Abstract
Malaria caused by Plasmodium ovale species is considered a neglected tropical disease with limited information about its characteristics. It also remains unclear whether the two distinct species P. ovale curtisi and P. ovale wallikeri exhibit differences in their prevalence, geographic distribution, clinical characteristics, or laboratory parameters. Therefore, this study was conducted to clarify these differences to support global malaria control and eradication programs. Studies reporting the occurrence of P. ovale curtisi and P. ovale wallikeri were explored in databases. Differences in proportion, clinical data, and laboratory parameters between the two species were estimated using a random-effects model and expressed as pooled odds ratios (ORs), mean difference (MD), or standardized MD depending on the types of extracted data. The difference in geographical distribution was visualized by mapping the origin of the two species. A total of 1453 P. ovale cases extracted from 35 studies were included in the meta-analysis. The p-value in the meta-analyses provided evidence favoring a real difference between P. ovale curtisi malaria cases (809/1453, 55.7%) and P. ovale wallikeri malaria cases (644/1453, 44.3%) (p: 0.01, OR 1.61, 95% CI 0.71–3.63, I2: 77%). Subgroup analyses established evidence favoring a real difference between P. ovale curtisi and P. ovale wallikeri malaria cases among the imported cases (p: 0.02, 1135 cases). The p value in the meta-analyses provided evidence favoring a real difference in the mean latency period between P. ovale curtisi (289 cases) and P. ovale wallikeri malaria (266 cases) (p: 0.03, MD: 27.59, 95% CI 1.99–53.2, I2: 94%), total leukocyte count (p < 0.0001, MD: 840, 95% CI 610–1070, I2: 0%, two studies) and platelet count (p < 0.0001, MD: 44,750, 95% CI 2900–60,500, I2: 32%, three studies). Four continents were found to have reports of P. ovale spp., among which Africa had the highest number of reports for both P. ovale spp. in its 37 countries, with a global proportion of 94.46%, and an almost equal distribution of both P. ovale spp., where P. ovale curtisi and P. ovale wallikeri reflected 53.09% and 46.90% of the continent’s proportion, respectively. This is the first systematic review and meta-analysis to demonstrate the differences in the characteristics of the two distinct P. ovale species. Malaria caused by P. ovale curtisi was found in higher proportions among imported cases and had longer latency periods, higher platelet counts, and higher total leukocyte counts than malaria caused by P. ovale wallikeri. Further studies with a larger sample size are required to confirm the differences or similarities between these two species to promote malaria control and effective eradication programs.
Highlights
Malaria caused by Plasmodium ovale species is considered a neglected tropical disease with limited information about its characteristics
P. ovale spp. infection is increasingly observed among travelers who return from P. ovale-endemic areas
Due to its lower mortality (0.15%)[2] than that of malaria caused by other non-P. falciparum spp. such as P. vivax and P. malariae, and due to mixed infection[54,55,56,57], there has been limited focus on P. ovale spp. in malaria research
Summary
Malaria caused by Plasmodium ovale species is considered a neglected tropical disease with limited information about its characteristics. A previous study suggested that differences in season, region, ecology, or host red cell invasion phenotype could maintain a physical barrier between the two s pecies[25] Another potential reason is that these two species have accumulated mutations through a genetic drift to prevent mating or recombination[26], and the differences in their recognition molecules that are essential for the mating process, such as the ookinete proteins, have been reported previously[27]. These two species are morphologically similar and cannot be differentiated using microscopic or RDT methods, there has been limited evidence of non-Schüffner’s stippling in P. ovale wallikeri-infected red blood c ells[28]. The genetic polymorphisms that can distinguish between P. ovale curtisi and P. ovale wallikeri, including P. ovale spp. tryptophan-rich antigen (potra)[6,7], P. ovale reticulate binding protein 2 (porbp2)[11,25,34], lactate dehydrogenase (ldh)[23], cytochrome (cytb b)[12], cytochrome oxidase subunit 1 (cox1)[12], glyceraldehyde-3-phosphatase (pog3p)[26], dihydrofolate reductase-thymidylate synthase (podhfr-ts)[12] and the k13 gene[35], were initially identified to differentiate between the two P. ovale species
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