Diagnosing Infection Levels of Four Human Malaria Parasite Species by a Polymerase Chain Reaction/Ligase Detection Reaction Fluorescent Microsphere-Based Assay

McNamara, David T.; Kasehagen, Laurin; Grimberg, Brian T.; Cole-Tobian, Jennifer L.; Collins, William E.; Zimmerman, Peter A.

doi:10.4269/ajtmh.2006.74.413

Cited by 122 publications

(169 citation statements)

References 33 publications

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Section: Improved Diagnosis Of P Malariae and P Ovale Infections Bymentioning

confidence: 99%

“…These assays enable detection of the four Plasmodium parasite species that infect humans at densities ~100 times lower than the limit of LM detection [47] and have evolved from simple species-specific amplification strategies to multiplex approaches that incorporate semiquantitative assessments [31,[49][50][51][52][53][54][55][56]. We have greatly extended the potential use of PCR diagnosis for a wide range of epidemiological studies through our recent efforts to develop a ligase detection reaction fluorescent microsphere assay (LDR-FMA) [52,57] to evaluate all four malaria parasites of humans in a single-well multiplex format.In a series of studies from PNG that have combined LM and molecular diagnostics [29,31,32], we have found that molecular methods consistently detected significantly increased prevalence of all four malaria species of humans, with the largest increases in P. malariae and P. ovale. In these studies from three different PNG populations, the prevalence of P. falciparum and P. vivax increased between 1.6 and 3.0-fold and 2.1 and 3.4-fold, respectively, and a 2.6 to 10.9-fold increase in P. malariae prevalence was observed (LM:…”

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

Müeller

Zimmerman

Reeder

2007

Trends in Parasitology

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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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Section: Improved Diagnosis Of P Malariae and P Ovale Infections Bymentioning

confidence: 99%

mentioning

confidence: 99%

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

Müeller

Zimmerman

Reeder

2007

Trends in Parasitology

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260

245

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“…Light microscopy (LM) and ligase detection reaction-fluorescent microsphere assay (LDR-FMA) were performed to identify samples infected with P. vivax as described. 21 The proportion of samples that was LMor LDR-FMA-positive for P. vivax infection was used to determine the infection prevalence for both provinces and each catchment. To increase the available template volume for analysis, whole-genome amplification (WGA) was performed using the Illustra GenomiPhi V2 DNA Amplification Kit as per the manufacturer's instructions (GE Healthcare, Rydalmere, New South Wales, Australia).…”

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confidence: 99%

High Genetic Diversity of Plasmodium vivax on the North Coast of Papua New Guinea

Arnott

Barnadas

Senn

et al. 2013

The American Journal of Tropical Medicine and Hygiene

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Abstract. Despite having the highest Plasmodium vivax burden in the world, molecular epidemiological data from Papua New Guinea (PNG) for this parasite remain limited. To investigate the molecular epidemiology of P. vivax in PNG, 574 isolates collected from four catchment sites in East Sepik (N = 1) and Madang (N = 3) Provinces were genotyped using the markers MS16 and msp1F3. Genetic diversity and prevalence of P. vivax was determined for all sites. Despite a P. vivax infection prevalence in the East Sepik (15%) catchments less than one-half the prevalence of the Madang catchments (27-35%), genetic diversity was similarly high in all populations (H e = 0.77-0.98). High genetic diversity, despite a marked difference in infection prevalence, suggests a large reservoir of diversity in P. vivax populations of PNG. Significant reductions in transmission intensity may, therefore, be required to reduce the diversity of parasite populations in highly endemic countries such as PNG.

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“…malaria species (13,20). The parasite density of P. vivax was determined by real-time quantitative PCR (14,21), and P. vivax-positive samples were genotyped for the highly polymorphic PvDBPII alleles (22).…”

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Naturally acquired Duffy-binding protein-specific binding inhibitory antibodies confer protection from blood-stage Plasmodium vivax infection

King

Michon

Shakri

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Individuals residing in malaria-endemic regions acquire protective immunity after repeated infection with malaria parasites; however, mechanisms of protective immunity and their immune correlates are poorly understood. Blood-stage infection with Plasmodium vivax depends completely on interaction of P. vivax Duffy-binding protein (PvDBP) with the Duffy antigen on host erythrocytes. Here, we performed a prospective cohort treatment/reinfection study of children (5-14 years) residing in a P. vivax-endemic region of Papua New Guinea (PNG) in which children were cleared of blood-stage infection and then examined biweekly for reinfection for 25 weeks. To test the hypothesis that naturally acquired binding inhibitory antibodies (BIAbs) targeting PvDBP region II (PvDBPII) provide protection against P. vivax infection, we used a quantitative receptor-binding assay to distinguish between antibodies that merely recognize PvDBP and those that inhibit binding to Duffy. The presence of high-level BIAbs (>90% inhibition of PvDBPII-Duffy binding, n ‫؍‬ 18) before treatment was associated with delayed time to P. vivax reinfection diagnosed by light microscopy (P ‫؍‬ 0.02), 55% reduced risk of P. vivax reinfection (Hazard's ratio ‫؍‬ 0.45, P ‫؍‬ 0.04), and 48% reduction in geometric mean P. vivax parasitemia (P < 0.001) when compared with children with low-level BIAbs (n ‫؍‬ 148). Further, we found that stable, high-level BIAbs displayed strain-transcending inhibition by reducing reinfection with similar efficiency of PNG P. vivax strains characterized by six diverse PvDBPII haplotypes. These observations demonstrate a functional correlate of protective immunity in vivo and provide support for developing a vaccine against P. vivax malaria based on PvDBPII.Duffy antigen ͉ immunity ͉ protective antibodies P rotective immunity against malaria is acquired by residents of endemic regions over a period of years after repeated exposure to malaria parasites (1). Naturally acquired immunity to Plasmodium falciparum and Plasmodium vivax malaria does not prevent infection by these parasites completely, but limits parasite densities, reduces the frequency of clinical malaria episodes, and prevents severe disease (2). Humoral immune responses against blood-stage antigens are an important component of naturally acquired immunity to malaria (2, 3). Therefore, parasite proteins engaged in erythrocyte invasion are potential targets of protective antibody responses.Interaction between P. vivax Duffy-binding protein (PvDBP) and the Duffy antigen receptor (DA) on host erythrocytes is central to blood-stage infection by P. vivax (4, 5). Adhesion to DA is mediated by the 140-kDa PvDBP (6-8). The receptor-binding domain of PvDBP maps to the conserved, N-terminal cysteine-rich region II (PvDBPII) (9, 10). Given the complete dependence of P. vivax on the PvDBPII-Duffy interaction for blood-stage infection and recent observations that PvDBPII-specific antibodies inhibit P. vivax invasion of human erythrocytes in vitro (11), we examined the hypothesis that...

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Diagnosing Infection Levels of Four Human Malaria Parasite Species by a Polymerase Chain Reaction/Ligase Detection Reaction Fluorescent Microsphere-Based Assay

Cited by 122 publications

References 33 publications

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

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

High Genetic Diversity of Plasmodium vivax on the North Coast of Papua New Guinea

Naturally acquired Duffy-binding protein-specific binding inhibitory antibodies confer protection from blood-stage Plasmodium vivax infection

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