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PubMed1987

Bovine cytotoxic T cell clones which recognize lymphoblasts infected with two antigenically different stocks of the protozoan parasite Theileria parva.

The Muguga and Marikebuni stocks of Theileria parva differ on the basis of cross-protection and in their schizont antigen profile determined with a panel of parasite-specific monoclonal antibodies. The phenotype and specificity of six cytotoxic T cell clones generated from an animal immunized against T. parva (Marikebuni) were investigated. All six clones had the BoT2+ BoT4- BoT8+ phenotype, were dependent on both specific antigen and T cell growth factor for proliferation and were restricted by determinants on class I major histocompatibility complex molecules. The clones killed target cells infected with either the Muguga or Marikebuni stocks of the parasite; the target cell lines tested included T cell clones which were infected in vitro with the two parasite stocks and subsequently recloned. The specificity of these cytotoxic T cell clones contrasts with that of T cell clones generated previously from animals immunized against T. parva (Muguga), in that the latter were specific for target cells infected with the Muguga stock of the parasite. Moreover, one of the clones generated against T. parva (Marikebuni) was restricted by the same major histocompatibility complex molecule as the Muguga-specific T cell clones. The difference in parasite strain-specificity between the two sets of clones appears to reflect the capacities of the two parasite stocks to cross-protect, since animals immunized against T. parva (Marikebuni) are protected against challenge with T. parva (Muguga) whereas a proportion of animals immunized with T. parva (Muguga) are susceptible to challenge with T. parva (Marikebuni). Another difference between the two sets of T cell clones was that those generated against T. parva (Marikebuni) only killed a proportion of cells of a given cell line in a 4-h cytotoxicity assay, whereas Muguga-specific T cells invariably kill the majority of cells. However, despite this partial killing, the clones markedly inhibited growth of parasitized cell lines when cultured with them for a period of 5 days.

Animals↗
PubMed1991

Bidirectional activating signals between Trypanosoma brucei and CD8+ T cells: a trypanosome-released factor triggers interferon-gamma production that stimulates parasite growth.

The hemoflagellate Trypanosoma brucei (T.b.) is the cause of African sleeping sickness. T. b. brucei which is pathogenic for rodents but nonpathogenic for humans was used to examine the interactions between the parasite and mononuclear cells (MNC). Co-cultivation in vitro of rat or human MNC and T.b. brucei resulted in a rapid non-antigen-specific release of interferon-gamma (IFN-gamma) which was dependent on CD8+ lymphoid cells. The parasites triggered MNC proliferation if IFN-gamma was blocked by a specific antibody in vitro. Separate cultures of parasites and MNC in a two-chamber system allowing exchange of soluble mediators showed CD8+ cell-dependent MNC triggering, indicating that a diffusable factor released by trypanosomes acts on the MNC. Gel filtration according to molecular mass of disrupted parasites and assay of the fractions revealed a peak activity at an approximate molecular mass of 185 kDa for the trypanosome-derived lymphocyte-triggering factor (TLTF). Conversely, there was a CD8+ cell-dependent action of MNC on the trypanosomes. MNC released a diffusable factor that in short-term experiments caused a striking increase in number of parasites. This effect was inhibited by antibodies against rat IFN-gamma. The increase in number of trypanosomes was promoted by rat MNC or rat IFN-gamma but not human MNC or human IFN-gamma suggesting a species-restricted recognition of IFN-gamma. An in vivo uptake of IFN-gamma by the parasites was suggested by immunohistochemical staining of T.b. brucei with an mAb against rat IFN-gamma and Western blot of the parasites showing a band with a molecular mass corresponding to IFN-gamma. The bidirectional signals we define here may explain certain features of trypanosomiasis, i.e. T cell activation, immunosuppression and host-range restriction. The seemingly important role of the TLTF indicates that it should be purified and explored as target for immune-specific intervention.

Animals↗
PubMed2001

Seasonal and age-related changes in blood parasite prevalence in Dark-eyed Juncos (Junco hyemalis, Aves, Passeriformes).

We determined seasonal changes in blood parasite infections in a free-living population of Dark-eyed Juncos (Junco hyemalis) breeding in interior Alaska (65 degrees N; 148 degrees W). The common parasites found in blood smears were Leucocytozoon fringillinarum (56%), Trypanosoma avium (33%), and Haemoproteus fringillae (9%). In males, parasite prevalences were relatively high at arrival on breeding grounds and increased during the breeding season. Intensity of infection with Leucocytozoon also increased between spring and summer, and then decreased at the time of migration (September). This decrease did not occur in adult females. Elevated prevalences during the breeding season probably reflected the addition of new cases via vector activity to positive status resulting from spring relapse. We observed neither an association between parasite species nor a consistent relationship between parasite intensity and body condition. To further study relationships between reproductive system activity and parasite infections, we compared prevalences in adult males that were undergoing their first cycle of gonadal development and regression (males in their second calendar year, or SY) with those of older males (males in their third or more calendar year, i.e., after-second-year males or ASY). Circulating testosterone concentrations declined in both groups between arrival on breeding grounds (end of April-early May) and the end of the reproductive period (July), and they were higher in May in ASY than in SY males. At the peak of the breeding season (June), ASY males also had a higher parasite prevalence than SY males. This difference may have resulted from immunosuppressive effects of gonadal hormones and/or from behavioral differences between SY and ASY males such that older males were exposed to more insect vectors than younger males. .

Age Factors↗
PubMed2003

Estimation of infection and recovery rates for highly polymorphic parasites when detectability is imperfect, using hidden Markov models.

A Bayesian hierarchical model is proposed for estimating parasitic infection dynamics for highly polymorphic parasites when detectability of the parasite using standard tests is imperfect. The parasite dynamics are modelled as a non-homogeneous hidden two-state Markov process, where the observed process is the detection or failure to detect a parasitic genotype. This is assumed to be conditionally independent given the hidden process, that is, the underlying true presence of the parasite, which evolves according to a first-order Markov chain. The model allows the transition probabilities of the hidden states as well as the detectability parameter of the test to depend on a number of covariates. Full Bayesian inference is implemented using Markov chain Monte Carlo simulation. The model is applied to a panel data set of malaria genotype data from a randomized controlled trial of bed nets in Tanzanian children aged 6-30 months, with the age of the host and bed net use as covariates. This analysis confirmed that the duration of infections with parasites belonging to the MSP-2 FC27 allelic family increased with age.

Algorithms↗
PubMed1998

Exploitation of manipulators: 'hitch-hiking' as a parasite transmission strategy.

For many parasites with complex life cycles, manipulation of host behaviour is an adaptation to increase the probability of successful transmission. Since manipulation is likely to be costly, other parasites may exploit hosts already manipulated so as to ensure their transmission without investing in manipulation. Such a cheating strategy, called 'hitch-hiking', could be adaptive in a range of situations. We first propose and discuss criteria that should be met by any parasite to be considered a hitch-hiker. Then, to understand the evolution of the hitch-hiking strategy, we use simple mathematical models to analyse the influence of several variables on the potential benefits for a nonmanipulative parasite of actively seeking a ride to the definitive host with a manipulative parasite. The models suggest that the prevalence or abundance of manipulative parasites will be a key determinant of whether hitch-hiking can be an advantageous option for other parasites. Copyright 1998 The Association for the Study of Animal Behaviour.

Journal Article↗
PubMed1998

Towards a functional explanation for the occurrence of anorexia during parasitic infections.

The development and occurrence of anorexia, the voluntary reduction in food intake during parasitic infections in animals, is somewhat paradoxical and contrary to conventional wisdom and expectation. We take the view that its occurrence is an evolved, costly behavioural adaptation which serves a function. Five such functional and general hypotheses to account for it are developed: (1) anorexia is induced by the parasite for its own benefit; (2) food intake decreases to starve parasites; (3) the negative effect on the host's energetic efficiency during parasitic diseases has a direct effect on food consumption; (4) food intake decreases for the purpose of promoting an effective immune response in the host; and (5) anorexia allows the host to become more selective in its diet, and thus select foods that either minimize the risk of infection or are high in antiparasitic compounds. Only hypotheses (4) and (5) survive the comparison for consistency with the physiological, metabolic and behavioural alterations that occur during the development of parasitic infections, and with the rule of generality (i.e. account for its occurrence in both protozoan and helminth infections). Both surviving hypotheses will need further experimental testing for their support or rejection, and such experiments are proposed. Also, the advantages and consequences of viewing anorexia during parasitic infections within a functional framework are discussed. These arise from the recognition that anorexia is a disease-coping strategy, part of the mechanism of recognition of parasite invasion by the immune system, which leads to a modification of the host's feeding behaviour. Copyright 1998 The Association for the Study of Animal Behaviour

Journal Article↗
PubMed1999

Retaliatory cuckoos and the evolution of host resistance to brood parasites.

We present a dynamic model of the evolution of host resistance to avian brood parasites, when the latter can retaliate against hosts that reject parasitic eggs. In a verbal model, Zahavi (1979, American Naturalist, 113, 157-159) suggested that retaliatory cuckoos might prevent the evolution of host resistance by reducing the reproductive success of rejecter hosts (i.e. by destroying their eggs or nestlings). Here we develop a model based on the association between the great spotted cuckoo, Clamator glandarius, and its main host, the European magpie, Pica pica, because this is the only system that has provided supportive evidence, to date, for the existence of retaliatory behaviour. Our aims were (1) to derive the conditions for invasion of the retaliation strategy in a nonretaliatory parasite population and (2) to investigate the consequences of retaliation for the evolution of host defence. If we assume a cost of discrimination for rejecter hosts in the absence of parasitism, and a cost paid by a retaliator for monitoring nests, our model shows cyclical dynamics. There is no evolutionarily stable strategy, and populations of both hosts and parasites will cycle indefinitely, the period of the cycles depending on mutation and/or migration rate. A stable polymorphism of acceptors and rejecters occurs only when parasites are nonretaliators. The spread of retaliator parasites drives rejecter hosts to extinction. Copyright 1999 The Association for the Study of Animal Behaviour.

Journal Article↗
PubMed1995

Comparison of the anti-laminin antibody response in patients with systemic lupus erythematosus (SLE) and parasitic diseases (filariasis).

In this study, we analyzed the presence of antibodies against the basement membrane antigen laminin (LMN) in patients with systemic lupus erythematosus (SLE), filariasis, and normal controls. By ELISA, 13.8% of SLE (12/87), 66.7% of parasitized patients (20/30), and two of the normal controls had these antibodies. IgG1 anti-LMN response was elevated in all groups, whereas IgG2 and IgG3 were also elevated in parasitized patients. The analysis of the IgG anti-laminin binding capacity in SLE and parasitized patients showed similar average antibody affinity. These antibodies did not react with fibronectin by a competition ELISA. By Western blot, the anti-laminin antibodies could be demonstrated in parasitized patient sera but not in SLE sera. Moreover, the ability of these antibodies to bind to heat-treated LMN (100 degrees C for 4 min) was different. The study of the binding capacity with native or denatured LMN by Western blot and dot-blot assays showed that the anti-LMN antibodies from parasitized patients were able to react with both native and denatured forms of LMN, whereas in SLE patients these antibodies were demonstrated only with native LMN. On the other hand, the reactivity detected in the normal control sera seems to be different from the anti-LMN antibodies from SLE and parasitized patients, and probably reflects the existence of natural antibodies in these sera. The presence of anti-LMN antibodies correlates significantly with the ability of inhibition of U937 cell adhesion to LMN-coated surfaces (P < 0.0025). The difference of anti-laminin reactivity suggests that antibodies produced following immunization with autoantigens or similar molecules present in parasites have different specificities from those spontaneously produced by individuals with autoimmune diseases.

Animals↗
PubMed1994

An abundantly expressed hemolymph glycoprotein isolated from newly parasitized Manduca sexta larvae is a polydnavirus gene product.

Cotesia congregata polydnavirus (CcPDV) is essential for successful parasitism of Manduca sexta larvae by the braconid wasp C. congregata. CcPDV virions are present in large numbers in the oviducts of C. congregata and injected with eggs into the hemocoel of M. sexta larvae during parasitization. Injection of sucrose density purified virions into nonparasitized larvae causes several of the parasitism-induced alterations in the physiology of host larvae that occur as a result of natural parasitism, including the synthesis of novel hemolymph proteins and abrogation of the host's immune response against the developing parasites. One of these proteins, early-expressed protein 1 (EP1), is a 190-kDa molecule which constitutes up to 5% of the total hemolymph protein by 24 hr following oviposition by the wasp. Using N-terminal sequence data for EP1 to construct primers for use in the polymerase chain reaction, we amplified and cloned a cDNA corresponding to the gene encoding EP1. This cDNA hybridized to DNA of the CcPDV genome, but not to DNA isolated from M. sexta larvae, suggesting that EP1 is a CcPDV gene product. A cDNA clone was isolated from an expression library generated from RNA extracted from newly parasitized M. sexta larvae. Sequence analysis of the cDNA clone revealed the presence of an open reading frame of 819 bp encoding a protein of 30.7 kDa. In vitro transcription/translation of the cDNA clone produced a protein of approximately 31 kDa, which was immunoprecipitated by EP1-specific polyclonal antiserum generated against purified deglycosylated EP1. EP1-like sequences also were amplified from male wasp genomic DNA, suggestive of integration of EP1-like sequences in the genome. This report constitutes the first evidence that a specific protein isolated from a parasitized host insect is a wasp polydnavirus gene product.

Amino Acid Sequence↗
PubMed1990

Antischistosomal action of mevinolin: evidence that 3-hydroxy-methylglutaryl-coenzyme a reductase activity in Schistosoma mansoni is vital for parasite survival.

The enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA reductase) plays an important role in regulating egg production in the human parasitic trematode Schistosoma mansoni. Infected mice treated with a low dose of mevinolin, an inhibitor of this enzyme, stopped egg production by the parasite and blocked the pathology associated with the infection. As an extension of this work, we exposed adult and developing schistosomes to higher doses of mevinolin for an extended period of time and observed the following: administration of 0.2% mevinolin in the diet of infected mice for 14 days resulted in 96-100% elimination of adult parasites. Administration of the same dose for 2 days before, and for 15 days after infection, resulted in 93-96% reduction of adult parasites. Co-administration of mevinolin with 0.5% mevalonate, but not 0.5% cholesterol, blocked the antischistosomal activity of mevinolin. We monitored schistosomal and mouse liver HMG-CoA reductase activity during the course of treatment and observed that HMG-CoA reductase activity was elevated in the liver but significantly reduced in the parasite. In vitro incubation of paired schistosomes with mevinolin, for up to 11 days, resulted in a dose- and time-dependent reduction of parasite motility and lactate production with eventual death. These in vitro effects were no evident when mevalonate was added to the culture system in place of, or in addition to, mevinolin. Collectively, the evidence suggests that mevalonate and/or metabolite not only plays a vital role in schistosome egg production, but is vital for survival of the parasite.

Animals↗
PubMed2003

Ceramide mediates growth inhibition of the Plasmodium falciparum parasite.

In mammalian cells, ceramide mediates death by chemotherapeutic drugs. We analysed, for the first time, the role of ceramide in inhibiting growth of the malaria-causing parasite Plasmodium falciparum. Added exogenously, ceramide significantly decreased the number of parasites, and this effect was abolished by sphingosine-1-phosphate, a biological antagonist of ceramide action. Ceramide can induce death of cancer cells by decreasing glutathione levels, and in our work it induced dose- and time-dependent depletion of glutathione in P. falciparum parasites. N-acetylcysteine, a precursor of glutathione, abrogated the cytotoxic effect of ceramide. Thus, ceramide can mediate growth inhibition of P. falciparum parasites by decreasing glutathione levels. The antimalarial drugs artemisinin and mefloquine induced the death of P. falciparum parasites by sphingomyelinase-generated ceramide and by decreasing parasite glutathione levels. Altogether, ceramide was identified as a signalling molecule capable of inducing growth inhibition of P. falciparum malarial parasites.

Animals↗
PubMed2006

First evidence of regular common cuckoo, Cuculus canorus, parasitism on eastern olivaceous warblers, Hippolais pallida elaeica.

Coevolution is defined as specialized relationships between species that lead to a reciprocal evolutionary change. A particularly suitable model system for studying coevolution is the interactions between obligate avian brood parasites and their hosts. The common cuckoo (Cuculus canorus, hereafter cuckoo) is a well-known brood parasite, which utilizes a range of smaller passerines as hosts. However, warblers of the genus Hippolais have rarely been reported as being victims of cuckoos, and furthermore, few data exist on the occurrence of antiparasite defenses in these hosts. In this study, we examined possible host-parasite coevolution between cuckoos and eastern olivaceous warblers (Hippolais pallida elaeica, hereafter olivaceous warblers) in three closely situated areas in northwestern Bulgaria. The olivaceous warbler has never been reported to be a regular cuckoo host. However, the present study, carried out in 2001-2003 shows that the olivaceous warbler is regularly and heavily parasitized by the cuckoo in this area. Parasitism rate was high (26.6%, 34/128) and consistent among years, with some variation between areas. The cuckoo egg mimicry was moderately good, and olivaceous warbler rejection rate of such eggs was 50%. Cuckoo eggs laid in olivaceous warbler nests had a whitish to whitish-green ground color, and the majority appeared to be distinctly different from cuckoo eggs found in other host species in the area. The olivaceous warbler proved to be a rather good host for cuckoos as 20.6% (7/34) of cuckoo eggs laid produced fledglings, a breeding success comparable to other suitable hosts in Europe. This is the first in-depth study of brood parasitism in a warbler of the genus Hippolais, and cuckoos parasitizing olivaceous warblers probably represent a previously unknown gens.

Animals↗
PubMed2004

Gastrointestinal parasite infestation.

Twenty-five percent of the world's population could be suffering parasitic infestation. Highest prevalence is in underdeveloped agricultural and rural areas in the tropical and subtropical regions. In some areas incidence may reach 90% of the population. In contrast, some major economic projects intended to promote local development have, paradoxically, caused parasitic proliferation, e.g. bilharziasis in Egypt and Sudan and Chagas disease in Brazil. The commonest cosmopolitan gastrointestinal parasite is Entamoeba histolytica. Some intestinal parasite are endemic in temperate climates, e.g. Entrobius vermicularis. The AIDS epidemic has increased the prevalence and severity of parasitic disease, particularly Strongyloides stercolaris. Tropical parasites are seen in Western people who travel to tropical countries. Radiology has acquired a major role in diagnosis and management of gastrointestinal parasite infestations and their complications.

Animals↗
PubMed2005

Immune responses to oral infection with Echinococcus multilocularis protoscoleces in gerbils: modified lymphocyte responses due to the parasite antigen.

Immune responses to oral infection with Echinococcus multilocularis protoscoleces in Mongolian gerbils were investigated. Gerbils not treated with prednisolone expelled most of the parasites within 3 days post-infection and induced parasite-specific intestinal IgA secretion after the oral inoculation with protoscoleces. In contrast, prednisolone-treated gerbils harbored notable numbers of parasites, and the parasite-specific intestinal IgA secretion was lower. In gerbils not treated and orally inoculated with protoscoleces (infected group), parasite-specific antibody levels in sera and intestinal washings were elevated, but blastogenesis against protoscolex antigens was observed only in cells from Peyer's patches at 14 days post-infection. Concanavalin A-induced proliferative lymphocytes from both infected and naive gerbils were suppressed by adding protoscolex somatic antigen. These data indicate that while parasite-specific antibody responses were observed, lymphocyte proliferative responses were suppressed by parasite infection/antigens in the Mongolian gerbil, prednisolone-untreated rodent definitive host model.

Administration, Oral↗
PubMed1998

Antibodies to nonrepeat sequences of antigen Pf155/RESA of Plasmodium falciparum inhibit parasite growth in vitro.

Immune responses to the repeat regions of the Plasmodium falciparum antigen Pf155/RESA have been extensively studied, and antibodies to the repeats are known to interfere with parasite growth both in vitro and in vivo. Less is known with regard to the effect on parasites of antibodies to the nonrepeat regions of the antigen. In the present study, rabbits were immunized with synthetic peptides corresponding to three different nonrepeated sequences of antigen Pf155/RESA. The reactivity of the antibodies with the particular peptides was analyzed by enzyme-linked immunosorbent assay (ELISA) and that with the parasite antigen, by immunoblotting and immunofluorescence. Although all antisera reacted strongly with the corresponding synthetic peptides, they reacted only weakly with full-length Pf155/RESA in either of the methods used. The specificity of the antibodies for Pf155/RESA was confirmed by their failure to stain Pf155/RESA-deficient parasites in erythrocyte membrane immunofluorescence, a method mainly detecting this antigen. Antibodies to the nonrepeat sequences also efficiently inhibited the merozoite invasion in vitro of Pf155/RESA+ parasites. However, these antibodies also inhibited Pf155/RESA-deficient parasites, indicating the presence of an antigen exhibiting a high degree of homology with Pf155/RESA. The results indicate that nonrepeat sequences of Pf155/RESA are immunogenic and may serve as targets for parasite-neutralizing antibodies, and, thus, the potential of the antigen as a vaccine candidate is emphasized.

Amino Acid Sequence↗
PubMed1988

Leishmania donovani: role of microviscosity of macrophage membrane in the process of parasite attachment and internalization.

Host macrophage infection by the parasite Leishmania donovani is heterogeneous, but it is not clear which factors are responsible for parasite recognition within the macrophages. One possible factor may be the alteration of the microviscosity of the macrophage membrane. This in turn may affect receptor expression and hence parasite infection. In this paper we describe alteration of the lipid composition and hence the microviscosity of the macrophage membrane in a controlled manner using liposome fusion technique. At a higher macrophage membrane microviscosity a larger number of parasites have been found to adhere to the macrophage surface. However, the proportion of parasites finally internalized when compared to parasites adhering to macrophages is inversely correlated with the artificially altered macrophage membrane microviscosity. The process of endocytosis has been examined in both native and lipid modified macrophages in the presence of several sugar antagonists. The results indicate (i) glucose and mannose are specifically involved in the binding process, and (ii) the microviscosity has a key role in controlling the macrophage parasite interaction. The results obtained so far support a model of endocytosis where expression of the receptor is a critical initial process dependent on the microviscosity of the membrane.

Animals↗
PubMed1990

Plasmodium chabaudi: in vivo effects of Ca2+ antagonists on chloroquine-resistant and chloroquine-sensitive parasites.

The effects of Ca2+ antagonists, verapamil, nicardipine, and diltiazem, on susceptibility to chloroquine were examined in mice infected with chloroquine-sensitive and chloroquine-resistant lines of Plasmodium chabaudi. In mice that received no chloroquine, daily injections of 50 mg/kg of verapamil, nicardipine, or diltiazem did not affect the growth of both sensitive and resistant parasites. When mice were injected daily with verapamil plus 2 to 3 mg/kg chloroquine, the chloroquine-sensitive parasite became more susceptible to chloroquine than the parasite in mice given chloroquine alone. On the other hand, in mice infected with chloroquine-resistant parasites, verapamil severely suppressed the growth of the parasite when accompanied by daily injections of 2 to 3 mg/kg of chloroquine, at which doses resistant parasites grew steadily in the absence of verapamil, indicating reversal of chloroquine resistance. This reversal was dose-dependent between 5 and 50 mg/kg of verapamil. Daily injections of nicardipine or diltiazem at 50 mg/kg also reversed resistance to chloroquine in resistant parasites. These results indicate that Ca2+ antagonists increase the susceptibility to chloroquine in a sensitive line of P. chabaudi and reverse chloroquine resistance in a resistant line.

Animals↗
PubMed1983

A comparison of knobby (K+) and knobless (K-) parasites from two strains of Plasmodium falciparum.

Erythrocytes infected with Plasmodium falciparum develop knob-like protrusions on their membranes. Knobby (K+) parasites of the FCR-3 (Gambian) strain have been shown to possess a histidine-labelled protein of apparent molecular weight 80 000 which is absent from knobless (K-) variants of the same strain. Here we report similar findings with K+ and K- parasites of another strain, the Malayan Camp strain, and also with cloned K+ and K- parasites of the FCR-3 strain. A histidine-labelled protein unique to the two K+ parasites was identified as a broad band with an apparent molecular weight of 89 000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The presence of this protein in both K+ Malayan Camp parasites and K+ FCR-3 (Gambian) parasites and its absence from K- parasites of both strains is consistent with this protein being a major component of knobs.

Animals↗