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PubMed1991

Antigenic analysis of Plasmodium yoelii liver stages by fluorescence antibody assays.

Little is known about the immune response against liver stage antigens which were first described for Plasmodium falciparum. In order to provide a basis for experimental studies, we analysed antigenically the liver stages of Plasmodium yoelii using sera of restricted specificity. Several distinct fluorescence patterns could be described in maturing liver forms. One pattern was identified as corresponding to antigens specific to the liver phase which are also species specific. Another pattern corresponds to sporozoite surface antigens which were predominant in liver trophozoites. Trophozoite-like liver forms were detected at least 7 days after the injection of irradiated sporozoites suggesting that parasites may persist and contribute to the immunity induced by this procedure.

Animals↗
PubMed1991

Possible mechanisms for the maintenance of polymorphisms in Plasmodium populations.

There are two views on the origin and maintenance of the high levels of polymorphism found in antigenic Plasmodium proteins. Immune selectionists consider that mutations which avoid stimulating a host response are frequent and advantageous. Proponents of the random genetic drift of selectively equivalent mutations hold that Plasmodium antigens are relatively unconstrained and can tolerate considerable structural diversity. Both sides agree that antigenic diversity is advantageous although selectionists see benefits in individual mutations whereas the proponents of random genetic drift see the advantage in the parasite's capacity to tolerate diversity per se.

Animals↗
PubMed1991

[Effect of nitroquine on protein synthesis of Plasmodium yoelii in vitro].

The erythrocytic stages of Plasmodium yoelii (BY 265 strain) were incubated with nitroquine (0.2 pmol.L-1 - 20 mumol.L-1), cycloheximide (0.1-10 nmol.L-1) and aminopterin (0.2 pmol.L-1 - 20 mumol.L-1) during 8 h in vitro. The results showed that the incorporation of [3H]-isoleucine into the protein by Plasmodium yoelii was inhibited by nitroquine (0.2 pmol.L-1) and cycloheximide (0.1 nmol.L-1), the inhibitory effect of nitroquine (IC50 = 0.16 nmol.L-1) was 397 times higher than that of cycloheximide (IC50 = 63.5 nmol.L-1). However, the incorporation of [3H]isoleucine into protein was not affected during at least 8 h of exposure to aminopterin (20 mumol.L-1). The results suggest that the inhibition of protein synthesis by nitroquine is one of the mechanisms of the early antimalarial action.

Aminopterin↗
PubMed1991

[The transplacental transport of Plasmodium falciparum in non-febrile parturient women in a holoendemic region].

Plasmodium falciparum parasitaemia measure, placenta print on microscope slide, immunofluorescence titration of Plasmodium antibodies and electrophoresis of haemoglobin were performed in 53 mothers and their child who did not shown any clinical signs of malaria. 51% from the mothers presented a patent parasitaemia associated with a high density of schizonts on uterine villi surface. Parasite density in children's blood was low and there was no correlation between mother's parasitaemia or placental schizogonia and newborn children's parasitaemia. We observed a higher prevalence of malaria attack, although the difference was not significant, in sickle cell women than in women whose haemoglobin was normal. In sickle cell women schizogonia occurred in placenta as in women whose haemoglobin was normal.

Anemia, Sickle Cell↗
PubMed1991

Wide distribution of the variant form of the human malaria parasite Plasmodium vivax.

We have found polymorphism in the repetitive and nonrepetitive regions of the sporozoite vaccine antigen, the circumsporozoite (CS) protein, in Plasmodium vivax malaria parasites from two geographically distant malaria endemic regions of the world. Like the recently described variant repeat sequence of P. vivax from Thailand, the CS protein repeat sequence of the variant P. vivax parasites from Papua New Guinea and Brazil is ANGA(G/D)(N/D)QPG, which differs from the previously identified CS repeat sequence, GDRA(D/A)GQPA, of P. vivax parasites from South America, Central America, and North Korea. Comparison of the P. vivax CS protein outside the repeat region revealed restricted polymorphism in regions that have exhibited T-cell immune function and sequence heterogeneity in the CS protein of Plasmodium falciparum. Our results show that P. vivax malaria parasites with the variant CS repeat sequences are widespread in nature and that the polymorphism in the CS protein of P. vivax is also present in the nonrepeat region.

Amino Acid Sequence↗
PubMed1991

[Plasmodium falciparum resistant to sulfadoxine/pyrimethamine in Senegal].

In 1983, the first African cases of malaria due to Plasmodium falciparum resistant to sulfadoxine/pyrimethamine, were described. Currently, this resistance is frequently found in Kenya and Tanzania. It has also been described in other African countries. A young Spanish woman contracted Plasmodium falciparum malaria in Senegal and was treated in our hospital with sulfadoxine/pyrimethamine. Fever and symptoms disappear within two days. The thick smears taken on the eighth and thirteenth days of treatment contained an abundance of gametocytes, but neither trophozoites nor schizonts. As the risk of transmission of malaria to the rest of the community was considered practically nil, no other treatment was administered. A month late, she was admitted to the hospital due to fever, shivering, fatigue, loss of appetite and hemolytic anaemia. The thick smear test again showed trophozoites of P. Falciparum. Thus, it proved to be a delayed grade I resistance to sulfadoxine/pyrimethamine, detected in far west Africa. An oral dose of mefloquine was administered as well as a red cell transfusion. Both fever and symptoms finally disappeared.

Adult↗
PubMed1991

Differential T cell responses to Plasmodium chabaudi chabaudi in peripheral blood and spleens of C57BL/6 mice during infection.

The definition of the immune status of a person is often taken as the responses obtained from lymphocytes isolated from peripheral blood. We therefore analyzed in a mouse model of Plasmodium chabaudi chabaudi the response of T lymphocytes taken from peripheral blood and compared it with the spleen during and after a primary erythrocytic infection. Using limiting dilution conditions, no malaria-specific T cell responses could be measured in the peripheral blood for up to 21 days after infection with P. chabaudi, whereas T cells responding to malaria Ag were readily detected in the spleen. This was true for T cells providing help and for those producing IFN-gamma. After clearance of the parasitemias to subpatent levels (75 days), qualitatively similar T cell responses were found in both compartments of the immune system, i.e., the Th cell response predominated over the inflammatory response. These data suggest that during an active infection with Plasmodium, T cell responses in peripheral blood are not necessarily indicators of the immune status.

Animals↗
PubMed1991

[Ultrastructural observation on the oocyst development and sporozoite formation of Plasmodium vivax].

The oocyst development of Plasmodium vivax was heralded by the appearance of cytoplasmic vacuoles and membraneous clefts. These clefts broke up oocyst cytoplasm into many sporoblasts. The onset of transformation from oocyst to sporozoite was heralded by forming pellicular complex, at some point of pelliculum of sporoblast dense inner membrane and subpellicular microtubules formed beneath the plasmalemma. The pellicular complex bulged out to form sporozoite buds appearing as small domes. Following enlargement of sporozoite buds the apical ends of the buds became conical in longitudinal sections with the newly formed apical rings at their truncated apices and then, newly formed dense inner membranes and subpellicular microtubules gradually extended backwards and finally enclosed the sporozoites. Beneath the inner membrane there were a total of 10-12 subpellicular microtubules arranged irregularly as 5 + 6, 6 + 5, 6 + 6, 7 + 4, 8 + 3, 10 + 1 and 11 + 1. During the formation of sporozoite, intranuclear spindle appeared in the nucleus, suggesting that the second meiosis in the life cycle of Plasmodium vivax occurred in developing sporozoites.

Animals↗
PubMed1990

[Tumor necrosis serum induce Plasmodium falciparum crisis form].

This paper reports that tumor necrosis serum (TNS) containing tumor necrosis factor (TNF) could inhibit Plasmodium falciparum in vitro. TNS was obtained from rabbits given macrophage-activating agent Mycobacterium tuberculosis (BCG) followed by intravenous administration of bacterial endotoxin (LPS). The results showed that TNS dilutions of 1:3, 1:6 and 1:12 could induce disappearance of Plasmodium falciparum (P less than 0.05) after being cultured 6 hours. TNS decreased red blood cell infective rate of the parasites as compared with the control (P less than 0.05) after 12 hours' cultivation. TNS of 1:3 dilution had further effect at 24 hours (P less than 0.05). Morphological observations showed that the growth of schizonts was retarded and abnormal merozoites were found.

Animals↗
PubMed1990

[Erythrocytes infected by Plasmodium falciparum activate human platelets].

Blood platelets are involved in Plasmodium falciparum malaria pathology as shown by thrombocytopenia and increased plasma level of two alpha granule proteins: beta thromboglobulin (beta TG) and platelet factor 4 (PF4). In this study we demonstrate that Plasmodium falciparum parasitized erythrocytes activate directly the secretion of beta TG and PF4 by human platelets. This secretion is related to parasitemia and occurs immediately after contact. Treatment of parasited erythrocytes by trypsin and diffusion chamber experiments suggest that platelet activation is triggered by parasitic substances shed on erythrocyte membrane and released in the culture medium.

Animals↗
PubMed1990

[In-vivo evaluation of Plasmodium falciparum sensitivity to chloroquine in Abidjan].

In vivo tests of Plasmodium falciparum chloroquine sensitivity were conducted in October and November, 1988 with 81 children aged 5 to 9 in several districts of Abidjan, Ivory Coast. The WHO standard scheme covering 7 days on basis of 25 mg per kilo spread over 3 days resulted in a therapeutic failure in 29.6 per cent cases. Nevertheless, a drop in overall parasitemia by over 80 per cent was noted from Day-0 to Day-2 in 70 per cent of visible resistance. Only in vivo tests conducted at a later stage with identification of chloroquine in the blood stream, with together in vitro studies will make it possible to know the actual level of resistance of Plasmodium falciparum strains to chloroquine.

Animals↗
PubMed1990

Ultrastructural features of host-parasite interactions in "in vitro" cultures of Plasmodium falciparum.

We carried out an electron-microscopy study on in vitro cultures of Plasmodium falciparum, whose general ultrastructural features are consistent with previous reports. In addition, whorled membrane-vesicles systems involving parasite and host-cells, never described to our knowledge up to now. As far as the parasite is concerned, these membraneous systems appear to be related to its growth and its connection with the external medium, with the possible involvement of Maurer's clefts. As for the erythrocyte, surface vesicles prove to be related to plasmodial infection in long-term in vitro culture. Richness in membranous structures of the complex host-parasite varies according to the metabolic demand of the plasmodium (i.e. on the life-cycle stage) and is influenced by external factors, possibly being a marker of drug action.

Animals↗
PubMedDate not supplied

[Evaluation of Plasmodium falciparum susceptibility to chloroquine and amodiaquine using a simplified, in vivo, 7-day test in southern Cameroon].

Plasmodium falciparum susceptibility to chloroquine and amodiaquine at a posology of 25 mg/kg per os in 3 days was evaluated in the pupils of 6 primary schools of South-West Cameroon during the first semester 1989. Parasitic index was 75%. Plasmodium falciparum was present in 96% of the infections 24% of the 357 children treated with chloroquine were carriers of trophozoites at D3 and 17% at D7. Complete resistance, at level R III, was observed in 4% of the children. By the 55 children treated with amodiaquine, 13% and 10% were carriers of few trophozoites at D3 and D7. The significance of these results is discussed.

Adolescent↗
PubMed1990

[Halofantrine hydrochloride in the treatment of Plasmodium falciparum malaria in a region of resistance. Analysis of 54 pediatric cases].

54 children (mean age: 43 months), with initial parasitemia up to 1,000 Plasmodium falciparum isolates per mm3, were treated with halofantrine hydrochloride 8 mg/kg twice daily at 6 hours intervals. 35 of these 54 children had received unsuccessful chloroquine and/or quinine treatment during 15 days before admission to the trial. Fever, which was observed in 52 of the children, and parasitemia disappeared respectively 18 hours and 37 hours after initial administration of the drug (mean values). Clinical and biological tolerance was excellent for all patients. Halofantrine is a new precious alternative for the treatment of malaria in regions with extensive multi-drug resistant strains of Plasmodium.

Animals↗
PubMed1990

[Effect of artesunate transdermal preparation on Plasmodium cynomolgi].

Artensunate transdermal preparation at 5, 10, or 15 mg/kg, bid, for 3 days applied locally on the shaved skin of the back of monkeys showed reliable therapeutic effects on Plasmodium cynomolgi, but recrudescence of the parasites was not controlled. If some azone was added in the artesunate transdermal preparation at the dosage of 5 mg/kg, bid, for 3 days, the parasitemia of Plasmodium cynomolgi could be cleared and recrudescence prevented, thus, the antimalarial effects was enhanced.

Administration, Cutaneous↗
PubMed1986

Antigen-specific, interleukin 2-propagated T lymphocytes confer resistance to a murine malarial parasite, Plasmodium chabaudi adami.

To explore cell-mediated immune mechanisms in host defense against malaria, we utilized a murine model system in which antibody-independent mechanisms of immunity are known to play a major role. Splenic T lymphocytes obtained from Plasmodium chabaudi adami-immune mice were maintained in vitro by using IL 2-containing medium and frequent antigenic stimulation. These IL 2-propagated T lymphocytes were characterized for their antigen reactivity, surface phenotype, and ability to confer protection to P. chabaudi adami in reconstituted mice. IL 2-dependent T lymphocytes maintained their capacity to proliferate in vitro to solubilized parasite preparations of homologous but not heterologous antigens. Antigen-specific proliferation was H-2 restricted, requiring antigen-presenting cells of the correct haplotype. More importantly, these propagated T lymphocytes were effective in adoptively transferring protection to both athymic nude mice and sublethally irradiated recipients. The protective response was dose dependent and antigen specific, because recipients resisted challenge infection with P. chabaudi adami but not with the heterologous parasite Plasmodium yoelii 17X. Pretreatment of the IL 2-propagated cells with anti-Thy-1.2 and complement abrogated their ability to transfer protection. Collectively, these results suggest that T lymphocytes obtained from P. chabaudi adami-immune mice, propagated and expanded in vitro, retain antigen specificity and passive protective activity in vivo.

Animals↗
PubMed1986

Antigen-specific and MHC-restricted Plasmodium falciparum-induced human T lymphocyte clones.

We established and analyzed human T lymphocyte clones induced by crude Plasmodium falciparum antigens of schizont-enriched asexual blood stages. Peripheral blood mononuclear cells (PBMC) were stimulated for 6 days with antigen, and the T cell blasts were separated and were transferred to limiting dilution cultures with antigen, irradiated PBMC, and recombinant interleukin 2. The following observations were made. Malaria antigen (M.Ag) induced similar proportions of T blasts in PBMC from infected individuals and noninfected controls, and the M.Ag-dependent clone frequencies (1/79 to 1/216) obtained with the blasts were similar. The majority of established clones derived from infected and noninfected subjects specifically recognized M.Ag and would not proliferate in response to red blood cells or autologous PBMC alone. They also required HLA class II determinant-compatible antigen-presenting (E-) cells. With three clones from one malaria patient, DR 1 or DR 5 specificities correlated with antigen presentation. Although T4+ and T8+ blasts were induced by M.Ag in PBMC, only T4 (Leu-3+) clones were obtained in our culture system. These clones secreted IL 2 in response to M.Ag. 4) Differential patterns of reactivity to native M.Ag, heat-stable antigens, and heat-precipitated antigens were exhibited by T cell clones, and the tested clones did not recognize Plasmodium berghei antigen. In conclusion, it is important with regard to previous observations on apparently nonspecific, mitogen-like effects of M.Ag in bulk T cell cultures that our results demonstrate specific recognition of P. falciparum by human T cells. The T cell clones obtained will be an important tool in the quest for a better understanding of the mechanisms involved in resistance to malaria infection.

Adult↗
PubMed1987

Antigenic analysis of the repeat domain of the circumsporozoite protein of Plasmodium vivax.

In the present study we analyzed the fine specificity of mouse monoclonal and human polyclonal antibodies directed against the repeat domain of the circumsporozoite (CS) protein of the human malaria parasite, Plasmodium vivax. Five synthetic peptides, representing monomeric and dimeric repeats of this malarial antigen, were assayed for their capacity to inhibit the binding of these antibodies to a yeast-derived recombinant CS protein. The results revealed the existence of at least two distinct repeated overlapping epitopes in the CS protein of P. vivax. Furthermore, polyclonal sera contain antibodies which recognize additional determinants not represented by the synthetic repeat peptides. Some of these sera contain antibodies recognizing a region flanking the repeat domain (region I). The present findings are in contrast with the antibody response in rodents and humans to the Plasmodium falciparum CS protein, which is directed against a single repeated immunodominant epitope.

Animals↗