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PubMed1975

Inducation of antibody against actin from myxomycete plasmodium and its properties.

Plasmodium actin was highly purified by gel filtration of crude G-actin on Sephadex G-100 followed by ultracentrifugation after polymerization in the presence of 1 M urea and 1 mM ATP. Purified actin showed a single band in the sodium dodecyl sulfate gel electrophoretic pattern. Antibody against this purified actin was induced in rabbits. The antibody obtained was immunologically monospecific for plasmodium actin, judging from the following results. (1) The addition of the antibody to a plasmodium F-action solution increased the turbidity of the mixed solution, showing the formation of the antibody-action complex. (2) In immunodiffusion and immunoelectrophoresis, the antibody formed single preciptin lines with the purified actin preparation and with the crude actin extract from the acetone-dried powder of plasmodium. (3) The antibody inhibited polymerization of plasmodium G-actin. (4) Plasmodium F-actin filaments were decorated with antibody in electron micrographs. The antibody reacted not only with plasmodium F- and G-actin, but also reacted with sea urchin egg actin, but it did not react with actin from rabbit striated muscle.

Actins↗
PubMed1979

[Production of interferon after infection by various doses of "Plasmodium berghei" in mice (author's transl)].

Groups of mice were inoculated with either low or high intraperitoneal doses of Plasmodium berghei infected erythrocytes (PIE). The course of infection was observed daily by counting new PIE which appeared in the red blood cells (RBC) of infected mice. At the same time, circulating interferon (IF) was tested. When low doses of infecting PIE were used (400 per mouse), circulating IF was first detected on the 5th day after inoculation. It increased to a maximal rate, when 5% of RBC were affected. It disappeared on the 8th day despite of a continuous rise of PIE. With high doses of PIE (60,000 per mouse), IF was detected on the 3rd day, when only 0.5% of RBC were parasitized. The maximal rate was observed on the 5th day when 20% of the RBC were affected. It disappeared on the 7th day, though the PIE rate would continue to rise. Treatment of mice by chloroquine (0.01 per g), at the time of first PIE appearance after Plasmodium infection, rapidly reduced the amount of PIE. In this case, no IF production was observed. Splenectomy resulted in an increased resistance of mice to the lethal effect of Plasmodium infection. IF production in such splenectomized mice was less important than in control. It was concluded that P. berghei was a good inducer of circulating IF at the beginning of the active disease, soon after infection. The fact was proven by the striking lowering effect of chloroquine and splenectomy that both reduced Plasmodium development and IF production.

Animals↗
PubMed1979

[Further observations of the course of Plasmodium berghei infection in the mouse].

Invasion of immature and mature erythrocytes by merozoites of Plasmodium berghei seems to obey the following rules: Merozoites prefer unparasitized immature erythrocytes. Multiple infections of immature erythrocytes occur in conditions of high merozoite production and low concentration of unparasitized immature erythrocytes, when frequently repeated contacts between merozoites and unparasitized or freshly parasitized immature erythrocytes become increasingly probable. Mature erythrocytes are invaded when the relative density of unparasitized immature erythrocytes drops below 0.2--0.5%, in other words, when merozoites do not meet unparasitized immature erythrocytes in 200--500 erythrocytes. Failure to invade mature erythrocytes is obviously not due to inability of the merozoites to penetrate the erythrocyte membranes.--Merozoites of Plasmodium vinckei, on the other hand, show random invasion of parasitized and unparasitized mature erythrocytes, leading to frequencies of unparasitized and singly or multiply parasitized erythrocytes approaching a Poisson distribution.--The Plasmodium berghei infection regularly leads to a lowered density of polychromatophilic erythrocytes in the peripheral blood. This depression of polychromatophilic erythrocytes uses to be of very different duration, form and intensity. The relative density of immature erythrocytes may show pronounced fluctuations in this phase. As has been seen in one animal, even monocytes and polymorphonuclear leucocytes may, alongside with the immature erythrocytes, for some time totally disappear from the peripheral blood. The depression of polychromatophilic erythrocytes evidently goes along with pronounced alterations of the erythropoesis in spleen and bone marrow. Leucocytes in the peripheral blood generally show rather uncharacteristic alterations of their concentration, they may form very high concentration peaks.

Animals↗
PubMed1979

[Plasmodium ovale malaria in France. Probability of of genetic control of the incubation period (author's transl)].

Plasmodium ovale as the causative parasite in attacks of malaria is rare. Nevertheless, the number of cases seen in France would seem to be on the increase. In 137 attacks of malaria collected between 1967 and 1978, Plasmodium ovale was found on 13 occasions. The main characteristics of this form of malaria are, apart from its benign nature, the usual absence of any recurrence and a very variable incubation period, ranging from fifteen days to several months or even a year (with an average of 3.2 months). It is thus important to bear this diagnosis in mind, even if a long period elapsed since return from an endemic area, and it will be realised that adequate chemoprophylaxis using a schizonticide does not offer protection from forms with a long incubation period. Genetic control of the duration of the period of maturation of exo-erythrocytic forms, i.e. the incubation period, is suggested, identical to that recently advanced in the case of Plasmodium vivax. This would account for the variability and possible long duration of incubation periods. A usual monoclonal character of these infections could explain the virtual absence of recurrences.

Adolescent↗
PubMed1978

An ultrastructural study of the sporogonic development of Plasmodium falciparum in Anopheles gambiae.

This paper describes the fine structure of the sporogonic development of Plasmodium falciparum in its natural vector Anopheles gambiae (Species A) as seen by scanning and transmission electron microscopy. The parasite was derived from naturally infected volunteers and the vector maintained under natural conditions at the MRC Laboratories, Fajara, The Gambia. Sporogonic development of P. falciparum is similar to that described for other Plasmodium spp. There are however greater similarities between P. falciparum and the avian malaria parasites, than those mammalian (primarily rodent) species described to date--particularly with respect to mitochondrial development, crystalloid morphology and nucleolar organization. Nuclear development is similar to that of the murine malaria parasites, but reconstruction of complete mitotic spindles from serial sections suggest the haploid genome of P. falciparum contains 14 chromosomes compared to eight to ten in the murine plasmodia. Sporoblast formation involves a unique process of cleft formation based on the expansion of the cisternal space of the endoplasmic reticulum. Sporozoite budding is almost exclusively confined to these inner membrane surfaces and results in a characteristic sporozoite distribution in the oocyst. High resolution scanning electron microscopy of free sporozoites provides the first surface view of the micropore of Plasmodium.

Anopheles↗
PubMed2026

Versatile, marker-free platform for life cycle-wide imaging of Plasmodium falciparum by integrating an exogenous gene cassette into a conserved intergenic locus.

The creation of transgenic Plasmodium falciparum lines with robust fluorescence across the entire life cycle is essential for advancing our understanding of parasite biology, which in turn informs the development of new drugs and vaccines. In this study, we utilized Plasmodium-optimized genome editing to integrate an mCherry expression cassette into a selected intergenic locus without gene disruption. The resulting marker-free line, NF54-mCh, exhibited intense fluorescence throughout all developmental stages, including asexual and sexual blood stages, as well as mosquito (ookinete, oocyst, and sporozoite) and liver stages. NF54-mCh showed normal proliferation, gametocytogenesis, and efficient transmission to mosquitoes. The ultra-high brightness in salivary gland sporozoites allowed for the non-invasive identification of infected mosquitoes. Sporozoites remained highly infectious to humanized mouse livers, thus enabling the completion of the full life cycle. NF54-mCh serves as a parental line for performing additional genetic modifications, because the CRISPR/Cas9-based genome editing method is free of introduced drug resistance markers. The broader applicability of this strategy was validated by generating similar reporter lines in Plasmodium species utilized in rodent malaria models. In summary, NF54-mCh represents a unique, versatile platform that will accelerate fundamental research and support the future development of malaria control strategies, including new vaccines and drugs.

Animals↗
PubMed2025

Plasmodium falciparum CyRPA Glycan Binding Does Not Explain Adaptation to Humans.

The human malaria parasite Plasmodium falciparum evolved from a parasite that infects gorillas, termed Plasmodium praefalciparum. The sialic acids on glycans on the surface of erythrocytes differ between humans and other apes. It has recently been shown that the P. falciparum cysteine-rich protective antigen (PfCyRPA) binds human sialoglycans as an essential step in the erythrocyte invasion pathway, while that of the chimpanzee parasite, Plasmodium reichenowi has affinities matching ape glycans. Two amino acid changes, at sites 154 and 209, were shown to be sufficient to switch glycan binding preferences and inferred to reflect adaptation of P. falciparum to humans. However, we show that sites 154 and 209 are identical in P. falciparum and P. praefalciparum, with no other differences located in or near the CyRPA glycan binding sites. Thus, the gorilla precursor appears to have already been preadapted to bind human sialoglycans.

Plasmodium falciparum↗
PubMed1976

Feeding mechanisms in extracellular Babesia microti and Plasmodium lophurae.

Although large hemoglobin inclusions are observed in intraerythrocytic Babesia microti parasites, they are absent from parasites freed of hamster red cells by immune lysis with anti-hamster erythrocyte serum. Babesia microti has no cytostome. This parasite, therefore, does not appear to feed by phagocytosis of large boluses of hemoglobin, as does Plasmodium. To determine whether Babesia can pinocytose protein, free parasites were fed ferritin in an in vitro system. Ferritin was taken up from the entire cell surface into narrow channels within 15 min at 37 C. Only merozoites, with their pellicular complex, failed to take up the protein. By 60 min, the ferritin was highly concentrated in many channels and vesicles, which formed interconnecting stacks. The ferritin-containing channels became associated with membrane whorls of the multimembranous structure. Membrane whorls were also observed in the process of extrusion in samples incubated for longer times. These events may represent steps in the digestion and excretion of the pinocytosed protein. Empty channels formed when Babesia was fed albumin. The diaminobenzidine reaction for hemoprotein was positive for the channels in both free and intraerythrocytic babesias. The staining reaction was completely inhibited by cyanide, but not at all by aminotriazole. These results further suggest that Babesia pinocytoses hemoglobin in vivo. Plasmodium lophurae parasites freed of red cells by immune lysis are surrounded by 2 membranes and apparently can ingest ferritin only through the cytostome. Extracellular cytostomal feeding involves both membranes, as it does in vivo. Ferritin was found in food vacuoles, some of which contained hemoglobin ingested before parasite isolation, connected to or near the cytostome. In both Plasmodium and Babesia low temperature inhibited ferritin uptake.

Animals↗
PubMed1978

Plasmodium durae Herman from the introduced common peafowl in northern Nigeria.

Plasmodium (Giovannolaia) durae Herman was originally described from Kenya, the type host being the common turkey, Meleagris gallopavo Linnaeus. There are no field records of this association outside of Africa, where the parasite, herein reported from another introduced and domesticated bird (the common peafowl, Pavo cristatus Linnaeus), was recently listed from 2 native Phasianidae of the genus Francolinus. The justification for the present identification is submitted against background data concerning malaria parasites from turkeys and other Galliformes in Africa and elsewhere, and restraint is urged in describing yet more "new species" of avian Plasmodium belonging to morphologically close taxa within Novyella and Giovannolaia. A near relative of P. durae, Plasmodium dissanaikei de Jong, is transferred from the former subgenus to the latter one.

Animals↗
PubMed1978

Checklist, host index, and annotated bibliography of Plasmodium from reptiles.

World literature on Plasmodium of squamate reptiles (1909-1975) includes 156 published accounts on 54 valid species and subspecies. AFRICA: 30 reports on 9 species; AUSTRALIA, ASIA & OCEANIA: 12 reports on 6 species and 2 subspecies; AMERICAS: 116 reports on 37 species. More than half of these reports and new species descriptions appeared during the last 10 years. Most concern plasmodia in lizards of the Neotropics, Georgia (Plasmodium floridense, a Neotropical-Caribbean parasite) and California (Plasmodium mexicanum). African host species are all lizards: 4 agamids, 3 skinks, 2 chamaeleonids, one chordyline, and one gerrhosaurine. Australasian host species are also all lizards: 6 agamids, 9 skinks, 2 lacertids, one (or two?) gekkonids, and one varanid. Known American host species include 12 snakes and 87 lizards: 34 anoline species, 12 sceloporines (plus 11 others experimentally infected), 4 basiliscines, 5 tropidurines, 2 iguanines, 2 skinks (one questionable), 2 anguids (a total of 4 animals), 4 sphaerodactylines, 2 gekkonines and 11 teiid species.

Animals↗
PubMed1978

Sickling rates of human AS red cells infected in vitro with Plasmodium falciparum malaria.

The kinetics of sickling of malaria-infected red cells from humans with sickle cell trait were studied in vitro in an attempt to obtain direct experimental evidence for a selective advantage of the hemoglobin S heterozygote in a malarious region. The sickling rates of cells infected with Plasmodium falciparum and of non-infected cells were studied both in the total absence of oxygen (by dithionite addition) and at several different concentrations of oxyhemoglobin which might obtain in vivo. In all cases, red cells containing small plasmodium parasite forms (ring forms) sickled approximately eight times as readily as uninfected cells. Cells containing large parasitic forms (trophozoites and schizonts) appeared to sickle less readily than uninfected cells, by light microscopy criteria, but electron micrographs demonstrated the presence of polymerized deoxyhemoglobin S with a high frequency. It is concluded that enhanced sickling of plasmodium-infected AS cells may be one mechanism whereby the hemoglobin S polymorphism is balanced in favor of the heterozygote.

Anemia, Sickle Cell↗