[78] 7,8-Dihydropteroate-synthesizing enzyme from Plasmodium chabaudi

1980 ◽  
pp. 564-570 ◽  
Author(s):  
Rolf D. Walter ◽  
Eberhard Königk
Keyword(s):  
Plasmodium Chabaudi

Blockade of TNF receptor 1 reduces disease severity but increases parasite transmission during Plasmodium chabaudi chabaudi infection

2008 ◽  
Vol 38 (8-9) ◽  
pp. 1073-1081 ◽  
Author(s):  
Gráinne H. Long ◽  
Brian H.K. Chan ◽  
Judith E. Allen ◽  
Andrew F. Read ◽  
Andrea L. Graham
Keyword(s):  
Disease Severity ◽  
Parasite Transmission ◽  
Tnf Receptor ◽  
Plasmodium Chabaudi

Interactions betweenTrypanosoma bruceiandBabesiaspp. andPlasmodiumspp. in mice

Parasitology ◽  
1985 ◽  
Vol 90 (2) ◽  
pp. 241-254 ◽  
Author(s):  
Stephanie M. Millott ◽  
F. E. G. Cox
Keyword(s):  
Trypanosoma Brucei ◽  
Babesia Microti ◽  
Cell Populations ◽  
Time Interval ◽  
Oxygen Species ◽  
Plasmodium Chabaudi ◽  
Subsequent Infection ◽  
Activated Oxygen ◽  
Large Numbers ◽  
Intracellular Parasites

Swiss mice with chronicTrypanosoma bruceiinfections become refractory to subsequent infection withBabesia microtiandB. rodhaini. Infection withB. microti7 days afterT. bruceiresulted in an obvious inhibition of the babesia parasitaemias and this inhibition became more profound as the time interval between the infections increased, until at 17–20 days the parasitaemias were totally abolished. Even after intravenous injection of large numbers of parasites parasitaemias were inhibited. Similar inhibition was obtained in BALB/c mice but not in C57BL/6 mice. Mice with establishedT. bruceiinfections also showed reduced susceptibility toB. rodhaini. In mice similarly infected withT. bruceiand the malaria parasitesPlasmodium chabaudi chabaudiandP. c. adamithe pre-patent periods were noticeably prolonged but the subsequent parasitaemias were unaffected. Infections withP. yoeliiwere unaffected.Trypanosoma bruceiinfections were not affected by the intracellular parasites. Among the mechanisms investigated to explain these findings were changes in red blood cell populations, cross-reacting antigens, the release of toxic factors and the generation of activated oxygen species. None of these could account for the inhibition observed.

Effect of dietary iron supplementation on the course of Plasmodium chabaudi malaria in weanling mice

2000 ◽  
Vol 20 (8) ◽  
pp. 1193-1199
Author(s):  
G.S. Ribeiro ◽  
M.R. Garnica ◽  
M.A. Cardoso ◽  
C. Colli ◽  
H.F. Andrade ◽  
...  
Keyword(s):  
Iron Supplementation ◽  
Dietary Iron ◽  
Plasmodium Chabaudi

Genetic studies on a major merozoite surface antigen of the malaria parasite of rodents, Plasmodium chabaudi

1991 ◽  
Vol 13 (4) ◽  
pp. 369-378 ◽  
Author(s):  
ANN P. McLEAN ◽  
F.ALEXANDER LAINSON ◽  
ANDREW MSHARKEY ◽  
DAVID WALLKER
Keyword(s):  
Surface Antigen ◽  
Malaria Parasite ◽  
Plasmodium Chabaudi ◽  
Genetic Studies ◽  
Merozoite Surface Antigen

Isolation and characterization of parasites and host cell ghosts from erythrocytes infected with Plasmodium chabaudi

1987 ◽  
Vol 23 (2) ◽  
pp. 103-115 ◽  
Author(s):  
Frank Wunderlich ◽  
Michael Helwig ◽  
Gabi Schillinger ◽  
Henry Vial ◽  
Jean Philippot ◽  
...  
Keyword(s):  
Host Cell ◽  
Plasmodium Chabaudi ◽  
Isolation And Characterization

Structure of the apical membrane antigen I (AMA-1) of Plasmodium chabaudi

1989 ◽  
Vol 37 (2) ◽  
pp. 281-283 ◽  
Author(s):  
Vikki M. Marshall ◽  
M.Gregory Peterson ◽  
Andrew M. Lew ◽  
David J. Kemp
Keyword(s):  
Apical Membrane ◽  
Plasmodium Chabaudi ◽  
Apical Membrane Antigen

Invasion of mature and immature erythrocytes of CBA/Ca mice by a cloned line of Plasmodium chabaudi chabaudi

Parasitology ◽  
1989 ◽  
Vol 99 (2) ◽  
pp. 157-163 ◽  
Author(s):  
W. Jarra ◽  
K. N. Brown
Keyword(s):  
No Reduction ◽  
Plasmodium Chabaudi ◽  
Equal Frequency ◽  
Early Stages ◽  
Parasite Replication ◽  
Parasite Populations ◽  
Peak Parasitaemia

SummaryDuring the early stages of the primary Plasmodium chabaudi chabaudi AS parasitaemia in CBA/Ca mice this parasite invaded normocytes, but as the parasitaemia developed increasing numbers of parasites were seen within reticulocytes. During and just after peak parasitaemia, as further parasite replication was controlled, the ‘crisis’ phase ensued, mice became increasingly anaemic and reticulocyte numbers were markedly increased. As the parasitaemia was resolved during crisis in excess of 25% of parasites had invaded reticulocytes. In phenylhydrazine-pretreated mice with artificially high reticulocyte levels and infected with P. c. chabaudi AS, normocyte/reticulocyte invasion occurred with equal frequency. No reduction in the infectivity of parasite populations developing in reticulocytes was observed.

Sign in / Sign up

Export Citation Format

Share Document