@article{Valea2009-ip,

title = {Performance of OptiMAL-IT compared to microscopy, for malaria 

 detection in Burkina Faso},

author = {Innocent Val\'{e}a and Halidou Tinto and Madi Nikiema and Lawrence Yamuah and Noel Rouamba and Maxime Drabo and Robert T Guiguemde and Umberto d'Alessandro},

year  = {2009},

date = {2009-03-01},

journal = {Trop. Med. Int. Health},

volume = {14},

number = {3},

pages = {338--340},

publisher = {Wiley},

abstract = {OBJECTIVE: To compare the performance of OptiMAL-IT, a rapid 

 diagnostic test for malaria, with that of microscopy in Burkina 

 Faso. METHOD: Finger-prick blood samples of 464 children 

 attending hospital for suspected malaria were tested for malaria 

 by microscopy and OptiMAL-IT. RESULTS: The sensitivity and specificity of OptiMAL-IT were 98.7% (CI 95% = 97.6-99.8) and 96.2% (CI 95% = 94.3-98.1) respectively, with a high positive 

 likelihood ratio (25.97). CONCLUSION: OptiMAL-IT can be 

 considered a good method to diagnose malaria in Burkina Faso, 

 particularly in remote areas with little or no access to 

 microscopy services.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Culleton2008-pj,

title = {Failure to detect Plasmodium vivax in West and Central Africa by 

 PCR species typing},

author = {Richard L Culleton and Toshihiro Mita and Mathieu Ndounga and Holger Unger and Pedro V L Cravo and Giacomo M Paganotti and Nobuyuki Takahashi and Akira Kaneko and Hideaki Eto and Halidou Tinto and Corine Karema and Umberto D'Alessandro and Virgilio Ros\'{a}rio and Takatoshi Kobayakawa and Francine Ntoumi and Richard Carter and Kazuyuki Tanabe},

year  = {2008},

date = {2008-09-01},

journal = {Malar. J.},

volume = {7},

number = {1},

pages = {174},

publisher = {Springer Nature},

abstract = {BACKGROUND: Plasmodium vivax is estimated to affect 75 million 

 people annually. It is reportedly absent, however, from west and 

 central Africa due to the high prevalence of the Duffy negative 

 phenotype in the indigenous populations. Despite this, 

 non-African travellers consistently return to their own 

 countries with P. vivax malaria after visiting this region. An 

 attempt was made, therefore, to detect the presence of P. vivax 

 parasites in blood samples collected from the indigenous 

 populations of west and central Africa. METHODS: Parasite 

 species typing (for all four human malaria parasites) was 

 carried out by PCR on 2,588 blood samples collected from 

 individuals from nine African malaria-endemic countries. 

 RESULTS: Most infections (98.5%) were Plasmodium falciparum, 

 Plasmodium malariae was identified in 8.5% of all infections, 

 and Plasmodium ovale in 3.9%. The prevalence of both parasites 

 varied greatly by country. Only one case of P. vivax was 

 detected from Sao Tome, an island off the west coast of Africa, 

 confirming the scarcity of this parasite in Africa. CONCLUSION: 

 The prevalence of P. vivax in local populations in sub-Saharan 

 Africa is very low, despite the frequent identification of this 

 parasite in non-African travellers.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Tinto2008-bs,

title = {Chloroquine-resistance molecular markers (Pfcrt T76 and 

 Pfmdr-1 Y86) and amodiaquine resistance in Burkina Faso},

author = {Halidou Tinto and Lougu\'{e} Guekoun and Issaka Zongo and Robert Tinga Guiguemd\'{e} and Umberto D'Alessandro and Jean Bosco Ou\'{e}draogo},

year  = {2008},

date = {2008-02-01},

journal = {Trop. Med. Int. Health},

volume = {13},

number = {2},

pages = {238--240},

publisher = {Wiley},

abstract = {We investigated the relationship between the two main molecular 

 markers for chloroquine resistance (Pfcrt T76 and Pfmdr-1 Y86) 

 and the clinical efficacy of amodiaquine in Burkina Faso. Before 

 treatment, the prevalence of Pfcrt T76, Pfmdr-1 Y86 or both 

 mutations in the same infection was significantly higher in 

 patients who experienced a recrudescence than in those who 

 successfully responded to the treatment. Therefore, these two 

 molecular markers could be useful in monitoring amodiaquine 

 resistance, particularly in countries where this drug is used in 

 combination with artesunate as first- or second-line treatment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Tinto2007-yx,

title = {Sulfadoxine-pyrimethamine efficacy and selection of Plasmodium 

 falciparum DHFR mutations in Burkina Faso before its 

 introduction as intermittent preventive treatment for pregnant 

 women},

author = {Halidou Tinto and Jean Bosco Ou\'{e}draogo and Issaka Zongo and Chantal Overmeir and Eric Marck and Tinga Robert Guiguemd\'{e} and Umberto D'Alessandro},

year  = {2007},

date = {2007-04-01},

journal = {Am. J. Trop. Med. Hyg.},

volume = {76},

number = {4},

pages = {608--613},

publisher = {American Society of Tropical Medicine and Hygiene},

abstract = {Sulfadoxine-pyrimethamine efficacy was determined with a 28-day 

 follow-up in 97 children between 6 months and 15 years of age. 

 The polymerase chain reaction (PCR)-corrected treatment failure 

 was 8.2% and the uncorrected was 21.6%. The presence of the 

 dihydrofolate reductase (DHFR) and dihydropteroate synthetase 

 (DHPS) mutations linked to sulfadoxine-pyrimethamine resistance 

 before and after treatment was determined by PCR-restriction 

 fragment length polymorphism (RFLP) and by a fluorogenic PCR 

 assay. Before treatment, the prevalence of the triple DHFR 

 mutations was higher among the patients having had a recurrent 

 parasitemia (either recrudescence or new infection; 28.6% versus 9.3%), although the difference was not significant (P = 

 0.1). The double mutation Ala-436/Gly-437 was observed in 67% 

 of samples, whereas no Glu-540 mutation was found. After 

 treatment, the triple DHFR mutation was found in 76.2% of 

 patients with recurrent parasitemia, recrudescence, and new 

 infection alike. Such high prevalence of mutant parasites 

 indicates that sulfadoxine-pyrimethamine should not be used as 

 monotherapy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Zongo2007-uv,

title = {Artemether-lumefantrine versus amodiaquine plus 

 sulfadoxine-pyrimethamine for uncomplicated falciparum malaria 

 in Burkina Faso: a randomised non-inferiority trial},

author = {Issaka Zongo and Grant Dorsey and Noel Rouamba and Halidou Tinto and Christian Dokomajilar and Robert T Guiguemde and Philip J Rosenthal and Jean Bosco Ouedraogo},

year  = {2007},

date = {2007-02-01},

journal = {Lancet},

volume = {369},

number = {9560},

pages = {491--498},

publisher = {Elsevier BV},

abstract = {BACKGROUND: Artemisinin-based combination regimens are widely 

 advocated for malarial treatment, but other effective regimens 

 might be cheaper and more readily available. Our aim was to 

 compare the risk of recurrent parasitaemia in patients given 

 artemether-lumefantrine with that in those given amodiaquine 

 plus sulfadoxine-pyrimethamine for uncomplicated malaria. 

 METHODS: We enrolled 521 patients aged 6 months or older with 

 uncomplicated falciparum malaria in Bobo-Dioulasso, Burkina 

 Faso. Patients were randomly assigned to receive standard doses 

 of either artemether-lumefantrine (261) or amodiaquine plus 

 sulfadoxine-pyrimethamine (260) for 3 days. Primary endpoints 

 were the risks of treatment failure within 28 days, either 

 unadjusted or adjusted by genotyping to distinguish 

 recrudescence from new infection. The study is registered at 

 controlled-trials.gov with the identifier ISRCTN54261005. 

 FINDINGS: Of enrolled patients, 478 (92%) completed the 28-day 

 study. The risk of recurrent symptomatic malaria was lowest in 

 the group given amodiaquine plus sulfadoxine-pyrimethamine 

 (1.7%vs 10.2%; risk difference 8.5%; 95% CI 4.3-12.6; p=0.0001); as was the risk of recurrent parasitaemia (4.7%vs 15.1%; 10.4%; 5.1-15.6; p=0.0002). Nearly all recurrences were 

 due to new infections. Recrudescences were four late treatment 

 failures with artemether-lumefantrine and one early treatment 

 failure with amodiaquine plus sulfadoxine-pyrimethamine. Both 

 regimens were safe and well tolerated, with pruritus more common 

 with amodiaquine plus sulfadoxine-pyrimethamine than with 

 artemether-lumefantrine. Each regimen selected for new isolates 

 with mutations that have been associated with decreased drug 

 susceptibility. INTERPRETATION: Amodiaquine plus 

 sulfadoxine-pyrimethamine was more effective than was 

 artemether-lumefantrine for the treatment of uncomplicated 

 malaria. For regions of Africa where amodiaquine plus 

 sulfadoxine-pyrimethamine continues to be effective, this less 

 expensive and more available regimen should be considered as an 

 alternative to blanket recommendations for artemisinin-based 

 combination treatment for malaria.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Tinto2006-iz,

title = {In-vitro susceptibility of Plasmodium falciparum to 

 monodesethylamodiaquine, dihydroartemisinin and quinine in an 

 area of high chloroquine resistance in Rwanda},

author = {Halidou Tinto and Claude Rwagacondo and Corinne Karema and Denise Mupfasoni and Waltruda Vandoren and Emmanuel Rusanganwa and Annette Erhart and Chantal Van Overmeir and Eric Van Marck and Umberto D'Alessandro},

year  = {2006},

date = {2006-06-01},

journal = {Trans. R. Soc. Trop. Med. Hyg.},

volume = {100},

number = {6},

pages = {509--514},

publisher = {Oxford University Press (OUP)},

abstract = {Plasmodium falciparum in-vitro susceptibility to chloroquine 

 (CQ), monodesethylamodiaquine, quinine and dihydroartemisinin 

 was investigated in Rwandan patients with a parasitaemia of at least >or=4000/microl. The study was carried out in 

 November-December 2003. Dihydroartemisinin was the most potent (GM IC(50)=2.6nmol/l, 95% CI 2.2-3.2) among the drugs tested. 

 Resistance to chloroquine was 45% (33/74) and that to 

 monodesethylamodiaquine 7% (5/74). All the tested isolates were 

 susceptible to quinine. The mean IC(50) of 

 monodesethylamodiaquine, quinine and dihydroartemisinin was 

 significantly higher for chloroquine-resistant than for 

 chloroquine-sensitive strains (P<0.05). The IC(50) of each drug 

 was significantly and positively correlated to that of the other 

 three drugs (P<0.005), and this correlation was higher between CQ and monodesethylamodiaquine (r=0.8). In-vitro CQ resistance 

 is linked to that of the other drugs tested. Most worrying is 

 the positive correlation between the IC(50) of 

 dihydroartemisinin and the other drugs, more particularly with 

 CQ, suggesting an increased tolerance of the parasites to all 

 drugs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Tinto2005-vz,

title = {Usefulness of the Plasmodium falciparum chloroquine resistance 

 transporter T76 genotype failure index for the estimation of 

 in vivo chloroquine resistance in Burkina Faso},

author = {Halidou Tinto and Boroma Sanou and Jean-Claude Dujardin and Jean Bosco Ou\'{e}draogo and Chantal VAN Overmeir and Annette Erhart and Eric VAN Marck and Tinga Robert Guiguemd\'{e} and Umberto D'Alessandro},

year  = {2005},

date = {2005-07-01},

journal = {Am. J. Trop. Med. Hyg.},

volume = {73},

number = {1},

pages = {171--173},

publisher = {American Society of Tropical Medicine and Hygiene},

abstract = {The prevalence of chloroquine (CQ) treatment failure and the 

 genotype failure index was determined in four sentinel sites in 

 Burkina Faso. In three sites, the genotype failure index varied 

 between 1.7 and 3, a result confirming the relationship between 

 the Plasmodium falciparum CQ resistance transporter (Pfcrt) T76 

 mutation and CQ resistance. In the remaining site, the genotype 

 failure index was unusually low, 1.1, which was significantly 

 different than that in the other sites (P < 0.00001). These 

 findings are discussed. Often but not always, the prevalence of 

 CQ resistance can be correctly estimated by the Pfcrt T76 

 genotype failure index.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Tinto2004-sw,

title = {Parasitological resistance of Plasmodium falciparum to 

 antimalarial drugs: what physicians should keep in mind},

author = {Halidou Tinto and Jean Bosco Ou\'{e}draogo and Maminata Traor\'{e} and Tinga Robert Guiguemd\'{e}},

year  = {2004},

date = {2004-04-01},

journal = {Sante},

volume = {14},

number = {2},

pages = {69--73},

abstract = {Plasmodium falciparum drug resistance has considerably modified 

 the attitude of physicians in terms of malaria case management. 

 However, a bad understanding of the resistance phenomenon can 

 lead to non-appropriate therapeutic and/or public health 

 practices. The objective of this paper was to contribute to 

 clarify the concept of parasitological resistance by analysing 

 the different types of resistance observed in vivo. We showed 

 through some examples that the precision of in vivo 

 parasitological results depends on the type of microscopical 

 technique used. We also showed that the classification system 

 into resistance levels RI, RII, and RIII does not correspond to 

 an increase in the resistance of the parasite itself but rather 

 to an increase in the proportion of the resistant strains 

 compared to the sensitive ones circulating in a given population. 

 Mutant strains are circulating in low proportions as long as 

 there is no selective drug pressure. They can be first detected 

 in vitro and, later on, when their proportion increase, they are 

 detected in vivo, first in non-immune subjects and later in 

 semi-immune subjects. Therefore, the role of the host immunity is 

 important in malaria drug resistance. To conclude, increasing use 

 of antimalarial drugs (especially in monotherapy) cannot thwart 

 the resistance, but rather leads to the selection of mutants 

 strains. As the proportion of the mutant strains increases 

 compared to the sensitive (wild) ones, it will reach the 

 microscopic detection level and then, the clinical level. It is 

 important that physicians involved in malaria case management 

 understand these notions in order to avoid non-appropriate 

 therapeutic decisions.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Tinto2003-pn,

title = {Relationship between the Pfcrt T76 and the Pfmdr-1 Y86 

 mutations in Plasmodium falciparum and in vitro/in vivo 

 chloroquine resistance in Burkina Faso, West Africa},

author = {Halidou Tinto and Jean Bosco Ou\'{e}draogo and Annette Erhart and Chantal Van Overmeir and Jean-Claude Dujardin and Eric Van Marck and Tinga Robert Guiguemd\'{e} and Umberto D'Alessandro},

year  = {2003},

date = {2003-11-01},

journal = {Infect. Genet. Evol.},

volume = {3},

number = {4},

pages = {287--292},

publisher = {Elsevier BV},

abstract = {The relationship between Pfcrt T76 and Pfmdr-1 Y86 mutations in 

 Plasmodium falciparum was explored in samples from patients with 

 uncomplicated malaria and tested in vitro and in vivo with 

 chloroquine (CQ) in Burkina Faso. The two mutations were 

 strongly related. The Pfcrt T76 mutation was found in 82% of 

 the samples having the Pfmdr-1 Y86 mutation too (odds ratio (OR)=4.8 [95% CI: 1.7-13.3]; P=0.002). However, only half 

 (16/34) of samples with Pfcrt T76 mutation had also the Pfmdr-1 

 Y86 mutation. The latter was apparently associated with in vitro resistance (OR=4.8 [95% CI: 1.4-16.5]; P=0.01) but such association disappeared (P=0.77) after adjusting for the 

 presence of the Pfcrt T76 mutation. This suggests that the 

 occurrence of the Pfmdr-1 Y86 mutation is dependent on that of 

 Pfcrt T76 mutation and could explain previous reports linking 

 the Pfmdr-1 Y86 mutation with CQ resistance (CQR). The isolates 

 carrying both the Pfcrt K76 and Pfmdr-1 N86 alleles (wild/wild 

 (WW)) and the single mutant Pfmdr-1 Y86 (WM) had the lowest IC50 

 geometric mean (GMIC50) values, while those carrying both Pfcrt 

 T76/Pfmdr-1 Y86 alleles (mutant/mutant (MM)), and the single 

 mutant Pfcrt T76 (MW) had the highest. Among pre-treatment 

 samples there was a strong linkage disequilibrium with an excess 

 of MM and WW and a deficit of single mutants (MW and WM), 

 suggesting that parasite fitness is higher for the former and 

 lower for the latter.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Ballin2002-cl,

title = {Antiplasmodial compounds from Cochlospermum tinctorium},

author = {Nicolai Zederkopff Ballin and Maminata Traore and Halidou Tinto and Archibald Sittie and Per M\olgaard and Carl Erik Olsen and Arsalan Kharazmi and S\oren Br\ogger Christensen},

year  = {2002},

date = {2002-09-01},

journal = {J. Nat. Prod.},

volume = {65},

number = {9},

pages = {1325--1327},

abstract = {Fractionation of an ethanol extract of roots of Cochlospermum 

 tinctorium afforded five compounds: 3-O-E-p-coumaroylalphitolic 

 acid (1), cochloxanthin (2), dihydrocochloxanthin (3), alphitolic 

 acid (4), and 1-hydroxytetradecan-3-one (5). This is the first 

 example of a 1-hydroxyalkan-3-one obtained from plant material 

 after gentle workup. The antiplasmodial activities of the 

 compounds were determined, and the IC(50) value of 

 3-O-E-p-coumaroylalphitolic acid was 2.3 microM.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}