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Effectiveness of a health education intervention on the use of long-lasting insecticidal nets for the prevention of malaria in pregnant women of Pakistan: a quasi-experimental study
research-article
Author(s):
Ramesh Kumar
1
,
5
,
,
Midhat Farzeen
1 ,
Assad Hafeez
1 ,
Baseer Khan Achakzai
2 ,
Muskan Vankwani
3 ,
Manohar Lal
4 ,
Rabia Iqbal
4 ,
Ratana Somrongthong
5
,
Publication date (Electronic):
29 June 2020
Journal:
Malaria Journal
Publisher:
BioMed Central
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Abstract
Background
About one quarter of pregnant women in the population of Pakistan are using long-lasting insecticide-treated bed nets (LLINs) for prevention of malaria. Past research reported that adequate information and education would act as mediator to change behaviour among patients for prevention of malaria infection. The effective use of LLINs would contribute to reduction of disease burden caused by malaria. The aim of this study was to determine the effectiveness of health education on the adoption of LLINs among pregnant women living in Tharparkar, a remote district in Sindh Province, Pakistan.
Methods
A quasi-experimental study design with control and intervention groups was conducted with 200 pregnant women (100 in each group). Women in the intervention group were provided with health education sessions on malaria for 12 weeks, while those in the control group obtained routine information from lady health workers (LHWs). Pre- and post-intervention assessment was done of knowledge about malaria and use of LLIN, which was statistically analysed using descriptive statistics and difference in difference (DID) multivariable regression analysis to test effectiveness of the intervention.
Results
Baseline was conducted with 200 pregnant women. Demographic characteristics were similar in both groups with slight differences in age, education, income, type of latrine, and source of drinking water. There were no significant differences between mean knowledge and use of LLINs scores between groups at baseline. However, the estimated DID value after the intervention was 4.170 (p < 0.01) and represents an increase in scores of knowledge in the intervention group compared to control. Similarly DID value of 3.360 (p < 0.05) showed an increase in use of LLINs score after the intervention which was significant, showing that the intervention had a positive effect.
Conclusions
Results proved that health education could be an effective intervention for improving knowledge and usage of LLINs among pregnant women for the prevention of malaria. Such educational interventions have a positive potential to be implemented at larger scale by incorporating them into routine health sessions provided by health workers.
Related collections
Most cited references28
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Quantifying the Number of Pregnancies at Risk of Malaria in 2007: A Demographic Study
Stephanie Dellicour, Andrew Tatem, Carlos Guerra … (2010)
Introduction Malaria in pregnancy can have devastating consequences to a pregnant woman and the developing fetus, but comprehensive estimates of the annual number of women who become pregnant each year in malaria endemic areas and are therefore at risk of malaria are not available, particularly for Latin America and the Asia-Pacific regions. These figures are an important first step towards informing policy makers and for estimating the regional needs for therapeutic and disease prevention tools for malaria in pregnancy. The most cited global estimate is from the Roll Back Malaria Partnership, which states that “each year approximately 50 million women living in malaria endemic countries throughout the world become pregnant” [1]. However, an explanation of the methods used to derive these estimates is not provided. More comprehensive estimates exist for Africa and are provided by the Africa Regional Office (AFRO) of the World Health Organization (WHO) in their widely quoted strategic framework document for malaria prevention and control during pregnancy in the African region [2]. Their estimate of 24.6 million pregnancies at risk of malaria (predominantly P. falciparum), is based on the number of live born babies delivered in malarious areas of Africa in the year 2000 using a combination of malaria risk maps [3] and estimates of the number of live births from UNICEF [4]. A more recent estimate by the WHO states that “In Africa, 30 million women living in malaria endemic areas become pregnant each year” [5]. Estimates for outside of Africa are less clear, particularly for P. vivax. P. vivax is the most widely distributed human malaria parasite and co-occurs with P. falciparum in tropical areas but also occurs in temperate regions outside the limits of P. falciparum transmission. It is the major cause of malaria in much of Asia and Latin America [6],[7], and recent evidence has shown that P. vivax infections are far from benign and can result in significant morbidity in pregnant women with serious consequences for maternal and infant health [8]–[10]. Here we define a global estimate of the number of pregnancies at risk of P. falciparum and P. vivax malaria in 2007 by combining malaria spatial limits developed by the Malaria Atlas Project (MAP; www.map.ox.ac.uk), which define the total population at risk of malaria [11], with country-specific demographic data on women of childbearing age provided by the United Nations and published data on induced abortions and spontaneous pregnancy loss. Methods Data Sources The global limits of P. falciparum malaria The initial focus of the Malaria Atlas Project has been P. falciparum [12] due to its global epidemiological significance [13] and better prospects for its control and local elimination [14]. The global spatial limits of P. falciparum malaria transmission in 2007 have recently been mapped. This was done by triangulating data on transmission exclusion using biological rules based on temperature and aridity limits on the bionomics of locally dominant Anopheles vectors, data on nationally reported case incidence rates, and other medical intelligence [15]. The resulting map stratifies the malaria endemic world by stable and unstable transmission in 2007 [15]. Unstable transmission refers to areas where transmission is plausible biologically, but limited, with a clinical incidence of less than one case per 10,000 population per year. Stable transmission refers to areas with a minimum of one clinical case per 10,000 population per year [15]. The global limits of P. vivax malaria Initial attempts to map the limits of P. falciparum and P. vivax transmission were made by Guerra et al. [16],[17]. The resulting maps and “masks” (mapped areas that are filtered and excluded from analyses) used were later tested against the Malaria Atlas Project parasite prevalence database to assess their feasibility [18],[19]. This testing revealed that the accuracy to define areas of zero transmission risk due to very low population densities was limited because of the coarse spatial resolution of the initial map. Moreover, in the initial mapping [16],[17], a high density population mask was used on the basis of the assumption that no transmission occurs in areas where the population density is so high that conditions become unsuitable for transmission through the process of urbanization. However, recent analyses [19] provide evidence suggesting that high density population masks and urban extent maps should not be used to map zero risk because some transmission can occur in high density urban areas, although this is significantly lower than in rural areas [18],[19]. Therefore, for the current analyses, the P. vivax limits were redefined using the same methods as in Guerra et al. [16],[17], but without applying the population-based masks. Also, previously excluded P. vivax endemic countries have now been added after a more extensive review of the literature; these include Comoros, Djibouti, Madagascar, and Uzbekistan. This refinement of the spatial limits of transmission for P. vivax accounted for an approximate 19% increase in the population at risk (PAR) compared with previous estimates [16],[17], principally (18%) due to the inclusion of major cities. Gridded population data The Global Rural-Urban Mapping Project (GRUMP) alpha version provides gridded population counts and population density estimates for the years 1990, 1995, and 2000, both adjusted and unadjusted to the United Nations' national population estimates [11],[20]. The adjusted population counts for the year 2000 were projected to 2007 by applying national, medium variant, intercensal growth rates by country [21] using methods described previously [22]. Annual number of pregnancies per country The number of pregnancies was calculated as the sum of the number of live births, induced abortions, and spontaneous pregnancy loss (including miscarriages and stillbirths) in 2007. Live births The annual number of live births in 2007 was estimated per country using demographic data on the proportion of women of childbearing age (WOCBAs) within a population and the total fertility rates. The data were abstracted from the United Nations' national population estimates, which provide publicly accessible demographic information by year, age, sex, and country for Africa, Asia, and the Americas [23]. The number of WOCBAs in each country, defined as the mid-year resident number of women aged between 15 and 49y, was obtained for the years 2005 and 2010 (interim years are not available), and the number of WOCBAs for 2007 was calculated as the midpoint between the 2005 and 2010 estimates. The fraction of WOCBAs per country was then calculated as the number of WOCBAs in 2007 divided by the mid-year resident population at risk in 2007 (available by year). The total fertility rate (TFR) is an age-standardised measure of fertility and corresponds to the total number of children that would be born alive to a woman entering her childbearing years at age 15y if she lived to the end of her childbearing years (age 49y) and if her fertility during these 35 reproductive years was the same as the average woman of childbearing age. The total fertility rate divided by 35 is the average number of live births per WOCBA per year and when multiplied by 1,000 this is expressed as the rate of live births per 1,000 WOCBAs per year. Induced abortions, miscarriages, and stillbirth rates Subregional data on induced abortion rates were obtained from a recently published review that calculated the worldwide, regional, and subregional incidence of safe and unsafe abortions in women of child bearing age in 2003 by use of reports from official national reporting systems, nationally representative demographic health surveys, hospital data, other surveys, and published studies [24]. Country-specific information on stillbirth rates was abstracted from model-based estimates published by Stanton et al. [25] that derived data from vital registration, demographic and health surveys (DHS), and data from study reports integrated into a regression model. Regional estimates were used for three malaria endemic countries for which country-specific estimates were not available (French Guiana, Mayotte, and Timor-Leste). Country-specific data on miscarriages (spontaneous abortions) are not available. To calculate the proportion of pregnancies resulting in miscarriage, a method was applied that uses multipliers to work backwards from the (known) number of live births and induced abortions to recover the (unknown) underlying number of pregnancies that “produced” them, as described in detail previously [24],[26]–[28]. The method takes account of pregnancies that are terminated voluntarily during the period of risk for miscarriage and estimates the number of spontaneous pregnancy loss (stillbirths and miscarriages) as 10% of induced abortions plus 20% of live births. It is based on clinical studies of rates of pregnancy loss by gestational age that indicate that for each 100 induced abortions an additional ten clinically recognised pregnancies will have aborted spontaneously prior to the average gestational age of induced abortions in that population, and that approximately 120 additional clinically recognised pregnancies are required to “produce” 100 live births [27],[28]. For example, in Afghanistan it was estimated that in 2007 1.182 million live births occurred among a population of 27 million and a further 0.284 million induced abortions occurred. The number of spontaneous pregnancy losses (the sum of the number of stillbirths and miscarriages) was therefore estimated at 0.2×1,182 plus 0.1×0.284 = 0.265 million, and the total number of pregnancies as 1.731 million. The reported number of miscarriages used in this manuscript represents the number of spontaneous pregnancy losses calculated through the multiplier method as described above, minus the country-specific number of stillbirths obtained from the review by Stanton et al. [25]. The estimates provided in this study refer to clinically recognised pregnancies and do not take into account the potentially large but unknown rates of embryonic loss that may occur in the first 4–6 wk of gestation. Estimating the annual number of pregnancies exposed to malaria To obtain the total population at risk, the limits of stable and unstable P. falciparum transmission and the limits of P. vivax transmission described above were overlaid onto the Global Rural-Urban Mapping Project (GRUMP) alpha surface, projected to 2007. For every malaria endemic country of the world, the population within each set of limits was extracted, following approaches described previously [13]. The number of pregnancies at risk of malaria was then calculated from the total annual number of pregnancies estimated to have occurred in 2007 in the entire country multiplied by the fraction of the total resident population living within the spatial limits of malaria transmission in that country. Results Tables 1 and 2 provide a summary of the total population living within the global spatial limits of malaria transmission in 2007, and the corresponding number of total population, pregnancies, and live births, stratified by species and transmission patterns (within areas of assumed unstable and stable P. falciparum transmission), globally and by WHO region. 10.1371/journal.pmed.1000221.t001 Table 1 Demographic data for malaria endemic countries. WHORO Region n of MECs Total Population (Both Sexes)a WOCBAsa Total n of Pregnanciesb TPRc Pregnancy Rate per 1,000 WOCBAs§ Percentage Pregnancies Ending in: Live-births Still-births Spontaneous Abortions Induced Abortions AFRO 43 755 178 36 7.16 204 72.4% 2.3% 13.3% 11.9% EMRO/EURO 19 544 142 19 4.76 136 68.8% 2.3% 13.1% 15.8% AMRO 21 530 143 16 3.81 109 63.2% 0.9% 14.0% 22.0% SEARO/WPRO 19 3,327 881 91 3.62 103 62.4% 1.6% 13.1% 22.8% Global 102 5,157 1,343 162 4.23 121 65.5% 1.8% 13.3% 19.5% a Source: United Nations Development Program (in millions). b The total number of pregnancies is the sum of the number of live-births, stillbirths, spontaneous, and induced abortions (in millions). c The total pregnancy rate (TPR) and the annual pregnancy rate per 1,000 WOCBAs are weighted means per region and is for illustration purposes only. The number of pregnancies was derived directly as the sum of the national estimates within each region and globally. MEC, malaria endemic countries; WHORO, World Health Organization Regional Office. 10.1371/journal.pmed.1000221.t002 Table 2 Total population at risk of P. falciparum and/or P. vivax malaria by WHO regional office in 2007 (in millions) (percent of the population in malaria endemic countries at risk). WHORO Region P. falciparum Transmissiona P. vivax Transmissiona Any Species Stable Transmissionb Unstable Transmissionb Overall Overall Overall AFRO 599.9 (79.4) 8.4 (1.1) 607.8 (80.5) 73.2 (9.7) 615.4 (81.5) EMRO/EURO 89.8 (16.5) 101.7 (18.7) 190.9 (35.1) 285.1 (52.4) 343.9 (63.2) AMRO 41.2 (7.8) 50.2 (9.5) 91.4 (17.2) 96.2 (18.2) 138.2 (26.1) SEARO/WPRO 654.9 (19.7) 824.9 (24.8) 1479.3 (44.5) 2,722.3 (81.8) 2,770.1 (83.3) Global 1,385.8 (26.9) 985.1 (19.1) 2,369.4 (45.9) 3,176.9 (61.6) 3,867.6 (75.0) Similar tables with risk estimates by continent and by pregnancy outcome (live-birth, induced abortions, stillbirths, and miscarriages) are provided in Tables S1, S2, S3. a Includes countries where P. falciparum and P. vivax co-exist. b Stable transmission, ≥1 autochthonous P. falciparum cases per 10,000 people per annum; unstable transmission, <1 autochthonous P. falciparum cases per 10,000 people per annum [15]. MEC, malaria endemic countries; TPR, total pregnancy rate; WHORO, World Health Organization Regional Office. The compiled data showed that, globally, 125.2 million women living in areas with P. falciparum and/or P. vivax transmission became pregnant in 2007: 77.4 million (61.8%) in the countries that fall under the regional office of the WHO for the South East Asian (SEARO) and the Western Pacific Region (WPRO); 30.3 million (24.2%) in AFRO; 13.1 million (10.5%) in the Eastern Mediterranean and European Region (EMRO and EURO); and only 4.3 million (3.4%) in the American Region (AMRO) (Table 3). Figures 1 and 2 display the same analysis by species, but depicted by continent rather than by WHO region. Of the 125.2 million pregnancies, 82.6 million (66.0%) are estimated to result in live births; 48.8 million (63.0%), 22.1 million (72.7%), 9.0 million (68.8%), and 2.7 million (63.1%) in the SEARO/WPRO, AFRO, EMRO/EURO, and AMRO regions, respectively (Table 4). It illustrates that the proportional distribution of pregnancies at risk resulting in live births is slightly different from the distribution of total pregnancies at risk, primarily reflecting the differences in the proportion of pregnancies ending in induced abortions, which is much lower in the AFRO region (11.9%) compared to the global average in the malaria endemic countries of 19.5% [24]. 10.1371/journal.pmed.1000221.g001 Figure 1 Malaria risk map for P. falciparum and corresponding number of pregnancies in each continent in 2007. 10.1371/journal.pmed.1000221.g002 Figure 2 Malaria risk map for P. vivax and corresponding number of pregnancies in each continent in 2007. 10.1371/journal.pmed.1000221.t003 Table 3 Number of pregnancies at risk of P. falciparum and/or P. vivax malaria by WHO regional office in 2007 (in millions) (column %). WHORO Region P. falciparum Transmissiona P. vivax Transmissiona Any Species Stable Transmissionb Unstable Transmissionb Overall Overall Overall AFRO 29.6 (54.1) 0.4 (1.2) 30.0 (35.1) 3.6 (3.9) 30.3 (24.2) EMRO/EURO 4.0 (7.3) 4.2 (13.7) 8.2 (9.6) 10.4 (11.2) 13.1 (10.5) AMRO 1.4 (2.5) 1.6 (5.2) 3.0 (3.5) 2.9 (3.1) 4.3 (3.4) SEARO/WPRO 19.7 (36.1) 24.5 (79.9) 44.2 (51.8) 76.0 (81.8) 77.4 (61.8) Global 54.7 30.6 85.3 92.9 125.2 Similar tables with risk estimates by continent and by pregnancy outcome (live-birth, induced abortions, stillbirths, and miscarriages) are provided in Tables S1, S2, S3. a Includes countries where P. falciparum and P. vivax co-exist. b Stable transmission, ≥1 autochthonous P. falciparum cases per 10,000 people per annum; unstable transmission, <1 autochthonous P. falciparum cases per 10,000 people per annum [15]. MEC, malaria endemic countries; TPR, total pregnancy rate; WHORO, World Health Organization Regional Office. 10.1371/journal.pmed.1000221.t004 Table 4 Number of live-births born to pregnancies at risk of at risk of P. falciparum and/or P. vivax malaria by WHO regional office in 2007 (in millions) (column %). WHORO Region P. falciparum Transmissiona P. vivax Transmissiona Any Species Stable Transmissionb Unstable Transmissionb Overall Overall Overall AFRO 21.6 (56.7) 0.3 (1.3) 21.8 (37.4) 2.5 (4.3) 22.1 (26.7) EMRO/EURO 2.8 (7.3) 2.9 (14.1) 5.6 (9.7) 7.1 (12.0) 9.0 (10.9) AMRO 0.8 (2.2) 1.0 (5.0) 1.8 (3.2) 1.8 (3.1) 2.7 (3.3) SEARO/WPRO 12.9 (33.8) 16.1 (79.5) 28.9 (49.7) 48.0 (80.6) 48.8 (59.1) Global 38.0 20.2 58.2 59.5 82.6 Similar tables with risk estimates by continent and by pregnancy outcome (live-birth, induced abortions, stillbirths, and miscarriages) are provided in Tables S1, S2, S3. a Includes countries where P. falciparum and P. vivax co-exist. b Stable transmission, ≥1 autochthonous P. falciparum cases per 10,000 people per annum; unstable transmission, <1 autochthonous P. falciparum cases per 10,000 people per annum [15]. MEC, malaria endemic countries; TPR, total pregnancy rate; WHORO, World Health Organization Regional Office. P. falciparum Malaria Of the 125.2 million pregnancies defined above, 85.3 million occur in areas with P. falciparum transmission, 51.8% of them (44.2 million) are in the combined SEARO-WPRO regions and 35.1% (30.0 million) in the AFRO region. The remainder live in the EMRO-EURO (9.6%) and AMRO regions (3.5%) (Figure 3; Table 3). As expected, the top five ranked countries with the highest number of pregnancies at risk of P. falciparum malaria were the malaria endemic countries with the largest overall populations: India (28.2 million), Nigeria (6.5 million), Indonesia (4.4 million), Pakistan (3.7 million), and the Democratic Republic of the Congo (3.3 million). Overall, 64.1% of 85.3 million pregnancies at risk of P. falciparum malaria live in areas with assumed stable transmission (Figure 3). However, this varies widely by region; from 98.7% in the AFRO region to none in the EURO region. As depicted in Figure 3, 55.3% of the 44.2 million pregnancies at risk of P. falciparum in the WPRO/SEARO region occur in areas of very low and unstable transmission. 10.1371/journal.pmed.1000221.g003 Figure 3 Distribution of the number of pregnancies in areas with P. falciparum malaria in 2007 by WHO regions and the corresponding proportion living under stable versus unstable transmission. Blue, SEARO and WPRO; green, AFRO; orange, EMRO; red, AMRO. P. vivax Malaria Globally, an estimated 92.9 million pregnancies occurred in areas endemic for P. vivax in 2007 (including in areas where both P. falciparum and P. vivax co-exist) (Figure 2). The top five ranked countries include: India (32.9 million), China (21.2 million), Indonesia (6.3 million), Pakistan (5.8 million), and Bangladesh (4.7 million). In the WPRO/SEARO region, where the majority of the populations at risk of P. vivax live (Figure 4), approximately 98.2% of those pregnancies in malaria endemic countries occur in areas with P. vivax transmission (alone or combined with P. falciparum). By contrast this was only 11.9% for the AFRO region where P. vivax transmission is principally restricted to the horn of Africa region, Madagascar, and the Comoros islands (Figure 4). 10.1371/journal.pmed.1000221.g004 Figure 4 Distribution of the number of pregnancies in malaria endemic areas in 2007 by WHO regions and by species (P. vivax transmission only, P. falciparum transmission only or transmission of both species). Blue, SEARO and WPRO; green, AFRO; orange, EMRO; red, AMRO. Pv, P. vivax; Pf, P. falciparum. The country-specific demographic data and population at risk estimates (Table S1), as well as total pregnancies at risk and by specific pregnancy outcomes (live births, induced abortions, stillbirths, and miscarriages; Table S2) and summary estimates by other regional categories (continents instead of WHO regions; Table S3), are provided as supplemental information. In addition, information is provided illustrating which countries are included in the different WHO regions (also see Figure S1) [29]. In brief, all malaria endemic countries on the African continent fall under the Africa Regional Office (AFRO), with the exception of Djibouti, Somalia, and Sudan, which fall under the EMRO office. Discussion This is the first time, to our knowledge, that contemporary species-specific estimates of the annual number of pregnancies at risk of malaria globally have been made. Our findings suggest that in 2007 approximately 125 million pregnancies occurred in areas with P. falciparum and/or P. vivax transmission, resulting in 83 million live births; representing approximately 60% of all pregnancies globally. Approximately 85 million pregnancies occurred in areas with P. falciparum transmission and 93 million in areas with transmission of P. vivax transmission, of which about 53 million occurred in areas where both species co-exist. The pregnancies at risk estimates for P. falciparum and P. vivax in Africa (32 million [30 million in the WHO-AFRO region]) are consistent with the previous estimates by WHO (25–30 million). By contrast, the numbers at risk outside Africa are much higher (95 million) than previously estimated (25 million). Comparisons between the estimates produced in this study and the previous WHO estimates are made difficult because details of the methodology used by the WHO is not provided and it is not clear if they included all transmission areas or only areas with stable malaria transmission. Inclusion of only those areas with stable P. falciparum transmission in our study resulted in global risk estimates of just less than 55 million pregnancies, 31 million in Africa and 23 million in the other regions, i.e., very similar to the previous WHO estimates. However, the numbers of pregnancies at risk outside Africa increase almost 4-fold if areas with unstable P. falciparum transmission are included (clinical incidence <1 per 10,000 population/year) (30 million) and areas situated in the temperate regions outside the limits of P. falciparum transmission that have P. vivax transmission only (40 million) are also included. It is also not clear if the previous WHO estimates included pregnancies resulting in live births only or included adjustments for induced abortions or spontaneous pregnancy loss. Since only approximately two-thirds of all pregnancies result in live births, estimates that include all pregnancies are about one-third higher than estimates based on live births only. Although risk estimates are widely quoted figures, it is important to place them in perspective. The estimates provided here merely define the global distribution of pregnancies that occur within the global spatial limits of malaria transmission. These estimates therefore represent “any risk” of exposure to malaria during pregnancy, and do not represent the distribution of actual incidence or health burden on mothers and unborn babies, which is beyond the scope of this paper. More than half (71 million) of the 125 million pregnancies occur in areas with unstable P. falciparum transmission (31 million) or with transmission of P. vivax only (40 million), and the risk of acquiring malaria in these areas is extremely low. Thus, although these 71 million pregnancies represent more than 50% of the global number of pregnancies at risk, they may only contribute a small proportion to the number of infections in pregnancy. For example, if the actual incidence of malaria infection in these very low transmission areas is 1 in 10,000 per person-year (52 wk), and if the average pregnancy resulting in a live birth takes 38 wk from fertilisation to term, then 71 million pregnancies at risk may result in only 5,188 actual malaria infections, whereas in areas with infection rates of 1.36 or higher per person-year, all term pregnancies have been potentially exposed to malaria. Furthermore, the definition of stable transmission for P. falciparum used included all areas with more than one clinical case per 10,000 population per year. This included almost all pregnancies at risk in the AFRO Region (99% of the 30 million pregnancies at risk) and 25 million of the 95 million (26%) pregnancies in the other WHO regions. However, these stable transmission strata cover a very wide range of transmission intensities and the actual risk of infection to the 55 million individuals and the impact on maternal and infant health varies enormously within this range. At the higher end of the transmission spectrum, the majority of malaria infections in pregnancy remain asymptomatic or pauci-symptomatic, yet are a major cause of severe maternal anaemia and preventable low birth weight, especially in the first and second pregnancies. In areas with stable, but low transmission, and certainly in areas with unstable and exceptionally low transmission, infections can become severe in all gravidae groups because most women of childbearing age in these regions have low levels of pre-pregnancy and pregnancy-specific protective immunity to malaria [30]. The most recent version of the World Malaria Map [28] from the Malaria Atlas Project shows that 89% of the populations in stable P. falciparum areas outside Africa live in areas characterised by low malaria endemicity (defined as P. falciparum parasite rate in children 2–10 y of age of ≤5%). This total includes all of the stable P. falciparum transmission areas in the Americas, and 88% of the populations at risk in the Central and South-East Asia-Pacific region [31]. Our estimates do not take seasonality into account and include all pregnancies occurring throughout the year, whereas those pregnancies that occur outside of the transmission season may be at no risk, or very low risk of exposure. Our risk estimates for P. vivax are likely to be less accurate than those for P. falciparum because of greater uncertainties about the basic biology of transmission and clinical epidemiology. For example, the climatic constraints on P. vivax transmission are less well defined, the accuracy of clinical reporting of P. vivax in areas with coincidental P. falciparum is poor, and the untreated hypnozoite stage of P. vivax, which can remain dormant in infected liver cells for months or years, provides an additional challenge to the interpretation of prevalence and incidence data [15]. We used a refined P. vivax risk map that resulted in a 19% increase over previous population at risk estimates (adjusted for population growth) [18],[19], principally resulting from the removal of the population density masks and thereby the inclusion of many large cities. In most of these cities, pregnancies will be at low or very low risk of autochthonous infections. Imported malaria associated with travel to rural areas may be a greater risk factor in these cities. We did not consider infections with P. ovale or P. malariae, as their distribution is not well described and the adverse effects on maternal health and the newborn infant are unknown. In the current analysis we used the map of the global spatial limits of P. falciparum malaria, which stratifies the malaria endemic world by stable and unstable transmission published in 2008 [15].This map uses a simple divide between very low risk and higher transmission intensities and a crude proxy to account for the corresponding levels of acquired immunity in women of childbearing age. As a next step, we will examine the burden of malaria in pregnancy in terms of health impact on the pregnant women (e.g., febrile episodes, impact on maternal anaemia and maternal mortality), the newborn baby (e.g., impact on the frequency of preterm births and low birth-weight) and the infant (e.g., susceptibility to malaria). For this project, we will use the more refined P. falciparum transmission intensity model of risk within the defined stable limits which was developed recently by the Malaria Atlas Project [31], allowing disease impact calculations across multiple transmission strata to be made. It is also important to take the different pregnancy outcomes into account in these further burden estimates. Of the 125 million pregnancies, one in five are estimated to be terminated voluntarily during the period of risk for miscarriage, and only about two-thirds (82.6 millions) are expected to result in live births. Although malaria in pregnancy is associated with miscarriages and stillbirths [30], the majority of the health and economic burden is likely through the impact on pregnancies that result in live births by increasing the risk of preterm births and low birth-weight [30] and by modifying the susceptibility to malaria in the infant [32]–[34]. Most of the existing research and policy guidance for malaria control in pregnancy has focussed on P. falciparum in the stable transmission regions of sub-Saharan Africa. The results of this study are consistent with the previous WHO-RBM risk estimates for areas with stable P. falciparum malaria in Africa, but our work offers advancement on the existing risk estimates for malaria endemic countries outside Africa. In these regions, the burden of malaria in pregnancy is less well defined, both in terms of the number of pregnancies and its actual impact on health. Policy guidelines for malaria control in pregnancy are also less well developed for these regions. These estimates of the number of pregnancies at risk of malaria provide a first step towards a spatial map of the burden of malaria in pregnancy and a more informed platform with which to estimate the associated disease and economic impact and its geographical distribution. Such global estimates provide guidance in terms of priority setting for resource allocation for both research and policy for the control of malaria in pregnancy. This project provides a dynamic framework that allows risk estimates to be updated when new risk maps of P. falciparum and P. vivax become available as the world attempts to move towards malaria elimination and eradication. Supporting Information Figure S1 Map of the WHO Regions (http://www.who.int/about/regions/en/index.html). (1.07 MB TIF) Click here for additional data file. Table S1 Demographic characteristics and total population at risk of P. falciparum and/or P. vivax malaria by malaria endemic country and by WHO regional office in 2007 (in millions). (0.38 MB PDF) Click here for additional data file. Table S2 Total number of pregnancies by pregnancy outcome in areas with P. falciparum and/or P. vivax transmission by continent in 2007 (in millions). (0.54 MB PDF) Click here for additional data file. Table S3 Total population, number of pregnancies, and number of live-births born to pregnancies in malaria endemic countries by continent in 2007 (in millions). (0.28 MB PDF) Click here for additional data file.
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The burden of malaria in pregnancy in malaria-endemic areas
BL Nahlen, C. Menendez, RW Steketee … (2001)
Pregnant women in malarious areas may experience a variety of adverse consequences from malaria infection including maternal anemia, placental accumulation of parasites, low birth weight (LBW) from prematurity and intrauterine growth retardation (IUGR), fetal parasite exposure and congenital infection, and infant mortality (IM) linked to preterm-LBW and IUGR-LBW. We reviewed studies between 1985 and 2000 and summarized the malaria population attributable risk (PAR) that accounts for both the prevalence of the risk factors in the population and the magnitude of the associated risk for anemia, LBW, and IM. Consequences from anemia and human immunodeficiency virus infection in these studies were also considered. Population attributable risks were substantial: malaria was associated with anemia (PAR range = 3-15%), LBW (8-14%), preterm-LBW (8-36%), IUGR-LBW (13-70%), and IM (3-8%). Human immunodeficiency virus was associated with anemia (PAR range = 12-14%), LBW (11-38%), and direct transmission in 20-40% of newborns, with direct mortality consequences. Maternal anemia was associated with LBW (PAR range = 7-18%), and fetal anemia was associated with increased IM (PAR not available). We estimate that each year 75,000 to 200,000 infant deaths are associated with malaria infection in pregnancy. The failure to apply known effective antimalarial interventions through antenatal programs continues to contribute substantially to infant deaths globally.
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Insecticide-Treated Nets for the Prevention of Malaria in Pregnancy: A Systematic Review of Randomised Controlled Trials
Carol Gamble, Paul J Ekwaru, Paul Garner … (2007)
Introduction Approximately 50 million pregnant women are exposed to malaria each year. Pregnant women are more susceptible to malaria, placing both mother and fetus at risk of the adverse consequences [1–3]. In areas of low and unstable transmission, such as in many regions in Asia and the Americas, women do not acquire substantial antimalarial immunity, and are susceptible to episodes of acute and sometimes severe malaria, and fetal and maternal death [4]. In areas with stable malaria transmission, such as in most of sub-Saharan Africa, infection with Plasmodium falciparum in pregnancy is characterised by predominantly low-grade, sometimes sub-patent, persistent or recurrent parasitaemia. These infections frequently do not result in acute symptoms yet are a substantial cause of severe maternal anaemia [5] and of low birth weight (LBW) [3], and as such are a potential indirect cause of early infant mortality [6–8]. Because most of these infections remain asymptomatic, and therefore undetected and untreated, prevention of malaria in pregnancy is especially important in these settings. The World Health Organization (WHO) advocates a three-pronged approach to malaria control in pregnancy that includes the use of insecticide-treated bednets (ITNs), intermittent preventive treatment (IPT), and case management (treatment) [9]. In areas of stable malaria transmission in sub-Saharan Africa, ITNs are highly effective in reducing childhood mortality and morbidity from malaria [10]. Although ITNs are promoted as a major tool in the fight against malaria in pregnancy, the available evidence about their efficacy in pregnancy has been inconsistent. In this review, we summarise the available data from randomised controlled trials that compared the effects of ITNs to no nets, or to untreated nets, on the health of pregnant women and birth outcome. Methods A protocol was developed for this review [11], and the standard search strategy of the Cochrane Infectious Diseases Group was used to identify potentially relevant trials [12]. The inclusion criteria were all trials that randomised individuals (pregnant women) or clusters (community or antenatal clinics) in areas where malaria transmission occurs. Where cluster-randomised trials were identified, the methods of analysis were checked to ensure that the precision of the data extracted from the reports was correctly estimated. The authors needed to have adjusted for clustering, as ignoring the clustering provides the correct point estimate of the magnitude of the trial effect but may overestimate the precision, resulting in potentially incorrect conclusions [13]. Primary outcomes selected were mean haemoglobin and anaemia, and mean birthweight and LBW; secondary outcomes included peripheral malaria in the mother assessed by finger prick during pregnancy or at birth, placental malaria assessed by microscopy, clinical malaria, pre-term birth, fetal loss (defined as miscarriage or stillbirth), and maternal death. Trial quality was assessed as adequate, inadequate, or unclear based on the methods used to generate the allocation sequence and allocation concealment [14]. Minimisation of loss to follow-up was considered adequate (≥90% of the participants randomised included in the analysis), inadequate ( 50% representing moderate heterogeneity) [17]. To minimise the anticipated heterogeneity, no attempt was made to combine trials that compared ITNs to no nets and those that compared ITNs to untreated nets [10]. Because all the included studies from Africa compared ITNs to no nets, and the one study comparing ITNs to untreated net was conducted in Thailand, this also resulted in stratification by the major malaria transmission regions (Africa versus non-Africa), which differ in transmission intensity, parasite species, predominant vector, and vector behaviour. The effect of ITNs was expected to be greatest in the first few pregnancies because women develop pregnancy-specific immunity against placental parasites over successive pregnancies as a consequence of repeated exposure [18]. Because gravidity was considered the greatest potential modifier of the effect of ITNs, analyses were stratified a priori by gravidity groups whenever this was possible based on the details provided. Other potential sources of effect modifications that were explored included concomitant use of IPT in pregnancy (IPTp), and differences between trials that used individual randomisation, in which women benefit primarily from personal protection by treated nets, and trials that used cluster randomisation. In the latter trials, ITNs were distributed to whole communities, which may result in a mass or community effect due to area-wide killing of the malaria-transmitting mosquitoes [19–21]. Women in the cluster-randomised trials were mostly provided with ITNs prior to becoming pregnant and were thus protected throughout pregnancy. In the individually randomised trials, nets were provided as part of antenatal care, i.e., typically from 20 to 24 wk onwards. We could not explore other potential sources of heterogeneity because the number of trials identified was too few. Results Description of Trials Six trials were identified; we excluded one trial as the analysis had not adjusted for clustering, and loss to follow-up was high (Text S1) [22]. Of the five included trials (Table 1), two were individually randomised [23,24], and three were cluster-randomised with analysis that took design effects into account [25–27]. Four trials were conducted in stable malaria-endemic areas in Africa (three in Kenya [24,26,27] and one in northern Ghana [25]), all with entomological inoculation rate (EIR) > 1/y, and one in Karen refugee camps along the Thailand–Myanmar border in an area with low and markedly seasonal malaria where P. falciparum and P. vivax coexist (EIR 0.5/y) [23]. The African trials compared ITNs to no nets; 6,418 women were enrolled [24–27]. The remaining trial from Thailand randomised individual women to receive either ITNs, untreated nets, or no nets [23]. In the “no nets” arm, a large proportion of women received nets from another donor independent of the study, and the researchers split the results in this control arm into women using donor nets and women not using donor nets. Because this compromised the validity of the control arm, we included only the comparison of ITNs with untreated nets (n = 223). All African trials gave double- or family-sized nets to each household. The nets used in Thailand were smaller single-sized nets (70 × 180 × 150 cm). All trials used the widely available insecticide permethrin (500 g/m2), except one trial that used cyfluthrin [24]. One trial included IPTp-SP in a factorial design [24]. Women were allocated to receive (1) ITNs plus IPTp-SP, (2) IPTp-SP alone, (3) ITNs plus IPTp-SP placebo, or (4) IPTp-SP placebo alone (“control”). None of the other trials included IPT. In the four trials from Africa, only women having their first baby were included in one trial [26], women having their first or second baby in another [24], and women of all gravidity in the remaining two trials (Table 1) [25,27]. In the trials including pregnant women of all gravidity, the authors analysed them differently: ter Kuile et al. grouped by gravidity 1 to 4 (G1–G4) and gravidity 5 and above (G5+) [27]. Browne et al. grouped by first pregnancy (G1), second pregnancy (G2), and third pregnancy and above (G3+) for continuous endpoints [25]. To allow for sub-group analysis by gravidity group, we grouped the G3+ group from Browne et al. and the G5+ group from ter Kuile et al. into one sub-group, referred to as “high gravidity”, and the G1 from Shulman et al., the G1 and G2 groups from Browne et al. and the G1–G4 group from ter Kuile et al. into another sub-group, referred to as “low gravidity” [25–27]. The study by Browne et al. also provided sub-group analyses for dichotomous endpoints, but unlike in the analysis for continuous endpoints they were not adjusted for cluster randomisation [25].The study by Dolan et al. in Asia did not provide estimates by gravidity group, with the exception of the effect on birth weight [23]. Treated Nets versus No Nets (Four Trials in Africa) Primary outcomes. All four trials reported the effect of ITNs on haemoglobin (Hb) levels and anaemia. Because of the variations in trial design and reporting, it was not possible to combine the results from all four trials for anaemia (Hb < 100 or 110 g/l) and severe anaemia (Hb < 70 or 80 g/l) [28]. The results for mean haemoglobin are provided by the time of assessment (third trimester or delivery) and by gravidity group (Figure 1). There was no evidence for improved haemoglobin levels in women having their first or second babies in the two trials that assessed haemoglobin levels in the third trimester [25,26]. The overall (i.e., all gravidae) summary odds ratio (OR) for any anaemia in the third trimester was 0.88 (95% confidence interval [CI] 0.71–1.10, p = 0.26, one trial) and for severe anaemia was 0.77 (0.56–1.08, p = 0.13, two trials). Insufficient details were reported to provide sub-group analysis by gravidity group. There was significant heterogeneity of treatment effect between the two other trials and sub-groups that assessed haemoglobin levels at delivery, with no evidence for a consistent effect overall (Figure 1) [24,27]. Mean haemoglobin levels were significantly higher in G1–G4 in the trial by ter Kuile et al., who also reported a significant delay in the time to the first episode of any anaemia (Hb < 110 g/l) in G1–G4 (hazard ratio [HR] 0.79, 95% CI 0.65–0.96, p = 0.02), but not in G5+ (HR 1.00, 0.86–1.18, p = 0.97) [27]. Njagi et al. did not find a significant increase in the mean haemoglobin levels of primi- and secundigravidae (Figure 1) or a significant overall reduction in any anaemia, although sub-group analysis by gravidity showed that a significant reduction in any anaemia was found in primigravidae and not secundigravidae (not shown) [29]. All four trials comparing nets to no nets reported on mean birth weight (Table 2; Figure 2). The average birth weight was 55 g higher in the ITN group in women of low gravidity, but no difference was detected in women of higher gravidity groups. For LBW, two trials contributed (Table 2), indicating women of low gravidity had a 23% reduction in LBW, but there was no apparent effect in women of high gravidity in the one trial measuring this [27]. There was also no evidence for an effect in women receiving IPTp with sulfadoxine-pyrimethamine (IPTp-SP) (one trial) (Figure 2). Browne reported the overall OR adjusted for clustering for all gravidity as 0.87 (95% CI 0.63–1.19); as no information was provided by gravidity group, and because LBW was a common event in this trial, the OR could not be pooled with the relative risk (RR) estimates from the other trials. Secondary outcomes. All four RCTs reported on malaria parasitaemia. One trial tested women every month and showed time to first infection in the ITN group was reduced (HR 0.67, 95% CI 0.52–0.86, p = 0.002) [27]. The prevalence of parasitaemia was less common in the ITN groups when assessed in the third trimester (OR 0.88, 073–1.06, p = 0.19, two trials) [25,26] or at the time of delivery (RR 0.76, 0.67–0.86, p < 0.001, two trials) [24,27]. Placental malaria parasitaemia was lower with ITNs by 23% (95% CI 10–34, three trials; Table 2). There was no evidence for an effect on the prevalence of peripheral or placental malaria in women who were provided IPTp-SP (one trial, Figure 3) [24]. Geometric mean parasite densities in peripheral blood tended to be lower in the ITN groups in women having their first or second baby, although the result was not statistically significant (geometric mean ratio 0.82, 95% CI 0.66–1.02, p = 0.07, two trials) [24,25]. There was no evidence for a beneficial effect in G3+ in the trial by Browne et al. (geometric mean ratio 1.28, 0.90–1.82, p = 0.17). Ter Kuile reported that maternal and placental parasite densities were identical in parasitaemic women from ITN and control villages, but insufficient details were provided for inclusion in this analysis [27]. Clinical malaria was reported in two trials, and episodes were less frequent in the ITN than in the control groups in both trials, but this was not significant. Shulman et al. reported on self-reported illness with parasitaemia (OR 0.85, 95% CI 0.47–1.54) [26], and ter Kuile et al. reported on any documented parasitaemia with documented fever based on monthly assessments in G1–G4 (HR 0.72, 95% CI 0.19–2.78) [27]. No effect was demonstrated in the one trial measuring pre-term delivery (<37 wk of gestation) [27] (Table 2). The three trials reporting on fetal loss (miscarriage or stillbirth) showed a consistent reduction in fetal loss associated with ITNs in low gravidity women (33%, 95% CI 3–53, p = 0.03; Figure 4; Table 2). Browne et al. [25] did not provide a breakdown by intervention group. Maternal death was reported by Njagi [24] (five deaths), with no trends evident by group; Shulman et al. [26] reported four deaths but did not specify the groups. ITNs versus Untreated Nets (One Trial from Thailand) This trial was conducted on the Thailand–Myanmar border, with individual randomisation [23]. Fewer women experienced peripheral malaria parasitaemia in the ITN group, but this was not significant (RR 0.73, 95% CI 0.47–1.04); however, in women infected with malaria, the geometric mean parasite density was lower in the ITN group (507 versus 1,096, p = 0.049), and anaemia (hematocrit < 30%) was less frequent with ITNs (RR 0.63, 95% CI 0.42–0.93). Mean birth weight was similar between the two groups (ITN group, 2,858 g, standard deviation 486, n = 94, versus untreated net group, 2,891 g, standard deviation 481, n = 85), as was LBW (RR 1.04, 95% CI 0.52–2.07) and pre-term delivery (RR 0.92, 95% CI 0.45–1.88). Fetal loss was significantly lower in the ITN group (2/102, 2%) than the untreated net group (10/97, 10%) (RR 0.21, 95% CI 0.05–0.92). The number of maternal deaths was similar (ITN group, 0/103, versus untreated net group, 2/100). Discussion This systematic review shows that ITNs were associated with some important health benefits for pregnant women and their babies. Women of low gravidity randomised to ITNs delivered fewer LBW babies and were less likely to experience fetal loss (miscarriage or stillbirth). Although the latter was not a primary endpoint in the trials, it is an important outcome. No significant decrease was observed in pre-term deliveries in the single trial that assessed this outcome. The consistent reduction observed in the miscarriage and stillbirth rates suggests that the attributable effect of malaria on fetal loss may be underestimated in malaria-endemic Africa, where most women remain asymptomatic when infected with P. falciparum. Despite the reduction in malaria infections, no overall effect on mean haemoglobin was demonstrated, and data on maternal anaemia were inconsistent. WHO currently recommends that women in malaria-endemic areas of Africa use both IPTp-SP and ITNs in pregnancy to prevent malaria. One of the two trials from western Kenya assessed the effect of ITNs and IPTp-SP simultaneously, using a factorial design. This trial showed that ITNs provided benefits in primigravidae when used alone, but it did not demonstrate additional benefits of the combined interventions over either of the single interventions [24,29]. The main benefit of ITNs in women protected by IPTp-SP may thus occur after birth through protection of infants from malaria, since infants typically share sleeping space with the mother for the first several months to years [30]. Similar considerations apply to the benefit of ITNs in grand-multigravidae (G5+), as no direct beneficial effect on the developing fetus in terms of birth weight or fetal loss was apparent in this group. The only trial included in this analysis that compared ITNs to untreated nets was also the only trial conducted outside of Africa, in an area with highly seasonal P. falciparum and P. vivax malaria on the Thailand–Myanmar border. It showed a statistically significant reduction in anaemia and fetal loss in all gravidae, but no evidence for a beneficial effect on birth weight or gestational age [23]. Extrapolation of results from the three cluster-randomised trials to predict the potential impact of programmes that distribute ITNs to individual pregnant women as part of antenatal care should be done with caution. Firstly, nets distributed as part of antenatal care will leave most women exposed to malaria in the first third or half of pregnancy, when the risk of peripheral malaria parasitaemia is greatest [3]. By contrast, most women in the cluster-randomised trials became pregnant after ITNs were distributed and were as such protected throughout pregnancy. Secondly, the effect of ITNs in the cluster-randomised trials reflects the combined effects of personal protection (individual barrier protection) and area-wide reductions in malaria transmission (community or mass effect) [19–21]. It is possible that the mass killing effect on mosquito populations in areas with a high ITN coverage will result in stronger treatment effects of ITNs than can be achieved with individual nets. It is also likely that the community effect in the cluster-randomised trials resulted in a slight underestimation of the magnitude of the effect of ITNs because women living in control households from adjacent villages not using ITNs will have benefited from the area-wide reductions in vector populations, as has been shown for effect estimates in young children [19]. Similar considerations apply to the trial comparing ITNs with untreated nets from the Thailand–Myanmar border [23]. Although, this trial randomised individual women, all trial participants lived in the same densely populated refugee camps and some mass effect by the treated nets cannot be excluded. The most recent trial from western Kenya by Njagi et al. is informative in this respect, as it is the only trial that compared the effects of ITNs versus no nets using simple randomisation by individual in an area with low ITN coverage (little or no mass effect) [24,29]. This trial and the community-randomised trial by ter Kuile et al. [27] were conducted simultaneously in contiguous areas with similar malaria transmission at baseline, and similar socioeconomic and educational status and ethnicity of the trial population. The effect estimates were similar between the two trials (in women not randomised to IPTp-SP), suggesting that ITNs may work equally well when provided to individuals as part of antenatal care in the second trimester or when provided to entire communities. The systematic review was informative, but there were some limitations stemming from the variety in trial designs and the number of trials. Outcome data were often expressed in different ways, and inclusion or analysis of gravidity groups was different. How anaemia and peripheral parasitaemia were detected and treated varied, with different periods of follow-up and different cut-offs, limiting our ability to provide summary estimates for some of the endpoints, or to provide sub-group analysis by gravidity group where desired. Shulman et al. and Njagi et al. tested and treated women only if they were suspected of being anaemic or of having malaria, but Dolan et al. performed weekly blood tests, and ter Kuile et al. tested monthly. The number of studies included in the analysis was limited. All four African studies were conducted in areas with stable malaria transmission with EIRs ranging from 10/y to 300/y. Three of the four were conducted in Kenya, and two of these in adjacent areas with similarly intense perennial transmission. These two studies had the greatest influence (expressed as the weight in the figures) on the overall results of the systematic review, particularly for the effect on placental malaria because in the trial by Shulman et al. [26] data were available for only 25.8% of women (those that delivered in the hospital). It is plausible that the 25.8% were different to those delivering at home and may not be representative of all those randomised. This may also explain some of the observed heterogeneity of the effect of ITNs on placental malaria. Although relatively few trials have been conducted and some questions on the efficacy of ITNs in pregnant women in Africa remain, the four trials comparing ITNs with no nets suggest significant beneficial effects of ITNs on birth weight and fetal loss in the first few pregnancies in areas with moderate to intense malaria transmission in sub-Saharan Africa. These findings are consistent with a non-randomised trial of the effect of socially marketed ITNs conducted in an area with intense perennial malaria transmission in southern Tanzania [31], and with an excluded randomised controlled trial from The Gambia, which has lower and highly seasonal transmission [22]. These observed beneficial effects of ITNs during the first few pregnancies, together with the absence of apparent harm to the developing fetus, the potential beneficial effect on the infant when the net continues to be used after birth [10], and the potential for ITNs to reduce malaria transmission through a mass killing effect on mosquito populations, support the current recommendations from WHO to provide ITNs for pregnant women in all regions with stable malaria transmission throughout sub-Saharan Africa, regardless of the degree of malaria transmission intensity. Further evaluation of the potential effect of ITNs on pregnant women and their infants is warranted in malaria regions including the Americas, Asia, and the southwest Pacific, which represent approximately half of all pregnant women exposed annually to malaria. The more complex vector populations with exophagic, exophilic, and early biting behaviour in some of these areas may result in lower efficacy of ITNs than in Africa, where Anopheles gambiae s.s. is the most important vector. These studies should include women of all gravidae, and ideally address the interaction between ITNs and drug-based prevention such as IPTp, which is also largely untested outside of Africa. In Africa, it took over a decade for the evidence of ITN or IPTp efficacy in pregnant women to accumulate. It would be more efficient if trials had a common design, and if systematic reviews used individual patient data to allow appropriate collection of design effects, more accurate and standardised handling of the data, and more robust sub-group analysis. In order to enhance the rate at which evidence becomes available and is translated into policy, future trials would clearly benefit from better co-ordination between research groups. Supporting Information Text S1 QUOROM Flowchart Screened, excluded, and included number of randomised controlled trials. (24 KB PPT) Click here for additional data file.
Author and article information
Contributors
Ramesh Kumar:
ORCID: http://orcid.org/0000-0002-9701-3179
drramesh1978@gmail.com
Ratana Somrongthong: sratana3@chula.ac.th
Journal
Journal ID (nlm-ta): Malar J
Journal ID (iso-abbrev): Malar. J
Title:
Malaria Journal
Publisher:
BioMed Central
(London
)
ISSN
(Electronic):
1475-2875
Publication date
(Electronic):
29
June
2020
Publication date PMC-release: 29
June
2020
Publication date Collection: 2020
Volume: 19
Electronic Location Identifier: 232
Affiliations
[1
]GRID grid.490694.6, Health Services Academy, , Ministry of National Health Services Regulation & Coordination, Government of Pakistan,
; Islamabad, Pakistan
Author information
Ramesh Kumar
http://orcid.org/0000-0002-9701-3179
Article
Publisher ID: 3298DOI: 10.1186/s12936-020-03298-2
PMC ID: 7325083
PubMed ID: 32600347
SO-VID: 8f39ae40-74d3-445e-b9d7-5658385e5006
Copyright © © The Author(s) 2020
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History
Date
received
: 1
December
2019
Date
accepted
: 17
June
2020
Categories
Subject:
Research
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issue-copyright-statement © The Author(s) 2020
ScienceOpen disciplines: Infectious disease & Microbiology
Data availability:
ScienceOpen disciplines: Infectious disease & Microbiology