Heterogeneity in filterability of erythrocytes from malaria (Plasmodium berghei)-infected blood

Summary Erythrocytes fromPlasmodium berghei-infected blood show a decrease in deformability with increasing parasitaemia, as measured by filterability through polycarbonate sieves. A major fraction of cells carrying mature parasites and a smaller fraction carrying ring-stage parasites account for the obstruction of filtration, while the remaining infected cells do not contribute to the decrease in filterability. The relation of filterability to metabolic status in infected cells is discussed. Acknowledgment. This investigation received the financial support of the UNDP/World Bank/WHO Special Programme for Research and Training in Tropical Diseases (TDR 800352) and the Rockefeller Foundation Programme for Great Neglected Diseases.     

Effect of Plasmodium berghei infection on benzoic acid metabolism in mice

The metabolism of benzoic acid was studied in Plasmodium berghei infected mice both in vitro and in vivo. Results of in vitro studies showed a considerable decrease in the ability of the infected liver to detoxify benzoic acid by hippuric acid formation. The in vivo study showed that hippuric acid formation decreases with increasing parasitemia and the emergence of benzoyl-glucuronide. This new pathway stops operating with further increase in parasitemia.     

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.     

Hepatic acid hydrolases of albino rats, Mastomys natalensis and albino mice during Plasmodium berghei infection

Changes in liver acid hydrolase activities during the infection of albino rats, Mastomys or mice with Plasmodium berghei are described. B-Glucosidase, B-galactosidase and N-acetyl-B-D-glucosaminidase exhibited widely different responses with acid phosphatase and cathepsin-B the least responsive and are likely to be causally related to immunity of animals.     

Pulmonary edema in mice infected with Plasmodium berghei. Involvement of catecholamines

Mice inoculated with Plasmodium berghei developed a drastic and significant pulmonary edema. Treatment of animals with phenoxybenzamine rendered mice hyporeactive to this physiopathological alteration.     

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.     

Effect ofPlasmodium berghei infection on benzoic acid metabolism in mice

Summary The metabolism of benzoic acid was studied inPlasmodium berghei infected mice both in vitro and in vivo. Results of in vitro studies showed a considerable decrease in the ability of the infected liver to detoxify benzoic acid by hippuric acid formation. The in vivo study showed that hippuric acid formation decreases with increasing parasitemia and the emergence of benzoyl-glucoronide. This new pathway stops operating with further increase in parasitemia.     

The course ofPlasmodium berghei infection in mice latently infected withToxoplasma gondii

Summary The course of infection with 2 different virulent strains ofPlasmodium berghei was investigated in mice latently infected withToxoplasma gondii. When given the highly virulent ANKA strain ofP. berghei all Toxoplasma-infected mice died but the survival time was prolonged. After infection with the less virulent strain K 173 mice could survive the subsequent infection. In these cases levels of parasitemia depended upon the duration of theT. gondii infection. Mice infected for about 6 weeks withT. gondii showed maximum protection. These studies were conducted in the Institut für Medizinische Parasitologie der Universit?t Bonn (D-5300 Bonn, Federal Republic of Germany).     

Mean cytoplasmic protein concentration of host erythrocytes and the reticulocyte response in Plasmodium berghei infected mice.

The decreasing mean cytoplasmic protein concentration (MPC) of P. berghei host cells is paralled by an increasing parasitemia and percent reticulocyte response. The reticulocyte response parallels the percent parasitemia except during a period of accelerated reticulocytosis noted during the midpoint of the infection at which time the percent reticulocytes increases at a rate more than double the rate of increase of percent parasitemia. Although the reticulocyte population and the host cell population are usually equivalent, the disparity noted suggests the existence of unique characteristics in the reticulocyte response of P. berghei infected mice.     

Of membranes and malaria: phospholipid asymmetry in Plasmodium falciparum-infected red blood cells

Cellular and Molecular Life Sciences - Malaria is a vector-borne parasitic disease with a vast impact on human history, and according to the World Health Organisation, Plasmodium parasites still...     

Hemoglobin concentration changes determined in populations of living host erythrocytes duringPlasmodium berghei infection in mice

Résumé On a mesuré la concentration en hémoglobine de cellules-hôtes vivantes pendant la période d'infection par lePlasmodium berghei de souris. Le premier jour de l'infection on n'a pas constaté de différence significative entre la concentration en hémoglobine des cellules-hôtes et celle des erythrocytes de contrôle. Le 5^e et le 9³ jour le niveau de concentration en hémoglobine des cellules-hôtes a nettement baissé. Le pourcentage de parasitémie était inversément proportionnel à la concentration en hémoglobine de la cellule-hôte, réaction érythropoiétique probable.     

Surface antigens of Plasmodium falciparum-infected erythrocytes as immune targets and malaria vaccine candidates

Understanding the targets and mechanisms of human immunity to malaria caused by Plasmodium falciparum is crucial for advancing effective vaccines and developing tools for measuring immunity and exposure in populations. Acquired immunity to malaria predominantly targets the blood stage of infection when merozoites of Plasmodium spp. infect erythrocytes and replicate within them. During the intra-erythrocytic development of P. falciparum, numerous parasite-derived antigens are expressed on the surface of infected erythrocytes (IEs). These antigens enable P. falciparum-IEs to adhere in the vasculature and accumulate in multiple organs, which is a key process in the pathogenesis of disease. IE surface antigens, often referred to as variant surface antigens, are important targets of acquired protective immunity and include PfEMP1, RIFIN, STEVOR and SURFIN. These antigens are highly polymorphic and encoded by multigene families, which generate substantial antigenic diversity to mediate immune evasion. The most important immune target appears to be PfEMP1, which is a major ligand for vascular adhesion and sequestration of IEs. Studies are beginning to identify specific variants of PfEMP1 linked to disease pathogenesis that may be suitable for vaccine development, but overcoming antigenic diversity in PfEMP1 remains a major challenge. Much less is known about other surface antigens, or antigens on the surface of gametocyte-IEs, the effector mechanisms that mediate immunity, and how immunity is acquired and maintained over time; these are important topics for future research.     

Pathogenesis of Plasmodium falciparum malaria: the roles of parasite adhesion and antigenic variation

Malaria results in up to 2.5 million deaths annually, with young children and pregnant women at greatest risk. The great majority of severe disease is caused by Plasmodium falciparum. A characteristic feature of infection with P. falciparum is the accumulation or sequestration of parasite-infected red blood cells (RBCs) in various organs, such as the brain, lung and placenta, and together with other factors is important in the pathogenesis of severe forms of malaria. Sequestration results from adhesive interactions between parasite-derived proteins expressed on the surface of infected RBCs and a number of host molecules on the surface of endothelial cells, placental cells and uninfected RBCs. Some receptors for parasite adhesion have been implicated in particular malaria syndromes, such as intercellular adhesion molecule 1 in cerebral malaria and chondroitin sulfate A and hyaluronic acid in placental infection. The principal parasite ligand and antigen on the RBC surface, P. falciparum erythrocyte membrane protein 1 encoded by a multigene family termed var, is clonally variant, enabling evasion of specific immune responses. An understanding of these host-parasite interactions in the context of clinical disease and immunity may reveal potential targets to prevent or treat severe forms of malaria. Received 25 June 2001; received after revision 22 August 2001; accepted 24 August 2001     

Hepatic acid hydrolases of albino rats,Mastomys natalensis and albino mice duringPlasmodium berghei infection

Summary Changes in liver acid hydrolase activities during the infection of albino rats,Mastomys or mice withPlasmodium berghei are described. B-Glucosidase, B-galactosidase and N-acetyl-B-D-glucosaminidase exhibited widely different responses with acid phosphatase and cathepsin-B the least responsive and are likely to be causally related to immunity of animals.