Wide distribution of <i>Plasmodium ovale</i> in Myanmar

Win, Thin Thida; Lin, Khin; Mizuno, S.; Zhou, Mian; Liu, Q.; Ferreira, Marcelo U.; Tantular, Indah Setyawati; Kojima, Satoshi; Ishii, Akira; Kawamoto, Fumihiko

doi:10.1046/j.1365-3156.2002.00857.x

Cited by 72 publications

(86 citation statements)

References 18 publications

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“…Blood samples were also examined by nested polymerase chain reaction (PCR)-based amplification of a species-specific segment of the 18S rRNA gene of human malaria parasites, as described by Kimura et al (1997) with the modifications introduced by Win et al (2002). DNA templates for PCR amplification were isolated from 200 ml of whole venous blood using Wizard genomic blood DNA purification kits (Promega, Madison, USA).…”

Section: Subjects Materials and Methodsmentioning

confidence: 99%

Naturally acquired antibodies to merozoite surface protein (MSP)-1(19) and cumulative exposure to Plasmodium falciparum and Plasmodium vivax in remote populations of the Amazon Basin of Brazil

Ladeia‐Andrade

Ferreira

Scopel

et al. 2007

Mem. Inst. Oswaldo Cruz

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Section: Subjects Materials and Methodsmentioning

confidence: 99%

Naturally acquired antibodies to merozoite surface protein (MSP)-1(19) and cumulative exposure to Plasmodium falciparum and Plasmodium vivax in remote populations of the Amazon Basin of Brazil

Ladeia‐Andrade

Ferreira

Scopel

et al. 2007

Mem. Inst. Oswaldo Cruz

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“…Infections with P. ovale, however, have also been reported in the Middle East [13], the Indian subcontinent [21] and different parts of Southeast Asia [11,22,23]. In West Africa (and to a lesser extent Central Africa), age specific LM prevalence of >10% have been observed [3,6] places where P. ovale is observed, it is relatively uncommon and its prevalence (as detected by LM) rarely exceeds 3-5% [22,[24][25][26].…”

Section: Geographical Distributionmentioning

confidence: 99%

Plasmodium malariae and Plasmodium ovale – the ‘bashful’ malaria parasites

Müeller

Zimmerman

Reeder

2007

Trends in Parasitology

270

245

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Although Plasmodium malariae was first described as an infectious disease of humans by Golgi in 1886 and Plasmodium ovale identified by Stevens in 1922, there are still large gaps in our knowledge of the importance of these infections as causes of malaria in different parts of the world. They have traditionally been thought of as mild illnesses that are caused by rare and, in case of P. ovale, short-lived parasites. However, recent advances in sensitive PCR diagnosis are causing a re-evaluation of this assumption. Low-level infection seems to be common across malaria-endemic areas, often as complex mixed infections. The potential interactions of P. malariae and P. ovale with Plasmodium falciparum and Plasmodium vivax might explain some basic questions of malaria epidemiology, and understanding these interactions could have an important influence on the deployment of interventions such as malaria vaccines. Geographical distributionAlthough distribution of Plasmodium malariae infection is reported as being patchy, it has been observed in all major malaria-endemic regions of the world [1]. P. malariae infections are most common in sub-Saharan Africa and the southwest Pacific, where age-specific prevalence in mass blood surveys have exceeded 15-30% [2][3][4][5][6][7][8]. By contrast, when P. malariae has been detected in malaria-endemic regions of Asia [9][10][11][12], the Middle East [13], South America [14] and Central America [15], it is observed as an infrequent infection, with blood-smear light microscopy (LM) prevalence rarely exceeding 1-2%. Much higher levels of infection were, however, found in montagnard refugees from the Cambodian-Vietnamese border [16]. In South America, P. malariae is thought to be a zoonotic infection because the genetically identical Plasmodium brasilianum infects new-world monkeys [17] and both monkeys and humans in endemic areas show high levels of seropositivity to P. malariae and P. brasilianum antigens [18].Plasmodium ovale was thought to have a much more limited distribution, with endemic transmission traditionally described as being limited to areas of tropical Africa, New Guinea, the eastern parts of Indonesia and the Philippines [19,20]. Infections with P. ovale, however, have also been reported in the Middle East [13], the Indian subcontinent [21] and different parts of Southeast Asia [11,22,23]. In West Africa (and to a lesser extent Central Africa), age specific LM prevalence of >10% have been observed [3,6] places where P. ovale is observed, it is relatively uncommon and its prevalence (as detected by LM) rarely exceeds 3-5% [22,[24][25][26].Indepth descriptions of the epidemiology of both infections based upon LM data are, thus, restricted almost exclusively to highly endemic areas in Africa and the Southwest Pacific. Detailed epidemiological studies from South America and Asia are lacking. Variation in parasite prevalenceIn West Africa, P. malariae prevalence has been reported to peak at ages similar to those of P. falciparum (i.e. in children under ten years of...

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“…Primer sequences and assay protocols are described by Win and others. 23 Drug treatment of vivax malaria. Plasmodium vivax malaria was treated according to the current therapy guidelines of the Ministry of Health of Brazil, 24 with 25 mg/kg of CQ base over 3 days (maximum adult dose, 1.5 g over 3 days) and 0.5 mg/kg/day of PQ base for 7 days (maximum adult dose, 30 mg/day).…”

Section: Study Areamentioning

confidence: 99%

Recurrent Parasitemias and Population Dynamics of Plasmodium vivax Polymorphisms in Rural Amazonia

Orjuela-Sánchez¹,

Silva²,

Silva‐Nunes³

et al. 2009

The American Journal of Tropical Medicine and Hygiene

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Abstract. Clinical trials documented alarming post-treatment Plasmodium vivax recurrence rates caused by recrudescence of surviving asexual blood stages, relapse from hypnozoites, or new infections. Here we describe high rates of P. vivax recurrence (26-40% 180 days after treatment) in two cohorts of rural Amazonians exposed to low levels of malaria transmission after a vivax malaria episode treated with chloroquine-primaquine. Microsatellite analysis of 28 paired acute infection and recurrence parasites showed only two pairs of identical haplotypes (consistent with recrudescences or reactivation of homologous hypnozoites) and four pairs of related haplotypes (sharing alleles at 11-13 of 14 microsatellites analyzed). Local isolates of P. vivax were extraordinarily diverse and rarely shared the same haplotype, indicating that frequent recurrences did not favor the persistence or reappearance of clonal lineages of parasites in the population. This fast haplotype replacement rate may represent the typical population dynamics of neutral polymorphisms in parasites from low-endemicity areas.

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Wide distribution of Plasmodium ovale in Myanmar

Cited by 72 publications

References 18 publications

Naturally acquired antibodies to merozoite surface protein (MSP)-1(19) and cumulative exposure to Plasmodium falciparum and Plasmodium vivax in remote populations of the Amazon Basin of Brazil

Naturally acquired antibodies to merozoite surface protein (MSP)-1(19) and cumulative exposure to Plasmodium falciparum and Plasmodium vivax in remote populations of the Amazon Basin of Brazil

Plasmodium malariae and Plasmodium ovale – the ‘bashful’ malaria parasites

Recurrent Parasitemias and Population Dynamics of Plasmodium vivax Polymorphisms in Rural Amazonia

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