Showing papers on "Malaria published in 2001"
TL;DR: It is speculated about the mechanisms that could cause malaria to have such a large impact on the economy, such as foreign investment and economic networks within the country, and a second independent measure of malaria has a slightly higher correlation with economic growth in the 1980-1996 period.
Abstract: Malaria and poverty are intimately connected. Controlling for factors such as tropical location, colonial history, and geographical isolation, countries with intensive malaria had income levels in 1995 of only 33% that of countries without malaria, whether or not the countries were in Africa. The high levels of malaria in poor countries are not mainly a consequence of poverty. Malaria is geographically specific. The ecological conditions that support the more efficient malaria mosquito vectors primarily determine the distribution and intensity of the disease. Intensive efforts to eliminate malaria in the most severely affected tropical countries have been largely ineffective. Countries that have eliminated malaria in the past half century have all been either subtropical or islands. These countries' economic growth in the 5 years after eliminating malaria has usually been substantially higher than growth in the neighboring countries. Cross-country regressions for the 1965-1990 period confirm the relationship between malaria and economic growth. Taking into account initial poverty, economic policy, tropical location, and life expectancy, among other factors, countries with intensive malaria grew 1.3% less per person per year, and a 10% reduction in malaria was associated with 0.3% higher growth. Controlling for many other tropical diseases does not change the correlation of malaria with economic growth, and these diseases are not themselves significantly negatively correlated with economic growth. A second independent measure of malaria has a slightly higher correlation with economic growth in the 1980-1996 period. We speculate about the mechanisms that could cause malaria to have such a large impact on the economy, such as foreign investment and economic networks within the country.
1,576 citations
TL;DR: It is estimated that each year 75,000 to 200,000 infant deaths are associated with malaria infection in pregnancy and the failure to apply known effective antimalarial interventions through antenatal programs continues to contribute substantially to infant deaths globally.
Abstract: 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.
1,078 citations
TL;DR: To decrease and stop transmission of this intolerable scourge, there is an urgent need for malaria vaccines, newer drugs, and better vector control methods as well as the ability to improve current technologies and use them more efficiently.
Abstract: Malarious patients experience asymptomatic parasitemia; acute febrile illness (with cerebral damage, anemia, respiratory distress, hypoglycemia); chronic debilitation (anemia, malnutrition, nervous system-related sequelae); and complications of pregnancy (anemia, low birth weight, increased infant mortality). These manifestations in patients, communities, and countries reflect intrinsic (human, parasite, mosquito) and extrinsic (environmental, social, behavioral, political, and economic conditions as well as disease-control efforts) determinants. At a minimum, between 700,000 and 2.7 million persons die yearly from malaria, over 75% of them African children. Between 400 and 900 million acute febrile episodes occur yearly in African children under 5 yr of age living in endemic areas. Although about half of these children are parasitemic, all merit consideration of malaria-specific therapy, which is becoming more problematic because of parasite resistance to drugs. These numbers will more than double over the next 20 yr without effective control. Fewer than 20% of these febrile episodes and deaths come to the attention of any formal health system. The relatively few ill patients who have any contact with the health services represent the "ears of the hippopotamus." Greatly intensified research activities and control of the intolerable burden of malaria are mandatory if economic development is to accelerate in Africa. In particular, support should be targeted to understanding and preventing malaria-induced anemia, hypoglycemia, effects on pregnancy, and neurologic and developmental impairment. To decrease and stop transmission of this intolerable scourge, there is an urgent need for malaria vaccines, newer drugs, and better vector control methods as well as the ability to improve current technologies and use them more efficiently.
1,025 citations
TL;DR: Feature of the transmission biology of P. vivax give this species greater resilience than the less robust Plasmodiumfalciparum in the face of conditions adverse to the transmission of the parasites, therefore, as control measures become more effective, the residual malaria burden is likely increasingly to become that of Pivax.
Abstract: We estimate that the global burden of malaria due to Plasmodium vivax is approximately 70-80 million cases annually. Probably approximately 10-20% of the world's cases of P. vivax infection occur in Africa, south of the Sahara. In eastern and southern Africa, P. vivax represents around 10% of malaria cases but 50% of all malaria cases. About 80-90% of P. vivax outside of Africa occurs in the Middle East, Asia, and the Western Pacific, mainly in the most tropical regions, and 10-15% in Central and South America. Because malaria transmission rates are low in most regions where P. vivax is prevalent, the human populations affected achieve little immunity to this parasite; as a result, in these regions, P. vivax infections affect people of all ages. Although the effects of repeated attacks of P. vivax through childhood and adult life are only rarely directly lethal, they can have major deleterious effects on personal well-being, growth, and development, and on the economic performance at the individual, family, community, and national levels. Features of the transmission biology of P. vivax give this species greater resilience than the less robust Plasmodiumfalciparum in the face of conditions adverse to the transmission of the parasites. Therefore, as control measures become more effective, the residual malaria burden is likely increasingly to become that of P. vivax.
1,018 citations
TL;DR: This study shows an association between the pfcrt T76 mutation in P. falciparum and the development of chloroquine resistance during the treatment of malaria, and this mutation can be used as a marker in surveillance forchloroquine-resistant falcIParum malaria.
Abstract: Background Chloroquine-resistant Plasmodium falciparum malaria is a major health problem, particularly in sub-Saharan Africa. Chloroquine resistance has been associated in vitro with point mutations in two genes, pfcrt and pfmdr 1, which encode the P. falciparum digestive-vacuole transmembrane proteins PfCRT and Pgh1, respectively. Methods To assess the value of these mutations as markers for clinical chloroquine resistance, we measured the association between the mutations and the response to chloroquine treatment in patients with uncomplicated falciparum malaria in Mali. The frequencies of the mutations in patients before and after treatment were compared for evidence of selection of resistance factors as a result of exposure to chloroquine. Results The pfcrt mutation resulting in the substitution of threonine (T76) for lysine at position 76 was present in all 60 samples from patients with chloroquine-resistant infections (those that persisted or recurred after treatment), as compared with a base-line p...
904 citations
TL;DR: Recent field studies suggest chloroquine resistance arose in > or = 4 distinct geographic foci and substantiate an important role of immunity in the outcomes of resistant infections after chlorquine treatment.
Abstract: The development of chloroquine as an antimalarial drug and the subsequent evolution of drug-resistant Plasmodium strains had major impacts on global public health in the 20th century. In P. falciparum, the cause of the most lethal human malaria, chloroquine resistance is linked to multiple mutations in PfCRT, a protein that likely functions as a transporter in the parasite's digestive vacuole membrane. Rapid diagnostic assays for PfCRT mutations are already employed as surveillance tools for drug resistance. Here, we review recent field studies that support the central role of PfCRT mutations in chloroquine resistance. These studies suggest chloroquine resistance arose in > or = 4 distinct geographic foci and substantiate an important role of immunity in the outcomes of resistant infections after chloroquine treatment. P. vivax, which also causes human malaria, appears to differ from P. falciparum in its mechanism of chloroquine resistance. Investigation of the resistance mechanisms and of the role of immunity in therapeutic outcomes will support new approaches to drugs that can take the place of chloroquine or augment its efficiency.
705 citations
TL;DR: In this paper, the interaction of iron and infection indicates a need for quantitative review of clinical morbidity outcomes and a balance must be struck in dose of oral iron and the timing of intervention with respect to age and malaria transmission.
Abstract: The continuing unresolved debate over the interaction of iron and infection indicates a need for quantitative review of clinical morbidity outcomes. Iron deficiency is associated with reversible abnormalities of immune function, but it is difficult to demonstrate the severity and relevance of these in observational studies. Iron treatment has been associated with acute exacerbations of infection, in particular, malaria. Oral iron has been associated with increased rates of clinical malaria (5 of 9 studies) and increased morbidity from other infectious disease (4 of 8 studies). In most instances, therapeutic doses of oral iron were used. No studies in malarial regions showed benefits. Knowledge of local prevalence of causes of anemia including iron deficiency, seasonal malarial endemicity, protective hemoglobinopathies and age-specific immunity is essential in planning interventions. A balance must be struck in dose of oral iron and the timing of intervention with respect to age and malaria transmission. Antimalarial intervention is important. No studies of oral iron supplementation clearly show deleterious effects in nonmalarious areas. Milk fortification reduced morbidity due to respiratory disease in two very early studies in nonmalarious regions, but this was not confirmed in three later fortification studies, and better morbidity rates could be achieved by breast-feeding alone. One study in a nonmalarious area of Indonesia showed reduced infectious outcome after oral iron supplementation of anemic schoolchildren. No systematic studies report oral iron supplementation and infectious morbidity in breast-fed infants in nonmalarious regions.
643 citations
TL;DR: The main ways to reduce morbidity and mortality are the use of insecticide-impregnated netting around the bed and chemoprophylaxis for specific groups at increased risk, such as nonimmune travelers to an area where malaria is endemic, pregnant women,1 and children with sickle cell anemia.
Abstract: Malaria caused by Plasmodium falciparum, a protozoan parasite of the blood, is responsible for up to 27 million deaths yearly, mainly in children in sub-Saharan Africa Worldwide there are over 300 million new cases of malaria per year Given the lack of a suitable vaccine, the main ways to reduce morbidity and mortality are the use of insecticide-impregnated netting around the bed and chemoprophylaxis for specific groups at increased risk, such as nonimmune travelers to an area where malaria is endemic, pregnant women,1 and children with sickle cell anemia However, in many areas the effectiveness of treatment and of efforts
605 citations
TL;DR: RTS,S/AS02 is safe, immunogenic, and is the first pre-erythrocytic vaccine to show significant protection against natural P. falciparum infection in semi-immune adult men in The Gambia.
552 citations
TL;DR: It is shown that since the late 1980s convincing evidence of a major public health impact of the spread of chloroquine resistance has been available and there is an urgent need to change treatment policies in Africa.
Abstract: Between 1978 and 1988 Plasmodium falciparum resistance to chloroquine has been reported in all countries of tropical Africa. Despite the intensification of resistance during the last 2 decades, chloroquine remains in 2000 the first-line treatment for malaria in most of these countries. Here we review published data on the public health impact of antimalarial drug resistance in Africa. These data show that since the late 1980s convincing evidence of a major public health impact of the spread of chloroquine resistance has been available. Hospital studies in various African countries have documented a 2- or 3-fold increase in malaria deaths and admissions for severe malaria, an increase temporally related to the emergence of chloroquine resistance. Data from sentinel demographic surveillance systems in Senegal indicated that mortality attributable to malaria in children increased by as much as 6-fold among populations where low levels of malaria mortality had been achieved because of efficient health services before the emergence of chloroquine resistance. Increasing incidence of severe malarial anemia also contributed to human immunodeficiency virus dissemination. The dramatic impact of chloroquine resistance on malaria mortality has long been underestimated because only a low proportion of malaria attacks are potentially lethal among persons continuously exposed since birth to high levels of transmission. There is an urgent need to change treatment policies in Africa.
539 citations
TL;DR: The tremendous growth in international travel increases the risk of importation of vector-borne diseases, some of which can be transmitted locally under suitable circumstances at the right time of the year, and it is unlikely that these diseases will cause major epidemics in the United States if the public health infrastructure is maintained and improved.
Abstract: Diseases such as plague, typhus, malaria, yellow fever, and dengue fever, transmitted between humans by blood-feeding arthropods, were once common in the United States. Many of these diseases are no longer present, mainly because of changes in land use, agricultural methods, residential patterns, human behavior, and vector control. However, diseases that may be transmitted to humans from wild birds or mammals (zoonoses) continue to circulate in nature in many parts of the country. Most vector-borne diseases exhibit a distinct seasonal pattern, which clearly suggests that they are weather sensitive. Rainfall, temperature, and other weather variables affect in many ways both the vectors and the pathogens they transmit. For example, high temperatures can increase or reduce survival rate, depending on the vector, its behavior, ecology, and many other factors. Thus, the probability of transmission may or may not be increased by higher temperatures. The tremendous growth in international travel increases the risk of importation of vector-borne diseases, some of which can be transmitted locally under suitable circumstances at the right time of the year. But demographic and sociologic factors also play a critical role in determining disease incidence, and it is unlikely that these diseases will cause major epidemics in the United States if the public health infrastructure is maintained and improved. Key words: dengue fever, encephalitis, global warming, hantavirus, leptospirosis, Lyme disease, malaria, plague, vectorborne diseases. — Environ Health Perspect 109(suppl 2):223‐233 (2001). http://ehpnet1.niehs.nih.gov/docs/2001/suppl-2/223-233gubler/abstract.html
TL;DR: These malaria-induced medical problems constitute major clinical, public health, and research challenges in that they may contribute to more than double the mortality than is generally acknowledged.
Abstract: Evaluations of the African childhood malaria burden do not fully quantify the contributions of cerebral malaria (CM), CM-associated neurological sequelae, malarial anemia, respiratory distress, hypoglycemia, and pregnancy-related complications. We estimated the impact of these malaria manifestations on members of the African population 2% of survivors of CM) 6 months. Severe malarial anemia heavily burdens hospitals with rising admission and CFRs and with treatments that are complicated by limited and sometimes contaminated blood supplies. Severe malarial anemia occurs 1.42-5.66 million times annually and kills 190,000-974,000 (> 13% CFR) children 225,000 (> 18% CFR) additional deaths among African children with malaria. Maternal, placental, or fetal malaria infection during pregnancy adversely affects development and survival of fetuses and newborns through low birth weight (LBW), maternal anemia, and possibly abortion and stillbirth. Between 167,000 and 967,000 cases of malaria-associated LBW occur yearly; malaria-induced LBW kills 62,000-363,000 (> 38% CFR) newborns each year. All the gaps in the burden comprise 0.4-1.7 million deaths annually, > 50% of which are due to severe malarial anemia. These malaria-induced medical problems constitute major clinical, public health, and research challenges in that they may contribute to more than double the mortality than is generally acknowledged.
TL;DR: The history of antigenic variation in malaria is covered and the more recent data are summarized with particular emphasis on Plasmodium falciparum, the etiological agent of the most severe form of human malaria.
Abstract: Many pathogens that either rely on an insect vector to complete their life cycle (e.g., Trypanosoma spp. and Borrelia spp.) or exist in a unique ecological niche where transmission from host to host is sporadic (e.g., Neisseria spp.) have evolved strategies to maintain infection of their mammalian hosts for long periods of time in order to ensure their survival. Because they have to survive in the face of a fully functional immune system, a common feature of many of these organisms is their development of sophisticated strategies for immune evasion. For the above organisms and for malaria parasites of the genus Plasmodium, a common theme is the ability to undergo clonal antigenic variation. In all cases, surface molecules that are important targets of the humoral immune response are encoded in the genome as multicopy, nonallelic gene families. Antigenic variation is accomplished by the successive expression of members of these gene families that show little or no immunological cross-reactivity. In the case of malaria parasites, however, some of the molecules that undergo antigenic variation are also major virulence factors, adding an additional level of complication to the host-parasite interaction. In this review, we cover the history of antigenic variation in malaria and then summarize the more recent data with particular emphasis on Plasmodium falciparum, the etiological agent of the most severe form of human malaria.
TL;DR: The molecular mechanisms of resistance to chloroquine are reviewed, and how to extend the therapeutic life of antifolate drugs is discussed.
01 Jan 2001
TL;DR: There are indications that chloroquine resistance is beginning to appear now also in P. vivax in the Southwest Pacific, indicating the emergence of multiple drug resistance in the malignant tertian parasite, Plasmodium falciparum.
Abstract: Half of the world's population live in regions where malaria is still endemic and about 2 million are killed by the disease every year. There is an exponential increase in the number of non-immune travellers who visit such areas and thousands develop malaria after they return home. The few drugs currently available for the prevention or treatment of malaria are discussed and the history of the emergence of multiple drug resistance in the malignant tertian parasite, Plasmodium falciparum, is traced from its origins in the late 1950s to the present time when it is found in the endemic regions of all continents. These are indications that chloroquine resistance is beginning to appear now also in P. vivax in the Southwest Pacific. The few new drugs under development and the uncertain future that they face are discussed.
TL;DR: P48/45 is shown to be a surface protein of malaria parasites with a demonstrable role in fertilization and only male gamete fertility of p48/ 45- parasites was affected, failing to penetrate otherwise fertile female gametes.
TL;DR: Children aged < 5 years of age were more likely than older children or adults to become anemic, and patients coinfected with P. vivax attenuates the anemia of falciparum malaria, presumably by modifying the severity of the infection.
Abstract: The factors contributing to anemia in falciparum malaria were characterized in 4,007 prospectively studied patients on the western border of Thailand. Of these, 727 patients (18%) presented with anemia (haematocrit 2 days) before admission, and pure Plasmodium falciparum infections rather than mixed P. falciparum and Plasmodium vivax infections. The mean maximum fractional fall in hematocrit after antimalarial treatment was 14.1% of the baseline value (95% confidence interval [CI], 13.6-14.6). This reduction was significantly greater in young children (aged < 5 years) and in patients with a prolonged illness, high parasitemia, or delayed parasite clearance. Loss of parasitized erythrocytes accounted for < 10% of overall red blood cell loss. Hematological recovery was usually complete within 6 weeks, but it was slower in patients who were anemic at admission (adjusted hazards ratio [AHR], 1.9, 95% CI, 1.5-2.3), and those whose infections recrudesced (AHR, 1.2, 95% CI, 1.01-1.5). Half the patients with treatment failure were anemic at 6 weeks compared with 19% of successfully treated patients (relative risk, 2.8, 95% CI, 2.0-3.8). Patients coinfected with P. vivax (16% of the total) were 1.8 (95% CI, 1.2-2.6) times less likely to become anemic and recovered 1.3 (95% CI, 1.0-1.5) times faster than those with P. falciparum only. Anemia is related to drug resistance and treatment failure in uncomplicated malaria. Children aged < 5 years of age were more likely than older children or adults to become anemic. Coinfection with P. vivax attenuates the anemia of falciparum malaria, presumably by modifying the severity of the infection.
TL;DR: For most of sub‐Saharan Africa, where malaria is stable, the introduction of crop irrigation has little impact on malaria transmission, and there is growing evidence that for many sites there is less malaria in irrigated communities than surrounding areas.
Abstract: The high population growth rate of the African continent has led to an increased demand for food and is in danger of outstripping agricultural production. In order to meet this need, many governments have sought ways of improving food production by initiating large-scale irrigation projects, involving reclamation of arid and semi-arid areas for the cultivation of crops. Although crop irrigation promises one solution to alleviating hunger and encourages economic growth, irrigation has often been blamed for aggravating disease in local communities. Malaria is one of the major tropical diseases associated with irrigation schemes, and changes in the transmission pattern of this disease following irrigation development have been a perennial subject of debate. It has often been assumed that high numbers of malaria vector Anopheles mosquitoes (Diptera: Culicidae) resulting from irrigation schemes lead inevitably to increased malaria in local communities. However, recent studies in Africa have revealed a more complex picture. Increased numbers of vectors following irrigation can lead to increased malaria in areas of unstable transmission, where people have little or no immunity to malaria parasites, such as the African highlands and desert fringes. But for most of sub-Saharan Africa, where malaria is stable, the introduction of crop irrigation has little impact on malaria transmission. Indeed, there is growing evidence that for many sites there is less malaria in irrigated communities than surrounding areas. The explanation for this finding is still unresolved but, in some cases at least, can be attributed to displacement of the most endophilic and anthropophilic malaria vector Anopheles funestus Giles by An. arabiensis Patton with lower vectorial capacity, as the latter thrives more than the former in ricefields. Similarly, among members of the An. gambiae complex, some cytotypes of An. gambiae sensu stricto are more vectorial than others. For example, the Mopti form has high vectorial capacity and breeds perennially in irrigated sites, whereas the savanna form is often sympatric but more seasonal. Also we suggest that many communities near irrigation schemes benefit from the greater wealth created by these schemes. Consequently irrigation communities often have greater use of bednets, better access to improved healthcare and receive fewer infective bites compared with those outside such development schemes. Thus, in most cases, irrigation schemes in Africa do not appear to increase malaria risk, except in areas of unstable transmission. However, developers should take the opportunity to improve health-care facilities for local communities when planning irrigation schemes wherever they occur.
TL;DR: The hypothesis that, in the long term and in the absence of malaria control, HbC would replace HbS in central West Africa is supported.
Abstract: Haemoglobin C (HbC; beta6Glu --> Lys) is common in malarious areas of West Africa, especially in Burkina Faso. Conclusive evidence exists on the protective role against severe malaria of haemoglobin S (HbS; beta6Glu --> Val) heterozygosity, whereas conflicting results for the HbC trait have been reported and no epidemiological data exist on the possible role of the HbCC genotype. In vitro studies suggested that HbCC erythrocytes fail to support the growth of P. falciparum but HbC homozygotes with high P. falciparum parasitaemias have been observed. Here we show, in a large case-control study performed in Burkina Faso on 4,348 Mossi subjects, that HbC is associated with a 29% reduction in risk of clinical malaria in HbAC heterozygotes (P = 0.0008) and of 93% in HbCC homozygotes (P = 0.0011). These findings, together with the limited pathology of HbAC and HbCC compared to the severely disadvantaged HbSS and HbSC genotypes and the low betaS gene frequency in the geographic epicentre of betaC, support the hypothesis that, in the long term and in the absence of malaria control, HbC would replace HbS in central West Africa.
TL;DR: Intermittent sulphadoxine-pyrimethamine treatment was well tolerated and no drug-attributable adverse events were recorded and Serological responses to EPI vaccines were not affected by the intervention.
TL;DR: The modest average coverage achieved by 1999 in the two districts suggests that insecticide-treated nets prevented 1 in 20 child deaths at that time, suggesting great potential for effective malaria control in rural African settings.
TL;DR: This article attempts to re-construct the evidence for the trends in childhood mortality as a result of Plasmodium falciparum infection over the last century in Africa.
TL;DR: This review considers the factors which have contributed to this gloomy picture of malaria, including those which relate to the vector, the female anopheline mosquito; to human activity such as creating new mosquito breeding sites, the impact of increased numbers of people, and how their migratory behavior can increase the incidence and spread of malaria.
Abstract: Malaria remains one of the world's worst health problems with 1.5 to 2.7 million deaths annually; these deaths are primarily among children under 5 years of age and pregnant women in sub-Saharan Africa. Of significance, more people are dying from malaria today than 30 years ago. This review considers the factors which have contributed to this gloomy picture, including those which relate to the vector, the female anopheline mosquito; to human activity such as creating new mosquito breeding sites, the impact of increased numbers of people, and how their migratory behavior can increase the incidence and spread of malaria; and the problems of drug resistance by the parasites to almost all currently available antimalarial drugs. In a selective manner, this review describes what is being done to ameliorate this situation both in terms of applying existing methods in a useful or even crucial role in control and prevention and in terms of new additions to the antimalarial armory that are being developed. Topics covered include biological control of mosquitoes, the use of insecticide-impregnated bed nets, transgenic mosquitoes manipulated for resistance to malaria parasites, old and new antimalarial drugs, drug resistance and how best to maintain the useful life of antimalarials, immunity to malaria and the search for antimalarial vaccines, and the malaria genome project and the potential benefits to accrue from it.
TL;DR: In view of fewer adverse ecological effects, increased sustainability and better uses of local resources and knowledge, environmental management – integrated with pharmacological, insecticidal and bednet interventions – could substantially increase the chances of rolling back malaria.
Abstract: Roll back malaria (RBM) aims at halving the current burden of the disease by the year 2010. The focus is on sub-Saharan Africa, and it is proposed to implement efficacious and cost-effective control strategies. But the evidence base of such information is scarce, and a notable missing element is the discussion of the potential of environmental management. We reviewed the literature and identified multiple malaria control programmes that incorporated environmental management as the central feature. Prominent among them are programmes launched in 1929 and implemented for two decades at copper mining communities in Zambia. The full package of control measures consisted of vegetation clearance, modification of river boundaries, draining swamps, oil application to open water bodies and house screening. Part of the population also was given quinine and was sleeping under mosquito nets. Monthly malaria incidence rates and vector densities were used for surveillance and adaptive tuning of the environmental management strategies to achieve a high level of performance. Within 3-5 years, malaria-related mortality, morbidity and incidence rates were reduced by 70-95%. Over the entire 20 years of implementation, the programme had averted an estimated 4173 deaths and 161,205 malaria attacks. The estimated costs per death and malaria attack averted were US$ 858 and US$ 22.20, respectively. Over the initial 3-5 years start-up period, analogous to the short-duration of cost-effectiveness analyses of current studies, we estimated that the costs per disability adjusted life year (DALY) averted were US$ 524-591. However, the strategy has a track record of becoming cost-effective in the longer term, as maintenance costs were much lower: US$ 22-92 per DALY averted. In view of fewer adverse ecological effects, increased sustainability and better uses of local resources and knowledge, environmental management--integrated with pharmacological, insecticidal and bednet interventions--could substantially increase the chances of rolling back malaria.
TL;DR: The evidence on the coincidental risks of malaria and anemia in Africa is reviewed and it is suggested that as many as 400,000 pregnant women may have developed severe anemia as a result of infection with malaria in sub-Saharan Africa in 1995.
Abstract: The paucity of precise information on the burden of malaria among pregnant women has hampered effective lobbying for the inclusion of preventative strategies against malaria in Safe Motherhood Initiatives. This article reviews the evidence on the coincidental risks of malaria and anemia in Africa and attempts to estimate the probable burden of malaria-related severe anemia in this susceptible group. Twenty-six studies on hemoglobin levels in all-parity pregnant women throughout this region could be matched with a malaria parasite ratio in children < 15 yr old (a measure of the intensity of transmission). In areas with no malaria, the mean hemoglobin levels were markedly higher than those found in areas with stable malaria transmission, though changes with increasing intensity of transmission were unclear. Eighteen studies from areas with stable malaria transmission in sub-Saharan Africa suggested that the median prevalence of severe anemia in all-parity pregnant women is approximately 8.2%. Assuming that 26% of these cases are due to malaria, it is suggested that as many as 400,000 pregnant women may have developed severe anemia as a result of infection with malaria in sub-Saharan Africa in 1995.
TL;DR: All cases of transfusion-transmitted malaria reported to the Centers for Disease Control and Prevention from 1963 through 1999 are reviewed to determine whether donors should have been excluded from donating blood, and their characteristics with the exclusion guidelines of the Food and Drug Administration and the American Association of Blood Banks.
Abstract: Background Transfusion-transmitted malaria is uncommon in the United States. After the report of three cases of complicated Plasmodium falciparum infection acquired by transfusion, we reviewed all cases of transfusion-transmitted malaria reported to the Centers for Disease Control and Prevention (CDC) from 1963 through 1999. Methods Information on the patients was from surveillance reports sent to the CDC. Information about the implicated blood donors came from the National Malaria Surveillance System. To determine whether donors should have been excluded from donating blood, we compared their characteristics with the exclusion guidelines of the Food and Drug Administration and the American Association of Blood Banks. Results Of 93 cases of transfusion-transmitted malaria reported in 28 states, 33 (35 percent) were due to P. falciparum, 25 (27 percent) were due to P. vivax, 25 (27 percent) were due to P. malariae, 5 (5 percent) were due to P. ovale, 3 (3 percent) were mixed infections, and 2 (2 percent) w...
TL;DR: Data support an interaction between symptomatic P. falciparum and HIV, and suggest an additional HIV-related public health problem in Africa.
Abstract: BACKGROUND: Falciparum malaria and HIV-1 infection are two of the most important health problems facing sub-Saharan Africa. No convincing evidence of an association between symptomatic malaria and HIV-1 infection has been found. OBJECTIVE: To investigate the effect of HIV-associated immunosuppression on malarial fever rates. DESIGN: An observational cohort study in HIV-specific, primary healthcare clinics in Entebbe, Uganda, on 1371 HIV-1-infected adults participating in a randomized trial of 23-valent pneumococcal vaccine. METHODS: Cohort members underwent routine 6 monthly surveillance and had open clinic access when sick. Episodes of fever were assessed according to standardized protocols. Rates of malaria are described according to HIV immune status determined by CD4 T cell counts. RESULTS: Incidence rates of Plasmodium falciparum malarial fever showed a marked inverse relationship with CD4 T cell count; 140, 93 and 57 cases per 1000 pyo for CD4 T cell groups 500 respectively, P < 0.001. Malarial fever definitions incorporating parasite density criteria (derived from asymptomatic surveillance) to correct for chance findings of fever and P. falciparum parasitaemia, did not affect the association of incidence rates with immunosuppression. CONCLUSION: These data support an interaction between symptomatic P. falciparum and HIV. Emphasis on mosquito avoidance measures should be an important component of education and counselling of HIV/AIDS patients in malaria-endemic areas, and suggests an additional HIV-related public health problem in Africa.
TL;DR: Demonstration in humans of elicitation of the class I restricted IFN-γ responses the authors believe necessary for protection against the liver stage of malaria parasites brings us closer to an effective malaria vaccine.
Abstract: We assessed immunogenicity of a malaria DNA vaccine administered by needle im or needleless jet injection [im or im/intradermally (id)] in 14 volunteers Antigen-specific IFN-γ responses were detected by enzyme-linked immunospot (ELISPOT) assays in all subjects to multiple 9- to 23-aa peptides containing class I and/or class II restricted epitopes, and were dependent on both CD8+ and CD4+ T cells Overall, frequency of response was significantly greater after im jet injection CD8+-dependent cytotoxic T lymphocytes (CTL) were detected in 8/14 volunteers Demonstration in humans of elicitation of the class I restricted IFN-γ responses we believe necessary for protection against the liver stage of malaria parasites brings us closer to an effective malaria vaccine