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      Genetic diversity of Plasmodium falciparum isolates from patients with uncomplicated and severe malaria based on msp-1 and msp-2 genes in Gublak, North West Ethiopia

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          Malaria infection can present with a wide variety of symptoms, ranging from mild to severe. Plasmodium falciparum isolates in uncomplicated and severe malaria infections may have different parasite genetic profiles. This study was conducted to assess differences in genetic diversity and allelic frequencies in P. falciparum isolates according to malaria severity and age of patients in the Gublack area, northwest Ethiopia.


          Cross-sectional health facility-based study conducted in Gublak, Ethiopia between July, 2017 and October, 2017. Symptomatic P. falciparum malaria patients with microscopically-confirmed infection were enrolled. Parasite DNA was extracted from filter paper blood spots and the polymorphic regions of the msp- 1 and msp- 2 genes were genotyped using allele-specific nested-PCR with fragment analysis by gel electrophoresis.


          A total of 118 patients were enrolled including 95 (80.5%) with uncomplicated infection and 23 (19.5%) with severe disease. In msp-1, the K1 allelic family was similarly prevalent in uncomplicated 42 (44.2%) and severe disease 12 (52.2%). In msp-2, FC27 was detected in 55 (57.9%) of uncomplicated infections and IC/3D7 in 14 (60.9%) of severe infections. 76 (64.4%) of the 118 isolates contained multiple genotypes; 56 (58.9%) in uncomplicated infections and 19 (82.6%) in severe infections. The overall of multiplicity of infection was 2.2 (95% CI 1.98–2.42) with 1.4 (95% CI 1.23–1.55) and 1.7 (95% CI 1.49–1.86) for msp- 1 and msp- 2, respectively. Multiplicity of infection was significantly higher in severe than uncomplicated infections (3.0 (95% CI 2.61–3.47) versus 2.0 (95% CI 1.83–2.23), respectively, p = 0.001). There was no difference in multiplicity of infection across age groups (p = 0.104).


          Patients with severe malaria were more likely to have multiclonal infections. Further studies are needed to describe the association between P. falciparum genotypes and malaria severity in different malaria transmission areas.

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          Most cited references 38

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          Vertical transmission of HIV-1 infection.

           M-L Newell (2015)
          Vertical transmission is the dominant mode of acquisition of infection for HIV infection in children, and about 1600 infants are newly infected each day worldwide. Without interventions the risk of transmission is between 15% and 35%, and associated with maternal disease progression, prematurity, duration of rupture of membranes, length of labour, and vaginal delivery. Breastfeeding approximately doubles the risk of vertical transmission; the additional risk of transmission through breastfeeding is approximately 15-20%, with about one-third of this accounted for by late postnatal transmission after 3 months of age. Current strategies to reduce the risk of transmission include a short course of anti-retroviral therapy, avoidance of breastfeeding and Caesarean section delivery. However, even if interventions late in pregnancy or around the time of delivery are highly effective in preventing perinatal infection, it is likely that as a public health policy they are of interest only if alternatives to breastfeeding are feasible, affordable, safe and available.
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            Association of transmission intensity and age with clinical manifestations and case fatality of severe Plasmodium falciparum malaria.

            There are concerns that malaria control measures such as use of insecticide-treated bed nets, by delaying acquisition of immunity, might result in an increase in the more severe manifestations of malaria. An understanding of the relationships among the level of exposure to Plasmodium falciparum, age, and severity of malaria can provide evidence of whether this is likely. To describe the clinical manifestations and case fatality of severe P falciparum malaria at varying altitudes resulting in varying levels of transmission. A total of 1984 patients admitted for severe malaria to 10 hospitals serving populations living at levels of transmission varying from very low (altitude >1200 m) to very high (altitude or =15 years: OR, 0.44; 95% CI, 0.27-0.73; P 1200 m: OR, 0.55; 95% CI, 0.26-1.15; P for trend = .03). The odds of cerebral malaria were significantly higher in low transmission intensity areas (altitude of residence 1200 m: OR, 3.76; 95% CI, 1.96-7.18; P for trend = .003) and with age 5 years and older (0-1 year: referent; 2-4 years: OR, 1.57; 95% CI, 0.82-2.99; 5 to or =15 years: OR, 6.24; 95% CI, 3.47-11.21; P<.001). The overall case-fatality rate of 7% (139 deaths) was similar at high and moderate levels of transmission but increased to 13% in low transmission areas (P = .03), an increase explained by the increase in the proportion of cases with cerebral malaria. Age and level of exposure independently influence the clinical presentation of severe malaria. Our study suggests that an increase in the proportion of cases with more fatal manifestations of severe malaria is likely to occur only after transmission has been reduced to low levels where the overall incidence is likely to be low.
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              Multiplicity of Plasmodium falciparum infection in asymptomatic children in Senegal: relation to transmission, age and erythrocyte variants

              Background Individuals living in malaria endemic areas generally harbour multiple parasite strains. Multiplicity of infection (MOI) can be an indicator of immune status. However, whether this is good or bad for the development of immunity to malaria, is still a matter of debate. This study aimed to examine the MOI in asymptomatic children between two and ten years of age and to relate it to erythrocyte variants, clinical attacks, transmission levels and other parasitological indexes. Methods Study took place in Niakhar area in Senegal, where malaria is mesoendemic and seasonal. Three hundred and seventy two asymptomatic children were included. Sickle-cell trait, G6PD deficiency (A- and Santamaria) and α+-thalassaemia (-α3.7 type) were determined using PCR. Multiplicity of Plasmodium falciparum infection, i.e. number of concurrent clones, was defined by PCR-based genotyping of the merozoite surface protein-2 (msp2), before and at the end of the malaria transmission season. The χ2-test, ANOVA, multivariate linear regression and logistic regression statistical tests were used for data analysis. Results MOI was significantly higher at the end of transmission season. The majority of PCR positive subjects had multiple infections at both time points (64% before and 87% after the transmission season). MOI did not increase in α-thalassaemic and G6PD mutated children. The ABO system and HbAS did not affect MOI at any time points. No association between MOI and clinical attack was observed. MOI did not vary over age at any time points. There was a significant correlation between MOI and parasite density, as the higher parasite counts increases the probability of having multiple infections. Conclusion Taken together our data revealed that α-thalassaemia may have a role in protection against certain parasite strains. The protection against the increase in MOI after the transmission season conferred by G6PD deficiency is probably due to clearance of the malaria parasite at early stages of infection. The ABO system and HbAS are involved in the severity of the disease but do not affect asymptomatic infections. MOI was not age-dependent, in the range of two to ten years, but was correlated with parasite density. However some of these observations need to be confirmed including larger sample size with broader age range and using other msp2 genotyping method.

                Author and article information

                Malar J
                Malar. J
                Malaria Journal
                BioMed Central (London )
                10 December 2019
                10 December 2019
                : 18
                [1 ]GRID grid.452387.f, Ethiopian Public Health Institute, ; Addis Ababa, Ethiopia
                [2 ]ISNI 0000 0001 2157 559X, GRID grid.1043.6, Menzies School of Health Research, , Charles Darwin University, ; Darwin, Australia
                [3 ]ISNI 0000 0004 0637 6869, GRID grid.414183.b, Internal Medical Services, Ballarat Health Services, ; Ballarat, Australia
                © The Author(s) 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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