Journal articles: 'Human malaria'

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BUTCHER, G. A., and G. H. MITCHELL. "The role ofPlasmodium knowlesiin the history of malaria research." Parasitology 145, no. 1 (November 10, 2016): 6–17. http://dx.doi.org/10.1017/s0031182016001888.

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SUMMARYIn recent years, a malaria infection of humans in South East Asia, originally diagnosed as a known human-infecting species,Plasmodium malariae, has been identified as a simian parasite,Plasmodium knowlesi.This species had been subject to considerable investigation in monkeys since the 1930s. With the development of continuous culture of the erythrocytic stages of the human malarial parasite,Plasmodium falciparumin 1976, the emphasis in research shifted away from knowlesi. However, its importance as a human pathogen has provoked a renewed interest inP. knowlesi, not least because it too can be maintained in continuous culture and thus provides an experimental model. In fact, this parasite species has a long history in malaria research, and the purpose of this chapter is to outline approximately the first 50 years of this history.

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Haldar, Kasturi, and Narla Mohandas. "Malaria, erythrocytic infection, and anemia." Hematology 2009, no. 1 (January 1, 2009): 87–93. http://dx.doi.org/10.1182/asheducation-2009.1.87.

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Abstract Malaria is a major world health problem. It results from infection of parasites belonging to the genus Plasmodium. Plasmodium falciparum and Plasmodium vivax cause the major human malarias, with P falciparum being the more virulent. During their blood stages of infection, both P falciparum and P vivax induce anemia. Severe malarial anemia caused by P falciparum is responsible for approximately a third of the deaths associated with disease. Malarial anemia appears to be multi-factorial. It involves increased removal of circulating erythrocytes as well as decreased production of erythrocytes in the bone marrow. The molecular mechanisms underlying malarial anemia are largely unknown. Over the last five years, malaria parasite ligands have been investigated for their remodeling of erythrocytes and possible roles in destruction of mature erythrocytes. Polymorphisms in cytokines have been associated with susceptibility to severe malarial anemia: these cytokines and malaria “toxins” likely function by perturbing erythropoiesis. Finally a number of co-infections increase susceptibility to malarial anemia, likely because they exacerbate inflammation caused by malaria. Because of the complexities involved, the study of severe malarial anemia may need a “systems approach” to yield comprehensive understanding of defects in both erythropoiesis and immunity associated with disease. New and emerging tools such as (i) mathematical modeling of the dynamics of host control of malarial infection, (ii) ex vivo perfusion of human spleen to measure both infected and uninfected erythrocyte retention, and (iii) in vitro development of erythroid progenitors to dissect responsiveness to cytokine imbalance or malaria toxins, may be especially useful to develop integrated mechanistic insights and therapies to control this major and fatal disease pathology.

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Sabbatani, Sergio, Roberto Manfredi, and Sirio Fiorino. "Malaria infection and the anthropological evolution." Saúde e Sociedade 19, no. 1 (March 2010): 64–83. http://dx.doi.org/10.1590/s0104-12902010000100006.

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During the evolution of the genus Homo, with regard to species habilis, erectus and sapiens, malaria infection played a key biological role, influencing the anthropological development too. Plasmodia causing malaria developed two kinds of evolution, according to a biological and philogenetical point of view. In particular, Plasmodium vivax, Plasmodium malariae, and Plasmodium ovale, would have either coevolved with human mankind (coevolution), or reached human species during the most ancient phases of genus Homo evolution. On the other hand, Plasmodium falciparum has been transmitted to humans by monkeys in a more recent period, probably between the end of Mesolithic and the beginning of Neolithic age. The authors show both direct and indirect biomolecular evidences of malaria infection, detected in buried subjects, dating to the Ancient World, and brought to light in the course of archeological excavations in some relevant Mediterranean sites. In this literature review the Authors organize present scientific evidences: these confirm the malarial role in affecting the evolution of populations in Mediterranean countries. The people living in several different regions on the Mediterranean Sea sides, the cradle of western civilization, have been progressively influenced by malaria, in the course of the spread of this endemic disease during the last millennia. In addition, populations affected by endemic malaria developed cultural, dietary and behaviour adaptations, contributing to decrease the risk of disease. These habits were not probably fully conscious. Nevertheless it may be thought that both these customs and biological modifications, caused by malarial plasmodia, favoured the emergence of groups of people with a greater resistance against malaria. All these considered factors decreased demographical impact, influencing in a favourable way the general development and growth of civilization.

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Lamikanra, Abigail A., Douglas Brown, Alexandre Potocnik, Climent Casals-Pascual, Jean Langhorne, and David J. Roberts. "Malarial anemia: of mice and men." Blood 110, no. 1 (July 1, 2007): 18–28. http://dx.doi.org/10.1182/blood-2006-09-018069.

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Severe malaria is manifest by a variety of clinical syndromes dependent on properties of both the host and the parasite. In young infants, severe malarial anemia (SMA) is the most common syndrome of severe disease and contributes substantially to the considerable mortality and morbidity from malaria. There is now growing evidence, from both human and mouse studies of malaria, to show that anemia is due not only to increased hemolysis of infected and clearance of uninfected red blood cells (RBCs) but also to an inability of the infected host to produce an adequate erythroid response. In this review, we will summarize the recent clinical and experimental studies of malaria to highlight similarities and differences in human and mouse pathology that result in anemia and so inform the use of mouse models in the study of severe malarial anemia in humans.

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Merrick, Catherine J. "Plasmodium falciparum." Emerging Topics in Life Sciences 1, no. 6 (December 22, 2017): 517–23. http://dx.doi.org/10.1042/etls20170099.

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Plasmodium falciparum is a protozoan parasite that causes the most severe form of human malaria. Five other Plasmodium species can also infect humans — P. vivax, P. malariae, P. ovale curtisi, P. ovale wallikeri and P. knowlesi — but P. falciparum is the most prevalent Plasmodium species in the African region, where 90% of all malaria occurs, and it is this species that causes the great majority of malaria deaths. These were reported by the WHO at 438 000 in 2015 from an estimated 214 million cases; importantly, however, figures for the global burden of malaria tend to have wide margins of error due to poor and inaccurate reporting. In this Perspective, features of P. falciparum that are unique among human malaria parasites are highlighted, and current issues surrounding the control and treatment of this major human pathogen are discussed.

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VON MÜHLEN, André. "COMPUTER IMAGE ANALYSIS OF MALARIAL PLASMODIUM VIVAX IN HUMAN RED BLOOD CELLS." Periódico Tchê Química 02, no. 1 (August 20, 2004): 42–51. http://dx.doi.org/10.52571/ptq.v1.n02.2004.agosto/9_pgs_42_51.pdf.

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This project aims to study computer image analysis of malarial parasites using morphological operators as its main method of approach. Malaria is a life-threatening parasitic disease transmitted through female Anopheles mosquitoes (1). It is found throughout the tropical and subtropical regions of the world (figure 1), and affects over 300 million people annually. As globalization, ease and frequency of travel increase, malaria cases may occur in any country (2). Over one million people die due to malaria every year (3).

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Aikawa, Masamichi. "Human Cerebral Malaria *." American Journal of Tropical Medicine and Hygiene 39, no. 1 (July 1, 1988): 3–10. http://dx.doi.org/10.4269/ajtmh.1988.39.3.

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OO, MAUNG MAUNG, MASAMICHI AIKAWA, THAN THAN, TIN MAUNG AYE, PE THAN MYINT, IKUO IGARASHI, and WILLIAM C. SCHOENE. "Human Cerebral Malaria." Journal of Neuropathology and Experimental Neurology 46, no. 2 (March 1987): 223–31. http://dx.doi.org/10.1097/00005072-198703000-00009.

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Slater, A. "Human malaria parasites." Biomedicine & Pharmacotherapy 46, no. 10 (January 1992): 502. http://dx.doi.org/10.1016/0753-3322(92)90014-x.

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Singh, Balbir. "Plasmodium knowlesi: an update." Microbiology Australia 37, no. 1 (2016): 39. http://dx.doi.org/10.1071/ma16014.

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There were only four species of Plasmodium that were thought to cause malaria in humans until a large number of human infections by Plasmodium knowlesi, a malaria parasite typically found in long-tailed and pig-tailed macaques, were reported in 2004 in Malaysian Borneo. Since then, cases of knowlesi malaria have been reported throughout South-east Asia and also in travellers returning from the region. This article describes the molecular, entomological and epidemiological data which indicate that P. knowlesi is an ancient parasite that is primarily zoonotic, and there are three highly divergent sub-populations. It also describes the detection methods for P. knowlesi, which is morphologicaly similar to P. malariae, and the clinical features and treatment of this malaria parasite that is potentially fatal.

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Weatherall, David J., Louis H. Miller, Dror I. Baruch, Kevin Marsh, Ogobara K. Doumbo, Climent Casals-Pascual, and David J. Roberts. "Malaria and the Red Cell." Hematology 2002, no. 1 (January 1, 2002): 35–57. http://dx.doi.org/10.1182/asheducation-2002.1.35.

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Abstract Because of the breakdown of malaria control programs, the constant emergence of drug resistant parasites, and, possibly, climatic changes malaria poses a major problem for the developing countries. In addition, because of the speed of international travel it is being seen with increasing frequency as an imported disease in non-tropical countries. This update explores recent information about the pathophysiology of the disease, its protean hematological manifestations, and how carrier frequencies for the common hemoglobin disorders have been maintained by relative resistance to the malarial parasite. In Section I, Dr. Louis Miller and colleagues consider recent information about the pathophysiology of malarial infection, including new information about interactions between the malarial parasite and vascular endothelium. In Section II, Dr. David Roberts discusses what is known about the complex interactions between red cell production and destruction that characterize the anemia of malaria, one of the commonest causes of anemia in tropical countries. In Section III, Dr. David Weatherall reviews recent studies on how the high gene frequencies of the thalassemias and hemoglobin variants have been maintained by heterozygote advantage against malaria and how malaria has shaped the genetic structure of human populations.

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Hernandez-Valladares, Maria, Pascal Rihet, and Fuad A. Iraqi. "Host susceptibility to malaria in human and mice: compatible approaches to identify potential resistant genes." Physiological Genomics 46, no. 1 (January 1, 2014): 1–16. http://dx.doi.org/10.1152/physiolgenomics.00044.2013.

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There is growing evidence for human genetic factors controlling the outcome of malaria infection, while molecular basis of this genetic control is still poorly understood. Case-control and family-based studies have been carried out to identify genes underlying host susceptibility to malarial infection. Parasitemia and mild malaria have been genetically linked to human chromosomes 5q31-q33 and 6p21.3, and several immune genes located within those regions have been associated with malaria-related phenotypes. Association and linkage studies of resistance to malaria are not easy to carry out in human populations, because of the difficulty in surveying a significant number of families. Murine models have proven to be an excellent genetic tool for studying host response to malaria; their use allowed mapping 14 resistance loci, eight of them controlling parasitic levels and six controlling cerebral malaria. Once quantitative trait loci or genes have been identified, the human ortholog may then be identified. Comparative mapping studies showed that a couple of human and mouse might share similar genetically controlled mechanisms of resistance. In this way, char8, which controls parasitemia, was mapped on chromosome 11; char8 corresponds to human chromosome 5q31-q33 and contains immune genes, such as Il3, Il4, Il5, Il12b, Il13, Irf1, and Csf2. Nevertheless, part of the genetic factors controlling malaria traits might differ in both hosts because of specific host-pathogen interactions. Finally, novel genetic tools including animal models were recently developed and will offer new opportunities for identifying genetic factors underlying host phenotypic response to malaria, which will help in better therapeutic strategies including vaccine and drug development.

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MAENO, Y., R. CULLETON, N. T. QUANG, S. KAWAI, R. P. MARCHAND, and S. NAKAZAWA. "Plasmodium knowlesi and human malaria parasites in Khan Phu, Vietnam: Gametocyte production in humans and frequent co-infection of mosquitoes." Parasitology 144, no. 4 (November 29, 2016): 527–35. http://dx.doi.org/10.1017/s0031182016002110.

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SUMMARYFour species of malaria parasite, Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae and Plasmodium knowlesi infect humans living in the Khanh Phu commune, Khanh Hoa Province, Vietnam. The latter species also infects wild macaque monkeys in this region. In order to understand the transmission dynamics of the three species, we attempted to detect gametocytes of the three species in the blood of infected individuals, and sporozoites in the salivary glands of mosquitoes from the same region. For the detection of gametocyte-specific mRNA, we targeted region 3 of pfg377, pvs25, pmg and pks25 as indicators of the presence of P. falciparum, P. vivax, P. malariae and P. knowlesi gametocytes, respectively. Gametocyte-specific mRNA was present in 37, 61, 0 and 47% of people infected with P. falciparum (n = 95), P. vivax (n = 69), P. malariae (n = 6) or P. knowlesi (n = 32), respectively. We found that 70% of mosquitoes that had P. knowlesi in their salivary glands also carried human malaria parasites, suggesting that mosquitoes are infected with P. knowlesi from human infections.

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Monteiro, Eliana Ferreira, Carmen Fernandez-Becerra, Maisa da Silva Araujo, Mariluce Rezende Messias, Luiz Shozo Ozaki, Ana Maria Ribeiro de Castro Duarte, Marina Galvão Bueno, et al. "Naturally Acquired Humoral Immunity against Malaria Parasites in Non-Human Primates from the Brazilian Amazon, Cerrado and Atlantic Forest." Pathogens 9, no. 7 (June 29, 2020): 525. http://dx.doi.org/10.3390/pathogens9070525.

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Non-human primates (NHPs) have been shown to be infected by parasites of the genus Plasmodium, the etiological agent of malaria in humans, creating potential risks of zoonotic transmission. Plasmodium brasilianum, a parasite species similar to P. malariae of humans, have been described in NHPs from Central and South America, including Brazil. The merozoite surface protein 1 (MSP1), besides being a malaria vaccine candidate, is highly immunogenic. Due to such properties, we tested this protein for the diagnosis of parasite infection. We used recombinant proteins of P. malariae MSP1, as well as of P. falciparum and P. vivax, for the detection of antibodies anti-MSP1 of these parasite species, in the sera of NHPs collected in different regions of Brazil. About 40% of the NHP sera were confirmed as reactive to the proteins of one or more parasite species. A relatively higher number of reactive sera was found in animals from the Atlantic Forest than those from the Amazon region, possibly reflecting the former more intense parasite circulation among NHPs due to their proximity to humans at a higher populational density. The presence of Plasmodium positive NHPs in the surveyed areas, being therefore potential parasite reservoirs, needs to be considered in any malaria surveillance program.

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Willimann, K., H. Matile, N. A. Weiss, and B. A. Imhof. "In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria." Journal of Experimental Medicine 182, no. 3 (September 1, 1995): 643–53. http://dx.doi.org/10.1084/jem.182.3.643.

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Cerebral malaria is a fatal complication of infection by Plasmodium falciparum in man. The neurological symptoms that characterize this form of malarial disease are accompanied by the adhesion of infected erythrocytes to the vasculature of the brain. To study this phenomenon in vivo, an acute phase severe combined immunodeficiency (SCID) mouse model was developed in which sequestration of P. falciparum-infected human erythrocytes took place. During acute cerebral malaria in humans, the expression of intercellular adhesion molecule-1 (ICAM-1) is induced in vascular endothelium by inflammatory reactions. Acute phase ICAM-1 expression can also be obtained in SCID mice. The endothelium of the midbrain region was the most responsive to such inflammatory stimulus. It is noteworthy that the reticular formation in the midbrain controls the level of consciousness, and loss of consciousness is a symptom of cerebral malaria. We found that infected human erythrocytes were retained 24 times more than normal erythrocytes in ICAM-1-positive mouse brain. Sequestration to the brain was reduced by anti-ICAM-1 antibodies. These in vivo results were confirmed by the binding of P. falciparum-infected erythrocytes to the ICAM-1-positive endothelium in tissue sections of mouse brain. We conclude that the SCID mouse serves as a versatile in vivo model that allows the study of P. falciparum-infected erythrocyte adhesion as it occurs in human cerebral malaria. Upregulation of ICAM-1 expression in the region of the midbrain correlates with increased retention of malaria-infected erythrocytes and with the symptoms of cerebral malaria.

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Swierczynski, Giovanni, and Maria Gobbo. "Atlas of Human Malaria (Atlante della Malaria Umana)." Journal of Travel Medicine 15, no. 2 (March 1, 2008): 143–44. http://dx.doi.org/10.1111/j.1708-8305.2008.00196.x.

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Sharp, Paul M., Lindsey J. Plenderleith, and Beatrice H. Hahn. "Ape Origins of Human Malaria." Annual Review of Microbiology 74, no. 1 (September 8, 2020): 39–63. http://dx.doi.org/10.1146/annurev-micro-020518-115628.

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African apes harbor at least twelve Plasmodium species, some of which have been a source of human infection. It is now well established that Plasmodium falciparum emerged following the transmission of a gorilla parasite, perhaps within the last 10,000 years, while Plasmodium vivax emerged earlier from a parasite lineage that infected humans and apes in Africa before the Duffy-negative mutation eliminated the parasite from humans there. Compared to their ape relatives, both human parasites have greatly reduced genetic diversity and an excess of nonsynonymous mutations, consistent with severe genetic bottlenecks followed by rapid population expansion. A putative new Plasmodium species widespread in chimpanzees, gorillas, and bonobos places the origin of Plasmodium malariae in Africa. Here, we review what is known about the origins and evolutionary history of all human-infective Plasmodium species, the time and circumstances of their emergence, and the diversity, host specificity, and zoonotic potential of their ape counterparts.

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Fonjungo, Peter N., Ibrahim M. Elhassan, David R. Cavanagh, Thor G. Theander, Lars Hviid, Cally Roper, David E. Arnot, and Jana S. McBride. "A Longitudinal Study of Human Antibody Responses toPlasmodium falciparum Rhoptry-Associated Protein 1 in a Region of Seasonal and Unstable Malaria Transmission." Infection and Immunity 67, no. 6 (June 1, 1999): 2975–85. http://dx.doi.org/10.1128/iai.67.6.2975-2985.1999.

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ABSTRACT Rhoptry-associated protein 1 (RAP1) of Plasmodium falciparum is a nonpolymorphic merozoite antigen that is considered a potential candidate for a malaria vaccine against asexual blood stages. In this longitudinal study, recombinant RAP1 (rRAP1) proteins with antigenicity similar to that of P. falciparum-derived RAP1 were used to analyze antibody responses to RAP1 over a period of 4 years (1991 to 1995) of 53 individuals naturally exposed to P. falciparum malaria. In any 1 year during the study, between 23 and 39% of individuals who had malaria developed immunoglobulin G (IgG) antibodies detectable with at least one rRAP1 protein. However, the anti-RAP1 antibody responses were detected only during or shortly after clinical malarial infections. RAP1 antibody levels declined rapidly (within 1 to 2 months) following drug treatment of the infections. No anti-RAP1 antibodies were usually detected a few months after the end of malaria transmission, during the dry season, or by the start of the next malaria season. Thus, RAP1 IgG responses were very short-lived. The short duration of RAP1 antibody response may explain the apparent lack of response in a surprisingly high proportion of individuals after clinical malarial infections. For some individuals who experienced more than one malarial infection, a higher anti-RAP1 antibody response to subsequent infections than to earlier infections was observed. This suggested secondary responses to RAP1 and thus the development of immunological memory for RAP1.

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Etkin, Nina L. "The co-evolution of people, plants, and parasites: biological and cultural adaptations to malaria." Proceedings of the Nutrition Society 62, no. 2 (May 2003): 311–17. http://dx.doi.org/10.1079/pns2003244.

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The urgency generated by drug-resistant strains of malaria has accelerated anti-malarial drug research over the last two decades. While synthetic pharmaceutical agents continue to dominate research, attention increasingly has been directed to natural products. The present paper explores the larger context in which plant use occurs and considers how the selection of medicinal plants has evolved over millennia as part of the larger human effort to mediate illness. First attention is directed to indigenous medicinal plants whose anti-malarial activity is based on an oxidant mode of action, by which intracellular constituents lose electrons (become more electropositive). Next, parallels are drawn between these plant substances and a suite of malaria-protective genetic traits: glucose-6-phosphate dehydrogenase deficiency; haemoglobins S, C and E; α- and β-thalassemias. These erythrocyte anomalies are classic examples of Darwinian evolution, occurring in high frequency in populations who have experienced considerable selective pressure from malaria. Characterized by discrete loci and pathophysiologies, they are united through the phenomenon of increased erythrocyte oxidation. In this model, then, oxidant anti-malarial plants are culturally constructed analogues, and molecular mimics, of these genetic adaptations. To further reinforce the scheme, it is noted that the anti-malarial action of pharmaceutical agents such as chloroquine and mefloquine duplicates both the genetic anomalies and the folk therapeutic models based in oxidant plants. This discussion coheres around a theoretical foundation that relates plant secondary metabolites (oxidants) to plasmodial biochemistry and human biological and cultural adaptations to malaria. Co-evolution provides a theoretical link that illuminates how medical cultures manage the relationships among humans, plants, herbivores and their respective pathogens.

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Chai, Jong-Yil. "Atlas of Human Malaria." Korean Journal of Parasitology 46, no. 2 (2008): 113. http://dx.doi.org/10.3347/kjp.2008.46.2.113.

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Carlton, Jane M. "Evolution of human malaria." Nature Microbiology 3, no. 6 (May 24, 2018): 642–43. http://dx.doi.org/10.1038/s41564-018-0170-2.

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Spring, M., M. Polhemus, and C. Ockenhouse. "Controlled Human Malaria Infection." Journal of Infectious Diseases 209, suppl 2 (May 28, 2014): S40—S45. http://dx.doi.org/10.1093/infdis/jiu063.

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Majeed, Muhammad Zafar, Muhammad Shahbaz Hussain, and Faiza Sarwar. "PREVALENCE OF HUMAN MALARIA." Professional Medical Journal 23, no. 06 (June 10, 2016): 655–59. http://dx.doi.org/10.29309/tpmj/2016.23.06.1602.

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Malaria is one of the devastating diseases worldwide. More than 3 billion peoplelive under the threat of malaria in endemic countries and kills more than one million each year.Malaria leads to multiple hematological (thrombocytopenia) and other abnormalities like renalsystem, nervous system with increased morbidity and mortality. Aim: The present study wasconducted to determine the prevalence of human malaria, its correlation with thrombocytopeniaand treatment in patients of District Rahim Yar Khan. Materials and Methods: A total of 200patients including 140 males and 60 females were the part of our study. Blood samples collectionwas done during September to November following monsoon season. Patients were diagnosedthrough peripheral blood smear. Both P. falciparum and P. vivax parasites against 300 white bloodcells (WBCs) were examined on the thick smear. Platelet count was done by using an automatedcell count analyzer. A platelet count of less than 150 x109/L defined thrombocytopaenia. Firstline of treatment was Chloroquine in cases of Plasmodium vivax whereas Neo fansidar incases of Plasmodium falciparum. Results: Gender wise distribution of patients was 140 (70%)males and 60(30%) females. We had 74 (37%) patients from urban and 126 (63%) from ruralpopulation. Malaria was most frequent 64% by P.vivax and 36% by P.falciparum. Fever was highduring admission to hospital and after usage of antimalarials recovery and improvement innumber of platelets was noted. Conclusion: The high prevalence rate of P. vivax pose a majorhealth hazard but of P. falciparum also may lead to serious complications. The high frequencyof human malaria infection should be a major concern for authorities in the fight against malariacontrol programs in Pakistan.

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Muerhoff, A. Scott, Larry G. Birkenmeyer, Ruthie Coffey, Bruce J. Dille, John W. Barnwell, William E. Collins, Joann S. Sullivan, George J. Dawson, and Suresh M. Desai. "Detection of Plasmodium falciparum, P. vivax, P. ovale, and P. malariae Merozoite Surface Protein 1-p19 Antibodies in Human Malaria Patients and Experimentally Infected Nonhuman Primates." Clinical and Vaccine Immunology 17, no. 10 (August 11, 2010): 1631–38. http://dx.doi.org/10.1128/cvi.00196-10.

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ABSTRACT Approximately 3.2 billion people live in areas where malaria is endemic, and WHO estimates that 350 to 500 million malaria cases occur each year worldwide. This high prevalence, and the high frequency of international travel, creates significant risk for the exportation of malaria to countries where malaria is not endemic and for the introduction of malaria organisms into the blood supply. Since all four human infectious Plasmodium species have been transmitted by blood transfusion, we sought to develop an enzyme-linked immunosorbent assay (ELISA) capable of detecting antibodies elicited by infection with any of these species. The merozoite surface protein 1 (MSP1), a P. falciparum and P. vivax vaccine candidate with a well-characterized immune response, was selected for use in the assay. The MSP1 genes from P. ovale and P. malariae were cloned and sequenced (L. Birkenmeyer, A. S. Muerhoff, G. Dawson, and S. M. Desai, Am. J. Trop. Med. Hyg. 82:996-1003, 2010), and the carboxyl-terminal p19 regions of all four species were expressed in Escherichia coli. Performance results from individual p19 ELISAs were compared to those of a commercial test (Lab 21 Healthcare Malaria enzyme immunoassay [EIA]). The commercial ELISA detected all malaria patients with P. falciparum or P. vivax infections, as did the corresponding species-specific p19 ELISAs. However, the commercial ELISA detected antibodies in 0/2 and 5/8 individuals with P. malariae and P. ovale infections, respectively, while the p19 assays detected 100% of individuals with confirmed P. malariae or P. ovale infections. In experimentally infected nonhuman primates, the use of MSP1-p19 antigens from all four species resulted in the detection of antibodies within 2 to 10 weeks postinfection. Use of MSP1-p19 antigens from all four Plasmodium species in a single immunoassay would provide significantly improved efficacy compared to existing tests.

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Kaur, Prabhjot, Arun Bhatia, Kanav Midha, and Mampi Debnath. "Malaria: A Cause of Anemia and Its Effect on Pregnancy." World Journal of Anemia 1, no. 2 (2017): 51–62. http://dx.doi.org/10.5005/jp-journals-10065-0012.

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ABSTRACT Malaria is one of the major health problems in the world. It remains an important cause of very high human morbidity and mortality, especially, among children and pregnant women. It results from the infection of parasites belonging to the genus Plasmodium. Plasmodium falciparum and Plasmodium vivax are the major pathogens responsible for causing human malaria. Approximately 75% of cases are caused by P. falciparum and associated with the mortality rate of approximately 0.5 to 1.0%. Both P. falciparum and P. vivax induce anemia during their erythrocytic stages of infection. Most of the malarial infections are related to some degree of anemia, the severity of which depends upon patient-specific characteristics (e.g., age, innate and acquired resistance, comorbid features, etc.) as well as parasite-specific characteristics (e.g., species, adhesive, and drug-resistant phenotype, etc.). Malarial anemia encompasses reduced production of erythrocytes as well as increased removal of circulating erythrocytes in the bone marrow. Susceptibility to severe malarial anemia is associated with the polymorphisms of the cytokines, which are likely to function by perturbing erythropoiesis. This article reviews the epidemiology, pathophysiology, clinical features, treatment, and various complications occurring due to malarial anemia. The second part of this article also focuses on the effect of malaria during pregnancy. Some significant effects of malaria during pregnancy include spontaneous abortion, preterm delivery, low birthweight, stillbirth, congenital infection, and maternal death. How to cite this article Saxena R, Bhatia A, Midha K, Debnath M, Kaur P. Malaria: A Cause of Anemia and Its Effect on Pregnancy. World J Anemia. 2017;1(2):51-62.

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Badell, Edgar, Claude Oeuvray, Alicia Moreno, Soe Soe, Nico van Rooijen, Ahmed Bouzidi, and Pierre Druilhe. "Human Malaria in Immunocompromised Mice." Journal of Experimental Medicine 192, no. 11 (December 4, 2000): 1653–60. http://dx.doi.org/10.1084/jem.192.11.1653.

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We have recently described that sustained Plasmodium falciparum growth could be obtained in immunodeficient mice. We now report the potential of this new mouse model by assaying the effect of the passive transfer of antibodies (Abs) which in humans have had a well-established effect. Our results show that the total African adult hyperimmune immunoglobulin Gs (HI-IgGs) strongly reduce P. falciparum parasitemia similarly to that reported in humans, but only when mice are concomitantly reconstituted with human monocytes (HuMNs). In contrast, neither HI-IgGs nor HuMNs alone had any direct effect upon parasitemia. We assessed the in vivo effect of epitope-specific human Abs affinity-purified on peptides derived either from the ring erythrocyte surface antigen (RESA) or the merozoite surface protein 3 (MSP3). The inoculation of low concentrations of anti-synthetic peptide from MSP3, but not of anti-RESA Abs, consistently suppressed P. falciparum in the presence of HuMNs. Parasitemia decrease was stronger and faster than that observed using HI-IgGs and as fast as that induced by chloroquine. Our observations demonstrate that this mouse model is of great value to evaluate the protective effect of different Abs with distinct specificity in the same animal, a step hardly accessible and therefore never performed before in humans.

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NIMRI, L. F., and H. N. LANNERS. "Glomerulonephropathies in Plasmodium inui-infected rhesus monkey: a primate model and possible applications for human quartan malaria." Parasitology 141, no. 12 (July 15, 2014): 1638–45. http://dx.doi.org/10.1017/s0031182014000900.

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SUMMARYNone of the few animal models proposed for the study of human quartan malaria nephritic syndrome have shown complete pathological findings that are similar to those seen in humans. This study investigated the histopathological changes in kidneys in 10 Plasmodium inui infected Macaca mulatta monkeys by light and electron microscopy in order to develop a suitable animal model for human quartan malaria. Ten healthy adult rhesus monkeys were infected with P. inui and clinical chemistry and haematologic tests were done before and after infection. A renal biopsy sample was collected before infection as a baseline control and another biopsy was collected after infection. Histopathological changes examined by light and transmission electron microscopy (TEM) revealed abnormalities in all infected monkeys to variable degrees. Several electron-dense discrete or diffused mesangial deposits, and increase in mesangial cells and matrix were associated with the morphological changes observed by light microscope. This pattern is consistent with membranoproliferative glomerulonephritis type reported in humans infected with Plasmodium malariae. Results strongly support that the P. inui-infected rhesus monkey develop an immune-complex-mediated glomerulonephritis in the course of the infection. Therefore, this experimental model represents a useful tool to better understand the different parameters and the consequences of quartan malaria infections comparable to situations in humans.

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MITRA, S., B. RAVINDRAN, B. K. DAS, R. K. DAS, P. K. DAS, and R. N. RATH. "Human cerebral malaria: characterization of malarial antibodies in cerebrospinal fluid." Clinical & Experimental Immunology 86, no. 1 (June 28, 2008): 19–21. http://dx.doi.org/10.1111/j.1365-2249.1991.tb05767.x.

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Brooke, Basil. "Mosquitoes and Malaria Control – A Complex Problem for Entomologists to Unravel." Outlooks on Pest Management 30, no. 5 (October 1, 2019): 213–16. http://dx.doi.org/10.1564/v30_oct_07.

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The control of malaria transmitting mosquitoes hinges on accurate species identification. This enables assessments of insecticide susceptibilities and important behavioural characteristics (such as feeding and resting behaviours) by species, leading to the design of coherent insecticide-based control strategies that can be enhanced by additional methodologies for malaria elimination. Malaria is a mosquito-borne parasitic disease that affects many vertebrates including humans. Prior to the 20th century the human malarias (Plasmodium falciparum, P. vivax, P. malariae, P. ovale and P. knowlesi) occurred in tropical and temperate regions but their distribution has since reduced to the tropical belt with by far the highest incidence in sub-Saharan Africa. Global incidence for 2017 was estimated by the WHO at 219 million cases corresponding to 435 000 deaths. It is also estimated that investment in malaria control and elimination amounted to $3.1 billion in 2017. The control (and elimination) of malaria largely hinges on the suppression of mosquito vectors, accurate diagnosis and case detection, and case management using appropriate antimalarial drug regimens. Controlling malaria vector mosquitoes (and of course other mosquito-borne diseases) means being able to identify that which needs to be controlled. This is not unlike the maxim of knowing one's enemy, and disease vector control is often phrased in militaristic terms. The arsenal of tools in the war against malaria vectors includes insecticides, bed nets, repellents, larvicides, endectocides, toxic baits and even modified genes. This call to arms against the transmitters of a deadly disease presupposes that the enemy can be identified, which, unfortunately, is not as easy as it sounds. Identifying malaria vectors to species has posed a significant challenge ever since Ronald Ross and Giovanni Grassi implicated dappled-winged Anopheles mosquitoes in malaria transmission. They could not have known the Pandora's Box they had opened, because several Anopheles species are cryptic. Many hide in cryptic species complexes and groups that confound straightforward morphological methods of identifying them. A species complex is a group of morphologically identical species that are very closely related, but nevertheless vary significantly in their feeding and resting behaviours, and mate assortatively (i.e. they recognise and tend only to mate with conspecific partners) enough that hybridisations between them are rare. Many member species of these complexes are sufficiently diverged that cross-mating between them yields infertile or non-viable offspring, but not in all cases. A species group is a looser assortment of related species whose morphological features match to a point where they are very nearly identical, often requiring specimens from more than one life stage to identify them. They also mate assortatively, and hybrids are rarer or simply never occur. The problem for malaria control is that several vector species, including many primary vectors, are members of cryptic complexes or groups. These invariably contain vector and non-vector species, requiring a complex and laborious system to unravel them and ascribe unambiguous genetic methods for their identification. Added to this complexity is the possibility that any Anopheles. species that takes human blood is a potential vector of the human malarias, with the added caveat that not all populations within a species are vectors. Some member species, and even populations within a species, feed either exclusively on humans (anthropophagy) and are potentially high transmission intensity vectors, or exclusively on livestock animals (zoophagy) making them non-vectors, or take blood from a range of sources including humans, becoming potential vectors of low to medium transmission intensity. An added layer of complexity is genetic heterogeneity between populations within a species. It can be argued that this complexity is not necessarily a problem for malaria control. After all, the aim of suppressing or even eliminating vector populations is the interruption of transmission, regardless of what species they are. But mosquito adaptability dictates otherwise. This is because the primary method of malaria vector control is deployment of specially formulated insecticides against adult mosquitoes, either by indoor residual spraying (IRS) or the treatment of bed nets. Mosquito adaptability has enabled a powerful response to these interventions, with resistance to insecticides becoming so widespread that fully insecticide susceptible malaria vector populations are now quite rare.

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Kho, Steven, Gabriela Minigo, Benediktus Andries, Leo Leonardo, Pak Prayoga, Jeanne R. Poespoprodjo, Enny Kenangalem, et al. "Circulating Neutrophil Extracellular Traps and Neutrophil Activation Are Increased in Proportion to Disease Severity in Human Malaria." Journal of Infectious Diseases 219, no. 12 (November 19, 2018): 1994–2004. http://dx.doi.org/10.1093/infdis/jiy661.

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AbstractBackgroundNeutrophil activation results in Plasmodium parasite killing in vitro, but neutrophil products including neutrophil extracellular traps (NETs) mediate host organ damage and may contribute to severe malaria. The role of NETs in the pathogenesis of severe malaria has not been examined.MethodsIn Papua, Indonesia, we enrolled adults with symptomatic Plasmodium falciparum (n = 47 uncomplicated, n = 8 severe), Plasmodium vivax (n = 37), or Plasmodium malariae (n = 14) malaria; asymptomatic P falciparum (n = 19) or P vivax (n = 21) parasitemia; and healthy adults (n = 23) without parasitemia. Neutrophil activation and NETs were quantified by immunoassays and microscopy and correlated with parasite biomass and disease severity.ResultsIn patients with symptomatic malaria, neutrophil activation and NET counts were increased in all 3 Plasmodium species. In falciparum malaria, neutrophil activation and NET counts positively correlated with parasite biomass (Spearman rho = 0.41, P = .005 and r2 = 0.26, P = .002, respectively) and were significantly increased in severe disease. In contrast, NETs were inversely associated with parasitemia in adults with asymptomatic P falciparum infection (r2 = 0.24, P = .031) but not asymptomatic P vivax infection.ConclusionsAlthough NETs may inhibit parasite growth in asymptomatic P falciparum infection, neutrophil activation and NET release may contribute to pathogenesis in severe falciparum malaria. Agents with potential to attenuate these processes should be evaluated.

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Carvalho, Leonardo J. M. "Murine cerebral malaria: how far from human cerebral malaria?" Trends in Parasitology 26, no. 6 (June 2010): 271–72. http://dx.doi.org/10.1016/j.pt.2010.03.001.

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Obiero, Joshua M., Seif Shekalaghe, Cornelus C. Hermsen, Maxmillian Mpina, Else M. Bijker, Meta Roestenberg, Karina Teelen, et al. "Impact of Malaria Preexposure on Antiparasite Cellular and Humoral Immune Responses after Controlled Human Malaria Infection." Infection and Immunity 83, no. 5 (March 16, 2015): 2185–96. http://dx.doi.org/10.1128/iai.03069-14.

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To understand the effect of previous malaria exposure on antiparasite immune responses is important for developing successful immunization strategies. Controlled human malaria infections (CHMIs) using cryopreservedPlasmodium falciparumsporozoites provide a unique opportunity to study differences in acquisition or recall of antimalaria immune responses in individuals from different transmission settings and genetic backgrounds. In this study, we compared antiparasite humoral and cellular immune responses in two cohorts of malaria-naive Dutch volunteers and Tanzanians from an area of low malarial endemicity, who were subjected to the identical CHMI protocol by intradermal injection ofP. falciparumsporozoites. Samples from both trials were analyzed in parallel in a single center to ensure direct comparability of immunological outcomes. Within the Tanzanian cohort, we distinguished one group with moderate levels of preexisting antibodies to asexualP. falciparumlysate and another that, based onP. falciparumserology, resembled the malaria-naive Dutch cohort. PositiveP. falciparumserology at baseline was associated with a lower parasite density at first detection by quantitative PCR (qPCR) after CHMI than that for Tanzanian volunteers with negative serology. Post-CHMI, both Tanzanian groups showed a stronger increase in anti-P. falciparumantibody titers than Dutch volunteers, indicating similar levels of B-cell memory independent of serology. In contrast to the Dutch, Tanzanians failed to increaseP. falciparum-specificin vitrorecall gamma interferon (IFN-γ) production after CHMI, and innate IFN-γ responses were lower inP. falciparumlysate-seropositive individuals than in seronegative individuals. In conclusion, positiveP. falciparumlysate serology can be used to identify individuals with better parasite control but weaker IFN-γ responses in circulating lymphocytes, which may help to stratify volunteers in future CHMI trials in areas where malaria is endemic.

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Riley, E. M. "The role of MHC- and non-MHC-associated genes in determining the human immune response to malaria antigens." Parasitology 112, S1 (March 1996): S39—S51. http://dx.doi.org/10.1017/s0031182000076654.

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SUMMARYIndividual susceptibility to malaria infection, disease and death is influenced by host genotype, parasite virulence and a number of environmental factors including malaria-specific immunity. Immune responses are themselves determined by a combination of host genes and environmental effects. The extent to which host genotype limits the spectrum of possible immune responses may influence the outcome of infection and has consequences for vaccine design. Associations have been observed between human major histocompatibility complex (MHC) genotype and susceptibility to severe malaria, but no similar associations have been observed for mild malarial disease or for specific antibody responses to defined malaria antigens. Epidemiological studies have shown that, in practice, neither T helper cell nor antibody responses to malaria parasites are limited by host MHC genotype, but have revealed that genes lying outside the MHC may influence T cell proliferative responses. These genes have yet to be identified, but possible candidates include T cell receptor (TcR) genes, and genes involved in TcR gene rearrangements. More importantly, perhaps, longitudinal epidemiological studies have shown that the anti-malarial antibody repertoire is selective and becomes fixed in malaria-immune individuals, but is independent of host genotype. These findings suggest that the antibody repertoire may be determined, at least in part, by stochastic events. The first of these is the generation of the T and B cell repertoire, which results from random gene recombinations and somatic mutation and is thus partially independent of germline genes. Secondly, of the profusion of immunogenic peptides which are processed and presented by antigen presenting cells, a few will, by chance, interact with T and B cell surface antigen receptors of particularly high affinity. These T and B cell clones will be selected, will expand and may come to dominate the immune response, preventing the recognition of variant epitopes presented by subsequent infections - a process known as original antigenic sin or clonal imprinting. The immune response of an individual thus reflects the balance between genetic and stochastic effects. This may have important consequences for subunit vaccine development.

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Prato, Mauro, and Giuliana Giribaldi. "Matrix Metalloproteinase-9 and Haemozoin: Wedding Rings for Human Host andPlasmodium falciparumParasite in Complicated Malaria." Journal of Tropical Medicine 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/628435.

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It is generally accepted that the combination of bothPlasmodium falciparumparasite and human host factors is involved in the pathogenesis of complicated severe malaria, including cerebral malaria (CM). Among parasite products, the malarial pigment haemozoin (HZ) has been shown to impair the functions of mononuclear and endothelial cells. Different CM models were associated with enhanced levels of matrix metalloproteinases (MMPs), a family of proteolytic enzymes able to disrupt subendothelial basement membrane and tight junctions and shed, activate, or inactivate cytokines, chemokines, and other MMPs through cleavage from their precursors. Among MMPs, a good candidate for targeted therapy might be MMP-9, whose mRNA and protein expression enhancement as well as direct proenzyme activation by HZ have been recently investigated in a series of studies by our group and others. In the present paper the role of HZ and MMP-9 in complicated malaria, as well as their interactions, will be discussed.

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Kirchgatter, Karin, Rosa Maria Tubaki, Rosely dos Santos Malafronte, Isabel Cristina Alves, Giselle Fernandes Maciel de Castro Lima, Lilian de Oliveira Guimarães, Robson de Almeida Zampaulo, and Gerhard Wunderlich. "Anopheles (Kerteszia) cruzii (DIPTERA: CULICIDAE) IN PERIDOMICILIARY AREA DURING ASYMPTOMATIC MALARIA TRANSMISSION IN THE ATLANTIC FOREST: MOLECULAR IDENTIFICATION OF BLOOD-MEAL SOURCES INDICATES HUMANS AS PRIMARY INTERMEDIATE HOSTS." Revista do Instituto de Medicina Tropical de São Paulo 56, no. 5 (September 2014): 403–9. http://dx.doi.org/10.1590/s0036-46652014000500006.

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Anopheles (Kerteszia) cruzii has been implicated as the primary vector of human and simian malarias out of the Brazilian Amazon and specifically in the Atlantic Forest regions. The presence of asymptomatic human cases, parasite-positive wild monkeys and the similarity between the parasites infecting them support the discussion whether these infections can be considered as a zoonosis. Although many aspects of the biology of An. cruzii have already been addressed, studies conducted during outbreaks of malaria transmission, aiming at the analysis of blood feeding and infectivity, are missing in the Atlantic Forest. This study was conducted in the location of Palestina, Juquitiba, where annually the majority of autochthonous human cases are notified in the Atlantic Forest of the state of São Paulo. Peridomiciliary sites were selected for collection of mosquitoes in a perimeter of up to 100 m around the residences of human malaria cases. The mosquitoes were analyzed with the purpose of molecular identification of blood-meal sources and to examine the prevalence of Plasmodium. A total of 13,441 females of An. (Ker.) cruzii were collected. The minimum infection rate was calculated at 0.03% and 0.01%, respectively, for P. vivax and P. malariae and only human blood was detected in the blood-fed mosquitoes analyzed. This data reinforce the hypothesis that asymptomatic human carriers are the main source of anopheline infection in the peridomiciliary area, making the probability of zoonotic transmission less likely to happen.

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Bargieri, Daniel Y., Irene S. Soares, Fabio T. M. Costa, Catarina J. Braga, Luis C. S. Ferreira, and Mauricio M. Rodrigues. "Malaria Vaccine Development: Are Bacterial Flagellin Fusion Proteins the Bridge between Mouse and Humans?" Journal of Parasitology Research 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/965369.

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In the past 25 years, the development of an effective malaria vaccine has become one of the biggest riddles in the biomedical sciences. Experimental data using animal infection models demonstrated that it is possible to induce protective immunity against different stages of malaria parasites. Nonetheless, the vast body of knowledge has generated disappointments when submitted to clinical conditions and presently a single antigen formulation has progressed to the point where it may be translated into a human vaccine. In parallel, new means to increase the protective effects of antigens in general have been pursued and depicted, such as the use of bacterial flagellins as carriers/adjuvants. Flagellins activate pathways in the innate immune system of both mice and humans. The recent report of the first Phase I clinical trial of a vaccine containing aSalmonellaflagellin as carrier/adjuvant may fuel the use of these proteins in vaccine formulations. Herein, we review the studies on the use of recombinant flagellins as vaccine adjuvants with malarial antigens in the light of the current state of the art of malaria vaccine development. The available information indicates that bacterial flagellins should be seriously considered for malaria vaccine formulations to the development of effective human vaccines.

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Antinori, Spinello, Laura Galimberti, Laura Milazzo, and Mario Corbellino. "BIOLOGY OF HUMAN MALARIA PLASMODIA INCLUDING PLASMODIUM KNOWLESI." Mediterranean Journal of Hematology and Infectious Diseases 4, no. 1 (March 9, 2012): e2012013. http://dx.doi.org/10.4084/mjhid.2012.013.

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Malaria is a vector-borne infection caused by unicellular parasite of the genus Plasmodium. Plasmodia are obligate intracellular parasites that in humans after a clinically silent replication phase in the liver are able to infect and replicate within the erythrocytes. Four species (P.falciparum, P.malariae, P.ovale and P.vivax) are traditionally recognized as responsible of natural infection in human beings but the recent upsurge of P.knowlesi malaria in South-East Asia has led clinicians to consider it as the fifth human malaria parasite. Recent studies in wild-living apes in Africa have revealed that P.falciparum, the most deadly form of human malaria, is not only human-host restricted as previously believed and its phylogenetic lineage is much more complex with new species identified in gorilla, bonobo and chimpanzee. Although less impressive, new data on biology of P.malariae, P.ovale and P.vivax are also emerging and will be briefly discussed in this review.

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Havlik, I., G. Mabera, D. Richardt, P. Thuma, P. Mabera, G. Biemba, S. Zuba, et al. "Curdian sulfate in human malaria." Parasitology International 47 (August 1998): 75. http://dx.doi.org/10.1016/s1383-5769(98)80141-4.

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Nussenweig, R. "Human trials of malaria vaccine." Science 236, no. 4803 (May 15, 1987): 763. http://dx.doi.org/10.1126/science.3554508.

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Tran, Tuan M., Babru Samal, Ewen Kirkness, and Peter D. Crompton. "Systems immunology of human malaria." Trends in Parasitology 28, no. 6 (June 2012): 248–57. http://dx.doi.org/10.1016/j.pt.2012.03.006.

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ESPINAL, CARLOS A. "Trial of human malaria vaccine." Nature 336, no. 6200 (December 1988): 626. http://dx.doi.org/10.1038/336626a0.

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WASSERMAN, MOISES. "Trial of human malaria vaccine." Nature 336, no. 6200 (December 1988): 626. http://dx.doi.org/10.1038/336626b0.

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ELKIN PATARROYO, MANUEL. "Trial of human malaria vaccine." Nature 336, no. 6200 (December 1988): 626. http://dx.doi.org/10.1038/336626c0.

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LACOMBE, J. M., B. FERRARI, R. ANDRIAMANANPISOA, and A. A. PAVIA. "Malaria invasion of human erythrocytes." International Journal of Peptide and Protein Research 32, no. 2 (January 12, 2009): 104–16. http://dx.doi.org/10.1111/j.1399-3011.1988.tb00670.x.

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Kariuki, Silvia N., and Thomas N. Williams. "Human genetics and malaria resistance." Human Genetics 139, no. 6-7 (March 4, 2020): 801–11. http://dx.doi.org/10.1007/s00439-020-02142-6.

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Capasso, L. "The origin of human malaria." International Journal of Anthropology 13, no. 3-4 (July 1998): 165–75. http://dx.doi.org/10.1007/bf02452663.

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Hermentin, P. "Malaria invasion of human erythrocytes." Parasitology Today 3, no. 2 (February 1987): 52–55. http://dx.doi.org/10.1016/0169-4758(87)90214-6.

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Hayakawa, Toshiyuki, Nobuko Arisue, Toshifumi Udono, Hirohisa Hirai, Jetsumon Sattabongkot, Tomoko Toyama, Takafumi Tsuboi, Toshihiro Horii, and Kazuyuki Tanabe. "Identification of Plasmodium malariae, a Human Malaria Parasite, in Imported Chimpanzees." PLoS ONE 4, no. 10 (October 12, 2009): e7412. http://dx.doi.org/10.1371/journal.pone.0007412.

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Jang, Ihn Kyung, Abby Tyler, Chris Lyman, John C. Rek, Emmanuel Arinaitwe, Harriet Adrama, Maxwell Murphy, et al. "Multiplex Human Malaria Array: Quantifying Antigens for Malaria Rapid Diagnostics." American Journal of Tropical Medicine and Hygiene 102, no. 6 (June 3, 2020): 1366–69. http://dx.doi.org/10.4269/ajtmh.19-0763.

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Martens, Pim. "Malaria on the Move: Human Population Movement and Malaria Transmission." Emerging Infectious Diseases 6, no. 2 (April 2000): 103–9. http://dx.doi.org/10.3201/eid0602.000202.

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Journal articles on the topic 'Human malaria'

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