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PubMed1979

[Malaria plasmodia in the mouse. Parasitization of mature and immature erythrocytes by Plasmodium berghei, Plasmodium yoelii and Plasmodium chabaudi (author's transl)].

Plasmodium berghei parasites (strain K173) in mice with developing immunity changed to a variant type with increased resistance against antibodies and enhanced invasion of mature erythrocytes; on passages in normal mice this variant type retransformed to the normal type (Kretschmar 1964). On detailed study, parasites of the variant type showed a markedly decreased predilection for polychromatophilic erythrocytes, leading to slowed multiplication during prepatency, increased invasion of mature erythrocytes and rapidly fatal course of the infection. Avoidance of parasitized immature erythrocytes remained unaltered in the variant type. In presence of antibodies many parasites invaded mature erythrocytes even in blood with high concentrations of immature erythrocytes. --Plasmodium yoelii (strain 17X) showed very high predilection for polychromatophilic erythrocytes, only slight lowering of immature erythrocyte concentration and low parasitization of mature erythrocytes. Parasites with altered preference for polychromatophilic erythrocytes were not observed in animals with parasitemia relapsing after spontaneous disappearance of the primary parasitemia or after injection of antiserum. It is suggested that in a variant of Plasmodium yoelii with high invasion of mature erythrocytes (Yoeli et al. 1975), the decisive virulence factor might be a lowered predilection for polychromatophilic erythrocytes. Avoidance of parasitized immature erythrocytes is less marked in Plasmodium yoelii than in Plasmodium berghei. In presence of antibodies more parasites invade mature erythrocytes. --Plasmodium chabaudi showed an appreciable preference for invasion of immature erythrocytes. Moreover, significantly more multiply parasitized mature and immature erythrocytes were found than would have been produced by random invasion of erythrocytes.

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PubMed1979

Soluble antigens released in vitro from erythrocytes infected with Plasmodium berghei.

Rat erythrocytes parasitized with Plasmodium berghei were found to release soluble antigenic products in vitro. The supernatants obtained by centrifugation of the disrupted cells induced specific transformation of non-adherent spleen lymphocytes of convalescent rats and produced precipitation lines with antiplasmodial antibodies. In a preliminary experiment they also immunized young rats against a viable challenge of P. berghei. It is suggested that the soluble material could serve for the purification of an effective protective antigen.

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PubMed1978

[Influence of a hot environmental temperature on the evolution of experimental paludism of the mouse with Plasmodium berghei berghei].

Swiss Mice infected with Plasmodium berghei berghei and maintained in permanence in a hot environmental temperature undergo a chronic infection whereas controls maintained at the laboratory temperature develop always an acute and lethal infection. The hot environmental temperature does not seem to have any action on the pathogenicity of the parasites. Host defences are stimulated.

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PubMed1978

Survival of parasites in mice immunized against Plasmodium berghei.

The rodent malaria parasite Plasmodium berghei may survive im immunized Swiss and C3H/StZ mice for a considerable period of time. Despite considerable differences in the observed survival time in animals of a given strain, a general, strain specific pattern is observed. Parasites generally survive longer in Swiss than in C3H/StZ mice. In some of the Swiss mice parasites survived throughout the experimental period, whereas in the others restricted survival was observed, possibly reflecting genetic disparity. Since booster infections did not affect the survival pattern, the effectiveness of elimination is not determined by "antigen" dependent, gradual differences in quality of the hosts' immune response. Repeated biotechnical manipulation of the animals may influence experimental results.

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PubMed1979

Lipid composition and activity of a lytic factor isolated from Plasmodium berghei.

A fraction was obtained from Plasmodium berghei which induced hemolysis of the erythrocytes of mice and hamsters. This fraction, called lytic factor (LF), was found to be composed of a large amount of lipid material. An examination of the lipids showed the major lipids to be monoglycerides, diglycerides, triglycerides, fatty acids, long-chain alcohol, sterol, sterol ester, sterol glycoside, and two cerebrosides. The most abundant component found in the LF was sterol ester, followed in order by cerebrosides, sterol, and sterol glycoside. Lytic activity was found to be lost when samples were boiled for 5 min. An examination of the lipid composition of LF before and after boiling showed changes which may be useful in studies on the mechanism of activity of this factor. The fatty acid composition of the total lipid fraction of LF was examined by gas-liquid chromatography. The major fractions were 18:1 and 16:0 in unheated LF and 16:0 in the heated LF.

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PubMed1979

Different appearance of parasitized erythrocytes in blood between normal and toxoplasma-infected rats after infection of Plasmodium berghei.

When normal rats were infected with Plasmodium berghei (Pb), both IgG and IgM immunofluorescent antibody titers were found to rise in the 1st week with increase of parasitaemia. After reinoculation of P. berghei into Pb-immune rats, IgG titer was further increased remarkably, although no parasitaemia was observed. No elevation of IgM titer was found. In rats infected with Toxoplasma gondii (Tg), IgG and IgM antibody activities were demonstrated in the 1st to the 3rd week postinfection but only IgG titer was maintained to the 16th week. The challenge with T. gondii to Tg-immune rats stimulated the further increase in IgG titer but not in IgM. When Tg-immune rats were infected with P. berghei, little or no parasitaemia appeared. In infection of P. berghei in Tg-immune rats which were treated with anti-rat thymocyte serum (ATS) beforehand, highly increased parasitaemia was usually found in the rats as compared with that in ATS non-treated rats. Pb-immune macrophages were more effective in phagocytosis of Pb-parasitized erythrocytes in vitro than normal or Tg-immune macrophages. When Pb-parasitized erythrocytes were preincubated with fresh Pb-immune serum, the phagocytosis rate of macrophages was clearly heightened. It was observed that the phagocytic activity of normal macrophages to Pb-parasitized erythrocytes was stimulated by addition of the supernatant (lymphokines) taken from the incubation of Tg-immune lymphocytes with Tg-antigen or Pb-antigen.

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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.

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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.

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PubMed1977

Cell mediated and humoral immunity in experimental Plasmodium berghei infection.

Adoptive passive transfer of immunity to Plasmodium berghei infection has been investigated in an inbred strain of Swiss mice. The mice were made hyperimmune by repeated passage of 10(3) parasites and subsequent therapy with an antimalarial drug. Immune sera and cells obtained from thymus, spleen and peritoneal exudate were transferred to normal animals which were subsequently challenged with standard doses of P. berghei. It was observed that: (a) immune serum in high doses (0.5 ml/mouse) enhanced parasitaemia; when used in smaller doses (0.1 ml/mouse), it afforded a considerable degree of protection; (b) viable immune lymphocytes obtained from thymus and lymph node afforded protection; (c) the mixed population of cells obtained from spleens of immunized mice, as well as peritoneal exudate, protected mice against challenge inoculum; (d) glutaraldehyde-treated spleen cells and material obtained after freezing and thawing the same number of spleen cells, macrophages and lymph node also afforded protection. These findings confirm that, under these experimental conditions, immunity against P. berghei is mediated through (i) specific antibody which is dose-dependent, (ii) cell-mediated immunity and (iii) effective response to processed antigen.

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PubMed1976

Serum-soluble malarial antigens and immune complex nephritis in Plasmodium berghei berghei infected mice.

Swiss albino mice infected with Plasmodium berghei berghi showed the serum-soluble malarial antigen and antibody on day 10 of infection onward. Immune complex nephritis in these mice developed on the seventh day after inoculation. The infected kidneys revealed the deposition of mouse gamma globulin, mouse beta1C globulin and malaria antigen along the capillary wall of the glomeruli. Proteinuria was detected on seventh day of infection. Serum-soluble malaria antigen in probably responsible for forming the soluble immune complex which causes glomerulonephritis in infected mice.

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PubMed1976

The chemotherapy of rodent malaria, XXIV. The blood schizontocidal action of erythromycin upon Plasmodium berghei.

Erythromycin inhibits chloroquine-induced pigment clumping in Plasmodium berghei in vitro. The drug was therefore tested against infections of P. berghei in mice and was found to be active at non-toxic doses. Given orally, the stearate salt was more effective than the base, but subcutaneously the base was more effective than the stearate. Erythromycin potentiated the action of chloroquine against two chloroquine-resistant strains of rodent malaria, the mildly resistant NS, and the highly resistant RC strains of P. berghei, but not against the drug-sensitive N strain.

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PubMed1979

Pathology of Anopheles stephensi after infection with Plasmodium berghei berghei. II. Changes in amino acid contents.

Infection with Plasmodium berghei results in the disease of a relatively high percentage of mosquitoes depending on the experimental conditions. The damage caused by the parasites may be so severe that the host dies. It can also become manifest for instance in a change in the amino acid content of the mosquito homogenate. The amino acid content of mosquitoes fed on a glucose solution, normal mouse blood, or the blood of infected mice was analysed qualitatively and quantitatively over a period of 14 days. The amino acids lysine, phenylalanine, proline, threonine, and tyrosine are always found in higher concentrations in infected mosquitoes. The content of leucine (and/or isoleucine) increased from the 6th day and glutamic acid from the 9th day compared to the controls. Lower concentrations were found for alanine, aspartic acid, glycine, and serine as compared to uninfected mosquitoes. Further investigations on this subject might help to find the causes for the susceptibility or resistance of individual mosquitoes to plasmodia.

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PubMed1977

Time-dependent loss of invasive ability of Plasmodium berghei merozoites in vitro.

UNLABELLED: The invasive ability of Plasmodium berghei merozoites in vivo was studied following their artificial removal from parasitized mouse red cells using complement-mediated immune lysis in vitro and in vivo. Time-course experiments revealed that lysed preparations contained two components contributing to the parasites' infectivity in mice. One component, presumed to be free merozoites released from mature schizont-infected cells, rapidly lost infectivity with time at 1 to 2 C. A second minor component appeared to have more stability at this temperature, and could be accounted for as intact parasitized cells containing mature schizonts not lysed by the complement in vitro, but lysed by the recipients' plasma complement in vivo. Further experiments revealed that suspension of parasitized cells in an isotonic diluent and centrifugation at moderate speeds substantially removes the number of invasive free merozoites insolable from a given sample of infected blood by immune hemolysis. CONCLUSIONS: merzoites, either contained within the confines of mature schizont-infected cells, or artificially removed from host cells, rapidly lose the ability to invade susceptible erythrocytes in vivo when suspended in an isotonic medium and held at 1 to 2 C in vitro.

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PubMed1978

Role of the surface coat in in vitro attachment and phagocytosis of Plasmodium berghei by peritoneal macrophages.

Evidence is presented to indicate that Plasmodium berghei merozoites, but not trophozotites, have an antiphagocytic capsule. The capsule appears to form around the developing merozoties of the schizont in the parasitophorous vacuole. Serum from animals immune to P. berghei reacts with this capsule. After reaction with immune serum, the antiphagocytic action of the capsule is lost. By the process of binding serum protein, the capsule becomes electron dense and can be readily visuallzed as the surface coat by electron microscopy. At physiological temperatures, phagocytosis by macrophages rapidly follows adhesion of antibody-coated parasites. Both tight and loose phagosomes are formed.

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PubMed1978

Nutritional studies of the south eastern state peasant diet: studies of the effect of malarial infection (Plasmodium berghei) on electrolyte changes in rats fed the peasants' diet.

1. Plasmodium Berghei (malaria infection) is not specifically related to the nutritional status of the host though nutritional status may aid the advance or elimination of the parasite. 2. The effect of the infection is more severe in low protein diets than in diets whose protein content was adequate. 3. There was no evidence of excessive urinary excretion of electrolytes in the infected rats. 4. It is suggested that low plasma levels of electrolytes in the infected rats were due to skin losses and these losses were independent of the protein content of the diet thus severity of malarial infection is unaffected by protein nutrition.

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PubMed1979

Exoerythrocytic merozoites of Plasmodium berghei in rat hepatic Kupffer cells.

Liver biopsies of white rates infected by Plasmodium berghei sporozoites were examined by electron microscopy. Intrahepatocytic schizont development was confirmed. In addition, at 60 and 70 h after sporozoite inoculation, exoerythrocytic merozoites were noted in Kupffer cells of liver sinusoids. Although it is theoretically possible that this observation may be of merozoite development in Kupffer cells, the authors suspect that this example of phagocytosis would be one of the host's natural defenses against sporozoite-transmitted malaria.

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PubMed1978

[Changes in Plasmodium berghei berghei in mice maintained at high temperatures].

The study of the evolution of Plasmodium berghei berghei is made in mice kept in a high temperature (35 degrees C) throughout the experiment. Some of these mouse parasites (less than 30%) show a gigantic atypical morphology. In the parasite growing in animals kept at 35 degrees C, the amount of DNA is higher than DNA rate of the parasites growing in control mice (20-22 degrees C). There is no evidence of any relation between the increase of DNA amount and the morphological modification of these parasites.

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PubMed1979

The use of membrane screen filters in the isolation of Plasmodium berghei sporozoites from mosquitos.

An improved procedure is presented for the isolation of Plasmodium berghei sporozoites from host mosquitos. The method employs filtration through a series of Nuclepore membranes followed by two consecutive centrifugations of the filtrate layered over Renografin-60 solutions of different densities. A Coulter Counter was used to compare isolations prepared by this technique with those prepared by a routinely employed discontinuous gradient method. When the sporozoite concentration in each preparation was standardized at 300 sporozoites per ml, isolations prepared by the new technique were significantly cleaner than isolations prepared by the discontinuous gradient method, containing an average of 1706 total particles per ml compared with 46 107 total particles per ml. The latter procedure was more effective, however, in removing viable microorganisms. Sporozoites isolated by both techniques were similar in immunogenicity and virulence.

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