 180; in muscle the earliest time at which minicircle DNA was detected was Day 7 and it was present until Day 180. Myocarditis was also observed; it developed from slight to severe in between Days 7 and 30, then gradually decreased, and cleared up. Mononuclear cell infiltrates in the myocardium were present from Days 7 to 180. Antigen and parasite nests were detected at Days 15 and 30 and disappeared at Day 180, although minicircle DNA was detected until the last day of observation. Both skeletal and heart muscles showed inflammatory reaction foci containing T. cruzi antigen. There was twice the number of foci in heart as in skeletal muscle. This ratio was maintained by Day 30; later skeletal muscle showed persistent inflammation which was practically cleared up in the heart. Parasites or antigen were not detected by Day 180 in both skeletal and cardiac muscle; however, minicircle DNA was amplified, indicating that an small proportion of parasites evaded immune response. According to these data, Mexican Ninoa Strain has a classification as biodeme 3.

Amino Acid Sequence↗

Plasmodium vivax: ookinete destruction and oocyst development arrest are responsible for Anopheles albimanus resistance to circumsporozoite phenotype VK247 parasites.

Anopheles albimanus and An. pseudopunctipennis differ in their susceptibilities to Plasmodium vivax circumsporozoite phenotypes. An. pseudopunctipennis is susceptible to phenotype VK247 but almost refractory to VK210. In contrast, An. albimanus is almost refractory to VK247 but susceptible to VK210. To investigate the site in the mosquito and the parasite stage at which resistance mechanisms affect VK247 development in An. albimanus, parasite development was followed in a series of experiments in which both mosquitoes species were simultaneously infected with blood from patients. Parasite phenotype was determined in mature oocysts and salivary gland sporozoites by use of immunofluorescence and Western blot assays and/or gene identification. Ookinete maturation and their densities within the bloodmeal bolus were similar in both mosquito species. Ookinete densities on the internal midgut surface of An. albimanus were 4.7 times higher than those in An. pseudopunctipennis; however, the densities of developing oocysts on the external midgut surface were 6.12 times higher in the latter species. Electron microscopy observation of ookinetes in An. albimanus midgut epithelium indicated severe parasite damage. These results indicate that P. vivax VK247 parasites are destroyed at different parasite stages during migration in An. albimanus midguts. A portion, accumulated on the internal midgut surface, is probably destroyed by the mosquito's digestive enzymes and another portion is most likely destroyed by mosquito defense molecules within the midgut epithelium. A third group, reaching the external midgut surface, initiates oocyst development, but over 90% of them interrupt their development and die. The identification of mechanisms that participate in parasite destruction could provide new elements to construct transgenic mosquitoes resistant to malaria parasites.

Animals↗

A model for estimating total parasite load in falciparum malaria patients.

We describe an age-structured mathematical model of the malaria parasite life cycle that uses clinical observations of peripheral parasitaemia to estimate population dynamics of sequestered parasites, which are hidden from the clinical investigator. First, the model was tested on parasite populations cultured in vitro, and was found to account for approximately 72% of the variation in that sub-population of parasites that would have been sequestered in vivo. Next, the model was applied to patients undergoing antimalarial therapy. Using individual data sets we found that although the model fitted the peripheral parasite curves very well, unique solutions for the fit could not be obtained; therefore, robust estimates of sequestered parasite dynamics remained unavailable. We conclude that even given detailed data on individual parasitaemia, estimates of sequestered numbers may be difficult to obtain. However, if data on individuals undergoing similar therapy are collected at equal time intervals, some of these problems may be overcome by estimating specific parameters over groups of patients. In this manner we estimated sequestered parasite density in a group of patients sampled at identical time points following antimalarial treatment. Using this approach we found significant relationships between changes in parasite density, age structure and temperature that were not apparent from the analysis of peripheral parasitaemia only.

Animals↗

Fine structure of the malaria parasite Plasmodium falciparum in human hepatocytes in vitro.

Recent advances in the ability to culture the hepatic forms of mammalian malaria parasites, particularly of the important human pathogen Plasmodium falciparum have provided novel opportunities to study the ultrastructural organisation of the parasite in its natural host cell the human hepatocyte. In this electron-microscopic and immunofluorescence study we have found the morphology of both parasite and host cell to be well preserved. The exoerythrocytic forms, which may be found at densities of up to 100/cm2, grow at rates comparable to that in vivo in the chimpanzee. In the multiplying 5- and 7-day schizogonic forms of the ultrastructural organisation of the parasite bears striking resemblances to other mammalian parasites, e.g., the secretory activity and distribution of the peripheral vacuole system, but also homology with avian parasites, e.g., in nuclear and nucleolar structure and mitochondrial form. The latter homologies support earlier suggestions of the close phylogenetic relationship of P. falciparum with the avian parasites. Evidence is also presented showing the persistence of the cytoskeleton of the invasive sporozoite within the cytoplasm of the ensuing rapidly growing vegetative parasites.

Animals↗

Labeled probes inserted in the macrophage membrane are transferred to the parasite surface and internalized during cell invasion by Toxoplasma gondii.

Tachyzoites of Toxoplasma gondii attach to the macrophage surface and are internalized either by a phagocytic process, which can be inhibited by cytochalasin D, or by an active process, independent of host cell actin. Previous studies have shown that parasite attachment induces the secretion of macromolecules found in the apical organelles (micronemes and rhoptries) and subsequent/concomitant parasite internalization with the formation of a membrane-bound vacuole known as the parasitophorous vacuole. In the present study we labeled the macrophage surface with fluorescent probes that bind to proteins (DiIC16) and lipids (DTAF) and then allowed control or cytochalasin-D-treated cells to interact with untreated or antibody-coated tachyzoites of T. gondii. The interaction was interrupted at different time points by fixation and the distribution of the probes was analyzed by confocal laser scanning microscopy. Following attachment of the parasites to the macrophage surface, intense labeling of the parasite surface was observed, suggesting transfer of components of the macrophage surface to the parasite surface. Nonadherent parasites were not labeled. Immediately after attachment, most of the parasites were internalized and labeling of the internalized parasites as well as of the parasitophorous vacuole, probably of its membrane, was evident, indicating that surface components of the macrophage are involved in the formation of the parasitophorous vacuole.

Animals↗