Plasma and in vitro levels of cytokines during and after a Plasmodium falciparum malaria attack in Gabon

Acta Tropica ◽  
2002 ◽  
Vol 83 (3) ◽  
pp. 195-203 ◽  
Author(s):  
Agnès Aubouy ◽  
Philippe Deloron ◽  
Florence Migot-Nabias
2002 ◽  
Vol 9 (3) ◽  
pp. 720-722
Author(s):  
Kåre Kemp ◽  
Jørgen A. L. Kurtzhals ◽  
Bartholomew D. Akanmori ◽  
Victoria Adabayeri ◽  
Bamenla Q. Goka ◽  
...  

ABSTRACT Levels of soluble CD30 (sCD30) in serum were elevated in patients with Plasmodium falciparum malaria but showed decline following treatment. The levels of sCD30 in serum were correlated significantly with the expression of gamma interferon by peripheral T cells. These data suggest that CD30+ cells are upregulated during a malaria attack and that they may play a regulating role at the site of inflammation.


Author(s):  
Mélissa Mairet-Khedim ◽  
Sandrine Nsango ◽  
Christelle Ngou ◽  
Sandie Menard ◽  
Camille Roesch ◽  
...  

Abstract Background Dihydroartemisinin/piperaquine is increasingly used for the treatment of uncomplicated Plasmodium falciparum malaria in Africa. The efficacy of this combination in Cameroon is poorly documented, while resistance to dihydroartemisinin/piperaquine readily spreads in Southeast Asia. Objectives This study evaluated the clinical efficacy of dihydroartemisinin/piperaquine in Cameroon, as well as the molecular profile and phenotypic susceptibility of collected isolates to dihydroartemisinin and piperaquine. Patients and methods Dihydroartemisinin/piperaquine efficacy in 42 days was followed-up for 138 patients presenting non-complicated falciparum malaria. Piperaquine concentration was determined at day 7 for 124 patients. kelch13 gene polymorphisms (n = 150) and plasmepsin2 gene amplification (n = 148) were determined as molecular markers of resistance to dihydroartemisinin and piperaquine, respectively. Parasite susceptibility to dihydroartemisinin and piperaquine was determined using validated in vitro survival assays. Results The efficacy of dihydroartemisinin/piperaquine treatment was 100% after PCR correction. The reinfections were not associated with a variation of piperaquine concentration at day 7. Ninety-six percent (144/150) of the samples presented a WT allele of the kelch13 gene. Two percent (3/150) presented the non-synonymous mutation A578S, which is not associated with resistance to dihydroartemisinin. No duplication of the plasmepsin2 gene was observed (0/148). All the samples tested in vitro by survival assays (n = 87) were susceptible to dihydroartemisinin and piperaquine. Conclusions Dihydroartemisinin/piperaquine has demonstrated excellent therapeutic efficacy with no evidence of emerging artemisinin or piperaquine resistance in Yaoundé, Cameroon. This observation suggests that dihydroartemisinin/piperaquine could be a sustainable therapeutic solution for P. falciparum malaria if implemented in areas previously free of artemisinin- and piperaquine-resistant parasites, unlike Southeast Asia.


2004 ◽  
Vol 71 (3) ◽  
pp. 294-296 ◽  
Author(s):  
AGNÉS AUBOUY ◽  
ANNICK KEUNDJIAN ◽  
MOHAMED BAKARY ◽  
PHILIPPE DELORON ◽  
JACQUES LE BRAS ◽  
...  

2013 ◽  
Vol 13 (12) ◽  
pp. 1043-1049 ◽  
Author(s):  
Benoit Witkowski ◽  
Chanaki Amaratunga ◽  
Nimol Khim ◽  
Sokunthea Sreng ◽  
Pheaktra Chim ◽  
...  

2020 ◽  
Vol 412 (16) ◽  
pp. 3915-3923
Author(s):  
Jia Liu ◽  
Olga Chesnokova ◽  
Irina Oleinikov ◽  
Yuhao Qiang ◽  
Andrew V. Oleinikov ◽  
...  

Blood ◽  
1983 ◽  
Vol 62 (4) ◽  
pp. 866-868 ◽  
Author(s):  
EF Jr Roth ◽  
C Raventos Suarez ◽  
A Rinaldi ◽  
RL Nagel

Abstract Previous data on in vitro culture of Plasmodium falciparum malaria demonstrated that red cell glucose-6-phosphate dehydrogenase deficiency (G6PD-) inhibited parasite growth in deficient hemizygous males. This study investigated the effect of heterozygosity for G6PD- on parasite growth. Blood was obtained from 8 female Sardinian G6PD- heterozygotes with G6PD normal cells ranging from 13% to 60%. For comparison, blood from a G6PD- hemizygous male, containing 100% deficient red cells, was mixed in different proportions with compatible normal blood. In both experiments, parasite growth was inhibited by the presence of deficient cells. In both cases, it was found that the inhibition could be explained by a simple dilution of normal cells by G6PD- cells. Thus, the typical female heterozygote is also protected to a significant extent. When considering the “malaria hypothesis” as it relates to G6PD, protection of the female heterozygote as well as the male hemizygote must be taken into account.


Author(s):  
Melissa Mairet-Khedim ◽  
Rithea Leang ◽  
Camille Marmai ◽  
Nimol Khim ◽  
Saorin Kim ◽  
...  

Abstract Background Artesunate-amodiaquine is a potential therapy for uncomplicated malaria in Cambodia. Methods Between September 2016 and January 2017, artesunate-amodiaquine efficacy and safety were evaluated in a prospective, open-label, single-arm observational study at health centers in Mondulkiri, Pursat and Siem Reap Provinces, Cambodia. Adults and children with microscopically-confirmed Plasmodium falciparum malaria received oral artesunate-amodiaquine once daily for three days plus single-dose primaquine, with follow-up on Days 7, 14, 21 and 28. The primary outcome was Day-28 PCR-adjusted adequate clinical and parasitological response (ACPR). An amodiaquine parasite survival assay (AQSA) was developed and applied to whole genome sequencing results to evaluate potential amodiaquine resistance molecular markers. Results In 63 patients, Day-28 PCR-adjusted ACPR was 81.0% (95% confidence interval [CI], 68.9–88.7). Day 3 parasite positivity rate was 44.4% (28/63; 95%CI, 31.9–57.5). All 63 isolates had the K13(C580Y) marker for artemisinin resistance; 79.4% (50/63) had Pfpm2 amplification. The AQSA resistance phenotype (≥45% parasite survival) was expressed in 36.5% (23/63) of isolates and was significantly associated with treatment failure (P = 0.0020). Pfmdr1 mutant haplotypes were N86/184F/D1246 and Pfcrt was CVIET or CVIDT at positions 72–76. Additional Pfcrt mutations were not associated with amodiaquine resistance, but the G353V mutant allele was associated with ACPR compared to Pfmdr1 haplotypes harboring F1068L or S784L/R945P mutations (P = 0.030 and P = 0.0004, respectively). Conclusions For uncomplicated falciparum malaria in Cambodia, artesunate-amodiaquine had inadequate efficacy owing to amodiaquine-resistant P. falciparum. Amodiaquine resistance was not associated with previously identified molecular markers.


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