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

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

Animals↗

[The parasite capacity of the host population].

The estimation of parasitic pressure on the host populations is frequently required in parasitological investigations. The empirical values of prevalence of infection are used for this, however the latter one as an estimation of parasitic pressure on the host population is insufficient. For example, the same prevalence of infection can be insignificant for the population with high reproductive potential and excessive for the population with the low reproductive potential. Therefore the development of methods of an estimation of the parasitic pressure on the population, which take into account the features the host population, is necessary. Appropriate parameters are to be independent on view of the researcher, have a clear biological sense and be based on easily available characteristics. The methods of estimation of parasitic pressure on the host at the organism level are based on various individual viability parameters: longevity, resistance to difficult environment etc. The natural development of this approach for population level is the analysis of viability parameters of groups, namely, the changing of extinction probability of host population under the influence of parasites. Obviously, some critical values of prevalence of infection should exist; above theme the host population dies out. Therefore the heaviest prevalence of infection, at which the probability of host population size decreases during the some period is less than probability of that increases or preserves, can serve as an indicator of permissible parasitic pressure on the host population. For its designation the term "parasite capacity of the host population" is proposed. The real parasitic pressure on the host population should be estimated on the comparison with its parasite capacity. Parasite capacity of the host population is the heaviest possible prevalence of infection, at which, with the generation number T approaching infinity, there exists at least one initial population size ni(0) for which the probability of size decrease through T generations is less than the probability of its increase. [formula: see text] The estimation of the probabilities of host population size changes is necessary for the parasite capacity determination. The classical methods for the estimation of extinction probability of population are unsuitable in this case, as these methods require the knowledge of population growth rates and their variances for all possible population sizes. Thus, the development methods of estimate of extinction probability of population, based on the using of available parameters (sex ratio, fecundity, mortality, prevalence of infection PI) is necessary. The population size change can be considered as the Markov process. The probabilities of all changes of population size for a generation in this case are described by a matrix of transition probabilities of Markov process (pi) with dimensions Nmax x Nmax (maximum population size). The probabilities of all possible size changes for T generations can be calculated as pi T. Analyzing the behaviour matrix of transition at various prevalence of infection, it is possible to determine the parasite capacity of the host population. In constructing of the matrix of transition probabilities, should to be taken into account the features the host population and the influence of parasites on its reproductive potential. The set of the possible population size at a generation corresponds to each initial population size. The transition probabilities for the possible population sizes at a generation can be approximated to the binomial distribution. The possible population sizes at a generation nj(t + 1) can be calculated as sums of the number of survived parents N1 and posterities N2; their probabilities--as P(N1) x P(N2). The probabilities of equal sums N1 + N2 and nj(t + 1) > or = Nmax are added. The number of survived parents N1 may range from 0 to (1-PI) x ni(t). The survival probabilities can be estimated for each N1 as [formula: see text] The number of survived posterities N2 may range from 0 to N2max (the maximum number of posterities). N2max is [formula: see text] and the survival probabilities for each N2, is defined as [formula: see text] where [formula: see text], ni(t) is the initial population size (including of males and infected specimens of host), PI is the prevalence of infection, Q1 is the survival probabilities of parents, Pfemales is the frequency of females in the host population, K is the number of posterities per a female, and Q2 is the survival probabilities of posterities. When constructing matrix of transition probabilities of Markov process (pi), the procedure outlined above should be repeated for all possible initial population size. Matrix of transition probabilities for T generations is defined as pi T. This matrix (pi T) embodies all possible transition probabilities from the initial population sizes to the final population sizes and contains a wealth of information by itself. From the practical point of view, however, the plots of the probability of population size decrease are more suitable for analysis. They can be received by summing the probabilities within of lines of matrix from 0 to ni--1 (ni--the population size, which corresponds to the line of the matrix). Offered parameter has the number of advantages. Firstly, it is independent on a view of researcher. Secondly, it has a clear biological sense--this is a limit of prevalence, which is safe for host population. Thirdly, only available parameters are used in the calculation of parasite capacity: population size, sex ratio, fecundity, mortality. Lastly, with the availability of modern computers calculations do not make large labour. Drawbacks of this parameter: 1. The assumption that prevalence of infection, mortality, fecundity and sex ratio are constant in time (the situations are possible when the variability of this parameters can not be neglected); 2. The term "maximum population size" has no clear biological sense; 3. Objective restrictions exist for applications of this mathematical approach for populations with size, which exceeds 1000 specimens (huge quantity of computing operations--order Nmax 3*(T-1), work with very low probabilities). The further evolution of the proposed approach will allow to transfer from the probabilities of size changes of individual populations to be probabilities of size changes of population systems under the influence of parasites. This approach can be used at the epidemiology and in the conservation biology.

Animals↗

Dose-dependent infection rates of parasites produce the Allee effect in epidemiology.

In many epidemiological models of microparasitic infections it is assumed that the infection process is governed by the mass-action principle, i.e. that the infection rate per host and per parasite is a constant. Furthermore, the parasite-induced host mortality (parasite virulence) and the reproduction rate of the parasite are often assumed to be independent of the infecting parasite dose. However, there is empirical evidence against those three assumptions: the infection rate per host is often found to be a sigmoidal rather than a linear function of the parasite dose to which it is exposed; and the lifespan of infected hosts as well as the reproduction rate of the parasite are often negatively correlated with the parasite dose. Here, we incorporate dose dependences into the standard modelling framework for microparasitic infections, and draw conclusions on the resulting dynamics. Our model displays an Allee effect that is characterized by an invasion threshold for the parasite. Furthermore, in contrast to standard epidemiological models a parasite strain needs to have a basic reproductive rate that is substantially greater than 1 to establish an infection. Thus, the conditions for successful invasion of the parasite are more restrictive than in mass-action infection models. The analysis further suggests that negative correlations of the parasite dose with host lifespan and the parasite reproduction rate helps the parasite to overcome the invasion constraints of the Allee-type dynamics.

Animals↗

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↗

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

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

Animals↗

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↗

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↗

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↗

[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↗

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↗

Immunization with Theileria parva parasites from buffaloes results in generation of cytotoxic T cells which recognize antigens common among cells infected with stocks of T. parva parva, T. parva bovis, and T. parva lawrencei.

Immunity to infection by the protozoan parasite Theileria parva in cattle is partially attributable to cytotoxic T cells, which kill lymphocytes infected with the schizont stage of the parasite. Here we evaluated five stocks of buffalo-derived T. parva lawrencei parasites and two stocks of cattle-derived T. parva parva parasites for their ability to induce in vivo cytotoxic T cells which can kill lymphocytes infected with a wide variety of strains of T. parva parasites. A group of seven full-sibling cattle, produced by embryo transfer and matched for at least one major histocompatibility complex class I haplotype, were immunized by infection and treatment with the parasite stocks. Target cells used in in vitro cytotoxicity assays were infected with five buffalo-derived parasite stocks and five cattle-derived parasite stocks, including T. parva parva and T. parva bovis. Immunization with any of the seven parasite stocks resulted in the generation of cytotoxic T cells which recognized parasite antigens on most if not all of the target cell lines tested, although the T. parva bovis stock was the least effective at doing so. Further in-depth analyses performed with peripheral blood mononuclear cells from one of the cattle immunized with T. parva lawrencei parasites showed that the pattern of killing of the panel of target cells was altered when either cells infected with different parasite stocks or clones of infected cells were used as stimulator cells in vitro, suggesting the presence of more than one population of parasite-specific cytotoxic effector cells in the peripheral blood mononuclear cells. However, clones of these cytotoxic effector cells recognized common or cross-reactive antigen epitopes expressed by the entire panel of infected target cells. These T-cell clones will be useful for identifying common T-cell antigen epitopes of T. parva and the parasite genes encoding them.

Animals↗

Impact of internal parasites on beef cattle.

Internal parasitism is a pervasive constant that reduces returns in beef cattle production. Parasitism may influence production sufficiently so that data derived investigating performance response will be erroneous. The interaction of internal parasites of cattle with other facets of their lives makes it imperative that more parasite research be done on cattle to consider their impact. Results of trials designed to determine forage production at various stocking densities may not reflect the nutritive value of the forage, but instead the severity of parasite exposure. Relative resistance or susceptibility to certain parasites vary with the breed of livestock and the species of parasite. Extensive work to evaluate the ability of various breeds and sires to influence parasitic numbers has been conducted in sheep but not in cattle. Some parasite trials have ignored the effects of nutrition on the establishment and retention of parasites. This becomes especially important where multiple parasite exposure may occur. Susceptible cattle, even on an optimal diet, will become parasitized, but if reexposed to the same species of parasite, cattle on an optimal diet may be able to resist reinfection, whereas those on deficient diets will not.

Animals↗

The population dynamics of competition between parasites.

A number of published studies of competition between parasite species are examined and compared. It is suggested that two general levels of interaction are discernible: these correspond to the two levels of competition recognized by workers studying free-living animals and plants: 'exploitation' and 'interference' competition. The former may be defined as the joint utilization of a host species by two or more parasite species, while the latter occurs when antagonistic mechanisms are utilized by one species either to reduce the survival or fecundity of a second species or to displace it from a preferred site of attachment. Data illustrating both levels of interaction are collated from a survey of the published literature and these suggest that interference competition invariably operates asymmetrically. The data are also used to estimate a number of population parameters which are important in determining the impact of competition at the population level. Theoretical models of host-parasite associations for both classes of competition are used to examine the expected patterns of population dynamics that will be exhibited by simple two-species communities of parasites that utilize the same host population. The analysis suggests that the most important factor allowing competing species of parasites to coexist is the statistical distribution of the parasites within the host population. A joint stable equilibrium should be possible if both species are aggregated in their distribution. The size of the parasite burdens at equilibrium is then determined by other life-history parameters such as pathogenicity, rates of resource utilization and antagonistic ability. Comparison of these theoretical expectations with a variety of sets of empirical data forms the basis for a discussion about the importance of competition in natural parasite populations. The models are used to assess quantitatively the potential for using competing parasite species as biological control agents for pathogens of economic or medical importance. The most important criterion for identifying a successful control agent is an ability to infect a high proportion of the host population. If such a parasite species also exhibits an intermediate level of pathology or an efficient ability to utilize shared common resources, antagonistic interactions between the parasite species contribute only secondarily to the success of the control. Competition in parasites is compared with competition in free-living animals and plants. The comparison suggests further experimental tests which may help to assess the importance of competition in determining the structure of more complex parasite-host communities.

Animals↗

Solute flux into parasitic plants.

Parasitic plants form intimate contacts with host tissue in order to gain access to host solutes. There are a variety of cell types within the host which parasitic plants could access to extract solutes. Depending on the degree to which the parasite has embraced the parasitic lifestyle, the extent of solute flux and the pathways used to transfer solutes from host to parasite will vary. To date, a variety of experimental approaches argue for diversity in the mechanisms and the routes by which parasites accumulate host solutes. Contact between host and parasite ranges from direct lumen-to-lumen links between host and parasite xylem and continuity between the sieve elements of host and parasite, to the involvement of transfer cells between host and parasite. Progress has been slow since Solms-Laubach distinguished types of parasitic plants that fed from host phloem or xylem in 1867, but advances in clearly delineating the pathways that link host and parasite should now be possible using fluorescent proteins expressed and restricted to particular cell types of the host. This will initially necessitate using Arabidopsis, but should allow the types of connection, i.e. symplasmic or apoplasmic, to be determined and then the identification of parasite transporters responsible for solute flux.

Adaptation, Physiological↗

[Role of host behavior in the life cycle of parasites].

Parasite is an organism which, at least in a part of its ontogeny uses another living organism as a proper environment for its life. In the "parasite-host" relationships, formed by both these components, the parasite itself bears the burden of formation and maintenance of these relationships in a balance. Three factors play the main role in this process: (1) physiological adaptations of the parasite, enabling survival in the host body and resistance against defence reactions of the host; (2) morphological adaptations, leading to changes in the body structure of the parasite, dependent on location in the host body; and (3) behavioural adaptations assuring contacts of parasites with their hosts. In the process of evolution most groups of parasites evolved a complicated life cycle, with change of host and outer environment, succeeding in maturation of the parasite and production of the offspring. To pursuit this aim the parasite takes advantage from the behaviour of its potential host, its food preferences (e.g. by inclusion into a food chain), periodic or circadian migrations, and generally from its mode of life. The parasite modifies behaviour of its hosts, sometimes to a high degree, especially the behaviour of intermediate hosts, making them more conspicuously displayed for predators, the most often their final hosts. The parasite itself changes also its behaviour to be more attractive for a potential host or to enhance the possibility of finding a proper host. Finally, in a host population the parasite bears upon the position of particular host individuals by degradation of dominants and shifting them from reproduction. This phenomenon may be considered as a self-defence of the host population against reproduction of ill individuals, weaken by a burden of parasites.

Animals↗

Community ecology of the metazoan parasites of grey mullets, Mugil platanus (Osteichthyes: Mugilidae) from the littoral of the state of Rio de Janeiro, Brazil.

One hundred and fifty specimens of grey mullets, Mugil platanus Günther, collected from the littoral of the State of Rio de Janeiro, Brazil, between June 1984 to August 1988, were necropsied to study their infracommunities of metazoan parasites. Twenty-five species of metazoan parasites were collected. One hundred and forty-nine (99.3%) fishes were parasitized by one or more metazoan species. According to their importance values, 13 species were considered dominant, 7 species codominant and 2 species subordinate (digeneans were the majority of the total number of parasite specimens collected, with 63.7%). The presence of larval stages of digeneans and cestodes suggest that M. platanus is at an intermediate level in the marine trophic web. The Simpson index for all parasite species was low (0.059) indicating lack of dominance by a particular species in the parasite community. The parasites of M. platanus showed a typical overdispersed pattern of distribution. The capture localities of the hosts were consolidated into 3 groups and its parasite communities showed high qualitative and quantitative similarity, with high values for the Sorenson similarity coefficient and Percent similarity coefficient. Six species had a positive correlation between the host's total body length and parasite intensity, while three species had a negative correlation. Four species had a positive correlation between the host's total body length and parasite prevalence and one species had negative correlation. Five parasite species had differences in prevalence and intensity in relation to sex of host, but these differences were confounded with the total length of male and female fishes. The mean diversity in the infracommunities of M. platanus was H' = 0.936 +/- 0.477, without correlation with the host's total length and without significant difference between male and female fishes. In the ectoparasites, the infracommunities showed overall positive association, 6 pairs of copepod species had a significant positive association. One pair of species showed a negative covariation between parasite intensities. Infracommunities of endoparasites also showed overall positive association, and four species pairs of digeneans had a significant positive association. Only one had a negative association. The specialist components with low prevalence values predominated in the parasite community, which, based on these factors, was considered closer to the isolationist type.

Animals↗

[The fate of parasites of animal origin transmitted to humans].

The fate of a parasite transmitted from an animal to man depends on the ability of the contaminating agent to reach a place where it can thrive, to find necessary nutrients, and to resist host defense mechanisms. The purpose of this study was to evaluate the incidence of transmission of parasites from animals to man and to determine to what extent transmission is followed by development. Stenoxenic parasites whose life cycle requires transmission from animals to man obviously develop in man and then return to animals. These parasites cause holozoonoses of the cyclozoonosis type. Some euryxenic parasites can develop as well in man as in animals. These parasites can cause holozoonoses of the amphixenoses type. Other presumably euryxenic parasites can be transmitted from animals to man but not vice versa. These parasites are hemizoonoses agents. Non-transmission back from man to animals can be observed under several circumstances: incomplete development in man with failure to reach the stage at which transmission back to animals is possible; full development but with immaturity or sterility of the elements of dissemination necessary for transmission back to animals; full development but no way of evacuating elements of dissemination; full development and evacuation but with failure of elements of dissemination to survive. In these four cases man constitutes a dead-end for the parasite. A fifth possibility is that the parasite reaches full development but transmission back to animals cannot occur because man is not preyed upon by a carnivorous animal. In this case parasites are potential agents of holozoonoses and man is a cul-de-sac for the involved parasites.

Angiostrongylus↗

Egg-laying behaviour by shiny cowbirds parasitizing brown-and-yellow marshbirds.

We studied the laying behaviour of shiny cowbirds, Molothrus bonariensis, parasitizing brown-and-yellow marshbirds, Pseudoleistes virescens. Shiny cowbirds lay two egg morphs, spotted and white immaculate. Brown-and-yellow marshbirds eject the white egg morph but accept the spotted morph. The incidence of parasitism in this host was 66.5%, and half of the parasitized nests had more than one shiny cowbird egg. There was a positive relationship between the number of parasitic events and the availability of nests in the laying stage, but parasitic events reached a plateau when the availability of nests was high. The distribution of parasitic eggs per nest was more clumped than expected by chance. Shiny cowbird females synchronized parasitism with host laying in 80% of the cases. They seldom parasitized nests before the host started laying or after the nest had been deserted or predated. The majority of multiply parasitized nests were parasitized by more than one female. Females that lay white eggs did not avoid parasitizing brown-and-yellow marshbird nests. Egg pecking by cowbird females resulted, on average, in one egg lost per parasitic event and the probability of being broken was greater for host eggs when host and parasitic eggs where both in the nest. Copyright 1999 The Association for the Study of Animal Behaviour.

Journal Article↗