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PubMedDate not supplied

[Congenital Plasmodium falciparum malaria. Apropos of a case in Paris].

A 28 years old parturient woman, coming back from Cameroon, was admitted with fever. Blood smear for malaria revealed trophozoïtes of Plasmodium falciparum. Because of fetal troubles, the infant was born by a caesarean. Physical examination of the new-born revealed an hepatomegaly. Cord blood film showed trophozoïtes of Plasmodium falciparum. With treatment with chloroquine, the child looked healthy in a few days. So, congenital malaria is not seldom in areas of high malaria endemicity, but we must be very careful with travellers parturient in other countries. The difference between congenital and perinatal malaria is discussed.

Adult↗
PubMed1983

Spirogermanium: a new drug with antimalarial activity against chloroquine-resistant Plasmodium falciparum.

Spirogermanium, a new investigational drug of novel structure currently under clinical studies in various neoplastic diseases, has revealed significant in vitro activity against chloroquine-resistant (FCB, FTA, FVO) and sensitive (FSL, FUI, FH) strains of Plasmodium falciparum. Inhibition of the growth and maturation of parasites after 36-h exposures to Spirogermanium started at concentrations ranging from 2.48 to 9.9 nM/ml. These concentrations appear to be within the range of Spirogermanium plasma levels reported in clinical studies with this drug. Since its clinical toxicities are unusually low in comparison with other anticancer drugs, our results on its in vitro activity against Plasmodium falciparum indicate Spirogermanium is an antimalarial drug of entirely novel structure, active in resistant strains.

Antimalarials↗
PubMed1984

Enhancement of phagocytosis of parasitized and nonparasitized red cells in acute Plasmodium berghei malaria.

The phagocytosis by mouse peritoneal macrophages of parasitized red cells (PRCs) and nonparasitized red cells (nonPRCs) separated from Plasmodium berghei infected blood was studied in vitro. Peritoneal macrophages from acutely infected mice and normal mice were cultured on coverslips. PRCs and nonPRCs were fractionated by Ficoll density gradient centrifugation from Plasmodium berghei infected blood. PRCs were fed in triplicate cultures to normal macrophages in normal serum, normal macrophages in acute serum, acute macrophages in normal serum, and acute macrophages in acute serum. Similarly, nonPRCs were fed to macrophages in the same combinations of normal and acute macrophages and serum. In acute serum, acute macrophages ingest PRCs significantly more readily than normal macrophages (p less than 0.05). Acute macrophages in acute serum ingest PRCs more readily than acute macrophages in normal serum, but the difference does not achieve statistical significance. Acute serum apparently decreases the phagocytosis of PRCs and nonPRCs by normal macrophages, perhaps because of an inhibitory antibody present in acute serum. As with PRCs, in the presence of acute serum, acute macrophages ingest nonPRCs significantly more readily than normal macrophages (p less than 0.05).

Acute Disease↗
PubMed1984

Studies on the Uganda I/CDC strain of Plasmodium malariae in bolivian Aotus monkeys and various anophelines.

A strain of Plasmodium malariae (Uganda I/CDC) was isolated from an infant who had been infected via blood transfusion from a donor who had entered the United States 8 yr previously. After passage through a splenectomized chimpanzee, the parasite was studied in 29 splenectomized Aotus azarae boliviensis monkeys. Maximum parasitemias were higher in Aotus monkeys without previous Plasmodium infection than in Aotus monkeys with a history of P. vivax infection. Animals with a history of infection with both P. vivax and P. falciparum had lower maximum parasitemias than did monkeys in either of the 2 preceding groups. The highest rates of mosquito infection were most often obtained during the 10-day period just after the parasite count rose above 500/mm3 of blood. The most susceptible mosquito was Anopheles freeborni followed by An. stephensi, An. gambiae, An. dirus, and An. maculatus. Two attempts to transmit the Uganda I/CDC strain of P. malariae to other monkeys by sporozoite inoculation were unsuccessful.

Animals↗
PubMed1984

Plasmodium berghei: characterization of antigens and their role in inducing immunity to infection.

In vitro, Plasmodium berghei infected erythrocytes incorporated 35S-methionine into 31 polypeptides with molecular weights from 21 kd to 300 kd. Hemoglobin and additional smaller molecular weight polypeptides were labelled with 35S-methionine by a population of uninfected, reticulocyte-rich rat erythrocytes. 3H-glucosamine was incorporated into at least 3 components by Plasmodium berghei infected erythrocytes. Uninfected, reticulocyte-rich rat erythrocytes did not incorporate 3H-glucosamine. Rabbit antisera against small, free plasmodia formed complexes which contained between 12 and 22 of the 31 labelled polypeptides in the 35S-methionine labelled antigen preparation. Rabbit antisera against soluble antigens washed from small, free plasmodia formed complexes containing many of the same labelled plasmodial polypeptides, however the reactions were particularly strong with those components which yielded polypeptides with molecular weights of 25 kd and 31 kd. Rabbit origin antisera against the 2 preparations did not form detectable complexes with the 3H-glucosamine labelled plasmodial components. Sera from rats undergoing progressive P. berghei infection formed complexes containing an increasing number of 35S-methionine labelled plasmodial polypeptides. Hyperimmune rat serum, the only serum protective upon passive transfer into mice, formed complexes containing 7 polypeptides with molecular weights of 35 kd, 75 kd, 80 kd, 92 kd, 100 kd, 150 kd and 190 kd. Antigens containing 1 or more of these polypeptides may be important in the induction of a protective antibody response against the parasite.

Animals↗
PubMed1984

Renal deposits of lipoprotein-immunoglobulin complexes in Plasmodium chabaudi-infected mice.

Lipoprotein metabolism is altered and immunoglobulin-lipoprotein complexes (Ig-Lp) are formed during malaria infection (1-5). Ig-Lp were detected in the sera of Plasmodium chabaudi-infected mice 9 days post-infection (1 or 2 days after parasitemia had peaked at about 50%) and reached a maximum on day 13 (when the parasitemia had decreased to less than 1%). Renal glomerular deposits of IgM were first detected at day 3 and were heavy from day 9 to day 29; deposits of IgG and low density lipoprotein (LDL) were present from days 9 to 62, and were more dense from days 22 to 29; deposits of C3 were observed from day 13 to day 29. Apoprotein B component was found in heparin eluates of kidneys on day 10, 14, and 29. Fractionated Ig-Lp, as well as whole sera from day-13 infected mice, were injected into uninfected mice that developed LDL glomerular deposits only when pre-treated with histamine. LDL glomerular deposits were also observed after i.v. injection of day-29 sera (containing free anti-lipoprotein antibody) into day-7 infected mice, but not when a mixture of day-29 and day-7 sera was injected into normal recipient mice. LDL glomerular deposits, however, were observed when recipient mice were treated with the Plasmodium-derived Insoluble Material (PDIM) 3 days before the injection of the day-29-day-7 sera mixture or day-13 serum. Two hours after the i.v. injection of 125I-Ig-Lp, the radioactivity of the kidneys was higher in histamine-treated, PDIM-treated, and P. chabaudi-infected mice than in controls. The clearance of 125I-Ig-Lp was higher in infected and in PDIM-treated mice than in controls. We suggest that the glomerular deposit of Ig-Lp that occurs during P. chabaudi infection requires an enhancing factor such as PDIM that is released during infection.

Animals↗
PubMed1984

Oxidative killing of the intraerythrocytic malaria parasite Plasmodium yoelii by activated macrophages.

The capacity of macrophages activated in vivo and in vitro to kill Plasmodium yoelii was investigated. Macrophages activated by BCG-, Con A-, or malaria-induced lymphokines (LK) were cultured with P. yoelii-parasitized erythrocytes (PE). In some experiments, effector and target cells were separated by a 0.45-micron filter. Parasite viability was assessed a) in vivo by injection of mice and quantitative detection of parasites by RIA or b) in vitro by the incorporation of 3H amino acids into parasite proteins. Activated macrophages killed target PE in a dose-dependent manner by elaborating a membrane-permeable soluble factor(s). The addition of small amounts of immune serum augmented the killing of the parasites. LK-activated macrophages underwent an oxidative burst upon the phagocytosis of PE as evidenced by the accumulation of reduced formazan in the NBT assay. The magnitude of the oxidative response corresponded to the number of parasites that were ingested. The phagocytosis-induced oxidative burst was necessary for subsequent killing of Plasmodium. Parasites incubated in microchambers separated from macrophages by a 0.45-micron filter were susceptible to H2O2 released by LK-activated macrophages incubated with PMA, opsonized zymosan, or P. yoelii antigen. Inhibition of protein synthesis by parasites exposed to products of activated macrophages was abrogated by preincubating macrophages with catalase but not with SOD, mannitol, or histidine. These results suggest that phagocytosis-associated oxidative mechanisms mediate the destruction of the malaria parasite. Hence, cell-mediated as well as antibody-dependent mechanisms cooperate in the immune response against malaria.

Amino Acids↗
PubMed1980

Purine base and nucleoside uptake in Plasmodium berghei and host erythrocytes.

The absorption of 3H-labeled adenine, adenosine, hypoxanthine, and 14C-labeled inosine by normal rat erythrocytes, Plasmodium bergheri-infected erythrocytes and saponin released "free parasites" was measured. The uptake of these labeled substrates by normal rat erythrocytes occurs both by diffusion and mediated transport systems. Similar absorptive mechanisms for these substrates also were observed for both Plasmodium berghei-infected erythrocytes and "free parasites." Data from inhibition studies using purine base and nucleoside analogues indicate the presence of three distinct transport loci in the normal erythrocyte for adenosine-inosine, hypoxanthine, and adenine and two loci in the infected erythrocyte and "free parasite" for adenosine-inosine-hypoxanthine and adenine. The initial metabolism of 3H-adenosine by the "free parasite" also was examined. A double isotope technique was used to follow the separate metabolic fates of the purine base and ribose moieties of adenosine. The data suggest a possible conversion of adenosine to the purine base and ribose moiety and subsequent uptake of the purine base by the parasite. In addition, a powerful adenosine deaminase inhibitor (2-deoxcoformycin) significantly reduced the uptake of 3H-adenosine by the "free parasites." Chromatographs of aliquots from postincubation media show the tritium label to be associated predominately with adenosine in the presence of 2-deoxycoformycin and with isoine and hypoxanthine in the absence of the inhibitor.

Adenine↗
PubMedDate not supplied

[Inflammation and resistance of mice against "Plasmodium berghei" (author's transl)].

An inflammatory reaction induced in mice by a subcutaneous injection of magnesium silicate embedded in a calcium phosphate gel is followed by an increased resistance against Plasmodium berghei. The occurrence of this increased resistance against Plasmodium berghei. The occurrence of this increased resistance is related to the time elapsed between the induction of the inflammatory process and the infection. The delayed mortality is correlated with a slowed development of parasitemia. It is hypothesized that the protective effect may be related to the capacity of the inflammatory reaction to promote in mice both specific and non-specific antiparisitic immune responses.

Animals↗
PubMed1982

Isolation of intracellular parasites (Plasmodium falciparum) from culture using free-flow electrophoresis: separation of the free parasites according to stages.

Parasitized human erythrocytes were concentrated from continuous cultures of Plasmodium falciparum from 5-7% up to 80-95% using Plasmagel. After aggregation of the cells with phythemagglutinin, the aggregated erythrocytes were fragmented by passing them, with minimal force, through successive nylon filters of decreasing pore size (100 microns-3 microns). The mixture of liberated, free parasites, intact erythrocytes and erythrocyte membrane vesicles was separated using free-flow electrophoresis. Most of the fractions containing free parasites did not show contamination with erythrocyte constituents as determined by light and electron microscopy, polyacrylamide gel electrophoresis, and enzymatic analysis. In addition, the various stages of free parasites of Plasmodium falciparum exhibited different electrical surface charges. Rings and trophozoites were highly negatively charged whereas schizonts and, in particular, merozoites showed low negative charges. Thus, the various stages could be isolated separate from each other.

Acetylcholinesterase↗
PubMed1982

Phospholipid biosynthesis by Plasmodium knowlesi-infected erythrocytes: the incorporation of phospohlipid precursors and the identification of previously undetected metabolic pathways.

Metabolic pathways leading to phospholipid biosynthesis in Plasmodium-infected simian erythrocytes were tested and quantified by incubating leucocyte-free erythrocytes in the presence of labelled precursors. Plasma fatty acids and lysophospholipids both served as sources of the fatty acids required for cellular phospholipid biosynthesis. However, the entry of free fatty acids and lysophospholipids appeared to be controlled by a competitive mechanism. A powerful deacylase-acylase system was detected, the nature and specificity of which remain to be defined. Glycerol-3-phosphate incorporation into cellular lipids accounted for most of the new phospholipid molecules formed in parasitized cells, and into cellular lipids accounted for most of the new phospholipid molecules formed in parasitized cells, and this compound, rather than the lysophospholipids, appeared to be the natural acceptor of the acyl groups. By incorporation of nitrogenous bases into cellular phospholipids, we identified significant pathways not previously detected in Plasmodium-infected erythrocytes: the formation of phosphatidylethanolamine by phosphatidylserine decarboxylation, and the formation of phosphatidylcholine by the methylation of phosphatidylethanolamine. These results, associated with the absence of lipid synthesis in host cells, mean that the enzymes controlling these two pathways could serve as enzymatic markers of parasites.

Animals↗
PubMed1975

[Perinatal transmission of Plasmodium falciparum malaria].

Two weeks after leaving Nigeria for temperate zones and a few hours after giving birth to twins, a nigerian mother suffered an acute attack of malaria due to Plasmodium falciparum accompanied by cerebral, renal and hematolgical complications. Both infants were apparently healthy at birth, and no parasites were found on peripheral blood smears. Both placentas were macroscopically normal. At two months of age the second infant, a boy, developed non-febrile hemolytic anemia due to Plasmodium falciparum. The clinical picture and pathogenic mechanisms of perinatal malaria are discussed. Possible protection of the twin sister by partial glucose-6-phosphate dehydrogenase deficiency is considered.

Adult↗
PubMed1993

Identification of Caucasian CD4 T cell epitopes on the circumsporozoite protein of Plasmodium vivax. T cell memory.

We have identified a population of Caucasians with a defined past history of infection with Plasmodium vivax malaria. Using purified synthetic peptides overlapping the sequence of the circumsporozoite protein, we determined the percentage of individuals whose T cells proliferated or secreted IFN-gamma in response to peptide stimulation, for both this population and a population of nonmalaria-exposed control individuals. A number of peptides were recognized by both groups, but 11 peptides were uniquely recognized by the exposed population, and thus represented malaria-specific T cell epitopes. CD4 T cells were found to be responsible for the proliferative response. Humans last exposed to vivax sporozoites as long ago as 49 yr responded as well or better to these malaria-specific epitopes as individuals exposed within the previous month. Since such malaria-induced memory response may not be a feature of Plasmodium falciparum infections, and since P. falciparum does not have a persisting hypnozoite stage, our data argue that the persistence of T cell memory to vivax epitopes may result from antigenic persistence in the liver.

Adult↗
PubMed1995

Inhibitory activity of the anti-malarial atovaquone (566C80) against ookinetes, oocysts, and sporozoites of Plasmodium berghei.

Ookinete formation from mature Plasmodium berghei gametocytes in vitro was partially inhibited by 0.05-0.1 microM atovaquone and almost totally blocked at a concentration of 0.25 microM. Microgametocyte exflagellation was not affected by atovaquone at concentrations up to 300 microM. Ookinete formation was also inhibited in culture when addition of 0.20 microM atovaquone was delayed by 4 hr, by which time DNA replication was likely to have been completed. Inhibition of ookinete formation by atovaquone was not reversed by orotic acid. Plasmodium berghei-infected Anopheles stephensi mosquitoes were fed a second blood meal 4, 7, 14, and 20 days postinfection (p.i.) from mice that had been treated with atovaquone or control diluent 8 hr previously. Atovaquone blood feeds on day 4 reduced oocyst numbers on days 6-12, although sporozoite numbers in the thorax and abdomen on day 20 were not significantly reduced. Blood feeds on day 7 slowed oocyst growth, blood feeds on day 14 did not significantly reduce sporozoite numbers, and feeds to mosquitoes on day 20 p.i. had no effect on transmission to naive mice. Sporozoite invasion of human hepatoma cells was unaffected by the presence of atovaquone.

Animals↗
PubMed1995

[Research on the factors influencing the sporogonic multiplication of Plasmodium vivax in the mosquito vector].

Volunteers with no previous malaria history infected with northern Guangdong isolate of Plasmodium vivax and mosquito vector, Anopheles stephensi, were the objects and materials used in the research. Totally there were 16 volunteers, half of them were infected by mosquito-bite and another half by blood-inoculation. Blood was drawn when parasitemia reached a certain level and the erythrocytic forms developed into large trophozoites. Mosquitoes fed on infected blood from 5 and 4 donors of the two groups gave high gland infection rate and high gland indices respectively, but the highest gland indices were got from volunteers infected by mosquito-bite. The time of blood-feeding is important, only those blood samples taken from the people 3 to 8 days after the first onset gave good sporozoite harvest and the gland infection was greatly reduced on the 9th day. During this period (d3-8), the density of gametocyte had obvious influence on the intensity of mosquito infection. When the sex ratio of gametocyte (female:male) was 4:1 or less, the result would be good. For the purpose of reflecting more perfectly the circumstance of the sporogonic multiplication of plasmodium in the mosquito vector, we suggest the concept of gut/gland infection intensity which equals the product of the infection rate and the index of oocyst/positive gland.

Adult↗
PubMed1994

Reinterpretation of the genetics of susceptibility of Aedes aegypti to Plasmodium gallinaceum.

Several studies have demonstrated a genetic basis for variation in susceptibility of Aedes aegypti to Plasmodium gallinaceum. Although 25 yr ago it was reported that P. gallinaceum susceptibility in Ae. aegypti is determined primarily by a single autosomal dominant gene, evidence for additional genetic factors has emerged. Two sublines, 1 refractory and 1 of intermediate susceptibility to P. gallinaceum, have been selected from the Moyo-In-Dry strain (MOYO) of Ae. aegypti. Prior to selection, the MOYO population was 20.3% refractory. Genetic crosses of the highly susceptible Rockefeller strain (ROCK) and the 2 selected sublines of the MOYO strain provide evidence for a complex mode of inheritance of Plasmodium susceptibility in Ae. aegypti.

Aedes↗
PubMed1994

[Detection of specific DNA fragment of Plasmodium falciparum by solid phase PCR].

Solid phase PCR for detecting Plasmodium falciparum was established and used to detect cultured FCCl/HN isolate and malaria patients in Yunnan Province. The results revealed that the sensitivity of the method for detecting FCCl/HN isolate DNA was as minimal as 0.2 pg, or about 10 parasites. The specificity of the method was confirmed by discriminating malaria patients infected with different species of Plasmodium. The results suggest that solid phase PCR is a specific and sensitive method for early detection of P. falciparum.

Animals↗
PubMed1993

[Malaria: two complementary methods for Plasmodium detection in hospital practice].

In non-endemic areas, malaria diagnosis must be reliable and sensitive. Using acridine orange staining of centrifuged parasites (QBC) and Giemsa- stained thin blood films, we detected Plasmodium in 170 blood samples (158 samples were positive with both methods; 7 were positive with the QBC technique only and 5 were positive with the thin smear only). The QBC technique is useful for rapid screening and thin smear is necessary for Plasmodium identification and parasitaemia determination. The two complementary methods provide rapid and efficient diagnosis of malaria in non-endemic areas as well as control of parasitaemia following therapy.

Animals↗