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PubMed1984

Intracellular parasite killing induced by electron carriers. I. Effect of electron carriers on intracellular Leishmania spp. in macrophages from different genetic backgrounds.

Mouse peritoneal macrophages were infected with Leishmania parasites from different species, then exposed to the electron carriers methylene blue (MB), toluidine blue O (TB), phenazine methosulfate (PMS) and crystal violet (CV). This led to killing of the intracellular parasites with no harm to the macrophages. On a molar basis, the potency of the electron carriers decreased in the following order: CV, TB, MB and PMS. MB and TB were more active against intracellular compared to free parasites, suggesting that the macrophages themselves might play a role in the observed anti-parasite toxicity. Intracellular killing could be achieved by a short pulse (30 min) of electron carrier. No difference could be detected between macrophages from different mouse strains as regards their capacity to kill intracellular parasites upon incubation with electron carriers. When macrophages from the L. major susceptible ('non-healer') BALB/c strain were infected with either L. enriettii (which is nonpathogenic to mice) or L. major, then exposed to an activating, lymphokine-rich supernatant, destruction of only L. enriettii was achieved, whereas L. major survived intracellularly. Incubation with MB, however, led to intracellular destruction of both parasites. Other Leishmania species could also be killed irrespective of the genetic background of the macrophages. These observations suggest that the triggering events in electron carrier- and lymphokine-mediated intracellular parasite killing are different.

Animals↗
PubMed1987

Isolation and characterization of parasites and host cell ghosts from erythrocytes infected with Plasmodium chabaudi.

A new procedure has been developed which allows the concomitant isolation of viable parasites and host cell plasma membranes from erythrocytes infected with Plasmodium chabaudi trophozoites. The average final yield of parasites is 56%. Free parasites reveal a well preserved ultrastructure, incorporate [14C]isoleucine for at least 3 h, and synthesize about the same proteins as parasites within erythrocytes as monitored by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE)-autoradiography. The host cell plasma membranes can be isolated in the form of ghosts with an average yield of 27%. The ghosts possess a structurally intact plasma membrane as revealed by freeze-etch electron microscopy. The ghosts are regularly associated with seven neo-proteins as identified by SDS-PAGE and isoelectric focusing (IEF)/SDS-PAGE. These neo-proteins have the following apparent molecular masses: 154 kDa, 145 kDa, 90 kDa, 72 kDa (pI 4.5), 67 kDa, 52 kDa, and 33 kDa (pI 5.7), respectively. The contamination of ghosts by parasite material and, conversely, the contamination of parasites by host cell plasma membranes is very low as demonstrated by light and electron microscopy, lactoperoxidase-mediated radioiodination and the distribution of the typical parasite marker enzymes such as choline kinase, cholinephosphotransferase and ethanolaminephosphotransferase.

Animals↗
PubMed1994

Recognition of the major cell surface glycoconjugates of Leishmania parasites by the human serum mannan-binding protein.

Activation of complement on the surface of parasitic protozoa of the genus Leishmania appears to be important for parasite infectivity in the mammalian host, as it allows these parasites to attach to and invade macrophages via their surface complement receptors. Serum mannan-binding protein (MBP) is a known activator of complement. Therefore, in the present study, we have investigated whether serum MBP binds to live Leishmania parasites, and to mannose-containing saccharides derived from the parasite cell surface. We have observed by fluorescence microscopy that biotinylated MBP binds to the surface of L. major and L. mexicana promastigotes. At this developmental stage the parasites are coated by a mannose-containing lipophosphoglycan (LPG). We have observed that radioiodinated MBP binds in a mannose-inhibitable manner to purified LPG which has been immobilized in plastic microwells, as well as to purified mannose-terminating di-, tri- and tetrasaccharide fragments ('cap' structures) which have been released by mild acid hydrolysis from the outer chains of the LPG, converted into neoglycolipids and resolved by thin-layer chromatography. 125I-MBP also binds in the chromatogram-binding assay to the mannose-containing glycoinositol-phospholipids that are expressed in high copy number on both the promastigote and the intracellular amastigote stages of most Leishmania species. These data suggest that MBP has the potential to opsonize the major developmental stages of Leishmania parasites, and provide a possible mechanism for the antibody-independent activation of complement on their surface.

Animals↗
PubMed1989

Characterization of adenine phosphoribosyltransferase from the human malaria parasite, Plasmodium falciparum.

Because of their inability to synthesize purines de novo, malaria parasites rely on purine phosphoribosyltransferases (PRTases) to convert purine bases salvaged from the host cell (the erythrocyte) into the corresponding purine nucleoside monophosphates. Our studies with late trophozoites of the human malaria parasite, Plasmodium falciparum, showed that virtually all of the purine PRTase activity is accounted for by two distinct enzymes. One enzyme utilizes hypoxanthine, guanine and xanthine (Queen, S.A., Vander Jagt, D. and Reyes, P. (1988) Mol. Biochem. Parasitol. 30, 123-134). The second enzyme utilizes only adenine and is the subject of this paper. This latter enzyme exhibits a biphasic pH-activity profile and is moderately to weakly inhibited by several divalent metal ions. Several of the properties of the P. falciparum enzyme were found to differ significantly from those of human erythrocyte adenine PRTase. (1) The molecular weight (18,000) of the parasite enzyme is smaller than that of the host cell enzyme. (2) The parasite enzyme, unlike the erythrocyte enzyme, is not significantly inhibited by sulfhydryl reagents. (3) 6-Mercaptopurine and 2,6-diaminopurine proved to be competitive inhibitors of the parasite enzyme (Ki 0.70 and 1.0 mM, respectively); on the other hand, the human enzyme is not inhibited by these agents. (4) The Km for adenine (0.80 microM) and 5-phosphoribosyl-1-pyrophosphate (0.70 microM) displayed by the parasite enzyme are significantly smaller than the corresponding Km values shown by the erythrocyte enzyme. These distinctions between the parasite and host enzymes point to the possibility that adenine PRTase of P. falciparum may represent a potential target for chemotherapeutic attack.

Adenine Phosphoribosyltransferase↗
PubMed1989

Parasite infections in AIDS.

'Illnesses no one's got' was the epidemiological clue that led to the identification of AIDS as a new disease in 1981 when a rare infectious organism Pneumocystis carinii was seen in previously healthy homosexuals. Since then a wide range of parasite infections has been recognized in AIDS patients. However, these patients are not susceptible to just any passing parasite. The human immunodeficiency virus (HIV) produces a specific immune defect and only parasites that can exploit that defect will be able to flourish. In this review Diana Lockwood and Jonathan Weber explore the spectrum of parasite diseases recognized in AIDS and also consider those parasites that occur infrequently in AIDS. Analysis of parasitic infections that AIDS patients do not suffer from will yield valuable information about immune recognition and handling of these parasites.

Journal Article↗
PubMed1995

Evolution of parasite life history traits: myths and reality.

Parasitism has evolved independently several times in many different animal lineages. Observations made on distantly related parasites have revealed a variety of adaptations to parasitism, including changes in physiology, morphology, and life history traits. These observations have led parasitologists to formulate general rules about the evolution of parasites, rules that define a common evolutionary path presumably followed by all parasitic organisms. Robert Poulin uses recent evidence to question the generality of these rules and to show that parasite evolution may take different roads. The selective pressures acting on parasites are diverse and may guide their evolution in any direction, just as they have shaped a wide variety of free-living organisms.

Journal Article↗
PubMed2004

Increased parasitaemia and delayed parasite clearance in Schistosoma mansoni and Plasmodium berghei co-infected mice.

Identifying factors that contribute to malaria susceptibility, severity and treatment failure remains one of the major research areas in malaria control strategies. In the present study, we superinfected Schistosoma mansoni infected mice with a lethal strain Plasmodium berghei ANKA to assess whether or not infection with S. mansoni affects parasite development, parasitaemia and parasite reduction or clearance following antimalarial treatment. Mice infected with P. berghei alone were used as control. The mice were followed for parasite development and parasitaemia between days 4 and 9 post-infection. On day 9, after taking blood samples, the mice were orally treated with 100mg/kg of chloroquine and then with 10mg/kg for three consecutive days. Parasite reduction/clearance and mortality were followed between days 10 and 13 post-treatment. The results showed, that superinfection with S. mansoni enhanced P. berghei parasite development, increased parasitaemia and mortality, and delayed reduction/clearance in parasitaemia. Hence, the results postulate that co-infections with schistosome and malaria parasites would aggravate malarial severity and prolong parasite reduction or clearance after chemotherapy in humans. This would necessitate the need for considering schistosome infection in clinical as well as therapeutic management of malaria patients in areas where the two diseases are co-endemic.

Animals↗
PubMed2005

The National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention: a new administrative structure for schistosomiasis control.

Since more than 5 decades, the overall responsibility for the national programme on schistosomiasis control in China resides at the government level, i.e. Ministry of Health. Day-to-day activities are carried out by independent provincial parasitic institutes situated in the endemic areas. Along with the general economic development and the steady progress in the medical sciences, successful developments in control and research of the parasitic diseases in the country were achieved. This necessitated a corresponding reorganization of the administrative structures which has taken place at several levels. In January 2002, the Chinese Centre for Disease Control and Prevention was reorganized and the Institute of Parasitic Diseases in Shanghai became part of this new organization under the name of the National Institute of Parasitic Diseases to better reflect its new role. By assigning all administrative tasks regarding research and control of parasitic diseases under the umbrella of one administrative central laboratory, the new task force for epidemiological surveys and direction of parasitic control programmes is well suited to respond to the daunting challenges of the future. The new institution has only existed for a few years but has already become a well-functioning force with a broad contact net of national and international experts on research and control of parasitic diseases.

Academies and Institutes↗
PubMed2006

Phylogeography of human lymphatic filarial parasite, Wuchereria bancrofti in India.

Wuchereria bancrofti, a nematode parasite causing human lymphatic filariasis is widely distributed in India. The phylogeography of this parasite was studied by constructing RAPD profiles of parasite populations collected from 71 microfilaria carriers residing in different geoclimatic regions of India. The analysis showed that the phylogeography of W. bancrofti populations is complex, with a high genetic divergence and gene flow among populations. The total genetic diversity (H(T)) and genetic differentiation (G(ST)) estimated for all the parasite populations were 0.0926 and 0.5859, respectively. The gene flow (Nm) between different regions indicated that two strains of W. bancrofti were prevalent in the country, one in the eastern side and the other on the western side of the Western Ghats. A highly significant genetic differentiation (F(ST) [theta] = 0.7978) was estimated between these two strains (chi 2 = 308.2789; P < 0.001). The gene flow between these strains was very low (0.2338). These two strains appear to have drifted genetically because of their geographic isolation by this thickly forested mountain range. The strain in the eastern side was found to be monophyletic in origin and is undergoing genetic divergence as the major parasite population in the country, spanning from eastern peninsular region to the northern plains. The variable geoclimatic factors and the antifilarial chemotherapeutical pressure on the parasite, which is in place for the past half a century, might have contributed for the high genetic heterogeneity its strains/populations in the country. The route of entry of the parasite into Indian sub-continent possibly appeared to be from an ancient origin from the countries of the Southeast Asian archipelago, through the eastern coastal line of the southern peninsula.

Animals↗
PubMed2004

Choline uptake into the malaria parasite is energized by the membrane potential.

The uptake by the intraerythrocytic malaria parasite of the phospholipid precursor choline was investigated in parasites 'isolated' from their host cells by saponin permeabilization of the erythrocyte membrane. Choline is transported across the parasite plasma membrane then phosphorylated and thereby trapped within the parasite. Choline influx was inhibited competitively by quinine. It increased with increasing extracellular pH, decreased on depolarization of the parasite plasma membrane with a protonophore or by increasing extracellular [K+], and increased in response to hyperpolarization of the membrane by decreasing extracellular [K+] or by addition of the K+ channel blocker Cs+. In ATP-depleted parasites choline was taken up but not phosphorylated. Under these conditions, imposition of an inwardly negative membrane potential using the K+ ionophore valinomycin resulted in the accumulation of choline to an intracellular concentration more than 15-fold higher than the extracellular concentration. Choline influx is therefore an electrogenic process, energized by the parasite plasma membrane potential.

Animals↗
PubMed2006

Plasmodium falciparum: chondroitin sulfate A is the major receptor for adhesion of parasitized erythrocytes in the placenta.

Plasmodium falciparum parasites that sequester in the placenta bind to the molecule chondroitin sulfate A (CSA). Women become resistant to malaria during pregnancy as they acquire antibodies that inhibit parasite adhesion to CSA, suggesting that a vaccine against placental malaria is feasible. Hyaluronic acid (HA) and non-immune IgG have also been proposed as receptors for P. falciparum adhesion in the placenta, but evidence for their roles is inconclusive. In this study, CSA, HA, and IgG were simultaneously assessed for their relative contributions to placental adhesion. Placental parasites collected in Tanzania uniformly adhered to the molecule CSA, and soluble CSA completely inhibited adhesion of most samples to placental cryosections. Three of 46 placental parasite samples also adhered to immobilized HA, but HA failed to inhibit adhesion of any placental parasites to placental cryosections. Similarly, non-immune IgG and protein A failed to inhibit adhesion of parasite samples to placental cryosection. P. falciparum adhesion in the placenta appears to be a non-redundant process that requires CSA as a receptor. Vaccines that elicit functional antibodies against CSA-binding parasites may confer resistance to pregnancy malaria.

Adolescent↗
PubMed2026

Parasite clearance in patients with Plasmodium vivax monoinfection treated with artesunate in Cambodia: an observational secondary analysis of trial data.

BACKGROUND: Artemisinin-based combination therapies are the frontline drugs for the treatment of malaria infections, but, for Plasmodium falciparum, the efficacy of artemisinin is threatened by the spread of resistance. Plasmodium vivax is the second most common cause of human malaria, but there is little information on its susceptibility to artemisinin due to the lack of an in-vitro culture system. This study aims to characterise the response of P vivax to artesunate using clinical, genomic, and transcriptomic data from infected individuals in Cambodia. METHODS: We analysed 161 P vivax infections from 87 patients (six female and 81 male; median age 20 years [IQR 17-26]) enrolled between Nov 10, 2021, and Nov 18, 2022, in a drug efficacy study in Cambodia and treated with 2 mg/kg/day of artesunate for 7 days. To determine clearance rates, we measured parasitaemia before, and 1 h, 2 h, 4 h, 8 h, and 16 h after the first dose of artesunate, and then at 24-h intervals during the 7 days of artesunate therapy. We also examined the parasites' genome sequences and used RNA sequencing of 31 infections to analyse changes in parasite gene expression upon treatment. FINDINGS: All infections were successfully cleared by day 3. However, 49 of the infections displayed a slow clearance after treatment, including nine (6%) infections with a parasite clearance slope half-life greater than 5 h. We observed no significant association between slow clearance and either patient or infection characteristics (including the infection's stage composition). Analyses of gene expression showed that, while fast-clearing parasites displayed significant changes in gene expression immediately upon treatment, slow-clearing parasites had a delayed gene expression response characterised notably by a downregulation of genes associated with haemoglobin endocytosis and digestion. INTERPRETATION: Some Cambodian P vivax parasites clear slowly after artesunate treatment, possibly due to a downregulation of haemoglobin metabolism that might reduce the efficiency of the artesunate. The slow clearance could allow parasites to outlast artesunate treatment and facilitate emergence of resistance to the artemisinin-combination therapy partner drug, threatening malaria elimination effort. FUNDING: US National Institutes of Health.

Adolescent↗
PubMed2004

Microscopy and the helminth parasite.

Microscopy has a long and distinguished history in the study of helminth parasites and has made a singularly outstanding contribution to understanding how these complex animals organise their lives and relate to their hosts. Increasingly, the microscope has been used as a powerful investigative tool in multidisciplinary approaches to parasitological problems, placing emphasis on functional correlates rather than anatomical detail. In doing so, microscopy has also uncovered a number of attributes of parasites that are of wider significance in the field of biology. Parasite surfaces have understandably demanded most of the attention of microscopists, largely as a result of the pioneering studies using transmission electron microscopy. Their findings focused the attention of physiologists and immunologists on the tegument and cuticle of helminths and in doing so helped unravel the complex molecular exchanges that are fundamental to understanding host-parasite interactions. Scanning electron microscopy succeeded in augmenting these data by revealing novel microtopographical features of the host-parasite relationship, as well as proving invaluable in helminth taxonomy and in assessing the efficacy of test substances in drug screens. Control of helminth parasites has never been more critical: problems of drug resistance demand urgent action to identify exploitable targets for new generation anthelmintics. In this regard, the neuropeptide signalling system of helminths is envisioned as central to nerve-muscle function, and thereby a crucial regulatory influence on their motility, alimentation and reproduction. The use of immunocytochemistry interfaced with confocal scanning laser microscopy has not only been instrumental in discovering the peptidergic system of helminths and its potential for chemotherapeutic exploitation, but through increasingly sophisticated bio-imaging technologies has continued to help dissect and analyse the molecular dynamics of this and other cellular systems within these important parasites.

Animals↗
PubMed2006

Phylogenetic analysis of coccidian parasites from invertebrates: search for missing links.

Apicomplexan parasites represent one of the most important groups of parasitic unicellular eukaryotes comprising such important human parasites such as Plasmodium spp. and Toxoplasma gondii. Apicomplexan radiation as well as their adaptation to the parasitic style of life took place before the era of vertebrates. Thus, invertebrates were the first hosts of apicomplexan parasites that switched to vertebrates later in evolution. Despite this fact, apicomplexan parasites of invertebrates, with the exception of gregarines, have so far been ignored in phylogenetic studies. To address this issue, we sequenced the nuclear SSU rRNA genes from the homoxenous apicomplexan parasites of insects Adelina grylli and Adelina dimidiata, and the heteroxenous Aggregata octopiana and Aggregata eberthii that are transmitted between cephalopods and crustaceans, and used them for phylogenetic reconstructions. The position of the adelinids as a sister group to Hepatozoon spp. within the suborder Adeleorina was stable regardless of the phylogenetic method used. In contrast, both members of the genus Aggregata possess highly divergent SSU rRNA genes with an unusual nucleotide composition. Because of this, they form the longest branches in the tree and their position is variable. However, the genus Aggregata branches together with adelinids and hepatozoons in most of the analyses, although their position within the scope of this cluster is unstable.

Animals↗
PubMed2006

Antigenic variation as an exploitable weakness of babesial parasites.

Babesia bovis and its bovine host interact in many ways, resulting in a range of disease and infection phenotypes. Host responses to the parasite elicit or select for a variety of responses on the part of the parasite, the full range of which is not yet known. One well-established phenomenon, thought to aid parasite survival by evasion of host adaptive immune responses, is the sequential expansion of antigenically variant populations during an infection, a phenomenon referred to as "antigenic variation". Antigenic variation in B. bovis, like that in the human malarial parasite, Plasmodium falciparum, is intimately linked to a second survival mechanism, cytoadhesion. In cytoadhesion, mature parasite-containing erythrocytes bind to the capillary and post-capillary venous endothelium through parasite-derived ligands. The reliance of these parasites on both functions, and on their linkage, may provide opportunities to develop anti-babesial and, perhaps, anti-malarial protection strategies. The development of inhibitors of DNA metabolism in B. bovis may be used to abrogate the process of antigenic variation, whereas small molecular mimics may provide the means to vaccinate against a wide range of variants or to prevent the surface export of variant antigen ligands. In this article, aspects of antigenic variation and cytoadhesion in bovine babesiosis are explored, with a discussion of opportunities for prophylactic or therapeutic intervention in these intertwined processes.

Animals↗
PubMed2002

Role of complex II in anaerobic respiration of the parasite mitochondria from Ascaris suum and Plasmodium falciparum.

Parasites have developed a variety of physiological functions necessary for existence within the specialized environment of the host. Regarding energy metabolism, which is an essential factor for survival, parasites adapt to low oxygen tension in host mammals using metabolic systems that are very different from that of the host. The majority of parasites do not use the oxygen available within the host, but employ systems other than oxidative phosphorylation for ATP synthesis. In addition, all parasites have a life cycle. In many cases, the parasite employs aerobic metabolism during their free-living stage outside the host. In such systems, parasite mitochondria play diverse roles. In particular, marked changes in the morphology and components of the mitochondria during the life cycle are very interesting elements of biological processes such as developmental control and environmental adaptation. Recent research has shown that the mitochondrial complex II plays an important role in the anaerobic energy metabolism of parasites inhabiting hosts, by acting as quinol-fumarate reductase.

Amino Acid Sequence↗
PubMed2003

Synthetic propeptide inhibits mosquito midgut chitinase and blocks sporogonic development of malaria parasite.

Incessant transmission of the parasite by mosquitoes makes most attempts to control malaria fail. Blocking of parasite transmission by mosquitoes therefore is a rational strategy to combat the disease. Upon ingestion of blood meal mosquitoes secrete chitinase into the midgut. This mosquito chitinase is a zymogen which is activated by the removal of a propeptide from the N-terminal. Since the midgut peritrophic matrix acts as a physical barrier, the activated chitinase is likely to contribute to the further development of the malaria parasite in the mosquito. Earlier it has been shown that inhibiting chitinase activity in the mosquito midgut blocked sporogonic development of the malaria parasite. Since synthetic propeptides of several zymogens have been found to be potent inhibitors of their respective enzymes, we tested propeptide of mosquito midgut chitinase as an inhibitor and found that the propeptide almost completely inhibited the recombinant or purified native Anopheles gambiae chitinase. We also examined the effect of the inhibitory peptide on malaria parasite development. The result showed that the synthetic propeptide blocked the development of human malaria parasite Plasmodium falciparum in the African malaria vector An. gambiae and avian malaria parasite Plasmodium gallinaceum in Aedes aegypti mosquitoes. This study implies that the expression of inhibitory mosquito midgut chitinase propeptide in response to blood meal may alter the mosquito's vectorial capacity. This may lead to developing novel strategies for controlling the spread of malaria.

Amino Acid Sequence↗
PubMedDate not supplied

Plasma profiles of albendazole metabolites after administration of netobimin and albendazole in sheep: effects of parasitism and age.

Netobimin and albendazole were administered to 3-month-old lambs with moderate infections of Nematodirus battus and to comparable parasite-naive lambs. Albendazole sulphoxide and albendazole sulphone concentrations were determined in the plasma of all lambs at frequent intervals after treatment. Both anthelmintic preparations were 100% effective in reducing nematode faecal egg output in the lambs. There were no significant differences in the concentrations of the sulphoxide or sulphone metabolites in parasitized compared with non-parasitized lambs given the same parent anthelmintic. The parasite-naive lambs were subsequently weaned and maintained indoors in conditions designed to preclude nematode parasite infection until they were 9 months old. Netobimin and albendazole were administered again and the plasma profiles of the albendazole sulphoxide and albendazole sulphone metabolites determined. There were no significant differences in the plasma distribution of these metabolites with age of the lambs. The area under the plasma concentration time curve, mean resident time and apparent half-life of the albendazole sulphoxide metabolite was determined following administration of each parent drug and the clearance of the metabolite/systemic availability of parent drug was determined as a marker of the amount of drug available for metabolism. There were no significant differences in pharmacokinetic variables between parasitized and non-parasitized animals nor with the age of the animals.

Aging↗