A mixed infection of vivax and falciparum malaria apparently resistant to 4-aminoquinoline: a case report

Schuurkamp, G J; Spicer, Paul E.; Kereu, Richard K.; Bulungol, Peter K.

doi:10.1016/0035-9203(89)90370-2

Cited by 34 publications

(14 citation statements)

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“…Resistance of the erythrocytic forms of P.vivax to chloroquine was reported as early as 1989 from subaequatorial islands between the Indian Ocean and the Pacific [8][9][10], a region largely affected by the Chesson strain of P. vivax. Later, the phenomenon was also encountered in northwestern Sumatra [11], India [12] and Myanmar [13].…”

Section: Introductionmentioning

confidence: 99%

Susceptibility to chloroquine, mefloquine and artemisinin of Plasmodium vivax in northwestern Thailand

Woitsch

Wernsdorfer

Congpuong

et al. 2007

Wien Klin Wochenschr

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The in vitro study had the objectives of monitoring the sensitivity of Plasmodium vivax to chloroquine and artemisinin, and to assess its baseline sensitivity to mefloquine in northwestern Thailand in an area near the border to Myanmar. The investigations were carried out in 2004 at the malaria clinics of Mae Sot, Chedi Ko and Mae Ka Sa, all in the district of Mae Sot, Province of Tak. The in vitro tests followed the method of Tasanor. Successful tests were obtained with 45 fresh isolates of P. vivax. The EC(50) and EC(90) values for chloroquine were 120.9 nM and 655.7 nM, respectively, the GMCOC was 1699.7 nM. There was a significant decrease of the chloroquine sensitivity since 1998/1999. However, results of parallel investigations continue to indicate clinical-parasitological sensitivity to chloroquine. With mefloquine the EC(50) and EC(90) the (baseline) values were 131.6 nM and 972.6 nM, respectively, the GMCOC was 1987.0 nM. For artemisinin the EC(50) and EC(90) values were 8.7 nM and 105.2 nM, respectively, the GMCOC was 310.5 nM. As compared to 2002, the sensitivity of P. vivax to artemisinin has shown a slight but not significant increase.

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Section: Introductionmentioning

confidence: 99%

Susceptibility to chloroquine, mefloquine and artemisinin of Plasmodium vivax in northwestern Thailand

Woitsch

Wernsdorfer

Congpuong

et al. 2007

Wien Klin Wochenschr

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“…3 In contrast, chloroquine-resistant P. vivax has been recognized only since ϳ 1990. Case reports from New Guinea appeared in 1989-1991, 4,5 and a prospective report from Indonesian New Guinea was published in 1993. 6 Myanmar has also reported resistant P. vivax since 1993.…”

Section: Introductionmentioning

confidence: 99%

Plasmodium vivax clinically resistant to chloroquine in Colombia.

Soto¹,

Toledo²,

Gutiérrez³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

106

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Abstract. Chloroquine-resistant Plasmodium vivax has been the subject of numerous case reports and prospective studies from Oceania and Asia. In contrast, only case reports exist from the Americas. We performed a prospective study with 28-day follow-up of clinical responses to chloroquine in 2 P. vivax-endemic regions of Colombia. Three (11%) of 27 patients failed to respond to treatment with the standard regimen of chloroquine (1,500 mg of base over 3 days). One patient demonstrated RI resistance on Day 26; one patient demonstrated RI resistance due to recrudescence of blood stages on Day 11; and one patient demonstrated RII resistance of blood stages by never displaying clearing of peripheral parasitemia. All patients were successfully treated with primaquine, which has some blood stage efficacy against P. vivax, combined with a second course of chloroquine. Clinical resistance of P. vivax to chloroquine is present in Colombia and should be monitored in the Americas.

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“…Its variants (VK210, are found in mixed infections; VK210 has also been found as a single infection [9]. Reduction in susceptibility to chloroquine has been reported from Papua New Guinea, India, Asia and South America [1,13,19], though no relationship between P. vivax genotypes and parasite clearance following treatment with chloroquine has been found. Kain et al (1993) suggested that response to chloroquine varies depending on the type of P. vivax, since the VK210 genotype and mixed infection with VK247 took longer to clear, while VK247 tended to have a shorter duration in Thailand.…”

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confidence: 99%

Correlation between Plasmodium vivax variants in Belém, Pará State, Brazil and symptoms and clearance of parasitaemia

Machado¹,

Filho²,

Calvosa³

et al. 2003

Braz J Infect Dis

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The aim of this study was to determine how different types of P. vivax affect clinical symptoms and parasitaemia clearance. Blood was collected from individuals from Pará State, Brazil. The patients were treated as chloroquine plus primaquine. P. vivax were typed daily till D7 and again on D30. Now we can confirm a previously reported correlation between P. vivax genotype and response to chloroquine. Clinical symptoms do not allow for objective identification of different P. vivax types in the Brazilian Amazon, since the VK247 and P. vivax-like have only been detected in mixed infections. Key Words: Plasmodium vivax variants, symptoms, chloroquine and primaquine treatment, clearence of parasitaemia. Plasmodium vivax has been the most common cause of human malaria in the Brazilian Amazon region during the last seven years. Its variants (VK210, are found in mixed infections; VK210 has also been found as a single infection [9]. Reduction in susceptibility to chloroquine has been reported from Papua New Guinea, India, Asia and South America [1,13,19], though no relationship between P. vivax genotypes and parasite clearance following treatment with chloroquine has been found. Kain et al. (1993) suggested that response to chloroquine varies depending on the type of P. vivax, since the VK210 genotype and mixed infection with VK247 took longer to clear, while VK247 tended to have a shorter duration in Thailand. A study conducted in Brazil showed no significant difference in the time of parasite clearance after treatment with chloroquine and primaquine, alone or combined [9]. Variants of P. vivax can produce different clinical signs and responses to treatment [5], as there is a correlation between P. vivax genotypes and the intensity of symptoms and vector preference, which can affect drug resistance and consequent failure of control measures [4]. We examined how different types of P. vivax affect clinical symptoms and parasitaemia clearance.Blood was collected from 30 individuals from Belém city (Pará State) who had signed the informed consent form. The blood samples were obtained before therapy was initiated (D0), and continued daily till day 5 (D5). Vacutainer tubes containing EDTA (Becton Dickinson, UK) were used to collected 5 mL of whole blood/ individual that was subsequently applied to glass-fibermembrane discs (Titertek, ICN Biomedicals Limited, UK) following the protocol described by Warhurst et al. [21]. The patients were treated as follows: 25 mg chloroquine/kg body weight during 3 days (10 mg/kg on day 1 and 7.5 mg/kg on days 2 and 3), plus 0.25 mg primaquine /kg for 14 days, starting on the fourth day. Plasmodium vivax types were identified by 176 BJID 2003; 7 (June) GFM/PCR/ELISA [9] for all samples. The patients were evaluated daily by a physician till D7, and again on D30.The typing of P. vivax genotype in D0 detected 16 samples with a single infection, all by VK210 (53%) and 14 samples with mixed infections (47%): four VK210 plus VK247 (13%), two VK210 plus P. vivax-like (7%), five VK247 plus P. v...

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A mixed infection of vivax and falciparum malaria apparently resistant to 4-aminoquinoline: a case report

Cited by 34 publications

References 0 publications

Susceptibility to chloroquine, mefloquine and artemisinin of Plasmodium vivax in northwestern Thailand

Susceptibility to chloroquine, mefloquine and artemisinin of Plasmodium vivax in northwestern Thailand

Plasmodium vivax clinically resistant to chloroquine in Colombia.

Correlation between Plasmodium vivax variants in Belém, Pará State, Brazil and symptoms and clearance of parasitaemia

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