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PubMed1977

A histidine-rich protein from Plasmodium falciparum and its interaction with membranes.

In previous studies, an unusual protein with 70% of histidine was isolated from Plasmodium lophurae. It was shown to have a possible function in the penetration of merozoites into erythrocytes. The results of the present study indicate the presence of a similar histidine-rich protein in Plasmodium falciparum. Like that of P. lophurae, the histidine-rich protein of P. falciparum is acid-soluble, but it has a slightly higher molecular weight.

Animals↗
PubMed1977

Comparison of treatment schedules for Plasmodium vivax infections in the Solomon Islands.

A total of 26 patients infected with Solomon Islands strains of Plasmodium vivax was treated with one of three regimens of cloroquine-primaquine, in an attempt to determine the relapse patterns and the response to treatment of the local strains of parasite. The results suggest that the standard course of chloroquine-primaquine provides a radical cure for the strains of Plasmodium vivax from the Solomon Islands, provided that strict supervision of drug administration is enforced.

Adolescent↗
PubMed1987

Vector incrimination and experimental transmission of Plasmodium floridense by bites of infected Culex (Melanoconion) erraticus.

A survey of mosquitoes which are attracted to and readily feed upon lizards in a northcentral Florida area where there is a relatively high prevalence of Plasmodium floridense in Anolis carolinensis was conducted. Culex erraticus and Cx. territans, collected in lizard-baited traps, readily fed on lizards in the traps and in the laboratory, and the former mosquito species is an experimental vector of Plasmodium floridense. Sporozoites were observed in the salivary glands from 11 to 14 days at 21-25 degrees C following an infective blood meal. The prepatent period of P. floridense in A. carolinensis at 18-24 degrees C was relatively long, 24-25 days (n = 2). At 32 degrees C, the prepatent period was decreased to 13-17 days (n = 4). The transmission rate of P. floridense by bite of Cx. erraticus and intraperitoneal inoculation of sporozoites from the salivary glands of Cx. erraticus, was relatively low (16.2%). Peak parasitemias ranged from 912 to 4,280 parasites per 10,000 red blood cells. Sporogonic development of P. floridense in Cx. territans which fed on infected lizards was not observed.

Animals↗
PubMed1986

Pathways for the reduction of oxidized glutathione in the Plasmodium falciparum-infected erythrocyte: can parasite enzymes replace host red cell glucose-6-phosphate dehydrogenase?

Plasmodium falciparum-infected human red cells possess at least two pathways for the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH): (1) the glucose-6-phosphate dehydrogenase (G6PD) pathway and (2) the glutamate dehydrogenase (GD) pathway using glutamate as a substrate. Uninfected erythrocytes lack the GD pathway. The NADPH generated can be used to reduce oxidized glutathione (GSSG), which accumulates in the presence of an oxidative stress. In red cell G6PD deficiency, this pathway is reduced or absent, and the host cells as well as the parasites within them are vulnerable to oxidant stress. In view of the presence of the GD pathway in parasitized red cells and the recent description of a parasite-derived G6PD enzyme, we have asked whether the pathways for the reduction of GSSG provided by the parasite can substitute for the host G6PD in red cells deficient in G6PD activity. We have devised a functional assay in which the reduction rate of GSSG is monitored in the presence of buffered infected or control red cell lysates and substrates. Infected G6PD-deficient erythrocytes were obtained from in vitro cultures after a single prior growth cycle of the parasites in G6PD deficient cells to eliminate contaminating normal red cells. The results show that only parasitized red cells can reduce GSSG via the GD pathway. In parasitized G6PD Mediterranean red cells (completely G6PD-deficient), there is a detectable GSSG reduction via the G6PD pathway, not found in uninfected lysates from the same individual. In G6PD A- (African type, featuring partial deficiency), a small increment in the G6PD-dependent reduction of GSSG can also be detected. However, when compared to G6PD normal red cells, the activities from the parasite-derived pathways are small and could not be considered substitutes for normal host enzyme activity. It is concluded that while the plasmodium provides additional pathways for the generation of NADPH that may serve its own metabolic needs, the host red cells and hence the parasite itself remain vulnerable to oxidant stress.

Erythrocytes↗
PubMed1986

[Bacterial infections and early Plasmodium falciparum malaria].

Two cases of Plasmodium falciparum malaria associated with bacterial infections--streptococcus A septicemia and Legionnaires' disease--are described. The association of these two infections is probably not incidental, and the hypothesis of Plasmodium falciparum induced immuno-deficiency is discussed.

Adult↗
PubMed1978

Plasmodium berghei adoptive transfer and immunosuppression of immunity in allogenic neonates.

Outbred female rats were hyperimmunized with Plasmodium berghei and mated to produce progeny. Spleen cells from the immunized rats and from normal control mothers were adoptively transferred to their 48 hr old neonates. Some neonates from immune mothers were fostered to normal mothers and vice versa. Weanling rats were challenged 35 days after birth with Plasmodium berghei; immune and normal litters which had not received cells were also challenged at the same time. Rats which had received immune spleen cells from their mothers but were fostered on to non-immune mothers showed significantly lower parasitaemias and higher fluorescent antibody titres than any other combination of cell transfer and maternal milk. GVH reaction was minimal. These results suggest that the immune response to P. berghei was suppressed in the presence of passively transferred maternal antibody.

Animals↗
PubMed1986

Studies on African saurian malarias: Plasmodium holaspi n. sp. from the flying lacertid Holaspis guentheri.

The African flying lizard Holaspis guentheri (Lacertidae) from the Uluguru Mountains, Tanzania was found infected by an undescribed malarial parasite, Plasmodium holaspi n. sp. Gametocytes were elongate, approximately twice the size of host cell nuclei, and showed prominent, irregular pigment granules. Schizonts were oblong or formed as rosettes, approximated the host cell nucleus in size, and produced 8-18 merozoites. Maturing gametocytes contained large masses or blocks of chromatin which can obscure sexual differentiation by staining reaction, while young gametocytes and asexual stages almost always occupy marginal positions in host cells. These characteristics distinguish P. holaspi from all other saurian Plasmodium species. This is the first malarial parasite described from African lacertid species.

Africa, Western↗
PubMed1986

The sporogonic cycle of Plasmodium reichenowi.

Plasmodium reichenowi, a malarial parasite of the chimpanzee, was infective to Anopheles freeborni, Anopheles quadrimaculatus, Anopheles stephensi, Anopheles maculatus, Anopheles dirus, and Anopheles culicifacies mosquitoes. Anopheles gambiae and Anopheles albimanus were not infected. Mean oocyst diameters of P. reichenowi were smaller than those of the other chimpanzee parasite, Plasmodium schwetzi. Sporozoites were present in the salivary glands of An. freeborni at 15 days when held at 25 to 26 C.

Animals↗
PubMed1979

In vivo and in vitro studies of quinine sensitivity of Plasmodium falciparum in Thailand.

Forty-four patients with falciparum malaria were studied. Nine patients were given quinine orally at a daily dose of 1.5 gm base for a period of 14 days. The mean parasite clearance in all 9 patients was 3.3 days, and none had recrudescence in follow-up examinations for 31 days. The in vivo study of these 9 patients showed sensitivity to quinine which correlated with the in vitro test, with concentration of quinine base 2.5-5.8 microgram/ml of blood that inhibited the maturation of Plasmodium falciparum parasites. The results of the in vitro test of 35 patients showed concentrations of quinine base 2.1-5.4 microgram/ml of blood were able to inhibit the maturation of P. falciparum parasites. Therefore, these studies indicate that Plasmodium falciparum are still sensitive to quinine and quinine remains to be the drug of choice for the treatment of falciparum malaria in Thailand.

Adolescent↗
PubMed1985

Production of IL 2 and IFN-gamma by T cells from malaria patients in response to Plasmodium falciparum or erythrocyte antigens in vitro.

T cells from patients acutely infected with malaria exhibit a disease-related stimulation of DNA synthesis in response to Plasmodium falciparum antigen in vitro. This response is weak and short-lived, suggestive of induction of suppressor mechanisms. Exogenous T cell growth factor (IL 2) that was added to antigen-stimulated T cell cultures enhanced proliferation in antigen-responsive cultures, indicating that the lymphocytes expressed IL 2 receptors. In contrast, the addition of IL 2 to cultures that did not respond to antigen had no effect. Antigen-responsive cultures contained endogenous IL 2 as well, and the antigen-induced lymphocyte proliferation was correlated with IL 2 production. However, the results suggested that IL 2 production by the patients' T cells was insufficient or actively shut off, and that this was responsible for the premature cessation of their DNA synthesis. Supernatants from 60% of the T cell cultures treated with malaria antigen and from 30% treated with RBC ghost antigen contained interferon-gamma (IFN-gamma), as determined by a cytopathic effect inhibition assay combined with acid treatment and antibody neutralization or by an IFN-gamma-specific ELISA. There was no obvious correlation between antigen-induced lymphocyte proliferation and the presence of IFN-gamma in the culture supernatants. A high IFN-gamma activity was also seen in antigen-treated cultures from P. falciparum-immune donors living in highly endemic malaria areas. In contrast, no IFN-gamma was found in supernatants of antigen-treated T cells from healthy donors or patients with Plasmodium vivax malaria. Thus, the IFN-gamma activity of these cultures appears to reflect the presence of antigen-reactive T cells and may be useful as a sensitive indicator of cellular immunity in P. falciparum malaria.

ABO Blood-Group System↗
PubMed1985

[Production of human monoclonal antibodies against various antigens of erythrocyte stages of Plasmodium falciparum].

Peripheral blood lymphocytes from 20 individuals living in a malaria endemic area (Burkina Faso) were transformed with Epstein-Barr virus. No antigen specific selection, nor stimulation of B-cells were performed prior to transformation. 20 cell lines were established, 14 secreted polyclonal antibodies directed against erythrocytic stages of Plasmodium falciparum. 4 lines were cloned and the supernatant analysed and characterised against Plasmodium falciparum antigens.

Animals↗
PubMed1979

A malarial parasite of Australian skinks, Plasmodium mackerrasae sp. n.

Plasmodium mackerrasae sp. n. parasitizes the Australian lizards Egernia cunninghami and E. striolata (Sauria: Scincidae). Described from an experimental host, E. whitei, it produces mature schizonts containing 6--12 nuclei arranged peripherally as a rosette, and round to oval gametocytes which are equal to or slightly smaller than host cell nuclei. Both schizonts and gametocytes parasitize all cells in the erythrocyte series. Presence of pigment in both asexual and sexual stages is correlated with maturity of the host cell. Asexual forms contain a single large vacuole, whereas mature gametocytes may show 1--4 vacuoles. Plasmodium mackerrasae resembles most closely P. sasai of Japan and P. tropiduri of tropical America. It differs from P. sasai by lacking fan-shaped schizonts and by having less heavily pigmented gametocytes, and from P. tropiduri by less variability in shape and greater vacuolation of the gametocytes. Host and geographic differences further support its distinction.

Animals↗
PubMedDate not supplied

[Plasmodium chabaudi: changes in the surface sialic acids of red blood cells during infection (author's transl)].

Surface sialic acids of mice red blood cells infected with the malarial parasite Plasmodium chabaudi are increased as compared to extracts of red cells from normal mice. This increase occurs coincidentally when reticulocytes increase in the peripheral blood. The same increase of surface sialic acids is shown by studies of reticulocytes from phenylhydrazine treated mice. Similarly, neutral hexoses, fucose, were found in greater quantities in surface glycopeptides obtained after incubation with trypsin of reticulocytes from phenylhydrazine treated mice than in surface glycopeptides of red cells from normal mice. This increase occurs also in Plasmodium chabaudi infected red cells with the development of reticulocytosis, in the same way. These facts suggest the contribution of reticulocytes to the biochemical changes observed during malaria infection.

Animals↗
PubMed1969

Active immunization against Plasmodium berghei malaria in mice, using different preparations of plasmodial antigen and different pathways of administration.

With regard to the effectiveness of the antigens in inducing clinical immunity against malaria parasites, the minimum amount of living antigen developed in mice during controlled low parasitaemia with Plasmodium berghei has been estimated and compared with the amount of non-living antigen obtained by various methods of freeing parasites from their erythrocyte hosts.Whereas about 100 mg of living antigen per kg of body-weight are sufficient to induce a degree of hyperimmunity, 1240 mg/kg of a freshly prepared crude antigen are necessary to enable the mice to survive a challenge infection while 3500 mg-7000 mg/kg of a vaccine prepared from freshly isolated plasmodia are necessary to produce a degree of immunity comparable with hyperimmunity. It appears, therefore, that every manipulation of the parasitized erythrocyte or the isolated plasmodium outside the host organism, as well as a storage time in excess of 36 hours, causes a reduction in antigenicity, up to a factor of 10(-2). However, this decrease in antigenicity is disproportionate compared with the reduced rate of infectivity of stored, parasitized erythrocytes and isolated parasites. After an incubation period of 18 hours, the ID(100) increases from 2 x 10 to 5 x 10(7) parasites. Therefore, the differences between the essential amount of living plasmodia and non-living antigen may be due to other, hitherto unknown, factors and not exclusively to degradation of the most important antigen.The saponin method of freeing parasites from their erythrocyte hosts was found to yield the purest antigen. Preparations of parasites obtained by treating parasitized erythrocytes with anti-erythrocyte serum or with formalin were highly contaminated with remnants of the host cells and showed no better antigenic qualities than the parasites isolated by means of saponin.Since the decrease of antigenicity associated with harvesting and isolation procedures is constant, vaccination with a fractionated antigen pool should be possible.

Animals↗
PubMed1977

Experimental infection with Plasmodium chabaudi in rats: antigen and antibody associated with anemia and glomerulonephritis of acute infection.

Rat-adapted Plasmodium chabaudi caused a syndrome characterized by hemolytic anemia, splenomegaly, and glomerulonephritis. All rats recovered and appeared normal after 4 weeks despite persistence of proteinuria. Serologic studies on the malarious rats revealed that the infection was associated with a soluble antigen which was present concurrently with antibody in plasma, in material eluted from blood cells, in extracts of kidney tissues, and in the urine. This antigen appeared to be identical with one extracted from P. chabaudi parasites and did not cross-react with antigens of Plasmodium gallinaceum. Tests for the cold-active hemagglutin (CAH) and the globulin associated serum antigen (SA) previously associated with acute malaria, revealed that CAH, but not SA, was present. From these observations it is suggested that soluble complexes of the parasite antigen and its antibody may have been causal in this syndrome.

Anemia↗
PubMed1982

The role of the Kupffer cell in the infection of rodents by sporozoites of Plasmodium: uptake of sporozoites by perfused liver and the establishment of infection in vivo.

The uptake of Plasmodium yoelii nigeriensis sporozoites by isolated perfused rat liver was very rapid and efficient. 67% of the initial load was removed from the perfusion media in the first passage through the liver, and 95% after 15 min of perfusion. Much of the uptake was explained by mechanical trapping in the liver. Up to 75% of the sporozoite load was retained after 15 min both by heat killed liver and liver cooled to 4 degrees C, therefore at least 20% of the sporozoite uptake in perfused normal livers was due to a biologically active process. In perfused normal livers, non-infective (heat-killed or trypsin-treated) sporozoites were taken up with an efficiency equal to infective sporozoite controls. However, a reduction in Kupffer cell number and activity, induced by silica treatment, resulted in a very significant decline in uptake of infective sporozoites by the perfused liver--and a parallel fall in the successful infection of the host by inoculated sporozoites in vivo. Since silica treatment produced no significant detectable pathological changes in hepatocytes, and infected blood passage results in a normal parasitaemia in silica treated animals it was concluded that the Kupffer cell was a component of the natural route of infection of the mammalian host by the majority of the infecting population of sporozoites of Plasmodium yoelii nigeriensis.

Animals↗
PubMed1983

[Plasmodium falciparum malaria acquired in Kenya with type II or type III resistance to amino-4-quinolines].

The authors report a case of Plasmodium falciparum malaria acquired in Kenya by a French tourist under correct chloroquine prophylaxis. She recovered under quinine and a sulfadoxine-pyrimethamine association. This is a new case of high level resistance (R II or R III) of Plasmodium falciparum to amino-4-quinolines recognized in East Africa. Malarial chemoprophylaxis recommended until now for this area may need to be reviewed.

Adult↗