Studies of splenomegaly in rodent malaria II. The course of splenomegaly, IgM, IgG levels and IgG immunofluorescent antibody titre in mice after infection with plasmodium berghei yoelii and/or plasmodium chabaudi

1971 ◽  
Vol 65 (4) ◽  
pp. 490-500 ◽  
Author(s):  
P. Suntharasamai ◽  
P.D. Marsden
Keyword(s):  
Antibody Titre ◽  
Plasmodium Berghei ◽  
Plasmodium Chabaudi ◽  
Rodent Malaria ◽  
Immunofluorescent Antibody

Plasmodium berghei and Plasmodium chabaudi chabaudi: development of simple in vitro erythrocyte invasion assays

Parasitology ◽  
1992 ◽  
Vol 105 (3) ◽  
pp. 355-362 ◽  
Author(s):  
J. McNally ◽  
S. M. O'donovan ◽  
J. P. Dalton
Keyword(s):  
Plasmodium Berghei ◽  
Plasmodium Chabaudi ◽  
Rodent Malaria ◽  
Erythrocyte Invasion ◽  
Malaria Species ◽  
Invasion Assays

SUMMARYErythrocyte invasion assays are described for two species of rodent malaria, namely Plasmodium berghei and P. c. chabaudi. These invasion assays are simple, are carried out using a candle jar and allow a number of assays to be performed simultaneously. Our results demonstrate that both rodent malaria species show an in vitro preference for reticulocytes although the preference of P. c. chabaudi for these cells is not as marked as that of P. berghei. The details of our invasion assays and our results obtained are discussed.

Eperythrozoon coccoides and rodent malaria: Plasmodium chabaudi and Plasmodium berghei

1967 ◽  
Vol 21 (1) ◽  
pp. 68-77 ◽  
Author(s):  
Karen J. Ott ◽  
Jan K. Astin ◽  
Leslie A. Stauber
Keyword(s):  
Plasmodium Berghei ◽  
Plasmodium Chabaudi ◽  
Rodent Malaria

scholarly journals Caspase-8 mediates inflammation and disease in rodent malaria

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Larissa M. N. Pereira ◽  
Patrícia A. Assis ◽  
Natalia M. de Araújo ◽  
Danielle F. Durso ◽  
Caroline Junqueira ◽  
...  
Keyword(s):  
Septic Shock ◽  
Human Disease ◽  
Caspase 8 ◽  
Inflammasome Activation ◽  
Plasmodium Chabaudi ◽  
Experimental Cerebral Malaria ◽  
Rodent Malaria ◽  
Canonical Pathways ◽  
Inflammatory Caspases

Abstract Earlier studies indicate that either the canonical or non-canonical pathways of inflammasome activation have a limited role on malaria pathogenesis. Here, we report that caspase-8 is a central mediator of systemic inflammation, septic shock in the Plasmodium chabaudi-infected mice and the P. berghei-induced experimental cerebral malaria (ECM). Importantly, our results indicate that the combined deficiencies of caspases-8/1/11 or caspase-8/gasdermin-D (GSDM-D) renders mice impaired to produce both TNFα and IL-1β and highly resistant to lethality in these models, disclosing a complementary, but independent role of caspase-8 and caspases-1/11/GSDM-D in the pathogenesis of malaria. Further, we find that monocytes from malaria patients express active caspases-1, -4 and -8 suggesting that these inflammatory caspases may also play a role in the pathogenesis of human disease.

scholarly journals Virulence, drug sensitivity and transmission success in the rodent malaria, Plasmodium chabaudi

2012 ◽  
Vol 279 (1747) ◽  
pp. 4677-4685 ◽  
Author(s):  
Petra Schneider ◽  
Andrew S. Bell ◽  
Derek G. Sim ◽  
Aidan J. O'Donnell ◽  
Simon Blanford ◽  
...  
Keyword(s):  
Drug Treatment ◽  
Drug Sensitivity ◽  
Resistance Mechanisms ◽  
Cellular Level ◽  
Plasmodium Chabaudi ◽  
Mixed Genotype ◽  
Rodent Malaria ◽  
Treatment Regimens ◽  
Drug Molecules ◽  
Evolutionary Advantage

Here, we test the hypothesis that virulent malaria parasites are less susceptible to drug treatment than less virulent parasites. If true, drug treatment might promote the evolution of more virulent parasites (defined here as those doing more harm to hosts). Drug-resistance mechanisms that protect parasites through interactions with drug molecules at the sub-cellular level are well known. However, parasite phenotypes associated with virulence might also help parasites survive in the presence of drugs. For example, rapidly replicating parasites might be better able to recover in the host if drug treatment fails to eliminate parasites. We quantified the effects of drug treatment on the in-host survival and between-host transmission of rodent malaria ( Plasmodium chabaudi ) parasites which differed in virulence and had never been previously exposed to drugs. In all our treatment regimens and in single- and mixed-genotype infections, virulent parasites were less sensitive to pyrimethamine and artemisinin, the two antimalarial drugs we tested. Virulent parasites also achieved disproportionately greater transmission when exposed to pyrimethamine. Overall, our data suggest that drug treatment can select for more virulent parasites. Drugs targeting transmission stages (such as artemisinin) may minimize the evolutionary advantage of virulence in drug-treated infections.

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